Index

S. No Disease condition
Cardiology
1. Hypertension
2. Ischemic heart disease
3. Unstable angina
4. Myocardial infarction
5. The diagnosis and treatment of non-ST elevation acute coronary syndrome
6. Consensus document for the diagnosis and treatment of ST elevation acute
coronary syndrome
7. Cardiac failure
8. Acute rheumatic fever and rheumatic heart disease
Pediatric cardiology
9 Cyanotic heart disease:
10 Acute rheumatic fever (RF) and rheumatic heart disease (RHD)
11 Non-surgical treatment of congenital heart disease
12
A. Transcatheter closure of congenital cardiac defects
13
1. Closure of atrial septal defect (ASD)
14
2. Transcatheter closure of Patent Ductus Arteriosus (PDA)
15
3. Transcatheter closure of ventricular septal defect (VSD)
16
4. Transcatheter closure of unwanted vessels or AV fistulas
17
B. Balloon dilatation of vessels and valves
18
1. Trans catheter dilatation of valves :
19
2. Vascular balloon dilatation
20 1. Dilatation of coarctation of aorta :
21 2. Dilatation of pulmonary artery stenosis:
22 3. Dilatation of pulmonary veins & systemic veins :
23 Atrial septostomy procedures
24
Other intervention procedures
25 Recent trends in management of heart failure
26 Management of common arrhythmias in children
27 Vasoactive agents in cardiogenic shock’
28 Recent trends in interventional cardiology
29 Timing of surgery for common congenital heart defects
Critical Care
30 Acute exacerbation of chronic obstructive pulmonary disease (COPD)
31 Acute severe asthma
32 Acute respiratory failure
33 Acute respiratory distress syndrome
34 Acute liver failure
35 Brain death test and ICU management
36 Evaluation of new fever in the critically ill patient
37 Hemodynamic monitoring in the ICU
38 Acute pulmonary embolism (PE)
39 Severe sepsis and septic shock
40 Severe community acquired pneumonia
41 Status epilepticus
42 Initial management of severe trauma
43 Traumatic brain injury
Nephrology and Hemodialysis
44 Acute nephritis
45 Nephrotic syndrome
46 Vascular access
47 Priming, connecting and disconnecting dialyser
48 Anticoagulation in haemodialysis
49 Dialysis dose/adequacy
50 Prevention of infections in hemodialysis unit
51 Emergency services
52 Laboratory backup
53 Nutrition

54 CVD monitoring & therapy

55 MBD monitoring & therapy
56 Hypertension & therapy
57 Diabetes monitoring & therapy
58 Renal replacement in intensive care setting

Endocrinology
59 Diabetes mellitus
60 Hirsutism
61 Hypothyroidism
62 Osteoporosis
63 Polycystic ovarian syndrome
64 Polycystic ovarian syndrome
65 Thyrotoxicosis
66 Obesity
ENT
67 Allergic rhinitis
68 Deviated nasal septum (DNS)
69 Epistaxis
70 Branchial cyst
71 Branchial fistula
72 Mouth ulcers
73 Acute parotitis
74 Submandibular sialadenitis
75 Thyroglossal duct cyst and fistula
76 Acute laryngotracheo bronchitis
77 Adenoiditis
78 Chronic laryngitis
79 Benign lesions of larynx
80 Deep neck space infection
81 Foreign body in aerodigestive tract
82 Goitre
83 Laryngopharyngeal reflux (lpr)
84 Carcinoma oral cavity
85 Carcinoma hypopharynx
86 Carcinoma larynx
87 Cervical lymphadenopathy
88 Peritonsillar abscess (quinsy)
Gastroenterology
89 Peptic ulcer disease
90 Approach to dysphagia
91 Achalasia cardia
92 Acute liver failure
93 Liver cancer or hepatocellular carcinoma (HCC)
94 Inflammatory bowel disease
95 Intestinal obstruction
96 Pancreatic carcinoma
General surgery
97 Blunt abdominal trauma
98 Cholecystectomy
99 Circumsion
100 Colectomy
101 Fistula in ano
102 Haemorrhoids
103 Hernia
104 Hydrocele
105 Parotid neoplasm
106 Peptic ulcer perforation
107 Skin and soft tissue lesions
108 Small bowel perforations
109 Varicose veins surgery
Pulmonology (respiratory diseases)
110 Acute respiratory distress syndrome
111 Bronchial asthma
112 Chronic obstructive pulmonary disease (copd)
113 Interstitial lung disease
114 Lung abscess
115 Lung cancer
116 Sleep disordered breathing
117 Pleural diseases
118 Community acquired pneumonia (bacterial)
119 Pulmonary hypertension
120 Sarcoidosis
121 Respiratory failure
Neurology
122 Guidelines for the management of epilepsy
Orthopedics
123 The infection of bones and joints
124 Osteoarticular tuberculosis
125 Name of condition: tuberculosis of spine
126 Degenerative cervical spodylolysis
127 Distal humerus fractures in adults
128 Upper limb fractures
129 Fracture of both bones forearm in adults
130 Fracture of shaft of the humerus
131 Radial head fracture
132 Hand injuries
133 Long limb trauma
134 Fracture neck of femur (intra-capsular
135 Trochanteric fractures (extra-capsular fracture neck femur)
136 Fracture shaft of femur
137 Fracture of tibia/fibula
138 Protocol for the management of pelvic fracture
139 Spinal injury
140 The neurological disorders: poliomyelitis and cerebral palsy.
141 Standard treatment guidelines for cerebral palsy
142 Radial head fracture
143 Ankylosing spondylitis
144 Bone tumours, tumourous conditions & developmental disorders mimicking bone
tumours
145 Gouty arthritis
146 Osteoarthritis
147 Osteomalacia
148 Osteoporosis
149 Rheumatoid arthritis
150 Rickets
151 Ankylosing spondylitis
Pediatrics & pediatric surgery
152 Protocol for dengue fever in children
153 Empyema thoracic
154 Inguinal hernia in children
155 Neonatal cholestasis
156 Urinary tract infection and vesico ureteric reflux
157 Neonatal jaundice-unconjugated hyperbilirubinemia
158 Neonatal intestinal obstruction
159 Protocol for neonatal seizures
160 Undescended testis in children

Urology
161 Haematuria
162 Urinary and male genital tract infections
163 Urolithiasis and ureteric colic
164 Benign hyperplasia of prostate (bph)
165 Renal cell carcinoma (rcc)
166 Bladder cancer
167 Prostate cancer
168 Testicular swelling – testicular torsion
General medicine
169 Pain
170 Headache
171 Abdominal pain
172 Chest pain
173 Other pains
174 Fever
175 Cough
176 Vomiting
177 Diarrhoea
178 Constipation
179 Chronic fatigue
180 Urinary problems
181 Pedal oedema (swollen feet)
182 Jaundice
183 Loss of consciousness
184 Weakness of one or more limbs
185 The unknown poisoning
186 Unknown bites
187 Typhoid fever
188 Malaria
189 Measles
190 Chicken-pox
191 Poliomyelitis
192 Diphtheria
193 Pertussis
194 Filariasis
195 Leptospirosis
196 Acute meningitis
197 Pneumonia
198 Tetanus
199 Tuberculosis
200 Leprosy
201 Acute hepatitis and fulminant hepatitis
202 Amoebic liver abscess
203 Anaemia
204 Sickle cell disease
205 Moderate / severe malnutrition
206 The management of dehydration

207 Primary surgical care

208 Dressings
Obstetrics and Gynecology
209 ANTE PARTUM HAEMORRHAGE
210 CARDIAC DISEASE IN PREGNANCY

211 BLEEDING IN FIRST TERM OF PREGNANCY

212 Ectopic Pregnancy

213 Molar pregnancy

214 Placenta praevia

215 ABRUPTIO PLACENTA

216 Uterine Rupture

217 POSTPARTUM HEMORRHAGE (PPH)

218 Hyperemesis gravidarum

219 ANEMIA IN PREGNANCY

220 Cervical incompetence

221 .Multiple gestation

222 Hypertension in pregnancy/Preeclampsia

223 Eclampsia

224 HIV in pregnancy

225 Hepatitis B during pregnancy

226 Hepatitis c virus during pregnancy

227 Urinary tract infections (UTI) in pregnancy

228 Pyelonephritis during pregnancy

229 Chorioamnionitis

230 DIABETES AND PREGNANCY

231 RHESUS ISOIMMUNIZATION

232 PRETERM LABOR AND PRETERM PREMATURE RUPTURE OF

MEMBRANES

233 LABOR DYSTOCIA

234 CORD PRESENTATION AND PROLAPSE

235 CESAREAN SECTION

236 INSTRUMENTAL VAGINAL DELIVERY

237 PERINEAL LACERATIONS

238 EPISIOTOMY

239 POST TERM PREGNANCY

240 INDUCTION OF LABOUR

241 NEONATAL RESUSCITATION

242 POST PARTUM COMPLICATIONS

243 Deep vein thrombosis and pulmonary embolus (DVT&PE)

244 Puerperal psychosis

GYNECOLOGY

245 INFERTILITY

246 PELVIC MASSES

247 DYSFUNCTIONAL UTERINE BLEEDING

248 Ammenhorea

249 CANCERS AND TUMORS

250 MENOPAUSE

251 PELVIC INFLAMMATORY DISEASES (PID)

252 VAGINAL DISCHARGE SYNDROMES

253 Mucopurulent cervicitis

254
Trichomonal vaginitis

255 Vulvo-vaginal candidiasis

Cardiology
1. HYPERTENSION
Hypertension is defined by a blood pressure consistently above 160/90 mm Hg in adult and 140/90 mm Hg
in pregnant woman.
Blood pressure (BP) must be measured several times with the subject lying down and at rest before we
confirm the diagnosis. Just one reading is not enough.
Diagnosis
Blood pressure above 160/90 on more than three occasions at least.
A diastolic between
Grade I (mild) hypertension, Between 90 to 99
Grade II (moderate hypertension). Between 100 and 109
Grade III hypertension. Above 110

For systolic the cut off is 180 for Grade II, above which it is Grade III.
Criteria to suspect secondary hypertension
1. Asymmetry of pulses,
2. Radiofemoral delay;
3. Pedal oedema or oliguria,
4. Mass per abdomen.
5. Orthostatic fall of BP (diastolic).
Many cases of hypertension present with head ache or giddiness or even angina and dyspnoea. Often patient
just feels easily tired and restless and ill without having fever or pain. Most cases are asymptomatic and
diagnosed incidentally. Even then it needs to be treated.
Untreated hypertensive patients are at increased risk of developing stroke, renal failure or myocardial
infarction. That is why it is advisable for everyone after the age of 45 to check the blood pressure of every
patient visiting the health centre for whatever reason -at least once a year. This is much more important if
the person is male, is overweight or is a smoker.
Similarly secondary hypertension may have no clinical indicators. Hence though most cases of hypertension
can be managed adequately at the primary health centre level, one consultation with a specialist is desirable
and should be made through the referral system.
Investigations:
1. Urine for albumin for acute renal dysfunction
2. Blood urea
3. Serum Creatinine for renal dysfunction
4. ECG and echocardiogram to assess impact on heart,
 5. For other causes of secondary hypertension it would need referral to tertiary care centre.
Treatment
Therapy must be regularly supervised and not abruptly interrupted; otherwise sideeffects can be serious.
Often the treatment is life long.
1. Patient Education
2. Low salt diet.
3. Weight reduction if obese.
4. Stop smoking if a smoker.
5. A regular isotonic exercise schedule especially if by nature of work one has to sit at one place all day
long.( like a 30 minute walk daily).
Drug Treatment-
One or two drugs that must be taken regularly. - As prescribed.
1. Atenolol (PO): one or two tablets once daily (25 to 100 mg, doses; never interrupt or abruptly stop
the treatment.
And / or
2. Hydrochlorothiazide (PO) : 25 to 50 mg/ d divided in 2 doses
3. Potassium supplementation (PO) or better advise eating potassium rich food (bananas for example)
If no improvement after two weeks add either:
4. Methyldopa (PO): start with one tablet 250 mg. thrice daily and increase progressively to reach 1500
mg per day or till BP is normalised. Or Amlodipine (PO) in single daily dose starting from 2.5 mg
going upto 10 mg per day. Or Enalapril (PO) in two divided doses, starting from 5 mg going upto 20
mg per day.
If atenolol is contraindicated one can start with amlodipine or enalapril.
If still uncontrolled refer to a specialist
Hypertensive crisis:
Abrupt, marked increase in blood pressure, usually over 200/130 which may lead to rapid damage to
kidneys, heart and the eye or lead to encephalopathy and coma. This needs urgent lowering of blood
pressure.
Tab. Nifedipine 5 mg to be chewed and swallowed or if in soft capsule to be squeezed under the tongue.
Repeat after half hour till blood pressure gets controlled. Meanwhile start on oral antihypertensive
medication as indicated earlier.
one can choose to add Inj hydralazine 10 mg IV every 10 to 15 minutes upto a maximum of 50 mg or
Injection sodium nitroprusside 0.25 to 10 micrograms/kg/min. as an IV infusion- diluting in 5% dextrose.
All such cases need to be evaluated for secondary hypertension later.
 2. ISCHEMIC HEART DISEASE
Compromise of heart function secondary to coronary insufficiency. This may take the form of recurrent
chest pain due to myocardial ischemia as in angina or may cause necrosis of myocardium as in myocardial
infarction.
a. STABLE ANGINA
Diagnosis :
1. Diagnosis is based on clinical pattern.
2. Chest pain – Retrosternal, dull aching, constricting or burning, radiating to neck, jaw, shoulders
or arms; usually precipitated by exertion or stress and relieved by rest or nitrates.
3. Other symptoms may include Dyspnoea, mild sweating, nausea or palpitations
On examination : Blood pressure may be high
Investigations and confirmation
1. ECG taken at that time may show ST elevation or depression or T inversion. In between anginal
episodes the ECG may be normal.
2. A treadmill stress test would confirm angina in over 95% of these cases. Echocardiography to
measure left ventricular function and rule out segmental dyskinesia suggestive of earlier myocardial
infarction would be useful.
Treatment General Guidelines
1. Daily exercise
2. Stop smoking
3. Dietary modification – low cholesterol, low fat diet with high roughage
4. Control of hypertension and Diabetes Mellitus.
Drug Treatment
1. Aspirin to be given for all the patients- half standard tablet once daily after meals. 75 – 300 mg PO
once daily
2. Nitrates : Isosorbide dinitrate 10 mg thrice a day.
3. When pain occurs one tablet can be kept sublingually.
4. If there is headache lower dose of 5 mg twice or thrice daily can be tried.
5. Betablockers : First line of therapy along with aspirin
Atenolol 25 – 100 mg / day (PO)
Metoprolol 50 – 450 mg / (PO)
If despite maximal medical treatment, angina is frequent enough to interfere with quality of life and
ischemia is confirmed by ECG with or without stress test then refer to higher centre for consideration of
coronary angiogram and revascularisation therapy.
 3. UNSTABLE ANGINA
Diagnosis
1. Based on Clinical Features
2. Angina of new onset
3. Angina at rest or with minimal exertion or
4. A crescendo pattern of angina with episodes of increasing frequency, severity and duration
Investigation and Confirmation
To differentiate from acute myocardial infarction.
ECG – Transient ST elevation or ST depression; T wave inversion during pain Positive treadmill stress test.
Treatment
If ECG facility is available Hospitalisation is advisable
Rest
Secure IV access
Sedation Diazepam 10 mg, If pain is severe morphine 2 - 4 mg IV
Aspirin - 160 – 325 mg PO once a day
Heparin - Unfractionated 5000 units IV followed with 1000 to 2000 units hourly – continued for 48 hours
Bolus 60 – 80 units / kg given as infusion 14 units / kg / hour with clotting time monitoring.)
Nitrates - isosorbide dinitrate 5 mg sublingually immediately and 10 mg thrice a day.
For uncontrolled pain one can give Injection nitroglycerine 5-100 micrograms/ min. IV diluted in 5%
dextrose titrated for 24 to 48 hours
Add morphine also if myocardial infarction is suspected.
ACE inhibitors – Enalapril 2.5 – 20 mg / day in divided doses twice a day.
Stool softeners – dulcolax 10 mg at night
 4. MYOCARDIAL INFARCTION
Diagnosis
1. Diagnosis is based on clinical presentation and ECG with enzyme studies contributing in case of
doubt.
2. Clinical Presentation
3. Retro-sternal crushing Chest pain radiating to neck, arms, lasting for more than ½ hours during rest.
4. Associated with
5. Nausea and vomiting
6. Increased sweating
7. Dyspnoea
8. Symptoms not reduced by rest or nitrates
9. Note that the pain can often present in atypical patterns including like heartburn or as epigastric
discomfort.
In addition there may be
10. Elevated JVP
11. Hypo / hypertension z Bilateral lung crepitation suggestive of pulmonary oedema
12. Presence of murmurs on auscultation
Investigations
ECG : diagnosis rests on ECG pattern - Convex ST – segment elevation with either peaked upright. or
Inverted T waves. Q waves in prolonged ischemia
Cardiac enzymes elevated: CK MB;
Echocardiogram : regional wall motion abnormality seen.
Treatment
1. Bed rest.
2. Sedation & pain relief : Morphine : 10 mg by slow intravenous infection (2 mg/mt) followed by a
further 5-10 mg if necessary.
3. Oxygen therapy : 2 – 4 l /min. via a nasal cannula.
4. Aspirin : 150 – 300 mg PO once a day.
5. Beta blockers : Atenolol 25 to 100 mg once daily. if pulse rate > 60/mm , BP > 90/60 mm Hg , and
lung fields are clear.
6. Reperfusion therapy :
If presenting within 12 hours of chest pain with ECG showing ST elevation > 1 mm then give
Inj. Streptokinase 1.5 million units over 1 hour
Contra indications (of Contra indications pre-perfusion therapy) include :
Active bleeding from any site.
Stroke/TIA < 1 year.
Pregnancy.
Active peptic ulcer disease etc.
Heparin : after 6 hours of completing the reperfusion therapy
Dose : same as that for unstable angina.
Nitroglycerin Infusion (as stated for unstable angina) :
If chest pain persists, to be followed by : Isosorbide dinitrate 10 mg thrice a day.

Complications:
1. Require referral to ICU setting
2. Arrhythmia
3. Ventricular ectopics
4. Supraventricular arrythmias
5. Conduction blocks
6. Ventricular tachycardia and fibrillation
7. Left ventricular dysfunction and Cardiogenic shock
 5. THE DIAGNOSIS AND TREATMENT OF NON-ST ELEVATION ACUTE CORONARY
SYNDROME
DIAGNOSIS OF NSTE ACS :

All patients presenting to a health care provider with symptoms suggestive of ACS should be considered as
high priority. For the purpose of this document, an arbitrary division is made to categorize the health care
facilities available in India for care of ACS patients (table 1). In big cities centers with varying degree of
sophistication are usually available. On the other hand, in parts of India (especially rural) even the basic
facilities are not available. Every health care centre should have a functioning ECG machine available 24
hours a day. Health workers at these centers should be trained to interpret the ECG so that treatment can be
initiated without delay. Telemedicine (fax, e-mail, and internet) is advancing in our country and a
networking between the centers can be of great value.

Definition of terms:
The term, NSTE-ACS includes UA and NSTEMI. These two conditions are closely related whose
pathogenesis and clinical manifestations are similar but of differing severity. The clinical presentation
depends on the severity of stenosis and the degree of thrombosis. In patients where ischemia is severe, there
can be myocardial damage with the release in troponin I (TnI), troponin T (TnT), or CK-MB and the
condition is referred to as NSTEMI. If there is no evidence of enzyme elevation, the condition is labeled as
UA. It is important to remember that the appearance of biomarkers may be delayed by up to several hours
after the onset of ischemic symptoms. The distinction between the terms UA or NSTEMI is retrospective. It
is also common to describe patients as Trop T- ve NSTE ACS (UA) or Trop T +ve NSTE ACS (NSTEMI).

Clinical presentation of NSTE ACS:

The clinical presentation of NSTE ACS encompasses a wide variety of symptoms. An accurate history
recording is very important. The important points in the history include nature of anginal symptoms, prior
history of IHD, sex (male), older age and an increasing number of traditional risk factors. The following
clinical presentations are usually included in NSTE ACS(3).
1. Prolonged (> 20 min) anginal pain at rest.
2. New onset (de novo) severe angina (class III of the classification of Canadian Cardiovascular
Society (CCS)(6).
3. Recent destabilization of previously stable angina with atleast CCS III angina characteristics
(crescendo angina) or
4. Post MI angina.
The typical clinical presentation of NSTE ACS is retrosternal pressure or heaviness (“angina”) radiating to
the left arm, neck or jaw which may be intermittent (usually lasting several minutes) or persistent. These
complaints may be accompanied by other symptoms such as diaphoresis, nausea, abdominal pain, dyspnea,
and syncope. There are several atypical symptoms and these include epigastric pain, recent onset
indigestion, stabbing chest pain, chest pain with pleuritic symptoms, or increasing dyspnea. Atypical
complaints are often observed in younger and older patients, in women, and in patients with diabetes.

Clinical assessment of NSTE ACS:

Physical examination: The clinical examination is frequently normal. The presence of tachycardia, heart
failure or haemodynamic instability must prompt the physician to expedite the diagnosis and treatment of
patients. It is important to identify clinical circumstances that may precipitate or exacerbate NSTE- ACS,
such as anaemia, infection, fever and metabolic or thyroid disorders. An important goal of physical
examination is to exclude non cardiac causes of chest pain and non-ischemic cardiac disorders (e.g.
pulmonary embolism, aortic dissection, pericarditis, valvular heart disease) or extra cardiac causes.
Electrocardiogram (ECG): The resting 12 lead ECG is the first diagnostic tool. It should be recorded as soon
as possible and immediately interpreted by a qualified physician. The finding of persistent ST elevation
suggests STEMI which requires a different treatment. ECG recordings should be repeated at least at 6 and
24 h, and in the case of recurrence of chest pain/symptoms. ECG should be compared with any previously
available recordings.
In NSTE ACS, ECG may show ST segment deviation, T wave changes or may remain normal. It should be
emphasized that a completely normal ECG does not exclude the possibility of NSTE ACS. In several
studies, around 5% patients with normal ECG who were discharged from the emergency department were
ultimately found to have acute MI or UA(7). ST segment shifts and T wave changes are the ECG indicators
of unstable CAD. The number of leads showing ST depression and the magnitude of ST depression are
indicative of the extent and severity of ischemia and correlate with the prognosis(8). ST depression of > 2
mm carries a increased mortality risk. Inverted T waves, especially if marked (greater than or equal to 2mm
(0.2 MV) also indicate UA/ NSEMI). Q waves suggesting prior MI indicate a high livelihood of IHD. The
utility of ECG becomes less if ECG is abnormal due to pre-existing intraventricular conduction defect or left
ventricular hypertrophy (LVH).Ischemia in the left circumflex coronary artery territory is frequently missed
in the common 12 lead ECG. It may be detected in lead V4-R, V3- R as well as in leads V7 – V9. These
leads should be recorded if clinically indicated.
Biochemical markers : Several biomarkers have been investigated in recent years to be used for diagnosis
and risk stratification. Cardiac troponin (CTn) is the biomarker of choice because it is the most sensitive and
specific marker of myocardial injury/ necrosis available. Unfortunately, there is a lack of understanding of
many of the analytical and clinical issues that govern the use of this important biomarker. The diagnostic cut
off for MI using cardiac troponins should be based on the 99th percentile of levels among healthy controls
as recommended by the consensus committee(9). All laboratories need to validate their values. The
diagnosis of NSTE- ACS should never be made only on the basis of cardiac biomarkers, the elevation
should always be interpreted in the context of clinical presentation. Troponin levels usually increase after 3-
4 hours. If the first blood sample for CTn is not elevated, a second sample should be obtained after 6-9 h,
and sometimes a third sample after 12-24 hours is required. Troponin level may remain elevated upto 2
weeks. Troponin elevation can occur in cardiac and non cardiac conditions including chronic renal failure.
In NSTE ACS, elevated CTn values signal a higher acute risk and an adverse long term prognosis. The
elevated troponin level is also useful for selecting appropriate treatment. Creatine Kinase MB is less
sensitive and specific for the diagnosis of NSTE ACS. However, it remains useful for the diagnosis of early
infarct extension (reinfarction) and peri-procedural MI because of its short half-life.
Many other biochemical markers like CRP, NT- Pro BNP, myoglobin are commercially available. At the
present time, there use is not recommended for the diagnosis.
Echocardiography: Echocardiography and Doppler examination should be done to assess the global left
ventricular function, any regional wall motion abnormality. Echocardiography also helps in excluding other
causes of chest pain.

Risk Stratification at presentation:

Many patients with NSTE- ACS require observation/hospitalization in an environment with continuous
electrocardiographic monitoring and defibrillation capability. The risk stratification at presentation is useful,
however, it is important to understand that patients who are stable initially, may become high risk
subsequently or vice versa. NSTE ACS includes a heterogeneous group of patients with a highly variable
prognosis. The risk stratification is necessary for prognosis assessment and treatment. A simple TIMI risk
score(10) which takes into consideration clinical variable can be used (Table 2). The TIMI risk score is
available at www.timi.org. A low TIMI score <3 usually indicates a low risk and a TIMI score > 3 indicates
intermediate or high risk. In general, patients having multiple coronary risk factors, advanced age, rest
angina, clinical left ventricular (LV) dysfunction, prior history of percutaneous coronary intervention (PCI)
or coronary artery bypass graft surgery (CABGS) indicate a high risk. Elevation of troponin or CK-MB
indicates myocyte necrosis and a high risk. It is important to note that the TIMI risk score is just a guide and
may not be reliable in young patients. There are other risk models based on PURSUIT trial (11) and
GRACE registry(12).
Data from western countries suggest that patients with acute chest pain might be better served by transport
to an adequately equipped facility (category A) than by sending them to a less equipped facility (category B,
C or D). It is well documented that early invasive therapy (early coronary angiography followed by
appropriate revascularization) is preferable in high risk patients. These patients should preferably be
admitted to category A hospitals or promptly transferred to such a facility. If a high risk patient is initially
admitted in Category B, C or D hospital, a decision for transportation should be taken. The decision is to be
individualized depending on the clinical, social and economic considerations.

Differential diagnosis:
A number of patients evaluated for suspected NSTE ACS are found not to have acute ischemia. This
includes patients with non cardiac pain (e.g. pulmonary embolism, musculoskeletal or esophageal
discomfort) or cardiac pain not caused by myocardial ischemia (e.g. pericarditis). These patients should be
evaluated as dictated by the individual presentation.

MANAGEMENT OF NSTE-ACS:
Patients who are awaiting hospitalization are advised to chew non enteric coated aspirin (162 to 325 mg).
They may receive sublingual nitrate or GTN spray for pain relief.
Patients with definite or probable NSTE-ACS who are stable should be admitted to an impatient unit for bed
rest with continuous rhythm monitoring and careful observation for recurrent ischemia. High risk patients,
including those with continuing discomfort and/ or haemodynamic instability, should be hospitalized in a
coronary care unit (CCU) and observed for at least 24-48 hours without any major complications.
What not to do ?
A. Fibrinolytic (thrombolytic) therapy using streptokinase, urokinase, tenecteplase or any other agent should
not be used in patients with UA and NSTEMI. These agents can prove harmful.
B. Glycoprotein IIb/IIIa agents like abciximab, tirofiban and eptifibatide are mostly useful in patients
undergoing percutaneous coronary interventions (PCI). The routine “upstream” use of the agents is not
recommended.
Anti- ischemic and analgesic therapy:
All patients must receive medication for relief of pain. Oxygen is useful for initial stabilization particularly
in those with hypoxemia.
Topical, oral or intravenous nitrates are recommended for pain relief. Intravenous nitroglycerin (NTG) is
particularly helpful in those who are unresponsive to sublingual NTG, in hypertension and in those with
heart failure. Nitrates should be used with caution if systolic blood pressure is below 100 mm of Hg.
Morphine sulfate (1 to 5 mg intravenously), if available, is a good option for pain relief in patients whose
symptoms are not relieved despite NTG or other anti ischemic therapy. The non steroidal anti inflammatory
drugs (NSAIDs) and COX-2 inhibitors should not be administered for pain relief due to increased risk of
cardiovascular events (13).
Oral beta blockers are useful for pain relief. The use of intravenous beta blockers should be avoided
particularly in haemodynamically unstable patients. Calcium channel blockers are of utility in vasospastic
angina and in patients with contraindications to beta blockade. Other antianginal drugs like ivabradine,
trimetazidine, ranolazine and nicorandil have limited role to play.
Antiplatelet agents:
Platelet activation plays a key role in NSTE- ACS and antiplatelet therapy should be administered once the
diagnosis is entertained. Aspirin (cyclo oxygenese inhibitor) should be administered to all patients unless
contraindicated.
Initial dose of chewed non-enteric aspirin from 162 to 325 mg is recommended. The subsequent dose of
aspirin can be 75 to 150mg daily on a long term basis. GI bleeding appears to increase with higher doses.
Clopidogrel is recommended in all patients with an immediate dose of 300 mg followed by 75 mg daily. In
patients considered for a PCI, a loading dose of 600 mg is advised to achieve more rapid inhibition of
platelet function. Clopidogrel should be maintained for 12 months unless there is an excessive risk of
bleeding.
A new antiplatelet agent, belonging to thienopyridine group of ADP receptor inhibitors has recently been
investigated in TRITON TIMI- 38 trial(14). Prasugrel reduces the platelet aggregation by irreversibly
binding to P2Y12 receptors on the platelets. Prasugrel is a prodrug and has rapid onset of action (1 hour). It
is converted to active and inactive metabolites. The active metabolite has half life of about 7 hours. In
patients undergoing PCI for ACS, the agent showed lower incidence of ischaemic events when compared to
clopidogrel. It was particularly effective in diabetics (4.2% absolute risk reduction for ACS). Bleeding
incidence was similar (2.2% vs 2.3%). The agent is correctly recommended for the following patients (1)
Patient presenting with STEMI (2) NSTEMI patient with diabetes mellitus or young male patients
undergoing PCI (3) Patient with history of stent thrombosis (4) non responders to clopidogrel. This agent is
contraindicated in patients with >75 years of age or in patient having history of TIA or any stroke. The
loading dose is 60 mg orally. The maintenance dose is 10 mg daily. In patient weighing <60 kg, the
maintenance dose has to be reduced to 5 mg daily.
Another new drug, ticagrelor has been found to be superior as compared to clopidogrel in ACS(15).
Ticagrelor is an oral, reversible, non thinopyridine P2Y12 antagonist. This is not a prodrug. This has a more
rapid onset of action (30 min) and rapid off sent of action (4-72 hours). In ACS, Ticagrelor was associated
with mortality reduction compared to clopidogrel (9.8% vs 11.7%, P=<0.001). However nonfatal bleeding
was higher (16.1% vs 14.6%, P=0.0084). The loading dose is 180 mg. Maintenance dose is 90 mg twice
daily thereafter.
All patients presenting with ACS/NSTEMI should receive aspiring plus any one of these three
(Clopidogrel/Prasugrel/Ticagrelor) agents.
The use of GP IIb / IIIa inhibitors has undergone a major change in the current era of high dose clopidogrel
and newer anticoagulants. These agents are used either upstream beginning prior to angiography or
administered after angiography during the PCI. The upstream use of GP IIb/IIIa inhibitors have
considerably reduced. Eptifibatide have not shown efficacy in reducing ischemic events in high risk NSTE-
ACS patients when used upstream and maintained during the PCI procedure. In routine practice, these days
patients are often taken to catheterization laboratory without prior use of GP IIb / IIIa agent(16). Any of the
three agents is used depending on the clinical and angiographic characteristics.

Anticoagulants:
Anticoagulation is recommended for all patients in addition to antiplatelet agents(3,4). An increasing
number of anticoagulants (previously referred to as antithrombins) are available and include unfractionated
heparin (UFH), low molecular weight heparin (LMWH), fondaparinux and bivalirudin.The choice of
anticoagulation depends on the risk of ischemic and bleeding events and choice of the initial management
strategy (e.g. urgent invasive, early invasive or conservative).
Enoxaparin (1mg/kg bw twice daily) is a preferred anticoagulant and is a good option in patients treated
conservatively or by invasive strategy. Enoxaparin can be stopped within 24 h after an invasive strategy
where as it should be administered up to hospital discharge (usually 3 to 5 days) in conservative strategy.
Fondaparinux is recommended on the basis of most favourable efficacy/ safety profile and the
recommended dose is 2.5 mg daily(17). This agent causes least bleeding complications. An additional UFH
in standard dose of 50-100 U/kg bolus is necessary during PCI due to slightly high incidence of catheter
thrombosis.
Bivalirudin is currently recommended as an alternative anticoagulant for urgent and elective PCI in
moderate or high risk NSTE ACS(18). Bivalirudin reduces the risk of bleeding as compared with
UFH/LMWH plus GP IIb/IIIa inhibitor.

Statins & other drugs:

Statins are recommended for all NSTE ACS patients, irrespective of cholesterol levels. Statin should be
initiated early after admission, with the aim of achieving LDLC levels <70 mg/dL. Atorvastatin is usually
the preferred agent. High dose (40-80 mg) is used for the initial period (1-2 months). Subsequent dosing is
bsed on the target LDL (<70 mg/dL) level.
ACE inhibitors are indicated in patients with reduced LV systolic function in diabetes and all other patient
of proven CAD. ARB are indicated in those patients who are intolerant to ACE inhibition.

CORONARY REVASCULARIZATION :
Revascularization for NSTE ACS is performed to relieve angina, ongoing myocardial ischemia and to
prevent progression to MI or death. The indications for revascularization and the preferred approach, PCI or
CABGS depend on the extent and severity of the lesions, the patient’s condition and co-morbidity(19).

Coronary angiography :
An invasive strategy always starts with angiography. The indications for urgent and routine early
angiography are shown in table 3 and 4.
Those patients who have no recurrence of chest pain, normal serial ECGs, no elevation of troponins and no
heart failure are considered as low risk. In these patients, a stress test is advised prior to discharge. Coronary
angiography is contemplated, if the stress test is positive.

Conservative and Invasive strategy :

There is a controversy which remains as to the optimal timing between hospital admissions, initiation of
medical therapy and invasive evaluation. There are large numbers of randomized controlled trials (RCT)
which have addressed this issue. The term invasive strategy refers to coronary angiography and subsequent
revascularization within 2 to 24 hours of hospitalization. Conservative strategy (selective invasive) refers to
initial medical stabilization followed by angiography and appropriate revascularization, usually within 72
hours or prior to hospital discharge. RCTS have shown that an early invasive strategy reduces ischemic end
points mainly by reducing severe recurrent ischemia and the need for re-hospitalization and
revascularization(20). This strategy reduces cardiovascular death and MI at up to 5 years of follow-up(21).
From the available data, following conclusions can be drawn. 1. High risk/unstable patients benefit most
from the early revascularization therapy & these patients should be promptly treated in advanced centers.
2. A systematic approach of immediate angiography is not necessary in patients who are stabilized with a
contemporary pharmacological approach. Likewise, immediate transfer of stabilized patients admitted in
hospitals without onsite cardiac catheterization facilities is not mandatory, but should be organized within
72 h. Figure 1 provides a flow chart for management of NSTE-ACS patients.

Percutaneous Coronary Intervention (PCI) and Coronary Artery Bypass Grafting (CABG) :
The mode of revascularization is usually based on the severity and distribution of the CAD. The PCI is
usually performed for the culprit lesion using drug eluting stents. Significant lesions in multiple vessels can
be treated either in same sitting or in staged fashion as considered appropriate. CABG is usually advised for
complex CAD not amenable to PCI, left main with triple vessel disease, total occlusions and diffuse disease.
It is important to consider the bleeding risk as these patients are on aggressive antiplatelet therapy. The
benefits of CABG are greatest after several days of stabilization with medical treatment and stopping the
antiplatelet agents.

LONG TERM MANAGEMENT:

Patients with NSTE ACS after the initial phase carry a high risk of recurrence of ischemic events.
Therefore, active secondary prevention is an essential element of long term management. Life style
alterations is very important. This is termed as therapeutic life style changes (TLC). Smoking cessation,
weight reduction, blood pressure control, management of diabetes, lipid intervention, antiplatelet agents,
beta blockers, ACE inhibitors (or ARB) remain extremely important interventions. Isotonic exercise like
brisk walk, swimming, cycling, jogging for 30-45 minutes daily or at least 150 minutes weekly should be
advised to all these patients. The exercise prescription (type, duration and intensity) should be
individualized based on the clinical status of the patient. Lastly psychological factors like anxiety and
depression are to be identified and treated(22). 24

Annexures:

Table 3: Indications for urgent coronary angiography and invasive strategy.

1. Refractory angina (e.g. evolving MI).

2.
deep negative T waves.
3. Clinical symptoms of heart failure or haemodynamic instability (‘Shock’).
4. Life threatening arrhythmias (ventricular fibrillation or ventricular tachycardia).

Table 4 : Indications for early coronary angiography :

1. Elevated troponin levels.

2. Dynamic ST or T wave changes.
3. Diabetes mellitus, reduced renal function.
4. Depressed LVEF < 40%.
5. Early post MI angina.
6. PCI within 6 months.
7. Previous CABG.
8. Intermediate to high risk according to risk score.
6. CONSENSUS DOCUMENT FOR THE DIAGNOSIS AND TREATMENT OF ST ELEVATION
ACUTE CORONARY SYNDROME

AIM AND SCOPE OF THESE RECOMMENDATIONS

Recent documents have described the evidence-based diagnosis and management of acute ST segment
elevation myocardial infarction (STEMI)1-4. While these are erudite and exhaustive, they are tailored to the
situation in developed countries. Because of the substantially different ground reality in India, there is a
need for modifications in the interpretation of the evidence and application of treatments to the Indian
context.
This statement attempts to provide guidance to Indian physicians and healthcare providers at the
grass-root level in making decisions for the optimal management of patients with STEMI.

DIAGNOSIS OF STEMI
Early diagnosis is the key to early treatment of STEMI. A history of chest pain or discomfort lasting 10-20
minutes should raise the suspicion of acute STEMI in susceptible individuals (middle-aged male patients,
particularly if they have risk factors for coronary disease). It must be recognized that pain may be atypical in
character or location. A 12-lead ECG must be performed as soon as possible. ECG should be interpreted
within ten (10) minutes of arrival in health care centre. If the initial ECG is not suggestive of STEMI but the
patient continues to have symptoms, repeat ECGs must be obtained (every 15 minutes, not after 12 hours or
next day) and compared to the first ECG. While markers of myocardial necrosis are useful in corroborating
the diagnosis, it must be emphasized that they may not be elevated early after the onset of symptoms. In
doubtful cases, echocardiography may be a useful adjunct in making the diagnosis, particularly among
young patients without prior history of coronary disease.

Equipment, personnel and training

Every primary health center should have a functioning ECG machine available 24 hours a day.
Health workers at these centers should be trained to recognize the cardinal features of STEMI so that
treatment can be initiated without delay. It may not be necessary for all health centers to have access to
facilities for cardiac biomarker testing. Use of qualitative test-strips in these centers may be expensive and
may lead to diagnostic confusion, and their use should be discouraged.
MANAGEMENT OF STEMI
Risk stratification
The initial assessment should include the rapid identification of patients who may be at high risk of
cardiogenic shock or death. The following characteristics have been most consistently associated with
adverse outcomes in patients with STEMI5-7:
i. Older age (age ≥75 years)
ii. Higher Killip class (class III or IV)
iii. Lower systolic blood pressure (<100 mm Hg)
iv. Higher heart rate (>100/min)
v. Anterior MI
The greater the number of risk factors, the higher is the risk. Therefore, after instituting initial treatment
(which may include fibrinolytic therapy), such patients are best transferred to hospitals with coronary care
units and catheterization laboratory facilities.
Initial treatment
The first treatment that should be given is 325 mg of (preferably) non enteric-coated aspirin to be chewed8.
All patients should receive aspirin. Clopidogrel should be administered at a loading dose of 300 to 600 mg
to all patients9-10. Patients undergoing primary PCI should receive a 600 mg loading dose11.
All patients should receive medications to relieve pain. These may include opioid analgesics (morphine
sulfate intravenously) where available. Sublingual or intravenous nitrates should be administered if systolic
blood pressure is ≥120 mm Hg. If systolic BP is ≥ 100 mm Hg but less than 120 mm Hg, nitrates must be
administered cautiously. Non steroidal anti-inflammatory drugs (NSAIDs, other than aspirin) should not be
given for analgesia
Choice of reperfusion therapy
Fibrinolytic therapy vs. primary PCI
Reperfusion therapy is the cornerstone of STEMI management and should be instituted in all patients
presenting within 12 hours of onset of symptoms8-13. The most efficacious reperfusion therapy available is
timely primary PCI, but it may not be the most effective in the Indian context, given the relative paucity of
PCI-capable centers14. Moreover, since most of these centers are located in urban areas, the distances
involved in transporting patients from rural areas become prohibitive. Fibrinolytic therapy therefore remains
the most practicable reperfusion strategy for India. The most recent data from India suggests that only about
8% of patients with STEMI receive primary PCI15. Nearly 60% of patients receive fibrinolysis with
streptokinase as initial treatment. It should be emphasized that even among urban/semi-urban dwellers (only
17% of patients enrolled in the CREATE registry 15 were from rural areas), a third of patients did not
receive any form of reperfusion therapy.
Patients presenting to PCI-capable centers should of course be treated with timely primary PCI if the door-
to-balloon time is anticipated to be less than 90 minutes from the time of arrival at the hospital4. It should
be recognized that door-to-balloon times may be greater than 2 hours even in PCI-capable centers during
off-duty hours, weekends and holidays, and immediate fibrinolysis may be the better option when delays are
anticipated. Such hospitals should implement processes to minimize and monitor door-to-balloon times.
Choice of fibrinolytic agent
Traditionally, streptokinase has been the most commonly used fibrinolytic agent in India. However,
streptokinase is not fibrin-specific, requires to be given as an infusion over one hour and may be associated
with hypersensitivity reactions. Recently, there is some favorable evidence for the use of tenecteplase in
Indian settings16-17. Tenecteplase has theadvantage of being fibrin-specific, can be given as a bolus dose,
and has a lower incidence of hypersensitivity reactions. TIMI 3 flow in the infarct related coronary artery
may also occur more frequently with tenecteplase when compared to streptokinase. Tenecteplase should be
administered at a dose of 0.5 mg/kg body weight18.
Personnel and training
Given that nearly a third of patients in urban India do not receive any reperfusion therapy, it may be
worthwhile for the government to consider making tenecteplase available at primary health centers as a
policy decision. This would also entail adequate training of medical and paramedical personnel at these
centers so that they can administer tenecteplase without delay. Studies conducted around the world have
found that administration of bolus-dose fibrinolytic agents by paramedical personnel is safe. The
government should commission studies to confirm the safety of such a practice in the Indian context before
its widespread implementation.
The case for pre-hospital fibrinolysis
Due to lack of awareness, lack of ambulance services and the distances involved, most patients with STEMI
living in urban/semi-urban India reach hospital after a delay of 5 hours15. This delay can be shortened by
institution of systems to initiate pre-hospital evaluation and fibrinolysis. Pre-hospital fibrinolytic therapy has
clearly shown to improve outcomes and has compared favorably with primary PCI19.
Transport of patients to centers with CCUs and/or PCI capability
Recent studies in Europe and North America have suggested that transport of patients to PCI-capable
centers may be a better strategy than immediate fibrinolytic therapy. Such a strategy may however not be
suitable for most parts of India because of the distances involved and the insurmountable logistics of
transport. Nevertheless, it may be possible for small geographic units (urban or rural) to develop systems for
the provision of efficient services for transporting patients to designated PCI-capable centers.
After administration of fibrinolytic therapy several situations may necessitate transfer of patients to centers
with CCUs and/or PCI capabilities. These are listed in table 2 below.

Adjunctive therapies
Antiplatelet treatment
Aspirin and clopidogrel should be administered as discussed in section 3.2. Glycoprotein IIb/IIIa antagonists
may be used in patients undergoing primary PCI although their role in patients pre-loaded with clopidogrel
is unclear. These agents may be administered in the catheterization laboratory, at the time of the procedure.
There is no role of administering these agents within the context of a strategy to bridge the time delay before
primary PCI (facilitated PCI)25. Abciximab, eptifibatide and tirofiban appear to be similarly effective and
may be used depending upon local preferences and availability3.
Antithrombotic therapy
Patients receiving fibrinolytic therapy
Following treatment with both fibrin-specific and non fibrin-specific fibrinolytic agents, there is strong
evidence for the use of antithrombotic agents for reducing reinfarction or recurrent ischemia13,24. Recent
studies suggest that low molecular weight heparins (LMWH) may be better than unfractionated heparin
(UFH) for this purpose24-26. The LMWHs enoxaparin or reviparin may be administered for up to 8 days
post-MI. Fondaparinux has recently been shown to reduce the occurrence of death or reinfarction while
concomitantly reducing the risk of major bleeding, and may therefore be considered among patients
undergoing treatment with streptokinase27. There is no role for bivalirudin among patients receiving
fibrinolytic therapy.
Patients undergoing primary PCI should receive periprocedural UFH or bivalirudin. Fondaparinux (without
added UFH) may increase the risk of catheter thrombosis.
Patients not receiving any reperfusion therapy Fondaparinux may be the preferred agent among patients who
have not received any reperfusion therapy29.
Beta adrenergic antagonists
Oral beta-blockers should be administered in the first 24 hours to patients who do not have heart failure, a
low output state, are not at increased risk of developing cardiogenic shock (see footnote in table 2), or do
not have other contraindications to beta-blocker therapy21. Intravenous beta-blockers may be administered
in the first 24 hours in the presence of hypertension or tachyarrhythmia, in the absence of the above
contraindications2.
ACE inhibitors and ARBs
ACE inhibitors improve survival in patients who have reduced left ventricular ejection fraction (LVEF ≤
40%) and those who are in heart failure following STEMI4. Benefits are proportionately lower among low
risk patients. ACE inhibitors should be started in the first 24 hours after STEMI in the absence of
contraindications. ARBs may be used in patients who do not tolerate ACE inhibitors30-31.
Other agents
Routine use of intravenous or oral nitrates does not improve outcomes in patients with STEMI. Nitrates may
be used for pain relief. There is no role for the routine use of calcium antagonists, intravenous magnesium,
antiarrhythmic agents or glucose-insulin-potassium infusions, and may be associated with adverse outcomes
in some cases4. High dose statins should be initiated as early as possible during hospital stay as part of
secondary prevention measures. The dose of statin to be used in Indian patients is not clear, but lowering
LDL levels to ≤70mg/dL may be a useful target.
Management post-fibrinolytic therapy
Several studies have suggested that routine angiography and PCI of the infarct related artery may reduce the
rates of re-occlusion or re-infarction 32-35. However, none of these studies have shown a reduction in
mortality with this strategy. Because of the resource intensiveness of this strategy and the absence of an
effect on survival, this panel favors a more conservative approach consisting of revascularization guided by
the results of risk stratification by early exercise stress testing. Angiography (and revascularization) should
of course be performed in the event of spontaneous ischemia or the development of mechanical
complications.
After the acute phase of STEMI, therapeutic lifestyle changes (including smoking cessation, exercise and
dietary modification) and drugs for secondary prevention assume critical roles in improving outcomes in the
medium and long-term. Patient counseling and education is the key to maintaining adherence to therapy in
the long run.
7. CARDIAC FAILURE
This is a condition caused by the inability of the heart to pump out as much blood per minute as it should.
Diagnosis
1. Clinical Features
2. Orthopnoea/pedal oedema
3. Tachycardia,
4. Elevated jugular venous pressure. Enlarged tender liver, pedal oedema, auscultation showing basal
lung crepitations
Investigation
1. Chest X –Ray to confirm failure and look for predisposing pulmonary disease,
2. ECG to rule out any ischemic causes for cardiac failure
3. Echocardiogram to diagnose:
4. Rheumatic valvular disease,
5. Ischemic heart disease
6. Cardiomyopathy is underlying cause of disease. Echo cardiography also helps assess severity of
ventricular dysfunction and rule out endocarditis.
Differential Diagnosis of causes
1. Rheumatic valvular disease (detected on auscultation and ultrasound)
2. Ischemic heart disease (detected on ECG)
3. Myocarditis and cardiomyopathies (detected on ultrasound)
4. On occasion it can be secondary to
5. Severe anaemia z Hypertension
6. Chronic lung disease.
7. Consider thiamine deficiency (beriberi) where appropriate.
Treatment
General Guidelines
1. Ensure salt is excluded or at least limited in diet.
2. In mild cases for restricting salt in diet it may be enough to avoid highly salted items like pickles,
papads etc. and put a bit less salt in cooking and not to add any salt while eating.
3. For severe cases cook separately without salt and give the day’s quota of salt- about half spoon of
salt in a small container, leaving to the patients choice to add it to whatsoever he chooses. The more
the leg swelling andbreathlessness the more the need to restrict salt.)
4. Avoid exertion- more severe cases would need bed rest.
5. Treat Anaemia if present
6. Prevention and prompt treatment of infections especially respiratory infections : Encourage to take
prescribed drugs;
 7. Treat cause – see relevant sections.
Drug Treatment
Tablet furosemide five days a week.
Adults 40 mg once daily
Children 1 to 2 mg/kg for preferably given in the morning hours, preferably
Tablet digoxin
0.25 mg orally daily – skipping dose on the last two weekend days may start initially with 0.125 mg.
Tablet enalapril 2.5 mg once daily if blood pressure is maintained (above 100 systolic), to be increased to
2.5 mg twice a day then further based on clinical judgement in two divided doses per day.
Potassium substitute liquid 0.5 to 1 daily – as one teaspoon thrice daily.
Especially if long standing treatment with furosemide and digoxin is being undertaken to prevent
hypokalemia and digoxin toxicity.
Treatment In emergency in severe cardiac failure (e. g. left ventricular heart-failure, acute pulmonary
oedema)
When breathlessness is considerable
Oxygen if available
If blood pressure is maintained
Put person in Half-sitting position, legs hanging down.
Give a diuretic like furosemide (IV)
Adult: 20 to 80 mg/ direct IV; to be repeated after 2 hours following clinical state Check blood pressure,
pulse and urine output.
Child: 1 mg / kg / direct IV; to be repeated after 2 hours following clinical state
Give isosorbide dinitrate or glyceryl trinitrate (sublingual): 0.25 to 0.5 mg, to be repeated after 30 minutes if
necessary.
Give Digoxin 0.25 mg orally; if patient is not on digoxin, then the dose can be repeated after 12 hours for
digitalization.
Enalapril 2.5 mg once daily to be increased to 2.5 mg twice a day then further as required- may be given if
not hypotensive
If blood pressure is not maintained – treat as shock. Transport to a hospital certified for this purpose
(functional CHC/district hospital)
If no definite cause is ruled out
Add Injection thiamine 100 mg/day for two days and continue with oral thiamine at same dose for several
weeks.
If there is evidence of endocarditis :
Treat with two antibiotics :
Benzyl penicillin 4 to 6 m. units IV 4 hrly and
Gentamicin (3 to 5 mg/kg as a loading dose followed by 1.5- 3 mg./kg/ day) in 3 divided doses for at least
three to six weeks
or AMOXICILLIN 250-500 mg thrice a day and
Ciprofloxacin (if oral treatment is essential as daily injection over along period cannot be organised).
If culture reports are available then choice of antibiotics would be guided by this.

8. ACUTE RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE

ACUTE RHEUMATIC FEVER
Disease affecting the heart valves and the joints due to antigenic cross reactivity between components of
cardiac tissue and Group B streptococci.
Diagnosis
1. jones criteria
Major - Carditis, migratory joint pains, chorea, subcutaneous nodules and erythema marginatum.
Minor - Clinical-Fever, Arthralgia, Laboratory-Elevated acute phase proteins including ESR Prolonged 2. 2.
PR interval on ECG
Essential - Evidence of recent Group B Streptococcal infection by one of the two ASLO titres > 400 IU. Or
Throat swab culture positive for Group B Streptococci
Presence of two major or one major and two minor plus one essential criterion required for diagnosis.
Where essential criteria test not available, one can initiate treatment based on major & minor Jones criteria
alone. Of these signs in most cases it is the typical migratory (flitting and fleeting) joint pains which is
diagnostic). For diagnosis of carditis the presence of tachycardia, new diastolic cardiac murmurs or muffling
of heart sounds, any evidence of pericarditis, or a persistent cardiac failure in a patient with rheumatic
valvular disease must be taken as “active carditis present”. An elevated ESR is the only available laboratory
test in most contexts.

Treatment
2. Anti streptococcal antibiotic therapy
3. Oral Penicillin V 500 mg twice a day for 10 days or
4. Procaine penicillin 8 lac units once daily IM for 7-10 days or
5. Injection Benzathine Penicillin 1.2 million units single dose or
6. Erythromycin 500 mg 6 hourly
7. Medical therapy for rheumatic fever
8. Aspirin -2 gm four times a day for 4-6 weeks, for children 100mg/kg/day in divided doses
9. After these taper depending on falling ESR or clinical improvement or
10. Prednisolone 1 mg per kg if active carditis is present. Carditis also needs strict and absolute bed rest.
Prophylaxis in rheumatic fever (to prevent further attacks)
Treatment for at least 5 yrs. following initial episode or 18 yrs. of age whichever is later. Drugs
Benzathine Penicillin
dult - 1.2 Million units of every 3-4 weeks
Child - 0.6 Million units of every 3-4 weeks
Or
Oral Penicillin V - 250 mg twice a day. If documented rheumatic valvular heart disease is present,
prophylaxis should be for life

RHEUMATIC HEART DISEASES

Presence of valvular heart disease – especially if multivalvular, most common form is stenosis of mitral
valve. There may be past history of rheumatic fever.
Clinical presentation
Signs of early cardiac dysfunction or failure
1. Dyspnoea
2. Orthopnoea
3. Tachycardia
4. Bilateral pitting pedal oedema
Signs of cardiac Failure :
1. Elevated JVP
2. Bilateral crepitations over base of lungs
3. Tender hepatomegaly
4. Ascites in long standing and severe cases.
5. They may also present with only :
6. Signs of stenosis
7. Fatigue
8. Syncope etc.
9. Arrhythmia (irregularly irregular pulse)
10. Endocarditis (fever).

Diagnosis
By auscultation clearly showing valvular heart disease.
Investigations and confirmation
1. Chest X ray showing pulmonary oedema, and helps assesses cardiac chamber enlargement most
often of left ventricle, left atria or right ventricle.
 2. ECG showing atrial fibrillation, chamber enlargement.
3. Echocardiography showing stenotic or incompetent valves
Treatment
General Guidelines
1. Precipitating factors causing congestive cardiac failure to be identified and treated, these include
2. Excessive exertion to be allayed by bed rest
3. Excessive salt in diet to be reduced
4. Diuretics added
5. Anaemia to be corrected (blood transfusion with packed cells if needed)
6. Antibiotics for respiratory or other intercurrent infections
7. Prophylaxis and prompt treatment against infective endocarditis
8. Control of rate in chronic atrial fibrillation with (digoxin)
Treatment of carditis (with prednisolone)
Drug Treatment
Ensure regular drug intake
Tablet furosemide preferably five days a week.
Adults 40 mg once daily
Children 1 to 2 mg/kg Preferably given in the morning hours.
Tablet digoxin 0.25 mg orally daily – skipping dose on the last two weekend days- may start initially with
0.125 mg.
Tablet enalapril 2.5 mg once daily if it is a predominantly regurgitant lesion and blood pressure is
maintained (above 100 systolic), to be increased to 2.5 mg twice a day and then further based on clinical
judgement in two divided doses per day.
Potassium substitute – potassium chloride liquid 0.5 to 1 daily – as one teaspoon thrice daily. Especially if
long standing treatment with furosemide and digoxin is being undertaken to prevent hypokalemia and
digoxin toxicity.

Definitive treatment
Early surgery if symptoms progress despite medical control :
Should be referred to a tertiary care centre, where the patient should be evaluated for the level of ventricular
function, valvular orifice area and the feasibility of surgery to correct the valvular defect.
Tertiary Prevention
The prevention of further complications.
Encourage him or her to continue the medicines without interruption.
Help the patient get a weekly supply of drugs from the PHC
Ensure that once in three weeks the patient takes an injection of benzathine penicillin. Alternatively he can
take oral penicillin tablets as prescribed by doctor.
Educate to avoid excessive salt intake, or excessive exertion or anaemia or infections. Prompt treatment of
respiratory infections and antibiotics( amoxicillin) if there are any wounds or cuts
If pregnant treat as high risk case and put under medical care.

Rheumatic heart disease can be prevented

Prompt treatment with full dose of antibiotics for sore throat with fever in children. If a child or adolescent
has fever with joint pains of the type seen in acute rheumatic fever this person must immediately take a full
course of amoxicillin or penicillin and then take once in three weeks an injection of benzathine penicillin
.Alternatively they can take oral penicillin tablets as prescribed by doctor.
Other than surgical correction and intractible failure all other aspects of treatment must be undertaken at a
specialist has confirmed diagnosis.
Pediatric cardiology
9. Cyanotic Heart Disease:
1. Introduction: Disease categories
2. Cyanotic Spells and their management
3. Timing of intervention for common lesions

Disease Categories:
Cardiac conditions that result in cyanosis are extremely diverse. The management guidelines are unique to
every lesion. Even within lesions there are numerous categories that require individualized attention. For
example Tetralogy of Fallot has numerous anatomic variations that can seriously influence how the
condition is managed. Broad principles have been listed in published guidelines (reference 3).
Common lesions in broad categories of cyanotic congenital heart disease (CCHD) that include conditions
associated with reduced pulmonary blood flow, CCHD with increased pulmonary blood flow and CCHD
associated with pulmonary hypertension are discussed in the published reference.
Cyanotic Spells:
Since cyanotic spells are common to a variety of CCHD conditions associated with reduced pulmonary
blood flow, it will be discussed in greater detail here:
Hyper cyanotic or Cyanotic spell is a pediatric emergency, which requires prompt recognition, and
intervention to prevent disabling cerebro-vascular insults and to save lives. A cyanotic spell needs to be
taken seriously not just because of the immediate threat but also because it indicates the need for early
operation.
How to recognize a spell?
1. Commonly seen below 2 years [peaks between 2 months to 6 months]
2. Onset is usually spontaneous and unpredictable
3. Occurs more often in early morning, although can occur at anytime in the day.
4. Infant cries incessantly, are irritable and often inconsolable.
5. Tachypnea is prominent and a cardinal feature. Typically these infants have a pattern of
6. Deep and rapid breathing without significant subcostal recession.
7. Cyanosis deepens as the spell progresses.
8. Later gasping respiration and apnea ensues, which leads to limpness and ultimately
9. Anoxic seizures.
10. Can last from minutes to hours.
11. Auscultation reveals softening or disappearance of pulmonary ejection murmur.
12. Occasional patient can have profound bradycardia.

Cardiac lesions which produce spells

1. Tetralogy of Fallot.
 2. TOF with Pulmonary atresia.
3. Tricuspid atresia and PS.
4. DORV with VSD and PS.
5. D-TGA or L-TGA with VSD and PS.
6. Single ventricle with PS.
7. Atrioventricular septal defect with PS.

Management of spells
1. Check airway and start oxygen. If child is uncomfortable with mask or nasal cannula, deliver oxygen via
tube whose end is held ½ - 1 inch away from nose. This corresponds to delivering 80% oxygen.
2. Knee - chest position.
3. Obtain a reliable intravenous access.
4. Sedate child with subcutaneous morphine 0.2 mg/kg/dose]or i/m ketamine [ 3-5 mg/kg/dose] if the access
is not obtainable expeditiously.
5. Soda -bicarbonate 1- 2 ml/kg given as 1:1 dilution or can be diluted in 10 ml/kg of isolyte-P which is
given bolus as the initial resuscitating fluid.
6. Correct hypovolemia (10ml/kg fluid bolus of isolyte P or dextrose normal saline).
7. Keep the child warm.
8. Start beta -blockade. Beta blockade is fairly safe unless a specific contraindication like bronchial asthma
or ventricular dysfunction exists. It should always be given with heart rate monitoring.
Medications and dosages:
1. IV metoprolol 0.1 mg/kg, given slowly over 5 min.
2. Can repeat every 5-min for a maximum of 3 doses.
3. Can be followed by infusion 1-2 mcg/kg/min
4. Monitor saturation, heart rates & BP
5. Aim to keep heart rate below 100/min.

Other options
1. I/v esmolol: 500mcg/kg over 1 min as loading dose, 50 mcg/kg/min for 4 minutes; if desaturation
persists without a significant decrease in heart rate the loading dose will need to be repeated and the infusion
rate can be increased in 50 mcg/kg/min increments until 300mcg/kg/min; this infusion should be maintained
at the rate that produces the desired result. Esmolol is relatively expensive but has the advantage of being
very short acting.
2. I/v propranolol [0.1 mg/kg].If desaturation persists and there is still no significant trend towards
improvement despite maximum beta blockage
3. Start vasopressor infusion.
Methoxamine given i/v at dose of 0.1mg-0.2 mg/kg /dose or i/m (0.1- 0.4 mg/kg/dose).
Phenylepherine: 5ug/kg as bolus and then 1-4 ug/kg/min as infusion.
4. If spells are persistent, consider paralyzing the child, elective intubation and ventilation and plan for
surgery, which can be corrective or palliative [BT shunt]
5. If convulsions occur- consider IV diazepam 0.2 mg/kg or IV midazolam 0.1-0.2 mg /kg/dose, as
slow push.

Appropriate and timely management of cyanotic spells can save lives and prevent CNS insults.

After a Spell:
1. After a spell is successfully managed, a careful neurological examination is mandatory. In case of
suspicion of neurologic insult during a spell, a CT scan is to be done to assess the presence and extent of
cerebral infarcts.
2. Initiate maximally tolerated beta-blockade (propranolol 0.5-1.5 mg/kg/dose 8hourly or 6 hourly).
The dose can be titrated by the heart rate response. Beta blockade may help improve restiniled segmental
analysis by 2D echo for complete diagnosis.
3. Plan towards early corrective or palliative operation (depending on the age and anatomy).
4. Correct anemia by packed cell transfusion. Hemoglobin levels < 12 gm/dl merit correction through a
blood transfusion in children with cyanotic spells; Continue therapeutic (if anemic) or prophylactic iron
therapy (if not anemic).

Preventing a Spell in a Child with a Cyanotic Congenital Heart Defect

Parents of patients diagnosed to have a cyanotic congenital heart defect should be counseled if the
possibility of occurrence of a spell is anticipated:
1. Explain to them the circumstances when a spell may occur.
2. Avoid dehydration.
3. Rapid control of temperature whenever fever occurs
4. Encourage early surgical repair Obtaining IV access in a cyanotic child can precipitate spells.
Difficulty in obtaining access can potentially be avoided by sedating child with IM ketamine [3-5 mg/kg]
and/or by using local anesthetic skin ointment before attempting for venous access or blood sampling.

Timing of Intervention in common cyanotic heart diseases:

Broad guidelines have been published (reference 3). Numerous anatomic variations dictate specific
decisions for individual patients. Additionally the paucity and variable capabilities of centers capable of
infant and newborn heart surgery in India will need to be recognized (reference 5). All these factors make
decision making in individual patients quite complicated and highly individualized.

Left to right shunts:

1. Introduction: Timing and indications of surgical or catheter-based intervention

2. Medical management while awaiting surgery or intervention
The timing of surgical or trans-catheter intervention for left to right shunts is a critical decision and one of
the most important tasks the pediatric cardiologist is asked to perform. Simply stated, the decision about
when to intervene requires carefully balancing the results of the procedure with the natural history of the
conditions. The extraordinary variety of conditions associated including unlimited combination of defects
complicates the decision making process. Further, during the last 30 years there have been numerous
advances in the field of pediatric cardiology and pediatric cardiac surgery. These advances have enabled
improved results from operations and trans-catheter interventions and have allowed the procedures to be
performed early. In addition, we now have information on the natural history of many congenital heart
conditions. An increasing number of studies are being published on the long-term results of operations and
interventions for congenital heart disease. Because of the wealth of information available to us the decision
about when to intervene in CHD" now involves careful consideration of a number of variables that influence
natural history and procedural outcome. There are no simple rules for the numerous CHD conditions and the
decision making process has to be individualized for every patient.
Detailed guidelines for individual left to right shunts are provided in reference number 1 and 2. These are
fairly contemporary and represent a consensus of national experts.
While awaiting surgery or catheter intervention, medications need to be administered. Specific guidelines
have been developed for this purpose and are published (reference number 4) through a consensus of
national experts.

10. ACUTE RHEUMATIC FEVER (RF) AND RHEUMATIC HEART DISEASE (RHD):

Figure 1 : Algorithm for initial Management of RF 12

In the past 4-5 decades there have been modest advances in our understanding of the disease process. There
have been minor changes in the diagnostic criteria and management practices for RF have also largely
remained unchanged for the last 20-30 years. However, there have been important changes in the
epidemiology both in India and the rest of the world. There appears to have been a sharp decline in RF and
RHD in parts of India that have shown improving indices of human development. Physicians living in these
parts of India need to be mindful of the prospect of over-diagnosis of RF. For most of India, however, the
disease is still quite common and it is important to not miss the initial episode of RF because secondary
penicillin prophylaxis still remains the most effective way of preventing RHD.
The algorithm displayed summarizes the initial management of RF.
 11. Non Surgical Treatment of Congenital Heart Disease

Therapeutic Cardiac Catheterization for treatment of Congenital heart defects has become a routine mode of
therapy in the present era. Catheter techniques have evolved to simplify future surgery, provide temporary
palliation or offer even definite repair. These procedures are categorized as established, investigational or
experimental.1 With improving hardware and increasing experience and expertise, more and more
procedures are being performed with great degree of safety and efficacy. The major advantage of non
surgical procedures is avoidance of scar, thoracotomy and cardiopulmonary bypass along with a shortened
period of hospitalization and lesser post-operative pain and recuperation period.
Although transcatheter interventional procedures have a relative low risk, there are potential complications
and therefore these procedures should not be used without an opportunity for benefit. These should
necessarily be performed in catheterization laboratories fully equipped with the various catheters, guide
wires, balloons and devices. They should be performed by a trained pediatric interventional cardiologist.
The American Heart Association has laid down guidelines and recommendations on indications for pediatric
therapeutic catheterization in various congenital heart diseases.2 These will need to be modified based on
our own data from surgical and interventional procedures with respect to immediate and long term results.
Pediatric interventions can be broadly classified into:
a. Transcatheter closure of congenital cardiac defects
b. Balloon dilatation of stenotic vessels and valves (Balloon Angioplasty and Valvuloplasty)
c. Atrial septostomy procedures
d. Others.
Given the relatively recent nature of these procedures, randomized control studies of their safety and
efficacy are still lacking. The results and complications of various procedures mentioned in this review are
taken from the prospective and retrospective observational studies and registry data reported in the literature
as well as from our own experience.3
A. Transcatheter Closure of Congenital Cardiac Defects

1. Closure of Atrial Septal Defect (ASD)

Device closure for ASD has been evolving since 1974, when Mills and King reported their experience with
the non-surgical technique. Last decade has seen a plethora of devices being used for ASD
closure. The important amongst them being Das Angel Wing, ASDOS, Button, Cardio Seal, Star
flex, Amplatzer septal occluder (ASO) and the Helex device. Some of them have been
withdrawn due to inadequate safety, sub-optimum efficacy or lack of being user friendly; while
the others are undergoing design modifications before being relaunched.
There is adequate data to indicate that transcatheter closure of secundum ASD is a viable alternative to
surgery in selected patients. In a large multicentric study using Clampshell occlusion device,
successful implantation was reported in 97% of the cases with 64% having complete closure and
35% having a small residual leak.4, 5 The prerequisites for ASD closure include (1) The
presence of a symptomatic or a large defect with pulmonary to systemic blood flow ratio of 1.5
or more (2) Weight greater than 8-10 kg (3) Central location of the defect with an adequate rim
on all sides to support the prosthesis (4)Defect size of 30 mm or less. (5) The ability to tolerate
short term antiplatelet therapy (6) The availability of an appropriate device.
Currently, the most common device used for ASD closure is the Amplatzer septal occluder (ASO). It can be
used effectively in defects as large as 40 mm (stretched diameter).With over tens of thousands of
implants used worldwide, its short term and intermediate term safety has been well established.
Some of the advantages of this device are the user friendly design, a smaller delivery system,
control over the device and the ease of retrieving and repositioning the device (without damaging
it) before release. Bulkiness of the device and the possibility of predisposition to thrombo-
 embolism may be some of the drawbacks of the device but no clinically significant problems
have been reported so far. Since October 1998, we have performed 236 cases using ASO at 17
different centers. ASD diameter of less than 30 mm with superior, inferior and posterior margins
of greater than 5 mm and separation of greater than 7 mm from anterior mitral leaflet were the
criteria for inclusion (Fig 1). The size of the ASD varied between 9 mm to 31mm(mean 17.6 +
5.1) with the device size varying between 11 to 40 mm. 9 patients were found to be unsuitable on
table since the device size equaling the stretched diameter of the defect was not available. In
patients, we failed to position the device in the appropriate position and hence the device was
removed and the patients were sent for surgery electively. Over a follow up period of 1.5 to 56
months (26 + 8.6), 1patient had a mild mitral regurgitation and 1 developed a small residual
shunt through a tiny satellite defect. There were no other adverse events including device
migration, thromboembolism or occurrence of arrhythmias.6 Very large ASDs (ASD requiring
devices > 30 mm) has also been found to be amenable to effective transcatheter closure in an
anaylsis of 31 patients with device requirement ranging from 30- 40 mm.Technical and clinical
success was seen in most patients.Complete absence of anterior rim with a tiny superior rim
appears to be an incremental risk factor for technical failure in this subset of patients. Similar
encouraging results in larger number of patients have been reported, both from India and
abroad.7 Major constraint to the use of such devices is their cost which currently is astronomical
and makes this procedure more expensive than surgery in most of the centres in India.

2. Transcatheter Closure of Patent Ductus Arteriosus (PDA)

Transcatheter closure of patent ductus arteriosus has been established as a safe and effective option to
surgical ligation. Transcatheter closure of a small PDA (<2.5mm) is done by using Gianturco
 coils which bring about closure of the PDA due to their thrombogenic potential. The immediate
angiographic success rates have been reported to be about 60-65% with a single coil and 90%
with the use of multiple coils.8 Our early experience using temporary balloon occlusion
technique for coil closure of PDA showed an immediate complete closure in 60% of cases which
increased to 95 % at end of 24 months as determined on Color Doppler. Only 3 out of 84 patients
needed a repeat procedure for a significant residual shunt9,10 (Fig 2). With modifications in
techniques(use of modified vertebral catheter, use of bioptome for coil delivery, use of multiple
coils and proper patient selection i.e PDAs less than 4 mm), results have shown significant
improvement in immediate angiographic closure which is now in the range of 90%. Other
techniques such as coil delivery using a snare or use of commercially available controlled coil
designs (PDA coils by Cook Inc, Duct occluder) have been described to increase safety and
improve efficacy. Rashkind’s double umbrella device, Sideris ’s Button device and Amplatzer
PDA device are some of the devices used for the closure of PDA; the former being withdrawn
from the market due to high incidence of arm fractures. Since October
Fig. 2 : Showing PDA closure by coil.

1998, we
have successfully deployed 174 Amplatzer PDA devices11 (Fig 3). All patients beyond the neonatal period
with no branch PA stenosis or aortic isthmic narrowing were considered suitable for the procedure (the
youngest being 3month old and weighing 3.2 kg). The minimum PDA diameter on angiogram varied
between 2-11 mm (mean 3.44 + 1.22), with a mean procedural time of 56.25 min and fluoroscopy time of
6.18 min.There were no major or minor complications during the procedure. All, except one had complete
closure of PDA, at the end of two weeks. At 6 weeks to 56 months of follow up, none had residual shunt
across the PDA.12 Two patients weighing less than 5 kg and requiring devices of greater than 6/4 size
developed significant gradients across LPA (velocity of greater than 2.5 m/sec).
Neonatal PDA, especially in a premature infant, does not have a well developed ductal diverticulum on the
aortic side. Moreover, many of these children have a high pulmonary artery pressure. None of
the currently available devices nor the coils can get anchored in these ducti. Thus surgical
ligation remains the procedure of choice in this subgroup. Residual shunts, coil / device
embolization, left pulmonary artery stenosis, aortic isthmus narrowing and hemolysis are some
of the complications reported with transcatheter closures. With increasing experience and
expertise, the complication rate has come down remarkably.

3. Transcatheter Closure of Ventricular Septal Defect (VSD)

Transcatheter closure of muscular VSDs using Amplatzer VSD occluder has been reported by Thanopoulos
et al with encouraging short and intermediate term results.13 Studies by the same author on the
transcatheter closure of perimembranous VSD with the Amplatzer septal defect occluder have
also shown promising preliminary results.14

4. Transcatheter closure of Unwanted Vessels or AV fistulas

Aortopulmonary collaterals arise from the thoracic aorta or its branches in patients with cyanotic congenital
heart disease and contribute to improved oxygen saturation. However, they can have adverse
effects before, during and after surgical repair. They are known to obscure the operative field,
reduce perfusion pressure on cardio pulmonary bypass, distend the left ventricle and compete
with effective sources of pulmonary blood flow in the pulmonary vasculature. Therefore all
significant collaterals need to be closed preferably before surgery. What constitutes a
“significant” collateral vessel is a matter of controversy but any collateral that has an
angiographically documented pulmonary venous return should be closed. A large collateral
which would reduce the saturation to below 70% or a collateral which is the only source of
pulmonary blood flow or the ones which can be easily accessed before establishing a CPB could
be left alone at the time of cardiac catheterization.
Although transcatheter closure of unwanted vessels can be accomplished by the use of vascular “glues” and
detachable balloons, Gianturco coils remain the most preferred technique (Fig 4). These coils are
versatile and flexible and can be delivered through catheters as small as 3F. Moreover they can
be reliably retrieved following inadvertent embolisation. Since the coils close the collateral
vessels due to clot formation, some groups soak the coils in thrombin solution to promote
thrombosis. The most common complication of coil closure of aortic collateral is embolism to
the lungs. Most of these coils can be retrieved with the use of snares. Other minor complications
include fever, pleural rub and occurrence of small pleural effusion.
Surgically created aortopulmonary shunts can lengthen or complicate intracardiac repair and can be closed
in the catheterization laboratory. However, the decision to close them preoperatively or
intraoperatively must be made jointly by the cardiologist and the cardiac surgeon.
Transcatheter techniques have also been used for the closure of pulmonary and coronary AV fistulas.
Although Gianturco coils are most commonly used, detachable balloons, Grifka bag,Amplatzer
PDA /ASD device have also been successfully used for transcatheter closure of these fistulae. In
our experience since 1995,of transcatheter closure of 11 patients (between the ages 1.17 to 9
years) with coronary cameral fistulas, we found the procedure safe and effective both in short
and immediate term follow up. Single or multiple Gianturco coils were used in 7 with 2 patients
requiring detachable balloons and coils and one patient requiring Gianturco and electrolysis-
released platinum coils.15 It is important to realise that different strategies consisting of route of
delivering the closure material and different types of anchoring devices need to be evolved
depending on the anatomy of the fistula, size of the patient and availability of the hardware.
Collaboration between interventional cardiologist and radiologist may be beneficial.
Fig. 4 : Transcatheter closure of coronary AV fistula

Balloon Dilatation of Vessels and Valves

Vascular or valvular stenoses are dilated by deformation or rupture through circumferential stress using a
balloon. Dilating balloons are usually made of transparent polyethelene with a diameter ranging from
2.5 –30 mm and with lengths of 2-10 cms.

1. Transcatheter dilatation of valves :

Stenotic valves can be opened by the use of balloon catheters which results in splitting of the commissures
and dilatation of the annulus. The balloon is rapidly inflated to a recommended pressure till the
waist in the balloon disappears. Pressure gradients are recorded before and after the dilatation to
assess the success of the procedure.Balloon valvuloplasty can performed for (a) Dilatation of
stenosed pulmonary valve (BPV) (b) Dilatation of stenosed aortic valve (BAV) (c) Dilatation of
membranous subaortic stenosis (d) Dilatation of mitral and tricuspid valve and (e) Dilatation of
bioprosthetic valves.
a. Balloon pulmonary valvuloplasty (BPV) : BPV is the treatment of choice for children with pulmonary
valvular stenosis (PS). It is effective and safe and provides relief of obstruction equivalent to
 that obtained following surgery.15 The only exceptions being those with dysplastic valves
and neonates with critical PS where the results are less gratifying. Balloon valvotomy is
recommended for transvalvular gradients above 50 mm Hg or if RV pressure is greater than
50% of systemic pressure (Fig. 5).
BPV can also be used as a palliation to reduce severe cyanosis in selected patients with congenital heart
lesions. The procedure is shown to have a significant improvement in the growth of
pulmonary annnulus and the pulmonary artery branches. We have limited experience of
palliating children having TOF with BPV with a success rate of 80% lasting for a period of 6
months(16, 17). In neonates and children with pulmonary valve atresia and intact IVS, it is
possible to perforate the pulmonary valve with the hardware of the GW or RF wire.Many
groups have reported successful perforation of pulmonary valve using these techniques.
b. Balloon aortic valvuloplasty (BAV) : In comparison to pulmonary balloon valvuloplasty, aortic dilation is
technically demanding and carries higher morbidity
Fig. 5 : Balloon Pulmonary Valvuloplasty

and mortality. This is particularly seen in infants with poor left ventricular function or those with hypoplasia
of left sided structures. At present BAV is indicated in children with peak systolic gradients greater than 60
mm Hg without significant aortic regurgitation and in infants with critical obstruction and left ventricular
dysfunction regardless of the gradient. The reported complications include transient left bundle branch
block, aortic valve incompetence, complete atrio-ventricular block and transient loss of femoral arterial
pulsations. In over 175 reported cases, the mean gradient reduced from 68-108mm to 24-41mm Hg post
procedure (Fig. 6) At follow-up, there was no re-stenosis or change in regurgitation. Significant
hemodynamic and clinical improvements were observed in 60-80% of the neonates with critical aortic
stenosis.18 Trans-carotid approach for neonates and trans-septal antegrade approach have also been
described for balloon aortic valvuloplasty. In our own experience, sick neonates with LV dysfunction are at
highest risk for procedure related complications.19
c. Dilatation of stenosed Mitral valve : Significant mitral stenosis can lead to pulmonary edema, alveolar
fibrosis, pulmonary artery hypertension and right ventricular failure. Balloon valvuloplasty
has supplanted closed surgical valvulotomy for symptomatic, non-calcified rheumatic mitral
stenosis. Although it can be used in children with congenital mitral stenosis, the results are
much less gratifying in terms of efficacy with high incidence of complications. Usually
patients with cuspal tear, papillary muscle avulsion and with pre-existing severe pulmonary
hypertension tolerate MR poorly and need early surgical intervention. Immediate success
rates range from 64-100% depending on the anatomy of the valve. Results of gradient
reduction persist for a long time in valves with good morphology.20
Fig. 6 : Shows Technique of Balloon Aortic Valvuloplasty

2. Vascular Balloon Dilatation

Successful vascular balloon dilatation involves controlled longitudinal or oblique, intimal and sometimes
medial tear.Current indications for vessel dilatation are : narrowing of pulmonary artery
branches, native CoA and stenosis of individual pulmonary veins and major systemic veins.
1. Dilatation of Coarctation of Aorta : There is a general agreement that percutaneous angioplasty represents
the procedure of choice for recoarctation of aorta following surgery. However, there is no
unanimity of opinion regarding the role of balloon angioplasty for native coarctation.This is
primarily due to early reports of aneurysm formation in as high as 6-45% of cases within 1-3
years after dilatation. However,with the present day practice of using smaller balloons at
lower pressures the incidence of such aneurysms has lowered.21 The major limitation of
balloon coarctoplasty in neonates and small infants (less than 3 months) is the high rate of
restenosis. The overall rate of complications in 230 reported procedures was about 6% (Fig
 7). The advantages are high primary success rate, low complication rate and shorter duration
of hospital stay in critically ill patients with high operative risks.
In children with tubular hypoplasia of the aortic isthmus, the use of intravascular stents has greatly reduced
the incidence of restenosis. Endovascular stents are extremely useful in preventing restenosis.
In our experience of primary stenting in 15 patients above 10 years of age with coarctation of
aorta, there was a marked decrease in the stenotic gradient from 59.13 + 8.8 mm Hg pre-
procedure to 5.26+ 12.93 mmHg post procedure. No major complications were seen except
in one patient who had delayed left femoral artery thrombosis requiring embolectomy. On a
follow up period of 3- 49 months there was no evidence of re-stenosis.22
2. Dilatation of Pulmonary artery stenosis: Pulmonary artery stenosis occurs as discrete isolated branch
stenosis, multiple distal stenoses or as a tubular hypoplasia. These are amenable to balloon
angioplasty and endovascular stents with an overall complication rate of 10% and mortality
rate of 1-2%. Most often these stenosis occur as a part of a congenital heart disease such as
TOF with pulmonary atresia.When it occurs in isolation or with other intracardiac defects it
could be a part of Rubella syndrome, William’s or Allagille’s syndrome.
3. Dilatation of Pulmonary veins & systemic veins : Therapeutic balloon dilatation of individual pulmonary
veins is still investigational and considered as the last resort due to lack of a realistic surgical
alternative. However, the overall long term results of balloon dilation of pulmonary veins
with or without stents appear dismal. Major systemic veins (SVC & IVC) are more amenable
to stent dilatation with gratifying results.
Fig 7 : Balloon dilatation of coarctation of aorta.

C. Atrial
Septostomy Procedures
Balloon atrial septostomy (BAS) is indicated as a palliative procedure for congenital heart lesions in
neonates and young infants in order to improve mixing as in d-TGA or to enlarge the obligatory,
restrictive,inter-atrial communication as in the case of mitral or tricuspid atresia. In infants older than 1
 month, a blade followed by balloon septostomy is recommended to achieve satisfactory results.The
overall complication rate is 8-10%.23 In our own experience of 73 cases who underwent echo guided
BAS for various indications, there was no mortality and there were no major complications.

D. Other Intervention Procedures

Catheter therapy is also used for :
1. Non-surgical foreign body removal – like catheter fragments, therapeutic occlusion devices, and
embolised foreign bodies. Commonly used retrieval devices are baskets, bioptomes and snares.
2. Transcatheter myocardial biopsy is helpful for etiological diagnosis of various myocarditis,
cardiomyopathies and for the diagnosis of rejection in patients with cardiac transplantation.
3. The transcatheter radiofrequency ablation of accessory pathways has revolutionized the treatment of
several forms of childhood arrhythmias.24
4. Laser balloon angioplasty has been reported in experimental animals to preserve the patency of ductus for
palliative shunting.
5. Collaborative therapeutic catheterization and surgical procedures have been attempted.e.g Transcatheter
completion of Fontan’s after a surgical bidirectional Glenn and peroperative transventricular
closure of VSD using a device on a beating heart.

Summary
Pediatric cardiac interventional program is not a one-man effort. It requires a well knit team consisting of
pediatric cardiologist, an intensivist, an anaesthesiologist, nurses and trained cardiac catheterization
laboratory personnel. It is necessary to have a surgical back up in case of complications warranting surgical
intervention.
In order to know whether or not these procedures are as effective and as safe as their currently available
surgical counterparts, it is essential to have a regular and complete follow up of these children. This is an
area where physicians and pediatricians can actively contribute by timely referral. Main issues that need to
be addressed during the follow up are short term success, long term success and procedure related
complications.
The major constraint for these procedures is their cost. However, it is expected that the prices will come
down in the next few years with increasing competition and indigenous production of some of these
materials.
In conclusion, pediatric cardiac interventions are here to stay given their track record of safety and efficacy.
However, it is important to realize their scope and limitations so that a right procedure is offered to the right
patient. With the current rate of growth in technology, they are bound to replace more and more surgical
procedures in the years to come.

28. RECENT TRENDS IN MANAGEMENT OF HEART FAILURE

Heart failure (HF) is a clinical syndrome characterized by the inability of the heart to supply cardiac output
at a pace necessary to meet the metabolic demands of the body. In case of children, this requirement
includes “growth and development”. To optimize the outcome one should have a sound knowledge of
common cardiovascular drugs and formulate protocols to optimize the clinical management of these
patients. At the same time one should be alert to new drug developments and be willing to modify one’s
approach to drug therapy as new information is available. This article attempts to fulfill the latter objective.
Pathophysiology and diagnostics of CHF: Target for therapeutics
Diagnostics: Search for the anatomical cause forms the most important aspect of evaluation of a child with
HF. Precipitating causes like rheumatic activity, infective endocarditis, intercurrent infections, anemia,
electrolyte imbalances, arrhythmia, drug interactions, drug toxicity or non-compliance and other systemic
disturbances etc should also be carefully looked for.
Therapeutics : The basic requirements for rational drug therapy are: 1) Complete correct diagnosis
(anatomical and pathophysiological cause of CHF) - This forms the most important aspect particularly in
pediatric population. With timely diagnosis and intervention of various conditions viz critical stenotic
lesions, shunt lesions, anomalous left coronary artery from pulmonary artery (ALCAPA), hypocalcemia,
dramatic improvement is achieved 2) Clear understanding of pharmacology of various drugs available
(includes pharmacokinetics, drug dosages, potential efficacy and side effects), 3) Meticulous monitoring of
patient for therapeutic end points and side effects 4) Readiness to modify or change the drug therapy if
ongoing treatment is not effective or unacceptably toxic.
Supportive care measures are extremely important
1) Airway and oxygen therapy, proper position and airway management is essential to keep it patent
and to clear the secretions. Assisted mechanical ventilation may be needed in some patients to help
in stabilizing hemodynamics by decreasing the work of breathing, 2) Maintenance of homeostasis:
warm environment, care of metabolic derangements, 3) Nutritional care, 4) Treatment of
precipitating factors: intercurrent infections, infective endocarditis, anemia, electrolyte imbalances,
hypo/hyperthyroidism, arrhythmias, rheumatic activity and drug toxicity
2) Hemodynamic monitoring
Invasive hemodynamic monitoring may be needed in the following patients with acute
decompensated HF (Class IIa)1 1)patients with uncertain fluid status, perfusion, systemic or
pulmonary vascular resistance 2)persistent symptomatic hypotension 3)worsening renal function
4)patients who require parenteral vasoactive agents.

Pharmacological intervention
Drug therapy has to be individualized as per clinical setting A-D which have been adapted from
consensus guidelines.2 Commonly used drugs are given in Table I.
 Clinical setting A: Patients at increased risk for heart failure, but no volume overload or ventricular
dysfunction as seen in exposure to cardiotoxic agents; family history of heritable cardiomyopathy;
univentricular hearts (pre and post Fontan); congenitally corrected transposition. Therapy consists of
the following: (i) avoid cardiotoxic drugs; (ii) periodic clinical assessment; (iii) periodic
echocardiographic evaluation for ventricular function; (iv) maintenance of sinus rhythm. There is no
role for ACE inhibitors/ betablockers (Class III).
Clinical setting B: Patients with abnormal cardiac morphology or function, but no symptoms of heart
failure as seen in mitral regurgitation (MR) or aortic regurgitation (AR) with left ventricular
enlargement; and univentricular heart. ACE inhibitors, beta blockers (Class I indication) are to be
used particularly when dysfunction sets in these cases.
Clinical setting C: Patients with past or current symptoms of heart failure (commonest group).
Diuretics, ACE inhibitors and digoxin main line of therapy in this subgroup.
Clinical setting D: Treatment for end-stage heart failure requiring continuous infusion of inotropic
agents, mechanical circulatory support, cardiac transplantation or hospice care.
Therapy: intravenous infusion of dopamine, dobutamine, milrinone, alone or in combination (details
described later in section on “Drugs in ICU setting”). Betablockers and ACE inhibitors should not be
used (Class III).
Conventional drugs Whatever new is new, we still stand by our old friend.
1. Digoxin: This glycoside has been shown to improve symptoms and signs of HF even if the
ventricular function is not very much affected or disturbed, as it has actions other than inotropic
effect in the form of neurohormonal activation, improvement in baroreceptor function, increased
vagal tone, sympathoinhibitory effect, decreased circulating norepinephrine levels, and possibly
aldosterone antagonistic effects. However, it has not been shown to provide survival benefit in
adults or in children.3 Lower dose may reduce the incidence of side effects and toxicity. Higher
digitalis levels can cause increased mortality.
2. Diuretics: Diuretics are currently recommended for all patients with HF who have volume
overload of the ventricle. Diuretics from different groups (a-c) can be combined for greater
efficacy : (a) Loop diuretics: eg. furose mide, torsemide. (b) Thiazides: viz hydrochlorothiazide
and metolazone. (c) Aldosterone antagonists: eg spironolactone and eplerenone.
Furosemide is beneficial for symptomatic relief.
Torsemide is a loop diuretic more potent than furosemide, (10 mg of torsemide is equivalent to 40mg of
furosemide), has a higher bioavailability and a longer duration of action. In an open label study on children,
torsemide was considered better than furosemide for control of HF.4
Thiazides: These are relatively milder diuretics (except for metolazone) primarily used in mild hypertension
and edema. Metolazone is ten times more potent than hydrochlorthiazide, useful in resistant cases of
hypertension and HF. Intermittent doses of metalozone may help to overcome diuretic resistance which may
occur due to fluid overload, mesenteric congestion (inadequate absorption) and low renal blood flow.
Spironolactone: This aldosterone blocking agent has been shown to improve survival in adult patients with
HF. Usually it is given in conjunction with furosemide as it is potassium sparing and has additive action as
diuretic. Small observational studies using spironolactone5 in children have shown benefit in controlling
HF.
3. Vasodilators: angiotensin converting enzyme inhibitors (ACEi) ACEi decrease the adrenergic
drive and blocks activation of renin angiotensin aldosterone system (RAAS). ACEi therapy can
be used as the first line treatment for HF, when it is not secondary to an obstructive lesion.
Improvement in symptoms and survival has been shown in adults with symptomatic HF on
ACEi.6 Enalapril is commonly started with 0.1 mg/kg/dose and increased gradually to a
maximum of 0.5 mg/kg dose. Lisinopril is another useful drug. High dose of lisinopril was more
beneficial than a low dose (ATLAS trial).7 One must up titrate the dose to the maximum
tolerable permissible dose. Several small observational studies have proven the efficacy of these
drugs in children and survival benefit with ACEi has been shown in children with idiopathic
dilated cardiomyopathy. ACEi have been found to be useful in valvular regurgitation, large left
to right shunts, if the systemic vascular resistance is elevated at the baseline and myocardial
dysfunction (without obstruction). As it can cause hyperkalemia, it should not be given along
with spironolactone.
4. Hydralazine: It is a non ACEi peripheral vasodilator that does not produce hyperkalemia, and is
safe in patients with renal impairment. It should be used in patients in whom ACEi are not
tolerated or contraindicated with a starting dose of 0.75 mg/kg/ day which may be increased
gradually up to maximum of 5mg/kg/day in four divided doses.
5. Angiotension receptor blockers (ARB) ARB are competitive antagonists for the angiotension
II receptors. A meta analysis of randomized trials in adults did not show any advantage of ARB
over ACEi. Studies in children are in progress. A combination of ACEi and ARB is currently not
recommended in pediatric patients.8
6. β blockers Several studies have shown the benefits of beta blocker therapy in adult patients with
HF. Carvedilol has been shown to decrease mortality and risk of clinical progression of HF. It
improves functional class and fractional shortening in children with ventricular dysfunction. In
the first multi centre, randomized, double blind, placebo controlled trial for carvedilol in children
there was no statistically significant difference due to unexpectedly low rate of events for
patients in worsened category and trial may have been underpowered.9
Various new drugs are in various stages of clinical application (Table II). Other new drugs which
are still experimental include adenosine antagonists, nitric oxide modulators, natriuretic peptides,
xanthine oxidase inhibitors.
Inotropic agents (acute decompensated HF) Current generation inotropes include
catecholamines, either endogenous (epinephrine, norepinephrine and dopamine) or synthetic
(dobutamine,isoproterenol) and afterload reducing agents milrinone, nitroglycerine. All these
drugs increase metabolic demands, induce maladaptive remodeling and also are proarrhythmic
secondary to accumulation of calcium. Newer agents aim to prevent the same, which includes
calcium channel sensitizers, nestritide, cardiac myosin activators, Na/K ATP ase inhibitor-
Istaroxime, (Table II). Despite the standard pharmacotherapy, some children and young adults
with HF remain in a chronic decompensated state requiring intravenous inotropes and vasodilator
medications. Some of these patients with endstage HF become inotrope-dependent, and are
candidates for newer therapies like ventricular assist device and also cardiac transplantation.

Other drugs
Intravenous immunoglobulins (IVIg)
IVIg is an immunomodulator, affecting function of B and T lymphocytes and is known to
neutralize pathogenic antibodies and suppress their synthesis.2 Drucker, et al reported a better
albeit non significant,survival with IVIg in suspected myocarditis in children. IVIg may be
useful in the initial stage of viral replication especially in cases where onset of symptoms is
preceded by a viral illness or history is short ((<3 months duration) or cardiac enzymes are
elevated (Class IIa). Some physicians use IVIg in all infants <1 year of age with idiopathic left
ventricular dysfunction (Class IIb) however its use in idiopathic left ventricular dysfunction
remains controversial. IVIg is contraindicated in patients with hypersensitivity to blood products
and in those with IgA deficiency. Relative contraindications include previous thrombotic
episodes and sepsis.Live vaccines should be postponed for at least 3 months after IVIg has been
administered and the recommended interval is 11 months. Similarly IVIg should be avoided for 3
weeks after a live vaccine has been given.2 (
Anticoagulation
Dilated cardiomyopathy or myocarditis with HF predisposes to stroke and pulmonary embolism.
Those with gross HF should receive oral anticoagulants (Class I). Oral anticoagulants are also
preferred for other children with cardiomyopathy who have significant ventricular
dysfunction(LVEF < 20 %) (Class IIa). The target INR is kept between 2.0 and 3.0. If
intracavitary thrombus or marked dilatation of atrial with spontaneous contract is present,
anticoagulant therapy is again warranted (Class I).2

Non pharmacological intervention: Mechanical interventions and devices

Ultrafiltration: UNLOAD trial (ultrafiltration versus intravenous diuretics for patients
hospitalized for acute decompensated congestive HF) showed ultrafiltration (UF) caused more
weight loss than conventional medical therapy but dyspnea assessment indicated similar scores
in both the groups. UF was associated with 50% reduction in number and length of
rehospitalization, and unscheduled medical visits for HF in adults. But there is paucity of data in
children.10
Cardiac resynchronization therapy (CRT):
Dyssynchrony in myocardial contraction commonly occurs in patients with HF and left bundle
branch block, leading to impaired LV function and worsening mitral regurgitation. CRT restores
normal contraction to the LV wall while improving overall heart function. This should be
considered after optimizing conventional pharmacological treatment. Indications for CRT for
adults (are given in ACC guidelines 2009):11 In pediatric patients CRT has been successfully
tried in post operative tetrology of Fallot patients with dysynchrony. Its long term benefit is yet
to be established.12

Implantable defibrillator: Antiarrhythmic medications have not been shown to decrease mortality
in adults with HF and in some instances have actually had harmful effect. Many studies have
shown that implantable defibrillator reduces the mortality in adults with HF. However, in
patients who are thought to be at risk for lifethreatening arrhythmias, one should consider
placement of intra cardiac defibrillator in children e.g. long QT Syndrome.
Continued positive airway pressure (CPAP): In adult population CPAP is an effective treatment
for sleep apnea seen with advanced HF. It improves LVEF, reduces urinary epinephrine levels
and improves cardiac output.
Assist device therapy: Assist devices improve survival and quality of life of patients ineligible
for a heart transplant. These also serve as a bridge to transplant and ventricular recovery. Since
the early report of pneumatic paracorporeal ventricular assist devices in children, there has been
increasing use of many devices such as the Berlin Heart VAD (Berlin Heart AG, Berlin,
Germany), MEDOS-HIA-VAD (Helmholtz Institute, Aachen, Germany), Thoratec Ventricular
Assist System (Thoratec Crop, Berkeley, California, USA), and Abiomed BVS-5000
(ABIOMED, Inc, Danvers, Massachusetts, USA) in children. Reports specifically addressing the
outcomes for the longer term ventricular assist device implantation in children do not exit and
what is known must be extrapolated from scattered experiences. As the number of pediatric
patients requiring ventricular assist device support increases, the science of long-term
mechanical circulatory support, cellular changes in cardiac remodeling and recovery and end-
organ perfusion of pulsatile flow in pediatric patients will likely to be refined in the coming
decade.
Surgery: Various surgical modalities have been proposed including mitral valve repair, left
ventricular reduction, endovascular patch plasty, dynamic cardiomyoplasty, prosthetic restraint
devices, but they still remain experimental.
Heart transplant in children of all ages is now accepted as a therapy for end-stage HF secondary
to cardiomyopathy, hypoplastic left heart syndrome, failure of Fontan and palliated congenital
heart disease when these diseases are life-threatening or are associated with a poor quality of
life.13 However, the facility is not well established in India. The approach and the criteria of
listing for heart transplantation in pediatric age are different from adults. Role of
cardiopulmonary exercise testing is limited by lack of consensus and limited data, the adult value
of peak oxygen consumption of 14 milliliter/ kilogram/minute guideline does not hold true for
children. The most important limitation is availability of donor heart for our growing population
of HF in pediatric age group and the need for continued medication and its cost. Keeping these
rare limitations in mind it is possible to use this rare resource to benefit as many children and
their families as possible12.
Genetic approach: Promising approach is still awaited Gene transfer: These target at least 3
different biological pathways that play a crucial role in the pathophysiology of CHF and form the
target for gene therapy. These include intracellular calcium signaling, β1-adrenergic receptor
(β1-AR) signaling, and antiapoptotic signaling. Invivo over expression of SERCA2a, achieved
by catheter injection of an adeno virus carrying the SERCA2a gene into the aortic root, restored
systolic and diastolic function to normal levels. Intracoronary delivery of a recombinant
adenovirus encoding ACVI (1.4x1012vp) improves global left ventricular function associated
with reduction in LV remodeling in a large animal model of HF. Stem cell forms another
promising future modality. Many cell types have been successfully transplanted into damaged
myocardium, including fetal cardiomyocytes, skeletal myoblasts, embryonic stem cells and bone
marrow-derived stem cells. The best characterized of these is skeletal myoblast, an immature
muscle cell that retains the ability to proliferate. Several studies have used human autologous
skeletal myoblasts transplantation to determine if engraftment of these cells leads to long-term
improvements in left ventricle function.14,15 However, these exciting progresses have many
unanswered questions including potential arrhythmic and oncogenic potential of these cells,
which can only be resolved by larger clinical trials with long-term follow-up which are not yet
available
In summary, standard therapy of vasodilators, diuretics, digitalis, ACE inhibitors and beta
blockers form the backbone of HF therapy. Innovative interventions directed at the failing heart
are being explored. Newer drugs and assist devices still are on the horizon particularly in
children and these need more research and evaluation.
26. MANAGEMENT OF COMMON ARRHYTHMIAS IN CHILDREN
In children, symptomatic arrhythmias commonly tend to be paroxysmal supraventricular
tachyarrhythmias (PSVT) while ventricular tachyarrhythmias (VT) are rare. The common PSVT
are AV reciprocating tachycardia (AVRT), Atrioventricular nodal re-entrant tachycardia
(AVNRT) and Permanent junctional reciprocating tachycardia (PJRT). Of these AVRT is the
most frequent PSVT in early life, accounting for 85% of arrhythmias in fetal life and 82% in
infancy. Up to 60% of AVRT resolve spontaneously by the end of infancy and the subsequent
incidence decreases by 65% in the 1-5 age group, 56% in the 6-10 age group and 68% in the
above 10 years age group.1 Wolf-Parkinson White (WPW) syndrome is a typical example of
AVRT. AVNRT is commoner in the school going age group with an incidence of about 23% in
the 1-5 age group, 34% in the 6-10 age group and 20% in those over 10 years of age. PJRT is
usually seen in the 3-4 year age group. All these tachyarrhythmias are paroxysmal (sudden onset)
as they are mediated by accessory tissue and the underlying mechanism is re-entry. Accessory
pathways are a result of embryological developmental anomalies that allows some atrial fibers to
penetrate the ventricular myocardium across the atrio-ventricular (AV) fibrous barrier, other than
at the AV node. As these fibers conduct electrical impulses faster than the AV node, they form
an alternate pathway through which earlier excitation (pre-excitation) of the ventricles occur.
The presence of two pathways with differing electrical characteristics facilitates re-entry. The
non-accessory pathway mediated (non-paroxysmal) SVT commonly observed in children are
Junctional ectopic tachycardia (JET) and Ectopic atrial tachycardia (EAT). Automaticity is the
underlying mechanism of these arrhythmias and is commonly seen in patients after surgical
repair for congenital heart disease. These are characterized by a slow onset and slow termination,
unlike the paroxysmal tachycardias. Ventricular tachyarrhythmias (VT) in children are seen in
association with Long QT syndrome (LQTS), Hypertrophic cardiomyopathy (HCM), Dilated
cardiomyopathy (DCM), Brugada syndrome and post cardiac surgery
Complete heart block (CHB) and Sick sinus syndrome are the bradyarrhythmias of note in
children. CHB is usually congenital with an incidence of 1 in 25000 live births1 and infrequently
sequelae to cardiac surgery. The underlying mechanism is block to conduction of electrical
impulse. Sick sinus syndrome results from an abnormality in impulse formation and conduction.
This may occur after surgery for closure of atrial septal defects, Senning/ Mustard procedures,
Fontan surgery and rarely be congenital.
To understand management of arrhythmia, it is required to be familiar with
• Basic electrophysiology of myocardial cell and conducting system in the heart,
• Mechanism and location of the arrhythmias
• Characteristics of the anti-arrhythmic drugs, and
• Non pharmacological modalities of arrhythmia management.
Cardiac tissue characteristics
The heart has two types of cells. Those responsible for contraction and those for impulse
formation & conduction. The conduction system is formed of the Sino-Atrial (SA) node, the
atrial internodal tracts, the Atrio-Ventricular (AV) node, the His bundle and the purkinje system.
The contractile cells are the myocardial cells and are activated by electrical impulses from the
purkinje fibers. There are important differences between the conducting and contractile cells.
Histologically, the conducting system is modified cardiac tissue with no contractile elements. It
can conduct and also initiate electrical impulses. Initiating an electrical impulse is owing to a
special ability of all cardiac cells to undergo spontaneous depolarization, the rate of which is
higher, the higher the tissue is positioned in the conducting system. As the threshold for
automaticity is highest in the sinoatrial (SA) node, it acts as the dominant pacemaker in a normal
heart, with the AV node, the specialized fibers of the atria and the HIS-Purkinje fibers following
in that order.
Cardiac cell electrical activity
The electrical activity from a single cell during depolarization and repolarisation is termed the
action potential. The surface ECG represents the sum of the electrical activity of all cardiac cells.
In the resting state of the cardiac cell, the Na+ K+ ATPase transmembrane ion exchange pump,
located in the cell membrane, actively pumps Na+ out and K+ in to the cells. This maintains a
resting membrane potential (RMP) of -90mv in HIS-Purkinje and working myocardial cells and
a lower RMP of -60mv in the SA and AV node. Spontaneous depolarisation in the SA and AV
node is facilitated by the lower RMP and the enhanced selective permeability of the cell
membrane of these tissues to K+. This threshold being lowest in SA node tissue, it acts as the
dominant pacemaker in a normal heart. Depolarisation in the non-conducting myocardial cells is
initiated and governed by the wave of electrical impulses from the conducting system. The HIS-
Purkinje cells and working myocardial cells use fast-sodium influx channels for depolarisation
and are termed fast response cells whereas the SA & AV nodal cells undergo depolarisation due
to a slow influx of calcium ions through calcium channels and are called slow response cells.
Repolarisation restores the RMP of the cardiac cell by allowing K+ and Ca++ influx in to the
cells and Na+ efflux with the help of Na+ K+ ATPase transmembrane ion exchange
pump.Pharmacological control of arrhythmias is mainly dependant on alterations of these ion
exchanges across the cardiac cell membrane.

Mechanism of arrhythmias
Re-entry phenomenon: In re-entry, the electrical impulse enters a tissue, depolarizes it and is able
to re-enter the tissue again to depolarize it a second time. This is possible only when an
accessory pathway combines with the existing normal conducting pathway to form an anatomical
circuit where there is slow conduction in one limb of the circuit and a transient or permanent
one-way block to electrical impulse in the other. The normal conducting pathway A has a slow
conduction velocity with short recovery time while the accessory pathway B has a fast
conduction velocity with long recovery period (Fig.1). This facilitates antegrade conduction
across one limb of the circuit and retrograde conduction back to the atria along the other limb,
thus setting up a fast, repetitive circuitous electrical movement. Re-entry can occur in the atrial
tissue, the AV node or the ventricular tissue. It could be macro re-entry (circus type) as in AV
reciprocating tachycardia, when the accessory pathway B is remote from the normal conducting
pathway A or Micro re-entry (focal) when the two limbs of the circuit are formed by functionally
dissociated pathways within the same tissue as in AV nodal re-entrant tachycardia.
In AVRT, as the conduction velocity through the accessory pathway B is faster than the nodal
pathway A, a normal sinus impulse that encounters these two pathways would travel faster
through the accessory pathway and activate the ventricle earlier. As the nodal pathway A also
gets partially activated, no re-entry occurs and the surface ECG demonstrates pre-excitation
(delta wave) with a short PR interval due to earlier excitation of the ventricular mass through the
accessory pathway. If an ectopic beat were to occur in this setting, it would find the accessory
pathway B non receptive because the refractory period of the accessory pathway B is longer than
that of the nodal pathway A. Therefore, the ectopic beat would travel antegrade down the slower
nodal pathway A. If after traversing the nodal pathway, this impulse finds the accessory pathway
to have recovered and receptive, it would travel retrograde through the accessory pathway B to
the atria thus initiating re-entry. This circus type, reciprocating movement similar to a dog
chasing its tail, could go on repetitively as long as the electrical impulse encounters cells which
have repolarised. A tachycardia using the slow A pathway for anterograde and fast B pathway
for retrograde conduction is termed “Orthodromic”. The impulse, when it reaches the HIS
bundle, spreads in an antegrade direction through the ventricles and again when it reaches atrial
muscle spreads in a retrograde direction through the atria resulting in a retrograde P wave
appearing after each antegrade QRS complex. In Orthodromic AVRT, the P wave is seen in the
ST segment (Fig.2) whereas with AVNRT the P wave may not be seen as it may be buried in the
QRS complex (Fig.3) since the retrograde activation of the atria is earlier. Up to 30% of AVRT
tend to have a concealed pathway and the surface ECG does not exhibit delta wave or a short PR
interval.
Automaticity is enhanced excitability causing the affected tissue to spontaneously depolarize at a
rate higher than the SA node, rendering it the new dominant ectopic pacemaker
Block is a mechanism by which the electrical impulses are not able to propagate due to block in
transmission.
Anti arrhythmic drugs:
The Vaughan Williams classification groups antiarrhythmic drugs in to Class I- fast sodium
channel blockers (Ia -quinidine, procainamide, disopyramide, Ib -lidocaine and Ic -flecainide,
propafenone).
Class II- beta-blockers (propranalol)
Class III- Potassium channel blocker (amiodarone, sotalol, dofetilide, ibutilide) Class IV – slow
calcium channel blockers. (verapamil, diltiazem)
Class I drugs exert a membrane stabilising effect by impairing the entry of sodium in to the cell.
This slows the rate of depolarization and reduces the excitability of atrial and ventricular tissue,
allowing the SA node to regain dominance of the cardiac rhythm. Also, prolongation of the
effective refractory period abolishes impulse re-entry. QT prolongation associated with this class
of drugs can be proarrhythmic. The negative inotropic effects make it unsafe for use in patients
with structural heart disease
Class II drugs reduces sympathetic activity which are known to be pro-arrhythmic and also
propagate re-entry mechanisms. Hence beta blockers are useful in treating arrhythmias
associated with long QT syndrome, Mitral valve prolapse syndrome, anaesthetic agent and
exercise induced arrhythmias. Beta blockade reduces the spontaneous firing rate of the SA node
and ectopic pacemakers, prolongs intranodal conduction and also prolongs the refractory period
of the AV node. This results in a negative chronotropic effect, reducing cardiac work. Beta
blockers are effective in prophylaxis of SVT by inhibiting the initiating atrial ectopic beat.
Class III drugs reduce K+ efflux out of the cells thereby prolonging the repolarisation phase.
This results in prolongation of the duration of action potential and refractoriness of the cardiac
tissues. The time interval required for re-excitation is prolonged and hence arrhythmias are
suppressed. The predominant advantage of this class of drugs is the indication to use them in the
presence of left ventricular dysfunction. Significant QT prolongation and attendant risk of
torsades is an adverse effect to be watched for.
Class IV drugs act by blocking slow inward calcium flow channels, especially affecting cells
whose depolarization depends on this such as the SA and AV nodes. They have no effect on
infranodal conduction and are negatively inotropic. This prevents their use in infants as the
myocardium is particularly sensitive to the negative inotropy of calcium channel blockers. Class
IV drugs are contraindicated when preexcitation is manifest, as they can facilitate antegrade
conduction during atrial fibrillation leading to ventricular fibrillation and arrest.
Digoxin has a dual mode of action on the myocardium. It acts directly on the heart by inhibiting
the Na+ K+ ATPase transmembrane ion exchange pump. This prevents active pumping out of
intracellular Na+ during repolarisation causing increased intracellular Na+ and Ca++
concentration and enhanced cardiac contractility. The indirect effect is through stimulation of
vagal efferents which reduces SA nodal rate and thereby heart rate. Digoxin also has a dose
related AV nodal conduction block that predominantly helps in reducing ventricular response to
atrial flutter/fibrillation.
Adenosine depresses the AV node conduction and produces transient AV block. Since the AV
node is part of the circuit in all PSVT, adenosine is the drug of choice for acutely terminating
such arrhythmias. Atrial arrhythmias, although not terminated by adenosine, may allow for
identification of the underlying mechanism during the transient AV block. Ventricular
arrhythmias are not affected whatsoever by this drug. The drug should be given as a fast
intravenous bolus as the half life is only 6 seconds.
Radiofrequency catheter ablation (RFA) is carried out in the catheterisation laboratory under
general anaesthesia. Percutaneous access is achieved through femoral artery and vein and
catheters with electrode sensors are advanced to various locations in the heart like the right
atrium, right ventricle, coronary sinus and the crux of the heart near the AV node. The abnormal
electrical connection causing the tachycardia is identified by the alterations that it causes of the
normal electrical signals. Once the pathway is located, extremely precise mapping of the same is
done using a special ablation catheter and the tissue under the exact location ablated using
alternating current of a frequency between 100 kHz and 1.5 MHz. This results in controlled
tissue desiccation through resistive tissue heating. The scarring results in replacement of
myocytes by fibrous and elastic tissue which in later life can potentially act as a substrate for
arrhythmias. As these scars have a tendency to increase in size with somatic growth of the child,
RFA is undertaken in very young children only when the arrhythmia is unlikely to resolve
spontaneously, or is refractory to medical management or associated with tachycardia induced
cardiomyopathy.2 However, reports of RFA in the paediatric population continues to be
encouraging with adverse events less than 1%, and long term freedom from the arrhythmias.3

Management of commonly encountered tachyarrhythmias in children

Tachyarrhythmias for a re-entrant tachycardia to be sustained, the arrhythmia cycle length must
be longer than the refractory period. Increasing the refractory period of one limb of the circuit
blocks conduction in that limb and terminates the re-entrant arrhythmia. In AVRT, the AV nodal
limb of the tachycardia circuit is the focus of attack, whereas in AVNRT, the antegrade A
pathway is the one most sensitive to intervention
A baby with PSVT typically exhibits a heart rate >200 bpm. An alert mother would notice the
baby to be irritable with incessant weak cry, refusing feeds and may appreciate the ‘fast heart
beat‘ while trying to calm the baby down on her shoulder. Very fast heart rate close to 300 beats
per minute compromises the cardiac output and the baby may present with features similar to
shock. When the PSVT is sustained for a long period then tachycardiomyopathy and congestive
heart failure is the mode of presentation. In a haemodynamically stable child, vagal maneuvers
should be attempted first. These maneuvers terminate PSVT by acutely increasing the refractory
period of the AV nodal limb / A pathway of the re-entry circuit. Recommended vagal maneuvers
are application of a plastic bag with ice cubes on the infant’s face for 10 seconds at a time or
applying pressure on the infant’s abdomen. Ocular pressure is no longer recommended. If these
measures fail, adenosine is administered at a dosage of 100 – 200 mcg/kg. This is given as a
rapid intravenous bolus injection through a large bore IV cannula with a three-way port to allow
follow up of the drug with a saline push. Rapidly escalating dose of adenosine can be
administered at very frequent intervals because of the short half life of the drug. If no satisfactory
response is achieved, intravenous infusion of esmolol or amiodarone is initiated. Amiodarone is
the preferred drug and is administered at a loading dose of 5mg/kg given over 20-30 minutes
followed by maintenance infusion at 5-15 mcg/kg/minute until the tachycardia terminates.4
When the child is haemodynamically unstable with the tachycardia, electrical cardioversion with
DC shock at 0.5 to 2 J/Kg is the recommended mode of management irrespective of the
mechanism of the underlying arrhythmia. Long term management of paroxysmal SVT depends
on the age of presentation and frequency. Considering the high incidence of spontaneous
resolution of AVRT and because they are not life threatening, a single episode of SVT in infancy
does not warrant treatment with drugs. Treatment of recurrent supra ventricular tachycardia is
ideally initiated with oral digoxin, propranolol or a combination of both. Digoxin is considered
safe for treating WPW syndrome (with pre-excitation) up to the age of two years, beyond which
propranolol would be the preferred drug.4 The loading dose of digoxin is 8-10 mcg/kg/24 hrs
followed by maintenance dosage of 6-8 mcg/kg in two divided doses. Propranolol is prescribed
at a dose of 0.2-0.5 mg/kg/dose 6-12 hourly up to a maximum of 1.5 mg/kg/dose 6-12 hourly.
Arrhythmias resistant to above measures could be managed with flecainide at a dose of 2-8 mg/
kg/day in 2-3 divided doses. Milk inhibits absorption of flecainide and therefore should not be
given together. It is best avoided when there is underlying structural heart disease or ventricular
dysfunction. QRS prolongation more than 25% is an indication to withhold the drug. Verapamil
(1-3 mg/kg/dose 8-12 hourly), a calcium channel blocker, though available for use in SVT in
children is generally not the preferred drug of choice. Amiodarone at a dosage of 4 mg/ kg/dose
at 8 hourly intervals for the first week followed by 12 hourly dosages for the subsequent week
and then once daily administration provide excellent relief from recurrence of PSVT in infants
and children, however the long term use is prevented by the wide range of adverse effects.
Therefore, children whose arrhythmias are non responsive to drugs other than amiodarone are
best referred for radiofrequency ablation. The dose of digoxin is halved when on concomitant
amiodarone as the latter increases the serum levels of digoxin.
PJRT is a re-entrant supraventricular tachycardia in children where the antegrade propagation of
the tachycardia circuit is down the AV nodal pathway and the retrograde activation of atrium is
through remotely located accessory pathway, usually in the posteroseptal region.5 The ECG
exhibits an inverted “p” wave in leads II, III, aVf and left lateral leads with PR interval shorter
than RP interval during the tachycardia. PJRT is usually incessant in character and when long
standing causes tachycardia induced cardiomyopathy. It commonly occurs around 3-4 years of
age. More than 20% of patients with PJRT exhibit spontaneous resolution of the tachycardia as
well as a good response to pharmacological therapy with amiodarone, verapamil or either drug in
combination with digoxin.6 This is in stark contrast to earlier held belief that PJRT does not
exhibit spontaneous resolution and is refractory to medical management. RFA is therefore,
reserved for children who have recurrences of the PJRT with or without tachycardia induced
cardiomyopathy despite drug therapy.
JET is the commonest (22%) arrhythmia seen in the immediate post-operative period following
intracardiac repair mostly following Tetralogy of Fallot correction.7 The underlying mechanism
is enhanced automaticity of the HIS bundle. ECG typically reveals a narrow QRS tachycardia
with a rate between 170-230 beats per minute, atrioventricular dissociation with the ventricular
rate faster than the atrial rate (Fig.4). JET usually responds to surface cooling to 34o C, atrial
pacing for AV synchrony, sedation & muscle relaxation to avoid stress and intravenous
amiodarone.
Atrial tachycardias commonly seen in children are intra atrial re-entry tachycardia (IART) due to
re-entry mechanism around atriotomy scars or Ectopic atrial tachycardia due to enhanced
automaticity of diseased or stretched atrial tissue. Multifocal atrial tachycardia is an ectopic atrial
tachycardia with multiple foci firing independently. Digoxin toxicity is an important cause of
multifocal EAT. The ECG shows multiple “p” waves of differing morphology with an isoelectric
baseline between the p waves differentiating it from atrial fibrillation. Drugs which are fast
sodium channel blockers and those that prolong the refractory period are more useful in
controlling arrhythmias arising in the atrial and ventricular tissues as they are the fast response
cells. RFA provides long term relief. EAT is more easily amenable to RFA than IART where
multiple circuits may be present.

Ventricular tachyarrhythmias results from either increased automaticity or re-entry in the

ventricular tissue. Ventricular arrhythmias are not affected by vagal maneuvers, as
parasympathetic innervations of the ventricles are minimal. Therefore, if vagal maneuvers result
in slowing of a broad complex tachycardia, VT is excluded. When the patient is unstable with
VT, cardioversion should be performed after adequately sedating the patient. Some may be
refractory to drug therapy while some respond to radiofrequency ablation. Beta blockers have a
role to play in VT associated with dilated and hypertrophic cardiomyopathies as well as in
LQTS. RV outflow tract VT is benign with a left bundle branch block pattern and inferior axis
on ECG. It responds to treatment with beta blockers and verapamil and is permanently relieved
with RFA. Idiopathic left ventricular VT is another benign tachycardia with a right bundle
branch block pattern with superior axis on ECG. This responds well to verapamil and is again
cured by RFA. Incessant VT occurs in the first two years of life and can induce tachycardia
induced cardiomyopathy and hence requires aggressive management with flecainide, amiodarone
and when resistant, RFA.
Automatic implantable cardioverter defibrillators (AICD) are indicated in children who are
susceptible to life threatening ventricular arrhythmia refractory to pharmacologic treatment and
those with syncope and family history of sudden cardiac death (SCD). This usually comprises
children with an underlying diagnosis of dilated and hypertrophic cardiomyopathies, LQTS with
QTc > 0.55 seconds, primary ventricular fibrillation, post surgical correction for Tetralogy of
Fallot and those who have undergone Mustard/Senning procedure for Transposition of the Great
Arteries. The challenge currently is to identify those at higher of SCD from ventricular
tachyarrhythmias to enable earlier intervention with AICD implantation.

Bradyarrhythmias:
The American Heart Association/American College of cardiology task force in 1991 recommend
cardiac pacing for symptomatic second and third degree AV block, third degree AV block
greater than 14 days following cardiac surgery, complete heart block (Fig.4) with a wide QRS
complex and in those with low escape rhythm variability and junctional instability.8 A
ventricular escape rate below 55 in neonates with structurally normal heart and below 70 when
associated with structural heart anomalies is an indication for permanent pacemaker implantation
(Fig.5&6).9 In the presence of CCF or cardiac defects, pacing is frequently necessary at a higher
underlying heart rate. Neonates with congenital complete heart block presenting with a very low
escape rate can be managed with intravenous infusion of isoprenaline (0.1mcg/kg/min) while
waiting for permanent pacemaker implantation. Inadequate response to isoprenaline and
haemodynamic instability with the bradycardia may infrequently warrant an emergency
percutaneous temporary cardiac pacing. The risk of sudden death in congenital AV block is
highest in early infancy but continues throughout adult life. Small single chamber pacemakers
weighing less than 20 gms are available nowadays and our practice is to implant these in extra
pleural, intrathoracic location in the left lateral chest wall with the lead secured to the epicardial
surface of the heart.10 This technique offers a secure position for the pacemaker in close
proximity to the cardiac mass without the risks associated with abdominal implantation. Once the
child grows to 5 years of age or weighs >10 kg, an endocardial pacemaker with subclavian
transvenous lead can replace the epicardial pacemaker which is then explanted.

27. VASOACTIVE AGENTS IN CARDIOGENIC SHOCK’

Shock is defined physiologically as inadequate delivery of oxygen and substrates to meet the
metabolic needs of the tissues. In essence,the perturbation of the primary equation that oxygen
delivery(DO2 ) is the product of oxygen content (CaO2 ) and cardiac output (CO) results in
shock.The CaO2 depends on how much oxygen-carrying capacity is available in terms of
hemoglobin (Hb) content and depends on how much oxygen the patient’s Hb contains, defined
as the arterial oxygen saturation (SaO2 ). Cardiac output is the product of heart rate (HR) and
stroke volume (SV) where stroke volume is determined by ventricular filling (preload),
impedance to ventricular ejection (afterload) and myocardial contractility. A state of hypoxic
shock may occur when CaO2 is impaired, or by acute profound anemia, which reduces the
amount of Hb and hence, reduces the body’s total oxygencarrying capacity. As cells are starved
of oxygen and substrate, they can no longer sustain efficient aerobic oxygen production and they
switch to anaerobic metabolism with resulting production and accumulation of metabolites that
ultimately lead to multisystem organ failure and if irreversible, cell death.
To summarize the equation:
Oxygen delivery (DO2 ) = oxygen content (CaO2 ) x cardiac output (CO)
CaO2 = (Hb X SaO2 X 1.34 mL O2 /g) +0.003 X (PaO2 )
CO = Stroke volume (SV) x heart rate (HR)
The clinical staging of shock includes compensated shock where the body responds to
hypoperfusion by vasoconstriction, tachycardia and redistribution of blood to vital organs,
resulting in falsely reassuring blood pressures. If untreated, this progresses to hypotensive shock
with multi-organ failure.
The etiologic types of shock may be physiologically compartmentalized into “hypovolemic,
cardiogenic, septic and distributive”.
Hemodynamic profiling of patients into sectors of “wet” or “dry” based on presence or absence
of congestion and “warm” or “cold” based on systemic perfusion can help determine therapy
Acknowledging the subtleties of how the age spectrum from neonate to early adult can result in
differing presentation and management is crucial as well. Understanding the interplay of
pathophysiology, staging, etiology, hemodynamic profile and age of the patient will facilitate an
intelligent use of vasoactive amines in managing pediatric shock
The shock continuum
Early in the evolution of compensated shock, hypoperfusion results in activation of the
sympathetic nervous system which stimulates the adrenals to produce catecholamines.1,2 This
increases the heart rate and systemic resistance via vasoconstriction. The renin angiotensin
system is also activated, leading to fluid retention by concentrating the urine and further
increasing vasoconstriction. This early compensatory phase also involves the redistribution of
blood from the skin, splanchnic and skeletal muscle systems to the vital organsthe brain, heart
and lungs. Clinically the primary equation manifests initially by an elevation in heart rate in
children, as the stroke volume component involving preload, contractility and afterload is
compromised. Vasoconstriction results in increased afterload, overall affecting stroke volume
and cardiac output. At this point, the role of maintaining an adequate preload becomes critical. In
summation, this phase clinically manifests as tachycardia with prolonged capillary refill, poor
peripheral pulses and most importantly preserved blood pressure.
Later hypotensive shock occurs when these mechanisms fail and hypotension develops,
compromising tissue perfusion and spiralling into vasomotor and microcirculatory multiorgan
failure. This phase clinically manifests as hypotension, lethargy with altered mental status,
decreased urine output, tachypnea, mottled extremities and multisystem abnormalities, which are
confirmed by laboratory testing.
The immature myocardium in infants has limited contractile reserve. The diastolic function also
gets easily compromised, leading to reduced compliance and rapid development of hypotensive
shock and death if not recognized and intervened on time.
Etiology
Hypovolemic shock is the commonest type of shock in children.It is multifactorial and may
occur secondary to hemorrhagic causes like surgery, trauma, hepatic or splenic rupture and from
non-hemorrhagic causes like gastro intestinal losses, burns, water deprivation and diabetes
insipidus or mellitus among other etiologies. It must be noted that hypotension may not occur till
about 25-40 % of intravascular volume is depleted. Using the primary equation, the decreased
intravascular volume leads to decreased preload from inadequate systemic vascular return,
resulting in decreased cardiac output.
Cardiogenic shock can occur from a myriad of congenital and acquired heart diseases affecting
preload, contractility and afterload with the final outcome being pump failure. These include
obstructive lesions, arrhythmias, large shunts, myocarditis, cardiomyopathies, ischemic injury
and post-operative low cardiac output syndromes.
Septic shock is defined as “severe sepsis leading to circulatory failure, manifesting as
tachycardia and tachypnea with fever or high leucocyte count and end organ dysfunction”,
according to the international consensus conference of the society of critical care medicine and
the American College of chest physicians2 . Up to 60 % of children with septic shock display
cold shock with decreased CO and elevated SVR. Clinically, these patients will have tachycardia
with initial preservation of blood pressure, with decreased capillary refill and decreased pulses.
About 20% of children have warm shock with low SVR and vasodilation, which will manifest as
tachycardia, decreased blood pressures, bounding pulses and delayed capillary refill. A smaller
percentage will demonstrate a decrease in both CO and SVR.1,2
Distributive or vasodilatory shock: One of the scenarios where this can occur is when
anaphylaxis results in activation of the cytokine cascade leading to an overwhelming loss of
systemic vascular tone and third spacing, culminating in shock. A neurological injury could
result in catastrophic hypotension from acute loss of sympathetic tone. The skin may appear
falsely reassuring being briskly perfused, with warm extremities, bounding pulses and brisk or
flash capillary refill ((<1-2 s). The presence of hypotension and tachycardia or other evidence of
metabolic disturbances, such as persistent lactic acidosis may point to the diagnosis of
distributive shock.
Hemodynamic profiling of cardiogenic shock:
An evolving framework translated from the adult literature is a useful paradigm in managing
pediatric heart failure and shock syndromes. Here patients are profiled hemodynamically, based
on presence or absence of elevated filling pressures/ pulmonary and systemic congestion (wet or
dry) and adequacy of perfusion (warm or cold). Profile A (warm and dry) is the preferred or
normal status, Profile B (warm and wet), Profile C (cold and wet) and Profile L (cold and dry).
Clinical evidence of a “wet profile” includes orthopnea, elevated jugular venous pressure,
accentuated second heart sound, edema and ascites. A “cold” profile would manifest with cold
extremities, mental status changes and narrow pulse pressure or pulsus alternans.
Clinically, Profile B, wet and warm, will present with pulmonary or systemic congestion,
manifesting as tachypnea, tachycardia, hepatomegaly, ascites, edema and elevated jugular
venous pressures, but are adequately perfused. Intuitively, therapy calls for diuretics and
standard medical management.
Profile C wet and cold, will have congestion and poor perfusion and the risk for death, where
need for transplantation greater than the previous profile. These are patients with poor
myocardial function and heart failure leading to shock. They will present with a picture of
pulmonary edema from left ventricular diastolic failure and hypotension from low cardiac
output. Management for this group would be inotropes and (judicious use of) afterload reducing
vasodilators for the “cold” presentation, before diuretics for the “wet” component of pulmonary
or hepatic congestion. In this situation the patient will need to warm up before you can succeed
in drying out. The choice of inotropes will depend on the clinical status of the patient but
milrinone intuitively would be optimal due to its inotropic, lusitropic (improve diastolic
function), and vasodilatory properties. The multicenter PRIMACORP trial demonstrated a clear
decrease in the incidence of post- operative low cardiac output syndrome (LCOS) with milrinone
use.4
Profile L so named to distance itself as a natural continuation of the three prior states is the cold
and dry patient with normal filling pressures but with poor perfusion. This unfortunately is the
most fragile situation where vasodilators though helpful can only be cautiously used with
inotropic support and ultimately may require ventilatory support.
Pharmacotherapy of shock
Table I summarises the sites of endogenous catecholamine receptors and effects of their
activation. In essence, α receptor activation results in vasoconstriction. β1 increases heart rate by
accelerating the sino- atrial node and ectopic pacemakers while enhancing myocardial
contractility while β2 is essentially vaso and broncho dilatory. Dopaminergic activation causes
diuresis and vasodilation.
Types of vasoactive amines
Table II explains the sites of action of select inotropes. Understanding their differential effects is
critical in managing shock.
Epinephrine: By its equally potent effects on all three receptors, epinephrine causes
vasoconstriction, inotropy and vasodilation. Lower dosages have predominantly ß inotropic
effects with α vasoconstriction taking over at higher levels. Clinically epinephrine is best used in
the patient with hypotension, myocardial failure and poor cardiac output and has special use in
patients with warm septic shock and postoperative cardiac surgery. In neonates, higher dosages
may cause irreversible myocardial damage. Note needs to be taken of its side effects which
include hyperglycemia and leukocytosis as well as oliguria in patients with poor renal perfusion.
Norepinephrine: Norepinephrine clearly is the most potent α stimulant vasoconstrictor, with
significant increase in systemic vascular resistance, arterial blood pressure and myocardial
oxygen consumption with minimal effect on contractility or cardiac output. Clinically
norepinephrine is rarely used in pediatric shock unless there is no response to the usual first line
medications. Occasional use maybe in the treatment of hypercyanotic spells of tetralogy of Fallot
due to its impressive effect on increasing the systemic vascular resistance diverting blood
through the dynamically narrowed right ventricular outflow tract. It may be briefly used in
conjunction with a vasodilator in early postoperative myocardial dysfunction
Dopamine: Low dosages (2-5 μg/kg/min) stimulate primarily the dopamine receptor which
increases renal, mesenteric, cerebral and coronary flow but without effect on inotropy or
systemic vasoconstriction. In the mid-range (5-10 μg/kg/min), through its direct ß adrenergic
effects, dopamine increases cardiac contractility without significant effects on heart rate or blood
pressure. Clinically low dose dopamine is best suited for the pediatric patient who has normal
blood pressures with oliguria and increased to medium dose when hypotension or lower heart
rates set in. Dopamine should be used with caution in patients with pulmonary hypertension and
congestive heart failure. Since 30% is protein bound, its efficacy is compromised in children who
are malnourished or have defective hepatic function. In the neonatal heart, the α effects of
dopamine may precede its ß effects due to variable maturation combined with decreased
norepinephrine stores.
Dobutamine: As noted in the accompanying tables, dobutamine stimulates the ß1 receptors
three times as much as it does the α1 and ß2 receptors. Hence its actions will primarily increase
myocardial contractility. Its ability to enhance chronotropy by accelerating the sino atrial node
and atrioventricular conduction is dose related. Dobutamine - “the great balancer”, by its ß2
activities, promotes some vasodilation which cancels out α1 induced vasoconstriction and
establishes balanced peripheral and systemic vascular resistances. This makes it optimal in post-
operative pulmonary hypertensive pediatric patients by not increasing pulmonary vascular
resistances and pressures.
It also facilitates a nice myocardial equilibrium by balancing its inotropic demand with
increasing coronary blood flow. This is achieved by dobutamine not having any action on
dopaminergic receptors which induce norepinephrine, the potent a stimulant coronary
vasoconstrictor.
As a bonus it also improves diastolic relaxation. These attractive features of dobutamine makes
its use preferable in cardiogenic shock and severe congestive cardiac failure To
summarize,dobutamine at doses of 2 to 8 mg/kg/min improves symptoms, increases cardiac
output and stroke volume while decreasing pulmonary capillary wedge pressures without
significant effect on heart rate, systemic and pulmonary vascular resistances. Of note,
dobutamine is less effective than dopamine in raising the blood pressure without enhancing
tachycardia in premature neonates, because of the unique properties of the immature
myocardium.
Isoproterenol: Isoproterenol has limited use in pediatric shock states due to its unfavorable
myocardial demands. However, it does have special use in patients with bradycardia or
atrioventricular block, even in the transplanted heart. It is occasionally used in post- operative
right heart failure states to help maintain heart rate and cardiac output. Its use should be avoided
in left ventricular outflow tract obstructive lesions like subaortic stenosis and hypertrophic
cardiomyopathy as it may potentiate the outflow gradient. It could also exacerbate hypercyanotic
spells in tetralogy of Fallot, because of its effect on reducing systemic resistance. Since it can
decrease diastolic pressure, avoid using isoproterenol in systemic to pulmonary shunts and
severe aortic regurgitation as this could lead to increased aortic runoff and reduced coronary
perfusion in diastole.
Milrinone: Milrinone belongs to a specific class of phosphodiesterase 3 inhibitors (PDEI 3) that
results in increased contractility without an appreciable effect on chronotropy. PDEI 3s are also
 potent peripheral and pulmonary vasodilators. Its ability to reduce pulmonary artery pressure is
through reduction in left ventricular end-diastolic pressure.4
Vasopressin: Arginine vasopressin is a noncatecholamine systemic vasoconstrictor which is
synergistic with the other pressors, and acts by enhancing the sensitivity of the vasculature to
catecholamines.Vasopressin has been shown to help in neonates with post- cardiopulmonary
bypass-vasodilatory shock.5
Levosimendan: Levomisendan belongs to a new category of drugs called calcium sensitizers
which increase myofilament sensitivity to calcium without increasing intracellular calcium
through binding to Troponin C.This leads to increased inotropy and vasodilation without the
increased oxygen consumption, impaired relaxation and tachyarrythmias that elevated calcium in
the cells usually induces.
Nesiritide: Nesiritide works to facilitate homeostasis through counter regulation of the renin-
angiotensin-aldosterone system leading to smooth muscle cell relaxation. In simpler terms, it
promotes vasodilation, natriuresis, and diuresis without significant hypotension.6
Algorithm for management of post-operative low cardiac output states (LCOS)
1) Initial baseline assessment after ensuring airway, breathing and circulation.
2) Cardiopulmonary monitoring of HR, BP, Oxygen saturations, vital signs trends
3) - Laboratory parameters: tissue perfusion markers- ABG- serum pH, base deficit,
bicarbonate, lactate
4) - Monitor for electrolyte imbalances especially calcium, magnesium and glucose. Assess
oxygen utilization via mixed venous saturations which should be > 70 %.
5) - Obtain chest X-ray to evaluate heart size, pulmonary blood flow, pneumoniaconsolidation
and pleural effusions/ pneumothorax.
6) - Echocardiography for cardiac function, pericardial effusion, valvular stenosis or
regurgitation besides assessment of pulmonary artery systolic pressure utilizing the tricuspid
regurgitant jet.
7) - ECG to assess atrio-ventricular synchrony.
8) - Evaluate if there are any significant residual anatomic lesions or surgical complications
necessitating re- operation or cardiac catheterization for diagnosis or intervention.
9) - Assess central venous pressure, pulmonary capillary wedge pressures and cardiac index if
indwelling catheters are available and interpret data based on clinical situation.
10) - Near infra red spectroscopy (NIRS):NIRS is being increasingly used in intraoperative as
well as critical care units for monitoring cerebral and tissue perfusion.
2)Respect hemodynamic principles of maintaining adequate preload, improving contractility and decreasing
afterload besides recognizing pulmonary hypertension and compromised coronary perfusion.
3) Minimize oxygen consumption by treating fever/infection and ensuring adequate sedation and paralysis.
Consider mild hypothermia to reduce the metabolic rate.
4) Maintain CVP appropriate for the lesion, with colloids or crystalloids. - Isotonic saline or colloid boluses
up to 60cc/kg
5) If the shock is unresponsive to fluid challenge, and hypotension is mild (10 -20% decrease in normal
mean arterial pressure for age), start with dopamine as first line inotrope at 5 μg/kg/min under central
venous and arterial monitoring
- if tachycardia persists consider milrinone load with 50 μg/kg IV over 20 minutes and infuse0.25- 0.5
mcg/kg/min or add dobutamine 5-10 μg/kg/min
- If SVR increased in cold and dry shock (profile L) attempt combination therapy with a vasodilator like
milrinone plus inotrope.
6) For fluid refractory- dopamine resistant severe shock (more than 30% decrease in mean arterial pressure)
- Consider epinephrine at 0.05-0.1μg/kg/min for cold shock in combination with vasodilators like milrinone.
Vasopressin in the dose range of 0.0003 to 0.008 units/kg/minute may help as rescue therapy in fluid and
catecholamine refractory shock and post-operative shock.
- Norepinephrine 0.01 -0.2 μg/kg/min for septic warm shock or as a bridge to mechanical support. Use with
caution due to its potent vasoconstrictor effect.
7) For sinus node dysfunction or atrioventricular block, consider isoproterenol (0.01-0.05 μg/kg/min) if
atrial pacing unavailable. Use with caution in hypotensive or hypovolemic states.
8) If persistent fluid and catecholamine resistant shock, consider mechanical support.
Goal should be normalization of capillary refill 1ml/kg/hour, normal mental status and an improving shock
index which is the HR/SBP ratio.7-13

28. RECENT TRENDS IN INTERVENTIONAL CARDIOLOGY

Advances in cardiac catheter based technology, improved understanding of the cardiac anomalies, modern
three-dimensional cardiac imaging tools with echocardiography and computed tomography have contributed
to development of various forms of non-surgical catheter based cardiovascular interventions. Interventions
originated from the days of balloon angioplasty of stenotic vessels by Gruentzig and stenotic valves by Kan
in 1980. Even though balloon atrial septostomy for transposition of great arteries was introduced by William
Rashkind 20 years earlier, it was not considered as beginning of the interventional era due to its palliative
nature. Newer hardware like low profile balloons, stents to keep dilated vessel open, devices used for
closing atrial and ventricular septal defects have shown promising intermediate term results over couple of
decades.
The rewarding results achieved by non-surgical treatment for many congenital heart lesions have
encouraged many centers to adopt these methods and that has increased experience in use of these devices.
The cost of treatment has also substantially reduced due to reuse of balloons, guide wires in developing
countries with effective sterilization strategies. This article will discuss the established indications of
catheter-based interventions, evolving technologies and new hybrid interventions.
Balloon dilation of stenotic valves
Balloon valvotomy works by splitting the fused commissures through circumferential wall stress. Balloon
pulmonary valvotomy (BPV) is the treatment of choice for typical isolated valvar pulmonary stenosis. The
presence of thick, dysplastic and less mobile valves and severe organic subvalvar obstruction portend
disappointing results. Peak echo doppler gradients of 50 mmHg or more is an indication for BPV that carries
a success rate of 98%. Complications like severe infundibular spasm referred as suicidal right ventricle can
be avoided if patients are adequately hydrated during the procedure. Congenital aortic valve stenosis with
gradients more than 50 mmHg can be progressive with a high incidence of sudden death. Valvotomy aims at
reducing the gradients, improving left ventricular function and reducing left ventricular hypertrophy, and
delay ultimate aortic valve replacement. Impaired left ventricular function will be an indication for balloon
aortic valvotomy, even if the gradient across the valve is low. A successful valvotomy is defined as fall in
gradients of more than 50% of pre dilation values. New or increase in aortic regurgitation occurred in 10%
of cases.
Neonatal balloon dilatation
Safety of neonatal pulmonary valvotomy is facilitated by maintaining adequate preprocedural pulmonary
blood flow using infusion of prostaglandin E1 to keep ductus arteriosus open, and use of low profile
polyethylene balloons. In pulmonary atresia with intact ventricular septum, perforation of the atretic valve is
achieved with radio frequency perforation or with the stiff ends of the guide wires. In these neonates, if
hypoplasia and non-compliance of the right ventricle results in poor antegrade flows even after relief of the
gradients, ductal stent with 4 mm coronary stents may help to wean the baby from PGE1 infusions.2 These
ductal stents will be a nonsurgical alternative to a Blalock Taussig shunt that may be needed in these
neonates. Neonatal aortic stenosis is associated with high mortality whatever the mode of treatment. Balloon
dilation can be offered as the initial modality of treatment. The procedural risk is higher if there is
cardiogenic shock at the time of presentation, endocardial fibroelastosis causing severe and persistent left
ventricular dysfunction, hypoplasia of left ventricle and associated cardiac anomaly
Balloon dilation of coarctation of aorta
Balloon angioplasty as the procedure of choice for patients with surgical re-coarctation is generally agreed,
however it is debated in native coarctation of the aorta. This is primarily related to the issues regarding re-
coarctation and aneurysm formation. Balloon size is chosen to the size of isthmus of aorta or descending
thoracic aorta beyond the post stenotic dilatation. Successful dilatation is defined as a residual gradient
below 20 mmHg. The factors, which contributed to suboptimal outcome in 19 % of cases, were higher pre
dilation gradients, isthmus hypoplasia, long tubular obstruction, increasing age and institutional experience.
The late results of balloon dilation in neonates are uniformly poor with a recurrence rate of 80%. Most
centers would opt for surgical resection of neonatal coarctation. Neonatal balloon dilatation is resorted to
only in poor surgical candidates like cardiogenic shock, very severe left ventricular dysfunction, metabolic
acidosis and anuria. The incidence of re-coarctation beyond neonatal period in less than 1 year of age
remains high at around 30% and so is a controversial method of treatment. In coarctation balloon dilated
beyond 1 year of age, recoarctation is very low at 8%. Ballooning is accepted as procedure of choice in
patients of re-coarctation following surgery because previous scar formation at the time of surgery reduces
incidence of aortic rupture and aneurysm formation. Aneurysm formation in the site of balloon dilatation
occurs in about 6% of patients and femoral vascular injury in around 5% of patients.

Stents in native / re-coarctation

Stents may decrease the rate of restenosis by preventing recoil thereby giving good procedural results
(Fig.1). It may also help in preventing acute or sub-acute dissection and prevent aneurysm formation by
providing circumferential support to the wall of the aorta. They have now been used to treat native
coarctation as well as re-coarctation. However the theoretical objection to its use in young age is that the
larger stents cannot be deployed and there is a limit to which the smaller stents, deployed at younger age,
can be re-dilated. Thus surgical removal of the stents may be required while correcting the lesion at a later
age. Once somatic growth is achieved, larger stents can be used which can be dilated up to 18-25 mm. The
chances of aortic rupture is largely minimized by the use of covered stents that are covered with
polytetrafluoroethylene in the past few years and they have increased the indications for interventional
therapy. Research on bioabsorbable magnesium based stents in neonates and young infants are yet to be
converted to clinical practice.
Device closure of atrial septal defects
Interventional therapy in ostium secundum ASD with right atrial and ventricular dilatation is widely adopted
in the absence of associated heart disease that would merit surgical intervention like partial anomalous
pulmonary venous connection and mitral valve disease.3 Sinus venosus, primum ASD, coronary sinus and
the IVC type of ASD are not amenable for device closures. A very careful preoperative evaluation by
echocardiography is very essential for planning the procedure. The defect should have adequate rims of
septal tissue all around separating it from vital structures such as mitral valve, pulmonary veins, coronary
sinus, etc. Patent foramen ovale in patients who have had cerebro-vascular accident due to paradoxical
embolism from venous side (with demonstrable right to left shunting on contrast echocardiography) can also
be closed using current devices. In view of the safety of these devices used for more than 20 years in over
100000 patients, interventional device closure of ASD is now a routine practice. Currently devices find
extended indications and are also used in patients with deficient margins, patients with multiple defects,
associated defects like ventricular septal defects, patent ductus arteriosus, and valvar stenosis (e.g.
Lutembacher syndrome – ASD device closure and balloon mitral valvotomy) that are amenable for
interventional therapy (Fig.2). Another extended indication for device closures are patients with severe
pulmonary hypertension with elevated pulmonary vascular resistance where fenestrated devices are used
and patients under 1 year of age weighing under 10 kg who have heart failure or growth failure.

VSD device closure

A majority of large ventricular septal defects that lead to heart failure in infancy are large and they need
surgical closure. Small to moderate sized defects that allow the infant to reach childhood without significant
heart failure or pulmonary hypertension may lead to persistent left ventricular dilatation, and are at risk of
endocarditis. Such defects merit closure. Inlet and sub pulmonary VSD are not amenable for interventional
therapy since their margins are shared by the tricuspid and pulmonary annulus respectively. A majority of
defects are perimembranous and a small proportion is in muscular location. These are considered for device
closure. Asymmetric nitinol double disc occluder devices have been used to close the perimembranous VSD
without affecting the aortic valve closure mechanism for over a decade in a large number of young patients.
One of the problems with perimembranous devices are early and late occurrence of atrioventricular nodal
conduction disturbances that may manifest as complete heart block, bradycardia or Stokes Adams attacks.
This complication is due to stretch of the infranodal conduction through the bundle of His along the margins
of the defect. Muscular defects are also suited for device closures using symmetric devices. In very small
infants who have muscular defects, per ventricular device closure after sternotomy using a catheter
advanced from the right ventricular anterior wall with avoidance of cardiopulmonary bypass has been
practiced in the recent years.

Coil embolization therapy

Transcatheter embolization with a variety of materials have been used to occlude abnormal channels but
stainless steel or platinum coils have emerged more popular and have assumed an important role in
congenital cardiovascular interventions. They are used in closure of patent ductus arteriosus, aorto
pulmonary collaterals in cyanotic heart diseases, pulmonary arteriovenous malformations, systemic and
coronary arteriovenous fistulae (Fig.3). Stainless steel coils made thrombogenic by inserting dacron strands
along its length used in the past are increasingly replaced with MRI compatible platinum coils since
ferromagnetic stainless steel coils may pose problems with cardiac magnetic resonance imaging evaluation
in future. Coil closure of small to moderate sized ductus arteriosus have been achieved by deployment of
single or multiple coils from either venous or arterial end. The availability of thicker (0.052 “coils) and
multiple coils have substantially simplified coil closure of large PDA.5

Device closure of PDA

Use of embolization coils in patients with large ducts may be complicated by (1) coil migration and
embolism to pulmonary bed or distal aorta and (2) left pulmonary artery stenosis in small children. Nitinol
based duct occluders have replaced coils in moderate to large ducts and are associated with a very high rate
of closure approaching 100% in 3 months. This device has the potential to close ducts even larger than
12mm in size (Fig.4).6 Even though there is a possibility of aortic protrusion in infants weighing less than 5
kg, these devices have been extensively used in these very small infants too.7 New modifications in device
shape and design like Amplatzer duct occluder II and vascular plugs have been used in various ductal
shapes through smaller delivery sheaths in the recent years. With extensive use of these coils and devices in
ducts, surgery seem to be indicated only in the neonates or premature babies with large ducts, where again
interventional therapy is done in experienced centers in many instances

Pulmonary artery and conduit dilatation

Native and postoperative pulmonary artery stenoses are usually not good surgical candidates due to very
high incidence of restenosis. Balloon dilatation and stenting of pulmonary arteries are technically highly
challenging and demanding interventions that need very meticulous planning of the hardware and technique.
After surgical reconstruction of right ventricle to pulmonary arteries using homografts and xenograft
conduits in various forms of cyanotic heart diseases, including tetralogy, pulmonary atresia, truncus
arteriosus and double outlet right ventricles, the conduits degenerate over time and lead to stenosis and
calcification as age advances. Conduits may also become inadequate due to smaller luminal diameter.
Conduit change will necessitate redosternotomy through the mediastinal adhesions. Balloon dilatation and
stenting hence will offer a valuable nonsurgical palliation since it may effectively postpone conduit
replacement. The distal conduit anastamosis is prone for stenosis due to fibrotic strictures and are effectively
relieved by balloon dilatation.

Atrial septostomy
Balloon atrial septostomy, a neonatal intervention done to improve intercirculatory admixture in
transposition of great vessels with an intact inter-ventricular septum before surgical correction has been in
clinical practice for nearly 5 decades. Specially designed balloon tipped septostomy catheters are used for
these purposes; these procedures are done in many neonatal ICU without fluoroscopy and under echocardio
graphic guidance. The procedure enlarges an already existing patent oval foramen and increases mixing of
blood, thus allowing more saturated blood to reach the systemic circulation. The effective pulmonary blood
flow is also increased because of right to left flow. In patients with transposition and large VSD and/or
PDA, balloon atrial septostomy relieves symptoms of heart failure by reducing the elevated left atrial
pressure created by the large pulmonary blood flow. In spite of reports that septostomy may increase
particulate and thromboembolism to the brain and potentiate left ventricular early regression, it stabilizes
patients before the arterial switch operation. A successful septostomy gives an arterial saturation of 75% or
more and less than 2mm Hg gradient across the atrial septum. In a small percentage no improvement in
mixing occurs for unexplained reasons in spite of adequate septostomy. In patients with rigid interatrial
septal tissues, more aggressive interventions like blade atrial septostomy using 10-15 mm blades, static
dilatation of interatrial septum using larger balloons is utilized, often in univentricular palliations with
associated stenosis or atresia of one of the atrioventricular valves.

Neonatal stenting of ductus arteriosus

In neonates with pulmonary atresia and critical right ventricular outflow tract obstruction, ductus arteriosus
may be the main source of pulmonary blood flow to maintain systemic oxygenation. In these neonates, the
natural duct closure that occurs in the first week may lead to calamitous drop in oxygen saturation that leads
to severe acidosis and death. These neonates are maintained on PGE1 infusion till they are operated upon
with a BT shunt. These surgeries in smallest of the neonates are morbid with chances of pulmonary over and
under circulation, ventilatory dependency, shunt thrombosis and other neonatal complications. Transcatheter
ductal stenting with coronary 4 mm stents will circumvent many of the problems of thoracotomy and may
provide a less morbid alternative especially in the compromised neonate.2 Larger stents are used in the
patients with duct dependent systemic circulation as in hypoplastic left heart syndrome, since the systemic
circulation is dependent on these ducts.

Post operative interventions

In view of the complexity of congenital cardiac surgical procedures, there are increasing recognition of
postoperative residual hemodynamically significant defects.8 Redo surgery to correct many of them will be
technically be more challenging and demanding. Table I details a large group of postoperative interventions
utilizing off-label uses of the occluder devices, stents and coils that are done to palliate these patients from
their hemodynamic disturbances.

Hybrid interventions
The bottleneck of application of interventional techniques in the smaller neonates and young infants is the
ability to have a safe vascular access to the heart to be able to deliver the occluder devices and stents in the
desired locations.9 Hybrid surgical techniques are performed with ease since the heart is directly exposed
after pericardial opening after sternotomy. Utilizing the advantages of sternotomy, introducer sheaths are
directly placed after placing purse string sutures on the right ventricular anterior free wall or anterior wall of
the main pulmonary artery. Under fluoroscopic guidance, guide wires and short sheaths are introduced
through muscular ventricular septal defects and branch pulmonary arteries. Once the sheath positions are
confirmed, devices can be placed across muscular ventricular septal defects for per ventricular device
closures (Fig.5). Similar placements of devices in atrial septum are referred as peratrial device closures.
Branch pulmonary artery stenosis can be dealt with direct stenting through sheaths placed across the main
pulmonary artery. These hybrid techniques avoid cardiopulmonary bypass in the smaller neonates and
infants and circumvent systemic side effects of extra corporeal circulation. Some surgical procedures like
Norwood stage I surgery in hypoplastic left heart syndromes associated with very high mortality and
morbidity are considerably simplified by adopting hybrid approach by avoiding cardiopulmonary bypass
and performing ductal stenting in the catheterization laboratory.1 These children grow for few months
before an extensive stage II surgery.

29. TIMING OF SURGERY FOR COMMON CONGENITAL HEART DEFECTS

Surgery remains the mainstay for most congenital heart defects (CHD), although many simpler CHD’s can
today be treated by nonsurgical catheter based interventions. Optimal results can be obtained with surgery
only if it is at an appropriate time in the natural history of the defect. Guidelines for management are
important for decision-making, however each patient needs to be evaluated on an individual basis. A
prerequisite for any management plan is an accurate anatomic and pathophysiologic diagnosis, which
ideally should be confirmed by a pediatric cardiologist. A surgical plan should then be made in conjunction
with the surgeon who is likely to do the surgery. It is not recommended that the treating pediatrician take a
decision on the treatment plan for any CHD in isolation, lest a disastrous error in the timing of intervention
occur.
Broad guidelines on optimal timing of intervention are given in Table I. These are presented keeping the
Indian scenario in mind and guided by current practice in the active pediatric cardiac units.
CRITICAL CARE
30. ACUTE EXACERBATION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
Rajesh Chawla,
Consultant Physician and Intensivist,
Indraprastha Apollo Hospital, Delhi
I. WHEN TO SUSPECT/ RECOGNIZE?
a) Introduction:
Chronic obstructive pulmonary disease (COPD) refers to a group of disorders characterized by chronic
airflow obstruction/limitation. The airway obstruction is persistent and largely irreversible. It includes two
distinct pathophysiological processes - chronic bronchitis and emphysema. Acute exacerbations of these
disorders occur during the natural history of progression of this disease. Exacerbations are frequent, more so
during winter, resulting in progressive loss of the functional capacity of the lungs leading to progressive
dyspnea.
b) Case definition:
For both situations of care (mentioned below*)
There are many definitions for what represents an acute exacerbation of COPD. One of the most widely
used definitions evaluates the severity of exacerbation based on three symptoms:
i. worsening dyspnea
ii. increase in sputum purulence
iii. an increase in sputum volume

Type I exacerbation (severe) have all three symptoms and Type 2 exacerbations (moderate) exhibit two of
three symptoms. Type 3 exacerbation (mild) include one of the symptoms and at least one of the following:
upper respiratory tract infection within the past 5 days,fever without apparent cause, increased wheezing,
increased cough, or a 20% increase in respiratory rate or heart rate over baseline.
II INCIDENCE OF THE CONDITION IN OUR COUNTRY
COPD is currently the fourth leading cause of death worldwide behind cardiovascular disease,cancer and
cerebrovascular diseases. The Global Burden of Disease Study estimated that in 1990, the worldwide
prevalence of COPD was 9.34 per 1000 men and 7.33 per 1000 women. Depending on the severity of the
disease, the 5-year mortality rate for patients with COPD varies from 40%to 70%. The three major causes of
death have been identified as COPD itself, lung cancer and cardiovascular disease. 3
The prevalence rates of COPD in males varied from 2.12% to 9.4% in studies conducted in north India and
from 1.4% to 4.08% in south India. The respective ranges for females were 1.33%–4.9% in north India and
2.55%– 2.7% in south India. A majority of cases with chronic COPD (57.4%) were found to suffer from a
mild form and only 16% had severe COPD.
A large-scale study in Hyderabad city and its surrounding municipalities, covering a population of more
than 54 lakh and 28 hospitals/health posts, was done in 2001 to collect cause-specific morbidity data. The
rates of hospital admissions of cases with COPD showed an age differential. While the rate was
47.84/100,000 persons at the community level, it was 57.28 for those 18–64 years of age and 546.17 for
those above 65 years of age. Treatment cost of a patient with COPD per year (in Rs)· according to
Guidelines is Rs 2126 for moderate to severe disease and Rs 10,538 for acute exacerbation.
III DIFFERENTIAL DIAGNOSIS
Acute exacerbation of COPD should be differentiated from the following disorders
1. Congestive cardiac failure
2. Bronchial asthma
3. Bronchiectasis
4. Interstitial lung disease
5. Chronic thromboembolic pulmonary disease
6. Obesity induced dyspnea
7. Chronic destructive lung disease due to old tuberculosis
8. Occupational lung disease

IV PREVENTION AND COUNSELING

Avoidance of smoking is the single most important factor in prevention of exacerbation of COPD. Yearly
influenza vaccine and 5 yearly Pneumococcal vaccine has also been found to be helpful. Education
regarding starting early antibiotics with evidence of exacerbation. Avoidance of pollution is advisable Early
consultation with physician should be strongly encouraged and patient should be educated about the
warning signs of acute exacerbation.
V OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,
TREATMENT & REFERRAL CRITERIA
*Situation 1: At Secondary Hospital/ Non-Metro situation: Optimal Standards of Treatment in
Situations where technology and resources are limited
a) Clinical Diagnosis:
Patient usually presents with a history of chronic cough and exertional breathlessness with recent increase in
cough,breathlessness, increased volume and purulence of sputum. There are usually associated
constitutional symptoms like fever, malaise and lack of appetite. Patient may be orthopneic and have
swelling of feet,
On examination there is increase in respiratory rate, tachycardia, flapping tremor and drowsiness ( if
retention of carbon dioxide) . Some patients who have predominant chronic bronchitis show features of
chronic corpulmonale (Blue Bloaters) like pedal edema, raised jugular venous pressure, puffy face, central
cyanosis, loud pulmonary heart sound and parasternal heave due to right ventricular hypertrophy. On the
other patient with predominant emphysema (Pink Puffers) are usually thin built, plethoric due to associated
secondary polycythemia, disproportionately dyspneic, features of hyper-inflated lungs like obliteration of
liver and cardiac dullness, silent chest.
b) Investigations:
1. Chest Xray – To rule out Pneumothorax. Look for consolidation, pleural effusion,cardiomegaly and
features of lung hyperinflation.Look for features of past tuberculosis
2. Pulse Oximetry
3. Sputum for gram stain, Culture and sensitivity, Acid Fast Bacilli stain.
4. Hemogram, blood urea, serum creatinine, serum electrolytes
5. Electrocardiogram

c) Treatment:
Oxygen therapy: Controlled humidified oxygen therapy with a Venturi mask (fixed performance device) or
low oxygen flow (1-2 litres) with nasal cannula or simple face mask (variable performance device) to keep
Spo2 90-92%. Higher oxygen saturation and high concentration of inspired oxygen should be avoided.
Bronchodilators:
Nebulised beta 2 adrenergic receptor agonists (salbutamol) in patients who are very dyspneic – 2.5-5 mg
nebulised every 4-6 hours and as necessary. Watch for tachycardia or arrhythmias
Inhaled beta 2 adrenergic receptor agonists in patients who are able to take metered dose inhalers (180 mcg)
every 2-4 hours
Nebulised anticholinergic agent (ipratropium bromide) 0.5 mg every 4-6 hrs
Inhaled Ipratropium bromide 18-36 mcg every 2-4 hours
Corticosteroids: Five to 10 days of oral or intravenous corticosteroids is advocated in most cases.
Prednisolone 40-60 mg orally or methylprednisolone 60-120 mg intravenously may be used. Appropriate
stress ulcer prophylaxis with Ranitidine or Proton Pump inhibitors should be started. Inhaled corticosteroids
may be added later when patient has stabilized.
Antibiotics: The most common organisms identified in acute exacerbation are Streptococcus pneumonia,
moraxellacatarrhalis and hemophilus influenza.In patients with more severe and recurrent disease gram
negative organisms like Klebsiella pneumonia and Pseudomonas aeruginosa should also be considered.
Initial antibiotic choice is empirical. Usually a macrolide antibiotic like azithromycin or clarithromycin or a
quinolone like levofloxacin or moxifloxacin is given. Broader spectrum antibiotics are used for severe
disease.
Methylxanthines like aminophylline. Though commonly used in India but given the frequent and severe
side effect profile,narrow therapeutic window and lack of evidence demonstrating improved outcomes
routine use of these agents is not recommended
There is no role of mucolytic or chest physiotherapy commonly used practices in acute exacerbation of
COPD.

d) Referral criteria:
Following category of patient should be referred to higher centre.
1. Patient who will benefit from non invasive ventilation and if this facility is not available in the
primary centre
2. Patients in need for intubation and mechanical ventilation
3. Patient with hemodynamic instability
4. Patient not responding to maximal medical treatment
5. Patient with acute exacerbation complicated by associated pneumonia,pneumothorax.
6. Patient in whom diagnosis is uncertain and needs further investigation.

*Situation 2: At Super Specialty Facility in Metro location where higher-end technology is available
a) Clinical Diagnosis: As in situation 1
b) Investigations:
1. Arterial Blood gas analysis – look for hypercarbia and respiratory acidosis
2. Echocardiogram- Low ejection fraction
3. D DIMER, Pro BNP – bio markers for venous thromboembolism and congestive cardiac failure
respectively
4. CT scan of Chest – look for other pulmonary disease, pulmonary thrombus
5. Venous Doppler of legs- to rule out deep venous thrombosis
c) Treatment:
1. Noninvasive ventilation should be applied simultaneously to a patient in acute respiratory failure in
addition to the rest of the treatment based on the clinical criteria, provided there is no contraindication
2. Non-invasive Positive Pressure Ventilation (NIPPV) is indicated in patients with appropriate
diagnosis with potential reversibility and if patient has any two of the following clinical criteria are fulfilled.
3. Moderate to severe respiratory distress
4. Tachypnea, (RR more than 25 / min)
5. Accessory muscle use or abdominal paradox
6. Blood gas derangement pH < 7.35, PaCO2 > 45 mm Hg
7. PaO2 / FiO2 < 300 or SPO2 < 92% with FiO2 0.5
CONTRAINDICATIONS
There are no absolute contraindications for the use of NIPPV. Some contraindications have, however, been
suggested
1. Non-availability of trained medical personnel
2. Inability to protect the airways -Comatose patients, patients with CVA or bulbar involvement,
confused and agitated patients. Upper airway obstruction
3. Hemodynamic instability- uncontrolled arrhythmia, patient on very high doses of inotropes, recent
myocardial infarction.
4. Inability to fix the interface -Facial abnormalities, facial burns, facial trauma, facial anomaly.
5. Severe GI Symptoms – vomiting, obstructed bowel. Recent GI Surgery., Upper G.I. Bleed
6. Life threatening hypoxemia
7. Copious secretions
8. Conditions where NIPPV has not been found to be effective

Protocol for application of NIPPV For successful noninvasive ventilation.

a) Patient interface –Nasal or oronasal mask
b) Mode of ventilation:
1) Bi-level positive airway pressure--Spontaneous or spontaneous timed mode in portable pressure
ventilators or NIV option on conventional ventilators
2) Pressure support /Pressure control /Volume control – conventional ventilators
c) Ventilator settings
Explain therapy and its benefit to the patient in detail. Also discuss the possibility of intubation.
a) Choose the correct size interface. Oronasal mask in acute respiratory failure is preferred.
b) Set the NIPPV portable pressure ventilator in spontaneous or spontaneous /timed mode. ,
c) Start with very low settings. Start with low inspiratory positive airway pressure (IPAP) of 6 – 8 cm H20
with 2 to 4 cm H20 of EPAP (Expiratory positive airway pressure). The difference between IPAP and EPAP
should be at least 4 cm H20.
d) Administer oxygen at 2 liters per minute.
e) Hold the mask with the hand over his face. Do not fix it.
f) Increase EPAP by 1-2 cm increments till all his inspiratory efforts are able to triggers the ventilator.
g) If the patient is making inspiratory effort and the ventilator does not respond to that inspiratory effort, it
indicates that the patient has not generated enough respiratory effort to counter auto PEEP and trigger the
ventilator (in COPD patients). Increase EPAP further till this happens. Most of the patients require EPAP of
about 4 to 6 cm H2O.Patient who are obese or have obstructive sleep apnea require higher EPAP.
h) When all the patient’s efforts are triggering the ventilator, leave EPAP at that level.
i) Now start increasing IPAP in increments of 1-2 cm up to a maximum pressure, which the patient can
tolerate without discomfort and there is no major mouth or air leak.
j) In some NIPPV machine, inspiratory time (Ti) can be adjusted. Setting the Ti at one second is a
reasonable approach.
k) Now secure interface with head straps. Avoid excessive tightness. If the patient has a nasogastric tube put
a seal connector in the dome of the mask to minimize air leakage.
l) After titrating the pressure, increase oxygen to bring oxygen saturation to around 90%.
m) As the settings may be different in wakefulness and sleep, readjust them accordingly.
When NIPPV is being initiated for acute respiratory failure, close monitoring and the capability to initiate
endotracheal intubation and other resuscitation measures should be available in the same setup. Start NIPPV
preferably in the ICU or in the emergency room in acute respiratory failure.

Application of NIPPV using a Critical Care Ventilator

a) The first step is to select a ventilator, which is capable of fulfilling the needs of the patient.
b) Explain the therapy to the patient
c) Choose the appropriate mode. Usually pressure support or pressure control modes are preferred. Standard
critical care ventilators using flow by system ( non invasive mode option ) allow the patient to breathe
without expending effort to open valves. In selected patients like those suffering from neuromuscular
diseases, volume assist or volume control mode may be used.
d) Choose an appropriate interface
e) Silent ventilator alarms
f) Keep FiO2 0.5

Using pressure support/control approach

1. Start with low settings like inspiratory pressure support at 5-6 cm H2O and PEEP at 2 cm H2O.
2. Initiate NIPPV while holding the mask in place and confirm optimum fit. If it is big or small or
loose, change it.
3. Hold the mask .do not fix the headgear
4. Now increase PEEP till all his inspiratory efforts are able to triggers the ventilator
5. If the patient is making inspiratory effort and the ventilator does not respond to that inspiratory
effort, it indicates that the patient has not generated enough respiratory effort to counter auto PEEP and
trigger the ventilator (in COPD patients). Increase PEEP further till this happens.
6. Once the patient’s all inspiratory efforts are triggering the ventilator then start increasing pressure
support further, keeping certain patient’ comfort in mind. (Reduce respiratory rate, reduced use of accessory
muscle etc. Ensure that there are no major leaks.
7. When there is significant mouth leak, there may be asynchrony. In that case, pressure control will be
the preferred mode of NIPPV and one can set up the inspiratory time to avoid asynchrony.
8. After adequate ventilation has been achieved, increase fraction of oxygen concentration to maintain
Oxygen saturation more than 90%.
9. Secure interface with headgear. It should be tight, but not over-tight. Small leaks are acceptable
10. A peak inspiratory pressure more than 25 cm is rarely required in COPD, but higher pressures can be
used when using NIPPV for other indications. PEEP is usually titrated between 5-10 cm H2O to improve
triggering and oxygenation.
Patient must be monitored very closely clinically. Look for sensorium,dyspnoea, respiratory rate ,respiratory
distress, use of accessory muscles, abdominal paradox, Mask comfort and vital signs pulse , blood pressure,
ECG monitoring and arterial oxygen saturation, All this must be documented every 15 minutes for the first
hour in the clinical notes. Patient will show improvement in parameters if NIPPV is effective. Arterial blood
gas sample should be sent after 30mts to 1 hr after the application of NIPPV. In ventilator setting look for
air leaks and patient–ventilator interaction.
Monitoring of noninvasive ventilation for acute respiratory failure
Subjective
1. Mask comfort
2. Tolerance of ventilator settings
3. Respiratory distress
4. Physical findings
5. Respiratory rate
Other vital signs
1. Accessory muscle use
2. Abdominal paradox
3. Ventilator parameters
4. Air leaking
5. Adequacy of pressure support
6. Adequacy of PEEP
7. Tidal volume (5–7 mL/kg)
8. Patient-ventilator synchrony

Gas exchange
1. Continuous oximetry (until stable)
2. ABGs, baseline and 1–2 hrs, then as indicated
Initially give NIPPV continuously or as long as possible. Once patient is tolerating periods off NIPPV, start
discontinuing during day time and give during nighttime. In two to three days patient can be weaned off
from the NIPPV.

1. Those who have failed NIV trial.

2. Those who have contraindications of NIV
3. Excessive secretions
4. Hemodynamic instability
5. Extreme obesity

1. Initial Ventilator settings in COPD patient should take into account patients need for prolonged
expiration. Appropriate initial ventilator settings would be volume assist control, Tidal volume 8 ml/kg
predicted body weight, rate 10-12/min, PEEP of 0-5 cm f H2O , FiO2 titrate for SpO2 90-92 % . High peak
flow 70-90 L/min to keep I:E ratio 1:4 or more .
2. Attempt should not be made to attain normal blood gas but to aim for patient’s baseline values.
3. Monitor for development of auto PEEP by end expiratory manouever or analyzing ventilator
graphics.
4. Judicious use of sedation and analgesia should be tried
5. Neuromuscular blockers should be avoided
6. Deep venous thrombosis prophylaxis, Stress ulcer prophylaxis and nutritional needs should be
addressed.

31. ACUTE SEVERE ASTHMA

WHEN TO SUSPECT/ RECOGNIZE?

Introduction:

It is a chronic inflammatory disease of the airways characterized by airway hyper reactivity and
inflammation, bronchoconstriction and mucus hyper-secretion. Asthma is associated with considerable
patient morbidity, a diminution in productivity and increase in health care utilization.
Case definition:
For both situations of care (mentioned below*)
Acute severe asthma or status asthmaticus is defined as a prolonged episode of severe asthma that is
unresponsive to initial standard medical therapy and may lead to respiratory failure.
The episode may be rapid in onset (in a matter of hours) or more typically progress during several hours to
days. The former is referred to as asphyxic asthma and occurs in a minority of cases.
INCIDENCE OF THE CONDITION IN OUR COUNTRY
The estimated prevalence of asthma in India is 2468 per 100,000 population. Prevalence of acute asthma in
age group 15-59 was found to be 40 per 1000,000 populations in India. Prognosis of asthma in general is
good but 10-20% of patents continue to have severe attacks throughout their lives. Approximately 10% of
patients hospitalized with asthma are admitted to the intensive care unit and 2% are intubated. Mortality rate
ranges from 0.5-3% in hospitalized patients.

DIFFERENTIAL DIAGNOSIS
The following should be should be considered in patients with severe breathlessness
1. Upper airway obstruction
2. Epiglottitis
3. Vocal Cord Dysfunction
4. Foreign Body aspiration
5. Congestive heart failure

V. PREVENTION AND COUNSELING

Morbidity and mortality from asthma disproportionately affects the economically disadvantaged, due to
prehospital factors such as access to health care, inadequate preventive therapy or delay in seeking medical
treatment
Rapid onset asthma is often triggered by exposure to allergens, irritants, exercise, psychosocial stress, and
inhaled illicit drugs. It may also develop after exposure to aspirin, non steroidal anti-inflammatory drugs, or
beta blockers in susceptible individuals. Asthma attacks may be triggered by viral or atypical pulmonary
infections.
Proper counseling regarding prevention of allergen or precipitating factors should be done. Compliance with
anti asthmatic drugs should be ensured and education in its proper use should be done. Early consultation
with physician during acute attack is advocated.
VI. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT & REFERRAL
CRITERIA

History and Physical Examination

Clinically patients present with dyspnea, cough, chest tightness and wheezing . Severity of asthma may be
assessed by the following
1. Unable to speak full sentences
2. Increased Respiratory rate
3. Use of accessory muscle
4. Increased Pulse rate
5. Pulsus paradoxus ( Inspiratory decrease in systolic blood pressure)
6. Decrease in sensorium, fatigue
7. Auscultation: Wheezes and crackles; silent chest signifies very severe airflow obstruction

b) Investigations:
1. Peak expiratory flow rate (PEFR) is an objective measure of airflow obstruction: <30% of
baseline/predicted would indicate likelihood of respiratory failure. Initially check every half hour to assess
response to therapy
2. SPO2: Hypoxia is usually correctable with supplemental oxygen. Refractory hypoxia should trigger
search for pneumothorax, atelectasis, pneumonia or occult sepsis.
3. Chest x-ray; To rule out pneumothorax, look for degree of hyperinflation, or any lung infiltrate
suggestive of atelectasis or collapse consolidation.

c) Treatment:
Initial medical management
1. Oxygen supplementation is continued to keep Spo2 more than 90%.
2. Nebulized salbutamol 2.5 mg (0.5 ml of 5% solution in 2.5 ml saline) or levosalbutamol, repeat
every 20 mins for 3 doses then less frequently dictated by patent’s clinical response.
3. More frequent and even continuous nebulization of salbutamol at a dose of 10 to 15 mg can be used
within limits of toxic effects such as tachycardia and tremors.
4. Ipratratropium 0.5 mg nebulization every 20 mts should be included in initial treatment
concomitantly with salbutamol for better bronchodilatation
5. If nebulizer is not available use 4 puffs of salbutamol MDI through a spacer device. Treatment
concomitantly with salbutamol for better bronchodilatation
6. Cortcosteroids should be initiated at the earliest to prevent respiratory failure.. The usual doses are:
Inj Hydrocortisone 100 mg every q 6 hourly or methylprednisolone 60-125 mg q 6-8 hourly. Oral
prednisolone 60 mg is equally effective.
7. Aminophylline may be used as a second-line agent although its role is much debated. A loading dose
of 5-6 mg/kg is followed by a continuous infusion of 0.6 mg/kg/hr. Avoid loading dose in case patient has
been on oral theophyllines earlier.
8. Antibiotics are not required routinely in bronchial asthma exacerbation and should be given only if
there is evidence of infection. Quinolones or macrolide may be used only if there is evidence of infection,
though most of these are viral in origin.

d) Referral criteria:
The following patients should be referred to higher centre as they have a probability of developing
respiratory failure and respiratory arrest.
1. Breathless at rest inspite of bronchodialtaors
2. Pulsus paradoxus > 25 mm Hg
3. Peak expiratory flow < 60% predicted
4. Oxygen saturation < 90%
5. Patient getting drowsy or confused
6. Bradycardia (<60/min)
7. Severe work of breathing and fatigue.

e) Investigation:
1. Arterial blood gases: In asthma normal or elevated PaCO2 signifies respiratory failure due to
respiratory muscle fatigue. pH < 7.28 would raise the need for ventilatory support
2. Doppler Echocardiogram – to rule out cardiac cause of breathlessness

f) Treatment:
1. Non-Invasive Ventilation: inspite of medical treatment if respiratory status worsens NIV may be
tried as a temporizing measure. IPAP reduces work of breathing and EPAP overcomes auto PEEP. Extended
trials of NIV may be warranted if the sensorium and patient comfort are improving. NIPPV is more useful
in patients with COPD; there is limited data on its use in acute severe asthma.
2. Monitor respiratory rate, SPO2, heart rate and blood pressure continuously. Reassess every 30 mins
until patient is stable and comfortable. Nursing attendance should be continuous.
3. Intubate if indicated
o Impending respiratory arrest
o Hypotension
o Altered sensorium: progressive drowsiness, agitation or severe restlessness
o In a conscious patient no improvement or deterioration after 3-4 hours of optimal medical therapy and
NIV support
o PCO2> 55 mmHg and Ph < 7.28. However more than the absolute values the general appearance and
degree of distress and fatigue of the patient are important.
4. Orotracheal intubation: As far a possible a tube size of 8 or more is employed and therefore
orotracheal route is preferred
5. Sedation and paralysis: At the time of intubation short acting sedative or anaesthetic such as
ketamine, propofol or midazolam and short acting neuromuscular blocking agent (succinylcholine or
rocuronium) are used. For maintenance of sedation to assist MV midazolam/ propofol infusion can be used.
Neuromuscular blocking agents should be avoided as infusion to prevent critical illness neuropathy.
6. Initial ventilator settings
Setting Recommendation
Respiratory rate 10-15 breaths/rain
Tidal volume 8-10 ml/kg
Minute ventilation 8-10 l/min
PEEP 0 cm H2O
Inspiratory flow ≥100 l/rain
I:E ratio ≥1:3
FiO2 1.00
The goals of ventilation are to
7. Maintain oxygenation (SpO2 > 90%)
8. Reduce work of breathing
9. Minimise auto-PEEP
10. Accept hypercarbia, do ont increase respiratory rate and tidal volume to reduce PaCO2 if it increases
auto-PEEP

Monitor: Hypotension is usual after mechanical ventilation due to dehydration,use of sedative and
intrinsic PEEP . It should be managed by giving fluid challenge

airway pressure reflects only proximal airway pressure and is generally high.

usion over 20 mins can also be tried in refractory cases although its role is
unproven.

Liberation from mechanical ventilation:

o Once the airway resistance decreases as reflected by decrease in Pplat and hypercarbia, spontaneous
breathing is then allowed by discontinuing paralysis and deep sedation.
o PEEP may be titrated cautiously to counteract auto PEEP for easier triggering
o The patient is given spontaneous breathing trials with a T-piece or low CPAP (equal to or less than 8 cm
H2O). After 30 -120 mins, if the trial is successful the ventilator is withdrawn.
o In the event of failure of the trial, the patient is placed on assist-control or Pressure support modes. While
on spontaneous breathing a PEEP of 5-8 cmH2O may be applied to reduce inspiratory threshold load
imposed by PEEP.
o Further attempts at liberation are carried out after 24 hours to allow for return of diaphragmatic function.
 Supportive Therapy. Adequate DVT prophylaxis and stress ulcer prophylaxis is mandatory in these
patients. Adequate nutrition support with less carbohydrate proportion to decrease CO2 production in COPD
patient is desirable.

32. ACUTE RESPIRATORY FAILURE

WHEN TO SUSPECT/ RECOGNIZE?

Introduction:

Respiratory Failure includes any condition that affects breathing and ultimately results in failure of the lungs
to function properly. The main tasks of the lungs and chest are to get oxygen into the bloodstream from air
that is inhaled (breathed in) and, at the same to time, to eliminate carbon dioxide (C02) from the
bloodstream through air that is exhaled (breathed out). In respiratory failure, either the level of oxygen in
the blood becomes dangerously low, and/or the level of C02 becomes dangerously high.

Case definition:
Respiratory failure is defined as a failure of gas exchange manifestedeither as hypoxemia (PO2 <60mm Hg
on room air) i.e. inadequate blood oxygenation or hypercapnia (PaCO2>45 mm Hg) i.e. excess of
circulating carbon dioxide or frequently a combination of both types of gas exchange abnormalities.
Practically/ clinically diagnosed as respiratory fatigue.

INCIDENCE OF THE CONDITION

The problem in US
1. 360,000 cases per year
2. 137 cases per 100,000 population
3. With 36% failing to survive the hospitalization
The problem in India: not known but respiratory failure is a common occurrence either as a complication of
other diseases or as a terminal event

DIFFERENTIAL DIAGNOSIS/ TYPES:

Type 1
Type 1 respiratory failure is defined as hypoxemia without hypercapnia, and indeed the PaCO2 may be
normal or low. The basic defect in type 1 respiratory failure is failure of oxygenation characterized by:
failure is failure of low (< 60 mmHg (8.0
oxygenation characterized kPa) on room air
by: PaO2
PaCO2 normal or low

This type of respiratory failure is caused by conditions that affect oxygenation such as:
1. Parenchymal disease (V/Q mismatch)
2. Diseases of vasculature and shunts: right-to-left shunt, pulmonary embolism
3. Interstitial lung diseases: ARDS, pneumonia, emphysema.

Type 2
The basic defect in type 2 respiratory failure is characterized by:
PaO2 decreasd
PaCO2 increasd

Type 2 respiratory failure occurs as a result of alveolar hypoventilation and results in inability to effectively
eliminate carbon dioxide.
The commonest cause of type II respiratory failure is COPD.
Other causes are:
1. Impaired central nervous system drive to breathe
1. Drug over dose
2. Brain stem injury
3. Sleep disordered breathing
4. Hypothyroidism

2. Impaired strength with failure of neuromuscular function in the respiratory system

1. Myasthenia Gravis
2. Guillian Barre Syndrome
3. Amyotrophic Lateral Sclerosis
4. Phrenic nerve injury
5. Respiratory muscle weakness secondary to myopathy,electrolyte imbalance, fatigue

3. Increased loads on the respiratory system

 1. Resistive-bronchospasm (Asthma ,Emphysema, Chronic Obstructive Pulmonary Disease)
2. Decreased lung compliance-Alveolar edema, Atelectasis, Auto peep
3. Decreased chest wall compliance- Pneumothorax, Pleural effusion, Abdominal distension
4. Increased minute ventilation requirement- pulmonary embolism by increase in dead space
ventilation, sepsis and in any patient with type I respiratory failure with fatigue.

Type 3 and 4 occur in setting of perioperative period due to atelectasis and muscle hypoperfusion
respectively.

PREVENTION AND COUNSELING

Treatment of underlying disease.

OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT & REFERRAL
CRITERIA
Clinical Diagnosis:

Dyspnoea at rest, tachypnoea, tachycardia, hypertension, nasal flaring, pursed lip breathing, using accessory
muscle of respiration.Evidence of central / peripheral cyanosis, asterexis or severe drowsiness in case COPD
is feature of severe hypercapnia

Investigations:

Pulse oxymetric assessment of SpO2 to assess blood oxygen content / hypoxia.

Chest x-ray:Details regarding evidence of consolidation, pulmonary edema, COPD and various other
pathology
Complete blood count, electrolytes
Electrocardiogram

Treatment:

Oxygen therapy:
In the hypoxic self-ventilating patient, delivery of oxygen to the alveoli is achieved by increasing the
environmental oxygen fraction (FiO2), which involves application of supplemental oxygen.
Oxygen therapy will suffice if muscle strength or vital capacity is reasonable and upper airway is not
compromised.
Pulse oxymetry is used to quickly titrate to the preferred levels of oxygen administration
Various oxygen delivery devices:
1. Variable performance:
Nasal cannula delivers oxygen at low gas flow 1-6lpm with FiO2 from 21-44 %. Best device for patient
with high PCO2as no rebreathing.
Face maskdelivers oxygen at low gas flow 6-10lpm with FiO2 upto 50%.
Nonrebreathingface maskwith reservoir bag delivers oxygen at flow rates 9-15 lpm with FiO2 from 85-90%.
Delivery of oxygen is dependent on the patient inspiratory flow rates.
2. Fixed performance:

1. Venture type mask –ensures fixed FiO2 above fixed flow.

2. Nebulised bronchodilators to relieve bronchospasm
3. Appropriate early antibiotics in case of pneumonia or in case of infective exacerbation of COPD or
antimalarials or antivirals as per case requirement.
4. IV steroids for acute exacerbation of COPD or bronchial asthma.
5. IV diuretics for acute pulmonary edema.

Referral criteria:
1. Need for invasive mechanical ventilation in cases of worsening hypoxemia or respiratory muscle
fatigue in spontaneous breathing patient or on NIV.
2. (Non-invasive ventilation in secondary care hospitals to be offered only if backed up by invasive
mechanical ventilation)
3. Need for non-invasive ventilation for worsening hypercapnic respiratory failure in COPD patients.
4. Unable to wean the patient off the ventilator in 48-72 hrs in small set up.
5. Need for specialized treatment.

Investigations:
1. Arteial blood gas analysis
2. Echocardiogram
3. Lung Function test (Spirometry)
4. Ventilation Perfusion Scan
5. CT scan of Chest
6. Other investigations to look for underlying cause of respiratory failure
Treatment:

Non invasive positive pressure ventilation or CPAP:

Using a comfortable reasonably tight nasal or full face mask with ventilators used in cases of hypercapnic/
type II respiratory failure like COPD, sleep apnoea, bronchial asthma and hypoxemic respiratory failure as
in acute cardiogenic pulmonary edema.
Mechanical ventilation with endotracheal intubation:
Indications:
1. Type I /hypoxemic respiratory failure where the patient is unable to meet the oxygen requirements of the
body or is able to do so only at a very high cost that results in haemodynamic and metabolic compromise.
2. Type II/ hypercapnic respiratory failure where the ventilarory pump has failed.

Goals of mechanical ventilation

1. Correct hypoxemia-PO2 ~60 mmHg/ SpO2 90%
2. Correct hypercapnic-PCO2 ~ 40mmHg
3. Reduce work of breathing
4. Reversal of respiratory muscle fatigue.

Complication of mechanical ventilation:

1. Related to intubation:
1. Loss of protective airway reflexes leading to aspiration
2. Autonomic stimulation causing either tachycardia and hypertension or bradycardia
3. Hypotension in fluid depleted patients post induction with sedations.

2. Complication secondary to endotracheal tube:blocked ,kinked and misplaced tube,unrecognised

esophageal intubation
3. Pneumothorax
4. Ventilator associated pneumonias
5. Ventilator associated lung injury like volutrauma, atelectotrauma and barotrauma.
Supportive care:
1. Suctioning: Maintains airway patency
Increases oxygenation and decreases work of breathing
Stimulates cough and prevents atelectasis.
2. Nebulisation: Inline jet nebulizer / MDI
Delivery of bronchodilator drugs in aerosolised form.
3. Humidification:Prevents drying of secretions and maintains mucociliary function.
4. Physiotherapy: Prevents atelectasis, facilitates postural drainage, and prevents complication of
mechanical ventilation.
5. Care of ETT: Proper fixing of the tube, measuring cuff pressure and maintaining it less than 25 mm of
Hg.
6. Nutritional support: early enteral feeding, provide adequate calories, protein, electrolytes, vitamins and
fluids, care of feeding tube.
7. Stress ulcer prevention: Early enteral feeding, H2 blockers or proton pump inhibitors for prophylaxis,
minimise use of steroids and NSAIDS
8. DVT prevention: DVT prevention either by low molecular weight heparin or conventional heparin or by
graduated compression stockings or sequential compression device in patient where heparin is
contraindicated.
9. Head end elevation of 35-45°.
10. Bowel bladder care
11. Care of eyes
12. Daily sedation interruption
13. Prevention of pressure sore: positioning, prevent soiling, use of air mattress, meticulous cleaning and
good wound care.
14. Adequate Analgesia for pain
15. Infection control.

Weaning:
Weaning is a gradual process, which involves withdrawal of mechanical ventilation and removal of artificial
airway. It represents the period of transition from total ventilatory support to spontaneous breathing.
Indications for weaning and extubation:
1. Resolution of disease and its acute phase
2. Patient is able to breathe spontaneously
3. Patient able to oxygenate
4. Patient able to protect the airway

Criteria for weaning

1. Resolution of disease and its acute phase
2. Patient has adequate cough
3. Adequate oxygenation:

PaO2 >60 mm Hg on
a) FiO2 < 0.5-0.6
b) PEEP < 5-10 cm of H2O

4. Stable haemodynamics without recent increase pressor requirement.

5. Adequate mentation or no recent deterioration in neurological status.
The best way to determine suitability for discontinuation of mechanical ventilation is to perform
spontaneous breathing trial, which can be performed in following ways,
1. Check respiratory rate and tidal volume on no pressor- support and calculate Rapid Shallow Breathing
Index and extubate.

(RSBI=respiratory rate/tidal volume in L)

If RSBI <105 breaths/min/L then patient is suitable for extubation
2. A T-piece trial involves patient to breathing through T piece for a set period of time (30 min to max 180
min) The chances of successful extubation are high if patient passes the T-piece trial.
3. An alternative variant is the use of CPAP(continuous positive airway pressure) via an endotracheal tube,
which overcomes the imposed work of breathing through ETT and prevents airway collapse.
During spontaneous breathing trial (SBT) presence of any of the following amounts to failure of SBT:
a. Change in mental status-somnolence, coma, agitation
b. Onset or worsening of discomfort
c. Severe diaphoresis
d. Signs of increased work of breathing- Use of accessory muscles, thoraco- abdominal paradox.
e. Increase in heart rate >20 bpm or blood pressure > 20 mm of Hg, or any evidence of haemodynamic
instability or new onset arrhythmias.
If a patient fails an SBT, then it is important to look for a reason like occult heart failure, neuromuscular
pathology, etc.
Suitability for extubation:
1. All of the above
2. The patient with adequate cough and gag reflexes.

Extubation failure:
The use of post extubation non invasive ventilators has decreased the use need for re-intubation.
Tracheostomy:
Tracheostomies to be considered if mechanical ventilation is expected for more than 7-10 days.

33. ACUTE RESPIRATORY DISTRESS SYNDROME

WHEN TO SUSPECT/ RECOGNIZE?
Introduction:
The acute respiratory distress syndrome (ARDS) is a sudden, life-threatening lung failure caused by an
inflammatory injury to the lung that is characterized clinically by acute hypoxemic respiratory failure
accompanied by pulmonary infiltrates.
Clinical disorders associated with the development of ARDS are divided into those associated with direct
injury to the lung and those that cause indirect lung injury (summarized in Table 1). Severe sepsis from any
cause is a common underlying disease. Falciparum malaria, leptospirosis,H1N1 influenza
pneumonia,hantavirus infection, scrub typhus and severe pneumonias due to Legionella and the
pneumococcus are common causes of ARDS and multiorgan failure in India.
Table 1. Clinical Disorders Associated INDIRECT LUNG INJURY
with the Development of ARDS
DIRECT LUNG INJURY
Common causes Common causes
Pneumonia Sepsis
Aspiration of gastric contents Severe trauma with shock and
Less common causes Multiple transfusions
Pulmonary contusion Less common causes
Fat emboli Cardiopulmonary bypass
Near-drowning Drug overdose
Inhalational injury Acute pancreatitis
Reperfusion pulmonary edema after Transfusion of blood products
lung transplantation or pulmonary
embolectomy

Case definition:
The American–European Consensus Conference Committee definition is commonly used. It defines a
spectrum of severity ranging from a milder form of lung injury, Acute Lung Injury (ALI), to a more severe
Acute Respiratory Distress Syndrome (ARDS)
Table 2. 1994 American–European Consensus Conference Committee Definitions

Condition Timing Oxygenation Chest Radiograph Pulmonary Artery

Occlusion
Pressure
Acute Lung Injury Acute Onset PaO2/FiO2 <300 Bilateral Infiltrates < 18 mmHg. when
(ALI) torr on Frontal chest measured or no
radiograph clinical evidence
 of left atrial
hypertension
Acute Respiratory Acute Onset PaO2/FiO2 <200 Bilateral Infiltrates < 18 mmHg. when
Distress Syndrome torr on Frontal chest measured or no
(ARDS) radiograph clinical evidence
of left atrial
hypertension

INCIDENCE OF THE CONDITION IN OUR COUNTRY

An early estimate by the National Institutes of Health (NIH) suggested that the annual incidence in the
United States was 75 per100, 000 population. Most studies report a mortality of 40 %-60% from ARDS
with most deaths being attributed to sepsis and multi-organ failure rather than a primary respiratory cause.
Recent studies have shown a decreasing mortality from this disease to as low as 36% and 34%. This may be
probably related to improved and more effective strategies for ventilation and treatment of sepsis and better
supportive care of the critically ill patients.
There are no reliable data from India.

DIFFERENTIAL DIAGNOSIS/ TYPES:

1. Cardiogenic pulmonary edema
2. Fluid overload
3. Bronchopneumonia
4. Aspiration pneumonia
5. Viral pneumonia
6. Alveolar hemorrhage
7. Pulmonary contusion
8. Miliary tuberculosis
9. Extensive pulmonary metastases
10. Vasculitis

PREVENTION AND COUNSELING

1. Management of the underlying condition

2. Early mangement and control of sepsis
3. Prognosis is guarded with mortality of about 50%
OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT & REFERRAL
CRITERIA

Clinical Diagnosis:
1. Features of the underlying condition
2. Breathlessness, tachypnea, respiratory distress, cyanosis, sweating, mental obtundation
3. Pulse oximetry show SpO2 below 90%, or is maintained above 90% only with high flow oxygen

Investigations:
1. Blood count, cultures, Ultrasonography and other investigations to diagnose the underlying
2. Chest X-ray : Bilateral parenchymal infiltrates
3. Arterial blood gases: low PaO2, low PaO2 / FiO2 ratio
4. Echocardiography: normal left ventricular function, may show signs of pulmonary hypertension and
right ventricular dysfunctionin severe cases

Treatment:
1. Treatment of the underlying illness
2. ALI / ARDS is not a disease of the lung alone; it is often a part of multiorgan dysfunction in
systemic inflammation and sepsis. Thus ventilatory and pulmonary management are part of the
overall management of the patient. Identifying and treating the inciting clinical disorder is of utmost
importance while supportive therapy with mechanical ventilation gives time for the lungs to heal.
3. Oxygen therapy
Intubation and mechanical ventilation
Use tidal volume of 6 ml/kg ideal body weight (approximately 350-400 ml for average height Indian male,
and 300ml for average height Indian female), respiratory rate 15-30/min
Give 5-10 PEEP

Plateau Pressure Pplat< 30 cm H2O

pH of 7.25-7.35
– 70mmHg, or SpO2 88%-95%

anical Ventilation

Mechanical Ventilation settings for Protective Lung Ventilation

Variable Protocol
Ventilator mode Volume assist-control
Tidal volume < 6 mL/kg ideal body weight
Plateau pressure Pplat< 30 cm H2O
Ventilation set rate/min 6–35/min, adjusted to achieve arterial
pH goal pH of 7.25-7.35
pH of 7.25-7.35 considered acceptable.
Inspiratory flow, I:E Adjust flow to achieve I:E of 1:1–1:3
Oxygenation goal PaO255-80mmHg
88% < SpO2 < 95%
Fio2/PEEP 0.3/5, 0.4/5, 0.4/8, 0.5/8, 0.5/10, 0.6/10,
(mm Hg) 0.7/10, 0.7/12, 0.7/14, 0.8/14, 0.9/14,
combinations 0.9/16, 0.9/18, 1.0/18, 1.0/22, 1.0/24
Weaning Attempts to wean by pressure support
required when FiO2/PEEP are .40

Referral Criteria
Undiagnosed underlying condition
Severe underlying illness and multiple organ dysfunction (e.g., severe sepsis, renal failure, etc)
Associated polytrauma with head injury
High FiO2 and PEEP requirement (FiO2 > 0.5 and PEEP > 10)
Requirement of deep sedation and neuromuscular blockade to allow smooth mechanical ventilation
High plateau pressures > 30 cmH2O despite tidal volume of 6 ml/kg
Development of complications such as pneumothorax, ventilator-associated pneumonia
Inability to wean patient

Investigations: as per situation 1 plus

Investigations to find the source of sepsis / underlying cause of ARDS
CT scan of the Chest: alveolar filling, consolidation, and atelectasis occurring predominantly in dependent
lung zone. lung injury in ARDS is non-homogeneous, and basal, dependent lung regions are more severely
affected by edema and consolidation.

Treatment:
Continue protective lung ventilation strategy, high FiO2 and PEEP
Permissive hypercapnia
Deep sedation and neuromuscular blockade
Recruitment manoeuvres
Prone ventilation
Nitric oxide
High frequency oscillation
Extracorporeal membrane oxygenation
Steroids may be considered but not recommended for routine use
Continue supportive Care
Prevent ventilator induced lung injury and ventilator associated pneumonia
Start weaning the patient as soon as possible

34. ACUTE LIVER FAILURE

AK Baronia,
Professor & Head,
Department of Critical Care Medicine,
SGPGI, Lucknow
Introduction
Acute Liver Failure (ALF) is defined as acute hepatitis (elevation in AST/ALT) accompanied by elevation
in INR >1.5 and any degree of mental alteration (encephalopathy) within 12 weeks of onset of symptoms, in
the absence of chronic liver disease. Its presentation is rapid, dramatic and frequently leads to death over the
course of a few days in the absence of emergency liver transplantation.
Incidence
The exact incidence of ALF in the Indian subcontinent is not known. However, viral hepatitis leading to
acute liver failure is the commonest cause in our country. In western countries, the commonest cause of
ALF is paracetamol poisoning and it is a relatively uncommon disease (e.g., it affects about 2500 patients in
the United States each year). Since there is a high load of hepatotropic viruses in India, the incidence of
ALF may probably be higher.
Prognosis
ALF carries a high mortality rate with 15-20% survival without orthotopic liver transplantation (OLT). In
developed countries, liver transplantation has revolutionized the prognosis of this disease and survival rates
are in the range of 59 to 79%, with liver transplantation. Moreover, it accounts for about 5-11 % of liver
transplants among adults.
Hepatitis A, paracetamol overdose and ischemic insults typically present as hyper acute liver failure, and
have a relatively good spontaneous survival rate of 36%, whereas idiosyncratic drug reactions and
indeterminate causes present later, with only a 14% survival rate without OLT. The other etiologies with
very poor prognosis include acute hepatitis B (and other non-hepatitis A viral infections), autoimmune
hepatitis, Wilson’s disease and Budd-Chiari syndrome. Patients presenting in grade III/IV encephalopathy
also have a very poor prognosis.
Differential diagnosis
Differential diagnosis includes severe malaria, leptospirosis, rickettsial diseases, enteric fever, and Hanta
virus infection.
Clinical features
The initial clinical features of ALF may be non-specific, and may include anorexia, fatigue, abdominal pain,
jaundice and fever before progressing to hepatic encephalopathy.
Hepatic encephalopathy is graded from I to IV based on clinical features and neurological signs.
Grades of Hepatic encephalopathy
I Changes in behaviour with minimal
change in level of consciousness
II Gross disorientation, drowsiness, possibly
asterixis, inappropriate behaviour
III Marked confusion, incoherent speech,
sleeping most of the time but arousable to
verbal stimuli
IV Comatose, unresponsive to pain,
decorticate or decerebrate posturing

This grading is clinically robust and increasing grades of hepatic encephalopathy have a strong negative
correlation with outcome. The evolution to grade III/IV HE is a grave prognostic sign as this group is at risk
of intracranial hypertension, and subsequent brain herniation.
Clinical signs suggestive of increasing intracranial pressure include worsening of hepatic encephalopathy,
systemic hypertension and bradycardia (Cushing reflex), altered pupillary reflexes and decerebrate rigidity.
All of these clinical signs occur late in the clinical course.
Etiological category Specific causes
Viral HAV, HBV±HDV, HRV, HSV
Human herpes virus 6, CMV, EBV, VZV, Parvovirus B19,
Yellow fever
Drug/toxin induced Paracetamol, Amanita phalloides, tetracyclines, Bacillus
(dose dependent) cereus, carbon tetrachloride
Drug/toxin induced Halothane, anti-tubercular therapy, co-amoxiclav, macrolides,
(idiosyncratic) ofloxacin, phenytoin, valproate, statins, NSAIDs, disulfiram,
metformin, dapsone, amiodarone, labetolol, methyl dopa,
HAART, etoposide, ecstasy/amphetamines, cocaine, herbal
remedies, etc
Vascular Ischemic hepatitis, Budd Chiari syndrome, right heart failure,
veno-occlusive disease
Metabolic Wilson’s disease, acute fatty liver of pregnancy, HELLP
Miscellaneous Autoimmune hepatitis, malignant infiltration, sepsis, heat
stroke
Others Cryptogenic
Criteria for hospital admission
All patients with clinical or laboratory evidence of moderate to severe acute hepatitis should have
immediate measurement of prothrombin time and careful evaluation for subtle alterations in mentation. If
the prothrombin time is prolonged by >4-6 seconds or more (INR>1.5) and there is any evidence of altered
sensorium, the diagnosis of ALF is established and hospital admission is mandatory.
Criteria for ICU admission
Patient with any one of the following:

However, rapidly worsening encephalopathy or grade III/IV encephalopathy warrants ICU admission.
m.

Optimal diagnostic criteria, investigations, treatment and referral

A. Non metro/ Secondary hospital
1.1Investigations
2) Prothrombin time(PT)/INR
3) Chemistries: serum sodium, potassium, chloride, bicarbonate, calcium, magnesium, phosphate, glucose
4) Liver function test: AST, ALT, alkaline phosphatase, GGT, total bilirubin, albumin
5) Renal function test : serum creatinine, blood urea nitrogen
6) Arterial blood gas (with arterial lactate, if possible)
7) Complete blood count
8) Blood type and screen
9) Viral hepatitis serologies: anti-HAV IgM, HBsAg, anti-HEV.
10) Ultrasound abdomen to look at the echotexture of the liver and rule out chronic liver disease/ Budd-
Chiari syndrome.
11) Blood culture
12) Blood smear for malaria, serology for Dengue and Widal test in selected cases (based on clinical
suspicion)
38

Laboratory monitoring
Frequency to repeat tests Tests
Twice daily Blood glucose (bedside
glucostix adequate)
Daily PT, serum sodium and
potassium
Arterial blood gas
Alternate day Blood count, serum creatinine
Twice weekly Magnesium, phosphate

1.2 Treatment
1) Nutrition: A carbohydrate rich diet with protein restriction (60 g/day) is recommended. If enteral feeds
are not tolerated, dextrose infusion should be started. A record of intake and output should be maintained
and a positive balance of no more than 500 ml is acceptable.
2) Bowel decontamination with lactulose and antibiotic for gut sterilization (ampicillin / metronidazole /
rifaximin)
3) Intravenous ranitidine or proton pump inhibitors.
4) Rehydration is required in many patients as they may be dehydrated at admission due to vomiting and
anorexia. Subsequently, maintain euvolemia.
5) Careful and repeated neurological examination for grade of encephalopathy and evidence of cerebral
edema is mandatory.
6) Avoid sedation in grades 1 and 2 encephalopathy.
7) All patients in grade 3 or 4 hepatic encephalopathy should be intubated electively for airway protection.
In addition, respiratory support and mechanical ventilation should be provided for those with inadequate
respiratory effort.
8) Treatment for clinical evidence of cerebral edema includes:

1. Elevation of head end of the bed to 15-30°

2. Head in neutral position
3. Limiting all nonessential physical examination
4. Maintaining normotension (mean arterial pressure atleast 70-80 mm Hg)
5. Hydrotherapy for fever control; judicious use of paracetamol to control fever
6. Prevent hypo and hyperglycemia
7. Parenteral mannitol (for raised ICP) in 0.5-1 gm/kg boluses
8. Look for and correct hypercapnia and hypoxemia

9) Give one dose of vitamin K. Fresh-frozen plasma transfusion is required for bleeding manifestations, as
and when required. Platelet transfusion is required for platelet counts <10,000/mm3 or invasive procedures.
10) N acetyl cysteine should be given in patients with acetaminophen induced ALF.
11) The role of antibiotics is not definitive. However, in grades 3 and 4 encephalopathy, prophylactic
antibiotics may be advisable. Third generation cephalosporin, e.g., Ceftriaxone, is adequate.

1.3 Referral
The following are reasons for referral to a higher centre:
1) Liver transplantation: Planning for transfer to a transplant center should begin in patients with grade I or
II encephalopathy because they may worsen rapidly. Early transfer is important as the risks involved with
patient transport may increase or even preclude transfer once stage III or IV encephalopathy develops.
2) Renal replacement therapy: Renal replacement therapy forms an integral part of care given to all patients
with renal failure. Continuous modes of dialysis such as continuous veno-venous hemofiltration are better as
hemodynamic stability is maintained and fluctuations in intracranial pressure are avoided.
3) Transfusion requirement: Patients with significant gastrointestinal bleed should be referred to an
institution where blood products can be arranged adequately.
B. Metro/ Super specialty situation
Investigations
All those listed in the previous section. In addition, the following may be added:
1) Toxicology screen including acetaminophen level
2) Serum Ceruloplasmin
3) Serum ammonia ( if possible)
4) Autoimmune markers: Antinuclear antibody, anti smooth muscle antibody, anti liver-kidney microsomal
antibodies, Immunoglobulin G level
5) HIV status (liver transplant)
6) Liver biopsy (via the transjugular route) may be done, if expertise with this technique is available.

Laboratory monitoring
Frequency to repeat tests Tests
Four times a day Blood glucose (bedside glucostix
adequate)
Twice daily Serum sodium and potassium,
Arterial blood gas
Daily PT/INR, blood count
Alternate day Serum creatinine, magnesium
Twice weekly Serum phosphate, Liver function
tests

Treatment
Treatment enumerated in the previous section should be instituted. The following are recommended, in
addition.
1) Enteral nutrition is preferred and should be started through a nasogastric tube. Total parenteral nutrition
may be considered, in case enteral nutrition is not tolerated or there are contraindications. However, the risk
of fungal infections increases with parenteral nutrition.
2) Invasive hemodynamic monitoring in the form of intra-arterial blood pressure and central venous
pressure monitoring.
3) Maintenance of adequate cerebral perfusion pressure
- Keeping mean arterial pressure >80mm Hg.
- PaCO2 in the range of 30-35 mm Hg.
4) In ventilated patients, sedation should be instituted to avoid coughing and bucking on endotracheal tube.
Bolus of lignocaine and sedation should be given prior to suctioning.
5) Pts with renal failure should be started on continuous renal replacement therapy to minimize fluctuations
in intracranial pressure during dialysis.
6) Urgent hepatic transplantation is indicated in acute liver failure where prognostic indicators suggest a
high likelihood of death.
7) Artificial and bio-artificial liver devices may be used as bridge to liver transplant

Complications
Infection
If antibiotics are not given prophylactically, surveillance for infection (including chest radiography and
periodic cultures of sputum, urine and blood for bacterial and fungal organisms) should be undertaken. In
case the patient develops ascites, spontaneous bacterial peritonitis should be ruled out. A low threshold for
starting appropriate anti-bacterial or anti-fungal therapy should be maintained.
Bleeding
Replacement therapy for thrombocytopenia and/or prolonged prothrombin time is recommended only in the
setting of hemorrhage or prior to invasive procedures. Prophylactic platelet transfusions are needed only for
platelet count <10,000/mm3.
Criteria for referral for liver transplant
Several prognostic indicators suggest a high likelihood of mortality and in these patients, liver
transplantation is the only option. Currently available prognostic scoring systems do not adequately predict
outcome; neverthless, the King’s college hospital criteria (KCH criteria) have been most commonly used
and most frequently tested of the several criteria proposed.

Kings College Hospital Criteria

Etiology of ALF
Acetaminophen overdose
Non-acetaminophen overdose
Criteria predicting death
Arterial pH <7.30
OR
All of the following:
PT > 100 seconds (INR > 6.5)
Creatinine level > 3.4 mg/dL
Grade III/IV encephalopathy
PT > 100 seconds (INR > 6.5 )
OR
Any three of the following:
Non A non B hepatitis/drug/halothane
Jaundice to encephalopathy interval > 7
days
Age < 10 years or > 40 years
PT >50 seconds (INR >3.5) and
bilirubin level >17.4 mg/dL

Prevention & Counseling: Hepatitis A & E, which spread mainly by faeco-oral contamination, can be
controlled by clean and safe water supply & other hygienic measures. . Universal precautions, viral
screening of blood for Hepatitis B & C should be made mandatory. Recycling of syringes should be
discouraged and declared unlawful.

35. BRAIN DEATH TEST AND ICU MANAGEMENT

WHEN TO SUSPECT/ RECOGNIZE?

Introduction:
It is important to recognize and diagnose brain death especially in patients who are potential organ donors.
Early diagnosis, documentation and initiation of the organ donation process and appropriate management of
brain-dead organ donorsforms an important part of intensive care unit management.
Definition
Brain death is defined as the irreversible loss of all function of the brain, including the brainstem. The three
essential findings to confirm brain death are coma (known irreversible cause), absence of brainstem
reflexes, and apnea.
An evaluation for brain death should be considered in patients who have suffered a massive, irreversible
brain injury of identifiable irreversible cause as established by history, clinical exam, lab testing or
neuroimaging (CT scan or MRI). Once brain death criteria are met a person clinically determined to be brain
dead is legally dead in the context of organ donation under the Transplantation of Human Organ Act 1994.
Always consider Medico legal, philosophical and religious perspective.

OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT & REFERRAL

CRITERIA

The diagnosis of brain death is primarily clinical. No other tests are required if the full clinical examination,
including each of two assessments of brain stem reflexes and a single apnea test, are conclusively
performed. In the absence of either complete clinical findings consistent with brain death, or confirmatory
tests demonstrating brain death, brain death cannot be diagnosed.
Differential Diagnosis
Neurologic states that can mimic brain death
1. Locked-in syndrome (Present in case of GBS); Patient cannot move the limbs, grimace or swallow,
but blinking and vertical eye movements remains intact.
2. Vegetative state; No awareness of self and environment using a series of stimuli after CPR may take
1 month to become fully apparent and is permanent if no change after 3 months is observed.

Investigation
Brain death Examination
Exam prerequisites
1. Irreversible loss of clinical brain function.
(Definitive cause leading acute brain catastrophe compatible with diagnosis of brain
death evidenced on clinical or neuroimaging)
2. Achieve Systolic Blood Pressure>100mmHg and core body temperature >32C (>90°F).
3. Exclusion of confounding factorin prognostication.
 Drugs (sedatives or neuromuscular blocking agents).
 Intoxication.
 Hypothermia (induced hypothermia therapy).
 Shock.
Brain death test
1. Sufficient time period has been passed to exclude possibility of possible recovery of meaningful
neurological function, several hours to days as per clinical factors.
2. The relevant family member or appropriate party has been notified of the intention to initiate the
determination of brain death.
3. Neurological exam then proceeds with aim of determining three principle findings in brain death:
coma, absence of brainstem reflexes and apnea (coma and apnea must coexist).
4. Two physician as per local institutional protocol do the brain death test
5. The second physician should not be involved in the patient’s care.
6. Neither physician should be involved with organ transplantation.
7. Intensivist, neurologist or any physician competent doing brain death test appointed by the institute
as per local law can do the brain death test, both physician do the test individually.

Determination of unresponsiveness (Coma)

Absence of supraspinal motor response to pain in all extremities and no eye opening to pain (standardized
painful stimuli - supraorbital pressure, TMJ pressure, sternal rub and nail bed pressure) Glasgow coma scale
3/15.
Examination of brain stem reflex
Pupillary reflex
Dilated pupils at mid position (4–6 mm).
Absence of bilateral pupillary responses to light.

Ocular movement
Absent oculocephalic reflex (doll’s eye )
Absent cold caloric responses (vestibulo-ocular reflex)

Absent Facial sensory and motor response

Absent Pharyngeal reflex and Tracheal reflex
Absence of gag reflex.
Absence of coughing in response to tracheal suctioning.

Apnea test
Prerequisites
1. SBP>100mmHg.
2. Core body temperature >36.5°C(>97°F).
3. Euvolemia with appropriate fluid balance in the previous 6 hours.
 4. Normal PaO2.
5. Normal PaCO2.

Procedure
1. Connect SpO2 probe and preoxygenation at 100% Fio2 for 10 minutes, draw baseline ABG, Pao2
>200 mmHg and Paco2 ~40mmHg (may require to reduce ventilator rate to get eucapnia) is needed.
2. Disconnect the ventilator.
3. Delivering oxygen by tracheal catheter at carina with flow of 6 liters per minute or T-piece system
using 12 l/min O2 flow or use CPAP of 10 cmH2O (less hypoxia with CPAP method).
4. Observe the chest and the abdominal wall movement for respiration for 8 to 10 minutes and monitor
the patient for changes in vital functions.
5. Rate of rise of PaCO2 is 3mmHg per minute so 8 – 10 minutes are sufficient for apnea test to get rise
of 20 mmHg of PaCO2.
6. Draw post test ABG and then reconnect the ventilator.
7. Positive apnea test - Absence of respiratory drive at a Paco2 of 60 mm Hg or 20 mm Hg above
normal base-line values, apnea is confirmed.
8. If respiratory movement occurs or any sign of hemodynamic instability, abandon the test, draw
sample for ABG and then reconnect the ventilator.
Ancillary test
Routine use is not recommended.
Observation period between two examination
Depends on the age of the patient;
1. 7 days to 2 month old minimum 48 hr interval.
2. 2 month to 1 year old minimum 24 hr interval.
3. >1 year to <18 years old minimum 12 hr interval.
4. >18 years old, interval is optional, minimum 6 hr.

Number of Confirmatory tests

Neonate < 7 days Brain death testing is not valid.
7 days to 2 months old, 2 confirmatory tests.
>2 months to 1 year old, 1 confirmatory test.
>1 year to <18 years old, optional.
>18 years old, optional.

Brain death declaration

If clinical criteria’s are met.
No need of confirmatory test.

Documentation of brain death

1. Etiology and irreversibility of condition.
2. Absence of brainstem reflexes.
3. Absence of motor response to pain.
4. Absence of respiration with Paco2 ≥ 60 mm Hg.
5. ming of first and repeat neurologic examination.
6. Justification for confirmatory test and result of confirmatory test.
7. Brain death time - time of rise of Pao2 >60mmHg after second set of test.
8. Two physician signatures should be obtained.

Primary or secondary health care centre

• Brain death test are clinical.
• Brain death can be declared at these centers if all three criteria’s are fulfilled.

Communication with family and further decision making

After the clinical criteria of brain death have been met, the physician should inform the next of kin, who can
be approached about organ donation. The physician is required to abide by state law with respect to organ
donation.
Treatment
Basic intensive care, cardivascular, respiratory, hemodynamic and metabolic support

Routine ICU care and monitoring

1. Nursing care.
2. Skin care.
3. Turning and positioning.
4. Care of lines.
5. Ryle’s tube to prevent risk of aspiration.
6. Pulse oximetry.
7. Arterial and central venous pressure monitoring.
8. Pulmonary artery catheter placement If necessary.
9. Foleys catheter for urine out put monitoring.
10. Core temperature monitoring.
11. Antibiotic therapy.
12. Anticipation of complications.
 13. Prevention and treatment of complications.
14. Frequent assessment and titration of therapies.
15. Nutrition.
16. Maintenance of vital organ function;
17. Resuscitation.
18. Oxygen delivery to the tissues.
19. Hydration and perfusion.
20. Routine laboratory testing ABG, CBC, SE, BUN, Cr and LFT.
21. Testing for HIV, HBV & HCV on all donors after first apnea test.
22. Additional tests may be necessary as per local protocol.
23. Support of the family.

Counseling
The family should be counseled that the patient cannot recover
Family should be counseled for organ donation
If the patient cannot become an organ donor, withholding or withdrawing of life support may be discussed
with the family.

Referral Criteria
If the patient is a potential organ donor, he should be transferred to a tertiary level centre that is certified by
the competent authority and is capable of supporting the brain dead organ donor
If in some cases further diagnostic studies are required to confirm brain death
o Difficulty to determine coma.
o Incomplete brain stem reflex testing.
o Incomplete apnea testing.
o Toxic drug levels.
o Facial trauma.
o Preexisting pupillary abnormality.
o Sleep apnea or severe pulmonary disease resulting in chronic retention of CO2 .
o Children younger than 1 year old (<1 year age not recommended).
o As required by institutional policy.

a)Clinical Diagnosis:

b)Investigations: as per situation 1 plus

1. EEG
 2. Bispectral index (BIS)
3. SSEP
4. Neuroimaging
5. Cerebral angiography (CTA, MRA) when ICP exceeds MAP angiography demonstrates absence of
blood flow beyond carotid bifurcation.
6. Cerebral scintigraphy (technetium tc-99m brain scan)
o Noninvasive study also knownas a cerebral blood flow study.
o Absent uptake of isotope in brain parenchyma is supportive of a diagnosis of brain death- Hollow skull
phenomenon.
o Single photon emission computed tomography(SPECT) at 48 hrs is 100 % diagnostic.
7. In case of barbiturate coma neuroimaging can be used without the necessary wait (5 half life
provided normal renal and hepatic function) for the medication to leave the system.
8. Transcranial Doppler Ultrasonography

However, the clinical criteria of brain stem death are considered adequate under the Transplantation of
Human Organ Act and special investigation are not mandatory to declare brain stem death in India.
Treatmentas in Situation 1 above plus
ICU management of Brain dead organ donor
1. ICU management of the potential organ donor plays a key role in maintaining and increasing current
number of donor organs aim is to improve organ survival.
2. Early identification of potential donors;
3. Critically ill patient in an intensive care unit - severity of acute brain injury is such that there is a
high probability of brain death occurring.
4. Early notification of Organ Procurement Organization(OPO), State Authorization Committee, Zonal
Transplant Coordinating Centre (ZTCC) or Local Authorization Committee(LAC)as per institutional
protocol.
5. Designated requestor – OPO or LAC coordinator, as per institutional protocol.
6. Requesting consent to organ donation from the family are ethical and professional responsibilities of
the intensive care specialist.
7. Preparation of the family.
8. Consider family’s psychological, religious and cultural needs.
9. Enquiring about the stated wishes of the patient.
10. Ensuring the wishes, dignity and privacy of the donor are respected.
11. Provide sufficient information and time.
12. Support family to make an informed decision concerning organ donation without undue pressure.
13. Clarification of ongoing physiologic support despite brain death.
The family should have adequate emotional and social support after giving consent to organ donation and
during the follow up period.
Details of all discussions with the families should be documented.

Supportive treatment should start early as soon as brain death has been recognized irrespective of the
consent.Switch the focus of the management for elevated intracranial pressure and brain protection, to
preservation of organ function and optimization of tissue oxygen delivery.
Hemodynamic support
Hypertension
1. Hypertension and bradycardia preceding brain death characterize the Cushing’s response.
2. Ischemia of the vagal nucleus in the medulla oblongata results in uncontrolled sympathetic
stimulation- catecholamine “storm” results in systemic hypertension, tachycardia and possibly tissue
ischemia including;
3. Pituitary ischemia.
4. Myocardial injury - right and/or left ventricular dysfunction.
5. Duration and severity of this “storm “ varies but within hours results in depletion of catecholamine
with subsequent generalized vasodilatation and homodynamic collapse.
6. Initial period of severe HTN – short acting ß-blocker esmolol.

Hypotension Most common problem seen in brainstem dead organ donors.

1. Chronic maintenance phase of brain stem dead donors is frequently characterized by hypotension.
2. Invasive monitoring of arterial and central venous pressure should be instituted.
3. Proper fluid management is the cornerstone of therapy;
Fluid resuscitation may require several liters of fluid.
Combination of crystalloids and colloids is used.
Relying on urine output alone to determine adequacy of fluid resuscitation is misleading because of
polyuria due to diabetes insipidus.
4. Vasopressors;
If possible use of vasopressors should be minimized because of their splanchnic vasoconstrictive
effects.
The first choice is usually Dopamine, preferably at a dose below 10mcg/kg/min.
Dobutamine should be used for impaired myocardial contractility; and
Norepinephrine or Epinephrine for severe systemic vasodilatation.
In donors who remain unstable despite routine management, pulmonary artery catheterization may
help in determining the problem.
5. Rule of 100’s for management of brain death organ donor;
 SBP 100 mmHg
U/O 100 ml/hr
PaO2 100 mmHg
Hb 100 g/L

Arrhythmias
1. Brady arrhythmias and tachyarrhythmia are common after brain death.
2. Brady arrhythmias occurring as part of the Cushing reflex, during coning, do not require treatment.
3. Correct acidosis, electrolyte abnormalities and try to optimize Inotropes.
4. Atropine is ineffective for Brady arrhythmias after brain death has occurred.

Respiratory support
Ventilatory support
1. Increase ET cuff pressure immediately after BD declaration.
2. HOB up 30°.
3. Turning q2h.
4. Pulmonary toilet.
5. Paco2 should be maintained in the normal range.
6. Routine use of PEEP at 5 cm H2O in brainstem dead organ donors is recommended to prevent
microatelectasis.
7. Plateau pressures should <35cmH2O to reduce the risk barotrauma.
8. FiO2 <0.6 to reduce the risk of oxygen toxicity.
9. PaO2 of >100 and a saturation >95%.
10. Monitor ABG’s q2h or as required.
11. Chest X-Ray.
12. Bronchoscopy in some cases.
13. CT chest in some cases

Renal support
1. Maintain urine output 1-3 ml/kg/hr.
2. Avoid nephrotoxic drug.
3. Maintain Euvolemia.
4. Oliguria;
5. Despite adequate filling pressures and blood pressure, loop diuretics or osmotic diuretics should be
used to initiate diuresis.
6. Polyuria, a frequent finding in brainstem dead organ donors;
 7. Diabetes insipidus.
8. Osmotic diuresis due to mannitol or hyperglycemia.
9. Physiologic diuresis due to massive fluid resuscitation.
10. Hypothermia.
11. Hypokalemia.
Neuro-Endocrine changes As neurologic death occurs, alteration in the hypothalamic-pituitary-adrenal
axis (HPA axis) is inevitable.
Diabetes insipidus
1. DI results in problems with homodynamic stability and fluid and electrolyte balance;
Urine volumes exceed 300ml/hr (or 7ml/kg/hr).
Hypernatremia (serum sodium greater than 150mEq/l).
Serum osmolality (>310mOsm/L).
Low urinary sodium concentration.
2. Desmopressin (dDAVP) preferred;
(DDAVP) 1 mcg IV, may repeat x 1 after 1 hour.
1-4 mcg every 8 to 12hrly SC.
Nasal spray.
3. Vasopressin - splanchnic and renal vasoconstrictive effects.
1-4 units/hr.
4. Hypernatremia (>155mEq/L)
Free water, i.e. D5% or half strength 0.45% Saline.

Hyperglycemia
1. Insulin 0.05-0.1U/kg/hour titrated to maintain glucose at 80-120.
2. Hourly glucose checks so as to avoid hypoglycemia.

Thyroid hormone replacement

1. Thyroid hormone administration typically with T3 (triiodothyronine) which is the active form of
thyroid hormone.
2. T3 is converted from T4 and T3 is 4 X more active than T4
3. Use T3 preferably if not available use T4 (T3 dose 0.05-0.15 mcg/kg/hour) titrate to keep SBP >100
4. Monitor Potassium levels closely.

Steroid
1. Protocols may use hydrocortisone 1.5 mg/kg IV Q 6 hours (max dose of 100 mg) or single dose of
methylprednisolone 15 mg/kg in adults and 1 mg/kg in children (max dose of 2 gm).
 2. The use of hormonal replacement therapy, Thyroxin, triiodothyronine (T3), corticosteroid and
insulin, has been advocated to improve cardiovascular stability. At present, such therapies are
regarded as experimental. Studies regarding ACTH and cortisol levels inconclusive. Unclear
whether steroids make any significant improvement in organ preservation.

Hypothermia
Core temperature should be monitored using rectal thermometers.
Maintain above 35°C.
• If core temperature <35°C
• Warm inspired gas.
• Warmed IV fluids.
• Warming lights.
• Warming blankets.
• Hot packs in the axilla.

Infection
1. Systemic infection is a relative contraindication to organ donation.
2. All unnecessary indwelling devices should be removed.
3. All lines and catheters must be inserted aseptically.
4. Care of dressings and wounds is vital.
5. Tracheal suction should be done with sterile precautions.
6. Appropriate samples from suspected sources of infection should be sent for culture and sensitivity.
7. Prophylactic antibiotics are indicated only immediately prior to organ retrieval.

Coagulopathy
1. If clinically significant mucocutaneous bleeding, treatment with appropriate blood components is
required.
2. Keep hematocrit > 30%.

Ischemic reperfusion injury

1. Keep FiO2 <0.6.
2. Avoid hyperthermia (>37°C).
3. Avoid hyperglycemia (>180 mg/dl).
4. Steroid and N-acetylcysteine may have sort term and long organ survival.

Absolute Contraindications to organ donation

 1. Malignancy (except primary brain tumors, low grade skin malignancies and carcinoma in situ of the
cervix).
2. Uncontrolled sepsis.
3. Active viral infections-hepatitis A and B, CMV, HSV, AIDS.

Age and Organ Harvesting

1. Corneas 0 - 100 years (poor eyesight is not a contraindication).
2. Heart Valves 0 - 60 years (Heart Attack not a contraindication).
3. Trachea 15 - 60 years.
4. Skin 16 - 85 years.
5. Kidneys 0 - 75 years (Pediatric donors consider weight and size).
6. Liver 0 - 70 years (size matching is usually recommended).

Organ Preservation Time

• Heart – 4 to 6 hours.
• Lungs – 4 to 6 hours.
• Small Intestines – 4 to 6 hours.
• Liver - 12 hours.
• Pancreas – 12 to 18 hours.
• Kidneys-72 hours.

Documentation
1. Cause of irreversible brain injury.
2. Absence of other potentially reversible causes of coma.
3. Clinical and other findings that confirmed brain death.
4. Time of brain death.
5. Information to the patient's family on brain death and organ donation.
6. Consent for organ or tissue donation.

Conclusion
A severe shortage of organs the world over has led to increased pressure on the intensive care staff for early
identification of the brain dead donor and optimum management of this condition. The diagnosis of brain
death as per the Transplantation Human Organ Act 1994 is based on simple clinical bedside tests,no need of
routine confirmatory test. This Act has made it possible in India to use this pool of patients for organ
retrieval and transplantation. The process of organ donation and transplantation requires co-ordination
between multidisciplinary teams operating almost simultaneously and sometimes in different locations like
getting surgeons from different specialties together for both donor and recipient surgery.

36. EVALUATION OF NEW FEVER IN THE CRITICALLY ILL PATIENT

When to suspect? Recognize?

INTRODCTION:New onset of fever in Intensive care unit is a very common finding, and triggers a
response of various investigations and addition of new antibiotics which may not be needed many times.
This leads to increasing cost and adds to increased utilizations of resources. All new fevers in ICU should be
evaluated in a prudent and cost effective manner.
CASE DEFINITION.
i. In non-immunosuppressed patient two consecutive temperature (core) of more than 101° F warrants
further investigation.
ii. In neutropenic patient a single temperature of 101° F should be considered important
iii. New onset of fever below this range, in a hemodynamically stable patient requires a bedside assessment
to look for a source of infection and non infectious fever and sending investigation appropriately.
iv. Recording fever
1. All patients in ICU should have hourly recording of temperature and recorded in nursing chart.
2. Uniformity of scale (Centigrade or Fahrenheit should be maintained)
3. The site of temperature recording should be recorded (Oral, axillary, rectal or tympanic)
4. Larger ICUs should have access to core temperature (rectal, tympanic or bladder) measurement device
5. The instrument should be properly calibrated and sterilized. Thermometers should not be shared between
patients to reduce cross infection

2. Incidence of the condition in our country

30% patients become febrile during hospitalizations. Up to 90% critically ill patients with severe sepsis
experience fever during ICU stay. ICU patients will generally present a newly elevated temperature at some
point during their stay. Fever in ICU could be infectious, non-infectious or mixed origin and confirmation of
source is difficult. A prudent, cost-effective assessment is necessary.
3. Differential diagnosis: Non-infectious causes of fever
a. CNS: SAH, ICH, Infarction
b. Cardiac: MI, Pericarditis
c. Pulmonary: Atelectasis, PE, fibro-proliferative phase of ARDS
d. Hepatobiliary & GIT: Acalculus cholecystitis, acute pancreatitis, active Crohn’s disease, toxic
megacolon, alcoholic hepatitis
e. Rheumatologic syndromes: Vasculitis, SLE, RA, Good pasture's syndrome
f. Endocrine: Hyperthyroidism, adrenal insufficiency, phaeochrocytoma
g. Other miscellaneous non-infectious causes:
i. Drug fever
ii. Transfusion reactions
iii. Neoplasms
iv. Malignant hyperthermia
v. Neuroleptic malignant syndrome
vi. Serotonin syndrome
vii. Opioid withdrawal syndrome
viii. Alcohol withdrawal syndrome
ix. Devitalized tissue secondary to trauma
x. Hematoma
h. Infectious causes of fever
i. CNS: Meningitis, Encephalitis, Brain abscess, Epidural abscess
ii. Head & Neck: Acute suppurative parotitis, Acute sinusitis, ASOM, Para and retropharyngeal abscesses.
iii. CVS: Endocarditis, Catheter related infection
iv. Pulmonary & Mediastinal: Pneumonia, Empyema, Mediastinitis
v. Hepatobiliary & GIT: Appendicitis, Diverticulitis, Peritonitis, Intraperitoneal abscess, Perirectal abscess,
Infected pancreatitis, Acute cholecystitis, Cholangitis, Hepatic abscesses, Acute viral hepatitis
vi. Genitourinary: Bacterial or fungal cystitis, Pyelonephritis, Perinephric abscess, Tubo-ovarian mass,
Endometritis, Prostatitis
vii. Breast: Mastitis, abscess
viii. Cutaneous: Cellulitis, Suppurative wound infection, Necrotizing fasciitis, Bacterial myositis, Herpes
zoster
ix. Osseous: Osteomyelitis

4. Prevention & Counseling

Staff working in the ICU should be familiar with drug fever and non- infectious causes of fever. Strict
asepsis, hand hygiene measures & universal precautions can bring down the infection related fevers.
Regular surveillance can help in identifying non-compliant staff, which can be appropriately counseled.
5. Optimal Diagnostic Criteria, Investigations, treatment & referral criteria

a. Clinical Diagnosis:
i. -threatening infection:
1. Elderly
2. Open abdominal wound
3. Large burns
4. Patients on ECMO, CRRT
5. CHF
6. End-stage liver disease, CRF
7. Patients on anti-inflammatory or antipyretic drugs.
ii. Symptoms and signs in the absence of fever, which mandate a comprehensive search for infection and
aggressive, immediate empirical therapy: Unexplained hypotension, tachycardia, tachypnea, confusion,
rigors, skin lesions, respiratory manifestations, oliguria, lactic acidosis, leukocytosis, leukopenia, immature
neutrophils (i.e., bands) of 10%, or thrombocytopenia

a. Key elements in evaluation: History & physical examination. Look at wounds, surgical incision sites,
vascular access and pressure ulcers. Obtain/review Chest Xray, look for new infiltrates or effusions.
Appropriate lab studies: Cultures, WBC, PBS. Remove CVC > 96 hrs Send tip for semi quantitative
culture.Send stool sample in patients on ABx for> 3 days.C difficile toxin. Diagnostic thoracocentesis,
paracentesis, LP, Ultrasound/CT
4. INITIAL ASSESSMENT
a. Focused history and bedside review of nursing chart and patients notes should be done. A detailed
medication history, line manipulation, blood transfusion, appearance of new rash, diarrhea, or any new
procedure performed should be enquired
b. Focused physical examination should be performed looking for any source of sepsis or non-infectious
cause of fever.
c. Common infectious causes of new fever in ICU
Hospital acquired or Ventilator associated pneumonia- Intubated for more than 48 hours. New fever,
purulent secretion, bronchial breathing
Central line sepsis-Line in place for more than 48 hours Erythema, purulent discharge at central line site.
Urinary catheter related infection – Catheter more than 48 hours in place,suprapubic tenderness cloudy urine
Surgical site infection – purulent discharge from wound site
Sinusitis- Nasogastric or nasotracheal tube, purulent nasal discharge
Parotitis- poor oral hygiene, unilateral tender parotid swelling
A calculus cholecystitis- abdominal tenderness, intolerance of feed
d. Common non infectious causes of fever in ICU

Rash- drugs (antibiotics,antiepileptics, NSAIDSetc.)

Unilateral painful swelling of limb- Deep Venous thrombosis
Thrombophlebitis
5. INVESTIGATION
Investigation to be performed (in all facilities)
a. Total and differential white count
b. Peripheral smear for toxic granules
c. CRP
d. Blood culture – All ICUS should have a protocol for sending blood culture. Recommendation for blood
cultures:

CULTURE NUMBER-

continuous bacteremia.

48–96 hrs after initiation of appropriate therapy for

bacteremia/fungemia.

Additional cultures should always bepaired.

For patients- without an indwellingvascular catheter

technique from peripheral sites

For cutaneous disinfection, 2% chlorhexidine gluconate in 70% isopropyl alcohol is the preferred skin
antiseptic; tincture of iodine is equally effective. Both require -30 secs of drying time before the culture
procedure. Povidone iodine is an acceptable a t be allowed to dry for 2 mins.
e. Wound swab for gram stain, culture and sensitivity
f. Endotracheal suction for gram stain C & S (semiquantitative)
g. Urine for gram stain C&S (semi-quantitative)
h. Central line tip for C&S
i. Chest x-ray
j. Abdominal USG
k. X-ray sinus
l. Transthoracic echocardiogram
Investigation to be performed in tertiary care center.
a. Procalcitonin
b. Chest CT
c. Bronchoscopy with lavage
d. CT sinus
e. CT abdomen for any collection
f. Four sets of blood culture
g. Blood for fungal culture
h. Stool for c. difficile toxin
e. MIC or e-test of antibiotics
f. Venous Doppler of legs
g. Transesophageal Echocardiogram
6. MANAGEMENT. It will depend on the underlying cause. Non specific treatment with antipyretic should
be instituted in patients with central nervous system disorder, extremes of age, poor cardiac reserve.

Referral Criteria: If higher diagnostic tests and imaging techniques are not available and the patient is not
improving, transfer to well equipped centres should be undertaken.

37. HEMODYNAMIC MONITORING IN THE ICU

WHEN TO SUSPECT/ RECOGNIZE?

h) Introduction:

Hemodynamic monitoring is an integral part of ICU care. Need for invasive monitoring should be assessed
carefully. Attention to technical details correct interpretation of data, and its application in selecting therapy
should be individualized within the clinical context.
a) Case definition:

For both situations of care

Basic hemodynamic monitoring: In any Secondary Hospital / non-Metro setup
1. Clinical examination- Central and peripheral pulses, Manual blood pressure- look at the trend,
compare with patients normal values, capillary refill, core temperature, peripheral temperature at
extremities
2. Noninvasive- Noninvasive blood pressure, Pulse oximetryplethysmographic signals
 3. Intraarterial pressure
4. Central venous pressure
5. Hourly urine output
6. Screening Echocardiography
7. Base deficit (ABG)
8. Central venous oxygen saturation
Advanced hemodynamic monitoring in selected cases:
These should be initiated in patients on high vasopressors, high ventilator support, compromised cardiac and
renal function, and where empirical fluid challenge may be harmful. These modalities include
o Cardiac output- minimally invasive

Pulse contour analysis (e.g. Flotrac, PICCO, LiDCO)

Esophageal Doppler
Pulmonary artery catheter
o Pulmonary artery occlusion pressure
o Continuous cardiac output
o Continuous mixed venous oxygen saturation (SvO2)
o Derived and calculated variables
o Pulse pressure/ Stroke volume variation
o Continuous Scvo2 monitoring
o Lactate levels

ARTERIAL CANNULATION
The ability of invasive blood pressure monitoring to identify beat to beat variability and long term trends is
unsurpassed by any other currently available technology. In addition, presence of arterial catheter enables
frequent sampling of arterial blood without arterial punctures in critically ill patients.
INDICATIONS:
a) Hemodynamic monitoring

- beat to beat monitoring of blood pressure

1. acutely hypertensive or hypotensive patients (shock)
2. use of vasoactive drugs
3. cardiac and cardiovascular surgery
4. induced hypotension

- pulse contour cardiac output monitoring

b) Frequent arterial blood gas sampling: critically ill patients including ventilated patient
c) Arterial administration of drugs, thrombolytics
d) Intra aortic balloon pump use
e) Noninvasive blood pressure monitoring not possible – e.g., too obese, burned extremity
ABSOLUTE AND RELATIVE CONTRAINDICATIONS:
1. Severe injury to the limb
2. Lack of collateral circulation
3. Coagulopathy
4. Arteriovenous fistula in the same limb
5. Pre-existing vascular insufficiency (Raynaud’s phenomenon)
6. History of surgery disrupting lymphatic drainage to that limb e.g., mastectomy with lymph node
dissection

Equipment:
1. Appropriate intravascular catheter
2. Fluid filled noncompliant tubing with stopcocks
3. Transducer
4. A constant flush device
5. Electronic monitoring equipment

Site selection:
1. The common sites of arterial line insertion are the radial, femoral, and dorsalis pedis arteries.
2. Other sites: axillary dorsalis pedis brachial, ulnar, posterior tibial and superficial temporal arteries

Arterial Cannulation:
1. The arterial line can be inserted using a simple catheter-over-needle arrangement (with or without a
guidewire) or a set based on the Seldinger technique.
2. Doppler or ultrasound can be helpful for difficult line insertion.

Set up of the pressure tranducing system

o The pressure transducing assembly consists of a coupling system, pressure transducer, amplifier and
signal conditioner, analog to digital converter, microprocessor which convert the signal received from the
vein or artery into a waveform on the a bedside monitor
o The flushing system – is set up using a 500 ml saline bottle encased in a bag
pressurized to 300 mm Hg. At this pressure the catheter will be flushed with 3 ml saline per hour and help
keep the catheter patent. Heparinised saline is no longer routinely used
 ucer is zeroed.

RESOURCES REQUIRED FOR ONE PATIENT/PROCEDURE (PATIENT WEIGHT 60 KGS)

SITUATION HUMAN INVESTIGATI DRUGS AND EQUIPMENT
RESOURCES ON OF 4-6 CONSUMABL
FOR 4- 6 WEEKS ES FOR 4-6
WEEKS WEEKS
One Each: Once a week or 1. Drugs for 4-6 1. Ultra
1. Intensivist / more for 4-6 week- Rs. 2000 sonography
Anaesthetist week long 2. Lab machine
2. ICU therapy investigation- 2. Invasive
Technician a. Ultrasound Rs. 2000 arterial
One in each 1. Doppler of 3. pressure
shift: the cannulated Consumables- monitor
1. ICU/Ward artery Rs.7000
Doctor 2. For arterial
2. Nurse canulation
3. Attendant b. Arterial tip
culture
(femoral
arterial line)
c. Blood culture
Central venous catheter insertion and Central Venous Pressure Monitoring
Definition: Insertion of a catheter in a central vein, usually the superior vena cava, but also in the inferior
vena cava or right atrium.
Indications: In recent years, central venous cannulation is practiced increasingly in anaesthesia and
intensive care for a variety of indications
Measurement of Central Venous Pressure (CVP)
1. Major surgery
2. Anticipated major blood loss
3. Anticipated major fluid shifts
4. Significant cardiac disease
5. Significant pulmonary disease
6. Pulmonary hypertension

Intravenous access
 1. Rapid administration of fluids and blood
2. Administration of Vasoactive agents and concentrated potassium infusions
3. Measurement of central venous oxygen saturation during resuscitation from shock
4. Measurement of cardiac output using some semi-invasive techniques
5. Total parenteral alimentation
6. Administration of Chemotherapeutic and other irritant drugs
7. Frequent blood sampling
8. Insertion of a pulmonary artery catheter
9. Inability to cannulate peripheral veins

Therapeutic procedures
1. Insertion of transvenous pacemaker
2. Insertion of catheters for haemodialysis and plasmapheresis
3. Aspiration of air emboli

Sites of central venous cannulation: The subclavian and internal jugular veins are the most commonly
cannulated veins. Other veins that may be used are the arm veins (basilic, cephalic), external jugular and
femoral veins.
Equipment Required
In all situations:
1. Location of the vein by anatomical landmarks
2. Appropriate intravascular catheter
o catheter over guidewire using the Seldinger technique
o cather through needle or cannula
o long cannula over needle
1. Fluid filled noncompliant tubing with stopcocks
2. Transducer
3. A constant flush device
4. Electronic monitoring equipment
5. Chest X-ray at the end of the procedure to confirm position of the CVC and rule out pneumthorax

In a superspeciality hospital in a Metro: in addition to the above

1. Location of the internal jugular vein by ultrasound
2. Portable ultrasound machine with a high frequency probe
3. Ultrasound probe with or without a needle guide
4. Sterile jelly
 5. Sterile sleeve for ultrasound probe
6. Antibiotic coated catheter may be used in case there is high risk of catheter related blood stream
infection
o Immunosuppressed patient
o High baseline CRBSI rate in the unit
o Anticipated prolonged duration of cannulation

Clinical Utilization of CVP Measurement

1. CVP is influenced not only by the volume status, but also by myocardial contractility, afterload,
intrathoracic and intra-abdominal pressures.
2. A single measurement of the CVP helps somewhat in defining circulatory status but leaves
considerable overlap in possible interpretations. Hence single values of CVP should not be relied
upon. Instead, response to fluid challenge and the trend of values should be used in clinical decision
making,
3. It is best not to remove PEEP for measurements.
4. DO NOT subtract half or any other proportion of PEEP value to the CVP measurement to get an
approximate of “true” CVP
5. In a non mechanically ventilated patient CVP of 8 -10 mm Hg is judged to be adequate.

Fluid Challenge
controlled fluid challenge and response of CVP is the best method of interpreting volume status. The fluid
challenge is performed in 4 steps:
o Select the type of fluid: usually normal saline or a colloid
o Infuse rapidly. Rate of infusion: 500ml of crystalloid or 200 ml of colloid over 20-30 minutes
o Target the Desired therapeutic response: the parameters are set empirically by the physician. These could
be mean arterial pressure (MAP >70mmHg), HR <100/min, hourly urine output > 0.5ml.kg/hr.
o Set the Danger / safety limits. Again set empirically by the physician. E.g. CVP 16mmHg, or 4-5mmHg
more than the baseline value
o Assess the response to the initial bolus of fluid
o Repeat bolus infusion of fluid if

o Discontinue fluid infusion if

o Reassess at frequent intervals

rule of thumb if the increase in CVP measured before and 5 minutes after a fluid bolus is 0-3 mmHg, more
fluid should be given. If it is 3-5 mmHg he is probably adequately filled. If the CVP increases >5mmHg
after the fluid bolus, fluid loading should be stopped.

Echocardiography
While resuscitation efforts are underway , a quick assessment with bedside echocardiogram can guide
clinician in rationalizing use of volume resuscitation, inotropes and vasopressors . This can be repeated to
assess response to therapy.
Using bedside Echocardiogram one can assess
o The Left ventricular (LV) function,
o Right Ventricular (RV) function,
o Presence of pericardial effusion and tamponade,
o Pre load assessment, fluid responsiveness
o Valve lesions.

Equipment requirement
Portable Echocardiography / Ultrasound machine with Probe

Introduction: Swan &Ganz introduced the balloon tipped pulmonary artery catheter into clinical practice in
early seventies. This brought the catheter out of the domain of radiologists and at the bedside of the patients
in intensive care. Notwithstanding the controversies regarding the utility of pulmonary artery catheter in
improving outcome, the clinician in the operating room and ICU needs to conversant with the use of
pulmonary artery catheter.
Indications for insertion of PAC: Pulmonary artery catheterization can be used for diagnostic purpose, to
monitor therapy, and to evaluate the effects of drugs. The indications for PAC insertion are:
Management of complicated myocardial infarction
• Hypovolemia vs cardiogenic shock
• Ventricular septal rupture (VSR) vs acute mitral regurgitation
• Severe left ventricular failure
• Right ventricular infarction
• Unstable angina

Assesment of respiratory distress

• Cardiogenic vs non-cardiogenic pulmonary edema
Primary vs secondary pulmonary hypertension
Assessment of type of shock
Assessment of therapy
• Afterload reduction
• Vasopressors
• Beta blockers
• Intra-aortic balloon counterpulsation
Assessment of fluid requirement in critically ill patients
• Hemorrhage
• Sepsis
• Acute renal failure
• Burns
Management of postoperative open heart surgical patients
• Assessment of valvular heart disease
• Assessment of cardiac tamponade/constriction
Contraindications / Cautions:
• Coagulopathy
• Inexperienced clinician
• Pulmonary hypertension
Pulmonary artery catheter insertion can only be performed at well equipped tertiary care centres.
Use of the Pulmonary Artery Catheter
The 4 most important measurements obtained from the PAC are
1. Pulmonary artery occlusion pressure (PAOP)
2. Pulmonary artery diastolic pressure (PADP)
3. Thermodilution cardiac output
4. Mixed venous oxygen saturation
5. The fluid challenge (as described with CVP) remains the best method of assessing the PAOP during
mechanical ventilation with PEEP.

Mixed venous oxyen saturation (Svo2) / Central venous oxygen saturation (ScvO2)
1. An SvO2 below 65% implies low oxygen delivery, while a value below 60% indicates that there is a
serious risk of tissue hypoxia if corrective measures are not taken.
2. A low SvO2 (< 40 % ) implies critical oxygen supply / demand imbalance. In some disease states,
cells in some tissues are unable to assimilate and/or process the needed oxygen.

3.
are unable to utilize oxygen.
 4. Thus a falling or low SvO2 is an important indicator that the oxygen delivery is compromised and is
deficient relative to the needs of the tissues.
5. An alternative is to measure central venous oxygen saturation (ScvO2). Central venous
catheterisation is a simpler and safer procedure, and is commonly used.
6. In this case a catheter is positioned in the Superior vena cava or upper Right atrium.
7. The goals of early resuscitation , within six hours of septic shock is to keep SVo2 > 65% or Scvo2 >
70%
8. SvO2 and ScvO2 can be measured continuously with oximetric catheters, or blood can be drawn
intermittently and the analysed using a co-oximeter on the blood gas machine

Cardiac Output monitoring

Cardiac output is the amount of blood being pumped to the body by the heart every minute. In some
patients, cardiac output monitoring may be useful to ake a diagnosis and to refine therapy.
Cardiac output monitoring should be perfromed only in well equipped tertiary care centres.
Indications
Management of complicated myocardial infarction
• Hypovolemia vs cardiogenic shock
• Severe left ventricular failure
Assessment of type of shock
Septic shock
Assessment of therapy
• Afterload reduction
• Vasopressors
• Beta blockers
• Intra-aortic balloon counterpulsation
Assessment of fluid requirement in critically ill patients
• Hemorrhage
• Sepsis
• Acute renal failure
• Burns
Management of postoperative open heart surgical patients

Methods of monitoring cardiac output

Thermodilution (intermittent or continuous) using the pulmonary artery catheter has been the classical
method of cardiac output monitoring. However insertion of a pulmonary artery catheter is demanding and
complicated. Other less invasive methods include
PiCCO: usingbolustranspulmonary thermodilution cardiac output and pulse contour derived continuous
cardiac output measurement are obtained. A central venous catheter, special thermistor tipped femoral artery
catheter and monitor are required.The main advantages over the pulmonary artery catheter is PiCCO is far
less invasive, easy to place requiring routine skills of placing a central line and arterial line. The additional
advantages are the values of extravascular lung water, global end-diastolic volume and the stroke volume
variation (a dynamic measure of preload).
Lithium Dilution Cardiac Output (LidCO): uses lithium dilution technique, instead of transpulmonary
thermodilution (used by PiCCO). The principle of pulse contour analysis for continuous cardiac output
measurement is similar.
o Advantages: Existing arterial line and venous lines can be used, even central venous access is not
mandatory. Therefore cardiac output monitoring can be established fast.
o Disadvantages: requires lithium injection
Flotrac: Arterial Pressure based Cardiac output (APCO) system calculates the stroke volume from
pulse pressure, which is the standard deviation of blood pressure. A special transducer is connected to an
existing arterial line and the cardiac output monitor.
o Advantages: does not require a central venous catheter or any bolus injection to estimate cardiac output,
easy and rapid set up

Preload Responsiveness
Preload responsiveness is the increase in cardiac putput in response to fluid loading.
Dynamic parameters predict the response to fluid loading without having to give a fluid challenge. Hence
they may avoid the potential hazards of a fluid challenge.
Stroke volume variation, Systolic pressure variation and Pulse pressure variation with respiratory cycle and
are referred to as dynamic indicators of preload responsiveness.
Values>13% is indicative of fluid responsiveness
These parameters are available on minimally invasive cardiac output monitors such as Flotrac, PICCO,
LIDCO.
Visible variation in the diameter of the inferior vena cava on echocardiography can also be used to predict
fluid responsiveness.
SPV, PPV and SVV cannot be used in patients with spontaneous breathing activity and / or with
arrhythmias. They are not reliable in patients ventilated with low tidal volume and in patients with increased
intraabdominal pressure
In these cases Passive leg raising is an alternative choice.
Passive leg raising maneuver is an endogenous fluid challenge. A continuous monitor of stroke volume or
SVV / PPV is required. Increase in stroke volume > 10%, increase of Aortic blood flow >10% in response
or decrease in SVV / PPV after PLR predict a good response to fluid loading
38. ACUTE PULMONARY EMBOLISM (PE)

I. WHEN TO SUSPECT/ RECOGNIZE?

i) Introduction:

Venous thromboembolic conditions leading to acute respiratory failure is common in critically ill medical
and surgical patients. This may be the presenting diagnosis on ICU admission or may develop secondarily in
patient admitted to ICU for other conditions. PE presentation is variable presenting suddenly as a cardio
respiratory arrest or may be asymptomatic .Mortality can be reduced by prompt diagnosis and therapy .
Despite significant advances in the prevention and treatment of VTE, pulmonary embolism remains the
most common preventable cause of hospital death, being responsible for approximately 150,000 to 200,000
deaths per year in the United States
j) Case definition:

For both situations of care (mentioned below*)

PE refers to obstruction to main pulmonary artery or one of its branches by material (e.g., thrombus, tumor,
air, or fat) that originated elsewhere in the body. This topic review focuses on PE due to thrombus. PE can
be classified as acute or chronic. Patients with acute PE typically develop symptoms and signs immediately
after obstruction of pulmonary vessels. In contrast, patients with chronic PE tend to develop slowly
progressive dyspnea over a period of years due to pulmonary hypertension
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY

The incidence of DVT in India as reported is one percent of the adult population after the age of forty and is
15% to 20% in hospitalized patients. The risk of DVT is 50% in patients undergoing orthopedic surgery,
particularly involving the hip and knee, and it is 40% in patients undergoing abdominal or thoracic surgery.
1/100 who developed DVT can develop PE which can be fatal. As per India-specific ENDORSE data
presented at Geneva, 1 of 2 hospitalized patients in India is at high risk of developing VTE at any point in
time.

An autopsy data from PGI Chandigarh, where 1,000 consecutive autopsies were performed between 1997
and 2002. 14.4% showed evidence of pulmonary thromboembolism (PTE). 1.45 % of all hospital deaths
were due to PTE
 1. The mean age was 37 years with a male preponderance in the ratio of 1.82:1
2. Clinical suspicion was present in 29.17 % of cases
3. The most common underlying cases were

o Sepsis (40.28%)
o Respiratory illness (10.42%)
o Malignancies (9.72%)
o Renal disease (8.3%)
o Hepatobiliary disease (7.64%)
o Cardiovascular disorder (6.94%)
o Gastrointestinal tract disorder (3.47%)
o Vasculitis (2.78%)

III. DIFFERENTIAL DIAGNOSIS /TYPES

Acute PE can be further classified as massive or sub massive:
Massive PE causes hypotension, defined as a systolic blood pressure <90 mmHg or a drop in systolic blood
pressure of ≥40 mmHg from baseline for a period >15 minutes. It should be suspected anytime there is
hypotension accompanied by an elevated central venous pressure (or neck vein distension), which is not
otherwise explained by acute myocardial infarction, tension pneumothorax, pericardial tamponade, or a new
arrhythmia.
All acute PE not meeting the definition of massive PE are considered submassive PE.
A saddle PE is a PE that lodges at the bifurcation of the main pulmonary artery into the right and left
pulmonary arteries. Most saddle PE are submassive.
Acute PE should be differentiated from other causes of acute breathlessness
o Pneumonia
o Pneumothorax
o Acute Left Ventricular failure
o Acute exacerbation of COPD
o Acute bronchial asthma

IV. PREVENTION AND COUNSELING

Most of the acute PEs originate from deep venous thrombosis (DVT) of legs. Assessing patients at risk for
DVT and preventing its occurrence decreases the incidence of acute PE
Assess the risk factors for PE and deep venous thrombosis (DVT) from past medical history as mentioned
below:
 1. Prior venous thromboembolism.
2. Immobility for more than 48 hours—congestive heart failure, septic shock, surgery with general
anesthesia, on mechanical ventilation.
3. Abdominal or lower extremity surgery or trauma.
4. Hypercoagulable states.
5. Malignancy.
6. Spinal cord injury.
7. Heparin-induced thrombocytopenia.
8. Pregnancy or use of oral contraceptives.
9. Indwelling central venous catheters
10. Obesity
11. Congestive heart failure

Initiate adequate DVT prophylaxis

1. Unfractionated heparin(UFH) 5,000 I.U. twice or thrice daily subcutaneously.
2. Fractionated Low molecular weight heparin – enoxaparin 40 mg sub cut once daily or equivalent
3. Fondaparinaux
4. In patients with high risk of bleeding mechanical methods like intermittent pneumatic compression
or graduated stockings may be tried.

V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,

TREATMENT & REFERRAL CRITERIA

i) Clinical Diagnosis:

PE should be suspected in all patients who present with new or worsening dyspnea, chest pain, or sustained
hypotension without any other obvious cause

ASSESS CLINICAL PROBABILITY OF PE: Clinical probability of PE is based on either clinical

judgment or clinical decision rules (Wells and Revised Geneva Score) mentioned below.

Therevised Geneva score:

j) Investigations:

) and ABG should be ordered in all these patients. Although these tests
are nonspecific they do increase the index of suspicion.

k) Treatment:
1. Provide oxygen to maintain saturation at more than 90%
2. 0 ml isotonic crystalloid. Any more volume
resuscitation should be given with caution as it may increase RV wall tension and cause ischemia
and worsening of shock.
3. While diagnostic confirmation is awaited, anticoagulant treatment withsubcutaneouslow molecular
weight heparin or intravenousunfractionated (UFH) heparin should be initiated as soon as possible in
patients with a high clinical probability of PE if there are no contraindications.
4. UFH is preferred in hemodynamically unstable patients in whom thrombolytic therapy is being
planned. UFH is also preferred in critically ill patients in the ICU with PE requiring numerous
procedures. It is also preferred in patients with renal failure. Patients are considered to be
hemodynamically unstable if they are in shock or have a systolic blood pressure of less than 90 mm
Hg or a drop in systolic pressure of more than 40 mm Hg for more than 15 minutes in the absence of
new onset arrhythmia, hypovolemia, or sepsis
5. Most patients with acute PE are candidates for initial anticoagulant treatment with subcutaneous
low-molecular-weight heparin or fondaparinux or intravenous UFH. LMWH and Fondaparinux are
preferred over UFH.
6. The usual doses of Anticoagulation for PE are:
h) Clinical Diagnosis:

i) Investigations:

1. If the patient has a high probability of PE clinically or on the basis of a high probability score, and is
safely transferable to CT room and is in a position to cooperate with breath holding, he should
undergo multidetector CT (MDCT) for CT Pulmonary Angiography irrespective of his
hemodynamic status.
2. If the patient is hemodynamically unstable and has a high probability of PE clinically or on the basis
of a high probability score and who is critically ill and can not be shifted, he should be subjected to
Trans-esophageal Echo (TEE,), lower extremity ultrasonography and his blood sample sent for a D-
Dimer level.A negative Echo and Venous Doppler, however, do not rule out clinically significant
PE.Efforts should be made to stabilize this patient hemodynamically and once the patient stabilizes,
he should be sent for MDCT CT Pulmonary Angiography, if doubt still remains about the diagnosis.
 3. If the patient is hemodynamically stable and has a low or medium probability score then order a high
sensitivity D- Dimer level (ELISA). If it is positive (level more than 500ng/ml) further testing with
CT chest is indicated.
4.
5. A V/Q scan may be done in patients with a high probability of PE and where there is a
contraindication for CT like renal failure or if CT scanning is not available.
6. In pregnant women with clinical findings suggestive of PE, an MDCTchest should be done. The
concern about radiation is overcome by the hazard of missing a potentially fatal diagnosis or
exposing the mother and fetus to unnecessary anticoagulant treatment. Multidetector CT delivers a
higher dose of radiation to the mother but a lower dose to the fetus than V/Q scanning. Venous
ultrasonography can be done in these patients before MDCT.

j) Treatment:
CONSIDER THROMBOLYSIS:
a) If the patient is hemodynamically unstable:
i. Admit in ICU
ii. Start anticoagulation, preferably IV unfractionated heparin or LMWH. Keep APTT time 1.5-2.5 to
normal.
iii. Administer thrombolytic therapy if there are no contraindications (Table1).
iv. Other supportive measure to stabilize the patient.
b) Hemodynamically stable patients with right myocardial dysfunction and injury suggested by TEE and
markers (raised Troponin and BNP) can also be given thrombolytic therapy if there are no contraindications
(Table 2).

CONSIDER SURGICAL TREATMENT

Hemodynamically stable patient with PE without myocardial dysfunction or injury:
Admit in ward.
Anti-coagulate with LMWH or Fondaparinux or UFH.
Closely watch for vitals and respiratory distress. Consider early mobilization.

INITIATE VITAMIN K ANTAGONIST (WARFARIN) THERAPY:

Vitamin K antagonist should be initiated as soon as possible preferably on the first treatment day and
Heparin should be continued. Heparin should be discontinued when INR reaches a level of 2.0 or higher for
at least 24 hours. Duration of treatment is from 3 to 6 months.
LMWH is preferred over Warfarin in Cancer and in pregnant women for longterm treatment.

: Inferior vena caval filters are indicated in the following conditions:

Recurrent thromboembolism despite anticoagulant therapy
Contraindication to anticoagulation therapy
Bleeding while on anticoagulants.
Patient should be put on long term anticoagulant treatment in the following conditions:
Idiopathic pulmonary embolism
Recurrent PE
Cancer

39. SEVERE SEPSIS AND SEPTIC SHOCK

I. WHEN TO SUSPECT/ RECOGNIZE?

Introduction:

Sepsis(from Greek sepein = to rot, putrefy)is a significant problem worldwide in the intensive care unit both
in terms of the burden on the healthcare and the morbidity and the mortality it causes. Despite the advances
in the treatment and the understanding of the pathophysiology of sepsis, the mortality has remained
unforgivably high. The site of infection is difficult to estimate and even among those patients where the site
is strongly suspected, cultures might be negative or of questionable significance. Though a positive blood
culture would be diagnostic, the rate of positivity is only 30 to 50 % percent. It is easy to confuse the
diagnosis of sepsis with conditions that simulate it such as pancreatitis or anaphylactic reactions or drug
fever. Early identification and prompt treatment is the key to reduce mortality
a) Case definition:

Till 2001 there was no clear definition of sepsis. As a result there was no uniformity in the treatment
guidelines. International sepsis forum defined sepsis in the following way

Systemic inflammatory response syndrome (SIRS)
Two or more of the following variables
(1) fever > 38°C (100.40°F) or hypothermia <36°C
(96.80°F)
(2) tachypnea (>20 breaths/min) or PaCO2 < 32
mmHg
(3) tachycardia (heart rate >90 beats/min)
(4) Leukocytosis or leucopeniai.eWBC > 12,000
cells/mm3, < 4,000 cells/mm3 or > 10% immature
band forms
Sepsis Systemic inflammatory response syndrome that
occurs due to a “known or suspected” pathogen
(bacteria, virus, fungal or parasite)

Severe sepsis Sepsis plus evidence of organ dysfunction or tissue

hypoperfusion as follows –
(1) Altered mental status.
(2) ALI PaO2/FIO2 <250
(3) Thrombocytopenia < 100,000/
(4)Bilirubin >2mg/dl
(5) INR >1.5 or aPTT> 60 seconds.
(6) Urinary output of 0.5 ml/kg for at least 2hr or
Scr>2mg/dl despite fluid resuscitation.
(7) Tissue hypoperfusion as suspected by mottled
skin, Capillary refilling time ≥ 2 seconds or lactate
>4 mmol/l
(8) Hypotension Systolic blood pressure ≤90
mmHg or mean arterial pressure ≤70 mmHg.
Sepsis induced hypotension SBP<90mmHg or MAP<70mmHG or SBP
decrease >40mmHg

Septic shock Sepsis induced hypotension despite adequate fluid

resuscitation.

II. INCIDENCE OF THE CONDITION IN OUR COUNTRY

The incidence of sepsis and the number of sepsis-related deaths are increasing, although the overall
mortality rate among patients with sepsis is declining. The mortality rates associated with severe sepsis and
septic shock are 25% to 30% and 40% to 70% respectively Though we do not have exact statistics from
India, one Indian study showed incidence of SIRS without organ dysfunction as 51.60%, SIRS with organ
dysfunction as 17.10% patients, of which 76.50% were due to sepsis and 23.50% were not due to sepsis.
ICU mortality of all admissions was 13.90% and that of severe sepsis was 54.10%. Hospital mortality and
28-day mortality of severe sepsis were 59.30% and 57.60%, respectively.

III. DIFFERENTIAL DIAGNOSIS

Severe Sepsis and Septic shock should be differentiated from other common cause of fever
and shock in ICU or hospital like -
1) Acute pancreatitis.
2) Drug fever.
3) Anaphylaxis and anaphylactoid reactions.
4) Adrenal crisis.
5) Cardiogenic shock, hemorrhagic shock or neurogenic shock.
6) Pulmonary embolism or pulmonary infarct.
7) Myxedema coma.
8) Thyrotoxicosis.
9) Poisoning or insect bite.
10) Burn, major surgery
11) SLE crisis.
12) Macrophage activation syndrome.

Although making the distinction of the above conditions from true sepsis becomes difficult, using different
biomarkers and imaging studies might be helpful in making the diagnosis. Close monitoring and optimising
the patient physiological variables will give us time to identify the exact insult.

IV. PREVENTION AND COUNSELING

Sepsis is a medical emergency. Awareness and recognition are the key of survival.The following action plan
should be used to reduce global mortality from severe sepsis.
1. Build awareness of sepsis.
2. Follow standards guidelines of care.
3. Improve early and accurate diagnosis.
4. Increase the use of appropriate treatments and interventions.
5. Educate staff about sepsis diagnosis, treatment and management.
6. Data collection for the purposes of audit and feedback

V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,

TREATMENT & REFERRAL CRITERIA

Clinical Diagnosis:
The presentation of sepsis varies. The most important step towards improving survival is to identify the
signs of sepsis very early.
General variables:
1. Altered mental status.
2. Fever.
3. Hypothermia.
4. Tachycardia.
5. Tachpnea.
6. Hyperglycaemia (plasma glucose >120 mg/dL or 7.7mmol/L) in the absence of diabetes.
7. Positive fluid balance.

Inflammatory variables:
1. Leukocytosis.
2. Leukopenia.
3. Normal WBC count with >10 % band forms.

Organ dysfunction variables:

1. Respiratory –Decreased oxygen saturation
2. Renal – Acute oliguria urine output <0.5ml/kg/hr for atleast 2 hrs or rise in Creatinine > 0.5 mg/ dL.
3. Haematological- Thrombocytopenia (platelet count <100,000/ μL) or coagulation abnormalities:
International Normalised Ratio INR >1.5 or activated partial thromboplastin time aPTT > 60 sec.
4. Liver - Hyperbilirubinemia (plasma total bilirubin>4.0 mg/ dL or 70 mmol/ L).

Tissue perfusion variables:

Decreased capillary refill or mottling

Haemodynamic variables:
Arterial hypotension, Systolic Blood Pressure SBP <90 mm Hg, Mean Arterial Blood Pressure MAP <70
mm Hg, or SBP decrease >40 mm Hg.
l) Investigations:

Investigations should be directed at diagnosis, assessing the focus of sepsis, and the severity of the sepsis.
1) Hb
2) TLC
3) DLC
4) Blood Glucose.
5) Renal function tests (SE,BUN,Cr)
6) Liver function test (Bi,AST,ALT,ALKP,GGT,PT,INR,PTT)
7) Cultures with gram stain
8) Urine R/M
9) X-Ray
10) ECG
m) Treatment:

Standard Operating procedure

a. In Patient
Sepsis should be treated in the ICU, if recognized out side the ICU. Immediately start fluid resuscitation,
collect blood culture and give broad spectrum antibiotics within 1 hr, culture collection should not delay
antibiotic administration, and simultaneously organize ICUtransfer.
b. Out Patient

Resuscitation with fluid in the emergency department collect blood culture and give broad spectrum
antibiotics within 3hrs , culture collection should not delay antibiotic administration, and shift the patient in
the ICU.
c. Day Care

Do not admit septic patient in Day care setting.

n) Referral criteria:
Generally, patients can be considered for transfer for diagnosis, source control or further monitoring when
they are hemodynamically stable with or without vasoactive drugs and when oxygenation and ventilation is
maintained.
a) Need Invasive monitoring devices such as arterial lines, centralline, flow trac.
b) Mechanical ventilation, dialysis or CRRT required.
c) Modern surgical facilities.
d) Ultrasound and CT scan or MRI

Always communicate with receiving hospital physician, document the reason for transport and arrange
appropriate staff, medication and instrument for transportation.

l) Investigations:

ABG
SCVO2.
Serum lactate
Procalcitonin (PCT)
These biomarkers may be useful to distinguish between infectious and non-infectious causes of SIRS.PCT
can be used to assess the severity of infection and prognostication. It also acts as a tool to guide
Antimicrobial Therapy.
1. Ultrasonography (source identification)
2. CT scan if it is safe to do(source identification)
3. USG or CT guided sample from the source – minimally invasive approach is advisable to prevent
change in physiology and keep in mind the risk of transportation to imaging department.

m) Treatment:
Follow the Surviving Sepsis Campaign (SSC) International guidelines for management of severe
sepsis.Rapid diagnosis, expeditious treatment multidisciplinary approaches are critical and necessary in the
treatment of sepsis. The management of patients with sepsis starts on arrival at the emergency room prior to
ICU admission. Special focus on fluid and hemodynamic resuscitation and early antibiotics.
(1) Within the first 6 hours (Early goal-directed therapy)
Fluid therapy
1. Start resuscitation with fluid boluses if hypotension or serum lactate >4mmol/L to maintain
 -12 mm Hg and 12-15mmHg in
mechanically ventilated patient or intra abdominal hypertension.
 an >65 mm Hg



concurrent hemodynamic improvement.

hematocrit of >30% and/or dobutamine infusion (up to a maximum of 20 μg/kg/min).
Diagnosis
1) Cultures with gram stain- Obtain appropriate cultures before starting antibiotics provided this does not
significantly delay antimicrobial administration.
1. Two or more blood cultures.
2. One or more BCs should be percutaneous.
3. One BC from each vascular access device in place for >48 hours.
4. Other site cultures as clinically indicated Eg. Tracheal culture, sputum culture, ascetic fluid culture,
Urine cultures. (should be sent in lab within one hour)
Antibiotic therapy
1. Begin intravenous antibiotics early within the first hour of recognizing
Severe sepsis or septic shock.
o Broad-spectrum agents
o Active against likely bacterial/fungal pathogens
o Good penetration into the source
2. Reassess antimicrobial regimen daily
3. Combination therapy in Pseudomonas infections and in neutropenic patient.
4. De-escalation after culture sensitivity report.
Early and appropriate antibiotic therapy and control of the source of infection arethe major therapies shown
to improve survival in sepsis.
Source identification and control
1. Source of infection should be established as rapidly as possible and start measures to control the source
within the first 6 hours of presentation as soon as the initial resuscitation is done e.g. abscess drainage,
tissue debridement and removal of central line. In pancreatitis avoid early surgical intervention.
2. Source control measures must be directed at achieving maximal efficacy with minimal physiological
upset.
Vasopressor
1. Use norepinephrine or dopamine through central line to keep MAP ≥ 65mmHg administered as the initial
vasopressors of choice.
2.Epinephrine, phenylephrine, or vasopressin should not be used as the initial vasopressor in septic shock
3.Vasopressin 0.01 to 0.04 units/min may be subsequently added.
4.Epinephrine as the first alternative agent in septic shock when norepinephrine is not effective.
5.Do not use low-dose dopamine for renal protection.
6.In patients requiring vasopressors arterial catheter should be put as soon as practical.

Inotropic support
1.In case of myocardial dysfunction as evidenced by increased cardiac filling pressures and decreased
cardiac output dobutamine can be used.
2.Dobutamine infusion (up to a maximum of 20 μg/kg/min) if mixed venous oxygen saturation Svo2 <65%.
3.Do not target predetermined supranormal levels of cardiac index.

(2) After initial resuscitation (24 hours goal)

Steroid
1. Consider use of low dose intravenous Hydrocortisone (≤300mg/day)
a. Septic shock poorly responsive to fluid and vasopressors
b. Endocrine or corticosteroid history warrants it
2.Do not use steroids to treat sepsis in the absence of shock and wean it once vasopressors are no longer
required
3. Hydrocortisone is preferred to dexamethasone
4. There is no role of ACTH stimulation test while determining whether the patient should receive
hydrocortisone to treat septic shock.

Blood product administration

1. Packed red blood cells should be given to patients with hemoglobin less than 7.0 g/dL (<7.0 g/L).
Achieve target hemoglobin of 7.0 -9.0 g/dL in adults.In certain special circumstances, A higher hemoglobin
level may be required. (e.g.: myocardial ischemia, severe hypoxemia, acute hemorrhage, cyanotic heart
disease, or lactic acidosis)
2. Erythropoietin must not be used to treat sepsis-related anemia
3. In case of active bleeding, fresh frozen plasma may be used. But its use for correcting laboratory clotting
abnormalities is contraindicated unless an invasive procedure is planned.
4.platelets should be transfused in case of -
- Counts< 5000/ μL regardless of bleeding.
- Counts between 5000 to 30,000/ μL and there is significant bleeding risk.
- Higher platelet counts ≥ 50,000/ μL in case of surgery or invasive
1. procedures.
Mechanical ventilation of sepsis-induced acute lung injury (ALI)/ARDS
1.Target a tidal volume of 6mL/kg (predicted) body weight and plateau pressure ≤30cmH2O in patients with
ALI/ARDS.
2. Positive end expiratory pressure (PEEP) should be set according ARDS NET protocol to avoid extensive
lung collapse at end expiration and prevent over distention of normal lung.
3. Allow permissive hypercapnia if needed, to minimize plateau pressures and tidal volumes
4. Weaning protocol and a spontaneous breathing trial (SBT) regularly to evaluate the potential for
discontinuing mechanical ventilation.(1A)
• Daily SBT (spontaneous breathing trial)
• Before the SBT, patients should:
– be arousable
– be hemodynamically stable without vasopressors
– have no new potentially serious conditions
– have low ventilatory and end-expiratory pressure requirement
– require FiO2 levels that can be safely delivered with a face mask or nasal cannula
5. Do not use a pulmonary artery catheter for the routine monitoring.
1. 6. Consider early prone position or rescue therapy for refractory hypoxia.
7. Use a conservative fluid strategy for patients with established ALI/ARDS after initial resuscitation.
Lung protective ventilation strategy using low tidal volume ventilation reduces ventilator-induced lung
injury like volutrauma, barotrauma, atelectrauma and biotrauma. This is the only ventilator manipulation
that has been shown definitively to reduce injury and absolute mortality reduction of 9%.
Sedation, analgesia, and neuromuscular blockade in sepsis
1. Use sedation protocols with a sedation goal for critically ill mechanically ventilated patients.
2. Avoid neuromuscular blockers where possible. Monitor depth of block with train-of-four when using
continuous infusions.

Glucose control
1. Aim to keep blood glucose 150 - 180mg/dL using a validated protocol for insulin dose adjustment.
Renal replacement
1. Consider early renal replacement therapy
2. Intermittent hemodialysis and continuous veno-venous hemofiltration (CVVH) are considered equivalent.
3. CVVH offers easier management in hemodynamically unstable patients.
Bicarbonate therapy
1. Do not use bicarbonate therapy to improve hemodynamics or reducing vasopressor requirements
with lactic acidemia and pH < 7.15.
Deep vein thrombosis (DVT) prophylaxis
1. Use either low-dose unfractionated heparin (UFH) or low-molecular weight heparin (LMWH), unless
contraindicated.
2. Use a mechanical prophylactic device, such as compression stockings or an intermittent compression
device, when heparin is contraindicated.
3. Combination of pharmacologic and mechanical therapy high risk for DVT.
Stress ulcer prophylaxis
1. Provide stress ulcer prophylaxis using H2 blocker or proton pump inhibitor.
Consideration for limitation of support
Discuss advance care planning with patients and families. Describe likely outcomes and set realistic
expectations.

40. SEVERE COMMUNITY ACQUIRED PNEUMONIA

1. When to suspect/Recognize?
a. Introduction

Community acquired pneumonia affects 2 to 3 million patients per year and carries high mortality of around
30% in severe cases. As life expectancy is increasing and many patients with chronic diseases like cardiac
failure,COPD are living longer , more patients in community like oncology and transplant with
immunosuppressive therapy , incidence of community acquired pneumonia is increasing and distinction
from hospital acquired pneumonia is getting blurred as these patients visit hospital frequently.
b. Case Definition

Patient usually presents with a constellation of respiratory symptoms like cough, purulent sputum and
sometimes pleuritic pain associated with constitutional symptoms like fever, lack of appetite and myalgia.
Chest x-ray revealing new infiltrate usually clinches the diagnosis.
c. Incidence of the condition

Community-acquired pneumonia is a major cause of morbidity and mortality, worldwide

Lower respiratory tract infections, including CAP, were ranked third in a list of the 30 leading causes of
death worldwide. About 4 million CAP cases occur annually in the US; with about 20% requiring
hospitalization. High mortality trends observed in patients hospitalized for CAP (5-20%) and in CAP
patients admitted in ICU (up to 50%). Overall mortality rate of CAP is about 7.3%.
Typical CAP- Sudden onset fever, chills, pleuritic pain, productive cough.Raised TLC, ESR, CRP. Chest x-
ray shows diffuse patchy opacities. 60-80% produced by bacteria like -Strep pneumoniae, Staphylococcus,
Kleibseilla, Haemophilus
Atypical CAP- The organisms: virus, mycoplasma, legionella, chlamydia psittaci, Coxeillaburnetii.
Presentation: Preceding airway symptoms, myalgias, fever without chills, headache, unproductive cough.
TLC, ESR, CRP are either normal or show a mild rise. Chest x-ray shows- diffuse, patchy or ground glass
shadows
Assessment of Severity
This is a crucial step as it will help in identifying patient who are prone to get complication and should be
admitted in intensive care unit.
CURB 65 is a useful mnemonic for this
2. Confusion
3. Urea > 20 mg/dl
4. Respiratory Rate >30/min
5. Blood Pressure Systolic <90 mmHg
6. Age > 65 years
INVESTIGATIONS
1. Complete Blood Count
2. CRP
3. Urea ,Creatinine
4. Liver Function Test
5. Blood Culture – Two sets
6. Prothrombin Time
7. Na, K
8. Sputum for microscopy, gram stain, AFB stain, fungal stain, cytology
9. Sputum for culture and sensitivity
10. Chest X-ray
11. ECG
Procalcitonin
2. Chest CT scan
3. Chest ultrasound
4. Bronchoscopy with lavage
5. Echocardiogram
6. Urine for legionella and pneumococcal antigen
7. Serology for H1N1, HIV, ANCA , Legionella
8. Nasal Swab for MRSA,Viral Panel
9. NT PRoBNP
10. Venous Doppler legs
11. D Dimer

Treatment: Initial Choice of Antibiotic

A detailed history should be taken to identify patients who are at high risk of drug resistant infection.
1. Previous hospitalization in 9 months
2. Previous antibiotic in 3 months
3. Comorbidity – steroid use, liver failure, renal failure, COPD
Cover common organisms responsible for pneumonia: both typical and atypical
1. Strep pneumoniae
2. Legionella
3. Staph aureus (MSSA)
4. Gram negative bacilli (non ESBL)
5. Hemophilus
Antibiotic choices in these patients
A beta-lactam (cefotaxime, ceftriaxone, or ampicillin-sulbactam) + azithromycin
OR
A beta-lactam (cefotaxime, ceftriaxone, or ampicillin-sulbactam) + a respiratory
Fluoroquinolone (levofloxacin or equivalent)
OR
For penicillin-allergic patients, a respiratory fluoroquinolone and aztreonam
Additional organisms to be considered in patients at risk of drug resistantInfection
If ESBL or pseudomonas is a concern- Anantipneumococcal, antipseudomonal beta-lactam (piperacillin-
tazobactam, cefepime, imipenem, or meropenem) + either ciprofloxacin or levofloxacin (750 mg)
OR
The above beta-lactam PLUS an aminoglycoside and azithromycin
OR
The above beta-lactam PLUS an aminoglycoside and an antipneumococcalfluoroquinolone
(for penicillin-allergic patients, substitute aztreonam for above beta-lactam)
If MRSA is a concern- Add vancomycin or linezolid. Availability of other cephalosporin with
betalactamase inhibitors combination (Cefoperazone – sulbactam, Cefepime Tazobactam, cetriaxone-
sulbactam) and Class 1carbapenem- Ertapenem can be used to cover ESBLs as per the hospital antibiotic
policy andlocal antibiogram.
Duration of Antibiotic therapy: Duration of antibiotic should be individualized based on clinical
response,type of organismbiomarker response, development of complications and comorbidities. Minimum
five days ofantibiotic is recommended. Prolonged antibiotics upto twoweeks should be considered
inselected cases like slow responders, pseudomonas and staph infection,lung abscess , empyema,metastatic
infection.
Identification of Non-Responders
With appropriate antibiotic therapy some improvement in patients clinical course should beseen within 48 to
72 hours. This should be assessed clinically as radiographic resolution takes alonger time. For non-
responders following conditions should be considered.
1. Organism not covered by empiric choice of antibiotic
2. Atypical organisms – Tuberculosis, strongyloidosis, meliodosis , H1N1 influenza etc
3 Complicated pneumonia- Lung abscess, empyema. Obstruction, Resistant organism
4. Nosocomial problem- Secondary infection.
Differential diagnosis: Heart failure, cryptogenic organizing pneumonia (COP), Malignancy, Pulmonary
embolism, Pulmonary eosinophilia pneumonia, Hypersensitivity pneumonitis, vasculitis –Wegners
granulomatosis
Referral Criteria
 -responders should be managed at a higher facility for appropriate workup.
shock, multi-organ dysfunction

41. STATUS EPILEPTICUS

I. WHEN TO SUSPECT/ RECOGNIZE?

l) Introduction:

Status epilepticus (SE) is a state of continuous seizure without return of consciousness. Any seizure type can
progress to status epilepticus. Status epilepticus is a serious medical and neurological emergency which
requires efficient management as delay is associated with worse outcome. The prognosis depends
predominantly on the cause and duration of the SE and is good in rapidly reversible causes. Overall
mortality is 15.8 %.( 1) Additional 10 to 23% of patients who survived from status epilepticus are left with
disability.
Case definition: For both situations of care (mentioned below*)
Clinically definition of SE based on manifestations of continuous seizure activity and incomplete recovery
of consciousness between seizures for a ‘particular duration’. The criterion for duration is still ambiguous
and evolving issue. For all practical purposes, a patient should be considered in status epilepticus if seizure
activity lasting more than 5 minutes as very few single seizures will last this long.
Refractory Status Epilepticus (RSE): Appropriate definition is still not available. RSE is commonly defined
as seizure activity that continues after failure of first and second line antiepileptic drug therapy (AED)
therapy.
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY

Chin et al in a recent systemic review reported incidence rates of SE between 3.86 to 38 per 100,000 per
year in children and 6 to 27 per 100000 per year in adults in Europe. (2) Incidence has bimodal distribution
with peaks in children less than a year (135 to 156 per 100000 per year) and elderly (14.6 to 86 per 100000
per year).The annual incidence of Non convulsive status epilepticus (NCSE) is 2.6 and 7.8 per100000.
NCSE was documented in 8 % of all comatose patients without signs of seizure activity. Frequency of
refractory status epilepticus in patients with SE ranged from 31 to 44 %.
There is hardly any incidence data available in India. In a recent study NCSE was documented as a cause of
altered mental status in 10.5% of comatose patients without signs of seizure activity. The incidence of RSE
in SE patients in Indian series ranges between 12 and 19 %. (3)
III. DIFFERENTIAL DIAGNOSIS
Disorders that may mimic seizures are benign conditions like myoclonus,
fasciculations, tremors, tics, panic attack, psychogenic seizures and potentially
dangerous conditions like basilar artery transient ischemic attack, metabolic
encephalopathy and syncope. When doubt regarding diagnosis is present one
should always request neurological consultation and electroencephalogram
(EEG). Video- EEG monitoring may be useful for detection of ongoing
subclinical seizures and should be considered in critically ill patient with
unexplained altered mental status.(4)

IV. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,

TREATMENT & REFERRAL CRITERIA

a) Clinical Diagnosis:
SE is best divided into three categories:
Convulsive status epilepticus (CSE)
Non convulsive status epilepticus (NCSE)
Partial status epilepticus (PSE)
CSE is the most common form of SE characterized by rhythmic jerking of the body, limbs, tongue biting
and loss of consciousness. With increasing seizure duration the movements may become reduced although
generalized electrical activity continues in the brain.
NCSE may be difficult to diagnose and may be more common in the elderly population. Although there is
no accepted classification of NCSE, two major types are partial complex –which is subdivided on the basis
that whether the patient has underlying epilepsy or is in coma and petit mal.
In partial complex SE stereotypical movements such as lip smacking, chewing or picking at ones’ clothes
may occur and alteration of consciousness lasts more than 30 minutes as result of abnormal cortical
electrical activity. Physical examination should look for signs of occult head trauma, substance abuse, fever,
meningismus and diabetes. Always check for Medical Alert bracelets or wallet information and try to
contact relatives to determine prior medical and seizure history.

b) Basic Investigations
Complete blood count , electrolytes ,Blood urea nitrogen(BUN),serum creatinine,glucose,liver function test

c) Treatment
Initial general management:
1. Assess basic life support
2. Start supplemental oxygen, monitor oxygen saturation
3. Initiate seizure precautions (e.g., padding bed rails)
4. Monitor vital signs and ECG
5. Adequate venous access and liberal hydration should be started with normal saline to prevent
dehydration and rhabdomyolysis.
6. Blood pressure should be monitored closely, especially if seizures persist for more than 30 minute
7. Consider thiamine 100 mg IV and dextrose 25-50 g IV if blood
8. glucose is less than 60 mg/dl
9. Treat fever with acetaminophen and icepacks

Initial Antiepileptic drug treatment

1. In the setting of acute brain injury, treatment usually should be initiated after a single self limited
seizure. Initial AEDs (viz. Lorazepam and phenytoin) should be given as soon as possible.
2. Management of SE should begin within 5 minutes of seizure activity or after two seizures without
full recovery in between.
3. Give IV Lorazepam 0.1 mg/kg IV at 2mg/minIf Lorazepam is not immediately available, diazepam
10-20 mg or midazolam 2-5 mg can be substituted
4. Midazolam given intramuscularly is the promising treatment in prehospital settings
5. Start phenytoin 20 mg/kg IV load at <= 50 mg/min

a) Clinical diagnosis (as per situation 1)

b) Investigation
1. Blood and urine toxicology screen and when indicated pregnancy test and arterial blood gases,
serum ammonia level
2. Anticonvulsant medication levels
3. CT or MRI scan and lumbar puncture may be necessary to establish underlying diagnosis once
seizures are controlled.
4. NCSE can only be diagnosed by EEG.
5. Investigate to find the underlying cause of seizure

Common Aetiologies of seizures in critical care unit:

Neurological :
Cerebrovascular disease: infarct, haemorrhage, vascular malformation
Vasculitis
Infection: meningitis, encephalitis, brain abscess
Head trauma
Anoxia
Brain tumours
Neurosurgical procedure
Hypertensive encephalopathy/eclampsia/posterior reversible encephalopathy syndrome
Complication of Critical illness:
Acute systemic insult, sepsis, hypotension
Electrolytes imbalances: hyponatremia, hypocalcaemia, hypomagnesaemia, hypophosphatemia (especially
in alcoholics), hypoglycaemia
Toxins
Illicit drug use, especially cocaine
Organ failure: renal, hepatic
Medications /substance withdrawal: Benzodiazepine, barbiturates, alcohol
If none of the above causes are identified consider following less common aetiologies:Anti NMDA
receptor limbic encephalitis(LE),Anti glutamate receptor LE,Paraneoplastic LE,Hashimotos'
encephalopathy.(5)
c)Treatment
Additional general management
1. Consider intubation to maintain airway patency
2. Monitor for arrhythmias, hypotension and respiratory failure

Antepileptic drug treatment

1. Start phenytoin 20 mg/kg IV load at <= 50 mg/min or Fosphenytoin at 20 mg phenytoin equivalents
(PE)/kg at =< 150 mg PE/min
2. Seizure activity not resolving with two anticonvulsants:
3. Give Phenobarbital 10-20 mg/kg IV at <70 mg/min.
4. Call for continuous EEG monitoring
5. Consider neurological consultation
6. Consider administration of following alternative agents:
7. Midazolam drip: 0.2 mg/kg slow IV push, followed by 0.1-2 mg/kg/hr to stop electrographic and
clinical seizures or
8. Propofol: 2 mg/kg load and 2-10 mg/kg/hr to stop clinical and electrographic seizures or maintain
burst suppression on EEG
9. Valproate 15 mg/kg IV load may be useful as an adjunctive agent.
 10. Pentobarbital 3-5 mg/kg IV to induce burst suppression; in most adults pentobarbital bolus 400 mg
over 15 min. every 15-30 min. until burst suppression appears is well tolerated, followed by infusion
at 0.3-9.0 mg/kg/hr to maintain burst suppression.(7),(8)
11. For all infusions, decrease infusion rate periodically to check EEG burst suppression pattern; if
electro cerebral silence occurs, decrease the dose till bursts are seen again.(4)

42. INITIAL MANAGEMENT OF SEVERE TRAUMA

1. When to suspect/Recognize?

a. Introduction: There is an increasing incidence of accidents and crimes in India with increasing
urbanization and attendant emergency admission of trauma victims. A comprehensive trauma care is lacking
in majority of places. As this malady affects predominantly young patients it is a heavy burden to the
exchequer. Improving organized trauma care with easy accessibility is an urgent need in our country.

b. Case definition: The American Trauma Society defines trauma as an injury caused by a physical force.
More often, trauma is the consequence of motor vehicle crashes, falls, drowning, gunshots, fires and burns,
stabbings, or blunt assaults.

Lot of emphasis has been placed on aggressive initial management of trauma. The concept of prehospital car
is highlighted by the Golden Hour, which may be defined as the period during which all efforts are made to
save a life before irreversible pathological changes can occur thereby reducing or preventing death in the
second and third phase. This period may range from the time of injury to definitive treatment in a hospital.
The first platinum 10 minutes becomes important to make this golden hour effective and should be
distributed as follows to make it fruitful.
Time lines: Assessment of the victim & primary survey- 1-minute, Resuscitation & stabilization – 5 min,
Immobilization & transport to nearby hospitals 4 minutes.
2. Incidence of the condition in our country

India contributes to 10% of world trauma with vehicular accident every 3 min & death every 10 min. Road
traffic injuries are a major cause of mortality responsible for 22.8% of death related to injuries.The lower
and middle-income group countries, including India contribute about 90% of the global burden of injury
mortality. Uncontrolled bleeding is a leading cause of death in trauma. In fact, death in trauma follows a
trimodal distribution of death. First peak occurs immediately after an accident. Second peak occurs 1-4
hours later and the third peak occurs 1-5 weeks later.
The initial management is usually done by paramedics, and an adequately trained team with skills in
maintenance of airway, control of external bleeding and shock, immobilization of the patient and
transportation. This has to be tied to early arrival of trauma ambulance and a system of triaging and
notifying the receiving hospital with a central coordination.
3. Differential diagnosis:

In Polytrauma, the assessment of the extent of injuries is very important. A head to toe examination
facilitates identifications of brain & cervical spine trauma, thoracic or abdominal or major skeletal trauma.
If shock persists after resuscitation, patient must be evaluated for any other covert internal injuries. All
patients with head injury should be assumed to have a cervical spine injury as well unless proved otherwise
clinically or radiologically.
4. Prevention & Counseling:

Road safety & pedestrian safety are two important issues. Most of the trauma victims are either pedestrians
or bicyclists. Strict implementation of traffic rules and measures like wearing helmets, lane driving and
implementing speed limits are important issues that need to be uniformly applied across India. A robust
prehospital ambulance system manned by qualified emergency medical technicians will help in improving
survival significantly.
Trauma victims are generally young and bread winners for their families. Any such death or disability is
associated with significant financial and psychological trauma to the victim and his family. Adequate
counseling and support is required for the trauma patients and their families.
5. Optimal diagnostic criteria, investigations, treatment & referral criteria

Facilities required
1. Medical Personnel with basic training in airway management and resuscitation
2. Basic Airway management equipment
3. Cervical collar
4. Spine Board
5. Scoop stretcher
6. Basic Volume resuscitation items like i.v fluids and i.v cannulas
7. Continuous oxygen supply and suction
8. Chest tube drainage system
9. Fracture stabilization material

10. Surgical sutures and hemostatic forceps.

11. X-ray & ultrasound facilities
12. Abdominal paracentesis equipment
13. Access to Blood Bank
14. Routine hematology, biochemistry, coagulation testing facility
15. Transport to higher center.
Clinical diagnosis: This remains the mainstay of diagnosis.
Investigations: Facilities like CT scan/MRI etc. are not available. Simple x-ray & Ultrasound should be
available. Basic investigations like hematology, biochemistry, coagulation parameters should be available.
Treatment: Quick identification and assessment of the extent of external injuries should be made. Basic
care like intravenous access, fluid or blood resuscitation should be done. Splinting & bandaging of injured
extremity or scalp should be done. Airway, breathing & circulation should get priority. Internal injuries and
head injuries cannot be managed and should be referred to higher centres. These centers should have a clear
policy on transfer of trauma patients and all patients who cannot be managed there should be shifted after
initial treatment and resuscitation.
Facilities required
1. Trauma Team with an on call rota and quick response time. The team should consist of a trauma surgeon
or a general surgeon, intensive care or emergency medicine physician,

Neurosurgical team, cardiothoracic team, orthopedician& anaesthesiologist.

2. The trauma team should be adequately supported by trained nurses and paramedical staff
3. Focussed abdominal ultrasound in trauma (FAST)
4. Portable X-ray facility
5. CT scan& MRI
6. Transport ventilator
7. Spine board
8. Scoop stretcher
9. Cervical immobilization devices
10. Difficult airway management equipment
11. Thoracotomy equipment
12. Portable echocardiogram
13. On site blood bank
14. Intravenous fluid warmed
15. Rapid i.v. infusion system
16. Central lines
17. Round the clock OT facility
18. Pericardiocentesis equipment
19. Trauma protocol to guide management
The principles followed in clinical diagnosis, investigations & treatment are same as above. However a
more organized approach is used, which is described below.
1. TRIAGE :Triage is a process of determining the priority of patients’ treatment based on the severity of
their condition and the resources available to provide that treatment. . In multiple casualty incidents, the
number of patients and the severity of their injuries do not exceed the ability of the trauma care facility. The
patients with life-threatening injuries are treated first. In mass casualty incidents, the number of patients and
the severity of their injuries exceed the capacity of the trauma care facility. Here, the patients with the
greatest chance of survival are treated first.

2. Primary Survey and Resuscitation: Primary survey involves rapid early assessment of the patient. The
life threatening conditions are identified and treatment priorities are established based on their injuries, vital
signs and injury mechanisms. During the primary survey, the following aspects are assessed and rapid
corrective measures taken.
a) Airway maintenance with C-Spine Control
b) Breathing and Ventilation
c) Circulation and /hemorrhage Control
d) Disability/ Neurological Status
e) Exposure/ Environmental Control

Airway with C-spine control

The patency of the airway should be assessed with special attention to foreign body or maxillo-facial
fractures that may result in airway obstruction. Chin-lift or Jaw-thrust maneuver may be used to achieve
airway patency simultaneously protecting the cervical spine. A definitive airway is warranted in a patient
with an altered level of consciousness or a Glasgow Coma Score of 8 or less. It is critical to protect the
spine. Spinal injury should be assumed in any patient of trauma unless specifically excluded.
Breathing and Ventilation
The patient’s chest should be exposed to adequately assess chest wall excursion. Auscultation to detect
adequate air entry, percussion to exclude air or blood in chest and visual inspection and palpation to detect
injuries to chest wall should be carried out. Specific life threatening problemssuch as tension pneumothorax,
massive hemorrhage, flail chest and cardiac tamponade should be identified immediately and addressed
during the primary survey
Circulation with Hemorrhage Control
Hemorrhage is the primary cause of shock in trauma patients. Rapid and accurate assessment of the patient’s
hemodynamic status and identification of the site of hemorrhage is therefore essential. It is critical to
establish adequate intravenous access in a trauma patient. While the primary survey is going on, two
intravenous lines should be established with short broad gauge cannula, preferably in the upper extremities,
and resuscitation started with crystalloids.
Disability / Neurological Status
A rapid neurological evaluation is carried out at the end of primary survey after the resuscitation and before
rapid sequence intubation. This assesses the patient’s level of consciousness, papillary size and reaction and
focal neurological deficit. The level of consciousness may be described in terms of Glasgow Coma Scale
(GCS).
Exposure / Environmental Control
The patient should be completely undressed to facilitate thorough examination and assessment. At the same
time care should be taken to prevent hypothermia to the patient.
Adjuncts to Primary Survey and Resuscitation
a) ECG Monitoring: The appearance of dysrhythmias may indicate blunt cardiac injury. Pulseless electrical
activity, the presence of cardiac rhythm without peripheral pulse may indicate cardiac tamponade, tension
pneumothorax or profound hypovolemia.
b) Urinary Catheter: Urine Output is a sensitive indicator of the volume status of the patient and reflects
renal perfusion. All trauma victims should be catheterized to enable monitoring of the urine output and plan
intravenous fluid therapy. Transurethral catheterization is contraindicated in patients urethral transaction is
suspected.
c) Gastric Catheter: A gastric tube is indicated to reduce stomach distension and decrease the risk of
aspiration. It should be passed via the orogastric route in patients with head injury and suspected base skull
fracture.
d) X-rays and Diagnostic Studies: The chest and pelvis x-ray help in the assessment of a trauma patient.
Any trauma patient entering the red area of the emergency should undergo blood sampling. The blood
should be sent for cross-match and arranging for packed cells, and important diagnostic parameters such as
hemoglobin, renal parameters, ABG should be checked. Pulse oximetry is a valuable adjunct for monitoring
oxygenation in injured patients.

e) FAST: Focused Assessment by Sonography in Trauma is a rapid non- invasive tool used to assess free
fluid in the abdomen, blunt abdominal injury and cardiac tamponade.
f) CT scan & MRI: For brain, spinal cord trauma and in injury to internal organs.
Secondary Survey
Once the primary survey is accomplished, life- threatening conditions are managed and resuscitative efforts
are underway, secondary survey is carried out. This is head to toe evaluation of trauma patient, which
includes a complete history and physical examination and reassessment of all the vital signs. Each region of
the body is completely examined. The care continues with regular re-evaluation of the patient for any
deterioration and new findings, so that appropriate measures can be taken.
Reevaluation
After the completion of the secondary survey, the patient should be reevaluated beginning with the
ABCs and thorough physical examination and examined for any missed injury such as fractures.
Constant monitoring of the severely injured patient is required and may necessitate rapid transfer to
the surgical intensive care unit, operating room or to another centre having better specialized
facilities. The transfer to another centre should not be delayed for the want of investigations.

43. TRAUMATIC BRAIN INJURY

I. a) When to suspect / recognize?

Traumatic Brain Injury is usually associated with road traffic accidents or criminal assault. It could also
happen due to a fall or due to industrial mishaps. Nevertheless the disorder is usually obvious and history is
generally clinching. In situations where the history is not forthcoming any injury or mishap associated with
the change in the level of consciousness of the individual should be deemed to be associated with brain
injury unless proved otherwise.
b) Case definition: The term TBI is self explanatory. However the course in hospital for a patient with TBI
is characterized by 2 major injuries – Primary and Secondary
Primary injury is the injury sustained by the patient and is related to the mechanism of injury. Secondary
injuries are those sustained during the transport and treatment of patients with TBI. This is the more
common cause of altered consciousness amongst TBI patients. Some of the causes of secondary injury are
1. Seizures
2. Hypotension
3. Hypertension
4. High and Low blood sugars
5. Elevated body temperature.
6. Electrolyte imbalance.
7. Hypoxia

II. Incidence of the condition in our country

Incidence of road traffic accidents in India is amongst the highest in the world, and is rising. As per the
report of the National Crime Records Bureau 2001, 2,710,019 accidental deaths, 108,506 suicidal deaths
and 44,394 violence-related deaths were reported in India. A significant proportion of the deaths due to
accidents and violence are due to head injuries. A study from NIMHANS revealed that minor, moderate and
severe brain injuries (due to RTIs) were recorded in 60%–65%, 16%–20% and 15%–20% of cases as per the
Glasgow Coma Scale (GCS) grading. Mortality was higher among those with severe brain injuries.
Polytrauma was documented in 1%–21% of cases. Facial, chest, abdominal and limb injuries were
documented in 48%, 3%, 1% and 10% of cases, respectively.
III. Differential Diagnosis:

The differential diagnosis of traumatic brain injury is generally straight forward. However when the history
is not forthcoming, differential diagnosis should include
1. Ischemic stroke
2. Sub arachnoid hemorrhage
3. CNS infections
4. Toxic encephalopathies

IV. Optimal Diagnostic criteria, investigations, treatment and referral criteria:

Situation 1: In non metro situation with limited resources:

Investigations:
1. CT Scan of the brain with or without contrast
2. Serum electrolytes
3. Blood sugar
4. Chest X-ray

Treatment
1. Maintenance of oxygenation and blood pressure: Hypoxia and hypotension are common causes of
secondary brain injury. Mortality amongst patients whose saturations are < 60% is close to 50%.
Duration of hypoxia is also a determinant of adverse outcomes.
2. Intubation when GCS < 8 is recommended. Mechanical ventilation is instituted to maintain PaO2
and control PaCO2
Similarly, both pre and intra hospital hypotension are predictors of adverse outcomes. It is
recommended that systolic blood pressure should not be less than 90 mm Hg. If hypotension does
occur initially, all precautions need to be taken to avoid recurrent episodes. In resource limited
settings management of TBI on the basis of Cerebral Perfusion Pressure may not be feasible and is
recommended as an optional strategy.
3. Hyperosmolar therapy: 20% Mannitol and Hypertonic Saline.Their use is indicated when raised
intracranial pressure is suspected.Mannitol can either be used as a single short term agent or as a
continuous therapy. However, repeated use of Mannitol over several days is not known to be
effective.
 4. Surgery, indicated for evacuation of extradural or subdural hematoma, intracranial hemorrhage,
depressed skull fracture, other surgery in case of associated polytrauma
5. Anaesthesia, analgesia and sedation: Providing adequate analgesia and sedation is crucial for a
patient with TBI with or without raised ICP. Morphine and midazolam can be used.
6. Infection Prophylaxis: Prevention of other systemic infections is also important in TBI. Early
extubation is recommended if the patient has an intact gag and cough reflex.
7. Thromboprophylaxis: Patients with TBI are at a high risk of deep venous thrombosis. This risk
increases with the increase in the severity of brain injury. Prophylaxis is either mechanical or
pharmacological or both. The use of mechanical intermittent pneumatic compression (IPC) devices
is strongly recommended for all patientswith TBI except when there are coexistent lower extremity
injuries.
8. A combination of IPC with low molecular weight heparin is superior to using either modality alone.
However, initiating LMWH or Heparin within 24 hrs of surgery is not recommended. No specific
agent is superior to the others. However, the use of pharmacoprophylaxis might be associated with a
higher chance of intra cranial bleeding.
9. Anti Seizure Prophylaxis: Post traumatic seizures can be early onset (<7 days) or late onset (>7
days). Both need to be prevented. Risk factors for PTS include
GCS<10
Cortical contusion
Depressed fracture
Sub dural hematoma
Epidural hematoma
ICH
Penetrating head wound
Seizure within 24 hrs of injury.

10. Phenytoin can be used for preventing early onset PTS. No role can be made out for prophylactic
drugs to prevent late PTS. Valproate is as effective as Phenytoin in preventing PTS but is associated
with higher mortality.
11. Hyperventilation: Prophylactic hyperventilation is not recommended. It is a temporary measure.
Whenever Hyperventilation is frequently required monitoring of SjVO2 or brain tissue oxygen
tension is recommended. Therefore such patients need to be referred to a centre with facilties to do
so.
12. Steroids: No role in the management of TBI

Transfer / Referral Criteria

 1. Non-availability of CT scan or neurosurgical expertise
2. Persistent unconsciousness with GCS < 8, seizures
3. Persistent high intracranial tension, clinically and on CT scan, despite medical and initial surgical
management
4. chest trauma
5. Ongoing requirement of mechanical ventilation, hemodynamic instability
6. Requirement for intracranial pressure monitoring

b)Investigations: as per situation 1 plus

1. MRI
2. Intracranial pressure and cerebral perfusion pressure monitoring
3. Serum osmolality
4. EEG monitoring

c) Treatment: as in situation 1 plus:

1. Hyperosmolar therapy: hypertonic saline. A close monitoring of the serum osmolality is warranted.
A central venous access is preferable for administration of hypertonic saline
2. Intra cranial pressure (ICP) Monitoring:

Indications:
1. Patients with TBI who have a GCS < 8 and for those who have an abnormal CT scan. The
abnormalities include hematomas, contusion, oedema, herniation and compressed basal cisterns.
2. Age of the patient is > 40 years, patient has systolic pressure <90mm Hg or there is abnormal motor
posturing.

The need for ICP monitoring is an indication for transferring the patient to a facility with the expertise in the
technique. It is not recommended for use in non metro areas and resource limited settings.
ICP Monitoring methods:
The ventricular catheter connected to an external strain gauge is the best available tool for ICP monitoring.
It is the least expensive and currently most accurate. It also gives a therapeutic option of CSF drainage.
Fibreoptic transduced monitors are also accurate but more expensive.
1. ICP Thresholds: Measures to regulate ICP should be initiated if the pressure exceeds 20 mm Hg.
Treatment should be tailored on the basis of clinical and CT findings with ICP as a guide.
2. CPP Thresholds: CPP should be maintained between 50-70 mmHg. Attempts to achieve CPP>70
are associated with a higher incidence of ARDS. CPP<50mm Hg should be avoided.
3. Brain oxygen monitoring: Wherever facilities for jugular saturation monitoring are available,
SjVO2 should be maintained >50%. If brain tissue oxygen tension is monitored then PbtiO2 should
be maintained > 15mm Hg. Jugular venous oxymetry is recommended when hyperventilation is used
with a therapeutic intent.
4. Anaesthesia, analgesia, sedation, neuromuscular blockade
5. Propofol is recommended in moderate doses as a sedative for its beneficial effects on ICP and
cerebral perfusion pressure. High dose propofol infusion can trigger Propofol Infusion Syndrome
and is therefore not recommended.
6. Opioid analgesics and benzodiazepines are recommended. Morphine and Midazolam can be
combined with opioid analgesics for sedation.
7. Barbiturate infusions are recommended for control of raised ICP.
8. If ICP remains high neuromuscular blocking agents may be considered.
9. Continuous EEG monitoring may be used wherever available to titrate the dose of sedatives.
10. Prophylactic Hypothermia: The use of prophylactic hypothermia in patients with raised ICP is
based on the fact that hypothermia decreases the metabolic activity of the injured brain. This reduces
the cerebral metabolic rate for oxygen and minimizes the extent of brain injury. The target
temperature is 32-330C to be maintained for atleast 48 hrs. However, monitoring patients on
hypothermia regimen needs core temperature monitoring and may not be available in resource
limited settings. If patients are considered fit for transport, it is advisable to transfer them to a centre
with the facilities and experience in using hypothermia.
Nephrology and Hemodialysis
46. VASCULAR ACCESS
Rationale: Vascular access has been described as the “Achilles Heel” of hemodialysis. Although a working
A V fistula should be ideally constructed prior to starting dialysis a large number of patients first come to
attention as end stage renal disease when they require emergency dialysis. These patients start and
sometimes continue dialysis with catheters, running all the attendant risks of infection and central vein
thrombosis. The regular monitoring of an AV fistula and early intervention for stenosis can prolong the life
of these accesses. Comprehensive care of a vascular access involves a team approach involving the patient
and several caregivers in order to obtain the best possible results and a basic approach to this is set down
here.
The responsibility of evaluating a patient, creating and preserving a vascular access should be a team effort
and should include the following members each of whom have specific responsibilities.
1. Dialysis Nurse / technician
2. Resident doctor/medical officer
3. Nephrologist
4. Vascular/General surgeon/Urologist
5. Interventional Radiologist/Nephrologist.

Types of Access
Permanent (Fistulae & grafts)
o Radio cephalic AV fistula
o Sephaneous vein forearm grafts
o Brachiocephalic AV fistula
o Brachiobasilic fistula with transposed vein
o Upper arm autologous sephaneous vein grafts
o PTFE grafts (straight or U) in any site.

An attempt should be made to provide every patient on Hemodialysis with a permanent vascular access in
the order listed above.
- 65% or more of patients starting HD should do so with an AV fistula, and 90% or
more of prevalent patients should dialyze with an AV fistula.
it is recommended
that these patients may begin dialysis with a temporary access and an attempt to construct a permanent
access should be made within the 1st 3 months on HD.

Autologous Sephaneous vein grafts may be preferred to PTFE grafts because of lower costs and
thrombogenicity.
Responsibility – Nephrologist.
Temporary

temporary access of choice either when

1. A permanent access has been created and is expected to mature within 90 days.

2. A period of waiting before the permanent access can be created is anticipated.

3. Partial or complete recovery is expected.
The sub-clavian vein should not be cannulated as a temporary access unless the internal jugular is unusable
and no permanent access is possible ipsilaterally. Even a single cannulation is associated with a 35% risk of
stenosis.
The femoral vein on the left side may be used as a temporary vascular access with rigid single lumened
cannulae in an emergency situation only. Cannulae in the femoral vein should not be retained for longer
than 5 – 7 days and should never be used in the outpatient setting. Right sided femoral vein cannulation
should be avoided if the patient is to undergo a future renal transplantation.
-Permanent

anterior chest wall should be utilized as semi-permanent access. The cuff should be placed subcutaneously
above the clavicle and at a distance of 3 – 4 cm from the exit site.

Selection and Site of vascular access.

All patients of CKD should have an AV fistula constructed at Stage IV or when the serum creatinine is > 5
mg% or the anticipated start of HD is < 6 months away.
Configuration:- The radiocephalic AV fistula on the non-dominant upper limb should be the 1st choice of
AV fistula.
The “ Rule of 6” should be followed in deciding when to use an AV fistula,
o 6 weeks from the time of creation,
o a vein of at least 6 mm in diameter with clearly distinguishable margins,
o a cannulation length of at least 6 cm from the anastomosis,
o flow of at least 600 ml/min and a depth of not more than 6 mm from the skin. Numerous collateral veins
should not be visible and there should be no evidence of venous hypertension.
Initial cannulation should be with 17G needles equipped with a “back eye”. Flows of upto 200 ml/min can
be obtained with a 17G needle. Subsequent cannulation should be with a 16G needle to obtain flows of 300
ml/min and with a 15G needle to obtain flows of > 300 ml/min.
Venous grafts, both autologous and PTFE may be used within three weeks of construction.
Design and performance of temporary accesses. The diameter of the cannula and the length are the 2
criteria responsible for the blood flow obtained.
1. Single lumened femoral cannulae should be at least 19 cm long to reach the IVC. Flows of > 200
ml/min are not obtained with standard femoral single lumened cannulae.
2. The length of a cannula in the right Internal jugular vein should be around 13.5 cm for an adult
Indian patient, while that of a left internal jugular cannula should be around 16 cm, that of a right
sub-clavian cannula should be 15 cm and a left subclavian vein cannula around 16 cm.
3. The cannulae should be at least 12 French to obtain flows of 300 ml/min and 14 french if higher
flows are to be obtained.
4. 8 & 10 French cannulae can be used in children.
5. Cuffed tunneled cannulae should have a total length of at least 35 cm for right internal jugular
cannulation and a length of 44 cm for left internal jugular cannulation.

Patient preparation and Evaluation prior to access

A history should be obtained regarding previous central venous cannulation, arterial cannulation, previous
attempted AV fistulae, and failure including the time and possible cause of access failure, presence of severe
cardiac disorders, malignancy and prothrombotic tendency or anticoagulation.

o Physical examination should include

a. Examination of peripheral pulses
b. Bilateral upper extremity blood pressure measurement.
c. Allens test & Modified Allens Test
Allen's test assesses collateral circulation in the hand, in 2 steps.
Step 1 occludes the radial artery for several minutes and compares the hand color to the other hand. The
hand is said to have sufficient collateral circulation through the ulnar artery if there is no change in color.
Step 2 occludes the ulnar artery. A change in hand color means the potential for radial artery occlusion is
high. That is a positive Allen's test, which contraindicates radial-artery use for an AV fistula
Modified Allen's Test
The procedure for performing a modified Allen's Test is as follows:
o Instruct the patient to clench his/her fist, or if the patient is unable, close the hand tightly.
o Apply occlusive pressure with the fingers to both the ulnar and radial arteries. This maneuver obstructs
blood flow to the hand.
o While applying occlusive pressure to both the arteries, have the patient relax his/her hand. Blanching of
the palm and fingers should occur. If it does not, you have not completely occluded the arteries with your
finger.
o Release the occlusive pressure on the ulnar artery. Flushing of the hand should occur within 5 to 15
seconds. This denotes that the ulnar artery if patent and has good blood flow. This normal flushing of the
hand is considered to be a positive modified Allen's test. A negative modified

Allen's test is one in which the hand does not flush within the specified time period. This indicates that ulnar
circulation is inadequate or nonexistent. The radial artery supplying arterial blood to that hand should not be
used for an AV fistula.
4. Presence of edema.
5. Presence of collateral veins
6. Collapsibility.

Pre op Imaging/mapping
1. Ultrasonographic mapping of venous drainage of the extremity is recommended in difficult cases. A
tourniquet should be applied to the upper arm and the vein diameter measured. The vein diameter
should be between 2 & 2.5 mm. This assessment should be done when patient has achieved near
ideal volume status.
2. In cases of previous 1 or more fistula failure and history of central vein Cannulation venography
should be done for patency & adequacy of peripheral & central veins.
3. Patients with 1 or more previous fistulae lost due to early thrombosis should have a thrombotic
screen done.

Preservation of peripheral and central veins

1. Patients with CKD IV or V should not have venipunctures or peripheral cannulae inserted in the
forearm or above the wrist once a decision to create an A V fistula for dialysis has been taken.
2. Patients admitted in hospital should be provided with bracelets labeled “No Venipuncture” to be
worn during admission.
3. Out patients should be educated about preserving of forearm veins.
4. The subclavian vein should not be cannulated as a temporary access unless the internal jugular is
unusable and no permanent access is possible ipsilaterally. Even a single cannulation is associated
with a 35% risk of stenosis.
Cannulation and Use of a Vascular Access
Every vascular access should be examined at each hemodialysis session prior to starting dialysis.
o Fistulae should be examined for a low pitched continuous bruit, and a thrill, absence of edema, normal
limb temperature, absence of ischemia, steal and large collateral veins.
o Fistulae should not have a water hammer pulse on examination.
o Veins should collapse upon raising the arm above the level of the heart.
The entire arm should be cleaned with 2% alcoholic chlorhexidine prior to needle insertion.
A railroading technique rather than a buttonhole technique should be followed for cannulation.
o Railroading – At each dialysis session, puncture of the fistula should be done 1 to 2 mm away from the
previous point and a return to the original site should occur after 6 – 7 sessions.
o Buttonhole – Every puncture is done through an identical point. This eventually leads to decreased pain
sensation at the site but also to weakening of the vein wall and aneurismal dilatation.
o The “arterial needle” should point towards the anastomosis and the “venous needle” should point away
from the anastomosis.
The skin at the site of puncture should be infiltrated with 2% Xylocaine using a 26G needle. Alternatively
the entire region should have been applied with a Lignocaine-Prilocaine gel, at least 30 minutes prior to
puncture to minimize pain.
Removal of needles should be accompanied by dusting of an antibacterial powder.
Firm digital pressure over a sterile guaze should be given to the site of needle insertion for 10 minutes after
removal of the needle followed by application of a sterile adhesive dressing.
Tight tourniquets should not be applied to a fistula limb.

Care of a vascular access

1. Dressings of a vascular access should be transparent, occlusive, and strong enough to resist the
weight of the dialysis cannula. Micropore or Tegaderm is a useful dressing
2. The skin around the exit site of the access site should be clipped of hair, and tincture benzoin should
be applied to the area prior to application of the dressing.
3. Mupirocin ointment should be applied to the exit site of both cuffed and uncuffed cannulae.
4. Mupirocin ointment should also be applied to the external nares, axilla and groin in patients using
cuffed tunneled cannulae as a vascular access, who have been found to be staphylococcal carriers.

5. Surveillance cultures should be carried out using nasal swabs of all patients and dialysis personnel
once a year and nasal staphylococcal carriers treated.
6. Patients and the attendants should wear a disposable surgical mask during any manipulation of the
cannula, dressing changes and connection and disconnection to the dialysis machine.
7. Dressings should be changed weekly and whenever wet, visibly soiled or stained with blood or other
material. Cannulae should not be unnecessarily manipulated.
8. The hubs of the cannulae should be cleaned with sterile swabs soaked in 2% alcoholic chlorhexidine,
the connection to blood tubings done without touching the hubs or connectors, and the joint wrapped
with a swab soaked in 2% alcoholic chlorhexidine or 10% povidone iodine for 10 minutes.
 9. The cannula should be flushed with sterile saline till free of blood prior to anticoagulant instillation
after each dialysis.

Monitoring and detection of Complications

The maximum blood flow obtained from the access should be documented at each dialysis.
1. A progressive drop in the flow obtained with needles of the same guage properly positioned should
prompt further investigation of the access for stenosis.
2. Venous pressure should not be used to monitor stenosis in an AV fistula vein but may be used to
monitor stenosis in an A V graft.
3. The venous pressure should be measured using 17G needles within the first 5 minutes of dialysis at a
blood flow of 200 ml/min. Serial readings are more useful than single. An increase of more than
20% or an absolute value persistently > 120 mm of Hg is indicative of a graft outflow stenosis.
4. Fistula and graft stenosis should be investigated by fistulograms. Ultrasonography is an alternative
but is highly operator dependant and can give fallacious readings due to deep collateral veins.
5. A fistulogram or CT fistulogram should evaluate the AV anastomosis, the draining veins, and the
central veins. (subclavian & SVC).
6. Fever or rigors during hemodialysis in patients with indwelling cannulae should prompt evaluation
of the vascular access as a source of infection.

Measures to prevent Access dysfunction

1. Antibiotic locks may be used in patients with cuffed tunneled cannulae. Citrate which has
antibacterial properties may be used alone as an alternative to heparin as a locking solution in a 4%
strength.
2. Prophylactic antibiotic lock solutions should never include drugs like Vancomycin which are to be
retained for therapeutic use.
3. Stenosis of AV fistulae should be treated to prevent the risk of thrombosis however overall life of
the AV fistula has not been shown to be increased by pre emptive intervention.

Preparation of Antibiotic Cannula Locks

1. Trisodium citrate is commercially available as a 46% solution. This may be diluted 10 times with
sterile water for injection to produce a 4.5% solution which is independently sufficient as an
antibacterial prophylactic lock solution.
2. Gentamicin – Citrate Lock solution:- 46% Trisodium citrate is diluted with sterile water 1:5 to
produce a 9.2% solution. 1 ml of this solution is mixed with 0.5 ml of 10mg/ml Gentamicin injection
and the resulting 1.5 ml injected into each limb of the cannula. The final solution contains 6.1%
citrate and 3.3mg/ml of Gentamicin can be used as either a prophylactic or therapeutic lock solution.
 3. Gentamicin – heparin solution - 1 ml of gentamicin inj containing 10 mg is mixed with 4 ml of
Heparin containing 1000 units/ml and up to 1.5 ml of the solution should be injected into each limb
of the cannula. The final solution contains 800 units/ml of Heparin and 2mg/ml of gentamicin, which
are physic-chemically compatible. Stronger concentrations should not be used and care should be
taken not to exceed the volume of the cannula to avoid systemic toxicity.

Treatment of permanent Access Complications

1. Surgical revision or percutaneous intervention should be attempted to salvage a stenosed AV fistula
or graft before attempting to construct a new access.
2. Thrombolysis or surgical thrombectomy should be attempted in case of an early acute access
thrombus.
3. Surgical thrombectomy is rarely successful in cases of late thrombus formation which are usually
due to an underlying stenosis.

Treatment of temporary Access Complications

1. Temporary cannulae in the femoral vein should always be removed if suspected to be infected.
2. Temporary cannulae in the internal jugular vein may be retained for a 24 to 48 hour period while
systemic antibiotics are administered, but should be removed if fever persists for longer than that and
subsequently replaced at a fresh site.
3. Cuffed tunneled cannulae may be retained for 72 hours or longer while antibiotic therapy according
to culture reports is administered. Systemic antibiotics should be accompanied by local antibiotic
lock solutions, the concentration of which can be several times higher than that of the MIC reported
for blood cultures.
4. Cannulae may be changed over a guidewire if fever persists for > 48 hours.
5. Cannulae should be removed and a fresh cannula inserted if

Bloodstream infection is accompanied by exit site & tunnel infection or abscess. (Fat necrosis should be
distinguished from pus)
Culture grows:
Staphylococcus aureus
Candida species
Gram negative bacilli.
Infection is accompanied by diminished cannula performance.
 1. Decreased flows or high venous pressures should be investigated with a catheterogram, which
should include visualization of the SVC for intraluminal thrombosis, migration or formation of a
fibrin sheath.
2. Local thrombolysis may be attempted for cannula thrombus or luminal thrombus.
3. Catheter change over a guidewire may be required for fibrin sheath formation.

47. PRIMING, CONNECTING AND DISCONNECTING DIALYSER

Rationale: The connection, starting stopping and disconnection of a patient from the extracorporeal circuit is
an integral part of the treatment and one which can give rise to complications both early and delayed if
improperly handled. The starting and stopping of dialysis also includes assessment of the patient as well as
noting developments during dialysis and in the interdialytic period. Because this is the period when both
patients and unit staff are under pressure to speed up the entire procedure strict adherence to a protocol and
perhaps the use of checklists is necessary to prevent complications. The following guidelines provide a
protocol for the procedure, designed to optimize treatment.

Rinsing & priming of dialyzer:

Thorough rinsing of dialyzer is important since it will reduce the incidence or severity of anaphylactic
reactions by removal of leachable allergens.
For new dialyzer it is advisable to rinse blood compartment with 1 litre of normal saline and with a dialyzer
that is being reused using 2 litres of normal saline. This is done to eliminate all the air and residual sterilant
from the dialyzer, blood lines and for priming of the circuit. The last 500 ml of normal saline is heparinized
with 1000 units of heparin.
Dialysate compartment of dialyzer is rinsed with dialysate for at least 5 minutes before initiating dialysis.
A label mentioning the name of the patient along with the hospital registration number of the patient should
be put on the new dialyser being used. In case a previously used dialyser is being reused the name and
registration number of the patient has to be checked by 2 persons and recorded in a register by the
individuals doing the activity.

Check all alarms

1. Blood circuit
a) Inflow (pre- pump) pressure monitor: Inflow pressure is 80 to -200 mm Hg. If there is poor blood flow
from the vascular access the alarm will beep and the blood pump will stop. Once the pump stops the suction
is relieved and the alarm is deactivated.
Important causes for excessive suction could be either a thrombus or fibrin plug at catheter tip (venous
catheter) or improperly placed arterial needle or clotting of arterial needle (AV fistula), drop in patient’s BP,
kinking of arterial line, use of a too small needle.
b) Outflow (venous) pressure monitor : It is usually +50 to +250 mm Hg. Causes could be clotting of the
venous blood line filter or venous line/needle, high blood flow rate when using a small venous needle,
kinked venous line, stenosis at the venous limb, improperly placed venous needle.
c) Air detector: Important alarm to prevent air embolism which can be fatal. Common sites for air entry
include the region around the arterial needle, via leaky tubing connections, via broken blood tubings, via
saline infusion tubing
d) Blood line kinking & hemolysis alarm

2. Dialysis solution circuit monitors

a) Conductivity : Most common causes of reduced conductivity are empty concentrate container or defect
in the proportioning pump
b) Temperature is automatically limited between 35 & 39oC for most machines in the dialysis mode.
A common cause of low temperature alarms could be either a loose heater cable, a tripping of the
safety switch or a faulty sensor in some machines
c) Blood leak: A blood leak alarm should be confirmed by testing the effluent dialysate with a test strip
used for detecting hemoglobin in the urine. If leak is confirmed, the dialysate compartment pressure should
be set to -50 mm Hg or lower to minimize entry of bacteria from the dialysis solution into the blood side of
the extracorporeal circuit. The blood should be returned and dialysis should be discontinued. Use new
dialyser to restart dialysis.
Patient assessment
It is recommended to follow the below mentioned steps.
1. Record weight of patient
2. Measure Blood Pressure in lying and standing position
3. Assess patient for any new symptoms and examine patient
4. Plan target UF and assess dry weight of patient

Vascular access
Percutaneous venous cannula:
1. Aspirate residual heparin or clot from each catheter lumen
2. Check patency of catheter lumina by irrigating with heparinised saline (100 units/ml)
3. During catheter connect and disconnect procedures, both dialysis staff and patient should wear surgical
masks. Face shield should not be used without surgical mask.
4. The lumen and catheter tips should never remain open to air. A cap or syringe should always be placed on
or in the catheter lumen while maintaining a clean field under the catheter connectors.
5. Caps should be soaked in povidone-iodine and kept wrapped in gauze soaked in povidone iodine for the
entire length of the dialysis. Alternatively the caps can be sterilised with ethylene oxide autoclaving during
the dialysis and can be reused after the dialysis is completed.
6. Catheter lumens must be kept sterile. Interdialytic infusions through the catheter are forbidden.
7. Always inspect the exit site for any evidence of infection (redness or purulent discharge)
8. If any evidence of exit site infection is seen a swab culture should be taken and sent to the laboratory
9. The exit site should be cleaned with betadine and then dried before it is dressed.
10. If there are infection appropriate systemic antibiotics either oral or parenteral can be started.
11. Local antiseptic ointment such as Mupirocin can be applied to the exit site
12. Exit site should never be immersed in bath water. Showering is best avoided but if the patient showers it
should be done prior to coming for dialysis where a new dressing and antibacterial ointment can be
promptly applied.
Arteriovenous fistula:
1. Check the fistula for patency and function after tying tourniquet
2. Both needles are placed in the vein downstream to the anastomosis
3. Arterial needle is placed distally as compared to the venous needle
4. If the patients has a poorly distended venous limb, briefly apply a tourniquet to define the location
5. A 16 or 15 gauge needle should be used in adults
6. Prepare the needle insertion site with povidone iodine for a full 10 mts
7. Arterial needle is inserted first 3 cm from the anastomosis site. The needle is inserted bevel up at a 45
degree angle pointing either upstream or downstream
8. The venous needle is inserted at a 45 degree angle pointing downstream (usually towards the heart)
9. The insertion point of the venous needle should be at least 3-5 cm downstream to the arterial needle to
minimize recirculation.

Arteriovenous graft:
1. Guidelines for placing the needles are similar to that of AV fistula

Initial heparin administration:

1. If heparin is used, heparin loading dose is administered into the venous port and flushed with saline
2. After 3 minutes of administration of heparin the blood flow is started (Some centres administer the
heparin into the arterial line leading to the dialyzer and start the blood flow immediately)

Initiating dialysis:
1. Blood flow rate is initially set at 50 ml/min, then 100 ml/min until the entire blood circuit fills with blood.
2. The priming fluid in the dialyzer can either be given to the patient in case the BP is low or disposed off to
the drain
3. Ensure proper blood levels in the venous drip chamber
4. Promptly increase blood flow rate to close to 250-300 ml/min
5. Record the pressure levels at inflow and outflow monitor
6. Set the pressure limits slightly above and below (10-20 mm Hg) the operating pressure to ensure that the
blood pump will stop in case of any change of operating pressure beyond the limits set
7. Dialysis solution flow is initiated
8. Enter the UF volume desired

Monitoring of patient:
The patient’s BP should be monitored and recorded as often as necessary. In an unstable patient the BP
should be checked every 15 minutes. In a stable patient BP is checked every 30-60 minutes.
In diabetic patients attempts should be made to measure the capillary blood glucose levels to detect any
episode of hypoglycaemia.
Termination of dialysis:
1. Blood in the extracorporeal circuit is returned using saline or air
2. If saline is used patient receives 100-200 ml of this fluid during the rinse back procedure
3. If air is used,
a) The blood pump is first switched off
b) The arterial blood line is clamped close to the patient.
c) The arterial blood line is disconnected just distal to the clamp, opening it to air.
d) The blood pump is restarted at a reduced rate of 20-50 ml/min and the air is allowed to displace the blood
in the dialyzer.
e) When the air reaches the venous air trap or when the air bubbles are first seen in the venous blood line,
the venous line is clamped
f) The blood pump stopped and the return procedure terminated.

Closure of vascular access:

1. AV fistula
a) Remove the needles from the AV fistula and apply gauze.
b) Tie the tourniquets at the sites of puncture over the gauze pieces
c) Patient advised to loosen the tourniquet straps after 4 to 6 hours and remove the tourniquets is there is no
oozing from the puncture sites
2. Venous catheters
a) After each dialysis session, the dead space of each lumen is filled with heparin through the injection ports
using 1000-5000 units/ml. Do not use higher concentration of heparin than suggested since it may result in
significant systemic anticoagulation.
b) The dead space of each catheter lumen varies among different manufacturers and also depends on the
length of the catheter. The required volume of heparin is usually labelled on the catheter hub. It should be
recorded on the patient’s chart. Do not inject a volume of heparin solution than necessary as it may be
hazardous in patients who are at risk for bleeding.
c) After each dialysis, catheter hubs or blood line connectors should be soaked in povidone-iodine for 3-5
minutes, then dried prior to separation.
d) The catheter should be covered with a sterile dry dressing. Nonbreathable or non porous transparent film
dressings should be avoided since they pose a greater threat of exit site colonization than dry dressings.

Post dialysis monitoring:

1. Measure blood pressure
2. Record the UF done
3. Measure post dialysis weight

48. ANTICOAGULATION IN HAEMODIALYSIS

Rationale: The patient receiving hemodialysis requires anticoagulation of the extracorporeal circuit both to
prevent blood clotting during a session and also to prolong the life of the dialyser therby improving reuse.
Although unfractionated heparin has been traditionally used for anticogulation in hemodialysis, low
molecular weight heparin, trisodium citrate, Fondaparinux, and prostacyclin, which are now available, may
have specific uses in individual patients on hemodialysis, but are more expensive. The safety of these agents
has also not been completely esablished in chronic kidney disease. Over-anticoagulation is associated with
both short and long term bleeding complications. This guideline attempts to provide an outline of the
rational use of anticoagulation, monitoring and special precautions for their use.
Background:
Clotting in the extracorporeal circuit is a major challenge in carrying out haemodialysis. The hemodialysis
circuit represents a large extracorporeal surface area and the simple passage of blood through the circuit
could potentially lead to the deposition and activation of plasma coagulation proteins thus initiating clotting.
The factors predisposing clotting of the extracorporreal circuit are given in table 1:
Consequences of clotting in the exrtacorporeal circuit:
The clotting in the extracorporeal circuit leads to blood loss and reduced solute clearance and
ultrafiteration due to reduction in dialyser surface area. Hence it is important to prevent clotting and
assess the adequacy of anticoagulation. The clues which help in assessing anticoagulation during
dialysis are given in table 2.

Guideline 1: The operator will make attempts to minimize clotting in the extracorporeal circuit by paying
attention to the following factors:
Technical or operator induced factors resulting in clotting
1. Dialyser priming
a. Following the correct priming technique and adequate priming to prevent retained air in dialyser. (Refer
guideline on priming technique).
b. Ensuring adequate priming of heparin infusion line
2. Heparin administration
a. Correct loading dose
b. Correct heparin pump setting for constant infusion
c. In time starting of heparin pump
d. Ensuring timely release of heparin line clamp
e. Adequate time interval after loading dose for systemic heparinisation to occur
3. Vascular access
a. Ensuring adequate blood flow by correct needle and catheter position.
b. Correct needle position to prevent recirculation.
c. Adequate uninterrupted blood flow by preventing repeated machine alarm situation
Guideline 2: Heparin administration techniques
The operator shall decide regarding the correct heparinisation schedule taking into consideration the risk of
haemorrhage and other comorbidities.
I. Routine anti coagulation with unfractionated heparin-
1. Indication – Those patients who do not have increased risk of hemorrhage or co morbidities like CNS
bleed, GI haemorrhage, uremic pericarditis are routinely treated with full dose heparinisation.
2. Delivery techniques
a. Intermittent bolus: Bolus loading dose 35-55units/kg followed by intermittent maintenance dose of 10-20
IU/kg boluses
b. Constant infusion: Bolus loading dose of 35- 55units/kg followed by constant infusion
3. Dose of unfractionated heparin
a. Body weight between 50 – 90 kg : no change in dose
b. Body weight outside these limits : bolus dose 75-100 units per kg; Infusion dose 750-1000 units per hour
4. Termination of heparin infusion
a. AV fistula-One hour before end of dialysis
b. Venous catheters- at the end of dialysis
5. Reversal of over heparinisation

Target clotting times during dialysis

ACT test baseline value 120 -150 seconds
Routine heparinisation: During dialysis desired range +80% (200-250 seconds); At the end of dialysis +40
% (170-190 seconds)
Tight heparinisation: During dialysis desired range +40% (170-190 seconds); At the end of dialysis +40 %
(170-190 seconds)
II. Tight heparinisation
1. Indication –
a. Patient at slight risk of bleeding
b. Heparin free dialysis unsuccessful due to frequent clotting
2. Delivery technique
a. Bolus dose followed by constant infusion
b. Do not try intermittent boluses as it will lead to rising and falling clotting times
3. Dose
a. Initial bolus dose : 750 units
b. Heparin infusion rate : 600 units per hour
c. Monitor and keep ACT at baseline +40
4. Termination of heparin infusion
a. Continue till end of dialysis
5. Target clotting times during dialysis

ACT test baseline value 120 -150 seconds

Tight heparinisation: During dialysis desired range +40% (170-190 seconds); At the end of dialysis +40 %
(170-190 seconds)
III. Heparin free dialysis
1. Indication
a. Pericarditis
b. Recent surgery with bleeding complications or risks
I. Vascular and cardiac surgery
II. Eye surgery ( retinal and cataract)
III. Renal transplant
IV. Brain surgery
c. Coagulopathy
d. Thrombocytopenia
e. Intracerebral hemorrhage
f. Active bleeding
2. Technique
a. Heparin rinse (avoid in case of thrombocytopenia) – rinse with saline containing 3000 units heparin per
litre
b. Drain out heparin containing saline by filling extracorporeal circuit with patients blood or unheparinised
saline at the start of dialysis
c. Keep blood flow to 400 ml per minute. In case high blood flow is not possible due to small patient size,
very high predialysis plasma urea level may use small surface area dialyser or reduce dialysate flow or
shorten treatment session.
d. Periodic saline rinse allows inspection of dialyser for evidence of clotting. In case clotting detected,
consider changing dialyser or terminating dialysis. Remove amount of saline infused by adjusting ultra
filtration.
Guideline 3: Anticoagulation in case Heparin use is contraindicated
In situations where the use of heparin is contraindicated and heparin free dialysis is not advisable, the
operator may choose alternative anticoagulants like
I. Bicarbonate dialysis solution with low concentration citrate
1. Indication
a. When heparinisation is contraindicated and heparin free dialysis not possible
b. To increase dialyser reuse
2. Technique: Dialysis solution contains 0.8 millimoles per litre citrate
II. Regional citrate (high concentration anti coagulation)
1. Indication – When systemic heparinisation Is not desirable
2. Technique
1. Infuse tri sodium citrate in arterial blood line
2. Use dialysate containing no calcium
3. Infuse calcium chloride in venous blood line

Advantage over heparin free dialysis –

1. Blood flow rate need not be kept high
2. Clotting rarely occurs

Disadvantage of Citrate –
1. Possibility of metabolic alkalosis- used with caution in patients with liver disease
2. chronic citrate used may result in aluminium overload

III. Low molecular weight heparin

1. Dose-
a. Loading dose : 125-250 aXaU IU/kg’
b. No intermittent bolus or infusion required.
2. Reversal –
a. Protamine of no use
b. Use plasma if needed

Advantages-
1. Less osteoporosis
2. Better lipid profile
3. Less hyperkalemia
4. Montioring not required

Complications-
1. Bleeding complications – seen in patients receiving clopidrel and aspirin
2. Anaphylactic reactions

IV. Heparinoids- heparin mixtures

Types-
1. danaparoid
2. fondaparinux
Use-
1. in patients with HIT

Guideline 4: The operator shall monitor the potential complications of use of heparin.
Heparin use may be associated with complications like heparin induced thrombocytopenia (HIT)
[Table 3], drug drug interaction [Table 4], bleeding events and osteopenia.
Characteristics HIT type 1 HIT type 2
Frequency 10 – 20 % 2-3%
Timing 1-4 days 5-10 days
Platelet Count 100 x 10 12 /L 30 -50 x 10 12 /L
Antibody No yes
Thrombosis No yes
Skin necrosis No yes
Repeated circuit clotting No yes
Access thrombosis No yes
Management Observe Withdraw Heparin

Table 4: Potential hazardous Drug interactions of heparin

1. Analgesics – Increased risk of bleeding with NSAID – avoid concommited use with IV
diclophenac, Increased risk of hemorrhage with ketorolac

2. Nitrates- Anti coagulant effect reduced by infusion of gyceryltrinitrate

3. Use with care in patients receiving oral anti couagulants, aspirin ,dextran

49. DIALYSIS DOSE/ADEQUACY

Rationale: Hemodialysis provides only a fraction of some of the numerous functions performed by the
native kidneys. Patients receiving inadequate dialysis suffer from malnutrition, inflammation, and a poor
quality of life. Additionally these conditions may lead to accelerated atherosclerosis. Since 1981 inadequate
dialysis has been shown to adversely affect survival, while increasing frequency and duration of dialysis
improved both survival quality of life and medication amounts. No single clinical or laboratory parameter
can assess adequacy of dialysis and overt signs may develop very late, hence it is necessary to develop a
comprehensive monitoring system of measuring adequacy of dialysis which is also easy to use and
reproducible. Some of these guidelines are set down in the following document.

Recommendations
Recommendations / guidelines suggested are based on International data and local experience.
1. Patients on MHD must receive 3 times dialysis in a week for at least 4 hrs each time with blood
flows of 300 ml/min and dialysate flows of 500 ml/min.
2. MHD less than twice a week (less than 8 hrs in 2 sessions) is not recommended.
3. For those on twice a week dialysis, may be given longer dialysis for 6 hrs i.e at night.
4. Residual renal function must be monitored every 3 months. Should be determined by average of 24
hrs urea and creatinine clearance.
5. It is recommended that kt/v or urea reduction ratio (URR) be used as a measure of dialysis
prescription.
6. URR is a simpler method to determine dialysis adequacy. URR should be targeted to > 65 %. Post
dialysis sample should be taken 2 minutes after dialysis or during slowing pump speed to 100
ml/min and sample taken 15 seconds later.
7. Kt/v of 1.4 – 1.6 should be achieved in each dialysis.
8. It is recommended that the minimally adequate dose of dialysis can be reduced among patients with
residual kidney function of greater than 2 mL/min per 1.73 m2, although the minimum single-pool
Kt/V should be no lower than 60 percent of the minimum target for those without residual renal
function.
9. An assessment of the dialysis dose in stable hemodialysis patients should be performed once per
month. More frequent measurements may be required in patients not doing well on dialysis.
10. The search for causes of a low Kt/V or URR should be done and these are:
o An assessment of fistula integrity
o Treatment duration
o Possible technical errors in the method of obtaining BUN samples
o Dialysis machine and patient specific variables such as:
 asures should be incorporated to improve effective hemodialysis treatment times, improve blood
flows, correct errors in blood sampling, or improve dialyzer clearance.

Dialysis adequacy is related also to other related variables. Lower death risk in dialysis patients is
associated with:
o Dialysis time greater than four hours
o Pre dialysis BUN between 70-90 mg/dl with adequate protein catabolic rate (PCR).
o Low requirement for erythropoietin & antihypertensive drugs.
o Plasma albumin greater than 4 gms/dl.
o Plasma cholesterol between
200-300 mg/dl
o Pre dialysis creatinine greater than 12.5 mg/dl
-being of the patient assessed
by a regular monthly clinical checkup of dialysis patients in the clinic along with monthly hematology and
biochemistry reports & other tests as required.

These need to be validated in more studies.

number of machines are being fitted with this module, it can be used as an adjunct to monthly urea based
measurements. It offers the advantage of being possible on each and every dialysis session, does not require
a lag time, and no blood collection is required. As the machine software uses the Watson formula to
calculate V, it is often overestimated and consequently Kt/V measured by online sodium or conductivity
monitoring underestimates urea based measurements by around 0.03.

Explanation & Discussion

ssessment of adequacy of hemodialysis is important. Monitoring the patient’s symptoms alone as is
commonly done in India, is insufficient as dialysis & erythropoietin to correct anemia may eliminate most
symptoms for many months even when patients are underdialyzed. Following BUN & creatinine is
insufficient because a low BUN & creatinine may reflect malnutrition & poor muscle mass rather than
sufficient dialytic removal, also a common clinical state in our dialysis population. Protein catabolic rate
(PCR) and timed average urea concentration have been shown to be important determinants of morbidity &
mortality as shown by National cooperative dialysis study (NCDS).
kt/v & shown to reflect the amount of dialysis
prescribed & delivered. Kt/v is defined as dialyzer clearance of urea (k obtained from manufacturer of
dialyzer & is available as ml/min), multiplied by duration of dialysis and divided by volume of distribution
of urea in the body (v in ml), which is approximately equal to total body water. Individualizing dialysis
prescription is a useful method to achieve a cost effective dialysis treatment. Dialysis dose can be
measured by Kinetic urea modeling (kt/v) or by simple urea reduction ratios (URR).
-pool Kt/V
of approximately 1.4 to 1.6 be achieved. These levels are consistent with the 2006 K/DOQI guidelines for
hemodialysis patients with minimal residual renal function (less than 2 mL/min per 1.73 m2).

Residual renal function facilitates the regulation of fluid and electrolyte balance, and may enhance survival.
The 2006 K/DOQI clinical practice guidelines. It is recommended that the minimally adequate dose of
dialysis can be reduced among patients with residual kidney function of greater than 2 mL/min per 1.73 m2,
although the minimum single-pool Kt/V should be no lower than 60 percent of the minimum target for those
without residual renal function.
Hemo study established that the risk of death (primary outcome) and secondary outcomes of combined
hospitalization & death were not different between high dose vs standard dose or high flux vs low flux
dialysis. In India, majority of patients on MHD receive twice a week dialysis. Dialysis dose received by
patients is mostly not measured & we do not have studies to provide any specific guidelines based on Indian
data. However such patients should have more frequent measurements of residual renal function and if it is
less than 2 ml/min/1.73 m2 then thrice a week dialysis should be recommended.

50. PREVENTION OF INFECTIONS IN HEMODIALYSIS UNIT

Rationale: The hemodialysis patient is particularly susceptible to several infections both bacterial
occasioned by the decreased immunity and blood borne viral infections. Studies have shown that bacterial
infections in addition to carrying a higher short term mortality also increase the risk of long term
cardiovascular complications. Viral infections like Hepatitis B and C progress to liver cirrhosis and increase
the morbidity and mortality on hemodialysis. In addition the staff of a dialysis unit are uniquely at risk of
contracting these viral infections from contaminated blood and dialysate. Preventing the transmission of
infections involves several links in the chain involving the patients, the dialysis procedure and ancillary
care, the staff of the unit and various administrative and waste disposal protocols. A comprehensive
infection preventive protocol includes hygiene measures, vaccination, dialyzer reprocessing and disposal of
biohazardous materials as set out in the following guideline.
Description:
The number of patients on maintenance hemodialysis is increasing rapidly in India. Chronic hemodialysis
patients have an increased infection risk. HD facility is very conducive for transmission of infection since
multiple patients receive dialysis concurrently. Transmission can occur directly or indirectly via
contaminated devices, equipment and supplies, environmental surfaces, or hands of personnel. Even in the
developed world, there are substantial deficiencies in infection control practices. These suggested reasons
include lack of awareness of the practices and their importance, and lack of clarity of difference between
universal precautions (recommended for all health-care settings) and the additional precautions necessary in
the hemodialysis setting.
The important infections that develop in these patients include viral infections such as hepatitis B and C,
HIV and bacterial infections, especially those involving vascular access. The prevalence of antimicrobial-
resistant bacteria has increased rapidly in health-care settings, including hemodialysis units in recent years.
Multi-resistant organisms (MRO) are defined as bacteria that are resistant to one or more classes of
antimicrobial agents. These include Methicillin Resistant Staphylococcus aureus (MRSA), Vancomycin
Resistant Enterococci (VRE), Extended Spectrum β-lactamase (ESBL)-producing Klebsiella pneumonia,
Carbapenem-resistant Acinetobacter baumannii (CRAB) and Clostridium difficile (antibiotic associated
diarrhoea). Antimicrobial use and direct contact transmission of resistant strains are the two main factors
that have contributed to this significant increase.
Infection control guidelines and surveillance system for infections in hemodialysis centers has been
implemented in most advanced countries to cut down infection risk and to determine the frequency and risk
factors for these complications. The suggested guidelines have been prepared by combining essential
features from several documents, and are meant to guide infection control implementation and surveillance
in HD units.
Units should establish written protocols for all procedures including cleaning and disinfecting
surfaces and equipment in the dialysis unit
Hand Hygiene
1. Staff should cover any cuts and abrasions with waterproof dressings. Staff who has extensive
untreated cuts or chronic skin disease, such as eczema, should not work in dialysis units when their
skin lesions are active.
2. Unwashed hands of healthcare workers are the major route of transmission of microorganisms in
healthcare settings.
3. Hand hygiene is includes hand washing with soap and water, and/or applying an alcohol-based hand
rub (e.g. sterilium)
4. Hands should be washed with soap and water when visibly dirty or contaminated with proteinaceous
material (e.g. blood or other body fluids).
5. If hands are not visibly soiled, an alcohol-based hand rub can be used.
6. Hand hygiene should be performed
7. before and after patient contact
8. after contact with a source of microorganisms (body fluids and substances, mucous membranes, non-
intact skin, or inanimate objects that are likely to be contaminated)
9. after removing gloves
 10. Hand hygiene facilities should be located as close as possible to the point of contact with patients
and dialysis equipment.
11. One hand wash basin should be provided for every 2-3 dialysis stations in the main dialysis area and
a minimum of one in an isolation room.
12. Soap solution must be provided in dispensers with disposable cartridges or single-use bottles, to
prevent bacterial contamination of the product.
13. Alcohol-based hand rubs should be placed at the point of contact, for example:
- Next to or attached to the frame of dialysis bed or chair
- At points of entry and exit of dialysis room
- At staff stations or chart and medication trolleys.

Use of gloves
1. Clean, non-sterile gloves should be worn when contact with blood or body fluids is anticipated; this
includes contact with patients and dialysis equipment.
2. Gloves must be changed and hands cleaned between patients and/or stations. ·
3. Gloves must also be changed and hands cleaned between different activities on the same patient (e.g.
moving from a contaminated to a clean body site).
4. Gloves should be worn for any cleaning activities.
5. Hands should be decontaminated or washed after removing gloves.
6. Gloves should not be washed or reused.

Personal protection
1. Face protection (eyewear/goggles, masks) is required to protect the mucous membranes of the eyes,
nose and mouth when performing procedures that may generate splashes or sprays of blood or body
fluids (e.g. during initiation and termination of dialysis).

2. Personal eyeglasses and contact lenses are not considered adequate eye protection.
3. Plastic aprons are indicated to prevent contamination of clothing with blood, body fluids, and other
potentially infectious material.
4. A long-sleeved, fluid-barrier (impervious) gown should be worn if exposed areas of the body e.g.
arms, body front, are likely to be contaminated by blood or body fluids.
5. All personal protection equipment (with the exception of eyewear/goggles unless soiled) must be
changed and hands cleaned
o between attending different patients.
o if it becomes splashed with blood or body fluids
o on leaving the work area.
Environmental Issues including Equipment and Consumables
1. Storage of equipment close to dialysis machines and patients should be minimized.
2. Where possible, regularly used equipment such as adhesive tapes, tourniquets, blood pressure cuffs
and clamps should be designated to each patient.
3. Consumables taken to the patient’s station should be used only for that patient and should not be
returned to a common clean area or used on other patients.

Cleaning of dialysis machines and chairs/beds

1. Dialysis machines should be internally disinfected, externally cleaned (and disinfected if indicated),
and dried after each patient.
2. The exterior of the machine should be effectively cleaned using protocols following manufacturer’s
instructions.
3. Special attention should be given to cleaning control panels on the dialysis machines and other
surfaces that are frequently touched and potentially contaminated with patients’ blood.
4. Cleaning of non-critical surfaces (e.g. dialysis bed or chair, countertops, external surfaces of dialysis
machines and equipment) should be done with neutral detergent and warm water.
5. The following procedure should be adopted for any surface/item that is visibly contaminated with
blood OR following dialysis of a patient infected with bloodborne virus:
o Clean with neutral detergent and water, and then
o Disinfect with sodium hypochlorite 1% (1,000 ppm available chlorine; 1:10 dilution).
o Remove chlorine residues from metallic surfaces with water as sodium hypochlorite in high
concentrations (>500 ppm) is corrosive to metals.

External transducer protectors

o should be fitted to the pressure lines of extracorporeal circuit.
o should be replaced if the filter becomes wet.
o Using a syringe to clear the flooded line may damage the filter and increase the possibility of blood
passing into the dialysis machine.

The machine should be decommissioned if spillage occurs at inaccessible locations, such as behind the
blood pump until proper cleaning and disinfection are done.

o Blood tubing draped or clipped to waste containers,

o Use of attached waste containers during priming of dialyzers
o Placing items on tops of machines for convenience (e.g., dialyzer caps and medication vials).
Due to the instability of chlorine compounds all diluted solutions should be discarded at the end of the day.
Disinfection of Haemodialysis Machines
1. Dialysis units must follow the manufacturer’s recommendations in relation to management of
haemodialysis machines
2. Manufacturers producing dialysis machines each recommend a different procedure for
decontamination, but they concentrate only on bacterial kill. It is recommended that efficacy of
decontamination procedure should additionally take into account level of biofilm and endotoxin
removal.
3. The development of bacterial biofilms in the hydraulic circuit of haemodialysis machines can be
prevented by frequent use of chemical and heat disinfection strategies.
4. Disinfection should include the following
5. Heat disinfection (80°C to 90°C) after each dialysis
6. Citric acid and heat disinfection at the end of the day
7. Bleaching (5% chlorine) once a month.
8. Frequent bleaching is not recommended because of possible damage to the machine.

Dialysates
1. Liquid bicarbonate dialysate concentrate can support rapid bacterial proliferation, and hence it not be
used more than 24 hours after opening.
2. Bottles containing unused dialysate should be immediately capped and the exterior of the bottle
wiped over with detergent and water as part of the overall procedure of cleaning the haemodialysis
machine.
3. The date and time of opening should be recorded on the bottle using an indelible pen.
4. Opened bottles containing unused fluid should be discarded after 24 hours.
5. Unfinished bottles used for infected patients must be discarded immediately after the dialysis
session.

Medications
1. Medications (including multiple dose vials) or supplies (syringes, swabs, etc) taken to the patient’s
station should be used only for that patient and should not be returned to a common clean area or
used on other patients.
2. Wherever possible, multiple dose vials should be used for the same patient.

3. Bags or bottles of intravenous solution should not be used as a common source of supply for
multiple patients
 4. When multiple dose medication vials (e.g., heparin, vials containing diluents) or solution bags are
used for multiple patients, individual patient doses should be prepared in a clean, centralised area
away from dialysis stations and delivered separately to each patient.
5. Do not carry medication vials from station to station.
6. Do not carry vials, syringes, swabs or other supplies in pockets.
7. If trays are used to deliver medications to individual patients, they must be cleaned between patients.
8. Clean areas should be clearly designated for the preparation, handling and storage of medications,
supplies and equipment.
9. Do not handle and store medications or clean supplies in the same or an adjacent area to that where
used equipment or blood samples are handled.
Needle and sharps
1. All needles and sharps must be disposed of into an approved closed, unbreakable container
according to the biomedical waste management rules.
2. Needles should not be manually recapped
3. No-touch technique should be used to drop the needle into the container, as it is likely to have a
contaminated surface.
4. These containers should be located as close as possible to the point of generation either attached to a
trolley or on a mobile stand.
5. Containers should be large enough to accommodate the types of devices being used in the area.
6. They should be closed and sealed when 2/3 full and disposed off in approved manner.

Blood spills
1. For minor spills on surfaces (e.g. benches, counter tops):
2. Wipe up with paper towel soaked in undiluted 1% sodium hypochlorite and then wash with neutral
detergent and hot water and allow to dry.
3. For major blood spills
4. Cover with chlorine powder (10,000 ppm available chlorine) and leave for two minutes OR Limit
spread using paper towels and slowly flood contaminated area with undiluted sodium hypochlorite
1% (5,000 - 10,000 ppm); leave for two minutes before cleaning up.
5. This should be followed by washing with neutral detergent
6. Common equipment including weighing scales should be cleaned after use with detergent and water
at least daily and when they become visibly soiled or come in contact with body fluids.

Blood Borne Virus Screening and Management

1. All patients should be tested for HBV, HCV and HIV on admission to the dialysis unit including
after transfer from another unit
 2. All maintenance dialysis patients should be retested at regular every 6 months for HBV, HCV and
HIV infection.
3. All HBsAg-negative patients must be vaccinated against hepatitis B using approved protocol.
4. Anti-HBs titers should be checked 4 weeks after the last dose and at 6 monthly intervals thereafter.
5. Non-responders (anti-HBs titers < 10 IU/ml) should receive 3 more doses of the vaccine.
6. All staff members should be vaccinated against hepatitis B, have their anti-HBs titer tested and be
aware of their serostatus, i.e., whether or not they have titers >10 U/ml
7. Testing of staff and carers for HCV or HIV is only recommended following a needlestick injury or
body fluid exposure
8. Patients with different bloodborne virus infections should be managed separately.
9. HBsAg, HBeAg and HBV DNA positive patients should be dialysed in a separate room.
10. Units with high (>20%) prevalence of HCV infection should strongly consider dialyzing anti-HCV
positive patients in a separate room.
11. Where there are no isolation facilities, positive patients should be separated from susceptible patients
(negative for HBsAg, anti-HBs, anti-HBc, anti-HCV, or anti-HIV), and undergo dialysis on
dedicated machines.
12. Patients with anti-HBs ≥10 mIU/mL may undergo dialysis in the same area as HBsAg-positive
patients. In case HBV patients are not dialyzed in a separate area, these patients should be placed as
buffer between HBsAg-positive and negative patients.
13. When a room/area/machine has been used for dialyzing infected patients, it should be used for
uninfected patients only after cleaning and disinfection.
14. Dialysis staff members caring for positive patients should not care for susceptible patients at the
same time (e.g. during the same shift or during patient change-over), but may change in different
shifts.
15. If staff members must care for both positive and negative patients during the same shift, they must
change their gown and gloves, and clean their hands in between patients.
16. Close contacts of positive patients should be tested for HBsAg and anti-HBs testing and if necessary,
vaccination.
17. If a staff member or carer experiences a needlestick injury or exposure to blood or potentially blood-
contaminated secretions from an infected patient, specialist opinion should be sought for
management.
Vaccinations
1. All patients over 5 years old should receive pneumococcal vaccine (23vPPV).

Optional
 1. Influenza vaccine should be given annually before the beginning of the influenza season
2. Non-immune future transplant candidates should receive varicella vaccine.

Multi-Resistant Organism (MRO) Screening

Dialysis units should institute measures to preventing transmission of MROs. These include
1. Access to good clinical microbiology laboratory to ensure prompt detection of MROs including
antimicrobial susceptibility.
2. Appropriate antimicrobial stewardship (optimal selection, dose, and duration of treatment)
3. active surveillance cultures (screening) to identify patients colonised or infected with MROs
4. decolonisation therapy where appropriate

Management of Patients Infected or Colonised with a MRO

ent of patients with the following because of
increased risk of transmitting a MRO:
o an infected/colonised wound that cannot be covered by a dressing
o urinary incontinence
o uncontrolled faecal incontinence or diarrhoea or enterostomies;
o exfoliative skin conditions (e.g. dermatitis, psoriasis) and burns

o the incidence of a MRO is increasing despite correct adherence to infection control precautions
o First case or outbreak of an MRO in the unit.

1. Dialyse MRO-positive patients in a separate room designated only for MRO-positive patients.
2. In a separate area in the main unit.
3. The main unit with ≥1 metre separation between beds/chairs

2. Staff caring for these patients must wear a gown and clean non-sterile gloves for all interactions that
with the patient or potentially contaminated areas in the patient’s environment.
3. Patients with different MROs should be managed separately.
4. The room where MRO-positive patients have previously been dialysed may be used for negative
patients only after cleaning and the area is dry.
5. Transport equipment (e.g. wheelchairs, trolleys) should be cleaned with detergent and water or
detergent or alcohol-impregnated wipes after use.
Prophylaxis for Staphylococcus aureus infection
1. The prevalence of S. aureus nasal carriage in many dialysis patients is higher than the normal
population (≥50%) and increases with duration of dialysis.
2. It is desirable that units should make efforts to ascertain rates of S. aureus nasal carriage amongst
patients in their units by performing surveillance cultures of anterior nares.

3. If the prevalence is found to be high, unit should institute regular surveillance for S. aureus carriage
and treatment of positive patients with twice a day intranasal mupirocin for 7 days, repeated every 3
months.
4. Routine use of mupirocin in dialysis patients to prevent S. aureus carriage is not recommended
because of risk of developing resistance

5. There should a prominent display at entry to the unit or reception requesting that patients and
individuals accompanying the patient promptly inform the staff if there are any symptoms of a
respiratory infection (e.g. cough, flu-like illness); gastroenteritis (e.g. diarrhoea, nausea, vomiting);
skin rash; or known exposure to a infectious disease (e.g. chickenpox, measles, pertussis).
6. Source containment measures should be implemented to prevent transmission of respiratory
infections. Coughing patients should be asked to wear a surgical mask or cover their cough.
7. All patients should perform hand hygiene as part of basic personal hygiene, including the use of
alcohol-based hand rubs
Preparing the Access for Cannulation
1. Wash hands.
2. Wash (or ask the patient to wash) the access site with antimicrobial or plain soap and water.
3. Apply clean gloves.
4. Cleanse the skin by applying any one of the following:
- 0.5 - 2% chlorhexidine gluconate in 70% ethyl or isopropyl alcohol
- alcoholic chlorhexidine (0.5% - 2% chlorhexidine gluconate in 70% ethyl or isopropyl alcohol).
- 70% isopropyl alcohol using sterile swabs
5. Cleanse in a circular, rubbing motion from the centre outwards, for 1 minute immediately prior to
cannulation. Do not use a backward and forward movement.
6. Wear sterile gloves for cannulation if the skin needs to be re-palpated.
7. Gloves should be changed if contaminated.

-
iodine and 2% mupirocin) should be applied to the exit site
Staff Training
ts should be trained in infection prevention and control practices including
o Proper hand hygiene technique
o Appropriate use of personal protection equipment
o Modes of transmission for BBV, pathogenic bacteria, and other microorganisms
o Infection Control Precautions for Dialysis Units
o Rationale for segregating patients
o Correct techniques for initiation, care, and maintenance of dialysis access sites.

New and inexperienced staff should be supervised until they are considered competent to practice safely on
their own.
Surveillance

o Rates of infection with blood borne viruses and bacterial infections overall and individually
o Results of serological testing for blood borne viruses.
o They should calculate incidence and conversion rates for blood borne viruses.

frequently if there is significant staff turnover.

Waste management
Wastes generated by the hemodialysis facility should be considered infectious and handled accordingly.
These solid medical wastes should be disposed of properly in an incinerator or sanitary landfill, according to
and regulations governing medical waste disposal (Bio-Medical Waste (Management & Handling) Rules,
1998).
Some relevant sections have been appended.
Option Waste Category Treatment & Disposal
Category No. I Human Anatomical Waste Incineration @/deep burial*
(human tissues, organs, body
parts)
Category No. 2 Animal Waste Incineration @ / deep
(animal tissues, organs, body burial*
parts carcasses, bleeding
parts, fluid, blood and
experimental animals used in
research, waste generated
by veterinary hospitals
 colleges, discharge from
hospitals, animal) houses)
Category No 3 Microbiology & local autoclaving / micro-
Biotechnology Waste waving / incineration@
(wastes from laboratory
cultures, stocks or specimens
of micro-organisms live or
attenuated vaccines, human
and animal cell culture used
in research and infectious
agents from research and
industrial laboratories,
wastes from production of
biologicals, toxins, dishes
and devices used for transfer
of cultures)
Category No 4 Waste sharps disinfection (chemical
(needles, syringes, scalpels, treatment @ 01/auto claving
blades, glass, etc. that may / micro- waving and
cause puncture and cuts. mutilation/ shredding"
This includes both used and
unused sharps)
Category No 5 Discarded Medicines and Incineration @/destruct ion
Cytotoxic drugs and drugs disposal in
(wastes comprising of secured landfills drugs
outdated, contaminated and disposal in secured
discarded medicines)
Category No 6 Solid Waste Incineration @ autoclaving /
(Items contaminated with micro-waving
blood, and body fluids
including cotton dressings,
soiled plaster casts, lines,
beddings, other material
contaminated with blood)
Category No. 7 Solid Waste disinfection by chemical
(wastes generated from treatment @ @
 disposable items other than autoclaving/micro-waving
the waste shaprs such as and mutilation/ shredding##
tubings, catheters,
intravenous sets etc).
Category No. 8 Liquid Waste disinfection by chemical
(waste generated from treatment@@ and discharge
laboratory and washing, into drains.
cleaning, house-
keeping and disinfecting
activities)
Category No. 9 Incineration Ash disposal in municipal landfill
(ash from incineration of
any bio-medical waste)
Category No. 10 Chemical Waste chemical treatment @@ and
(chemicals used in discharge into drains for
production of biologicals, liquids and secured landfill
chemicals used in for solids
disinfection, as insecticides,
etc.)

51. EMERGENCY SERVICES

Rationale: The process of hemodialysis is akin to a major surgical operation. At any given time a fixed
amount of blood is in the extracorporeal circuit which is not under the physiological control and the normal
feedback mechanisms of the patient. Although most dialysis machines are equipped with a fail safe mode, a
self-test, alarms and a safety profile of less than 1 event per 100 million treatments, emergencies related to
personal error, and patients intrinsic condition ranging from minor discomfort to cardiac arrests on
hemodialysis have been reported in dialysis units. The following guideline elaborates the personnel
protocols and equipment required for managing emergencies in the dialysis unit.
Description:
Hemodialysis unit may be located in the premises of a hospital or it may be a standalone HD unit. In either
case emergency equipment, personnel and medicines are to be kept ready in the unit for urgent use before
the patient is shifted to ICU.
The common haemodialysis emergencies are:
1. Hypotension
2. Dialyzer reactions
a. Type A (anaphylactic reaction)
b. Type B (non-specific reaction)
3. Haemolysis
4. Air embolism
5. Disequilibrium syndrome
6. Chest pain, MI
7. Arrhythmias
8. Sudden cardiac arrest

Personnel
1. Nephrologist
2. Resident doctors-One per shift in three shifts
3. Dialysis technologists – one per two machine-- in three shifts
4. Nurses—one per three patients—in three shifts
5. Anaesthesiologists during day time and on call
6. Anaesthesia technician

Nephrologist should be available roud the clock, atleast on call, for managing emergencies. Resident
Doctors should be trained in identifying cardiac arrhythmias, cardioversion and intubation technique. Nurses
should be able to handle EKG machine and cardiac monitors. All should be ACLS certified. An
Anesthesiologist should be available on call.
Equipment required to prevent and treat these emergencies
1. Accurate weighing scale to exactly measure weight.
2. Dialysis machines with ultrafiltration controller and sodium modelling to prevent hypotension. Spare HD
machine is advisable
3. Micro-haematocrit tube for manual measurement
4. Activated clotting time machine.
5. Glucometer.
6. Multichannel cardiac monitor, Signal-averaged ECG (SAECG) and defibrillator.
7. Laryngoscopes, Endotracheal tubes, Suction apparatus or wall mounted suction, Central oxygen supply &
suction tubes, mouth gag and Ambu Bag
8. Ryles tube.
9. Arterial blood gas analysis machine.
10. 24 hour emergency power generator to ensure uninterrupted power supply.
Equipment not required for an emergency, but useful in preventing an emergency
1. Implantable cardioverter-defibrillator.
2. Ambulatory blood pressure monitor.
3. Portable ultrasound for abdominal emergencies.
4. Hand held doppler device for vascular access assessment.

These are optional equipments and may be made available depending on the size of the unit.
Medicines to be available for emergency use
1. Ionotropes: Injections: Dopamine, Dobutamine, Nor-adrenaline, vasopressin
2. Solutions: 25% dextrose; 3% saline; 5% dextrose
3. Injection Protamine
4. Injections: Lignocaine, amiodarone
5. Injection Hydrocortisone
6. Injection Adrenaline
7. Injection Atropine
8. Injection and tablet Pheniramine maleate
9. Capsule and tablet Nifedepine
10. Tablets: Clonidine, paracetamol, sorbitrate
11. Injection Nitroglycerine
12. Injections: Ondansetron, metoclopramide, pantoprazole, ranitidine
13. Injection vitamin K
14. Anti-convulsants Medozolam, Dilantin
15. Salbutamol

An Intensive Care and a Respiratory Care Unit are to be within the reach so that a critically ill patient may
be shifted there, without delay.

52. LABORATORY BACKUP

Rationale: Assessment of adequacy of dialysis, nutritional status, bone mineral disorders, anemia and
monitoring for infections all require frequent laboratory investigations. Since various biochemical and
serological parameters are dependent on the methodology used and the standardization and calibration of
equipment widespread inter laboratory variation may be observed. It is therefore necessary for a unit
performing hemodialysis to have access to a laboratory with reliable and reproducible results and to
establish protocols of investigations for patients dialyzing with them. Some of the basic protocols and
requirements of the laboratory for a hemodialysis unit are laid out in the following guidelines.
Description:
Most of the Hemodialysis units are located in large hospitals and the hospitals have clinical, biochemical,
and microbiology facilities attached to them. Usually imaging facilities are also available with these
hospitals. A ‘stand-alone’ HD centre may not have an attached laboratory or a imaging facility.
In either case, a laboratory with equipment for carrying out tests required for monitoring the management of
patients on maintenance Hemodialysis is essential
Investigations recommended for patients on maintenance haemodialysis:

Parameter When to check Remark Reference

Blood urea Once a month - -
Serum creatinine Once a month - -
Serum sodium Once a month - -
Serum potassium Once a month - -
Kt/V Once a month More frequently http://www.kidney.o
Non-compliant rg/
patients, problems in professionals/kdoqi/
delivery of HD like guidelines_updates/d
poor blood flow, oqiuphd_ii.html#6
clotting of dialyzer,
delivered dose is
widely different
from prescribed one
& recent
modification of dose
Hemoglobin Once a week - -
Platelet count Once a month Once in 2 weeks if -
heparin induced
thrombocytopenia is
suspected

Total leucocyte Once a month - -

count

ESR Once a month - -

Serum calcium Once a month if the Once a week when Handbook of

patient is on cinacalcet was Dialysis Daugirdas
calcitriol/doxercalcif started for SPTH JT, Blake PG, Ing
erol/paricalcitol TS, 4rth edition

Serum phosphorus Once a month if the Once a week when HBD: Daugirdas
patient is on cinacalcet was
calcitriol/doxercalcif started for SHPT
erol/paricalcitol

PTH Once a month Once a month when HBD: Daugirdas

being treated for
SHPT

Serum uric acid Once a month - -

SGPT, SGOT, ALP Once a month - -

Iron studies Once a month if - http://www.kidney.o
Patients not attained rg/
target Hb, on EPO, professionals/
not receiving iron kdoqi/
Once in three guidelines_updates/
months if Patients doqiupan_iii.html
not attained target
Hb, on EPO,
receiving iron
Once in three
months if Patients
has attained target
Hb, on EPO

Guidelines for testing for HBV and HCV in haemodialysis patients (where universal precautions are
strictly followed)

Patient status On admission Monthly Semiannual Annual

All patients HbsAg, Anti-HBc, - - -
Anti-Hbs,
Anti-HCV, ALT
Anti-HCV
In HD units with a
low prevalence of
HCV, initial testing
with enzyme
immunoassay
[EIA]; (if positive,
followed
by nucleic acid
testing [NAT])
should be
considered.
In HD units with a
high prevalence
of HCV, initial
 testing with NAT
should be
considered.

HBV susceptible like - HbsAg

nonresponders to vaccine Screening should be repeated
every 3–6 months once
on HD depending on the
prevalence of HBV infection in
the unit
Anti-Hbs positive (> - - -
10 mIU/mL), anti-HBc
negative
Anti-HBs and anti- - - No additional testing
HBc positive needed
Anti HCV negative - ALT Anti-HCV
For patients on HD
therapy who test
negative for HCV,
retesting every 6 to
12 months with EIA
should be considered.
Testing for HCV with
NAT should be
performed for HD
patients with
unexplained
abnormal ALTs.
If a new HCV
infection in an HD unit
is
suspected to be
nosocomial, testing
 with NAT should be
performed in all
patients who may have
been exposed.
Repeated testing with
NAT is
suggested
within 2 to 12 weeks
in initially
NAT-negative
patients.
Screening should be
repeated at least every
6 months
once on HD. HCV
screening should
include an ELISA
assay and a
confirmatory testing
with a more specific
assay (RIBA)

HIV Screening for HIV

infection should be
done in all
patients starting HD or
transferring from
another unit
after getting informed
consent. Once on
routine HD,
screening is not
recommended.
Equipment required for investigations:
A. Biochemistry
1. Semi auto analyser / Bench Top auto analyser
2. Electrolyte Analyser (Ion selective electrode)
3. Semi auto coagulation analyser

B. Imaging facility.
1. 500 ma X-ray
2. Ultra Sound, Echocardiography, Doppler
C. Clinical Pathology
1. Cell counter
2. Urine analyser / Binocular Microscope
3. pH meter

D. Microbiology
1. Manual Elisa Reader / Immunoassay analyser
2. Bacterial cultures

E. Blood Bank
Rationale:
A.1.
Auto analyzers are recommended as analysis by enzymatic method is accurate compared to calorimetric
method. Bench top analyzers are good and less expensive, whereas semi auto / auto analyzers are more
expensive. Units may choose the equipment depending on the work load and expertise available. Analysers
and kits for doing all the tests listed below have to be made available in the attached laboratories.
A.2.
Electrolyte analysis with Ion selective analyzer is accurate and reliable. Flame photometers are not
recommended.
A.3.
For coagulation test like clotting time, PT and APTT, manual methods may be used. However, depending
on workload, semi auto coagulation analyser may be installed which is preferable.
B.1.
500ma X-ray machine is necessary for radiological evaluation.
B.2.
Ultra sound ,echo and Doppler are required for cardiovascular and other organ evaluation .
C.
Cell counters for quick and accurate cell counts and urine analyser for various urine test are important.
However, a good binocular microscope and routine equipments for cell counts and urine microscopy is also
adequate.
D.1.
Manual Elisa readers for screening for HBs Ag. HCV and HIV are good and adequate. However, depending
on the work load and need for other investigations, Immunoassay analyser may be used in place of Elisa
readers
E. HD centres must have access to Blood Bank which has facilities for component separation.
References:
1. CDC guidelines; accessed on http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5005a1.htm#
2. European Best Practice Guidelines for Haemodialysis (Part 1)

Nephrol Dial Trans Volume 17 suppl 7 July 2002

3. Gordon CE, Balk EM, Becker BN, Crooks PA, Jaber BL, Johnson CA, Michael MA, Pereira BJ, Uhlig K,
Levin A, US Commentary on the KDIGO Clinical Practice Guideline for the Prevention, Diagnosis,
Evaluation, and Treatment of Hepatitis C in CKD Am J Kidney Dis 52:811-825, 2008

53. NUTRITION
Rationale: Anorexia has been documented in a very large number of patients on both hemodialysis and
CAPD and been to shown to be multifactorial. Most patients entering hemodialysis are on protein restricted
diets, which may not be liberalized after starting on maintenance hemodialysis. Indian patients who
traditionally consume a lower protein than their Western counterparts may be at a particularly higher risk of
malnutrition. Malnutrition and low serum albumin have been shown in the dialysis population to directly
correlate with mortality. As development of malnutrition may be subtle in patients on dialysis who are
losing or gaining weight due to fluid shifts, extremely close monitoring by subjective and objective, clinical
and biochemical parameters are required to assess nutritional status, and avoid hypercatabolism and
malnutrition.

Guideline 1. Prevalence of malnutrition and goals of nutritional intervention

Protein energy malnutrition (protein energy wasting (PEW)) is common (18%-70%) among patients on
maintenance hemodialysis (MHD). PEW is the strongest predictor of morbidity and mortality, therefore,
goals of nutritional therapy in dialysis patients are i) to prevent malnutrition, ii) improve nutritional status,
iii) build up body stores for good transplant outcome (if planned) and iv) improve quality of life.
Hemo study has demonstrated that progressive renal insufficiency is associated with a spontaneous decline
in protein intake. Predialysis patients appear to have a spontaneous protein intake of <0.7 g/kg/day, which is
below the minimal recommended daily intake so by the time patient starts hemodialysis, patient is already
malnourished. Therefore, nutritional status should be assessed at the start of maintenance haemodialysis
(MHD), PEW should be avoided during MHD because of poor patient outcome, and in the absence of
malnutrition, nutritional status should be monitored every 2 months in patients <50 years of age and in
patients >50 years of age nutritional status should be monitored every month.
In India, protein intake of an average middle class individual is less than 0.7g/kgbw/day. Also recommended
cut offs for Asian population for BMI are lower than those of Western population because of difference in
body size. Although recommendations for dietary protein intake are based on recommended dietary
allowances for Indian population, which are quite similar to those of western population, but for an Indian
patient to switch over from moderately low protein diet to a very high protein diet may be difficult because
of i) body may not accept such high quantity of protein instantneously, ii) it may affect residual renal
function, iii) patient can get uremic because of excessively high protein intake and iv) affordability.
Therefore, although, patient should be put on high protein diet, but the target should be achieved gradually
over a period of time depending upon how much the patient can easily tolerate and digest. Patient should be
given high calorie diet to ensure proper utilization of protein.
Guideline 2 – Evaluation of Protein Energy Nutritional Status
Nutritional status in maintenance dialysis patients should be assessed with a combination of valid
complementary measures rather than by any single measure alone because no single measure provides a
comprehensive indication of nutritional status. Measures of intake, visceral and somatic protein stores, body
composition, and functional status identify different aspects of nutrition status. Therefore, using
combination of nutritional measures provides an assessment of visceral and somatic protein body pools,
body weight and hence fat mass and nutrient intake. These can be divided into three categories: Category I:
Measurements that should be performed routinely (every visit, monthly or three monthly), Category II:
Measures that can be useful to confirm the findings of category I (as and when needed) and Category III:
Clinically useful measures if low might suggest more rigorous examination of protein energy wasting:
2a ) Measurements that should be performed routinely (every visit, monthly or three monthly)
Category I
2a i.) Every visit Assessment: Protocol should include a) medical history, b) physical examination
(including deficiency signs on skin), c) hydration status, 4) difference between actual weight and dry
weight. Malnutrition may be identified with greater sensitivity and specificity using a combination of factors
including calculating weight loss <85% of ideal weight.
Stabilized serum albumin, percent of usual edema free post dialysis weight, dietary diaries (dietician’s role)
should be evaluated monthly.
2a ii) Serum albumin is a valid and clinically useful measure of protein energy nutritional status in
maintenance dialysis patients. Serum albumin is recommended for routine measurement because there is a
large body of literature that defines the normal albumin values. Predialysis or stabilized serum albumin
should be checked monthly, maintained at ≥ 4.0g/dL using Bromcresol Green (BCG) method. Since half life
of albumin is ~20 days, it should evaluated once month. However, the limitations of using serum albumin as
a nutritional marker are that the levels decrease in Inflammation & Infection.
2 a iii) Serum prealbumin (optional): Serum prealbumin is a valid and clinically useful measure of protein
energy nutritional status in maintenance dialysis patients. In Indian scenario cost inhibits regular use of
serum prealbumin as a nutritional marker though its advantage is a much shorter half life ~2-3 days.
However, depending upon affordability, serum prealbumin can be used as a marker of nutritional status.
Prealbumin should be greater than 30 mg/dL
Serum prealbumin is a negative acute phase reactant protein, as its levels decrease in Inflammation & stress,
so therefore prealbumin may not correlate well with other nutritional parameters. Also levels are increased
in renal disease due to impaired degradation by kidneys.
2 a iv) Adjusted edema free body weight. Body weight should be obtained post dialysis. For individuals
whose edema free body weight is between 95th and 115th percent of median standard weight, the actual
edema free body weight may be used. Following equation can be used to calculate edema free adjusted body
weight (aBWef)
aBW ef= BWef + SBW-BWef x 0.25
Where BW ef is the actual edema free body weight and SBW is standard body weight as determined from
NHANES II data. Because of interdialytic weight gain, aBW ef should be calculated based on post dialysis
values.
2 a v.) Three Monthly Assessments: Clinician must examine fat deposits/ depletion, muscle mass (Mid-
upper arm circumference (cm)/3.14-triceps skinfold mm)
2 a vi) Subjective global assessment (SGA) is recommended because it gives a comprehensive overview
of nutritional intake and body composition including a rough assessment of both muscle and fat mass and
because it is correlated with mortality rates. It is recommended that SGA scoring be determined by 4 item,
7- point scale used in CANUSA Study. SGA scorecorrelates with objective measures
(albumin/weight/intake/anthropometry). Change in SGA rating by 1 point decreases relative risk of death by
25%. A higher SGA score is associated with a lower RR of death and fewer hospitalized days/year
(CANUSA study) SGA should be six monthly.
Recommendations for future Research: Should BMI, Serum albumin and serum TIBC be included in SGA
scoring as is done in malnutrition inflammation scores (MIS).
2 a vii) Assessment of Dietary Intake should be done using 1.) Diet History Questionnaires, 2.) Food
weighing and 3.) Observation. Food weighing is difficult for patients who visit dialysis units on out patient
basis. Assessment of food intake using diet history questionnaires is therefore more appropriate for such
patients. Dietary interviews and diaries can be used to assess intake not only of protein and energy but
also of a variety of other nutrients as well as pattern and frequency of meals. Dietary interviews and diaries
should be followed once in 3 months.
2 b) Measures that can be useful to confirm the findings of category I (as and when needed)
2b i) Anthropometric measurements are valid and clinically useful indicators of protein energy
nutritional status in maintenance dialysis patients. These measures include, percent usual body weight,
percent standard body weight, height, Body mass index (BMI), Mid- upper arm muscle circumference
(MUAC), skinfold thickness (biceps, triceps, subscapular, suprailliac) and waist/hip ratio. For
anthropometric calculations, post dialysis actual edema free body weight should be used. Patients in the
lower 50th percentile of weight for height clearly have a reduced survival rate. Differences in
anthropometric measurements among MD patients and normal individuals may indicate a nutritional
disorder or other clinical abnormality. Standard international methods should be followed for performing
anthropometry and calculating body composition from measurements.
2b ii) BMI: Because height may decrease with aging in MHD patients particularly those with bone disease,
height should be measured once annually. Skeletal frame size must also be determined to calculate
individual’s standard body weight percent (%SBW).
2b iii) Mid- upper arm muscle circumference (MUAC) should preferablybe measured every three months.
2 b iv) Skinfold thickness (biceps, triceps, subscapular, suprailliac) should preferably be measured every six
months.
2 b v) Body composition assessment (Optional): Depending upon availability of the equipment, bioelectrical
impedance analysis (BIA), Infrared reactance, or DEXA can be used to assess long term adequacy of
protein-energy nutritional status. Measurement can be repeated every six months. Accurate data on body
composition are helpful to. Although whole body DEXA is less influenced by abnormalities in hydration
status which are common in HD patients, it does not distinguish between intracellular and extracellular
water compartments. Every dialysis centre may not have DEXA because of prohibitive cost and also it is not
a bed side tool. Routine use of DEXA is not recommended.
2c) Clinically useful measures if low might suggest more rigorous examination of protein energy
wasting: Predialysis creatinine, blood urea nitrogen, cholesterol, serum and urine electrolytes , serum and
Urine Urea Nitrogen, serum and visceral protein. A low predialysis or stabilized serum urea level may
indicate a low intake of protein and amino acids. Depending upon availability of test facility and reliability
and financial affordability: serum and blood cell vitamin levels, plasma amino acid levels (Essn/NonEssn &
valine/glycine) (Optional).
2c i) Predialysis Serum Creatinine:
Low stabilized predialysis creatinine of between 2.0-4.5 mg/dL with negligible renal function should be
investigated for low dietary protein intake and skeletal muscle wasting and risk for high mortality
This is a direct indicator of protein intake and muscle mass. It is directly proportional to skeletal muscle
mass & dietary muscle intake According to NKF/KDOQI guideline 5 predialysis Serum Creatinine of
<10mg/dL is considered as high risk for Protein Energy Wasting (PEW) which warrants thorough
evaluation of Protein Energy Wasting (PEW). Mortality risk increases with creatinine below 9-11 mg/dL in
patients on MHD or PD. But these data are based on Western population with significantly different body
frame and size.
A predialysis serum creatinine of higher than 10mg/dL is not tolerated by Indian patients and they become
highly uremic (anorexia, vomiting, loss of taste) . Therefore, the threshold levels of predialysis serum
creatinine for Indian are much lower than those recommended by NKF/KDOKi guidelines.
A low predialysis or stabilized serum creatinine level in MHD patients suggests decreased skeletal muscle
mass and or low dietary protein intake. Therefore in Indian patients, low stabilized predialysis creatinine of
between 2-4.5 mg/dL with negligible residual renal function should be investigated for low dietary protein
intake and skeletal muscle wasting and risk for high mortality.
Recommendations for future research: To create threshold for predialysis creatinine for Indian patients
for evaluation of PEW.
2 c ii) Serum Cholesterol is a valid and clinically useful measure of protein energy nutritional status in
maintenance dialysis patients may be influenced by comorbid conditions. Hypocholesterolemia is associated
with chronic protein-energy intake/deficits and or the presence of co morbid conditions including
inflammation. Individuals with low normal <150-180 mg/dL or declining serum cholesterol concentrations
should be evaluated for nutritional deficit and indicate as they have increased mortality risk. In stable
patients the recommended dietary intake of cholesterol is <200mg/d.
2c iii) Protein Equivalent of Total Nitrogen Appearance (PNA) (Optional):
Protein catabolic rate (PCR) is a valid and clinically useful measure of net protein degradation and protein
intake in maintenance dialysis patients. In a clinically stable patient PNA provides a valid estimate of
protein intake.
There are a number of technical problems with measuring PNA in individuals undergoing HD. PNA
approximates protein intake only when the patient is in zero nitrogen equilibrium. PNA may fluctuate from
day to day as a function of protein intake and a single measurement may not reflect usual protein intake.
When dietary protein intake (DPI) is high total nitrogen appearance (TNA) underestimates protein intake.
PNA may overestimate DPI when protein intake is less than 1 g/kg/d possibly due to endogenous protein
catabolism. Finally normalizing PNA to body weight can be misleading in obese, malnourished and
edematous patients.

Guideline 3. Management of Acid-Base Status

Guideline 3a Measurement of Serum Bicarbonate: Serum bicarbonate should be measured in
maintenance hemodialysis (MHD) patients once monthly. Low serum bicarbonate concentrations in MHD
patient almost always indicate metabolic acidosis. Acidemia associated with metabolic acidosis is associated
with increased oxidation of branched chain amino acids (valine, leucine and isoleucine), increased protein
degradation and PNA and decreased albumin synthesis.
Guideline 3b Treatment of Low Serum Bicarbonate: Predialysis or stabilized serum bicarbonate levels
should be maintained at or above 22 mmol/L. Normalization of predialysis or stabilized serum bicarbonate
concentrations can be achieved by higher basic anion concentrations in the dialysate and/or by oral
supplementation with bicarbonate salts. Higher concentrations of bicarbonate in hemodialysate (38mmo/L)
have been shown to safely increase predialysis serum bicarbonate concentrations. Oral dose of sodium
bicarbonate usually about 2 to 4 g/d or 25 to 50 mEq/d can be used to increase bicarbonate concentration.
Correction of academia due to metabolic acidosis increases serum albumin and decreases protein
degradation rates. Most trials report that normalizing predialysis or stabilized serum bicarbonate
concentrations is beneficial for protein, amino acid and bone metabolism and protein-energy nutritional
status.
Guideline 4 Inflammation
Many patients undergoing HD show evidence of chronic inflammation with intermittent or persistently
elevated levels of acute phase proteins. C Reactive protein (CRP) levels should be checked every 3 months.
An elevated CRP is often associated with reduced serum albumin levels secondary to impaired albumin
synthesis. In this context hypoalbuminemia is an inflammatory marker, rather than an index of poor dietary
intake.
Guideline 5. Management of dietary protein and energy intake
Guideline 5a. Eliminate/Treat any potentially reversible or treatable condition (anemia) or
medication that might interfere with appetite or cause malnutrition.
Guideline 5b. Anorexia: Major proportion of patients treated with HD consume less protein and energy
than is recommended due to loss of appetite. Factors that contribute to anorexia are i) underdialysis (switch
over to thrice weekly dialysis in place of twice weekly dialysis therapy), ii) comorbidity, iii) medication (in
such circumstances discontinuing phosphate binders and iron and vitamin supplements for a short period of
time helps improve appetite) and iv) psychosocial factors . These factors should eliminated.
Guideline 5c Dialysis regimen should be regularly monitored and modified to treat intensification of the
patient’s uremic state that is caused by superimposed illness. Maintain KT/V of 1.2 in HD patients.
Guideline 5c) Detailed Nutrition counseling on patient’s first visit.
New patients require proper counseling on disease, its causes, what has caused disease in the patient,
progression of disease, how to control progression, importance of nutritional counselling. Clinician’s
personal involvement in nutritional counseling is important for better compliance.
Guideline 5d) Dedicated renal dietician: Each center should have a dedicated renal dietician who can
follow up the patients. Patient must visit dietician regularly. Telephonic follow-ups: Dietician should
contact patients telephonically in order to motivate them to improve compliance. Regular telephonic
follow-up results in better nutritional status and QOL (KDQOL).
Dietician should advise patients to maintain dietary diaries. Dietician should evaluate nutritional status
which should be evaluated every month. Even small decrease in nutritional indices together with decrease in
protein and energy intake strongly suggest need for frequent nutritional monitoring (MDRD Study).
Dietician should evaluate changes in body composition, loss of muscle mass and weight with longitudinal
anthropometry.
Guideline 5e) Dietary Protein Intake (DPI): Dietary protein intake for clinically stable MHD patients
should be 1.2 g/kgbw/d (Table 1). This amount is necessary to ensure neutral or positive nitrogen balance.
At least 50% of protein should be of high biological value (HBV)Proteins of HBV have an amino acid
composition that is similar to human protein and is likely to be utilized more efficiently by humans to
conserve , body proteins. Egg white, fish, chicken, milk and milk products (curd, chenna/paneer), dehusked
(without outer covering to prevent hyperphosphatemia) lentils kidney beans, soy protein (milk and cheese
marketed as Tofu) are good sources of protein with HBV. Include two cereals in one meal eg:- rice and
wheat.to improve protein quality the ratio of cereal protein to pulse protein should be 4:1.
Guideline 5f) Intradialytic protein intake: Patients should be advised to eat high protein food (high
protein snack/chenna/curd/egg whites/protein biscuits etc) during dialysis to prevent protein catabolism and
to make up for losses due to dialysis procedure. Protein snacks should be taken anytime after half an hour of
initiation of dialysis.
Guideline 5g) Dietary Energy Intake: Recommended energy intake for MHD patients is 35 kcal/kg b.w if
the patient is less than 60 years of age and 30 kcal/kg bw if the patient is more than 60 year.
Recommendations for children are based RDA for chronological age (Table 2) It is recommended that 50-
60% of total calories should come from carbohydrate, 30% of total calories should come from fat (saturated
fats <7%), and 20% of total calories should come from protein. Energy intake of patients having diabetes
mellitus should be 25 to 30 Kcal/kg/d. Blood sugar levels should be monitored to avoid hyperglycemia.
Guideline 5h) Individualize dietary prescription: Renal diet has numerous restrictions therefore
adherence to such a diet can be difficult and stressful. Prescribed diets should be individualized to help
accommodate each patient’s unique circumstances in terms of palatability, cost, comorbid medical
conditions and cultural eating habits.
Guideline 6) Management and treatment of Undernutrition
Guideline 6a) Correct inadequate dietary protein intake: Patients who do not have adequate DPI should
first receive dietary counseling and education. If DPI remains inadequate oral supplementation should be
prescribed. If oral supplements are not tolerated or effective and protein malnutrition is present consider
tube feeding to increase protein intake.
Guideline 6b) Assess patient’s compliance: Assessment of patient compliance to dietary prescription and
nutritional intervention should be done on every visit. Patients who do not have adequate dietary Intake
should first receive dietary counseling and education. Meal plan should be Individualized Patient should be
motivated to eat enough calories for proper utilization of protein.
Guideline 6c) Detect Lack Of Appetite: Appetite assessment tools are a valid and clinically useful
measure of estimating nutritional intake. It is recommended to use one or more of these tools. (i) Appetite
and diet assessment Tools (ADAT) for appropriate nutritional intervention. Rating is based on prompt
questions like during the past week how would you rate your appetite? Rating may be1) Very good, 2) good,
3) fair, 4) poor and 5) very poor. (ii) Subjective Global Assessment (SGA). Scores are based on prompt
question “how would you grade your appetite in the last week? Scoring may be 1) Good, 2) sometimes bad,
3) often bad, and 4) always bad.Dietary Intake is assessed in terms of 1) overall change, 2) no change, 3)
change and 4) duration of change in weeks. Type of change is assessed in terms of 1) suboptimal solid diet,
2) hypocaloric diet, 3) full liquid diet, 4) starvation.(iii) Kidney Disease Quality of Life-Short Form
(KDQL)Rating is based on question “To what extent were you bothered during past four weeks by lack of
appetite”? Scoring may be 1) Not at all, 2) somewhat, 3) moderately, 4) very much 5) extremely.
Guideline 6 d) Indications of nutritional support: Patients who are unable to meet protein/energy
requirements with food for an extended period of time should receive nutrition support. Extended period is
defined as days to 2 weeks depending upon the severity of patient’s clinical condition, degree of
malnutrition,and degree of inadequacy of their nutritional intake. Complete nutritional assessment is needed
before intervention.
Guideline 6 d i) Protein Supplementation: In dialysis patients if DPI remains inadequate oral
supplementation should be prescribed.
Guideline 6 d ii) Oral Supplements: 1). Special Calorie Dense Commercial Formulas provide 2kcal/ml
with high protein and low electrolytes. 2). Provide smaller water load than intravenous feeds. Use of Alpha
Keto-analogues (optional) may improve protein utilizationand reduce degree of catabolism. Standard
recommended dose of ketoacid dosage is 6 to 14 g daily. However,high cost of Alpha Keto-analogues deters
their use.
In case of children, supplemental nutritional support should be considered when a patient is not growing
normally or fails to consume the RDA for protein and/or energy. Supplementation by oral route is preferred
followed by enteral tube feeding.
Guideline 6d iii) Nasogastric feeding: If oral supplements are not tolerated or effective and malnutrition is
present consider tube feeding should be considered as it provides balanced nutrients.
But who decides regarding tube feeding? In India, most of the patients want to escape tube feeding and
because patient is reluctant to go for tube feeding because of discomfort caused by Ryle’s tube, malnutrition
worsens. It is the clinician’s responsibility to explain the potential risks of worsening malnutrition and
convince and motivate the patient and his attendants for tube feeding.With tube feeding, overnight
enteral supplements can improve nutritional status. Tube feeding provides smaller water load than
intravenous feeds, lowers risk of infection than TPN , is less expensive, overnight supplementation
improves nutritional status.
Guideline 6 diii
Recommendations for Tube feeding. 1. Start with 50-100 ml feeds every 6 hours and gradually increase
to 300-400ml per feeding. 2) If continuous feedings are started, then start feeding from 20-50ml/hr, then
increase 20ml every 2-8hrs until requirement is reached.
Guideline 6d iv) Indications for Intra dialytic Parenteral Nutrition: If tube feedings are not used then
intra dialytic parenteral nutrition (IDPN) should be considered. In any case IDPN should be given if
spontaneous intake of energy is >20 & <25 kcal/kgIBW and if protein is > 0.8g but < 1g/kg/IBW. Consider
regular use of IDPN during hemodialysis or SLED in anuric or oliguric patients as because of fluid
restriction IV nutrition cannot be used aggressively. An equivoluminous degree of ultrafiltration should be
added to regular UF rate to maintain fluid balance. Minerals : Include sodium, potassium and Magnesium
in the IDPN/TPN solution as per patient’s requirement.
Guideline 6d v) Indications for Total Parenteral Nutrition: If combination of Oral and IDPN is
insufficient then total parenteral nutrition (TPN) should be considered. In any case TPNshould be given if
spontaneous intake is <20 kcal/kgIBW and < 0.8g protein/kgIBW.
Guideline 6e ) Monitoring Side Effects of Parenteral Nutrition:It is recommended to monitor side effects
of parenteral nutrition. 15-25% of the patients may get nausea and vomiting when IDPN is initiated. In such
cases, 1) decrease infusion rate, 2) reduce total IDPN by half for 1 to 2 weeks. Intradialytic cramping may
occur in rare cases of low plasma osmolality if sodium profiling is not used. It is recommended that
1gNaCl/250ml of infusion should be added to IDPN. 3) Glucose metabolism should be checked. 4)Prevent
hyperglycemia (>300mg/dL) by administer ing 2-6 units short acting insulin.
Guideline 7 Electrolytes:
Guideline 7a Sodium: It is recommended that patients on HD should restrict sodium intake to no more than
2 g/d. Patients with limited residual renal function and uncontrolled hypertensionshould restrict its use to 1.5
grams/d. In case of hyponatremia (Na < 135 mmol/dL), depending upon deficit, salt capsules made out of
measured quantity of salt (prescribed for correction) should be advised. In case of hypernatremia, correct
hydration and rule out all medical conditions which can cause hypernatremia. Restrict foods with high salt
content (papadams, pickles, chutney, sauce), dry fruits, popcorns, coconut water.
Guideline 7b Potassium: Potassium intake for a patient on HD should be 1mEq/kg BW/d. Patients should
be advised to leach potassium from green vegetables. Fruit juices and vegetable soup should be avoided.
Patients on HD should be allowed to take fruits with low potassium content (<100mg/100g). Recommended
fruits are apple, banana, pineapple, pear, orange, guava and papaya (approximately 50-60 g/d). Patients
should avoid green leafy vegetables and vegetables with very high (>300mg/g) potassium content. Diabetic
patients should not take banana and orange. Hypokalemia may develop in patients who are on diuretics or
who have low protein intake. To correct hypokalemia, 60-80 mEq (or as per s. potassium level) of
potassium should be administered either orally or through intravenous route (if deficit is large). Anuric
patients on HD should have stricter control of potassium and advised to stop fruit intake if serum potassium
level approaches 4.9 mEq. Potassium binders should be prescribed in case of hyperkalemia.
Guideline 8 Carnitine (Optional)
Administration of L-Carnitine may improve subjective symptoms such as malaise, muscle weakness,
intradialytic cramps, and hypotension, and quality of life in HD patients. It should, therefore, be used
keeping in mind patients’ condition. However, the totality of evidence is insufficient to recommend its
routine use. Carnitine may enhance responsiveness to erythropoietin stimulating agents (ESA) in
erythropoietin resistant anemia.
Guideline 9 Fluid restriction and controlling thirst
Recommended fluid intake for HD patients is 24 hour urine output + 500 ml for insensible. Fluid includes
all liquids (for example water, tea, milk, curd) consumed by the patient. However, if the patient is in volume
overload, the +500 ml for insensible losses should be reduced and diuretic therapy should be started.
However if the patient is anuric, diuretics should be avoided to prevent. Electrolytes should be closely
monitored. Salt should be restricted in order to control thirst. Rinsing mouth when ever patient feels thirsty
may bring down fluid intake.
Guideline 10 Monitoring Serum Calcium and serum phosphate levels
Hypocalcemia should be treated with IV or oral calcium supplements. Stop calcium based phosphate
binders in hypercalcemia and shift patient on non-calcium based phosphate binders. Consider discontinuing
phosphate binders for few weeks if i) patient’s serum levels are within normal range with strict instructions
for avoiding foods rich in phosphates and ii) in case of loss of appetite.
Guideline 11 Minerals and Vitamins
Recommended daily dietary intake of minerals and vitamins is given in Table 3.0. Zinc needs special
mention. Zinc supplements are recommended for patients having proteinuria.
In children 100% of the recommended dietary allowance is a reasonable starting point for water soluble
vitamin (thiamine, pyridoxine B12 and folic acid) requirement in children on MHD. Nutritional status of
water soluble vitamins be monitored. Supplementation should be considered if dietary intake alone does not
meet or exceed the RDA, if measured blood vitamin levels are below normal values (monitor 4-6 months),
or if clinical evidence of deficiency is present (low folic acid or Vitamin B12 levels giving rise poor
responsiveness to recombinant human erythropoetin). An intake of 100 % of RDA should be the goal for
vitamins A,C,E, K, zinc and copper. Supplements of fat soluble vitamins should be avoided due to reduced
renal clearance. Vitamin K supplementation may be considered during antibiotic therapy.
Guideline 12 Monitoring Lipids
Restrict dietary fat and sugar intake. The therapeutic goal should be to achieve a low density lipoprotein
(LDL) cholesterol of <100 mg/dL and a fasting triglyceride level of <500 mg/dL. Therapeutic life style
changes diet, weight reduction, increased physical activity and treatment of hyperglycemia if present. Diet
should contain < 7% saturated fats, with polyunsaturated fat <10% of total calories and monounsaturated fat
<20% of total calories and with total fat at 20-30% of total calories. Carbohydrates should not exceed 60%
of total calories. In HD patients 20-30g of fibre per day should be consumed to reduce dyslipedemia. If
required drug therapy should be started.
Guideline 13 Protein intake during Acute illness
Acutely ill patients on HD should receive at least 1.2-1.3g/kg/d depending upon catabolic rate. Patient may
require nasogastric feeds along with parenteral nutrition. Fluid overload should be checked in patients on
TPN.
In case of acute pancreatitis, oral intake should be stopped and IV fluids and parenteral formulations
containing medium chain triglycerides (MCTs) should be administered. In diabetic patients blood sugars
must be monitored and dose of insulin adjusted as per the requirement.
Guideline 14 Energy intake during Acute illness
Recommended energy intake for a maintenance dialysis patient who is acutely ill is at least 35
kcal/kg/d for those who are below 60 years and 30-35 kcal/d for those above 60 years of age. In
diabetic patients blood sugar levels should be monitored to avoid hyperglycemia.

Table 1 Protein Requirement and Dietary Allowance for Indian Infants, Boys, Girls and
Adults on Hemodialysis
Age Group Requireme Body for HD Requireme Body for HD
nt weight Patient nt weight Patient
g/protein/k (Kg) Total daily g protein/d (Kg) Total daily
g/d Requireme Requireme
nt nt
g protein/d g protein/d
+ 0.4 + 0.4
g/kg/d & g/kg/d
+0.2 for and
adults +0.2.g/kg
for adults
Infant 1-5 months 2.2 5.0 11.0
Infant 6-9 months 1.69 7.9 16.5
Infant 9-12 months 1.69 8.8 18.39
Boys Girls
1-2 years 1.47 10.3 19.26 1.47 9.6 17.9
2-3 years 1.25 12.8 21.1 1.25 12.1 19.9
3-4 years 1.16 14.8 23.0 1.16 14.5 22.6
4-5 years 1.11 16.5 24.9 1.11 16.0 24.1
5-6 years 1.09 18.7 27.8 1.09 17.7 26.3
6-7 years 1.15 20.4 31.62 1.15 20.0 31.0
7-8 years 1.17 22.7 35.6 1.17 22.3 35.0
8-9 years 1.18 25.2 39.8 1.18 25.0 39.5
9-10 years 1.18 28.0 44.2 1.18 27.6 43.6
10-11 1.18 30.8 48.6 1.18 31.2 49.2
years
11-12 1.16 34.1 53.1 1.15 34.8 53.9
years
12-13 1.15 38.0 58.9 1.14 39.0 54.6
years
13-14 1.15 43.3 67.1 1.13 43.4 66.4
years
14-15 1.14 48.0 73.9 1.12 47.1 71.5
years
15-16 1.13 51.5 78.7 1.09 49.4 73.6
years
16-17 1.12 54.3 82.5 1.07 51.3 75.4
years
17-18 1.10 56.5 84.75 1.06 52.8 75.9
years
Adult male 1.0 60 72
Adult female 1.0 55 66

Table 2 Energy Requirement and Dietary Allowance for Indian Infants, Boys and Girls on
Hemodialysis
Age Group Requireme Body for HD Requireme Body for HD
nt weight Patient nt weight Patient
Energy (Kg) Total daily Energy (Kg) Total daily
kcal/kg/d Requireme kcal/kg/d Requireme
nt nt
Kcal/kg/d Energy
kcal/kg/d
Infant 115 4.58 526
0-1month
Infant 105 5.50 577
2 months
Infant 95 6.28 596
3 months
Infant 6-9 months 80 7.9 632
Infant 9-12 months 80 8.8 704
Boys Girls
1-2 years 85 10.3 875.5 80 9.6 768
2-3 years 85 12.8 1088 80 12.1 968
3-4 years 80 14.8 1184 75 14.5 1087
4-5 years 80 16.5 1320 75 16.0 1200
5-6 years 80 18.7 1496 75 17.7 1327
6-7 years 75 20.4 1530 70 20.0 1400
7-8 years 70 22.7 1589 70 22.3 1561
8-9 years 70 25.2 1764 65 25.0 1625
9-10 years 70 28.0 1960 65 27.6 1794
10-11 65 30.8 2002 60 31.2 1872
years
11-12 65 34.1 2216 60 34.8 2088
years
12-13 60 38.0 2280 55 39.0 2145
years
13-14 60 43.3 2598 50 43.4 2170
years
14-15 60 48.0 2880 50 47.1 2355
years
15-16 55 51.5 2832 50 49.4 2470
years
16-17 55 54.3 2986 45 51.3 2308
years
17-18 55 56.5 3107 45 52.8 2376
years

Table 3.0 Recommended daily dietary intake of minerals and vitamins for patients on MHD
Nutrients RDA
Sodium <2 g
Potassium 2.0 mmol
Calcium 2000 mg (total elemental
calcium
provided by phosphate
 binders should not exceed
1,500 mg/d)

Phosphorus 800 mg (serum

phosphorus >5.5 mg/dL)
Magnesium 0.2-0.3 g
Iron
Vitamin A None
Β-Carotine None
Retinol None
Thiamine (mg) 1.5
Riboflavin (mg) 1.7
Vitamin B6 (mg) 10
Vitamin B12 mg 0.006
Niacin (mg) 20
Folic Acid (mg) >1.0
Pantothenic acid (mg) 10
Biotin (mg) 0.3
Vitamin C (mg) 60-100
Vitamin E (mg) None
Vitamin D In nonuremic patients
200-400 IU
Vitamin K 7.5 mg/ week Deficiency
occurs if patient is taking
antibiotic.
Table 4 Exchange list of common foods for Protein Content
Protein Found in Food
Meat: 7 grams of protein per: 1 ounce meat, fish or poultry, 1 egg , 1/4 cup tuna , 1/2 cup baked beans, dried
peas, and lentils, 2 tablespoons peanut butter
Dairy: 8 grams of protein per:
1 cup milk (8oz)
1 cup yogurt (8oz)
1 ounce cheese
1/3 cup cottage cheese
2 cups ice cream
 Breads and cereals: 3 grams or protein per: 1 slice of bread , 1/2 cup rice, noodles, pasta, cereal
Vegetables: 1 gram of protein and fruit have .5 grams or protein per: 1/2 CUP

54. CVD MONITORING & THERAPY

Rationale: The largest contribution to mortality in Chronic Kidney disease patients on dialysis is from
Cardiovascular Disease. A large number of patients especially those dialyzing in free standing units may not
attend outpatient clinics and cannot be completely assessed during a dialysis session. Hemodialysis itself
may impose an additional stress on the patient with pre existing cardiovascular disease and patients on
dialysis have both traditional and non traditional risk factors. It therefore becomes necessary that every
patient on dialysis be adequately monitored and treated early for Cardiovascular disease. This document
attempts to provide guidelines on the optimum time and methods of monitoring patients for cardiovascular
disease.
Description:
The burden of Cardio-vascular disease (CVD) in chronic kidney disease (CKD) is very high in HD
population. Beyond, traditional risk factors like diabetes mellitus, hypertension, smoking, dyslipidemia,
obesity in HD population many more non-traditional risk factors like volume overload, anemia, mineral and
bone disease, inflammation, oxidative stress etc contribute significantly to very high prevalence of CVD.
In patients on MHD common types of CVD are; atherosclerotic vascular disease especially involving
coronary and cerebro-vascular arteries and Left Ventricular Hypertrophy. Other common CVD
manifestations are Congestive Heart Failure and peripheral vascular disease. The CVD is major cause of
morbidity and mortality in these patients. It is therefore important that CVD is diagnosed and adequately
monitored in a proactive manner.
ALL PATIENTS STARTING MHD MUST HAVE FOLLOWING DIAGNOSTIC EVALUATION
FOR CVD
On entry into HD unit:
Patients who are initiated for the first time, usually they are having significant hemodynamic, metabolic,
biochemical and volume imbalance. Hence, the investigation for CVD should be deferred till the based
weight, appropriate Hb, volume, electrolyte and divalent balance is achieved.
It is mandatory to perform baseline 12 lead ECG, Chest X-ray and Echocardiogram in all patients to assess
their baseline status of CVS and to identify and stratify their risk for future CVD.
Electrocardiography (Mandatory)
All dialysis patients should have baseline ECG at the start of maintenance hemodialysis and then it should
be ordered as and when clinically indicated. Interpretation of ECG should take into account the shifts of
volume, changes in electrolytes and anemia.
Two-dimensional and M mode echocardiography provides a noninvasive assessment of left ventricular
structure and function, together with imaging of valves and pericardium. Systolic dysfunction, diagnosed by
low fractional shortening or ejection fraction can be determined, as can LV geometry and LV hypertrophy.
The degree of hypertrophy can be identified by increased LV wall thickness or by calculating LV mass
index according to various formulae. LV mass measurement varies over the course of a hemodialysis
session by as much as 25 g/m. Therefore where possible, imaging should be carried out when the patient has
achieved their “base dry weight”. Diastolic LV function can be assessed noninvasively using pulsed
Doppler analysis of flow across the mitral valve during diastole. Baseline and annual assessment of
echocardiography should be followed in all dialysis patients.
(Optional) could be utilized as a screening tool for ischemic heart
disease in HD patients. It can also be used in patients with valvular disease or impaired systolic function to
assess underlying systolic reserve. Since the sensitivity and specificity are operator dependent the
interpretation should be correlated with clinical context.

OR
Nuclear Scintigraphic Scanning(Optional)

Nuclear scintigraphy can be used both for assessment of myocardial systolic function and for ischemia. The
predominant role for nuclear scanning techniques, however, is in the assessment of myocardial ischemia.
Exercise-based studies as well as the use of dipyridamole to enhance vasodilatation are commonly used,
together with one or other of Tc-labelled thallium, methoxyisobutylisonitrile (MIBI), or
metaiodobenzylguanidine (MIBG).
Inherent problems with scintigraphy must be taken into consideration. Blood pressure may be too high or
too low to permit safe administration of a vasodilatory agent; high endogenous circulating levels of
adenosine may blunt the efficacy of dipyridamole; coronary flow reserve may be reduced due to LV
hypertrophy and small vessel disease; and symmetrical coronary disease and/or a blunted tachycardic
response due to autonomic neuropathy can mask significant pathology. Both on-site expertise and the
recognized testing limitations in patients with HD negatively influence the utility of nuclear scanning.
Electron-Beam Ultrafast Computed Tomography(Optional)

Electron-beam ultrafast computed tomography (EBCT)-derived coronary artery calcification is a reliable

surrogate for significant coronary atherosclerosis. Evidence is accumulating that increased calcium content
per se is a poor prognostic sign. It should be utilized for diagnosis and monitoring the coronary
calcifications load and should influence the treatment of MBD including P binders, Vit D or its analogues,
calcium supplementations, cinacalcet etc.
During an Acute Event:
During on acute event it is mandatory to perform ECG 12 lead and biochemical markers of ischemia. Once
the event is controlled, every patient with acute event should be considered stress test and CAG.
Stress test and CAG should be considered whenever the other tests during baseline evaluation and/or follow
up assessment suggest significant CVD and/or warrants intervention.
1. Coronary Angiography (Only to be done for clinical indication such as acute coronary syndrome and
angina)

Coronary Angiography remains the gold standard for diagnosis of coronary artery disease. It should be
ordered whenever there is CAD is clinically suspected and non invasive tests are positive or inconclusive. In
situations where non invasive tests like ECG, DSE are negative the clinical suspicion should determine
regarding CAG.
2. Biochemical Markers of Ischemia

The elevated levels of CPK MB, Troponin T or I, LDH in the serum can be used to assess acute ischemia.
Troponin I is more specific in CKD and HD group. Interpretation should be cautious in asymptomatic
individuals as these enzyme levels go up in HD population by 1 to 3 times. These enzymes should be
ordered when there is acute coronary ischemia is suspected; they have no role in routine screening for
coronary artery disease.
Annual Monitoring:
It is desirable to perform 12 lead ECG, Chest X-ray and Echo cardiogram in all HD patients on regular
annual basis. Whenever, these tests are inconclusive or negative with strong clinical suspicion stress test
(stress ECG, Echo or Scintigraphy) should be considered.
Advanced Testing:
Various investigations like Duplex Ultrasonography and Doppler Color-Flow Imaging, Intravascular
Ultrasound, Plethysmography and Brachial Artery Reactivity, Ankle-Brachial Index etc should be
considered depending on the clinical condition and suspicious, availability of resources and expertise. These
tools are indicator of quantitative load of vascular disease rather than one time event hence these
investigations should be followed on regular basis and before and after any therapeutic intervention.

55. MBD MONITORING & THERAPY

Rationale: Disorders of Mineral metabolism in patients of Chronic kidney disease are highly vaable. They
may overlap, and treatment of one form may worsen the other, and are ultimately associated with vascular
calcification and worsening of ischemic heart disease and peripheral vascular disease. In childhood they
may also be associated with growth retardation and gait abnormalities. All disorders of bone mineral
metabolism require intensive monitoring, frequent treatment adjustments and especially vascular
surveillance. The guideline attempts to provide a comprehensive and easy to follow protocol for monitoring
bone and mineral disorders in CKD.
Description:
Abnormalities of mineral metabolism in CKD include hyperphosphatemia, hypocalcemia, elevated
parathyroid hormone (PTH), and reduced 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and other
vitamin D metabolites and growth hormone. Though they start early, abnormalities are very obvious in
patients on dialysis (CKD-MBD). The abnormal mineral and endocrine functions critically impair the
regulation of both bone formation, and structure and function and bone abnormalities universal in this
population. Deranged mineral and bone metabolism as well as the therapy used to correct these
abnormalities can lead to extraskeletal calcification. There is a strong association between CKD-MBD and
bony fractures, cardiovascular disease, and mortality. The latter two have received increased attention
recently. It is therefore, important to identify and correct these abnormalities in dialysis patients.
Evaluation for detecting CKD-MBD
Biochemical assessment
d alkaline phosphatase should be
monitored regularly

levels, the monitoring should be at longer intervals and for unstable levels or after any change in treatment,
more frequent monitoring intervals are recommended to monitor for trends and treatment efficacy and side-
effects
a. Serum calcium and phosphorus 1-3 months
b. Alkaline phosphatase 3 months
c. PTH 6-12 months.

and the entire clinical picture should be taken into consideration rather than just the one parameter.
-phosphorus product should be abandoned for making therapeutic decisions

following a patient longitudinally and for comparing readings between patients.

inform them of any change in assay method.

-charge of drawing samples should be familiar with the requirement of sample source
(whole blood, plasma or serum), drawing requirements (e.g. vacutainers, needle size etc.) and sample
handling specifications (such as storage and transport conditions, temperature etc.) to prevent inappropriate
interpretation.

should be contacted and the test repeated before making a therapeutic decision.

Imaging
1. Bone mineral density testing should not be performed for assessment of CKD-MBD.
2. Use of any test other than the ones mentioned here is not recommended for evaluation of CKD-MBD
3. An abdominal X-ray (lateral view) should be obtained at baseline and repeated annually.
4. If available, echocardiogram should be done to detect the presence or absence of valvular calcification

1. For infants, the length should be measured at least once every 3 months
2. Older children should be assessed for linear growth at least annually.

Management of CKD-MBD
Goals of treatment
o If the serum phosphorus levels are elevated, the goal should be to reduce them towards the reference range
using phosphate binding agents.
o Serum calcium levels should be maintained in the reference range.
o The iPTH levels should be maintained in the range of approximately 2-9 times of the upper limit for the
assay.

Treatment of hyperphosphatemia
1. All patients with hyperphosphatemia (values above the reference range) should be started on dietary
phosphate binders
2. Patients should be expressly instructed to take phosphate binders with meals.
3. Calcium containing phosphate binders should be used as first choice agents unless there are
contraindications (see below).
4. Non-calcium containing binders can be used either alone or in combination with each other or with
calcium containing binders.
5. Calcium-based phosphate binders should be avoided in patients who exhibit persistent hypercalcemia or
vascular/valvular calcification.
6. The use of aluminum-containing phosphate binders should be restricted to exceptional situations and be
restricted to a maximum of 6-8 weeks.
7. Dialysate water should be treated adequately to ensure removal of aluminum.
8. The dialysate calcium concentration should be kept between 5 and 6 mg/dl to allow optimal use of
calcium-containing phosphate binders.
9. Limiting dietary phosphate intake for treatment of hyperphosphatemia should be considered only in
patients who do not show evidence of malnutrition.
10. If the serum phosphate levels do not come down with maximal doses of phosphate binders, the dialysis
duration and/or frequency should be increased to ensure dialytic removal.

All patients with 25 (OH) vitamin D levels in insufficient or deficient range should be treated with
oral cholecalciferol.

Treatment of hyperparathyroidism
1. In patients with persistently high serum PTH levels, treatment vitamin D analogs (calcitriol or
doxercalciferol) should be initiated.
2. The iPTH levels should be maintained in the range of approximately 2-9 times of the upper limit for the
assay. However, treatment should be initiated if the levels show a consistent increase or decrease in one
direction, even when whey are within this range. This is suggested to avoid progression to levels outside of
this range.
3. In patients who fail to show a decline or show an increase in PTH levels despite use of vitamin D
analogues, calcimimetics may be started, either alone or in combination with vitamin D analogs.
4. In selected patients, it might be appropriate to start cinacalcet as a first line therapy for
hyperparathyroidism.
5. The dose of phosphate-binder dosage should be adjusted to appropriately control changes in phosphorus
and calcium levels that may occur following institution of vitamin D analogs or calcimimetics.

Caution
1. Vitamin D analog use should be avoided in patients with hypercalcemia and/or if serum PTH levels are
persistently low.
2. Vitamin D analogues should be reduced or stopped in patients with persistent hyperphosphatemia.
3. Vitamin D analogs, and/or calcimimetics should be reduced or stopped if iPTH levels decrease to less
than two times upper limit of normal.
4. Calcimimetics be reduced or stopped in patients with hypocalcemia, especially if it is severe and/or
clinical signs and symptoms appear

levels despite adequate vitamin D and/or calcimimetics

should be worked up to evaluate for development of parathyroid adenoma using ultrasound and/or CT scan
and MIBI scan.
o Patient who continue to exhibit high iPTH levels and are found to have a solitary adenoma should be
treated with alcohol injection by an experienced operator and/or surgical removal.
o Patients with persistently high iPTH levels who do not show an adenoma should undergo a
parathyroidectomy.

and biochemical abnormalities of CKD-MBD should be treated with recombinant human growth hormone
when additional growth is desired.

56. HYPERTENSION & THERAPY

Rationale: Of all modifiable risk factors for mortality and especially cardiac deaths, the greatest benefit has
been shown for blood pressure lowering. Blood pressure in patients on hemodialysis possesses several
unique features, and wide fluctuations occur during dialysis and in the interdialytic interval. Benefits have
also been shown for different classes of drugs used to control blood pressure. The aim of treatment outlined
in this guideline includes optimizing blood pressure control avoiding hypotension and obtaining maximum
cardiovascular benefits and quality of life.
Recommendations
1. All dialysis patients benefit by a comprehensive evaluation of their cardiovascular status. Blood
pressure control is an important component for this. MHD patients should have frequent interdialysis
blood pressure monitoring, predialysis & post dialysis B.P. monitoring. Blood pressure should be
monitored every hour during every dialysis session in stable patients & more frequently in unstable
patients.
2. The target goals should generally be realized based upon individual patient characteristics, with the
lowest target BP values being consistent with patient well-being and the absence of intradialytic
hypotension.
3. Post dialysis blood pressure target of < 140 / 90 mmHg is recommended. This correlates better with
interdialysis blood pressure. Wherever possible monitor interdialysis blood pressure which should
also be less than 140 / 90 mmHg. In patients with variable blood pressure levels during dialysis,
ambulatory blood pressure monitoring is recommended whose mean should be targeted at <135/85
mmHg during day time & < 120/80 mmHg at night time.

To attain this level of control, the following measures may be utilized:

1. If the blood pressure remains elevated despite the attainment of ‘dry weight’, antihypertensive
medications should be administered. The choice of drug is based upon the benefits and adverse
effect profile, but an antihypertensive agent is preferably administered during the evening with a
 once per day dosing schedule. ACE inhibitors or angiotensin II receptor blockers may be preferred
because they may provide greater benefits, such as relatively more LVH regression and
cardiovascular benefits.
2. Patients should be adequately dialyzed. (Please see dialysis adequacy)
3. Large interdialytic weight gains must be discouraged. Management of increased fluid accumulation
should be accomplished in consultation with dietician to achieve a low sodium intake, increased
ultrafiltration, and/or increased dialysis treatments.
4. Low initial doses of subcutaneous erythropoietin should be administered, and the target hematocrit
should be slowly achieved

To achieve recommended target blood pressure levels in MHD following recommendations:

1. Based on clinical assessment of volume status including edema, fluid in lungs, JVP and serous
cavities, blood pressure, chest x-ray, echocardiography, the clinician must try to set a ‘target dry
weight’ and achieve that weight over 3-6 weeks in young adults and 12-14 weeks in older
individuals & those with vascular pathology.

2.
withdrawn depending on blood pressure control. Once dialysis is started and hypervolumenia is
improved.
3. For patients who have difficulty in achieving ‘target dry weight’ or whose blood pressures are labile
or develop LVF despite achieving dry weight, should be evaluated by echocardiography,
bioimpedence, plethysomography, inferior vena cava diameters, plasma or brain natriuretic peptide
levels & and true dry weight determined.
4. Dry weight is dynamic and frequent clinical assessment must be made to reassess dry weight.
Explanation & Discussion
Hypertension is common in dialysis patients. Based upon multiple studies, over 50 to 60 percent of
hemodialysis patients (up to 85 percent in some reports) and nearly 30 percent peritoneal dialysis patients
are hypertensive. These values are lower than the 80 percent incidence of hypertension at the initiation of
dialysis, due largely to better volume control in most patients.
Clinicians should strive for an even better blood pressure control rate. Since poorly controlled hypertensive
hemodialysis patients are more likely to have large interdialytic and excessive weight gains, persistent
hypertension often reflects volume control that remains imperfect despite the initiation of dialysis.
Poor blood pressure control has also been reported in children undergoing dialysis. In one study,
approximately one-half of children had uncontrolled hypertension after one year of dialysis therapy.
Uncontrolled hypertension is perhaps the most important risk factor for increased cardiovascular disease in
dialysis patient.
Pathogensis
The single most important cause of hypertension in CKD & dialysis patients is:
1. Sodium and volume excess due to diminished sodium excretory capacity

2. Other are:
3. Activation of the renin-angiotensin-aldosterone system due to primary vascular disease or to regional
ischemia induced by scarring.
4. Increased activity of the sympathetic nervous system.
5. Calcification of the arterial tree.
6. An increase in endothelium-derived vasoconstrictors (such as endothelin) or a reduction in
endothelium-derived vasodilators (such as nitric oxide).
7. The administration of erythropoietin may be associated with increase in blood pressure or poor
control of blood pressure.
8. Preexistent essential hypertension

Method of blood pressure measurement

A reliance upon immediate predialysis and/or postdialysis BP measurements alone to detect hypertension in
patients undergoing hemodialysis may be misleading. The predialysis systolic BP may overestimate the
mean interdialytic SBP by 10 mmHg, while the postdialysis systolic BP may underestimate the mean
systolic BP by 7 mmHg. Some studies, however, have suggested that the postdialysis BP may be more
reflective of interdialytic BP.
Continuous monitoring is therefore warranted in patients suspected of poor control (such as those with large
interdialytic weight gain). The results with ambulatory blood pressure monitoring appear to be more
reproducible.
Optimal blood pressure
Current blood pressure target ranges for dialysis patients have been extrapolated from those suggested for
the non-dialysis patient population. For some dialysis patients, we suggest that goal BP levels be a
predialysis value of below 140/90 mmHg and a postdialysis value of below 130/80 mmHg. If clinical
characteristics permit and ambulatory pressures are measured, a "normal" BP, defined as a mean ambulatory
BP less than 135/85 mmHg during the day and less than120/80 mmHg by night, is a reasonable target.
The target goals should generally be based upon individual patient characteristics. In some younger patients,
the target BP may even be set as low as 120/80 mmHg.
Treatment
Control of volume status — Control of volume status can either normalize the BP or make the
hypertension easier to control in the great majority of dialysis patients. Heavy reliance is placed on the
dialysis procedure to gradually remove fluid over a period of days to weeks until a stable "dry weight" is
achieved.
Accurate setting of the "dry weight" — The ‘dry weight’ is the weight below which further ultrafiltration
will always produce hypotension and unacceptable symptoms such as cramps, nausea & vomiting. The ‘dry
weight’ is highly variable in many patients, and can fluctuate with intercurrent illnesses (such as diarrhea or
infection) as well as nutritional status.
Numerous attempts have been made to utilize alternative methods to more accurately assess dry weight.
These include bioimpedance plethysmography, and measurement of the inferior cava diameter, plasma
natriuretic peptide (particularly atrial and brain) concentrations, blood volume, and other parameters.
However, these methods are frequently impractical, are not necessarily accurate, and a large prospective
study has not yet been performed that compares these methods to clinical assessment alone. The clinician
must therefore define the dry weight and goal blood pressure for each dialysis patient based upon his or her
best clinical judgment.

Prolonged and/or more frequent hemodialysis — Patients in a large dialysis center in Tassin, France and
some home hemodialysis patients undergo long, slow hemodialysis in which the standard regimen is eight
hours, three times per week. This regimen is associated with the maintenance of normotension without
medications in almost all patients. Although these results have been largely attributed to optimal volume
control, other factors may also contribute, such asmore complete control of uremia which, as noted above,
may decrease afferent renal nerve activity and efferent sympathetic activation.
Nocturnal hemodialysis, — a procedure in which dialysis is performed six or seven nights a week during
sleep for a variable amount of time based upon the length of sleep desired (usually 6 to 12 hours in total), is
also associated with excellent blood pressure control. Almost all patients become normotensive without
medications. To achieve this, the "target weight" is progressively decreased until all antihypertensive agents
are discontinued.
The 2007 European Best Practice Guidelines recommend that the treatment time and/or frequency of
dialysis should be increased in patients with hypertension despite optimal volume removal.
Antihypertensive medications
Therapy with antihypertensive drugs is primarily indicated in the 25 to 30 percent of dialysis patients in
whom hypertension persists despite seemingly adequate volume control. Some evidence suggests that the
administration of such agents may provide significant clinical benefits, including improved mortality.
Calcium channel blockers — Calcium channel blockers are both effective and well tolerated in dialysis
patients, even in those who are volume expanded. The only randomized prospective study found that
amlodipine, compared with placebo, improved overall mortality among hypertensive dialysis patients.
Calcium channel blockers are particularly useful in patients with left ventricular hypertrophy and diastolic
dysfunction. Calcium channel blockers do not require supplementary postdialysis dosing.
ACE inhibitors — ACE inhibitors are well tolerated and are particularly effective in patients with heart
failure due to systolic dysfunction and in many patients after an acute myocardial infarction. The 2006
K/DOQI guidelines also suggest that these agents and/or angiotensin II receptor blockers are preferred in
dialysis patients with significant residual renal function. These agents may help preserve native kidney
function.
ACE inhibitors and angiotensin II receptor blockers [ARBs], are associated with a decrease in left
ventricular mass among hemodialysis patients. There are conflicting data concerning the effect of ACE
inhibitors on mortality among hypertensive patients undergoing maintenance dialysis.
ARBs — A number of angiotensin II receptor blockers (ARBs) are currently available. Among
hemodialysis patients, ARBs (and ACE inhibitors) are associated with a decrease in left ventricular mass.
Beta blockers — Beta blockers are particularly indicated in patients who have had a recent myocardial
infarction. As in nonuremic subjects, patients with end-stage renal disease who have heart failure due to
systolic dysfunction may also benefit from therapy with a beta blocker. Such therapy should be initiated at
very low doses to minimize the risk of hemodynamic deterioration.
Potential side effects include central nervous system depression (an effect that may be more prominent with
lipid-soluble drugs that cross the blood-brain barrier), hyperkalemia (particularly with non-selective beta
blockers), bradycardia, and possible exacerbation of heart failure. In addition, beta blockers should be used
cautiously in patients also taking a calcium channel blocker, since there are often additive negative
chronotropic and inotropic actions.
Central sympathetic agonists — The central sympathetic agonists, such as methyldopa and clonidine, are
used less frequently because of their adverse effects involving the central nervous system.
Reduced dialysate sodium concentration — A variable dialysate sodium concentration may result in
lower antihypertensive medication requirements and decrease in postdialysis blood pressure. A fixed lower
dialysate sodium concentration in combination with dietary salt restriction may also help control
hypertension.
Refractory hypertension
Some dialysis patients are resistant to both volume control and antihypertensive medications. Factors to be
considered in this setting are concurrent use of a medication that can raise the BP (such as nonsteroidal
antiinflammatory drugs), renovascular hypertension, noncompliance to medical regimen, and expanding
cyst size in polycystic kidney disease. If a treatable cause cannot be found, minoxidil may be effective in
reducing the BP.
Patients undergoing hemodialysis who are noncompliant and in whom volume status and hypertension
cannot be controlled may also benefit by switching to peritoneal dialysis. Nearly all peritoneal dialysis
patients can become normotensive with strict adherence to volume control.
The efficacy of peritoneal dialysis in controlling blood pressure in refractory patients is related to its
smoother volume removal and its more consistent maintenance of dry weight.
Hypertension during hemodialysis
Although hypotension during hemodialysis is a frequent complication, some patients develop paradoxical
hypertension in the later stages of dialysis, a time at which most of the excess fluid has already been
removed. This problem is intermittent in a given patient with a widely variable frequency. The pathogenesis
is unclear, although some evidence suggests that altered nitric oxide/endothelin-1 balance may contribute.
Various medical modalities (such as the administration of an angiotensin converting enzyme inhibitor or an
alpha-blocker at the time of hypertension, or pretreatment with antihypertensive medications to lower the
blood pressure before dialysis) have not been predictably effective. Sometimes, the administration of
isotonic saline to presumably treat hypovolemia-induced excessive reflex sympathetic activation may be
helpful. Limited observational evidence suggests that this increase in blood pressure is associated with
adverse outcomes.

57. DIABETES MONITORING & THERAPY

Rationale: Diabetes mellitus is the single largest contributor to chronic kidney disease (31.3% in the 2010
annual report of the CKD Registry of India). Patients on dialysis often require low or no antidiabetic
medication. However other systemic complications of Diabetes may continue even after a patient has
reached ESRD. Glucose control and monitoring may retard or prevent other complications. Several oral
drugs may have to be discontinued in CKD or have major modifications in the dosages used. The targets of
HbA1c, and blood glucose in CKD(5) may have to be adjusted taking into account the risks of
hypoglycemia, the contributions of CKD to AGEs and the possible benefits of strict blood glucose control.
Guidelines presented here elaborate the available drugs and their use in CKD along with the methods to be
used for monitoring.
Description
It is well known that blood glucose levels need to be well controlled in ESRD patients. Several
observational studies have shown that high levels of HbA1C are associated with higher death rates
The recommendations for control of blood sugar in diabetic patients on dialysis are as follows
1. Glycemic control & monitoring in ESRD are complex
2. Patients with ESRD are susceptible to hypoglycaemia and therefore drug therapy requires special caution
3. ESRD patients need ongoing diabetes education with an emphasis on how to recognize and treat
hypoglycaemia
4. All patients should have a baseline measurement of their blood sugar levels (fasting & postprandial) and
HbA1C at the time of initiation of dialysis therapy
5. Therapy for control of blood sugar should be individualized. The targets of therapy are HbA1C between
6-7%, fasting blood sugar < 140 mg% and post prandial blood sugar < 200 mg%
6. Patients can be maintained on Insulin (preferably) or oral hypoglycaemic agents. However the risk of
hypoglycaemia is more with OHAs.
7. Long acting insulin (glargine or NPH) for basal requirements along with rapid acting insulin before meals
two to three times daily
8. Newer basal insulin (glargine) and rapid acting insulin analogues (lispro or aspart) insulin are more
favourable than NPH and regular insulin but are more expensive
9. Some patients may prefer a premixed insulin combination for convenience of dosing. In that case NPH +
lispro insulin may be better than NPH + regular insulin
10. For Type 1 diabetes, insulin therapy should be started at 0.5 IU/kg which is half the dose in patients
without renal failure
11. For ESRD patients with ype 2 diabetes, insulin therapy should be started at a total dose of 0.25 IU/kg
12. Further adjustments to the regimen should be individualized based on the self monitored blood glucose
testing
13. Of the oral antidiabetic drugs available, glipizide, gliclazide, sitagliptin and saxagliptin may be used in
ESRD patients. Glipizide starting 2.5 mg daily should be reserved for ESRD patients with HbA1C value
less than 8.5 %. Maximum dose used is 10 mg. Avoid sustained release forms of the drug. The usual dose of
Sitagliptin is 100 mg orally once daily, with reduction to 50 mg for patients with a GFR of 30 to 50 mL/min,
and 25 mg for patients with a GFR less than 30 mL/min. Sitagliptin may be used at doses of 25 mg daily in
ESRD, irrespective of dialysis timing. Other drugs of this class are being developed. Saxagliptin can be used
at a dosage of 2.5 mg daily after dialysis. Valdagliptin is not to be used.
14. Thiazolidinediones (Pioglitazone & Rosigliyazone) do not need any dose adjustments. The main adverse
effect is oedema and fluid overload and thus should be avoided in ESRD since they may precipitate heart
failure.
15. It is recommended that diabetic ESRD patients should have a fixed schedule for dialysis since the blood
sugars are affected by dialysis.
16. It is advisable to consult an endocrinologist with expertise in managing diabetes in ESRD

Insulin preparations:
INSULIN ONSET OF PEAK EFFECTIVE DOSING
PREPARATIO ACTION ACTION DURATION CHANGE IN
N RENAL
FAILURE
Rapid-acting Reduce dose by 25% when glomerular
filtration rate (GFR) is 10–50 mL/min, and by
50% when GFR < 10 mL/min
Regular 30–60 min 2–3 hr 8–10 hr
Lispro (Humalog) 5–15 min 30–90 min 4–6 hr
Aspart (NovoLog) 5–15 min 30–90 min 4–6 hr
Long-acting Reduce dose by 25% when GFR is 10–50
mL/min, and by 50% when GFR is less than
10 mL/min
Neutral protamine 2–4 hr 4–10 hr 12–18 hr
Hagedorn (NPH)
Glargine (Lantus) 2–4 hr None 20–24 hr
Detemir (Levemir) 3–4 hr 3–14 hr 6–23 (19.9) hr
Premixed Reduce dose by 25% when GFR is 10–50
mL/min, and by 50% when GFR is less than
10 mL/min
70/30 human mix 30–60 min 3–12 hr 12–18 hr
70/30 aspart mix 5–15 min 30–90 min 12–18 hr
75/25 lispro mix 5–15 min 30–90 min 12–18 hr

Discussion & Rationale

Blood glucose levels can fluctuate widely due to various effects of uremia and dialysis
The HbA1C levels can be falsely high in ESRD but is still a reasonable measure of glycemic control
Most anti diabetic drugs are at least in part excereted by the kidneys, so patients with ESRD are at greater
risk of developing hypoglycaemia
Insulin is the main drug used for control of diabetes since most oral anti diabetic drugs are contraindicated
or not recommended.
A variety of insulin preparations are available, including rapid-acting, intermediate-acting, and long-acting
forms and premixed combinations, each with its specific onset, peak, and duration of action.
Studies have shown that the pharmacokinetic profile of insulin lispro (Humalog), which has a short onset of
action and a short duration of action, may not only facilitate the correction of hyperglycemia but may also
decrease the risk of late hypoglycemic episodes, which is of increased relevance in hemodialysis patients.
On the basis of the available evidence it is recommended to use a long-acting insulin such as insulin
glargine (Lantus) or NPH insulin for basal requirements, along with a rapid-acting insulin analogue such as
lispro or insulin aspart (NovoLog) before meals two or three times daily.
When the GFR drops to between 10 and 50 mL/min, the total insulin dose should be reduced by
25%; once the filtration rate is below 10 mL/min, as in ESRD, the insulin dose should be decreased
by 50% from the previous amount

58. RENAL REPLACEMENT IN INTENSIVE CARE SETTING

Rationale: The patient with acute kidney Injury (AKI) in the intensive care unit (ICU) may have
hemodynamic instability a circulation supported by inotropic agents, large fluid requirements for nutrition
and drugs, coagulopathy and is often anuric. Many modalities of renal replacement therapy are available for
such patients yet the individual patient may require a treatment “tailor made” for his condition at different
stages of his illness. The different therapies vary in their labor intensiveness, costs, availability and centre
expertise often producing a dilemma when choosing the best modality. In addition the critically ill patient
may have frequent treatment interruptions for other life saving procedures, a temporary vascular access,
drug dosing requiring adjustment, and intensive monitoring. Guidelines presented here attempt to elaborate
the indications, timing of initiation, modality choice and intensity of treatment required for managing the
ICU patient with AKI often in the setting of multi organ failure.
Description:
Acute kidney injury is common in intensive care unit, occurring in about 50% of patients. Dialysis support
is needed in up to a quarter of AKI patients in ICU. Dialysis dependent AKI in ICU carries high mortality in
excess of 50%. AKI patients in ICU differ from end-stage renal disease (ESRD) patients on maintenance
hemodialysis in that 1) the rate as well as the amount of nitrogenous waste products generated is much
higher due to increased catabolic rate and 2) cardiovascular instability is more likely in them. The choice of
renal replacement therapy (RRT) in them should take in to account these factors.
Recommendations for initiation of RRT in AKI in ICU.

RRT in the intensive care setting may need to be initiated irrespective of the serum creatinine if any of the
following conditions exist. Formulae for estimating GFR should not be used in the setting of AKI.
1. Azotemia (BUN > 100 mg/dl or blood urea >200 mg/dl).
2. Clinically significant organ edema not responding to high dose diuretics.
3. Weight gain of more than 10% above baseline in AKI, which does not respond well to frusemide.
4. Severe acidemia due to metabolic acidosis. ( pH < 7.1)
5. Hyperkalemia (plasma K+ > 6.5 meq/L or rapidly rising).
6. Uremic organ involvement. (pericarditis, encephalopathy, neuropathy, myopathy)
7. Progressive severe dysnatremia (Na+ > 160 or < 115 meq/L).
8. Non-obstructive oliguria (< 200 ml/12 hrs) or anuria ( < 50 ml/12 hrs).
9. Malignant Hyperthermia.
10. Overdose with a dialysable drug.
11. Coagulopathy requiring large amounts of blood products in patients at risk of pulmonary edema or
ARDS

Type of initial modality of RRT in ICU:

The main four modalities of RRT available for patients in ICU are intermittent hemodialysis (IHD),
continuous renal replacement therapy (CRRT), hybrid therapy such as sustained low efficiency dialysis
(SLED) and peritoneal dialysis (PD).
 Recommendations for initial choice of type of RRT in ICU.

these are contraindicated.

1. Adult patients who are septic and hypercatabolic may not achieve adequate small solute clearance
with PD and may carry an increased risk of mortality. Hence PD should not be the initial modality of
RRT in them. However if all other modalities of RRT are not available or contraindicated, PD may
be used for RRT in them.
2. Pediatric patients in an intensive care setting may be managed with either PD or a form of
Hemodialysis or CRRT
3. Neonatal and pediatric patients weighing < 10 kg should probably be managed with PD except
where expertise is available to perform CRRT.
4. Hemodynamically stable patients should be managed with IHD, which is effective and provides a
standardized urea clearance of around 20 ml/min with standard 4 hour treatments. The frequency of
dialysis will be determined by the ultrafiltration requirement and the catabolic state of the patient.
5. Patients with hypotension or who require vasopressor drugs to maintain their circulation should be
treated with either SLED or CRRT.
6. The duration of SLED should be determined by the requirement of ultrafiltration which should
probably not exceed 300 ml/hr.

A continuous form of SLED known as C- SLEDD may be used to achieve ultrafiltration targets while
maintaining hemodynamic stability.
1. The form of CRRT either veno-venous hemofiltration, (CVVH), veno-venous hemodialysis
(CVVHD), or a combination (CVVHDF), should be chosen according to clinician expertise
available and the capabilities of the machines available.
2. For patients who do not require biochemical clearance but only ultrafiltration, either isolated UF on a
hemodialysis machine or slow continuous ultrafiltration (SCUF) should be used.
3. All therapies should be veno-venous and pump driven using dedicated machines with safety devices
including blood leaks, transmembrane pressure and air detection alarms. Arteriovenous techniques
should not be used as efficacy & safety monitoring may be inadequate.

Recommendations for vascular access for dialysis in ICU:

and should not be used for

administering drugs or TPN or measurement of central venous pressure.
If high volume hemofiltration or hemodiafiltration is being delivered a 14F cannula or 2 cannulae in
different veins should be used.
1. The vascular access should be sited distant from vascular cannulae delivering TPN, antibiotics or
catecholamine infusions.
2. Antibiotic lock such as gentamicin may be used in patients who are at increased risk of catheter
related infection.

Recommendations for selection and use of machines for ICU RRT

1. Standard Hemodialysis machines used for maintenance hemodialysis can be used for dialysis in the
intensive care settings. They should be equipped with accurate volumetric controlled UF, and slow
flow options for SLEDD, both parameters should be easily and frequently calibrated. Most machines
deliver minimal dialysate flow rate of 300 ml/min, ArrT plus delivers flows of 200 ml/min.
2. Machines capable of generating fluid for online fluid may be used for Hemodiafiltration and
SLEDD-f. These should be equipped with at least 2 and preferably a 3rd ultrafilter in the
replacement fluid delivery circuit. All machines should be of a “fail safe” design.
3. All machines used for CRRT should be dedicated, with their own disposables. The machines should
have a minimum of 3 and preferably 4 or more pumps to make all forms of treatment possible. The
machines should have an error of < 2.5% in measurement of ultrafiltration volumes. Gravimetric
balancing scales are preferable to flow measurements. A few of the available machines are shown in
Table 1.

Recommendations for Dialysate & Replacement Fluids

1. For IHD and SLED, bicarbonate based dialysate should be used. Acetate or Lactate based dialysate
should be avoided for IHD or SLED.
2. Bicarbonate or Lactate based dialysate may be used in CRRT.
3. Isotonic bicarbonate based fluid may be preferred as replacement fluid in CRRT. If commercially
made bicarbonate replacement fluid is not available or if is too expensive for routine use, a custom
made replacement fluid may be used instead. This could be 0.9% saline of isotonic fluid with sodium
concentration equal to or very close plasma sodium, as shown in Table 2. Fluid recommended for
intravenous use alone should used as replacement fluid.
4. Lactate based dialysate for CRRT may be avoided in patients with liver failure and cachectic
patients with poor muscle mass.
5. Potassium concentrate in the dialysate fluid and replacement fluid may vary from 0-4 mmol/L
depending on the need. Cardiac patients and those with arrhythmias should have dialysate and
replacement fluids with K+ of 4 meq/L.
6. Where online hemodiafiltration or SLEDD-f is carried out the water used for dialysis should be of
ultrapure standard. Dry powder concentrates should be used for these therapies. Where possible,
endotoxin levels should be carried out prior to starting therapy.

Recommendations for Dialyzers & Hemofilters for RRT in ICU.

1. Standard intermittent hemodialysis and SLEDD may be carried out with low flux dialyzers.

2. SLEDD-f and CHFD (continuous high flux dialysis) may require high flux, ultra flux or special high
porosity dialyzers.
3. All dialyzers should be of biocompatible materials, either fully substituted cellulose or synthetic
material. Bio-incompatible Cupraphane dialyzers should be avoided in ICU since they carry
increased risk of mortality compared to bio-compatible membranes.
4. CRRT requires special hemofilter sets, usually as part of a complete set, each of which is compatible
with specific machines only.
5. Blood flow and ultrafiltration Rates
6. The total ultrafiltration rate should be predetermined by the patients requirement and the blood flow
set thereafter so that the filtration fraction is < 15% of the blood flow. ( specially applicable to
hemofiltration and hemodiafiltration)
7. For intermittent hemodialysis blood flows should be around 200– 300 ml/min to achieve adequate
clearances.
8. For SLED blood flow rate is set at approximately 150 - 200 ml/min in anticoagulant free sessions.

Anticoagulation for ICU RRT

1. Unfractionated heparin should be the anticoagulant of choice during intermittent hemodialysis and
CRRT when not contraindicated.
2. Heparin should be administered as a continuous infusion in patients on CRRT with aPTT monitoring
every 4-6 hours and the dose adjusted. After an initial loading dose of 1500 to 2000 units, an
infusion of 250 to 500 units per hour may be initiated and adjusted according to the aPTT reports.
The aPTT should be maintained at between 45-60 seconds or around 1.5 times the control value.
3. In patients receiving LMWH as DVT prophylaxis the same can be continued with the doses given
just before a session of IHD or SLED. Monitoring is not possible and the risk of bleeding is
increased with the use of these agents in AKI.
4. In patients with DIC or who are bleeding, IHD and SLEDD can be carried out without any
anticoagulation with little compromise of duration and efficacy.
5. A dialysate containing citrate may be useful in enhancing dialyzer life.
 6. CRRT almost always requires anticoagulation and in patients with DIC, regional anticoagulation
with citrate and calcium or heparin and protamine may be used. If the risk of bleeding is high, CRRT
may be performed without anti-coagulation. In such a situation periodic saline flushes (150 ml every
4 hours) may be given to increase the life span of the filter.
7. In regional citrate anticoagulation the blood levels of ionic Calcium require to be monitored 4 hourly
and the infusion rates adjusted.
8. In heparin protamine regional anticoagulation the aPTT of both the patient and the extracorporeal
circuit between the sampling ports should be monitored. For an infusion of 500 units /hour of
heparin a neutralizing infusion of 5 mg /hour of protamine will be required.

Adequacy of RRT in AKI

Thrice weekly intermittent hemodialysis giving a Kt/V of ≥1.2 per session may be sufficient in most cases.
This is equivalent to a urea clearance of 21 ml/min, when normalized to a week
1. Increased frequency of dialysis may be required to achieve appropriate fluid balance or acidosis,
hyperkalemia correction or for urea clearance if extremely hypercatabolic.
2. SLED may be performed thrice a week with 8 – 12 hourly sessions to achieve a clearance of around
33 ml/min. More frequent or longer sessions will be determined by the need for ultrafiltration and
acidosis correction rather than enhanced urea clearance.
3. The prescribed times may be slightly higher to account for failure to achieve the time prescribed, the
blood flow with temporary access and the risk of circuit clotting.
4. In CRRT, a total effluent (dialysate plus ultrafiltration) rate of 20-25 ml/kg/min is generally
sufficient in most cases of AKI. However in an extremely catabolic or septic patient, a higher dose
may be used.
5. The proportion of diffusive and convective clearance in CRRT may vary. A proportion of 50:50 or
65:35 for diffusion (dialysate) and convection (ultrafiltration) may be generally preferred for regular
CRRT.
6. Replacement fluid may be administered either pre-filter or post-filter. However if rate of
replacement fluid administration is more than one third of blood flow rate, it is better to administer it
post-filtration to prevent excessive dilution of pre-processed blood. However this strategy may
increase the risk of filter clotting.

Other Modalities of Extracorporeal Therapy

No generalized recommendations can be made for the following therapies which are currently under
research, and which may have to be individualized for certain patients.
1. High Volume Hemofiltration
 2. Coupled plasma filtration hemadsorption
3. Cascade hemofiltration
4. Polymixin B hemoperfusion for Endotoxin removal.

Table 1:- Machines for ICU dialysis & SLEDD

Company Machine for each modality
Intermittent hemodialysis SLEDD CRRT
Fresenius 4008 Series H & S Arrt plus online Multifiltrate
B. Braun Dialog plus Dialog plus Diapact
Baxter/Edwards Tina Tina BM 25
Nikisso DBB series Nikisso DBB series Acquarius
Minntech - - HF 400
Gambro AK series AK 200 ultra Prisma & Prisma
plus
Medica - - Equasmart
Nx stage - - Nx stage
Nipro Surdial & Diamax Surdial & Diamax -

Table 2:-Replacement Fluids for CRRT

Component Lactated Dianeal Hemasol In house
Ringers (Peritoneal (Gambro) prepared*
Solution dialysis
fluid)

Glucose - 1360mg% - May be added

if risk of
hypoglycemia
is present.
Na+ 130 meq/L 132 140 134.5
K+ 4 meq/L - - 4
Cl- 109 meq/L 96 109.5 87
Ca++ 2.7 meq/L 3.5 3.5 2.6
Mg++ - 0.5 1 -
Lactate 28 meq/L 40 3 14
Bicarbonate - 32 37.5
*The above solution is prepared by adding 75 ml of NaHCO3 (3 ampoules) of 7.5% to 825 ml of 0.45%
saline along with 2 ml of 15% KCL and 100 ml of 50% dextrose.
10%
Calcium gluconate is added.

Recommendations for pediatric CRRT.

CRRT is being used increasingly in pediatric ICU world over, and is the preferred modality of RRT
in the developed world. No clear evidence based recommendations are available for pediatric CRRT,
but some recommendations may be made based on the experience of units doing pediatric CRRT.
Recommendations for use of CRRT in children are summarized in Table 3.
Weight of the child Filter (Surface area) Blood flow (ml/min) Total effluent volume
(ml/hour)
Up to 5 kg M10 (0.04 m2) 25-30 100-150
5-20 kg FX20 (0.2 m2) 30-75 150-500
20-40 kg M60 (0.62 m2) 75-100 500-1000
>40 kg M100 (0.95 m2) ≥100 ≥1000

Femoral catheter is preferred to jugular catheter in small children.

1. F5 catheter may be used for small children of ≤20 kg weight.
2. There are no clear recommendations for the dose of dialysis in children. A Kt/V of 1 per day may be
a reasonable target dose in them. If For example, if the weight of the child is 20 kg, total daily
effluent may be equal to total body water, i.e., 20X0.6= 12 liters per day or 0.5 liters per hour.

Recommendations for goals of RRT.

1. Steady level in CRRT and pre-dialysis level in IHD or SLED of BUN of ≤60mg/dl (Blood urea ≤120
mg/dl) should be achieved within 48 hours after initiating dialysis.
2. Volume status as close to euvolemia as possible.
3. Correction of acidosis to maintain pH ≥7.2.
4. Maintain serum electrolyte levels within reasonably normal limits (sodium: 130-148 mmol/L,
potassium: 3.5-5.5).
 Recommendations for stopping RRT.
Guidelines for termination of RRT in AKI are unclear and are empiric. An attempt may be made to
withdraw RRT if urine output is consistently more than 30 ml/min for at least 6-12 hours and pre-dialysis
BUN is < 100 mg/dl (Blood urea 200 mg/dl) and serum creatinine is <5 mg/dl and patient does not exhibit
any uremic symptoms.
Antibiotic Dose Adjustment in CRRT

CRRT provides a clearance of around 35 ml/min for most antibiotics, hence doses should be increased to
provide adequate peak and trough levels.
For many drugs ideal dosing schedules are unavailable and further studies of plasma concentrations are
required.
The ideal dosing schedule should be based on plasma levels, especially where there is a narrow therapeutic
window, as with aminoglycosides and Vancomycin
Failure to increase the doses may provide subtherapeutic doses of drugs like Vancomycin.
However for most of the commonly used antibiotics used in a critical care setup there exists a wide
therapeutic to toxic ratio and a general guideline for dosing is provided in the table. All doses are for
intravenous drugs
Drug dosing in CRRT

Drug Practical dose in CRRT

Acyclovir 1500 mg in 3 doses
Amikacin 500 mg od (7.5 mg/kg)
Netilmicin 150 mg od (3mg/kg)
Tobramycin 120 mg od (3mg/kg)
Vancomycin 500 – 1000 mg od (15 mg/kg)
Teicoplanin 300 mg od (5 – 6 mg/kg)
Cefotaxime 2000 mg bd (100 mg/kg)
Ceftazidime 1000 mg bd (50 mg/kg)
Ceftriaxone 2000 mg od 50 mg/kg)
Ciprofloxacin 200 mg od
Imipenem 500 mg tds
Metronidazole 500 mg tds
Piperacillin tazobactum 4500 mg tds (300 mg/kg
Piperacillin)
Cefuroxime 1500 mg bd (75 mg/kg)
Amoxycillin clavulunate 1250 mg bd (50 mg/kg)
Fluconazole 400 mg od
Gentamicin 120 mg od 3 mg/kg)
linezolid 600 mg bd (10mg/kg/dose)
Meropenem 1000 mg tds (40 mg/kg/dose)
Penicillin 2MU tds (50000
Units/kg/dose)
Endocrinology
59. DIABETES MELLITUS
Introduction
Diabetes Mellitus (DM) is a global epidemic. Type -2 diabetes which forms almost 95 % of the total
diabetes in India is largely a preventable disorder. India harbours more than 50 million diabetics. DM is
associated with development of specific long-term organ damage (chronic complications) including
retinopathy with potential blindness, nephropathy with a risk of progression to renal failure requiring
lifelong dialysis or renal transplantation, neuropathy with risk for foot ulcers, amputation, and Charcot joints
and autonomic dysfunction such as sexual, bowel and bladder impairment. Patients with diabetes are at a
particularly high risk for vascular complications like cardiovascular, cerebrovascular, and peripheral artery
disease. A recent rise in the number of adolescent and young Type -2 diabetics in India is an alarming
trend. This is largely due to lifestyle factors.Recent Indian data suggest prevelence rates of 15 to 20 % in
urban areas and about half of it in ruralareas.
DM poses a great threat to the health of our nation, it costs dearly the exchequer as the treatment of acute
and chronic complications of diabetes are expensive. Beside this is the cost of day to day medication, tests,
monitoring and loss of productive work due to illness.
Hence it is important to recognise this disorder as early as possible. Attempt should be made to detect
hyperglycemia in prediabetes stage to prevent progression to diabetes. And finally the aim is to treat this
disorder effectively to prevent the devastation of the chronic complications.
Definition
DM is a chronic metabolic disorder ofcarbohydrate, fat, and protein metabolism characterized by
hyperglycaemia,resulting from defects of insulin secretion, insulin action, or a combination of both 1 . Type
1 diabetes is due to an absolute lack of endogenous pancreatic insulin production, whereas in Type 2
diabetes, insulin resistance is the basic defect which is contributed by a combination of genetic
predisposition, physical inactivity, and obesity.
Classification
Old terms like IDDM (insulin dependant DM), NIDDM (non insulin dependant DM)adult onset diabetes or
juvenile diabetes have been abondoned.
ADA classification of 1997 which was later accepted by WHO is the most widely accepted classification of
DM .
Classification of Diabetes Mellitus
Classification of Diabetes Mellitus
1. Type 1 -(beta -cell destruction, usually leading to absolute insulin deficiency)
A. Autoimmune
B. Idiopathic
Type 2 -(may range from predominantly insulin resistance with relative insulin deficiency to a
predominantly secretory defect with or without insulin resistance)
3. Other specific types (see Table ) Genetic defects of b-cell function -MODY 1 to 9, mitochondrial
DNA. Genetic defects in insulin action Diseases of the exocrine pancreas (pancreatitis trauma,
pancreatectomy,neoplasm cystic-fibrosis etc) Endocrinopathies (acromegaly, Cushing's syndrome,
gucagonoma, pheochromocytoma, hyperthyroidism etc)
Drug-or chemical-induced
Infections
Uncommon forms of immune-mediated diabetes
Other genetic syndromes sometimes associated with diabetes, e.g.: Down’s syndrome, Friedreich’s ataxia,
Klinefelter’s syndrome, Wolfram’s syndrome
4. Gestational diabetes
Characteristics ofDiabetes In India
1. Onset is about one decade earlier than the west
2. Occurs at a lower BMI
3. Central obesity is more common
4. Type 1-less than 5% of the total diabetes
5. Cardiovascular complications occur early
6. PVD is less common than the west
7. Foot problems more common
8. No structured treatment protocol
9. Lack of trained manpower like diabetes educators,endocrinologists
10. Cost of the treatment is a big hinderance
11. Social and religious factors play an important role

Diagnosis
Any one of the following:
1. Symptoms of diabetes + casual plasma glucose concentration> 200mg/dl (Casual -any time of the
day without regard to time since last meal)
2. Fasting plasma glucose> 126mg/dl (Fasting -no caloric intake for atleast 8 hours)
3. 2 Hour plasma glucose during OGTT > 200mg/dl (OGTT according to WHO criteria)
4. Note-HbA1c > 6.5% indicates diabetes, however it cannot be considered as a diagnostic tool in
isolation.
Impaired glucose metabolism
Impaired Fasting Glucose (IFG):
FPG > 100 and 125 mg per dL
Impaired Glucose Tolerance (IGT):
1. 2hr PGPG > 140 and 199 mg per dL
2. FPG > 100mg/dl and> 125mg/dl be classified as having IFG.
3. Prevalenceof diabetes is increasing rapidly in developing countries like India
4. Occurs due to relative insulin deficiency in an individual with insulin resistance
5. Usually asymptomatic and detected during evaluation for unrelated indications, but may present with
hyperglycemic symptoms-
6. Frequent urination, excessive thirst, excessive hunger
7. Weight loss, delayed healingof wounds, pain in calves, burning feet
8. Tiredness, Itching -especially in genital area
9. Tingling and numbness, blurring of vision, lethargy, somnolence,
10. Sometimes the symptoms are due to complications of diabetes when patient presents to a clinician
for the first time with a complication like erectile dysfunction.
Type 1 DM:
Absolute insulin deficiency due to autoimmune destruction of pancreatic beta cells.
Onset is mostly in childhood or in young adults before 35 years, about may rarely occur in elderly.
Symptoms
1. Abrupt onset of severe hyperglycemic symptoms. Sometimes the child may present with just
weakness, lethargy, bedwetting.
2. May present as diabetic ketoacidosis .
MODY-Maturity onset diabetes of the young:
Monogenic form of diabetes associated with mutation in a single gene

Diagnostic Criteria

1. Autosomal dominant transmission of diabetes with three generations involved

2. Absence of ketosis at any time
3. Controllable without insulin at least in the early stages of the disease

Clinical criteria are no longer acceptable and genetic analysis is needed to confirm the diagnosis.
Clinical Features
-obese.Respond better to sulphonylureas in initialfew years of diabetes.
1. Do not need insulin initially-later may become insulin-requiring (MODY 1, 3 and 5)
2. Isolated Mild fasting hyperglycemia-MODY 2-no treatment required
3. Diabetes with renal cysts/ renal agenesis RCAD (renal cysts and diabetes syndrome)-MODY
Fibrocalculous pancreatic diabetes-(FCPD):
Severe hyperglycemia in a lean patient from a tropical country like India with recurrent pain abdomen,
evidence of chronic pancreatitis after excluding other causes of chronic pancreatitis like alcoholism ,should
be considered for FCPD.Absence of ketosis and presence of pancreatic calculi is the characteristic feature.
Latent Autoimmune Diabetes Of Adults (LADA):Type 1 Diabetes Which Presents Late
1. GAD(Glutamic acid decarboxylase) autoantibody positive
2. Age at onset >35 years
3. Lean patient
4. Insulin treatment required within one year of onset
5. Many patients with Type 2 diabeteswho are lean, have no family history of diabetes and who require
insulin early in the course of the disease actually have LADA
Screening for Diabetes:
Ethnically every Indian falls into a high risk category however it may not be feasible to screen everyone.
The following population group need screening.
1. Family history of diabetes
2. Cardiovascular disease, Hypertension
3. Overweight or obesity, males with a waist >90cm females with a
waist >80cm
4. Sedentary lifestyle
5. Patients who are on steroids
6. Previously H/O IFG ,IGT
7. Dyslipidemia
8. History of gestational diabetes
9. People who were born with a birth weight >9 poundsor LBW
10. Polycystic ovary syndrome

If normal, repeat screening in 3 yrs for low risk subjects and every year for high risk subjects. If IGT or IFG
repeat screening in 1 year.
All pregnant ladies should be screened at -24-28 weeks if the risk is low,or at first ante natal visit if she
belongs to a high risk group.
Risk factors for GDM:
1. Risk factors for GDM-
2. Overweight or obesity
3. Family history of diabetes mellitus
4. History of IGT,IFG
 5. Poor obstetric history
6. History of delivery ofan infant with a birth weight >9 pounds
7. History of polycystic ovary syndrome
8. Fasting plasma glucose concentration >90 mg/dL or 2-hour postprandial glucose
>140 mg/dL
Physical Examination :
1. Height, weight, BMI
2. Blood pressure measurement, including postural variation if indicated
3. Thyroid examination
4. Skin examination of insulin injection site and for acanthosis nigricans.
5. Xanthelesma

Comprehensive foot examination

1. Inspection-see for redness or cracks or dryness of skin and shape of the foot
2. Palpation of dorsalis pedis and posterior tibial pulses
3. Ankle and knee jerks
4. Proprioception, vibration and monofilament sensation
5. Dilated retinal examination
6. Dental examination

Investigations at the time of diagnosis:

Fasting and postprandial plasma glucose

1. HbA1c
2. Fasting lipid profile
3. AST/ALT
4. Urine complete exam, including assessment of microalbuminuria
5. Serum creatinine, and estimated GFR
6. TSH if there is dyslipidemia and in women >40
7. ECG

Markers of glycemic status

1. Plasma glucose
2. Whole blood glucose (glucose meters)
3. Urine glucose
 4. Glycosylated hemoglobin (HbA1c) .HbA1cis an index of long term Glucose Control, performed on
venous blood

Test results are not affected by

-Time of the day
-Meal intake
-Exercise
-Just administered diabetes drugs
-Emotional stress
-Patient cooperation
In certain situations HbA1c can be falsely high(uremia,alcoholism etc) or low(blood loss iron defeciency
anemia,pregnancy,hemoglobinopathies ,reduced RBC survival).
C-Peptide
in in the proinsulin molecule ,by-product of insulin biosynthesis
For every molecule of insulin in the blood, there is one molecule of C-Peptide.

Very low levels:

-Type 1 diabetes
-Complete surgical removal of pancreas
-peptide measurement is very limited .Its measurement and interpretation of the
results should be done by an Endocrinologist.

Microalbuminuria
microalbuminuria annually in all Type 2 diabetics starting at diagnosis and Type 1
diabetic with DM more than 5 years

Methods
Measurement of the albumin to creatinine ratio in a random spot collection or 24 hour urine collection for
creatinine and albumin with simultaneous measurement of serum creatinine.
Albumin excretion rate (AER)-It is based on the albumin concentration ,the duration of the urine collection
and the urine volume, and has the advantage of giving results which are independent of the ingested fluid
quantity.AER is the gold standard for the diagnosis of microalbuminuria.
Foot examination-this should include examination of the shape of feet, bony prominences, calluses,
deformities of the toes. Skin examination for texture ,color and loss of sweating, loss of hair. Nail
examination for thickening, ingrowings, fungal infections. Inspection of interdigital webspaces for fungal
infections and minor traumas Sensory examination of foot. Palpation of dorsalis pedis and posterior tibial
arteries. Joint movements for checking the power of the muscles (muscle wasting) and joint integrity.
Vibration test (128Hz), nylon monofilament test, ankle brachial index, peripheral doppler may provide very
important information.
Continuous glucose monitoring(CGM) is indicated in pregnancy,brittle diabetes,insulin pump users.For
Type -1 diabetics and elderly it can be used periodically to study hypoglycemia more closely.
Monitoring
Glucose Frequency depends on the the kind of
treatment and the severity of illness.It may be
as low as twice a month to as high as 6-7 times
in a day.#
A1C Once in 3-4 months and six monthly if
glycemic control is good
Lipids Quarterly if uncontrolled, otherwiseOnce in 12
months*
Creatinine Once*
Urine complete exam Once*
Urine microalbumin Once in a year*
ECG Once in a year*
Fundoscopy Once in a year for all Type -2 diabetics from
the time of diagnosis*.In Type -1 once every
year from 4-5 years after diagnosis or at the
age of 10 years.More frequent exams are
needed in advanced retinopathy
Urine complete exam Once*
Urine microalbumin Once in a year*
ECG Once in a year*
Fundoscopy Once in a year for all Type -2 diabetics from
the time of diagnosis*.In Type -1 once every
year from 4-5 years after diagnosis or at the
age of 10 years.More frequent exams are
needed in advanced retinopathy
# monitoring should include fasting,preprandial and 2-hour postprandial and bed time glucose levels
.Occasionally between 2:00 -3:00AM glucose measurement is indicated to detect nocturnal
hypoglycemia.Self monitoring of glucose by Glucose measuring devices at home is desirable for all
diabetics.Patients on insulin need to monitor more frequently as compared to those on OADs.
Nutrition therapy: Diet therapy has to be individualised based on the likes and dislikes, calorie
requirement (overweight or underweight), lifestyle and comorbidities. Carbohydrates should form 50-65 %
of the total calories, proteins should form 15-20% (like non diabetics) and fats -15-25%. Average Indian
diets usually contain the desired fiber content (15-25 gm/1000 cal). The saturated fat consumption should be
minimised to < 10% of the total calories. If the LDL is >100 than it should be further reduced to <7%.Trans
fats should preferably be eliminated completely from the diet. Vegetable oils should be used
interchangeably so that the desired omega 3:6 ratio is achieved .No one kind of oil can be recommended.
Coconut and palm oils should be avoided. There is no role of any additional multivitamins, trace elements
,antioxidants or any kind of neutraceuticals except Vit D. Consumption of fresh fruits ,salads and green
vegetables shouldbe encouraged which would supply all the multivitamins, trace elements, antioxidants.
Absolute restriction of sucrose is not essential however it should be minimised. Restricted protein intake of
0.8 to 1.0 g/kg per day is required in patients who are inthe earlier stages of chronic kidney disease and to
0.8 g/kg per day in patients who are in the later stages of chronic kidney disease .
Artificial sweeteners: Sucralose,Aspartame,Saccharin,Acesulfamec and a few others are non caloric
sweeteners.Their consumption should be minimised .The scientific data favouring their safety is scanty
hence they can be used in smaller quantities with a caution although the accepted daily intake for Aspartame
is 50 mg/kg/day and for Sucralose and saccharin is 5 mg/kg/day.
Vaccination-Pneumococcal vaccine may be recommended for all diabetics.
Life style interventions –The Diabetes Prevention Program found that people at risk of developing type 2
diabetes were able to cut their risk by 58% (it was 74% in subgroup ofasians) with moderate physical
activity (30 minutes a day) and weight loss (5 to 7% of body weight, or about 15 lb). For people over age
60, the risk was cut by almost 71% .Adopting healthy lifestyle with increasing physical activity and weight
reduction is key for achieving success in diabetes management. The effect ofphysical activity and other life
style interventions on glucose and BP is comparable to pharmacological treatment. The goals of the life
style interventions should be to achieve at least 5%reduction in body weight in obese. The individuals with
high risk should be systematically targeted with lifestyle interventions regardless of their glucose status.
Regular daily physical activity of 45 minutes or more is recommended for all diabeticsin general. Besides
leisure time physical activity, other forms of activity like walking ,occupational or daily commuting on foot
or

bicycle, household chores ,activity at work place is also helpful and should be encouraged. Later the
intensity and duration of exercise can be increased according to one's general health and age. To begin with
it could be just brisk walk. The aim is to raise and sustain the heart rate for 15-20 minutes to 60-85% of the
maximal heart rate for that age. Maximal heart rate is 220 minus age. Exercise should be preceded by an
additional 05 minute warmup and followed by a 05 minute cool down. Thorough examination before
starting physical activity is mandatory in view of associated comorbidities like CAD, proliferative
retinopathy, autonomic neuropathy, arthritis, feet problems etc. Cessation of smoking, tobacco and
moderating alcohol intake(only for those who are already taking alcohol, it cannot be recommended in any
form for those who are not taking alcohol) should be reemphasised on every clinic visit.
Stress management: Relieving stress by adopting healthy lifestyle or by any other method including the
traditional Indian methods is helpful.
Oral drugs: Oralanti diabeticdrugs (OADs)have no or very little role inType -1 diabetes. Theycan be
initiated at the time of detection of diabetes or after a trial of lifestyle measures for 6-8 weeks. Choice of an
oral agent depend on many factors like duration of the diabetes, age and weight of the patient, presence of
other comorbidities ,lifestyle of the patient ,degree and type of hyperglycemia(fasting /postprandial)and
susceptibility to hypoglycemia. Metformin(MF) and Sulphonylureas (SU) alone or in combination should
form the base or the first line therapy in most of the OAD requiring diabetics.Sensitisers (like MF ,
Pioglitazone )and Alpha glucosidase inhibitors (AGI) are useful throughout the lifespan of a diabetic.
Secretagogues like SU and Glinides are not very useful in long duration of diabetes and progressively lose
their efficacy as their action is dependant on residual beta cell mass which progressively decline in all Type
-2 diabetics. Glinides are useful as monotherapy in elderly where a potent long acting SU is relatively
contrindicated. DPP-4 inhibitors are not suitable for burnt out or long standing diabetes. As cost is often an
issue for choosing an OAD ,DPP-4 inhibitors can be added if mono or dual therapy fails. At present they
cannot be recommended as first line therapy. Pioglitazone can be used as mono,dual or tripple
therapy.Alpha glucosidase inhibitors are useful adjunct with any of the above mentioned drugs if
postprandial hyperglycemia is the main target, though by themselves they are weaker drugs if used alone.
Two OADs from a same group should not be used together. If HbA1c is mildly elevated (around 7%)
monotherapy may be sufficient. For moderately elevated HbA1c (around 8%)dual drug therapy as seperate
or in fixed combination can be initiated. However MF or SU as monotherapy in higher doses may be
sufficient even for these patients. For HbA1c of more than 9%, combination therapy is initiated or
intensified as dual or tripple therapy or insulin can be added as single bed time dose if fasting
hyperglycemia is the main target .Insulin as multiple doses(premixed or split mixed )can be added to the
OADs. In some situations where other measures fail, insulin can be used along with a combination of OADs
and GLP-1 analogues.
IGT-MF and Acarbose can be used to delay the onset of diabetes.
Side effects of OADs
Sulphonyureas:Hypoglycemia, nausea, constipation, pain abdomen, weight gain, hematological
abnormalities, headache, skin disorders. Not very useful with higher doses of insulin,avoided in advanced
renal failure.
Glinides: Hypoglycemia,nausea,constipation,pain abdomen,diarrhoea.

Metformin:Pain abdomen, nausea, vomiting, diarrhoea, anorexia, weight loss, flatulence, B-12 defeciency.
Contraindicated if serum creatinine is >1.4 in women and >1.5 in males, also contraindicated in CHF,
advanced hepatic and respiratory failure.Avoided in periop period.
Alpha glucosidase inhibitors-Flatulence, constipation, pain abdomen, diarrhoea, vomiting. Avoided in
serious GI disorders.
DPP-4 inhibitors-constipation, pain abdomen, diarrhoea, swelling ,headache, URI, arthralgia, anorexia. Not
very useful in long standing diabetes.
Pioglitazone:fluid retension, anaemia, weight gain, sinusitis, worsening of retinopathy, Fractures in
postmenopausal women. Contraindicated in CHF, fluid overload states and in advanced hepatorenal
dysfunction.Recent data impicates it in bladder cancer. It has been banned in Germany. A great caution is
required in patient selection for its use .
Mechanism of action of Sulphonylureas,Glinides
OADsInsulin secretagogues
Insulin sensitisers Pioglitazone,Metformin
Drugs acting locally on gut Alpha glucosidase inhibitors
Potentiating Incretin DPP-4 Inhibitors
axis,glucagon suppression

When HbA1c is high ,fasting glucose should be the target first and when Its relatively better or
towards normal side the postprandial glucose should be targeted first to achieve better
glycemic control.
Insulin –Insulin is a potent anabolic hormone .The effects other than glucose lowering are
important in many clinical situations where anabolic activity is desired.
Indications
Type -1 DM, pregnancy, severe infections, severe catabolic states, OAD failure,acute stressful
situations like acute coronary syndrome, stroke, acute renal or hepatic failure, periop period.
Secondary diabetes, post transplant diabetes ,congestive heart failure are also indications for
insulin usage. Insulin can be added to existing OADs for short durations (e.g. steroid use in a
diabetic on OADs) or long durations.
Insulin preparations Onset Peak Effective
and their Duration
pharmakokinetics-
Insulin
Rapid-actingAnalogue
Aspart ,Lispro 5-15 min 30-90 min <5 h
Glulisine 5-15 min 30-90 min <4 h
Short-acting
Regular 30-60 min 2-3 h 5-8 h
Intermediate
NPH 2-4 h 4-10 h 10-16 h
Long-acting
Glargine 2-4 h No peak 20-24 h
Detemir 3-8 h No peak 5.7-23.2 h
Premixed
75% insulin lispro 5-15 min Two 10-16 h
protamine
suspension/25%
insulin
50% insulin lispro 5-15 min Two 10-16 h
protamine
suspension/50%
insulin
70% insulin aspart 5-15 min Two 10-16 h
protamine
suspension/30%
insulin
70% NPH/30% 30-60 min Two 10-16 h
regular
75%NPH/25% 30-60 min Two 10-16 h
regular
50%NPH/50% 30-60 min Two 10-16 h
regular

Animal insulin is no longer preferred as more safe and cheap synthetic human insulin is easily
available inabundance.
Basal insulin therapy -if only fasting hyperglycaemia is the concern and patient is already on
OADs then basal may be added to OADs.
Shifting to rapid acting analogues or their premixed preparations are preferred in the following
situations:
1. When good control is not possible with short acting or premixed human insulins,
2. Occurrence of frequent hypoglycemia,
3. When lifestyle of the patient demands immediate intake of food after insulin injection
4. Renal or hepatic failure where more predicted and shorter action of insulin is desired.
 5. Allergic reactions to human insulin.

Insulin should be injected on anterior abdominal wall as the first preferred site,other sites can be
thighs,buttocks and lastly the arms.Injecting repeatedly at one site can cause lipodystrophy and
erratic insulin absorption.
Other injectable therapies-GLP-1 analogues-Currently available GLP-1 analogues Exenatide
and Liraglutide are a good choice in an obese Type-2 diabetic. They can be used as an adjunct
with any OAD except DPP-4inhibitors for reducing both fasting and postprandial hyperglycemia.
Hypoglycemia is uncommon if used alone. Nausea, vomiting, abdominal pain, distension,
dyspepsia, diarhoea and headache are the common side effects. Usage should be avoided in
patients with associated severe GI disorders like pancreatitis. Exenatide is given twice daily
subcutaneously before meals andLiraglutide once daily with disregard to the meals but almost at
the same time daily. Weight loss is an advantage with these agents which make them a useful
tool for obese diabetics. They are contraindicated in Type-1 DM and acute hyperglycemic
complications.
Insulin pump: At present due to its prohibitive cost its usage is very limited. All patients who
qualify for insulin pump therapy should be referred to a centre where expertise for a pump is
available. Pump therapy requires a lot of motivation and time from both -the patient and the
clinician.
Indications
1. All Type -1 diabetics who are poorly controlled with basal-bolus therapy.
2. Pregnancy
3. Frequent hypoglycemia or hypoglycaemic unawareness
4. Persistently elevated fasting glucose (Dawn phenomenon)
5. Multiple chronic complications with labile glucose requiring fine tuning of glycemic
control
6. Management of labile diabetes after renal or hepatic transplant
7. In situations where insulin requirement is very high a trial of pump therapy can be given.

Hypertesion in diabetics:
Lifestyle measures form the cornerstone of hypertension management. Salt intake should be
restricted to less than 6 gmper day. Restriction of salt intake should however be individualised
.Care has to observed in elderly and in people who sweat much particularly in summers. The
target BP is 130/80 for all diabetics and 120/70 in established nephropathy (creatinine >1.5 or
proteinuria >1 gm per day) .BP should be measured at each visit .Measuring postural variation in
BP is useful in autonomic dysfunction. Therapy should be individualised based on the associated
comorbidities and side effects of drugs. Lifestyle measures and dietry adjustments are essential
to attain the desired goals.
ACE (Angiotensin Converting Enzyme )Inhibitors and ARBs (Angiotensin Receptor Blockers)
can be used interchangeably as a first line antihypertensive agent in all diabetics. Second line
agentcould be calcium channel blockers or cardioselective betablockers. Diuretics and alpha
blockers can also be used whereever needed. Glucose intolerence due to any of these agents is
not clinically significant.
Diabetic dyslipidemia-Classically, DM induces elevation in triglyceride and LDL, and
low HDL levels.It should be treated aggressively with a LDLc target of <100mg/ dlwithout
CAD and <70 mg/ dl with CAD.Goal for triglycerides is <150mg/dland for HDLc is
>45mg/dl.Statins form the cornerstoneof lipid lowering therapy.Statins are also useful if
microvascular complications like nephropathy and retinopathy are present.Addition of fibrate or
ezitimibe is indicated when desired goals are not met.Triglycerides of >400 is an indication for
the use of fibrate as a primary therapy.Combination of niacin can be useful if HDL is persistently
low.Usually anti lipid therapy is lifelong and doses need adjustments based on periodic lipid
profile.Dietarymodifications and lifestyle measures can alonebe sufficient sometimes.Statins can
produce myalgias and rarely myopathy .
Aspirin(ASA) usage in diabetes-Low dose(75-150mg)ASA prophylaxis should be given to all

diabetics over 50 years of age with one additional cardivascular risk factor. Watch for adverse
events -GI bleed and hemorrhagic stroke .
Management of diabetes in pregnancy-prepregnancy counseling for the desired goals for
glucose and blood pressure,lifestyle measures ,nutrition.Shifting to insulin and withdrawl of
ACE inhibitors and lipidlowering drugs is required in prepregnancy period.Folic acid 10 mg
daily should be started to prevent neural tube defects.
Screening for GDM
Glycemic targets in pregnancy-fasting-95 mg/dl,2hours post prandial-<120 and one hour <140.
Diabetic Foot: Even a small ulcer should be given full attention .Neglecting small ulcers or
trauma can finally become the reason for limb loss.
Diabetic foot results predominantly due to neuropathy ,associated with infection and ischemia.X-
ray of the foot may expose foreign body or gas and must be done .Shifting these patients to
insulin helps in better glycemic control and early healing. Infections of the foot are
polymicrobial and require wide spectrum coverage. Limb and life threatening infections must be
treated with parenteral antibiotics. Pus collection of any magnitude should be drained out and
explored widely. Early surgery is always desired .Iodinated solutions , H2O2 and other strong
antiseptics should be avoided for cleaning the wound as they prevent angiogenesis. Planter
lesions will heal only with offloading the affected foot.
Referral to a higher center necrotising fascitis, any chronic non healing ulcer, lesion associated
with systemic involvement, presence of significant ischemia charcot's joint, requirement of
advanced imaging and customised footwear or orthotic support.
BMI 21-25
Fasting glucose 80-120
2 hours postprandial glucose 130-160
HbA1c 6.5-7.0
BP 140 / 80
Total Cholesterol <150
LDLc <100
Triglycerides <150
HDLc >40for males, > 50 for
females

Hospitalised patient -periop period

Targets-Preprandial glucose-<110
2 hours Postprandial glucose-<180
Critically ill patients-140-18018
Most of these patients will be on insulin which preferably should be given as bolus -basal
therapy i.e.3-4 boluses of short acting insulin and a bedtime dose of NPH or long acting insulin.
Stable patients who are eating well can be managedwith 2-3 time insulin (premixed or split
mixed)In all hemodynamically compromised situations, acute myocardial infarction, stroke, high
dose steroid therapy, immediate post op period of major cardiac surgery, severe sepsis, very high
glucose levels ,patients on ventilator.IV infusion of short acting insulin with glucose monitoring
every 1-2 hours is preferred. Basal insulin requirement must be assessed for all patients to
prevent fasting and interprandial glucose peaks. Patients who are nil by mouth may also need
some basal insulin. Overlap between subcutaneous and IV insulin for 30-60 minutes should be
done to prevent sudden hyperglycemia relapse when shifting from IV to subcutaneous insulin.
Hypoglycemia: more common in following situations
Patients who are older, have renal or liver disease
Have a long duration of diabetes, autonomic neuropathy, hypopituitarism
Regularly miss meals, erratic meal pattern
unusual exercise
Take greater than the prescribed dose of their medication
Concomitant medication –Levofloxacin*, beta blockers,
* hyperglycemia is more common with Levofloxacin though rarely hypoglycemia can occur.
Diabetes Education: Educating the patient for lifestyle modifications, hypoglycemia, insulin
therapy, foot care, benefits of quitting smoking and tobacco, reducing alcohol helps in achieving
the targets of therapy.
Sick day guidelines: The objective of these guidelines is to avoid hospitalisation during
situations like acute diarrhoea, vomiting febrile illness. And if at all it is required the patient is
able to prevent DKA or other diabetes related acute complications. All diabetics should be taught
these simple rules or a handout may be given mentioning-In any febrile illness or whenever there
is poor intake of food and water due to any illness dehydration and ketosis must be avoided
.Never omit your medication -insulin or OAD. Infact sometimes a higher dose is required when
we are sick even when we are not eating. Blood glucose and urine ketones must be checked
frequently -every 4-6 hourly. Type 1 diabetics may require monitoring 2-4 hourly. Try to eat
small amounts of carbohydrates every 2-4 hourly ,soft food or liquids are easier to take .!00-
120ml of fluid every hour (carbohydrate free if glucose is >250 and with carbohydrates if
glucose is less than 250. Fluids and carbohydrates are required to maintain hydration and calorie
requirement and preventing hypoglycemia. Dehydration and worsening ketosis are ominous
signs . Physician must be consulted if nausea or vomiting persists with ketosis .If blood glucose
is persisting more than 300 on two consecutive times .If breathing becomes rapid or laboured,
fever >100 degree F persisting more than 24 hours, persisting diarrhoea or vomiting or pain
abdomen. Inability to take fluids for more than 4 hours due to vomiting drowsiness or altered
sensorium or anyother unexplained symptoms. Drug treatment adjustments during sickdays-stop
metformin, and preferably other OADs except sulphonylureas, increase or decrease
sulphonylureas according to the glucose readings. Addition of short acting insulin may be
required to OADs.In situations where patient is already on insulin, long acting or intermediate
insulin should be continued in the same doses. Dose of short acting insulin can be adjusted by
measuring sugars 4-6 hourly.Premixed insulins should be supplimented by short acting insulins
usually 20-25 %extra or more dose of insulin is required in addition to the usual dose of
insulin.However if vomiting or diarrhoea persists hypoglycemia can occur.
Prevention of diabetes: Identify the high risk population .Fasting glucose and OGTT should be
used for identifying IFG and IGT.No drug is recommended for the prevention of diabetes.MF
and Acarbose can be used in IGT and IFG.Lifestyle measures mentioned in section 2.3 should be
persued for prevention of diabetes.
Referral to a tertiary center /Endocrinologist: In the following situations a referral to a
tertiary center where endocrinologist is available should be done at least once or more in a year.
Diabetes in a neonate or an infant, all Type -1 diabetics with polyendocrinopathy, Coeliac
disease orwith growth hormone defeciency. Diabetes with complications, brittle diabetes,
pregnancy with diabetes, diabetes with endocrine tumors like pheochromocytoma, pituitary
tumor, rare varieties of diabetes like diabetes with lipodystrophies or rare syndromes,requirement
of CGM or insulin pump. Diabetes after liver or renal transplant. In any other situation where
glycemic control is not achieved despite of all efforts.
Referral to a nephrologist: serum creatinine >1.5 ,proteinuria more than >1
gm/day,nephropathy in absence of retinopathy ,suspicion of a nondiabetic renal disease.
Referral to a retinal surgeon:when early NPDR is progressing ,CSME,advanced retinopathy.
Referral to a neurologist: severe neuropathic symptoms not responding to the standard
treatment, suspicion of non diabetic neuropathy, amyotrophy, stroke, mononeuropathy.
Referral to a cardiologist: angina or its equivalent ,diabetic cardiomyopathy,peripheral vascular
disease requiring further workup
Who does what
Doctor-history taking, physical examination, ordering investigations, prescrbing treatment.
Nurse-patient education -like explaining the basics of diabetes and its complications, foot care,
exercises, hypoglycemia, self monitoring of glucose, insulin injection devices and techniques.
Dietician-calorie calculation, explaining the concept of carbohydrate counting, food exchanges,
glycemic index, modifications in diet during special situations like pregnancy, renal impairment.
Technician-drawing blood ,doing ECG, installing CGMS, insulin pump installation and its
management except the insulin dose calculation and its modifications . Biothesiometry and use
of other gadgets for foot care.

60. HIRSUTISM
I. WHEN TO SUSPECT /RECOGNISE
a) Introduction:

Hirsutism is the presence of excessive growth of terminal hair that appears in a male pattern in a
woman. Though the presence of hirsutism may be a purely cosmetic and social concern to the
affected woman, medically it can be indicative of conditions like Polycystic Ovarian Syndrome
(PCOS), non classic Congenital Adrenal Hyperplasia (CAH) or virilizing tumours of the ovaries
or adrenals.
Androgens are essential for the conversion of vellus (small, straight and fair) hairs into terminal
(larger,thicker,coarser, curlier and darker) hairs. This conversion is dependent on the level of the
circulating androgens, their metabolism locally at the pilo-sebaceous unit by the enzyme 5 alpha
reductase into dihydrotestosterone, and the subsequent binding of the latter to its receptor. This
local metabolism and androgen-receptor interaction is highly variable. As a result pilosebaceous
units vary in their sensitivity to androgen. Therefore, the degree of hirsutism may be very
different between individuals with similar levels of circulating androgens.
b) Case definition:
Hirsutism is a clinical diagnosis. Hirsutism should be distinguished from hypertrichosis which is
generalised excessive vellus hair growthin a non sexual pattern. Hypertrichosis is androgen-
independent. Its origin is hereditary or secondary to systemic conditions and certain drugs.
Typically, hirsutism is defined clinically by judging the severity of hirsutism (graded
subjectively from 1 to 4) in each of nine defined body areas. A total score of more than 8 out of a
maximum of 36 is considered significant. This is the Ferriman-Gallwey hirsutism scoring
system. Apart from its subjective nature and other drawbacks, the total score does not reflect the
significance of higher degrees of hirsutism in one area alone (“focal hirsutism”) if the other areas
are unaffected. Thus focal hirsutism which is causing distress to a woman may not lead to a
“significant” total FG score of 8. This has led to the concept of “patient-important hirsutism” –
i.e. hirsutism that is significant for the individual seeking medical attention.
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY:
About 5 % of women in the west have hirsutism. Data for our country are lacking.It is
encountered commonly in practice.
III. ETIOLOGY:
Polycystic ovary syndromeIdiopathic (hirsutism without hyperandrogenemia)Late-onset or non-
classic congenital adrenal hyperplasiaAndrogen-secreting tumoursOvarian tumoursAdrenal
tumoursCushing's syndromeHyperprolactinaemiaAcromegalyThyroid
dysfunctionIatrogenicAndrogen therapy (testosterone, anabolic steroids)DanazolAndrogenic
progestins (levonorgestrel, norethindrone and norgestrel)
Glucocorticoids
Polycystic ovaries, idiopathic hirsutism and drug-induced hirsutism constitute the largest
proportion of cases.
Hypertrichosis can occur in the following conditions or with some drugs as indicated below
Porphyria
Phenytoin
Cyclosporine
IV. COUNSELLING
Patients have to be informed of treatment options and time frame of efficacy of various
modalities –especially the delayed onset of pharmacologic therapy and that laser and intense
pulsed light (IPL) modalities are methods of long term hair reduction and not “permanent”
removal. The need for continued therapy for sustained control should also be explained.
V.OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT AND
REFERRAL CRITERIA:
1) Diagnosis:
Hirsutism is a clinical diagnosis. The presence of excess terminal hairs in a male pattern has to
be documented. The Ferriman Gallewey score of > 8 is helpful if the scoring is feasible. A
baseline FG score is also useful for assessing treatment response.
Strict requirement of FG score >8 for diagnosing and treating hirsutism is not applicable. Some
patients have already removed their hair or have been treated before their first medical encounter
precluding any scoring attempt. One also has to bear in mind the situation of “focal hirsutism”
and “patient-important hirsutism”.
The Ferriman Gallwey Scoring System
Hirsutism is scored from 0 (none) to 4 (severe) in each of nine defined areas, and the total score
added.
Clinical evaluation is also directed at discerning clues to specific etiologies.
----Drug use
----Androgen secreting neoplasm: Sudden onset, rapid course, progression, virilisation
(clitoromegaly, temporal hair recession, muscularity, voice change) or abdominal/pelvic mass
suggest the possibility of androgen secreting neoplasm. ----PCOS : Perimenarcheal onset of
menstrual irregularity, infertility, acne, male-pattern alopecia, obesity, acanthosis nigricans.
---Non-classic CAH: history of consanguinity in parents, family history of infertility, hirsutism,
menstrual irregularity or both
---Cushing’s syndrome: Hypertension, striae, easy bruising
---Hyperprolactinemia: Galactorrhoea
---Primary hypothyroidism: Goitre, other clinical features
---Acromegaly: Acral enlargement, coarse features, prognathism
2) Investigations:
Patients with isolated, mild hirsutism need not have any tests done.
Patients with the following need to be investigated:
Moderate or severe hirsutism, i.e. FG score >15
Hirsutism of any degree when it is
sudden in onset and/or rapidly progressive
progressing despite therapy
associated with menstrual irregularity/infertility/obesity/acanthosis nigricans
associated with features of virilization
1. Serum Testosterone:
Serum testosterone should be checked early morning. In women who are having regular cycles it
should be checked between days 4-10. In others,either a random sample or one obtained after
progesterone induced bleeding should be used. Testosterone levels in the upper normal range or
mildly elevated (70 -150 ng/dl) is usual for PCOS. Serum testosterone values in the adult normal
male ranges (200 –1100 ng /dl) are seen in virilizing neoplasms. If serum total testosterone is
normal in the situation where elevated levels are expected, serum albumin and SHBG should be
checked in addition and the free androgen index calculated. Commercially available free
testosterone assays may be unreliable.
2. Other tests are to be chosen according to the suspected etiology
i) Ultrasound : PCOS, adrenal/ovarian neoplasm
ii) Serum basal 17 hydroxy progesterone and if this is between 3 -10 ng/ml a
Synacthenstimulation test : non classic CAH
iii) Serum DHEAS : Adrenal neoplasm
iv) Additional tests for hypothyroidism, hyperprolactinemia, acromegaly, Cushing ’s syndrome,
when suspected
c) Treatment :
Treatment has to be prolonged and often continuous for control of hirsutism. When cosmetic
measures alone are insufficient treatment, it has to be complemented with (a) pharmacologic
therapy, or (b) direct long term hair removal methods. The choice between pharmacological
therapy and hair removal methods depends on patient preference, cost, and the area needed to be
treated (wider areas require pharmacologic therapy). In those with hyperandrogenemia,
pharmacologic therapy needs to be combined with hair removal methods to achieve better
control of hirsutism.
1. Pharmacologic therapy :
Any chosen pharmacologic therapy needs to be given a trial of at least six month before
augmenting dosage, combining, or changing drugs.
i) Oral contraceptives :
OCPs containing progestin with less (norgestimate, desogestrel) or no (drospirenone) androgenic
potential are better than those containing levonorgestrel.
ii) Antiandrogens :
Because of their teratogenic potential, antiandrogens should not be used alone in all those who
can conceive and are not on effective contraception.
Spironolactone is the most commonly used antiandrogen at 100-200 mg/day in divided doses.
Finasteride at 2.5 to 5 mg per day is less effective. It is a type 2 alpha reductase inhibitor and
inhibits conversion of only one of the isoenzymes responsible for formation of
dihydrotestosterone from testosterone.
Flutamide (250-500 mg per day) is rarely used because of its hepatotoxic potential but can be
used with periodic monitoring of LFT in severe refractory cases.
Topical eflornithine cream is used for focal hirsutism (e.g. facial hirsutism). It inhibits ornitihine
decarboxylase which catalyses the rate limiting step for polyamine synthesis which is necessary
for hair growth. It does not remove hair but reduces the growth and appearance of facial hair.
2. Hair removal/reduction methods :

Depilation - Removal of hair shaft from the skin surface e.g. shaving and chemical depilatory
creams
Epilation – Removal of hair shaft from above the bulb – waxing and plucking

Electrolysis – destruction of hair follicles by insertion of a needle and use of electric current can
be used for limited focal hairs as it is time consuming. The cost is less than photoepilation.
Photoepilation (laser or intense pulsed light) is a costly modality, but can be used for treating
relatively wider areas. The energy absorbed by the melanin destroys the hair follicles. There is a
reduction of 30 % or more in the number of terminal hair after a given setting. More than one
sitting is therefore required. Vellus hair follicles remain and can exhibit conversion into terminal
hairs when androgen excess is not taken care of.
Standard Operating Procedure :
1. Confirm hirsutism. Distinguish from hypertrichosis.
2. Ascertain history of development and progression of hirsutism.
3. Check for other features of hyperandrogenism (acne, male-pattern alopecia), virilisation
4. Rule out exposure to androgens, and features
of PCOS, Cushing’s syndrome, acromegaly, hyperprolactinemia and hypothryoidism.

Isolated mild hirsutism in women with normal cyclical menstruation, does not require further
testing unless there is inadequate response to or progression despite empirical treatment.
6. Total testosterone should be checked in all others. Free testosterone index in case the latter is
unexpectedly normal.
7. Other tests would depend on the endocrinopathy clinically suspected.
8. Treatment is offered to all women with patient-important hirsutism despite cosmetic measures.
9. Pharmacotherapy and electrolysis/photoepilation are the available options – choice for latter
measures being made on patient preference, availability, affordability and extent of area affected.
Pharmacotherapy often needs to be combined with hair reduction methods in women with
hyperandrogenemia to achieve better and sustained control.
10. Pharmacotherapy is precluded in all those trying to or likely to conceive
11. OCPs alone are an option for most. Antiandrogens alone can be used only in those who
follow effective contraception. Antiandrogens and OCPs are therefore often used in combination.
12. Any pharmacotherapy should be given a trial of at least 6-9 months before modification.
d) Referral criteria
1. When endocrinological conditions like acromegaly, Cushing’s syndrome, CAH are suspected
2. When facilities for photoepilation or electrolysis is not available.

61. HYPOTHYROIDISM
Hypothyroidism is the second most common endocrine disorder after diabetes and affects
individuals of all ages from new born to elderly population. The prevalence of congenital
hypothyroidism varies from 1 in 2500 to 1 in 3000 newbornsand the prevalence of primary
hypothyroidism in adults is around 5-40%. However, the incidence of subclinical thyroid
dysfunctions is on rise possibly because of increasing awareness about the disease among
masses ,easy and wide spread availability of thyroid hormone assays and possibly universal salt
iodization programme.
Screening is recommended for the following high risk groups:
-All new born infants
-Pregnant women
-Strong family history of thyroid disorders/or autoimmune disorders
-Having an autoimmune disease like T1DM
-Patients with depression, dyslipidemia and infertility
Primary hypothyroidism constitutes around 95% of the patients with hypothyroidism and in rest
5% it is due to secondary hypothyroidism and drugs. The majority of patientswith
hypothyroidism are due to Hashimoto’s thyroiditis and postablative therapies particularly 131I
radioablation and thyroid surgery in patients with Graves’ disease. Hypothyroidism in few
patients is related to thyroiditis and drugs like lithium and amiodarone. Iodine deficiency is a
rare cause of hypothyroidism .
The symptoms and signs include weakness (99%), dry coarse skin (76%), slow speech (34%),
periorbital puffiness (60%), constipation (40%) and others like pallor and cold skin(48%).
Presence of goitre (40%) and delayed deep tendon reflexes (77%) are usual finding on
examination.
Diagnosis of primary hypothyroidism is easily established by low T4, low T3 and high TSH
(≥10µU/ml). Serum T3 levels are usually normal as increased 5’ monodeiodinase activity and
preferential secretion of T3 by the thyroid gland maintains it until the disease advances.
Subclinical hypothyroidism is diagnosed by normal T3 and T4 levels and serum TSH is above
the reference range. Secondary hypothyroidism is characterized by low T3, T4 and low TSH
which may be accompanied with other hormone deficiencies as well.
Management
Management of adult hypothyroidism requires treatment with L-thyroxine which is built-up
gradually over a period of weeks from 25 µg and increasing to 100-125 µg daily. The tablet is to
be taken in the morning fasting state 45 min, prior to intake of food. The doses may be required
to built up more gradual in elderly patients and patients with coronary artery disease. The
concurrent administration of iron, calcium and antacids interfere with L-thyroxine absorption and
therefore these medications should be administered 6-8h later after L-thyroxine administration.
The L-thyroxine replacement is unambiguous in pregnant women with subclinical
hypothyroidism (SCH), while in other patient with SCH, presence of goitre, TMA positivity,
high LDL-Ch or signs/symptoms related to hypothyroidism warrants L-thyroxine replacement.
If there is no benefit in symptoms with L-thyroxine over a period of 3-6 months,then treatment
can be withdrawn.
Clinical improvement with therapy with L-thyroxine is marked by dieresis, weight loss, increase
in heart rate, appetite and feeling of well being. However, change in voice and improvement in
myopathy may take a longer time to recover.
Periodic monitoring of thyroid function is required to assess the adequacy of therapy. The target
TSH to be maintained is between 0.5 to 2.5 µU/ml. Initially at 6 weeks and later once in 6
months estimating TSH is usually sufficient to assess the adequacy of replacement therapy.

62. OSTEOPOROSIS
I. WHEN TO SUSPECT/ RECOGNIZE?
a) Introduction:Osteoporosis is a skeletal disease characterized by low bone mass and
microarchitectural deterioration of bone tissue with a consequent increase in bone fragility and
susceptibility to fracture.
Osteoporosis is a silent disease until it is complicated by fractures—fractures that can occur
following minimal trauma. These fractures are common and place an enormous medical and
personal burden on aging individuals and a major economic toll on the nation. Osteoporosis can
be prevented and can be diagnosed and treated before any fracture occurs. Importantly, even
after the first fracture has occurred, there are effective treatments to decrease the riskof further
fractures.
b) Case definition:According to the World Health Organization (WHO) diagnostic
classification, osteoporosis is defined by bone mineral density (BMD) at the hip, spine or
forearm, that is less than or equal to 2.5 standard deviations below the young normal mean
reference population (1).
The categories in WHO definition are:
1. Normal: BMD higher than 1 SD below the young adult mean
2. Osteopenia, or low bone mass: BMD between 1 and 2.5 SD below the young adult mean
3.Osteoporosis: BMD lower than 2.5 SD below the young adult mean
4. Established (or severe) osteoporosis: BMD lower than 2.5 SD below the young adult mean
and the presence of one or more fragility fractures
Thus, osteoporosis is defined in practice by a surrogate marker (i.e., BMD), not a health outcome
(fracture), even if other factors can influence the likelihood of fractures. The relationship
between BMD and fractures is very similar to that between hypertension and stroke and stronger
than thatbetween serum cholesterol and coronary heart disease.
II.INCIDENCE OF THE CONDITION IN OUR COUNTRY
Osteoporosis affects an enormous number of people, of both sexes and all races, and its
prevalence will increase as the population ages. It is estimatedthat with this 2.5 SD threshold,
30% of white women older than 50 years haveosteoporosis (2),a fraction that is similar to the
lifetime risk of fracture at the hip, spine, and forearm for a 50-year-old woman(3).By this
definition, about 0.6% of young adult women haveosteoporosis, and 16% have low bone mass.
Though there is paucity of large population based data that define the prevalence of osteoporosis
and fracture from India, recent reviewsestimate there are over 25 million people in India with
osteoporosis, which is expected to reach about 36 million by 2013(4, 5). Osteoporosis was
attributed to widespread vitamin D deficiency and reduced dietary calcium intake. Vitamin D
deficiency is very common in India.
III.DIFFERENTIAL DIAGNOSIS
Evaluation of a patient suspected of havingosteoporosisincludes an adequate history and physical
examination and assessment of the potential causes of secondaryosteoporosisand diseases
mimickingosteoporosis like osteomalcia. Occasionally metastasis to spine can mimic
osteoporotic fractures.
Risk factors for secondary osteoporosis
1. Endocrine disorders -Hyperparathyroidism,hypogonadism,hyperthyroidism, diabetes
mellitus, Cushing disease,prolactinoma,acromegaly,adrenal insufficiency
2. Gastrointestinal/nutritional conditions -Inflammatory bowel disease,celiac disease,
malnutrition, gastric bypass surgery, chronic liver disease,anorexia nervosa, vitamin D or
calcium deficiency
3. Renal disease -Chronic kidney disease, idiopathichypercalciuria
4. Rheumatologic diseases -Rheumatoid arthritis,ankylosing spondylitis,systemic lupus
erythematosus
5. Hematologic disease – Multiple myeloma, thalassemia, haemophilia, systemic
mastocytosis, lymphoma, leukemia, sickle cell disease,
 6. Genetic disorders -Cystic fibrosis,osteogenesis imperfecta,homocystinuria,Ehlers-Danlos
syndrome, Marfan syndrome,hemochromatosis,hypophosphatasia
7. Others -Porphyria, sarcoid, immobilization, pregnancy/lactation,chronic obstructive
pulmonary disease (COPD), parenteral nutrition, HIV/AIDS

Medications known to cause or accelerate bone loss

1. Corticosteroids -Prednisone (≥ 5 mg/d for ≥ 3 mo)
2. Anticonvulsants -Phenytoin, barbiturates, carbamazepine (These agents are associated
with treatment-induced vitamin D deficiency.)
3. Heparin (long-term)
4. Chemotherapeutic/transplant drugs -Cyclosporine, tacrolimus, platinum compounds,
cyclophosphamide, ifosfamide, methotrexate
5. Hormonal/endocrine therapies -Gonadotropin-releasing hormone (GnRH) agonists,
luteinizing hormone-releasing hormone (LHRH) analogs, depomedroxyprogesterone,
excessive thyroid supplementation
6. Lithium
7. Aromatase inhibitors -Exemestane, anastrozole

IV.PREVENTION AND COUNSELING

Several interventions to reduce fracture risk can be recommended to the general population.
These include an adequate intake of calcium and vitamin D, lifelong participation in regular
weight-bearing and muscle-strengthening exercise, avoidance of tobacco use, identification and
treatment of alcoholism, and treatment of other risk factors for fracture such as impaired vision.
V.OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA
Target group: Postmenopausal women and men age 50 and older.
a. Counsel on the risk of osteoporosis and related fractures.
b. Check for secondary causes.
c. Advise on adequate amounts of calcium (at least 1,200 mg per day) and vitamin D
(1000-2,000 IU per day) including supplements if necessary for individuals age
 50 and older. Serum vitamin D level of > 30 ng is required to prevent vitamin D
deficiency
d. Recommend regular weight-bearing and muscle-strengthening exercise to reduce
the risk of falls and fractures.
e. Advise avoidance of tobacco smoking and excessive alcohol intake.
f. In women age 65 and older and men age 70 and older, recommend BMD testing.
g. In postmenopausal women and men age 50-69, recommend BMD testing when
there is concern based on their risk factor profile.
h. Recommend BMD testing to those who have had a fracture, to determine degree
of disease severity.
i. Initiate treatment in those with hip or vertebral (clinical or morphometric)
fractures.
j. Initiate therapy in those with BMD T-scores ≤ -2.5 at the femoral neck or spine by
dual-energy x-ray absorptiometry (DXA), after appropriate evaluation.
2. • Initiate treatment in postmenopausal women and men age 50 and older with low bone
mass (T-score between -1.0and -2.5, osteopenia) at the femoral neck or spine and a 10-
year hip fracture probability ≥ 3% or a 10-year major osteoporosis-related fracture
probability ≥ 20% based on WHO absolute fracture risk model (FRAX®).FRAX tool
computes the 10 year probability of hip fracture or a major osteoporotic fracture in a
specific population.Till It is validated for Indian population data from other asian
countries can be used.
a. Current pharmacologic options for osteoporosis prevention and/or treatment are
bisphosphonates (alendronate, ibandronate, risedronate and zoledronic acid),
calcitonin, estrogens and/or hormone therapy, parathyroid hormone (teriparatide)
and estrogen agonist/antagonist (raloxifene). Adequate vitamin D is also required
for maintaining bone health. The daily requirement of vitamin D is 1000-2000 IU.
Mega doses of vitamin D (sachets containing 60,000 IU ,Injection of
cholicalceferol as 3.0 lacs or 6.0 lacs IU) is appropriate in most
situations.Toxicity due to over dose of vitamin D is rare.
b. BMDtesting performed in DXA centers using accepted quality assurance
measures is appropriate for monitoring bone loss. For patients on
 pharmacotherapy, it is typically performed two years after initiating therapy and
every two years thereafter; however, morefrequent testing may be warranted in
certain clinical situations.Ideally DXA scan of three sites (hip, spine and
forearm)should be done .Results of DXA should be interpreted with caution in
situations like spondylosis,and other degenerative diseases of hip and spine .Other
conditions like fluorosis,metallic implants in bone can also lead to falsely elevated
DXA score.DXA will not differentiate between low calcium content in the bone
being caused by osteoporosis (quantitative abnormality)and osteomalacia which is
a qualitative abnormality.

By definition, diagnosis of osteoporosis requires assessment of BMD by DXA. Formal diagnosis

of osteoporosis thus can only be made in the centers where DXA is available. Monitoring of
therapy for osteoporosis also requires serial analysis of BMD by DXA preferably by the same
machine.
a)Clinical Diagnosis: Osteoporosis is to be suspected in situations like occurrence of fractures
following trivial trauma and presence of risk factors for osteoporosis.
b)Investigations: DXA is an essential modality for establishing the diagnosis and monitoring
therapy for osteoporosis. X-ray ofspine can show an osteoportic vertebral fracture. Biochemical
parameters like serum calcium, phosphate, alkaline phosphatase are within normal range in
osteoporotic patients. Serum intact parathyroid level is also in the normal range.
c)Treatment: Bisphosphonate or teriperatide along with adequate calcium and vitamin D
supplementation can be instituted in all settings. Oral Bisphosphonates because of their
efficacy,safety and ease of administration are the first line therapy for osteoporosis.GI toxicity
with oral Bisphosphonates can be avoided with appropriate precautions.The cost of treatment
with teriperatide can be a constraint.Teripartide should be given under supervision of an
endocrinologist.It is important to remember and recognise atrial fibrillation and osteonecrosis of
jaw ,which are rare side effects of Zolidronic acid therapy.
Standard Operating procedure: Orthopedic interventions can be required for management of
osteoporotic fractures.
a.In Patient -NA
b.Out Patient –Treatment can be instituted in outpatient settings.
c.Day Care –Injection of zolidronate once every year
d)Referral criteria: For DXA
For biochemical and hormonal investigations

DXA facilities are usually available in speciality centers. Otherwise, the basic treatment remains
the same.
a)Clinical Diagnosis: same for situation 1
b)Investigations: do
c)Treatment: do
Standard Operating procedure: do
a.In Patient
b.Out Patient
c.Day Care
d)Referral criteria: NA

VI.WHO DOES WHAT?

a.Doctor: Endocrinologist, orthopedician or a physician who can assess the risk factors for
osteoporosis and assess the need for ordering a DXA scan, interpret the BMD report and institute
appropriate therapy.
b.Nurse: Educate the patient about injecting teriperatide and administration of bisphosphonates
c.Technician: DXA technician, laboratory staff for biochemical and hormonal assay.

63. POLYCYSTIC OVARIAN SYNDROME

I. WHEN TO SUSPECT/ RECOGNIZE?

a) Introduction:

Polycystic Ovarian Syndrome (PCOS) is the commonest endocrine disorder of the reproductive
age group females. Though the structural term “polycystic” is an integral part of its name, the
presence of polycystic ovaries is not an essential component of the condition. In fact, PCOS is a
functional disorder of the ovaries characterised by complete or incomplete triad of chronic oligo-
/anovulation, hyperandrogenism and, sonologically detectable “polycystic” ovaries.
PCOS is known to have significant association with some very important medical conditions like
metabolic syndrome, diabetes, cardiovascular disease, endometrial cancer and, obstructive sleep
apnoea.
The syndrome typically begins around menarche but may appear later in life especially in
women who experience weight gain.
PCOS is to be suspected in women with one or more of the following :
Oligomenorrhoea/amennorhoea
Subfertility/infertility
Hirsutism/acne/androgenic alopecia
Incidental sonologic detection of “polycystic” ovaries
b) Case definition:

A universally accepted definition has been lacking. It is currently diagnosed by applying the
diagnostic criteria proposed at the 2003 Rotterdam international consensus conference. As PCOS
is a syndrome, it is defined by a combination of features rather than any one single manifestation.
It is also a diagnosis of exclusion. Other conditions which can mimic PCOS by causing
menstrual irregularity and/or hyperandrogenism must be excluded.
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY

The prevalence in the west is between 5-7% and increasing with the trend of increasing obesity.
The prevalence in our country is undetermined but is a common condition encountered in
practice specially by endocrinologists, gynaecologists and dermatologists.
III. DIFFERENTIAL DIAGNOSIS

Non classic congenital adrenal hyperplasia Cushing’s syndrome Primary hypothyroidism

Hyperprolactinemia Acromegaly Virilising adrenal and ovarian tumour
Drugs
IV. PREVENTION AND COUNSELING
The only mode of prevention is prevention of obesity. Women with PCOS need to be counseled
about the condition itself along with its associations, specially metabolic and cardiovascular. A
properly informed patient would be better equipped to choose between different modalities of
treatment, especially in case of hirsutism.
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,

TREATMENT & REFERRAL CRITERIA

1) Clinical Diagnosis:
The current definition of PCOS is the one that was evolved in 2003 at the Rotterdam
ESHRE/ASRM-sponsored PCOS consensus workshop. According to this definition PCOS can
be diagnosed if ANY two out of the three features mentioned below are present, and other
mimicking conditions (e.g. congenital adrenal hyperplasia, androgen-secreting tumours,
Cushing's syndrome) have been excluded:
1. Oligo-and/or anovulation
2. Clinical and/or biochemical signs of hyperandrogenism
3. Polycystic ovaries
It is a condition arising out of functional abnormalities of the ovaries and the documentation of
polycystic ovaries is not an essential criterion. By the same token, the presence of polycystic
ovaries alone does not suffice to make the diagnosis.
History and physical examination is important to determine the presence of features of the
syndrome, their temporal profile, and relevant family history. Clinical clues to ascertain
likelihood of other mimicking medical conditions are to be looked for. Similarly clinical
evaluation should also focus on the possibilities of other known associations of PCOS.
Clinical Features of PCOS :
1. Oligo-and/or anovulation
2. Oligomenorrhoea (i.e.fewer than 9 menstruations in a year) amenorrhoea
3. Dysfunctional uterine bleeding
4. Subfertilty /infertility.
5. Hyperandrogenism
6. Hirsutism
7. Acne
 8. Male pattern alopecia
Associations of PCOS::
1. Metabolicsyndrome and insulin resistance
2. Obesity
3. Hypertension
4. acanthosis nigricans
5. Sleep apnoea
6. excessive snoring and daytime sleepiness
Differential diagnosis of PCOS :
1. Non-classic CAH: family history of infertility, hirsutism or both
2. Cushing’s syndrome: Hypertension, striae, easy bruising
3. Hyperprolactinemia : Galactorrhoea
4. Primary hypothyroidism : Goitre, other clinical features
5. Acromegaly : Acral enlargement, coarse features, prognathism
6. Virilising adrenal/or ovarian neoplasm : clitorimegaly, extreme hirsutism and male-
pattern baldness, abdominal/pelvic mass
7. Drug history for exposure to androgens, anabolic steroids, valproic acid, cyclosporine

2) Investigations:

To confirm diagnosis :
i) Ultrasound of ovaries.

Regularly menstruating women should be scanned in the early follicular phase (cycle days 3-5).
Oligo-/amenorrhoeic women should be scanned either at random or between days 3 and 5 after a
progestin-induced withdrawal bleeding.Presence of 12 or more follicles, measuring 2-9mm in
diameter in either ovary, and/or increased ovarian volume (>10ml) is consistent with the
diagnosis. Whenever feasible, transvaginal approach should be used specially in obese
individuals.
ii) Serum testosterone.
It should be measured in the morning preferably in the follicular phase. A level in the upper
normal range or slightly elevated is generally seen in PCOS. A level in the range of normal adult
males is suggestive of virilising disorders. If total testosterone is normal, a reliable free
testosterone level if available should be asked for.
For differential diagnosis :
i) TSH

TSH should be measured to rule out primary hypothyroidism. Hypothyroidism can cause
ovulatory dysfunction but not significant hyperandrogenism. Therefore the role of
measuringTSH in women with significant hyperandrogenism is to rule out a chance co-existence
of a common disorder responsible for ovarian dysfunction and subfertility.
ii) Prolactin

Prolactin levels should be measured in the fasting state in the morning to rule out
hyperprolactinemia resulting from prolactionomas. Like hypothyroidism, hyperprolactinemia
can cause ovulatory dysfunction but not significant hyperandrogenism. Importantly, many
patients with PCOS may have prolactin levels in the upper normal range or slightly elevated and,
therefore, this should not be considered indicative of prolactinomas.
iii) Gonadotropins and Estradiol
Measurement of FSH and LH levels is not required for diagnosis of PCOS
These are useful for differential diagnosis in the group of females with oligo-or anovulation
withoutfeatures of hyperandrogenism, namely :
a) Pre mature ovarian failure (high FSH/LH)
b) Hypogonadotropic hypogonadism (normal/low FSH/LH and low estradiol).

PCOS, in contrast, has normal FSH, with or without elevated LH, and normal estradiol
iv) Serum 17-hydroxyprogesterone

This is to be measured in the follicular phase of menstrual cycle in the morning only in those in
whom non-classic CAH is considered to be a possibility.
v) Serum DHEAS

In those whom virilising adrenal neoplasms need to be ruled out.

vi) Tests for acromegaly and Cushing’s syndrome need to be done only in those with suspicious
clinical features.

Ancillary Studies to look for associations of PCOS :

i) Oral Glucose Tolerance Test
ii) Fasting Lipid Profile
iii) Polysomnography

Only when there is a suspicion of sleep apnoea

3) Treatment:

Treatment choice depends on the component of the condition which is desired to be addressed in
a given clinical situation.
Applicable to all :
i) Weight loss in those overweight.

All overweight/obese individuals with PCOS, weight reduction is recommended. A 5-7 % weight
loss can help improve Insulin resistance and thereby improve ovulatory dysfunction,
hyperandrogenism, metabolic abnormalities
ii) Metformin
By reducing hepatic glucose output reduces insulin levels and can have a wide effect like weight
loss. Effect of metformin is evident regardless of baseline body weight.
Applicable to those with menstrual irregularity and desire to conceive:
i) Metformin

ii) ovulation induction with antiestrogens (clomiphene) or aromatase inhibitor (lerotrozole), or

gonadotropins
Metformin can be used in combination with other ovulation inducing agents.
Applicable to those needing treatment for menstrual irregularity alone :
i) cyclical progesterone
ii) OCPs

Applicable to those needing treatment for hirsutism :

i) Cosmetic measures (bleaching, waxing, shaving, chemical depilation)
ii) Permanent hair reduction (electrolysis, photoepilation)
iii) Pharmacologic therapy (not for those desiring/likely to conceive)

OCPs
iv) Antiandrogens (spironolactone) and

5 alpha reductase inhibitor (finasteride)

OCPs are commonly combined with antiandrogens
Standard operating procedure
1. Consider PCOS in women with hirsutism and/or other cutaneous markers of
hyperandrogenism, oligo- or amenorrhoea, subfertility.
1. Rule out pregnancy in amenorrhoeic women.

2. Check testosterone level

3. Pelvic sonography
4. Exclude other conditions mimicking PCOS to confirm diagnosis of PCOS. Choice of test
would depend on the clinical situation. TSH and prolactin should be checked in all those with
menstrual irregularity and/ or infertility.
5. Check for associated features of metabolic syndrome – including glucose intolerance and
dyslipidemia.
6. Consider possibility of sleep apnoea
7. Insulin resistance reduction with weight loss (in those overweight) and metformin can help
ameliorate all features
8. For oligo- or amenorrhoea : cyclic OCPs or progestin alone
9. For hirsutism : cosmetic measures along with pharmacologic therapy and/or
electrolysis/photoepilation
10. For infertility : metoformin and/or other ovulation induction measures

65. THYROTOXICOSIS
Thyrotoxicosis refer to clinical syndrome of toxicosis associated with excess circulating thyroid
hormones which may or may not be associated with increased gland activity while
hyperthyroidism is associated with increased gland activity and increased levels of circulating
thyroid hormones. Therefore, all patients with hyperthyroidism are thyrotoxic while vice versa
is not true.
The common cause of thyrotoxicosis include Graves’ disease, toxic multinodular goitre (MNG),
toxic adenoma and thyroidits. The symptoms associated with thyrotoxicosis include weight loss,
despite increased appetite, palpitation, heat intolerance, fatigue, weakness, frequent motions and
trembling. The signs include tachycardia, tremor, warm moist skin, goitre (96%), hyperreflexia
eye signs and dermopathy®.Grades of goiter grading as per WHO classification include a) Grade
0: Thyroid neither palpable nor visible. b). Grade 1: Thyroid palpable but not visible with neck in
normal position c). Grade 2:Thyroid palpable and visible with neck in normal position The
monosymptomatic manifestation of thyrotoxicosis include malabsorption syndrome, loan atrial
fibrillation, attention deficiency disorder, tall stature & hypokalemic/hyperkalemic
periodicparalysis.
The diagnosis of hyperthyroidism is based on increased T3, T4 and suppressed TSH (<0.05
µU/ml) with clinically evident toxicosis. The usefulness of 99mTc scan is only in a situation
when there is a clinical suspicious of thyroiditis particularly when there is history of fever, neck
pain, rapid weight loss and tender goitre. 99mTc scan is also useful in establishing a diagnosis
of toxic adenoma. Estimation of TPO antibody is not required, however it is positive in
significant titres in 70-80% of patients with Graves’ disease and its presence is a marker of
autoimmune thyroid disease. Ultrasonography is useful for establishing a diagnosis of
multinodular goitre as sometimes a single large nodule is only present clinically.
Treatment of thyrotoxicosisinclude drugs, (thionamides) 131radioablation after failure of drug
treatment and rarely surgery if goitre is very large (III/IV). The drug treatment include the use of
neomercazole (NMZ) in doses of 30-40 mg per day usually in a single dailydose preferably in
the morning fasting state. The doses higher than this does not yield any additional benefit.
However, the NMZ should be administered in three divided doses if patient is severely toxic.
Use of non iodized salt is currently recommended along with NMZ to avoid iodine as a fuel to
hyperthyroid gland. The NMZ doses are gradually tapered once the patient becomes euthyroid
that usually spans over 3 months and continued for 24 months usually in doses of 5mg as even
this minimum dose possesses immunomodulatory action. There is no extra-benefit of extending
the treatment beyond 24 months in preventing the recurrence of disease. The disease is said to
be in remission
when the patients remains euthyroid at least for a period of one year afterstoppage of treatment.
However, remission rate is around 40-50%, therefore majority of the patients required
reintroduction of drug or ablative treatment. Management ofassociated thyroid orbitopathy
include methyl prednisolone in low dose pulse therapy(4.5 gm over 8 weeks) and if failed to
response addition of azathropine is recommended. Recently rituximab has been used for
orbitopathy with success.

66. Obesity
Obesity is an increasingly important health problem worldwide including the developing
countries. In India, obesity is emerging as an important health problem particularly in urban
areas. Almost 30-65% of adult urban Indians are either overweightor obese or have abdominal
obesity. The rising prevalence overweight and obesity in India has a direct correlation with the
increasing prevalence of obesity-related co-morbidities; hypertension, the metabolic syndrome,
Dyslipidemia, Type 2 diabetes mellitus (T2DM), and cardiovascular disease (CVD).
"obesitygenic" lifestyle of excess caloric intake and decreased physical activity, these same
genes contribute to obesity and poor health. Obesity is commonly considered to be one of the
most important preventable causes of premature death, second only to smoking. Therefore, this
marked increase in obesity has enormous public health implications
Definitions and measurement of overweight and obesity
Obesity is generally defined conceptually as the condition of excess body fat. However, There is
no precise definition of excess. The degree of adiposity is a continuous trait not marked by any
clear division into normal and abnormal. In addition, direct measurement of body fat is difficult.
Thus, for practical purposes, obesity is often defined as excess body weight rather than as excess
fat. In epidemiologic studies, for both children and adults, body mass index (BMI) is used to
express the degree of obesity. This index is calculated as the body weight (kg) divided by the
stature ([height in Meter]2squared) (wt/M2), BMI correlates well with body fat and is relatively
unaffected by height.
BMI = Weight in Kg
(height in meter)2
Waist Circumference (WC) and Waist Hip Ratio (WHR) Cut-offs for Obesity
Abdominal obesity is increasingly being recognized as an important cardiovascular risk factor.
The cardiovascular risk associated with abdominal obesity can be attributed to excess abdominal
adipose tissue (visceral Fat), both intra-abdominal adipose tissue (IAT) and subcutaneous
adipose tissue (SCAT). Common surrogate measures of abdominal obesity are Waist
Circumference (WC) and Waist Hip Ratio (WHR). Waist circumference is a simple, easily
obtainable anthropometric parameter, which can be assessed in the outpatient setting.
Measurement of WHR is more difficult as accurate measurement of hip circumference may not
always be possible since it requires difficult task especially in women in India. Further, changes
in WHR may not accurately reflect the extent of obesity or changes in weight. As with BMI, the
relationship of central fat to risk factors for health varies among populations as well as within
them. Current classifications of obesity are based on BMI and waist circumference. The one
recommended by the World Health Organization and the NHLBI is shown in Table-1. BMI has a
curvilinear relationship to risk. Several levels of risk can be identified using the BMI.
Table –1. Definitions for adults
Classification of Overweight & Obesity and risk ofdisease as Recommended by the WHO &
NHLBI.
Asian Indians exhibit unique features of obesity; excess body fat, abdominal adiposity, increased
subcutaneous and intra-abdominal fat, and deposition of fat in ectopic sites (liver, muscle, etc.).
Obesity is a major driver for the widely prevalent metabolic syndrome and type 2 diabetes
mellitus (T2DM).The proposed cut-offs for defining overweight and obesity by WHO are not
appropriate for Asian Indians, and that Asian Indians are at risk of developing obesity related co-
morbidities at lower levels of BMI and waist circumference (WC).
The currently recommended cut-offs of WC (>102 cm in men and >88 cm in women) are also
not be applicable to all the populations due to heterogeneity and different relationship with
cardiovascular risk. Asian Indians appear to have higher morbidity at lower cut-off for WC than
do White Caucasians.
-stretchable flexible
tape in horizontal position, just above the iliac crest, at the end of normal expiration, in the
fasting state, with the subject standing erect and looking straight forward and observer sitting in
front of the subject.
-and clinic-
based risk stratification.

For Japanese, a BMI of 23 or 24 kg/m2has the same percent fatas that of a BMI of 25 in
Caucasians or 28 to 29 in African-Americans. On the basis of these differences and the
observations that the risk for diabetes and hypertension had doubled when the BMI was 25
kg/m2, a taskforce from the Asia-Oceania section of the International Association for the Study
of Obesity has proposed an alternative table, where obesity is defined as a BMI >25 kg/m2and
high-risk waist circumference at >90 cm for men and >80 cm for women.
Hence it is also recommended for Asian Indian population.
Classification of Obesity as Recommended by the Asia -Pacific Task force –
Risk of co morbidities with waist circumference<80 cm (women)> 80 cm (women)
Weight categoryBMI< 90 cm (men)> 90 cm (men)Underweight <18.5LowAverageHealthy
weight18.5-22.9AverageIncreasedOverweight>23At Risk23 –24.9IncreasedModerateObesity
class I25 –29.9ModerateSevereObesity class II> 30SevereVery Severe
Classification of Obesity as per fat distribution
Obesity can also be classified based on the regional distribution of the fat
Android(or abdominal or central, males) -Collection of fat mostly in the abdomen (above the
waist)
-shaped

Gyneoid (below the waist, females) -Collection of fat on hips and buttocks
-shaped
nical problem

Definitions of Obesity for children and adolescents

In children with 2-19 years old
BMI : > 85thto 95thpercentile for that age –Possible risk of overweight and should undergo
further evaluation.
BMI : > 95thpercentile for that age –Overweight
In the United States, the 2000 CDC BMI for age growth charts are recommended for screening
of individuals who are overweight and those who are at risk for overweight.
No BMI for age reference exist for children younger than 2 years. Nor are there any consistent
recommendations for the definition of overweight in this age group.
1. Overweight
 2. BMI between 85thto 94thpercentile for age and sex
3. Obese
4. BMI ≥95thpercentile for age and sex -or-BMI ≥30 kg/m²
5. Severe obesity
6. ≥99thpercentile (equivalent to BMI of 30-32 kg/m² for 10-12y.o. -or-≥34 kg/m² for 14-
16y.o.)
7. Weight for length is used in the under 2-yr age group

For the evaluation of obesity in Indian children IAP growth charts are used. At present, IAP
suggeststo use WHO growth charts and Growth charts by Agrawal DK. IAP expect to come out
with its own new growth charts. Till the time IAP comes out with IAP Charts, it is suggested to
use WHO growth charts, which can be accessed at
http://www.who.int/childgrowth/standards/chart_catalogue/en/index.htmlHowever with secular
trends growth charts often change & periodic revision of Growth charts done should be accepted.
Obesity is associated with various organ System Dysfunction & they are
Cardiovascular
Hypertension, Coronary artery disease, Congestive heart failure, Cor pulmonale, Varicose veins,
Pulmonary embolism.
Musculoskeletal
Hyperuricemia and gout, Immobility-Osteoarthritis (knees and hips), Low back pain
Psychologic
Depression, low self-esteem, Body image disturbance, Social stigmatization
Respiratory
Dyspnea, Obstructive sleep apnea, Hypoventilation syndrome, Pickwickian syndrome, Asthma
Gastrointestinal
Gastroesophageal reflux disease (GERD), Nonalcoholic fatty liver disease (NAFLD),
Cholelithiasis, Hernia, Colon cancer
Genitourinary
Urinary stress incontinence, Obesity-related glomerulopathy, Hypogonadism (male), Breast and
uterine cancer, Pregnancy complications
Neurological
Stroke, Idiopathic intracranial hypertension, Meralgia paresthetica
Integument
Striae (stretch marks), Stasis pigmentation of legs Lymphedema, Cellulitis, Intertrigo,
carbuncles, Acanthosis nigricans, skin tags, Hirsutismin patients with PCOS.
Endocrine
Metabolic syndrome, Type 2 diabetes, Dyslipidemia, PCOS, Hyperandrogenemia, menstrual
disorders, Amenorrhea, infertility.
There two ways by which endocrine system is affected in Obesity.

Obesity and Obstructive Sleep Apnea

Obesity is the most powerful risk factor for obstructive sleep apnea (OSA). Several
pathophysiologic mechanisms relates obesity to the development of OSA These mechanisms
include anatomic and functional obstruction of the pharyngeal airway. Sleep deprivation,
daytime somnolence and metabolic dysregulation may also contribute to obesity in the setting of
OSA. Although history and physical examination may help predict OSA in obese individuals,
polysomnography is the gold standard for making the diagnosis of OSA and assessing effects of
therapy. Weight loss is an important strategy for treating OSA. However, the cornerstone of
current management is continuous positive airway pressure.
Clinical Evaluation
Basic evaluation in clinics is measurement of Height, Weight, BMI, Waist Circumference.
Detection of acanthosis nigricans or skin tags should suggest significant insulin resistance. A
number of physical features of an obese individual may help identify a specific cause for the
individual's problem. Features of the hypothalamic syndrome, Cushing's syndrome, Polycystic
ovarian disease (Which is a common in younger women) should be looked for. Among the
various genetic diseases that produce obesity, Prader-Willi is the most common. It includes
hypotonia, mental retardation, and sexual immaturity, and can usually be recognized clinically.
Bardet-Biedl syndrome, with its polydactyly and retinal disease, is distinctive. Obesity and red
hair in a child might suggest a defect in the processing of POMe.
Laboratory Evaluation
Common laboratory tests which should be done as a part ofthe obesity evaluation are -Plasma
Glucose (Fasting & Post glucose or postprandial), Plasma Lipids, Thyroid Functions, serum uric
acid, Liver function tests, Prostate-Specific Antigen in Males, Ultrasound of the Gall Bladder.
Other tests like overnight dexamethasone suppression test, serum gonadotropins, etc may be
done depending on the patients clinical profile. (Serum insulin has no role in the evaluation of
obesity in day today practice except in suspected cases of Insulinoma which is very rare.)
Management of Obesity
Obesity prevalence has increased markedly over the past few decades. The obesity pandemic has
huge implications for public health and our society.
There are many Health benefits of moderate weight loss (5-1 0% of present body weight)
Reduction in Death-20% overall, 30% diabetes-related & 40% cancer
deaths
Blood pressure Reduction -10 mmHg decrease
Improvement in Lipids -15 % decrease in cholesterol & improvement in other lipids
Improvement in Glycemic control in patients with Diabetes.
Hence weight loss program should be achieved by following principles
–Diet control, Exercise, & Behavioural Modification.
Lifestyle Modification
Principles of weight loss
1. Decrease total energy intake (TEl), Maintain a balanced deficit diet
2. Increase physical activity (Adjust energy balance to prevent weight regain) appropriate
for that age.
3. Behavior modification;
4. Maintenance program -monitoring and long term follow-up.

5. While managing obesity we should remember certain facts that

6. Do not recommend Rapid weight loss (i.e. >5-10% weight loss in 6 months), it should be
slow so that maintainance becomes easy. Rapid weight loss is associated with rebound
weight gain which sometimes can be more than initial weight.
7. We should have realistic expectations of 5-10% weight loss in 1 year.
8. Passive exercise, Heat or Vibration therapy, etc should not be recommended.

Obesity management programs

The therapies and degree of intensity of any weight loss program should be based on an
assessment of the degree of adiposity (anthropometry) and the presence or absence of medical
risk factors. Mild to moderate uncomplicated overweight and obesity may require advice with a
specific eating and physical activity program. Greater degrees of obesity and risk, or the presence
of disease, require more intensive lifestyle interventions, the use of pharmacotherapy, or surgery
& treatment of basic cause of Obesity if any. Any weight management program must provide a
weight maintenance component. Regular and long-term follow-up visits and interventions are
part of the management of Obesity.
Diet intervention
Although energy (calorie) restriction produces good weight loss, some individuals may find this
irksome and impossible to maintain. It is the total calorie intake which decides patients weight
rather than the type of food. However for some patients, a low-fat eating plan may prove
effective. Such plans may be maintained for several years. Greater losses may be obtained by
additionally reducing energy intake. Men may also need to reduce energy intake by limiting their
alcohol intake. There is no long term difference between low calorie diet (LCD) & Very low
calorie Diet (VLCD).
Physical activity /exercise program
Emphasis should be placed on increasing total daily activity to between 60 and 90 min each day.
Although exercise and fitness are important, the initial emphasis should be on increasing the
activities of daily living, in particular more walking. A formal written exercise prescription has
been shown to increase effectiveness in general practice. Giving patients the opportunity to use
or purchase a pedometer and then setting the number of steps they need do in a day may prove an
effective method of increasing activity. For patients with arthritis or other disabilities,
hydrotherapy (exercising in water) may be a way of initiating movement and this type of activity
can assist weight loss. Patient can do any type of exercise which is suitable for his/her age &
associated comorbid condition.
Behavior modification
This therapy is important and central to any weight loss program. There are many components to
behavior modification, but one simple is the use of a food and exercise diary. This allows habit
recognition and changes accordingly. All subjects, but most particularly those who are
overweight or obese, under-report food intake and over report the activity they undertake. A
diary provides an important starting point for discussion and suggestspossible interventions.
Additional behavioral therapies include discussion about habits, change and alternative ways of
approaching situations. Other techniques involve stress management, improving self-esteem and,
occasionally, more spe-cific counseling or psychiatric intervention.
Such a lifestyle program should involve a team of health professionals (dietitians,
physiotherapists, nurses, psychologists). Good results and satisfaction are usually obtained by the
involvement of multidisciplinary teams. Some commercial groups use conventional therapy (e.g.
Weight Watchers or programs used in some gyms), whereas others rely on alternative or natural
therapies and still others use magic treatments that sound plausible but which really have neither
have any scientific basis nor effectiveness. Examples of the magic type of therapy would be
total-body wrapping, some herbal and bulking agents. Few have been tested rigorously and very
are costly, but the very existence of such program and therapies shows that manyindividuals
desire to lose weight but need to be guided into the correct approach and provided with effective
therapy.
Maintenance program, Monitoring and longer term follow-up
This is an essential part of any weight loss program but the most neglected part. Follow-up
programe are essential and very effective.
Patients involved in an obesity treatment program require the following
Monitoring of weight (ideally monthly, no greater than bimonthly);
Monitoring of pulse rate and blood pressure;
Monitoring ofobesity-related risks and diseases (e.g. dyslipidemia, type 2 diabetes).
Drug therapy
The decision to give pharmacotherapy for obesity is made from clinical judgment requirement of
the each individual patient in terms of potential benefitsbalanced against potential risks. BMI
between 25and 30 with comorbid conditions is the definite indication to start pharmacotherapy
along with lifestyle intervention.
The various drugs which have been used for obesity are :
1. Appetite suppressants
a. Adrenergic agents (e.g. amphetamine, methamphetamine phenylpropanolamine, Phentermin)
2. Serotonergic agents (e.g. fenfluramine desfenfluramine, SSRIs like setoraline, fluoxetine)
3. Thermogenc agents -Ephedrine, caffeine
4. New ones
a. Serotonin and Noradrenaline reuptake Inhibitor -Sibutramine;
b. Intestinal Lipase inhibitors -Orlistat
c. The CB1blocker -Rimonabant,

Among all these drugs currently only Orlistat is approved drug for the medical management of
obesity. All other drugs are either not approved or banned fortheir use in obesity. Orlistat is an
intestinal lipase inhibitor. It irreversibly inhibits the action of gastric and pancreatic lipases
which are required to hydrolyse dietary fat before absorption. Unabsorbed triglycerides and
cholesterol are excreted infaeces. It can cause Weight loss of 5-8.5 % at the end of 1 yr.
Side effects include steatorrhoea, flatus, fecal incontinence and oily spotting. Absorption of fat
soluble vitamins may be lowered with orlistat. Hence vitamin supplementation is recommended.
The maximum effect of orlistat is achieved at a dose of 120 mg thrice daily with every fatty
meal. In patients with Fat restricted diet this drug is of no use.
There is no good scientific evidence for the alternative therapies.
Surgical Treatment of Obesity –Overview
Gastrointestinal surgery is the most effective approach for inducing major weight loss in
extremely obese patients. Bariatric surgery has evolved over the last half century as a treatment
option for patients suffering from morbid obesity. It involves modification of the digestive
system by either decreasing the gastric volume (restrictive) or altering the path of the food bolus
causing an element of malabsorption (Malabsorptive). These alterations effect appropriate
changes in eating behavior and aid lifestyle modifications to help weight loss.
Indications for Bariatric Surgery -

.0 to 39.9 kg/m2 (with comorbidiry) and one or more severe

medical complications of obesity (e.g., hypertension, heart failure, Type 2 Diabetes Mellitus,
sleep apnea).
ntional
therapy, acceptable operative risks,

The Surgical Options for Weight loss Surgery Restrictive Procedures

Combined Procedures
• Roux-en-Y gastric bypass (RYGBP)
Malabsorptive Procedures
Bilio-pancreatic diversions (BPD)
-pancrearic diversion with duodenal switch (BPD-DS)
Experimental Procedures
-jejunal bypass
Over the years, minimally invasive surgery has evolved from general laparoscopic surgery to
advanced laparoscopic surgery. Given the advantage of laparoscopy with other general surgery
procedures, it was a logical step to attempt these complex bariatric procedures using minimally
invasive approach. Laparoscopic BPD-DS has higher complication rate compared to gastric
bypass or banding and a mortality rate as high as 5%.
Bariatric Surgery Outcomes -Weight Loss
Bariatric surgery is currently the most effective method to treat severe obesity. The amount of
excess weight loss (EWL) varies according to procedure. Long term data is now emerging that
shows maintenance of weight loss 5-15 years after modern bariatric procedures. This sustained
weight loss has a major impact on individual patient health and longevity.
Approach to Obesity management
Prevention:
With Limitedoptions of drug treatment prevention becomes an important step. Prevention should
start from Childhood so that we can prevent future health hazards. Balanced diet & regular
Aerobic physical activity is must for everyone & should be educated since childhood.
ENT
67. ALLERGIC RHINITIS
WHEN TO SUSPECT/ RECOGNIZE
A. Definition: Allergic rhinitis is allergic inflammation of nasal airways.
B. Introduction: When a foreign protein (allergen) is inhaled by a previously sensitized
individual, a reaction between the allergen and the antibodies takes place on the nasal mucosa.
This inflammatory reaction presents as itching in the nose, sneezing and nose block.
C. Allergic rhinitis may be seasonal or perrineal. Allergic rhinitis is found to co exist with
Bronchial asthma, nasal polyps, sinusitis, adenoid hypertrophy, Eustachian tube dysfunction and
otitis media.

INCIDENCE IN OUR COUNTRY

D. No exact data are available in our country.
DIFFERENTIAL DIAGNOSIS
The diagnosis is clinical. The differential diagnosis would include
1. Vasomotor rhinitis
2. Hormonal rhinitis in pregnancy, hypothyroidism etc
3. Nasal block due to deviated nasal septum
4. Immotile cilia syndrome
5. Specific rhinitis caused by granulomatous diseases like wegener’s and sarcoidosis.

PREVENTION AND COUNSELLING

Allergic rhinitis can be prevented by environmental control measures and allergen avoidance by
reducing outdoor exposure during pollen season. For indoor allergens prevention would include:
1. Covering mattresses with impermeable covers
2. Washing of bed linen every two weeks in hot water
3. Avoidance of exposure to pets

OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &

REFERRAL CRITERIA
AT SECONDARY HOSPITAL/ NON METRO SITUATION
CLINICAL DIAGNOSIS: the diagnosis is essentially based on history. The basic evaluation
should include:
1. Complete ENT examination
2. Nasal examination for condition of nasal mucosa and polyps if any.
3. Evaluation of respiratory system to exclude asthma

INVESTIGATIONS:
1. Complete blood count,
2. Absolute eosinophil count.
3. X Ray of paranasal sinuses.
4. Other investigations based on associated conditions
I. TREATMENT:
1. OUT PATIENT:
1. Nasal decongestants: avil, cetrizine, fexofenadine etc
2. Nasal Steroid sprays: Fluticasone, Mometasone, Budesonide etc
3. Oral steroids: for refractory cases and those with asthma.
2. DAY CARE: nil
3. INPATIENT:
1. Surgical procedures like septoplasty, adenoidectomy with or without grommet insertion,
polypectomy may be required.
2. Manangement of comorbities.
REFERRAL CRITERIA:
1. Extensive nasal polyposis
2. Associated complications not manageable in the centre.

CLINICAL DIAGNOSIS: nasal examination is complemented with nasal endoscopy under local
anaesthesia.

INVESTIGATIONS:
1. Allergy skin testing
2. IgE estimation if available
3. CT Scan of paranasal sinuses

TREATMENT: Additional measures which may be required are

1. OUT PATIENT: antihistamines, nasal steroid sprays, leukotrienne antagonists and oral
steroids.
2. DAY CARE/ INPATIENT:
1. Septoplasty
2. Endoscopic sinus surgery
3. Management of comorbidiites.
REFERRAL CRITERIA:
1. In adequate facilities for any of the above.

68. DEVIATED NASAL SEPTUM (DNS)

WHEN TO SUSPECT/ RECOGNIZE
Definition: Deviated Nasal Septum is deflection of nasal septum from midline.
Introduction: Deviated Nasal Septum (DNS) may be caused by birth trauma, trauma to face
during life or due to asymmetric growth of cartilages and bones of nose. They may present with
nose block, recurrent nasal discharge, infections of nose and sinuses, bleeding from nose or
headaches. In gross DNS, there may be a concomitant deviation of external nose also.

INCIDENCE IN OUR COUNTRY : Very few people have absolutely straight nasal septum.
Most minor DNS are not symptomatic and do not require treatment. Only symptomatic DNS
need be mentioned to the patient and treated.

DIFFERENTIAL DIAGNOSIS
The differential diagnosis includes:
1. Acute or chronic Rhinosinusitis
2. Nasal Allergy
3. Large Adenoid mass in children
4. Foreign Body/ Rhinolith in children
5. Nasal Polyps
6. Growths/ Tumors of nose

PREVENTION AND COUNSELLING

DNS cannot be prevented. Minor deviations do not require treatment. Symptomatic DNS can be
corrected by surgery through the nostrils under Local or General Anaesthesia. Surgery is usually
done after the age of 16 years when the facial growth is complete. Surgery in younger patients
may be undertaken if grossly symptomatic and not amenable to medical management for nasal
obstruction.
In septoplasty, the deviated portion of the nasal septum is removed. The nose is packed for 1 -2
days to prevent bleeding. Patient is discharged after removal of packs. The nose takes 1 -2 weeks
to heal completely.

69. EPISTAXIS
WHEN TO SUSPECT/ RECOGNIZE
Definition: Epistaxis is bleeding from nose. Blood may flow anteriorly or go posteriorly. It may
be clotted or flow from nose .
Introduction: Nose bleeds are common as nose is rich in blood supply and is prominent on the
face. Most epistaxis are minor and are managed at home. Only a small percentage comes for
medical attention.

INCIDENCE IN OUR COUNTRY

No exact data are available in our country.

DIFFERENTIAL DIAGNOSIS
The diagnosis is clinical. Hence it has no differential diagnosis. The various common causes of
epistaxis may be local or systemic.
Local causes
1. Low humidity: as in dry climate in summers and winters
2. Infection- Rhinitis, sinusitis
3. Trauma: Injury to nose by direct trauma or by nose picking.
4. Surgery: Septoplasty or endoscopic sinus surgery
Systemic causes:
1. Hypertension
2. Blood thinning drugs like aspirin, clopidogrel, warfarin
3. Benign growths like Angiofibroma and Rhinosporidiosis
4. Cancers like Sinonasal cancers and Carcinoma of nasopharynx

PREVENTION AND COUNSELLING

Epistaxis can be prevented by keeping the nasal mucosa moist in dry climates by douching with
water, applying creams and nasal sprays
Most epistaxis are mild and can be dealt effectively at home. The soft parts of nose are pinched
tightly for 10-20 minutes. The head is bent forward and kept above the level of heart. Any blood
flowing in to throat should be spit into a bowl. Ice can be applied locally. After the epsitaxis is
controlled, patient is advised not to blow nose, keep the nasal mucosa moist and blood pressure
under control.
OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA
CLINICAL DIAGNOSIS: When the epistaxis is not controlled with local pressure for over 20
min, expert medical care is required. The basic evaluation should include:
1. Pulse, BP monitoring,
2. General evaluation of clinical condition
3. Complete ENT examination
4. Nasal examination to identify cause and site of bleeding.
5. Evaluation of extent and site of trauma to face if any

INVESTIGATIONS:
1. Complete blood count,
2. Bleeding and clotting time.
3. X RAY of paranasal sinuses and nasal bones in trauma.
4. Other investigations based on general clinical condition

TREATMENT:
1. OUT PATIENT: General condition of the patient is stabilized.
2. DAY CARE:
1. If the site of bleeding is identified, chemical or electro cautery is done to stop the bleeding.
2. If not, then anterior nasal packing is done with ribbon gauze soaked in liquid paraffin and
antibiotic solution, gelfoam or hemostatic sponge. The packs are kept in place for two to three
days.
3. INPATIENT:
1. It the bleeding still continues, a posterior nasal packing with gauze or Foley’s catheter may be
done.
2. Manangement of comorbities.

REFERRAL CRITERIA:
1. Massive blood loss
2. Bleeding not controlled with anterior and posterior nasal packing.
3. Midface fractures would require a maxillofacial consultation.
4. Other co morbidities requiring appropriate cross consultations.

CLINICAL DIAGNOSIS: When the epistaxis is not controlled with anterior and posterior nasal
packing, the evaluation should include:
1. Review of general evaluation of clinical condition
2. Complete ENT examination
3. Nasal Endoscopic examination under Local/ General Anaesthesia to identify cause and site of
bleeding.
4. Evaluation of extent and site of trauma to face if any
INVESTIGATIONS:
1. complete blood count,
2. bleeding and clotting time.
3. Prothrombin Time/ PTTK/ INR
4. Contrast enhanced CT Scan of paranasal sinuses
5. MR Angiography
6. Digital substraction angiography (DSA) of carotid and vertebral artery system

TREATMENT: Additional measures which may be required are

1. OUT PATIENT/ DAY CARE: Endoscopic electro cautery
2. INPATIENT:
1. Septoplasty
2. Maxillofacial reduction of fracture and wire and plate fixation.
3. External carotid artery ligation
4. DSA embolisation of bleeding vessel
5. Biopsy and / or excision of tumor if any
6. Management of comorbidiites.
REFERRAL CRITERIA:
1. In adequate facilities for any of the above.
70. BRANCHIAL CYST
Introduction: Branchial cleft cysts are congenital epithelial cysts, which arise on the lateral part
of the neck from a failure of obliteration of the second branchial cleft in embryonic development.
Phylogenetically, the branchial apparatus is related to gill slits. (Branchia is Greek for gills).
Definition: At the fourth week of embryonic life, the development of 4 branchial (or pharyngeal)
clefts results in 5 ridges known as the branchial (or pharyngeal) arches, which contribute to the
formation of various structures of the head, the neck, and the thorax. The second arch grows
caudally and, ultimately, covers the third and fourth arches. The buried clefts become ectoderm-
lined cavities, which normally involutes around week 7 of development. If a portion of the cleft
fails to involute completely, the entrapped remnant forms an epithelium-lined cyst with or
without a sinus tract to the overlying skin.
Incidence in India: Unknown. Branchial cleft cysts are the most common congenital cause of a
neck mass. An estimated 2-3% of cases are bilateral. A tendency exists for cases to cluster in
families.
Differential diagnosis:
1. Lymphadenopathy (reactive, neoplastic, lymphoma, metastasis) 2. Vascular neoplasms and
malformations 3. Capillary hemangioma 4. Carotid body tumor 5. Lymphatic malformation
(cystic hygroma) 6. Ectopic thyroid tissue 7. Ectopic salivary tissue
Prevention and Counseling: NA
Optimal Diagnostic Criteria, Investigations, Treatment & Referral Criteria
Clinical Diagnosis: Diagnosis is usually made clinically. Many branchial cleft cysts are
asymptomatic. Depending on the size and the anatomical extension of the mass, local symptoms,
such as neck swelling, dysphagia, dysphonia, dyspnea, and stridor may occur.
A branchial cyst commonly presents as a solitary, painless mass in the neck of a child or a young
adult. A history of intermittent swelling and tenderness of the lesion during upper respiratory
tract infection may exist. Discharge may be reported if the lesion is associated with a sinus tract.
Branchial cysts are smooth, non-tender, fluctuant, translucent masses, which occur along the
lower one third of the antero-medial border of the sternocleidomastoid muscle between the
muscle and the overlying skin.
Secondary branchial cleft cyst lesion: The lesion may be tender if secondarily inflamed or
infected. When associated with a sinus tract, mucoid or purulent discharge onto the skin or into
the pharynx may be present.
Investigations:
1. Fine-needle aspiration may be helpful to distinguish branchial cleft cysts from malignant neck
masses. Fine-needle aspiration and culture may help guide antibiotic therapy for infected cysts.
2. A sinogram may be obtained. If a sinus tract exists, radio-opaque dye can be injected to
delineate the course and to examine the size of the cyst.
3. Ultrasonography helps to delineate the cystic nature of these lesions.
4. A contrast-enhanced CT scan shows a cystic and enhancing mass in the neck. It may aid
preoperative planning and identify compromise of local structures.
5. MRI allows for finer resolution during preoperative planning. The wall may be enhancing on
gadolinium scans.
Treatment: Surgical excision is definitive treatment for branchial cleft cysts. A series of
horizontal incisions, known as a stair step or stepladder incision, is made to fully dissect out the
occasionally tortuous path of the branchial cleft cysts
Standard Operating Procedure: As in patient surgery should be performed
Referral Criteria: depends upon competency of operating surgeon and available resources.

71. BRANCHIAL FISTULA

Introduction: Branchial fistulas are uncommon anomalies of embryonic development of
branchial apparatus. Second branchial arch and pouch anomalies are common anomalies of
branchial apparatus.
Definition: During embryonic development, the second arch grows caudally; envelop the third,
fourth and sixth arches and form the cervical sinus by fusing with the skin caudal to these arches.
The edges of cervical sinus fuse and the ectoderm within the fused tube disappears. Persistence
of ectoderm gives rise to branchial cyst.
The branchial fistula results from the breakdown of the endoderm, usually in the second pouch.
A persistent fistula of the second branchial cleft and pouch pass from the external opening in the
mid or lower neck in the line of the anterior border of the sternocleidomastoid muscle, deep to
platysma along the carotid sheath, then pass medially deep between the internal and external
carotid arteries after crossing over the glossopharyngeal nerve and hypoglossal nerve. Finally, it
opens internally in the tonsillar fossa usually on the anterior face of the upper half of the
posterior pillar of the fauces or in the intratonsillar cleft.
Most of the times it is a simple sinus opening that extend up the neck for a variable distance.
Complete branchial fistula with internal opening into tonsillar region is rare.
Incidence in India: Unknown. Although branchial fistulas may occur in any age group,
commonly patients present to clinician in first and second decades of life.
Differential diagnosis: sinus from an infected lymph node
Prevention and Counseling: NA
Optimal Diagnostic Criteria, Investigations, Treatment & Referral Criteria
Clinical Diagnosis:
1. History - Diagnosis is usually made clinically. Patient complains of mucopurulent discharge
from an opening in lower lateral part of neck.
2. Examination – A small punctum in the skin at the junction of upper two third and lower one
third of anterior border of sternocleidomastoid muscle.
Investigations:
The tract of fistula can be diagnosed by a dye test or fistulogram and sometimes negative
preoperative test might become positive under general anaesthesia because of muscle relaxation.
Occasionally the fistula tract may be blocked by thick secretions or granulation tissue.
Treatment: Surgical excision
Standard Operating Procedure: As in patient surgery should be performed
Referral Criteria: depends upon competency of operating surgeon and available resources.

72. MOUTH ULCERS

Mouth ulcers are sores or open lesions in the mouth.
Causes, incidence, and risk factors
Mouth ulcers are caused by many disorders. These include:
Canker sores
Gingivostomatitis
Herpes simplex
Leukoplakia
Oral cancer
Oral lichen planus
Oral thrush

The skin lesion of histoplasmosis may also appear as a mouth ulcer.

Canker sores are more common in young adults than in children or older adults.
Symptoms
1. Open sores in the mouth
2. Pain or discomfort in the mouth

The appearance and exact location of lesions varies with the specific disorder.
Signs and tests
A health care provider or dentist usually diagnoses the type of mouth ulcer, based on its
appearance and location. Blood tests or a biopsy of the ulcer may be needed to confirm the
cause.
Treatment
The goal of treatment is to relieve symptoms. The cause, if known, should be treated. Gentle,
thorough oral hygiene may relieve some of the symptoms. Topical (rubbed on) antihistamines,
antacids, corticosteroids, or other soothing preparations may be recommended for applying
directly to the ulcer. Avoid hot or spicy foods, which often increase the pain of mouth ulcers.

73. ACUTE PAROTITIS

Parotitis is an inflammation of one or both parotid glands, the major salivary glands located on
either side of the face, in humans. The parotid gland is the salivary gland most commonly
affected by inflammation.
CAUSES :
Infectious parotitis
Acute bacterial parotitis:
Parotitis as Extrapulmonary Tuberculosis:
Acute viral parotitis (mumps):
HIV parotitis:
Autoimmune causes
These are also collectively known as chronic punctate parotitis or chronic autoimmune parotitis.
Sjögren's syndrome:
Mikulicz disease:
Lymphoepithelial lesion of Godwin:
Blockage
Blockage of the main parotid duct, or one of its branches, is often a primary cause of acute
parotitis, with further inflammation secondary to bacterial superinfection. The blockage may be
from a salivary stone, a mucous plug, or, more rarely, by a tumor, usually benign.
Chronic nonspecific parotitis:
Recurrent parotitis of childhood
Sialadenosis (sialosis):
Sarcoidosis:
Pneumoparotitis:

Symptoms
Abnormal tastes, foul tastes
Decreased ability to open the mouth
Dry mouth
Fever
Mouth or facial pain, especially when eating
Redness over the side of the face or the upper neck
Swelling of the face (particularly in front of the ears, below the jaw, or on the floor of the mouth)

Signs and tests

An examination by the health care provider or dentist shows enlarged salivary glands. Pus may
drain into the mouth. The gland may be painful, particularly with bacterial infections. Viral
infections such as mumps may cause painless swelling of the glands. A CT scan or ultrasound
may be done if the doctor suspects an abscess.
Treatment
In some cases, no treatment is necessary.
If there is pus or a fever, or if the infection is known or thought to be bacterial, antibiotics may
be prescribed. Antibiotics are not effective against viral infections.
If there is an abscess, surgical drainage or aspiration may be done.
Good oral hygiene, with thorough tooth brushing and flossing at least twice per day, may aid
healing and help prevent an infection from spreading. If you are a smoker, stop smoking as it
helps in recovery.
Warm salt water rinses (1/2 teaspoon of salt in one cup of water) may be soothing and keep the
mouth moist.
Drink lots of water and use sugar-free lemon drops to increase the flow of saliva and reduce
swelling. Massaging the gland with heat may help.

74. SUBMANDIBULAR SIALADENITIS

INTRODUCTION:
The submandibular gland, along with the parotid and sublingual glands, comprise the major
salivary glands. The minor salivary glands are scattered along the upper aerodigestive tract,
including the lips, mucosa of the oral cavity, pharynx, and hard palate.
The submandibular gland is the second largest (approximate weight, 10 g) of the major salivary
glands (the parotid gland is the largest). Anatomically, it is situated in the submandibular triangle
of the neck.
DEFINITION:
Sialadenitis of the submandibular gland is a relatively commonly encountered yet infrequently
discussed topic. Causes range from simple infection to autoimmune etiologies.
Causes
Acute sialadenitis
Chronic sialadenitis
Sialolithiasis
Autoimmune sialadenitis
Sialadenosis

Differential Diagnoses
The differential diagnosis of submandibular sialadenitis and sialadenosis includes the following:
1. Infectious (acute) cause - Bacterial or viral disease
2. Inflammatory cause - Sialolithiasis, radiation-induced disease
3. Autoimmune cause - Sjögren disease, lupus
4. Granulomatous cause - Tuberculosis, tularemia, sarcoidosis, catscratch disease, actinomycosis
5. Drug-related cause - Thiourea
6. Neoplastic (benign) cause - Pleomorphic/monomorphic adenoma, oncocytoma, ductal
papilloma, hemangioma, foreign body, ranula, lymphoepithelial cyst
7. Neoplastic (malignant) cause - Adenoid cystic carcinoma, mucoepidermoid carcinoma,
adenocarcinoma, undifferentiated carcinoma, malignant oncocytoma, squamous cell carcinoma
8. Endocrine cause - Hypothyroidism, diabetes mellitus
9. Metabolic cause - Vitamin deficiency, cirrhosis, obesity, bulimia, malabsorption

INVESTIGATIONS
1. Ultrasonography
2. Sialography
3. Computed tomography scanning
4. Magnetic resonance imaging
5. Fine-needle aspiration and biopsy

TREATMENT :
One management scheme is as follows:
1. Acute sialadenitis
1. Medical management - Hydration, antibiotics (oral versus parenteral), warm compresses and
massage, sialogogues
2. Surgical management - Consideration of incision and drainage versus excision of the gland in
cases refractory to antibiotics, incision and drainage with abscess formation, gland excision in
cases of recurrent acute sialadenitis
2. Salivary calculi
1. Medical management - Hydration, compression and massage, antibiotics for the infected gland
2. Surgical management - Duct cannulation with stone removal, gland excision in recurrent cases

75. THYROGLOSSAL DUCT CYST AND FISTULA

Introduction: Thyroglossal duct cyst is a rare but occasional cause of a benign midline neck
mass.
Definition: The cyst is usually located at the midline of the neck. Thyroglossal duct cysts result
from the dilatation of a remnant tract at the site where the primitive thyroid descended from its
origin at the base of the tongue to its permanent location, low in the neck. Failure of subsequent
closure and obliteration of this tract predisposes to thyroglossal cyst formation.
It most often occurs before age 20, but may be found in the older population as well. It is more
common in males. The thyroglossal duct cyst may rupture spontaneously and present as a
draining sinus, which has been erroneously called a thyroglossal fistula, although communication
with foramen caecum (true fistula) is extremely rare.
Incidence in India: Unknown
Differential diagnosis: Dermoid Cyst
Lipoma
Lymph Node
Minor Salivary Gland Tumour
Sebaceous Cyst
Hypertrophied Pyramidal Lobe
Prevention and Counseling: NA
Optimal Diagnostic Criteria, Investigations, Treatment & Referral Criteria
Clinical Diagnosis: Diagnosis is usually made clinically. Thyroglossal duct cysts most often
present with a palpable asymptomatic midline neck mass at or below the level of the hyoid bone.
The neck mass moves with swallowing and on protrusion of tongue. Some patients will have
neck or throat pain, or dysphagia (difficulty in swallowing).
Investigations:
1. Fine needle aspiration cytology
2. Ultrasound,thyroid function tests to ensure nomal thyroid gland
3. Radionuclide scanning if normal thyroid not located

Treatment: Excision (Sistrunks operation). The intimate association of the tract with hyoid bone
mandates simultaneous removal of the central portion of the hyoid bone to ensure complete
removal of the tract.
Standard Operating Procedure: As In patient the surgery should be performed
Referral Criteria: depends upon competency of operating surgeon and available resources.

76. ACUTE LARYNGOTRACHEO BRONCHITIS

Introduction:
Acute laryngotracheo bronchitis or Croup is most of the times a viral infection caused by
parainfluenza type 1 and 2 virus in children between 6months to 3years of age. Secondary
bacterial infection by gram positive cocci may occur.
Definition:
It is an inflammatory condition of the larynx, trachea and bronchi.
Differetial diagnosis:
It has to be differentiated from acute epiglottitis.
Acute epiglottitisAcutelaryngotracheobronchitis
H.influenza type b Parainfluenza type 1 and 2
2-7years of age 3months to 3years
Supra glottis involved subglottic area
No prodromal symptoms prodromal symptoms present
Sudden onset slow onset
High grade fever low grade or no fever
Cough absent present barking seal like cough
Stridor present present
Odynophagia present absent
Thumb sign on lateral view steeple sign- anteroposterior view
Clinical diagnosis:
Hoarseness of voice, croupy cough, fever, inspiratory stridor, suprasternal, intercostal recession.
Steeple sign on anteroposterior radiograph of neck. Examination of larynx is avoided, it may
precipitate complete obstruction.
Investigations:
Complete blood count,serum electrolytes, radiograph of neck and chest.
Treatment:
Intravenous antibiotics, humidification, parenteral fluids, streroids to relieve oedema, racemic
adrenaline via respirator, intubation/tracheostomy if respiratory obstruction increases despite of
medical management. Tracheostomy if intubation is required beyond 72hours.

77. ADENOIDITIS
Introduction:
The nasopharyngeal tonsils, commonly called “adenoids” are situated at the junction of roof and
posterior wall of the nasopharynx. Adenoid tissue is present at birth, shows physiological
enlargement upto the age of six years, and then tends to atrophy at puberty and almost
completely disappears by the age of 20.
Definition:
Adenoiditis is the infection of the adenoids. Enlarged and infected adenoids may cause nasal
obstruction, mouth breathing, nasal discharge, sinusitis, epistaxis, change of voice, Eustachian
tube blockage leading to conductive hearing loss, recurrent attacks of acute otitis media, serous
otitis media, typical facial appearance known as adenoid facies, pulmonary hypertension in long
standing cases.
Differential Diagnosis:
1.Congenital
2.Infection- bacterial, viral
3.Allergy
4.Malignancy- adenoid cystic carcinoma
5.Nasopharyngealangiofibroma
6.Causes of nasal obstruction

Clinical Diagnosis:
History, general examination, local examination with posterior rhinoscopy mirror, flexible or
rigid nasopharyngoscope, lateral radiograph nasopharynx.
Investigations:
Complete blood count, blood grouping, prothombin time, bleeding time, clotting time,serum
electrolytes, renal and liver function tests,xray chest and nasopharynx, electrocardiogram.
Treatment:
When symptoms are not marked breathing exercises, decongestant nasal drops and
antihistaminics. When symptoms are marked adenoidectomy is done.
Adenoidectomy is the standard operating procedure. Done under general anesthesia with oral
intubation. Boyle davis mouth gag is inserted, adenoids palpated digitally and removed with the
help of adenoid curette with and without guard. Hemostasis is achieved by packing the area for
sometime.

78. CHRONIC LARYNGITIS

Chronic Laryngitis Without Hyperplasia
It is a diffuse inflammatory condition symmetrically involving the whole larynx, i.e. true cords,
ventricular bands, and root of the epiglottis.
Aetiology
1. It may follow incompletely resolved acute simple laryngitis or its recurrent attacks.
2. Presence of chronic infection in paranasal sinuses, teeth and tonsils .
3. Occupatonal factors, e.g. exposure to dust and fumes such as in miners, strokers, gold or iron
smiths and workers in chemical industries.
4. Smoking and alcohol.
5. Persistent trauma of cough as in chronic lung disease.
6. Vocal abuse.

Clinical Features
1. Hoarseness. This is the commonest complaint.
2. Constant hawking. There is dryness and intermittent tickling in the throat and patient is
complited to clear the throat repeatedly.
3. Discomfort in the throat.
4. Cough. It is dry and irritating.

Treatment
1. Eliminate infection of upper or lower respiratory tract. Infection in the sinuses, tonsils, teeth or
chronic chest infection should be treated.
2. Avoidance of irritating factors, e.g.smoking, alcohol or polluted environment.
3. Voice rest and speech therapy.Voice rest has to be prolonged for weeks or months.
4. Steam inhalations.They help to loosen secretions and give relief.
5. Expectorants.They help to loosen viscid secretions and give relief from hawking.

Chronic Hypertrophic laryngitis

It may be either a diffuse and symmetrical process or a localised one, the latter appearing like a
tumour of the larynx.
Aetiology
Same as discussed under chronic laryngitis without
Hyperplasia.
Pathology
Pathological changes starts in the glottis region and later may extend to ventricular bands base of
epiglottis and even subglottis .
Initially there is hyperaemia ,oedema and cellular infiltration in the submucosa. The mucous
glands suffer hypertrophy at first but later undergo atrophy with diminished secretion and
dryness of larynx.
Clinical features
This disease mostly affects males (8:1) in the age group of 30-50 years.
Hoarseness ,constant desire to clear the throat, dry cough and discomfort in throat when the
voice has been used for an extended period of time, are the commom presenting symptoms.
Examination:
On examination, changes are often diffuse and symmetrical.
1. Laryngeal mucosa, in general, is dusky red and thickened.
2. Vocal cords appear red and swollen.
3. Ventricular bands appear red and swollen and may be mistaken for prolapsed or eversion of
the ventricle.
4. Mobility of cords gets impaired due to oedema and infiltration, and later due to muscular
atrophy or arthritis of the cricoarytenoid joint.

Treatment
Conservative: Same as for chronic laryngitis without hyperplasia.
Surgical: Stripping of vocal cords, removing the hyperplastic and oedematous mucosa, may be
done in selected cases.Damage to underlying vocal ligament should be carefully avoided. One
cord is operated at a time.

79. BENIGN LESIONS OF LARYNX

TYPES
Solid lesions
1. Vocal nodule
2. Vocal polyp
3. Reinke’s oedema
4. Contact ulcer
5. Intubation granuloma
6. Leukoplakia or keratosis
Cystic lesions

Vocal cord nodule

Vocal cord nodule is a mass of tissue that grows on the vocal folds (vocal cords). Typically this
mass will appear on the junction of the anterior and middle two-thirds of the vocal fold, where
contact is most forceful.
Vocal cord polyp
A polyp is usually a red or reddish lesion that has a sharp margin and is clearly different from
surrounding tissue. It can be either broad-based or narrow-necked. It may be smooth and round,
or it may have lobes. Some polyps that have been present for a long time can take on odd shapes.
There is a lot of variability in size. Polyps may occur singly or in pairs, one on each vocal fold
directly opposite one another. Almost always, they occur at the midpoint of the vocal fold.
Reinke's edema
Reinke's edema, also known as polypoid degeneration, is the swelling of the vocal folds due to
fluid collection (edema).
Granuloma
A granuloma is a benign growth that results from irritation or trauma. It is usually found at the
back of the vocal fold, over a part of cartilage called the vocal process which lies just underneath
the membrane covering the larynx.
Contact Ulcer
Contact granuloma, also known as a contact ulcer, is a condition where an ulcer is found in the
vocal fold. The most common cause of the condition is sustained periods of increased pressure
on the vocal folds, and is commonly seen in people who use their voice excessively.
Gastroesophageal reflux disease is also thought to be a contributing factor in the development of
contact ulcers.
Treatment :
5. Voice rest,
6. To remove the source of the irritant (e.g. smoking cessation, vocal rest, etc.).
7. Microlaryngoscopic surger

80. DEEP NECK SPACE INFECTION

INTRODUCTION
Deep neck space infections most commonly arise from a septic focus of the mandibular teeth,
tonsils, parotid gland, deep cervical lymph nodes, middle ear, or sinuses. These deep cervical
space infections have become relatively uncommon in the postantibiotic era. Consequently,
many clinicians are unfamiliar with these conditions. In addition, with widespread use of
antibiotics and/or profound immunosuppression, the classic manifestations of these infections,
such as high fever, systemic toxicity, and local signs of erythema, edema, and fluctuance, may be
absent.
Deep neck space infections often have a rapid onset and can progress to life-threatening
complications. Thus, clinicians must be aware of such infections and should not underestimate
their potential extent or severity.
SPACES:
Submandibular space
Parapharyngeal space
Retropharyngeal space
Prevertebral space
Peritonsillar space
Parotid space
Potential routes of spread — The deep cervical fascial spaces are normally bound together by
loose connective tissue and intercommunicate to varied degrees. A thorough understanding of
the potential anatomic routes of infection not only provides valuable information on the nature
and extent of infection but also suggests the optimal surgical approach for effective drainage.
CLINICAL FEATURES
A. Peritonsillar, parotid, parapharyngeal, and submandibular abscesses are generally associated
with sore throat and trismus (the inability to open the jaw). Trismus indicates pressure or
infection of the muscles of mastication (the masseter and the pterygoids) or involvement of the
motor branch of the trigeminal nerve. Findings on physical examination include swelling of the
face and neck, erythema, and purulent oral discharge. There may be pooling of saliva in the
mouth and asymmetry of the oropharynx. Lymphadenopathy is usually present.
B. Dysphagia and odynophagia are secondary to inflammation of the cricoarytenoid joints.
C. Dysphonia and hoarseness are late findings in neck infections and may indicate involvement
of the tenth cranial nerve
D. Unilateral tongue paresis indicates involvement of the twelfth cranial nerve.
E. Stridor and dyspnea signify airway obstruction and may be manifestations of local pressure or
spread of infection to the mediastinum.

INVESTIGATION
IMAGING
Computed tomography (CT) is the imaging modality of choice for the diagnosis of deep neck
space infections . CT allows the critical evaluation of soft tissues and especially bone from a
single exposure. In addition, the axial imaging format of CT is particularly well suited to the
head and neck. Because CT can localize a process and define its extent, particularly extension
into the mediastinum or the cranial vault, it is also an invaluable tool for planning and guiding
aspiration for culture or open drainage.
Magnetic resonance imaging (MRI) is useful for assessing the extent of soft tissue involvement
and for delineating vascular complications. However, MRI takes significantly longer than CT to
obtain good quality images, which may cause discomfort or claustrophobia. In addition,
individuals with certain implanted devices cannot undergo MRI.
Plain radiography is of limited utility for the evaluation of deep neck space infections; it is
sometimes helpful for detecting retropharyngeal swelling or epiglottitis
TREATMENT — Appropriate antibiotics in conjunction with surgical drainage of loculated
infection are essential for a successful outcome of deep neck space infections.

81. FOREIGN BODY IN AERODIGESTIVE TRACT

Introduction:
Foreign body aspirated into air passage can lodge in the larynx, trachea or bronchi. Children
below 4 years are more often affected. Non irritating foreign bodies like plastic, glass or metalls
may remain symptomless for a long time. Irritating foreign bodies(vegetative) like peanuts,
beans, seeds, etc gives a diffuse violent reaction leading to congestion and oedema of
tracheobronchial mucosa-vegetal bronchitis
Symptoms:
Choking, gaging, wheezing: lasts for short time. Foreign body can be cuffed out or it may
lodgein arynx or tracheobronchial tree.
Symptomless interval
Later symptoms depend on site of its lodgement:
→Laryngeal: Large foreign body complete can lead to sudden death
Partial: pain, harseness, croupy cough,aphonia, dyspnoea, wheezing and hemopptysis.
→Traheal: loose- palpatory thud, audible slap
→Bronchial:Right>left. Can lead to atelectasis or check valve
Diagnosis:
Xray
Fluoroscopy
CT scan
Bronchograms
D/D
Acute laryngotraheo bronchitis
Acute Simple laryngitis
Laryngismus Striduluz
Management:
Antibiotics
Steroids
Laryngeal Foreign Body:
In complete obstruction Pound on back, turn patient upside down, follow Heimlichs
Manoeuvre(stand behind the person¸and place your arms around his lower chest and give four
abdominal thrusts)
If this fails: Cricothyrotomy or emergency tracheostomy
Once acute respiratory emergency is over: Direct laryngoscopy/ laryngofissure
Tracheal/Bronchial Foreign bodies:
→Conventional rigid Bronchoscope
→Rigid Bronchoscope with telescopic aid
→Bronchoscopy with C arm fluroscopy
→Dormia Basket/ Fogarthy Balloon
→Thoracotomy and bronchotomy for peripheral foregn bodies
→Flexible Fibre optic bronchoscopy

82. GOITRE
A goiter or goitre (Latin gutteria, struma), is a swelling in the thyroid gland which can lead to a
swelling of the neck or larynx (voice box). Goitre rarely occurs when the thyroid gland is
functioning properly. Worldwide, over 90% cases of goitre are caused by iodine deficiency.
Classification :
They can be classified in several ways by morphology, appearance, cause and other
characteristics.
Non-Toxic:
1. Simple (struma diffuse)
2. Multinodular (struma nodosa)
3. Uninodular (struma uninodosa)
Toxic:
1. Diffuse (Graves)
2. Toxic multinodular
3. Toxic nodule
Special:
1. Cancer
2. Thyroiditides
3. Inflammatory
Various causes:
1. Chronic infection
2. Actinomycosis
3. Amyloidosis

Other type of classification:

1. Class I - palpation struma - in normal posture of the head, it cannot be seen; it is only found by
palpation.
2. Class II - the struma is palpative and can be easily seen.
3. Class III - the struma is very large and is retrosternal; pressure results in compression marks.

Causes :
Worldwide, the most common cause for goiter is iodine deficiency. Selenium deficiency is also
considered a contributing factor. In countries that use iodized salt, Hashimoto's thyroiditis is the
most common cause.
Further causes include
1. Thyroid autonomy
2. Autoimmune conditions of the thyroid (Hashimoto thyroiditis, Morbus Basedow)
3. Medications and substances such as lithium, antithyroid agents, thyocyanate
4. Inflammations (thyroiditis)
5. Cysts
6. Benign and malignant neoplasms
7. Pituitary problems
8. Acromegaly
9. Thyroid hormone insenstitvity
10. Sarcoidosis, amyloidosis
11. Hydatiform mole

Signs and symptoms :

Goiter associated with hypothyroidism or hyperthyroidism may present with symptoms of the
underlying disorder although the symptoms are often unspecific and hard to Diagnose.
Goiter not associated with hormonal abnormalities will not cause any symptoms aside from the
presence of anterior neck mass. However, for particularly large masses, compression of the local
structures may result in difficulty in breathing or swallowing. In those presenting with these
symptoms, malignancy must be considered.
Toxic goiters will present with symptoms of thyrotoxicosis such as palpitations, hyperactivity,
weight loss despite increased appetite, and heat intolerance.
Treatment :
Goiter caused by suspected iodine deficiency is very frequently treated by a combination of
levothyroxine and iodine supplementation depending on thyroid hormone levels.
Treatment may not be necessary if the goiter is small. Goiter may be related to hyper- and
hypothyroidism (especially Graves' disease) and may be reversed by treatment. Graves' disease
can be corrected with antithyroid drugs (such as propylthiouracil and methimazole),
thyroidectomy (surgical removal of the thyroid gland), and iodine-131 (131I - a radioactive
isotope of iodine that is absorbed by the thyroid gland and destroys it). Hypothyroidism may
raise the risk of goiter because it usually increases the production of TRH and TSH.
Levothyroxine, used to treat hypothyroidism, can also be used in euthyroid patients for the
treatment of goitre. Levothyroxine suppressive therapy decreases the production of TRH and
TSH and may reduce goiter, thyroid nodules, and thyroid cancer. Blood tests are needed to
ensure that TSH is still in range and the patient has not become subclinically hyperthyroid. If
TSH levels are not carefully monitored and allowed to remain far below the lower limits of
normal (below 0.1 mIU/L or IU/mL), there is epidemiologic evidence that levothyroxine may
increase the risk of osteoporosis and both hip and spinal fractures.[4] (Such low levels are
therefore not intentionally produced for long periods, except occasionally in the treatment of
TSH-dependent thyroid cancers.)
Thyroidectomy with 131I may be necessary in euthyroid goitrous patients who do not respond to
levothyroxine treatment, especially if the patients have difficulty breathing or swallowing. 131I,
with or without the pre-injection of synthetic TSH, can relieve obstruction and reduce the size of
the goitre by thirty to sixty-five percent. Depending on how large the goitre is and how much of
the thyroid gland must be removed or destroyed, thyroidectomy and/or 131I treatment may
destroy enough thyroid tissue as to produce hypothyroidism, requiring life-long treatment with
thyroid hormone pills.

83. LARYNGOPHARYNGEAL REFLUX (LPR)

INTRODUCTION ;
Laryngopharyngeal reflux (LPR), also extraesophageal reflux disease (EERD) refers to
retrograde flow of gastric contents to the upper aero-digestive tract, which causes a variety of
symptoms, such as cough, hoarseness, and asthma, among others.
Although heartburn is a primary symptom among people with gastroesophageal reflux disease
(GERD), heartburn is present in fewer than 50% of the patients with LPR. Other terms used to
describe this condition include atypical reflux, and supraesophageal (or supra-esophageal) reflux.
Signs and symptoms :
Extraesophageal symptoms are the result of exposure of the upper aerodigestive tract to the
gastric juice. This causes a variety of symptoms, including hoarseness, postnasal drip, sore
throat, difficulty swallowing, indigestion, wheezing, chronic cough, globus pharyngis and
chronic throat-clearing.
Diagnosis :
As there are multiple potential etiologies for the respiratory and laryngeal symptoms,
establishing LPR as the cause based on symptoms alone is unreliable. Further laryngoscopic
findings such as erythema, edema, laryngeal granulomas, and interarytenoid hypertrophy have
been used to establish the diagnosis; but these findings are very nonspecific, and have been
described in the majority of asymptomatic subjects undergoing laryngoscopy. Response to acid-
suppression therapy has been suggested as a diagnostic tool for confirming diagnosis of LPR, but
studies have shown that the response to empirical trials of such therapy (as with proton-pump
inhibitors) in these patients is often disappointing.
Treatment :
Management of symptoms for patients within this subgroup of the GERD spectrum is difficult.
Several studies have emphasized the importance of measuring proximal esophageal, or, ideally,
pharyngeal acid exposure in patients with clinical symptoms of LPR, to document reflux as the
cause of the symptoms. Once these patients are identified, Nissen fundoplication should be
offered to the patients in the early phase of disease, as medical treatments often don’t provide
any benefit, and a delay in referring patients for surgical treatment is associated with poor
outcome

83. ACUTE PHARYNGITIS

INTRODUCTION : It is acute inflammation of pharynx.
AETIOLOGY:
VIRAL:
Rhinovirus
Influenza
Parainfluenza
Measles
Chickenpox
Harpes simplex

BACTERIAL
1. Streptococcus
2. Diphtheria
3. Gonococcus
FUNGAL
1. Candida albicans

CLINICAL FEATURES
1. Mild phyaryngitis : Discomfort in throat ,malaise,low grade fever
2. Moderate tosevere : Pain in throat ,malaise,dysphagia,headache,high fever,phyaryng show
erythema,exudates,enlargement of tonsils and lymphoid follicles on the posterior phyryngeal
wall
3. Very severe : Oedema of soft palate and uvula with enlargement of cervical nodes

DIAGNOSIS
1. Culture of throat swab is helpful in the diagnosis of bacterial pharyngitis.Itcan detect 90% of
group A Streptococci.Diphtheria is cultured of special media.Swab from a suspected case of
gonococcal phyaryngitis should be cultured immediately without delay.

TREATMENT
1. General measures : Bed rest ,plenty of fluids,warm saline gargles or pharyngeal irrigations and
analgesics form the mainstay of treatment.
2. Specific treatment :
3. Streptococcal pharyngitis treated with penicillin G
4. Dipthera is treated with penicillin and arythromycin
5. Gonococcal treated with tetracyclin
6. Fungal pharyngitis : Nystatin is the drug of choice

THE VIRAL INFECTION CAUSING PHARYNGITIS

Herpangina : It is caused by group A coxsackie virus and mostly affects children. Characteristic
features include fever,sore throat and vesicular eruption on the soft palate and pillars. Vesicles
are small and surrounded by a zone of erythema.
Infectious mononucleosis : It is caused by Epstein-Barr virus.It affects older children and young
adults, and is characterised by fever ,sore throat, exudative pharyngitis,Lymphadenopathy,
splenomegaly and hepatitis.
Cytomegalovirus : It most affects immunosuppressed transplant patients.Clinically,it mimics
infectious mononucieosis but heterophil antibody test is negative.
Measles and chickenpox : Measles is characterised by the appearance of Koplik’s spots on the
buccal mucosa opposite the molar teeth.The spots appear 3-4 days before the appearance of rash.

84. CARCINOMA ORAL CAVITY

Introduction-
Tumours of lips and oral cavity often present a significant problem to the surgeon with regards to
early diagnosis and staging, access for resection and reconstruction of both soft tissues and bone.
Tumour of lips are now included within the UICC classification for oral cavity tumours.
Surgical Anatomy-
Anatomic Sites and Subsites for Lip and Oral Cavity-
Lip
External upper lip (vermilion border)
External lower lip (vermilion border)
Commissure
Oral Cavity
Buccal mucosa
Mucosa of upper and lower lips
Cheek mucosa
Retromolar areas
Bucco-alveolar sulci, upper and lower (vestibule of mouth)
Upper alveolus and gingiva (upper gum)
Lower alveolus and gingiva (lower gum)
Hard palate
Tongue
Dorsal surface and lateral borders anterior to circumvallate papillae (anterior two thirds)
Inferior (ventral) surface

Floor of mouth
Epidemiology-
The lip is the most common site of cancer in the mouth. It is most common in white people and
approximately 93% of the tumour present in the lower lip and the male to female ratio 80:1. The
most common tumour is squamous cell carcinoma.
In case of oral cavity cancer an estimated 387500 new cases are diagnosed annually worldwide.
It constitutes 30-40% of head and neck cancer in India and the country ranks among the top few
in the world in the incidence of these cancers. Buccal mucosa is a common subsite in Indian
population, probably aided by the chewing habit that is prevalent in this country. In India, buccal
mucosa cancer is the most common cancer in men and third most common cancer in women.
The oral cancers assume importance in the cancer control programme of the country because of
its impact on the overall health of the population as well as potential as a target for early
detection and prevention
Predisposing Factors-
 between
redox-active metals in saliva and the low reactive free radicals in cigarette smoke. The incidence
of oral cavity cancers in persons who smoke is approximately 6 times that of those who do not. It
causes sequential histological changes in oral mucosa. Over a prolonged period of exposure,
these changes eventually lead to neoplastic transformation.
- alcohol beverages may contain carcinogens or pro-carcinogens
including nitrosamine and urethane contaminants and ethanol. Ethanol is metabolized by alcohol
dehydrogenage and to some extent by cytochrome p450 to acetaldehyde, which may be
carcinogenic. The combined effect of alcohol and cigarette is synergistic. The risk for a person
who smokes and drink is 15 that of an individual who neither habit.
- it cause damage to buccal mucosa.

Precancerous Conditions-
Oral cancer can occur as denovo or on existing pre-malignant conditions. These include-
1. Leucoplakia- this is a clinical term without a definitive histological definition. Leukoplakia is
a white mucosal based keratotic plaque that cannot be wiped free from the underlying tissue. It is
defined as white patch in oral mucosa that cannot be characterized clinically or pathologically as
any other disease. Most frequent sites are the buccal mucosa and the commissures. Leukoplakia
with epithelial dysplasia (20%) is found to have greater chance of malignant transformation.
Only 6% of lesion eventually progressed to SSC. A biopsy is indicated if the lesion is suspicious.
2. Erythroleukaplakia- the associated risk for malignant transformation is greater than
leukoplakia.
3. Submucosal fibrosis- most frequently encountered in individuals who chew betel nut, or poor
oral hygiene, or periodontitis. The risk of developing oral carcinoma is 7.6% over a 10 year
period.
4. Lichen planus- it also been associated with the development of oral carcinoma.
Symptoms of Oral Cancer-
hite or red patches in your mouth

Differential Diagnosis-
1. Chronic non-healing ulcer in oral cavity- characteristic findings in favor of malignant ulcer
are-

otic debries and looks dirty gray

3. Pre-malignant conditions like leukoplakia and erytholeukoplakia

TNM Staging-
T1: Tumor 2 cm or less in greatest dimension
T2: Tumor more than 2 cm but not more than 4 cm in greatest dimension
T3: Tumor more than 4 cm in greatest dimension
T4a: Moderately advanced local disease. Lip: Tumor invades through cortical bone, inferior
alveolar nerve, floor of mouth, or skin of face, ie, chin or nose
Oral cavity: Tumor invades adjacent structures only (eg, through cortical bone [mandible,
maxilla], into deep [extrinsic] muscle of tongue [genioglossus, hyoglossus, palatoglossus, and
styloglossus], maxillary sinus, skin of face)
T4b: Very advanced local disease. Tumor invades masticator space, pterygoid plates, or skull
base, and/or encases internal carotid artery
Prognostic Markers-
Various features of the cancer allow to prognosticate the outcome of the treatment.

-stage
- chance of nodal metastasis is maximum with tumour thickness >5mm.
- the chance of treatment failure is high when the margin of resection is
closed (<5mm) or involve.

Evaluation-
1. History & Examination - Almost 90% of the cancers are of squamous cell variety. Buccal
mucosa is the most common site affected in India. The sump area or ‘coffin corner’ at the
posterior tongue/ floor of the mouth is a common site for cancer but may be missed by cursory
inspection. So, a through history and physical examination is very important for its early
detection.
2. Biopsy can be taken at OPD if lesion is large otherwise it can be taken under GA.
3. Endoscopies can be carried out to rule out other synchronous malignancy.
4. Chest imaging, CT/MRI if indicated.
5. Preanesthesia studies.
6. Dental evaluation.
Treatment protocol-
1. For T1–2, N0 disease
a) Excision of primary (preferred) ± unilateral or bilateral selective neck dissection.

- If it is associated with No adverse features like (extracapsular nodal spread, positive margins,
pT3 or pT4 primary, N2 or N3 nodal disease, nodal disease in levels IV or V, perineural
invasion, vascular embolism) then only follow up is required.
- If it is associated with one positive node without adverse feature RT can be given optional. If it
is associated Adverse features then planned for Re-excision or Chemo/RT and follow up.
b) An alternative to surgery - External-beam RT ± brachytherapy 70 Gy to primary 50 Gy to
neck at risk.
- If pt came with No residual disease then follow up is required.
- If pt landed with Residual disease then Salvage surgery can be better choice.
2. For T3, N0 disease Excision of primary and reconstruction as indicated and unilateral or
bilateral selective neck dissection is the treatment of choice.
- If it is associated with No adverse features like (extracapsular nodal spread, positive margins,
pT3 or pT4 primary, N2 or N3 nodal disease, nodal disease in levels IV or V, perineural
invasion, vascular embolism) RT can be given optional.
- If it is associated adverse features then planned for Re-excision or Chemo/RT and follow up.
3. T4a, Any N; T1-3, N1-3 disease Surgery is treatment of choice.
a) For N0, N1, N2a-b, N3 Excision of primary, ipsilateral comprehensive neck dissection ±
contralateral selective neck dissection (reconstruction as indicated) can be considered.
b) For N2c (bilateral) disease Excision of primary and bilateral comprehensive neck dissection
(reconstruction as indicated) can be planned.

- In both cases if there are No adverse features RTc (optional) can be given and then follow up.
- If it is associated Adverse features (extracapsular nodal spread, positive margins, pT3 or pT4
primary, N2 or N3 nodal disease, nodal disease in levels IV or V, perineural invasion, vascular
embolism) then planned for Re-excision or Chemo/RT and follow up.
Treatment Protocol for Pre-Malignant Lesion-
1. Full history and examination.
2. Biopsy
a) Biopsy negative- Discharge
b) Leukoplakia and other pre-malignant lesion- Excision biopsy, Laser etc- Follow up in H & N
clinic
c) Other pathology like Lichen planus, candidiasis- Oral medication
d) Biopsy positive- EUA and imaging- Definitive treatment
Preventive Measures-

-healing ulcer mouth

85. CARCINOMA HYPOPHARYNX
Introduction- Hypopharynx is a highly important anatomical site as physiologically it is a
component upper aero-digestive tract and it also represents a common conduit for both
respiration and deglutition. Hence, any tumor or treatment of tumors in this area will produce
disturbances in swallowing and inevitable aspiration. Tumors arising in this area often present in
advanced state and so, key to cure lies in early and accurate diagnosis and prompt treatment.
Surgical Anatomy- It is triangular space extending from the level of hyoid bone above to the
lower border of cricoid cartilage below. The hypopharynx consists of three regions- pyriform
sinus on each side, the posterior pharyngeal wall, and the post cricoid region.
Pyriform sinus (PFS)- It represents channels formed on either side of the larynx. It is bounded by
pharyngoepiglottic fold superiorly, the apex inferiorly, thyroid cartilage laterally and
hypopharyngeal surface of AE fold medially.
Posterior pharyngeal wall- It extends form floor of ventricle superiorly to inferior border of
cricoids cartilage inferiorly and from one apex of PFS to the other.
Post-cricoid region- It extends from at the level of arytenoids cartilage and connecting folds to
inferior border of cricoids cartilage.
The hypopharynx is lined throughout by squamous epithelium. The pyriform sinus has rich
lymphatic supply. In general, the lymphatic in this area drain in deep cervical lymph node at
level IV but inferior part of PFS and post cricoid area also drain in paratracheal lymph node in
level VI and posterior pharyngeal wall drain in retropharyngeal area.
Almost all carcinoma of hypopharynx are SSC carcinoma in type. PFS comprise maximum of
around 50% of total, postcricoid tumors make up around 40% and posterior pharyngeal wall
make up remaining around 10%. Tumors of PFS can be divided into those which primarily
involve the lateral wall or the medial wall. Those arising from medial wall are more extensive
and involve AE fold and paraglottic space and can therefore fix the hemilarynx on that side.
Occasionally it can involve postcricoid area where vocal cord fixation can occur if
cricoarytenoid joint is involved.
As PFS is rich in lymphatic supply, 70-75% patients of pyriform fossa tumor have palpable neck
mass at presentation which usually involve level II-IV deep cervical node and 5% have bilateral
node at presentation.
Epidemiology- Age specific incidence of pharyngeal cancer show an increase risk of developing
disease with increasing age for both men and women. Postcricoid tumors remain the only SSC of
head and neck that is more common in women. The overall incidence of tumor in UK is
approximately 1-3 per 100000.
Etiological Factors-
Alcohol and tobacco remain the two principal carcinogen implicated in the tumors of the upper
aerodigestive tract, to include the hypopharynx and they are synergistic to each other. A major
dietary risk factor (iron deficiency) in relation to postcricoid carcinoma has been described
particularly in patients with Plummer-Vinson syndrome. This syndrome is associated with
anemia, glossitis, esophageal web, koilonychias and achlorhydria. Some also have a history of
radiation to the neck.
Symptomatology-
phagia

The clinical picture caused by a large tumor is often unmistakable, but in the early stages the
symptoms may be indefinite. Whilst the feeling of lump in the throat, which is worse on
swallowing saliva is rarely of serious significance (e.g globus pharyngicus) or persistent
soreness, should always be treated with extreme suspicion, especially in elderly patients who
smoke and drink. Persistent pharyngeal pain is nearly always a sinister symptom and if
associated with malignancy it reflects deep invasion in larynx and pharyngeal structures. It is
often associated with referred pain to ipsilateral ear.
Differential Diagnosis-
1. Globus pharyngicus- It usually presents in young women as a sensation of a lump in throat in
midline between hyoid and suprasternal notch but more commonly at cricoid level. It is
intermittent and typically occurring between meals, when swallowing saliva, in the evening or
during stress and, although uncomfortable but never painful.
2. Pharyngeal oesophageal motility disorder- in patients with throat symptoms who have no
abnormality found on examination and investigation and diagnosis can be confirmed by barium
video fluoroscopic swallow examination.
3. Benign tumors like Leiomyomas common in hypopharynx and upper oesophagus.
4. Lipomas and fibrolipomas occur occasionally.

TNM CLASSIFICATION-
T1 Tumor size ≤ 2 cm and limited to one sub-site
T2 Tumor size > 2 but ≤ 4 cm or more than one sub-site
T3 Tumor size > 4 cm or hemilarynx fixation
T4a Tumor invades Thyroid / cricoid cartilage, hyoid bone, thyroid gland esophagus, central
compartment soft tissue
T4b Prevertebral fascia, mediastinal structures, Internal carotid artery
Work up- History and physical examination, Biopsy ,HPV testing suggested, Chest imaging, CT
with contrast or MRI or PETCT and CT with contrast of primary and neck, Dental evaluation,
including panorex as indicated, Speech & swallowing evaluation as indicated, Examination
under anesthesia with endoscopy and Pre-anesthesia studies.
Examination - All patients presenting with a throat complaint or a mass in the neck requires a
full head and neck and general examination. Patients can be examined in OPD using either
indirect laryngoscopy, a rigid Hopkin’s endoscope or FOL passed through the nose. Particular
attention should be paid to obvious swelling or ulceration and also to the presence of pooling of
saliva in pyriform fossa (Chevalier Jackson’s sign) and oedema of arytenoids. Presence or
absence of laryngeal crepitus should be look for. Absence of crepitus means any postcricoid or
posterior pharyngeal wall involvement.
It is important to carry out any imaging studies prior to endoscopy and biopsy if possible since
FNAC; endoscopic and open biopsy can all create artifactual features on both CT and MRI.
Specific Uses of Imaging-

paraglottic space
Barium swallows extremely useful investigation in tumour involving postcricoid and cervical
oesophagus.
Treatment Protocol-
1. T1, N0, selected T2, N0 (not requiring total laryngectomy) disease -
a) Definitive RT can be considered
- If Primary site: complete response then only follow up is required. - If pt presented with
Primary site: residual tumor then Salvage surgery + neck dissection as indicated.
b) Alternatively Surgery: Partial laryngopharyngectomy (open or endoscopic) + Ipsilateral or
bilateral selective neck dissection is the treatment of choice.
- If there are no adverse features like extracapsular nodal spread, positive margins, pT3 or pT4
primary, N2 or N3 nodal disease, Perineural invasion, vascular embolism only follows up is
required.
- With Adverse features Chemo/RT can be consider.
2. T1, N+; T2-3, any N (if total laryngectomy required) disease –

a) Induction chemotherapy x 2 cycles and follow-up.

- If Primary site: Complete response then Definitive RT can be considered.
- If patient presents with residual tumor in neck then Neck dissection can be done.
- If primary site: Partial response then planned for Induction Chemotherapy 3rd cycle and follow
up.
- If primary site: CR then Definitive RT can be considered.
- Primary site: PR then Chemo/RT and follow up
- If CR: only observation required.
- If Primary site: < PR then planned for Surgery.
- If pt is having no adverse features RT can be considered.
- With any adverse features Chemo/RT can be given.
b) An alternative to induction chemotherapy - surgery Laryngopharyngectomy + selective (N0)
or comprehensive (N+) neck dissection, including level VI can be consider.
- Patient with no adverse features only follow-up required
- With adverse features Chemo/RT and follow up required.
c) Third option is CCRT.
- If Primary site: complete response but with Residual tumor in neck then Neck dissection can be
consider.
- In case of complete response of neck then Post-treatment evaluation (minimum 12 wks) with
PET, Contrast-enhanced CT or MRI and physical exam is required. - If inv are negative only
observation is required. And if inv are positive then Neck dissection is considered.
- If patient presented with Primary site: residual tumor then Salvage surgery + neck dissection as
indicated.
3. For T4a, any N disease –
a) Surgery + comprehensive neck dissection (preferred) is treatment of choice followed by RT or
Chemo/RT.

b) Or alternatively Induction chemotherapy x 3 cycles and follow-up.

- If patient presented with Primary site: CR or PR and stable disease in neck then consider
Chemo/RT.
- If Primary site: complete response but Residual tumor in neck then Neck dissection can be
consider.
- If patient presented with Primary site: residual tumor after chemo/RT then Salvage surgery +
neck dissection as indicated.
- If pt presented with Primary site: < PR or progression in neck after NACT then Salvage surgery
+ neck dissection as indicated.
c) Third option is CCRT.
- If patient presented with Primary site: complete response but Residual Tumor in neck then
Neck dissection can be considered.
- If pt presented with Primary site: residual tumor Salvage surgery + neck dissection is indicated.
Prognostic Factors-
 olve

5 year survival rates in the Liverpool series-

- 31%
- 29%
- 20%

Prevention And Counseling- Abstinence of alcohol and cessation of smoking is first and
foremost for prevention.

87. CERVICAL LYMPHADENOPATHY

Introduction-
Lymphadenopathy is an abnormal increase in size and/ or altered consistency of lymph nodes. It
is a clinical manifestation of regional or systemic disease and serves as an excellent clue to the
underlying disease. Cervical lymphadenopathy (C.L.) is a fairly common clinical presentation.
Surgical anatomy and classification - Cervical lymph nodes are lymph nodes found in the neck.
There are approximately 300 lymph nodes in the neck
Cervical lymph nodes are classifieds into 7 groups. They are-
bmental and submandibular nodes
o Level Ia: Submental triangle
o Level Ib: Submandibular triangle
 -tracheal, pre-laryngeal and post-tracheal

Incidence
- Age < 30 - 79% benign; 15% lymphomatous; 6% carcinomas
- Age > 50 - 40% benign; 16% lymphomatous; 44% carcinomas
- 0.6 annual incidence of generalized lymphadenopathy
Differential diagnosis-
Common infectious causes of lymphadenopathy
1. Adenovirus
2. CMV
3. Enterovirus
4. EBV
5. Varicella
6. Herpes simplex
7. Staphlococcus infection
8. Group A hemolytic Streptococcus
9. Tularemia
10. Brucellocis
11. Tuberculosis
12. Atypical mycobacteria
13. Klebsilla
14. AIDS
15. Bubonic plague
16. Anthrax

Common non-infectious causes of lymphadenopathy

1. Hodgkin's disease
2. Lymphomas
3. Leukemia
4. Metastatic disease
5. Histiocytosis
6. SLE and JRA
7. Kawasaki Disease
8. Sarcoidosis

Symptoms and signs-

1. Neck Swelling

Lymph node character

i) Stone hard: typical of cancer usually metastatic
ii) Firm rubbery: can suggest lymphoma
iii) Soft: infection or inflammation
iv) Matting: tubercular

2. Pain-
(i) Painful lymph node present in acute inflammatory condition.
(ii) Painless lymph node mainly present in granulomatous or malignant conditions
3. Size - Rapid increase in size could be due to malignancy.
Evaluation
1. Laboratory studies
a) CBC count, including a careful evaluation of the peripheral blood smear. An erythrocyte
sedimentation rate is nonspecific but may be helpful.
b) Evaluation of hepatic and renal function and a urine analysis are useful to identify underlying
systemic disorders that may be associated with lymphadenopathy.
c) Additional studies, such as lactate dehydrogenase (LDH), uric acid, calcium, and phosphate,
may be indicated if malignancy is suspected. Skin testing for tuberculosis is usually indicated.
d) In evaluating specific regional adenopathy, lymph node aspirate for culture may be important
if lymphadenitis is clinically suspected.
e) Titers for specific microorganisms may be indicated, particularly if generalized adenopathy is
present. These may include Epstein-Barr virus, cytomegalovirus (CMV), Toxoplasma species,
and human immunodeficiency virus (HIV).
2. Imaging studies
a) Chest radiography is usually the primary screening imaging study. Additional imaging studies
are usually based on abnormal chest radiograph findings. Chest radiography is often helpful in
elucidating mediastinal adenopathy and underlying diseases affecting the lungs, including
tuberculosis, coccidioidomycosis, lymphomas.
b) CT scan and MRI especially helpful in case of metastatic disease to know the extent of
involvement.
c) Nuclear medicine scanning is helpful in the evaluation of lymphomas.
d) Ultrasonography may be helpful in evaluating the changes in the lymph nodes and in
evaluating the extent of lymph node involvement in patients with lymphadenopathy.
3. Fine Needle aspiration Cytology
4. Lymph Node Biopsy / Excisional Biopsy
Management
1. Treatment with antibiotics (covering the bacterial pathogens frequently implicated in
lymphadenitis) followed by re-evaluation in 2-4 weeks is reasonable if clinical findings suggest
lymphadenitis. Benign reactive adenopathy may be safely observed for months.
Infectious lymph adenopathy usually requires treatment with appropriate antibiotics.
2. Granulomatous condition requires address of general condition, and treatment with steroids
and immunoglobins depending on conditions.
3. In cases of malignant conditions, patient can be managed on different modality of treatment
viz chemotherapy, radiotherapy or surgery depending on type and stage of malignancy.

88. PERITONSILLAR ABSCESS (QUINSY)

Introduction: Peritonsillar abscess is a common infection of Head & Neck region. Although not
generally considered as a deep neck space infection physicians must be aware of the typical
clinical presentation & diagnostic strategies in order to quickly diagnose & appropriately treat
these patients to prevent complications.
Case Definition: PTA is a collection of pus between the fibrous capsule of the tonsil usually at
the upper pole & the superior constrictor muscles of pharynx.
Incidence in our Country: 0.9/10000/yr (Age Range- 3-91 yrs)
Differential Diagnosis
1. Infectious - Peritonsillar Cellulitis
Parapharyngeal abscess
Dental - Upper 3rd molar abscess
Co-existing Infectious Mononucleosis
2. Inflammatory-Kawasaki disease
3. Vascular-Post traumatic Internal Carotid Artery Aneurysm
4. Benign lesions-Benign Lympho-epithelial Cysts
5. Neoplastic –Large tonsil tumours with extra tonsillar spread (eg. Squamous cell carcinoma);
Tonsillar lymphoma; Rhabdomyosarcoma
6. Peritonsillar space tumours-Minor Salivary gland tumours
7. Anterior Pillar Mucosal tumours-Squamous cell carcinoma
Prevention and Counselling
1. Do not smoke.
2. Maintain good oral hygiene
3. Promptly treat oral infections.
4. If recurrent tonsillitis, tonsillectomy can be considered.
5. Always finish the course of antibiotics given in prescription even if you feel better within few
days of starting the course.

Optimal Diagnostic Criteria & Investigations

1. Clinical diagnosis-
a) History
(i) Progressive, usually unilateral sore throat over 3-4 days.
(ii) Odynophagia
(iii) Dysphagia for solids then liquids
(iv) Ipsilateral otalgia
(v) Headache, body ache
(vi) Fever,chills& rigors
b) General Examination
(i) Muffled & thick speech (hot potato voice / plummy voice)
(ii) Foul breath
(iii) Vitals – Fever; tachycardia
c) Local Examination
(i) Limited mouth opening (Trismus)
(ii) Torticollis
(iii) Oral cavity- Dental caries
(iv) Oropharynx- Soft Palate-Congested ,Bulging
Anterior Tonsillar Pillar- Congested, Edematous
Tonsil-Edematous (May not appear enlarged as it gets buried in edematous pillars
Uvula-Edematous, pushed to opposite side.
2. Investigations
a) Complete Blood counts
b) Serum electrolytes
c) Needle aspiration of pus
(i) Culture
(ii)Sensitivity
d) Imaging
(i) Orthopantogram
(ii) X- Ray Neck
AP view – Distortion of soft tissue
Lateral view- Rule out other differential diagnosis
Treatment & Referral Criteria
Standard Operating Procedure
1. Needle Aspiration
- Infiltration of 2% Lignocaine with Adrenaline (1: 100,000) given.
- Using Needle 16-18 gauge & 10 ml syringe aspirate from the area which is most fluctuant.
- Aspirate at superior pole initially because it is the most common area where abscess is present;
then middle 1/3rd followed by lower 1/3rd if pus is not returned from superior pole.
- Needle guard is used to prevent accidental injury to Internal Carotid Artery due to tip of needle
migrating too far posteriorly. Only 0.5 cm of needle needs to be exposed.
- If needle guard is unavailable a curved clamp can be used to expose a small portion of needle
before inserting it into area of aspiration.
2. Incision & Drainage
- Local infiltration of 2 percent Lignocaine with Adrenaline ( 1: 100,000) given.
- Using No.11 blade scalpel / Quinsy knife a large peritonsillar abscess is incised.
- It allows free flow of pus as the abscess cavity decompresses.
- To prevent risk of aspiration, allow patient to hold Yankauer catheter tip & do suction of pus.
3. Abscess /Hot Tonsillectomy
4. Interval Tonsillectomy
5. In-Patient Care
a) Airway- Tracheostomy may be essential in case of compromised airway
b) Breathing
c) Circulation- IV Fluids
d) Antibiotics- IV until acceptable swallowing is feasible.
e) Antibiotic of choice-
- Penicillin G Benzathine (Adult- 600mg iv q 6 hr for 12-24 hr Paediatric- 12,500- 25000 U/kg iv
q 6hr)
- Erythromycin (Adult- 15-20 mg /kg/day PO /iv divided q6h; Not more than 4 g/day; Paediatric-
30-50mg/kg/day PO/iv divided q6h)
f) Analgesics- Paracetamol - 500 mg TDS; Pethidine
g) Hydrogen peroxide/ Saline mouth wash
h) Single dose iv Steroid
5. Out Patient Care
a) Analgesics
b) Antibiotics
c) Hydrogen peroxide gargles

1. Clinical Diagnosis - same

2. Investigations
a) Complete blood count
b) Serum Electrolytes
c) Monospot /Heterophile Antibody Test for Infectious Mononucleosis
d) Needle Aspiration of Pus - Culture & Sensitivity
e) Blood Culture - If Septicemia.
f) Imaging
(i) Orthopantogram
(ii) X- ray Neck - AP view; Lateral view
(iii) CT-Scan Neck with Contrast
Indications for CT Scan
- Failure of I&D
- Presence of Trismus
- Young age (less than 7 yrs)
Findings in CT Scan
- Hypodense fluid collection with rim enhancement in tonsil.
- Foreign body (fish/chicken bone) as an inciting factor.
g) USG - Intraoral or Transcutaneous
h) MRI Angiography
3. Treatment - same
Gastroenterology
89. PEPTIC ULCER DISEASE
Disease characterized by ulcers in the stomach or duodenum, associated with epigastric pain and
discomfort.
High association with infection with H. Pylori and with excessive intake of drugs especially
NSAIDs.
Diagnosis
� Epigastric pain or discomfort related to food intake. Clinical assessment may be adequate to
make diagnosis and initiate treatment.
� Upper gastro-intestinal endoscopy confirms diagnosis and is advised in all non responsive
patients.
Treatment
� Non-drug measures :
� stop smoking and alcohol
� avoid food associated with dyspeptic symptoms
� avoid all pain killer drugs.
� Antacids : more effective if in liquid form and more effective at about 20 to 30 ml given four
times a day. To be given about 20 minutes after a meal. If taken as tablet it is to be chewed and
not swallowed.
� Tablet ranitidine : 150 mg twice daily for at least three months.
Other antiulcer drugs are better prescribed only after endoscopic confirmation of ulcer
Complications include Gastro-intestinal bleeding, gastric outlet obstruction and perforation all of
which would require hospitalization for acute supportive management and surgery.

90. APPROACH TO DYSPHAGIA

I. When to suspect/recognize?
a. Introduction:
Dysphagia is an important symptom of esophageal or orpharyngeal disorder. It usually indicates
the presence of an underlying disease process and, therefore, requires prompt evaluation.
b. Case definition:
Dysphagia is defined as difficulty or inability to transfer food from the oral cavity to the
stomach.
II. Incidence of Dysphagia 1,2
Dysphagia has been shown to be present in 20% of patients seen at primary care level and 15%
of elderly patients in the community. Many of the elderly patients do not seek medical advice.
Incidence data from India are lacking.
III. Differential Diagnosis 3,4
Dysphagia is sub classified into two types depending on the location of the lesion. Inability or
difficulty in transferring food from oral cavity to upper esophagus is referred to as
oropharyngeal dysphagia. Inability or difficulty in transferring food from upper esophageal
region to stomach is termed as esophageal dysphagia.
A careful history is vital in identifying the type and underlying cause of dysphagia. Difficulty in
initiating a swallow suggests oropharyngeal dysphagia. This may be accompanied by sensation
of food getting stuck above suprasternal notch, choking sensation, nasal regurgitation of food,
aspiration, dysarthria and dysphonia. When swallow is initiated but a few seconds later the
patient feels food is getting stuck in esophagus (below suprasternal notch), esophageal dysphagia
is likely. Dysphagia may occur due to structural lesions in the pathway of food bolus transit
(Mechanical dysphagia) or neuromuscular dysfunction (Motor dysphagia). Difficulty in
swallowing liquids and solids from the onset of dysphagia suggests motor dysphagia while
difficulty in swallowing solids alone at the onset of illness indicates mechanical dysphagia. A
short duration of progressive symptoms with significant weight loss is suggestive of malignancy.
Presence of pain during swallowing (odynophagia) may occur in infective lesions (Candida,
CMV, etc,) or acute ulcerating lesions (pill esophagitis). History of gastroesophageal reflux
symptoms, systemic illness (Stroke, 4 Parkinson’s disease, myasthenia gravis, muscular
dystrophy, scleroderma, AIDS, etc.), drug/corrosive ingestion, exposure to radiation and
surgeries in past may provide further clues to the diagnosis. Clinical examination for
thyromegaly, cervical lymph nodes, oral cavity lesions and central nervous system function may
be helpful. Hence, a careful history usually enables a physician to narrow down the list of
differentials. Table 1 shows the differential diagnosis of dysphagia.
2. Appropriate labelling of corrosive substances and keeping them away from the reach of
children may prevent corrosive injuries of esophagus.
3. Swallowing pills in upright position with plenty of fluid may prevent pill esophagitis.
4. Prompt therapy of gastroesophageal reflux disease with proton pump inhibitors may heal
esophageal ulcers and prevent development of peptic stricture.
5. Adequate chewing of food reduces the chance of food bolus impaction.
6. Counselling patients that dysphagia is an alarm symptom which requires prompt medical
attention may help in early diagnosis and management of malignancy of esophagus.
V. Optimal diagnostic criteria, Investigations, Treatment and Referral Criteria5-8

a. Clinical diagnosis: Dysphagia is a symptom and hence a history of difficulty/inability to

initiate or complete a swallow is sufficient to confirm its presence. Further probing about the
duration, nature (solids alone or for both solids and liquids), course (progressive or intermittent)
of the symptom as well as associated symptoms (see section on differential diagnosis) helps to
reduce the number of possible etiologies and plan appropriate focussed investigations.

b. Investigations:
or oropharyngeal/esophageal lesions, systemic illnesses causing
dysphagia (stroke, Parkinson’s disease, Myasthenia gravis, etc.) should be considered and
appropriately evaluated.

opriate. Specimen
from lesions should be obtained for histopathology and/or microbiological evaluation. For motor
oropharyngeal dysphagia, video-fluoroscopic swallowing study is the best modality.

gastrointestinal endoscopy is
appropriate as it enables better characterisation of lesion and collection of specimen for
histopathology and/or microbiological evaluation. In suspected esophageal motility disorder,
barium swallow study may be the appropriate initial test. For further characterisation of the
motility disorder, patient may be referred to a higher center for esophageal manometry.

c. Treatment:
Oropharyngeal dysphagia:
1. Treatment of neuromuscular causes is difficult but in conditions like myasthenia gravis and
Parkinson’s disease medical therapy may be useful.
2. Adequate nutrition is crucial. Thick fluids or soft solids are better tolerated.
3. If risk of aspiration is high, feeding through nasogastric tube may be considered or surgical
gastrostomy/jejunostomy may be performed for feeding.
4. For infective lesions, antibiotics may be used.
5. Malignant lesions require a multidisciplinary approach at a higher center.

Esophageal dysphagia:
1. Both structural and motor lesions require therapeutic endoscopic procedures or surgery and,
hence, are better managed at a higher center.
2. Calcium channel blockers provide some relief in achalasia cardia or diffuse esophageal spasm.
3. Proton pump inhibitors may be given for peptic strictures.
4. Soft foods should be recommended in case of esophageal webs and rings.

Standard Operating Procedure

Out Patient: Patients without systemic illness and with adequate hydration and good sensorium
can be managed as outpatients.
In Patient: Patients with severe systemic illness, dehydration and impaired level of
consciousness should be managed as inpatients.
Day Care: Patients with dehydration can be managed on a day care basis and discharged after
proper hydration and intervention if they can subsequently adequately nourish themselves at
home.

Referral criteria:
1. Oropharyngeal dysphagia: Non-availability of video fluoroscopy or gastrointestinal
endoscopy facilities or for management of malignant lesions
2. Esophageal dysphagia: For further evaluation and management after barium swallow study
3. Patients with systemic illnesses requiring specialised care

a. Clinical diagnosis: Same as in situation 1.

b. Investigations:
1. Prior to investigations for oropharyngeal/esophageal lesions, systemic illnesses causing
dysphagia (stroke, Parkinson’s disease, Myasthenia gravis, etc.) should be considered and
appropriately evaluated. Consultation with a neurologist and imaging of brain as well as
electrophysiological study of nerve/muscles may be warranted.

2. Structural oropharyngeal dysphagia:

(i) Consultation with an ENT specialist for nasopharyngeal endoscopy is appropriate. Specimen
from lesions should be obtained for histopathology and/or microbiological evaluation.
(ii) If no lesion is found, a computed tomography of the lower head and neck region would be
required.

3. Motor oropharyngeal dysphagia:

(i) Video-fluoroscopic swallowing study is the best modality.
(ii) Manometric study may be undertaken to assess for upper esophageal sphincter dysfunction
and cricopharyngeal achalasia.

4. Structural esophageal dysphagia:

(i) Upper gastrointestinal endoscopy is appropriate as it enables better characterisation of lesion
and collection of specimen for histopathology and/or microbiological evaluation.
(ii) If a peptic stricture is suspected, a 24 hour esophageal ph study would confirm the presence
of gastroesophageal reflux.
(iii) If the esophageal mucosa is normal during endoscopy, extrinsic compressive lesions should
be suspected and computed tomography of mediastinum or endoscopic ultrasonography from
esophagus is required to locate these lesions.

5. Esophageal motility disorder:

(i) Barium swallow study may be the appropriate initial test.
(ii) For further characterisation of the motility disorder, esophageal manometry should be
performed.
Figure 1 shows the approach to a patient with dysphagia.

c. Treatment:
Oropharyngeal dysphagia:
1. Treatment of neuromuscular causes is difficult but in conditions like myasthenia gravis and
Parkinson’s disease medical therapy may be useful.
2. Adequate nutrition is crucial. Thick fluids or soft solids are better tolerated.
3. If risk of aspiration is high, feeding through nasogastric tube may be considered or
percutaneous endoscopic gastrostomy may be performed. If percutaneous endoscopic
gastrostomy is not feasible, surgical gastrostomy/jejunostomy may be performed for feeding.
4. For infective lesions, antibiotics may be used. For malignant lesions a multidisciplinary
approach involving the surgeon, radiotherapist and oncologist is required.

Esophageal dysphagia: Treatment depends on the disease.

1. Achalasia Cardia:
a) For surgically low risk patients, graded pneumatic dilatation should be performed.
b) If two sessions of pneumatic dilatation does not provide adequate symptom relief, surgical
(laparoscopic or open) myotomy of lower esophageal sphincter should be performed. Direct
referral of patients for surgery is also an option.
c) For high risk surgical patients, botulinum toxin injection in the LES region may provide short
term symptom relief.
2. Strictures (Corrosive, Radiation, Peptic and Anastomotic):
a) Endoscopic dilatation (bougie dilators) is the preferred initial treatment if feasible. Repeated
dilatations may be required.
b) For long, tight strictures or those with frequent recurrence of symptoms after endoscopic
dilatation, surgery may be considered. For short strictures dilatation using CRE (Controlled
Radial Expansion) under endoscopic vision is effective. For Anastomotic strictures, dilatation
using CRE balloons is beneficial.
c) Anti-reflux therapy with proton pump inhibitors reduces the need for further dilatation in
peptic strictures.
3. Esophageal tumours:
a) Benign tumours causing dysphagia should be surgically resected.
b) If lesion is small and does not extend beyond submucosa (assessed using endoscopic
ultrasonography), endoscopic mucosal resection/endoscopic submucosal dissection are less
invasive options.
c) For operable malignant tumours, chemoradiation followed by surgery is the treatment of
choice.
d) Most malignant lesions of esophagus are inoperable at diagnosis and hence palliation is the
only option. Palliative options include – i) placement of a nasogastric feeding tube over a guide
wire (placed during endoscopy), ii) esophageal stenting using self expandable metal stent
(SEMS), iii) radiation therapy and iv) surgical gastrostomy/jejunostomy for feeding.
4. Esophageal webs and rings: Esophageal webs and rings should be managed with endoscopic
dilatation.
5. Other conditions:
a) Nitrates or calcium channel blockers can be used for diffuse esophageal spasm.
b)Systemic illness like scleroderma requires appropriate medical therapy.
Standard Operating Procedure
Same as in situation 1.
Referral criteria:
While a super speciality center is expected to have all the diagnostic and therapeutic facilities,
patients may be referred if required equipments/expertise are not available.
VI. Who does what and timelines?
a. Doctor:
1. Within one hour of patient’s arrival at the hospital
Initial resuscitation if patient is sick, dehydrated, etc,.
History and clinical examination
Need for hospitalisation
After the patient is stabilised
Planning further diagnostic tests
Explaining the condition to patients and relatives and obtaining informed consent for procedures
Definitive treatment of the patient
Referral to other specialists in the same hospital or to other centers
b. Nurse:
1. On patient’s arrival at the hospital - Measure blood pressure, pulse rate, breathing rate and
level of consciousness and inquire about the chief complaint. The doctor should be accordingly
informed.
2. Obtain intravenous access, collect blood samples for investigations and carry out treatment
orders for patients requiring emergency care.
3. Assist the doctor in performing procedures, surgery, etc.
c. Technician
1. Set up and maintenance of equipments required for emergency or elective care
2. Assist the doctor during endoscopic or surgical procedures
3. Keep a ready stock of instruments/accessories required for emergency or elective procedures
*Patients with absolute dysphagia (unable to swallow at all) should be stabilised prior to
evaluation of the cause
#Key points in history – character (solid/liquid food), duration, course (progressive/intermittent),
weight loss, pain during swallowing, medications/corrosive ingestion, radiation, systemic illness
CT – Computed Tomography; UGI – Upper Gastrointestinal
Figure 1: Approach to a patient with dysphagia

91. ACHALASIA CARDIA

When to suspect/recognize?
a. Introduction 1: Esophageal dysphagia involves difficulty in transferring food from the upper
esophageal region to the stomach. It is subdivided into mechanical dysphagia (caused by
structural lesions in the path of food bolus transit) or motor dysphagia (caused by neuromuscular
dysfunction). Mechanical dysphagia is generally progressive in nature with dysphagia to solids
being noticed at first followed in time by dysphagia to liquids. On the other hand, in motor
dysphagia, there is simultaneous dysphagia to both solids and liquids from the onset. Among the
various causes of motor dysphagia, achalasia cardia remains the most recognised. Besides
dysphagia, clinical features of achalasia include regurgitation, chest pain, hiccups, halitosis,
weight loss, aspiration pneumonia and heartburn. The exact pathophysiology of this entity is
unknown although increasing evidence suggests that loss of ganglion cells within the myenteric
plexus supplying the smooth muscles of the esophagus (including the lower esophageal
sphincter) to be responsible.
b. Case definition1: Achalasia (a Greek term meaning "failure to relax") is a disease of
unknown etiology characterised by loss of peristalsis in the distal esophagus and a failure of
lower esophageal sphincter (LES) relaxation.
II. Incidence2-4: In the West, the incidence of achalasia cardia is reported to be approximately
1/100,000 population per year with prevalence being 7.1 to 13.4/100,000 population per year.
There is hardly any data on the incidence and prevalence of the disease in India. A recent
retrospective study from Lucknow conducted in a tertiary care centre reported that achalasia
cardia constituted 77% of the patients who presented with motor dysphagia. This disease affects
people of both genders equally and presents between 25 to 50 years age.
III. Differential Diagnosis1:
Other motor disorders: Diffuse esophageal spasm
Nutcracker esophagus
Hypertensive LES
Diseases with distinct etiology but with functional consequences mimicking achalasia:
Pseudoachalasia (associated with malignancies and infiltrative diseases)
Chagas disease
Post surgical (following fundoplication and bariatric surgery)
IV. Prevention and Counselling5:
There are no particular preventive measures for achalasia cardia. Long standing dilatation of
esophagus can result in development of squamous cell carcinoma of the esophagus although
there are no recommendations for surveillance.
V. Optimal diagnostic criteria, Investigations, Treatment and Referral Criteria
Situation 1: At Secondary Hospital/Non-Metro situation
a. Clinical diagnosis1,6: Presence of insidious onset, gradually progressing dysphagia to both
solids and liquids with varying combinations of regurgitation, chest pain, hiccups, halitosis,
weight loss, heart burn and aspiration pneumonia may suggest achalasia cardia. The patient may
give history of adopting certain manoeuvres like lifting the head or throwing the shoulders back
to facilitate esophageal emptying.
b. Investigations1,6:
widening with presence of air fluid level and absence of gastric
bubble maybe seen.

i) Dilated esophagus with a characteristic “bird beak” deformity in the lower esophagus
ii) Massively dilated esophagus may produce a “sigmoid” esophagus
copy: Typical findings include
i) Dilated esophagus with food or fluid residue
ii) Esophageal mucosa that is generally normal may show inflammation caused by retained food,
pills or Candidiasis
iii) Contracted LES that can be negotiated with a gentle push of the endoscope.
Endoscopy is essential to rule out neoplasms in the cardia and the fundus.
c. Treatment1,7: Treatment of achalasia cardia maybe pharmacological, endoscopic or surgical.
ed in secondary hospitals.

and preferably, a surgical backup are available.

given
immediately before meals. These have the advantage of being non-invasive but they are not as
effective as the other therapeutic options. Side effects and tachyphylaxis limit their use.
Generally these are given to patients who cannot tolerate or are unwilling for invasive therapies.

Standard Operating Procedure

If adequate facilities of investigation and invasive therapy are available, patients in secondary
hospitals are generally managed as outpatients. If endoscopic therapy is possible, this can be
done as a day care procedure.
Referral criteria:
- Non-availability of endoscopy, endoscopic accessories, manometry, fluoroscopy and surgery
- Patients with systemic illness requiring specialised care

a. Clinical diagnosis: Same as in situation 1.

b. Investigations1,6-8: In addition to those discussed in situation 1, other investigations that can
be performed include conventional manometry and high resolution manometry of the esophagus.
- Characteristic findings on conventional manometry include failure of the LES to relax, elevated
basal LES pressure and aperistalsis of the esophageal body.
- High resolution manometry (HRM) of the esophagus is an advanced form of manometry. Based
on HRM, achalasia is classifed into 3 subtypes:
Type 1(Classic) achalasia, where swallowing results in no significant change in esophageal
pressurization.
Type II achalasia, where swallowing results in simultaneous pressurization that spans the entire
length of the esophagus.
Type III (spastic) achalasia, where swallowing results in abnormal, lumen-obliterating
contractions (spasms).
Responses to all types of achalasia treatment (both endoscopic and surgical) were best in type II
patients and worst in type III patients.
- It is preferable to quantify the basal LES pressure by manometry prior to endotherapy or
surgery to assess the efficacy of the same on follow up especially in the event of recurrence of
symptoms.

c. Treatment1,9,10: Pharmacological treatment would be same as in situation 1.

The other forms of therapy are broadly divided into endoscopic or surgical.
1) Endoscopic therapy:
a. Pneumatic dilatation: Forceful stretching of the LES is accomplished using a Rigiflex
pneumatic balloon dilator in a graded fashion under fluoroscopy. Although this is quite effective
and can be done as a day care procedure, there is a 3-5% risk for perforation which can warrant
additional surgery. If two sessions of pneumatic dilatation are unsuccessful, surgery should be
performed.

b. Botulinum injection: Botulinum toxin A is injected into the LES so as to reduce its pressure.
Its effect may not be as durable as that following pneumatic dilatation. Minor side effects of this
procedure include rash and transient chest pain. It is ideal for high risk surgical patients in
providing short term relief.

2) Surgery:
a. Open Heller’s myotomy (either transabdominal or transthoracic)
b. Minimally invasive (either laparoscopic or thoracoscopic)
Surgical therapy is more effective and long lasting than endotherapy. Reflux esophagitis can be a
problem after surgery but can be ameliorated by performing an antireflux procedure
(fundoplication). Overall mortality from Heller’s myotomy is less than 2%. Current evidence
suggests that a laparoscopic approach is associated with similar efficacy, reduced morbidity, and
shorter hospital stay when compared with surgical myotomy via other approaches. Direct referral
for laparoscopic surgery can be considered for a low risk patient rather than pneumatic dilatation.

Standard Operating Procedure

Out Patient: Patients who do not have major comorbidities can be managed as outpatients. Post
procedure patients can also be followed up.
In Patient: This would be required for those with major comorbidities that need stabilisation, for
postoperative care and for monitoring those with anticipated complications following
endotherapy. This may also be required for those who have copious food residue on initial
endoscopy for clearing the contents (using a Ryle’s tube) before the next endoscopy.
Day Care: This would be required for patients who are dehydrated for stabilisation following
which they can nourish themselves at home. Endotherapy can also be performed as a day care
procedure.

Referral criteria:
A superspecialty center is expected to have the required diagnostic and therapeutic facilities for
management of achalasia. However, a patient maybe referred if required equipment or expertise
is unavailable.
VI. Who does what and timelines?
a. Doctor:
If patient is sick (within 1 hour of arrival to hospital)
Initial resuscitation and assess if patient is dehydrated, has pneumonia, etc and requires
admission.
If patient is otherwise well
History and clinical examination
Planning diagnostic tests
Discussion of condition and management options with patients and responsible well wishers and
relatives and obtaining informed consent
Definitive treatment
Referral to other specialists in the same hospital or to a higher center
b. Nurse:
Measure vital signs and assess level of consciousness
Inquire chief complaints and inform the doctor accordingly
Obtain intravenous access for blood investigations
Carry out treatment orders as directed by the doctor
Assist the doctor in performing therapeutic procedures
c. Technician:
Maintain equipment required for emergency or elective care
Assist the doctor and the nurse during therapeutic procedures

92. ACUTE LIVER FAILURE

. WHEN TO SUSPECT /RECOGNIZE?

a. Introduction:

Acute liver failure is a syndrome of varying aetiology resulting in rapid loss of hepatic metabolic
and immuological functions, manifesting as altered mentation and coagulopathy and in many
cases progressive multi-organ failure, in a previously normal individual. The condition is
associated with high mortality and is a frequent indication for liver transplantation.
b. Case definition:
Various terminologies and definitions have been used.
Fulminant Hepatic Failure: Potentially reversible disorder that is the result of severe liver injury
with onset of encephalopathy within eight weeks of symptoms and in the absence of pre-existing
liver disease.
Acute Liver Failure: Evidence of coagulopathy (INR>1.5) and any degree of mental alteration
(encephalopathy) occurring within 26 weeks of onset of illness in a patient without preexisting
liver disease.
Note: Diagnosis of hepatic encephalopathy is clinical; West Haven grading of
encephalopathy is followed:-
Legend to above table: HAV= Hepatitis A virus ; HBV = Hepatitis B virus; HEV = Hepatitis E
virus; PCM= Paracetamol
4. PREVENTION AND COUNSELING

The prevention of ALF due to viral hepatitis entails prevention of hepatitis and avoiding use of
hepato-toxic drugs after onset of hepatitis, including paracetamol. Immunization against hepatitis
B is recommended for all. In India over 95% adults are exposed to HAV. Vaccine for HAV is
available and may be used in children. Use of potable water is recommended for prevention of
HAV and HEV.
5. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,TREATMENT &
REFERRAL CRITERIA
a. Situation 1: At secondary hospital / non-metro situation
i. Clinical Diagnosis: Patients presenting with acute hepatitis should be monitored for altered
sensorium or asterixis. Liver span (normal 12-15 cm) should be examined daily. Spleen tip may
be palpable in 20% patients with acute hepatitis due to reticulo-endothelial cell hyperplasia.
Evidence of chronic liver disease in the form of spider naevi, gynecomastia, palmar erythema,
splenomegaly or ascites goes against the diagnosis of ALF.
ii. Investigations: For severity and aetiology of liver failure and to exclude acute on chronic
liver failure and chronic liver disease.

CBC, LFT, INR, Creatinine, Electrolytes, Sugar, USG upper abdomen, HbsAg.
iii. General Measures:
1. Patients with altered mentation should be admitted to ICU.
2. Avoid stimulation, avoid sedation.
3. Nurse with head end elevation to 30®
4. Consider intubation if grade III/IV encephalopathy.
5. Fluid and electrolyte maintenance. Any fluid may be used.
6. Enteral nutrition preferred till grade 1 /2 encephalopathy. Protein intake 1G/Kg.
7. Inj PPI (proton pump inhibitor) IV once daily to prevent stress induced erosive gastritis /
ulcers.
iv. Specific Measures
1. Inj Vitamin K 10 mg IV single dose.
2. Inj Mannitol bolus 0.5-1g/Kg if signs of cerebral edema: systolic hypertension, bradycardia,
irregular respiration or unequal pupils or posturing. Use mannitol only if plasma Osmolality is <
320 mosmol/L.
3. Antibiotics. Surveillance blood culture followed by prophylactic antimicrobials. Suggested
protocol : Piperacillin + Tazobactam, Teicoplanin, Metronidazole and Fluconazole. Modify as
per prevalence of local flora / sensitivity pattern.
4. Inj N-acetyl cysteine 150mg/Kg over 1 hour, 12.5mg/Kg/hour over next 4 hours and then
6.25mg/Kg/hour over 67 hours. Start early in course of illness i.e., for patients with grade 1 or 2
hepatic encephalopathy.
5. Treatment directed at aetiology:
a. Acetaminophen: N-Acetyl Cystine
b. HSV: Acyclovir: Skin lesions in 50% only
c. Amanita phalloides: Penicillin G 1 million units/kg/day
d. HELLP/AFLP: Terminate pregnancy
e. HBV: Tenofovir. Concerns of lactic acidosis with Entecavir
v. Avoid
1. Fresh frozen plasma (FFP) as it interferes with assessment for liver transplantation. Use only if
invasive procedure planned.
2. Platelet transfusion with platelets >10,000/cmm unless invasive procedure planned
3. Protein restriction to <1G/Kg
4. Branched chain amino acids
5. Lactulose
6. Inj L-Ornithine L-Aspartate
7. Prophylactic anticonvulsants
8. Hypothermia

vi. Referral Criteria

1. Diagnosis not clear: ALF Vs ACLF / CLD
2. Aetiology not clear
3. Worsening clinical condition
4. Transfer to tertiary care facility may be considered early in the course of illness (Grade 2
encephalopathy).

i. Clinical Diagnosis: same as level 1

ii. Investigations: Same as level 1. In addition:-

IgM-anti HBc if HbsAg positive, IgM-antiHEV. If viral markers negative then ANA, SMA,
serum ceruloplasmin, examination for KF rings. In ICU setting: ABG, arterial ammonia.
iii. Treatment: Same as at level 1. In addition:-
3% saline infusion @ 30 ml/hour till serum Na 145 mEq/L, then maintain 10-15 ml/hour (aim
serum Na 145-155 mEq/L). Monitor serum sodium 12 hourly.
iv. Referral criteria for liver transplantation

The approach to liver transplantation for ALF has to be clear and mathematical. The following
questions to be answered:-
Step 1. Is liver transplantation indicated?
Apply modified King’s College Hospital (KCH) criteria:-

If answer to step 1 is yes, proceed to step 2. If answer to step1 is no, keep looking for indication
for liver transplantation as the negative predictive value of KCH criteria is low. Give due
consider ation to MELD score (>30) and arterial ammonia (>124).
Step 2: If answer to step 1 is yes, is there a contraindication to transplantation? Contraindications
include sepsis and posturing due to severe cerebral edema. Get in touch with the nearest liver
transplant centre for advise before deciding aginst transplantation.
Step 3: If answer to step 2 is no, can the family afford liver transplantation?
Step 4: If answer to step 3 is yes, is there a suitable donor?
Test blood group of patient and willing near relatives aged 18 to 50 years. If ABO compatible
donor is available, counsel on success and risk of liver transplantation and donor surgery.
Step 5: Transfer patient and ABO compatible willing near relative to transplant centre. Consult
the nearest liver transplant centre for precautions during the process of transfer.
93. LIVER CANCER OR HEPATOCELLULAR CARCINOMA (HCC)
I. WHEN TO SUSPECT/ RECOGNIZE?

a) Introduction:

Liver cancer or primary liver cancer or hepatocellular carcinoma (HCC) is, as the name suggests,
a primary malignant tumor arising from the liver cells or hepatocytes. It usually arises on a
background of cirrhosis, but it may even arise in non-cirrhotic livers. The etiology of cirrhosis
may be hepatitis B, hepatitis C, alcohol or even non-alcoholic steatohepatitis. Liver cancer has
been reported as the 5th most common cancer and the third most common cause of cancer related
mortality in the world literature.
b) Case definition:

For both situations of care (mentioned below*)

Secondary care centers: Any space occupying lesion (SOL) or a nodule in the liver detected
either on ultrasonography, CT scan or MRI, in a patient who has underlying cirrhosis, should be
considered as an HCC unless proved otherwise. The presence of high AFP >400ng/ml confirms
the diagnosis of the SOL/nodule being HCC. However, normal AFP levels do not exclude the
presence of HCC. Appearance of a new SOL in liver even in patients, who do not have
underlying cirrhosis, should be investigated with HCC being the first differential diagnosis.
Tertiary care centers:
1. In a patient who has cirrhosis any SOL, more than 2 cm, if it shows enhancement in the
arterial phase and washout in the delayed phase, on at least one dynamic imaging (either a triple
phase contrast CT scan of abdomen or dynamic contrast enhanced MRI of the abdomen), should
be labeled as HCC unless proved otherwise, irrespective of alpha feto protein (AFP) levels.

2. In a patient who has cirrhosis, and the SOL is between 1-2 cm, then the typical contrast
enhancement and washout pattern needs to be demonstrated on at least two imaging modalities to
make a diagnosis of HCC
3. Patients who have SOL in the liver but do not have cirrhosis, or those who have atypical
enhancement characteristics on dynamic imaging, the diagnosis of HCC can be confirmed by
characteristic microscopic features on a biopsy of the lesion or fine needle aspiration cytology of
the lesion. Where ever possible efforts should be made to make a non-invasive diagnosis of
HCC, that is, without putting any needle in to the tumor
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY

In our country, the reported incidence of HCC is 1.2 /100,000 females per year and 2.7/100,000
males per year and a prevalence of 1.9% of all cancers, based on population cancer registry data.
In a prospective study in patient with cirrhosis, the reported incidence is 1.6 per 100 person years
of follow up.
III. DIFFERENTIAL DIAGNOSIS

Differential diagnosis include all other causes of mass /SOL in the liver. These can be
either benign or malignant

These lesions can be differentiated from HCC by means of characteristic imaging findings of
these lesions as well as the clinical setting of presentation.
IV. PREVENTION AND COUNSELING

The most important risk factors for the development of liver cancer are hepatitis B infection,
hepatitis C infection, alcoholic cirrhosis, non-alcoholic steatohepatitis related cirrhosis, and other
causes of cirrhosis. Therefore the most important preventive measures would be to prevent
development of these diseases. The following measures can me considered to be preventive
strategies for HCC:
1. Vaccination against hepatitis B
2. Universal screening of donated blood for hepatitis B and C and discarding of infected units
3. Preventive strategies for diabetes and obesity
4. Strategies to prevent alcoholism

At present there is no recommended chemopreventive strategy, once a patient becomes cirrhotic.

V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &

REFERRAL CRITERIA

*Situation 1: At Secondary Hospital/ Non-Metro situation: Optimal Standards of

Treatment in Situations where technology and resources are limited
a. Clinical Diagnosis:

All patients with cirrhosis of liver who develop recent worsening of their clinical status should
be suspected of having developed liver cancer and should be appropriately investigated. It should
be suspected when:
1. A patient who has stable cirrhosis develops new ascites
2. A cirrhotic patient develops a difficult to control ascites.
3. A stable cirrhotic develops severe constitutional symptoms, such as weight loss or anorexia.
4. Any patient, especially one who has cirrhosis, develops prolonged fever of unknown origin
(FUO)
5. A patient of cirrhosis develops pain in the upper abdomen.

b. Investigations:

The initial investigations should include:

1. Abdominal ultrosonography which can pick up features of cirrhosis and presence of any SOL
in the liver.
2. Alpha feto protein (AFP) levels: Levels of more than 10 ng /ml should raise the suspicion of
HCC and should be investigated further.

c. Treatment:

Standard Operating procedure

Comprehensive treatment of Liver cancer involves:
1. Treatment of the tumor
2. Treatment of cirrhosis
3. Treatment of complications of cirrhosis
4. Treatment of the virus if the cause is hepatitis B or C.

Treatment of the tumor is based on the stage of the tumor. The most commonly used staging and
treatment plan followed is based on the BCLC (Barcelona clinic liver cancer) staging system.
This system incorporates, not only the size and number of tumors, but also, 26

the residual liver function, the functional status of the liver and presence or absence of
extrahepatic spread. The BCLC staging system is given below:
e. Out Patient
Only in cases requiring symptomatic treatment
Referral criteria:
Patients requiring curative or palliative therapies for HCC [ such as liver transplantation, liver
resection, radiofrequency ablation, percutaneous ethanol injection, trans-arterial
chemoembolization, trans arterial radioembolization, and biological therapy (tyrosine kinase
inhibitors or monoclonal antibodies)], should all be referred to a hepatologist or
gastroenterologists with interest in managing HCC at a tertiary care center
Even patients requiring advanced treatment for complications of cirrhosis, should be referred to
tertiary care centers.

a) Clinical Diagnosis:
All patients with cirrhosis of liver who develop recent worsening of their clinical status should
be suspected of having developed liver cancer and should be appropriately investigated. It should
be suspected when:
1. A patient who has stable cirrhosis develops new ascites
2. A cirrhotic patient develops a difficult to control ascites.
3. A stable cirrhotic develops severe constitutional symptoms, such as weight loss or anorexia.
4. Any patient, especially one who has cirrhosis, develops prolonged fever of unknown origin
(FUO)
5. A patient of cirrhosis develops pain in the upper abdomen.

b) Investigations:

The initial investigations should include:

1. Abdominal ultrosonography which can pick up features of cirrhosis and presence of any SOL
in the liver.
2. Alpha feto protein (AFP) levels: Levels of more than 10 ng /ml should raise the suspicion of
HCC and should be investigated further. The further investigations required are:
3. Triple phase contrast enhanced CT Scan of abdomen
4. Dynamic contrast enhanced MRI of the abdomen
5. Contrast enhanced ultrasonography
6. PET CT scan of the abdomen
7. Bone scan
8. Biopsy or FNAC of the tumor with immunohistochemical staining
9. Other tumor markers such as PIVKA-II and AFP-L3
The investigations from number 3-9 may all be required or may be required selectively for
confirming the diagnosis, determining the stage of the disease, determining extrahepatic spread
and suitability for treatment.
c) Treatment:
As has been mentioned earlier, treatment depends on the BCLC stage of the disease
Standard Operating procedure
a. In-Patient
Curative forms of therapy for liver cancer include:
1. Liver resection (surgical removal of a part of the liver involved by the tumor)
2. Percutaneous ablative therapies [burning the tumor with either radiofrequency current
(radiofrequency ablation) or with injection of 100% alcohol or with injection of 50% acetic acid]
or
3. Liver transplantation.
Palliative therapies include:
1. Transarterial chemoembolization,
2. Transarterial radio-embolization
3. Systemic chemotherapy.
4. Continuous intra-arterial chemotherapy through implatable port.
As mentioned earlier, BCLC staging system guides therapy as follows:
Patients with very early HCC (stage 0)and early HCC (stage A): Can be offered all forms of
curative therapy:
1. Liver transplantation
2. Liver resection
3. Percutaneous ablative therapies (radio frequency ablation, percutaneous ethanol injection or
percutaneous acetic acid injection therapy)
Patients with intermediate HCC (stage B): Can be offered therapy with:
1. Transarterial chemoembolization (TACE).
2. Oral chemotherapy with biological such as sorafenib
3. Liver transplantation can be offered to patients with single large tumor or even multiple
tumors, but only at experienced centres. (these would be patients outside Milan’s criteria [single
tumor < 5 cm or up to 3 tumors with diameter < 3 cm])

Patients with (stage C):

Can be offered
1. Systemic chemotherapy with Sorafenib
2. Radioembolization with yttrium 99 theraspheres
Patients with end-stage disease (stage D):
Can be offered
1. Oral chemotherapy with Sorafenib
2. Symptomatic therapy

b. Out Patient

Patients being given symptomatic therapy or oral chemotherapy can be managed in the out
patient setting. Follow up after curative therapies would also be done in the out patient setting.
Following percutaneous ablative therapies, patients need to undergo regular FU with a dynamic
contrast imaging (either a CT or MRI scan), liver function profiles and tumor markers at regular
intervals or as indicated.
d) Referral criteria:
Patients fit for undergoing liver transplantation should be referred to a hepatologist at a liver
transplant center
VI. WHO DOES WHAT? and TIMELINES
a. Doctor
1. Diagnosis and treatment(medical, radiological and surgical) of cases
b. Nurse
1. Nursing care to patients undergoing treatement at in-patients.
2. Endoscopy nurse
c. Technician
1. Endoscopy technician
2. Interventional radiology technician
3. Liver surgery technician
4. Lab technician, biochemistry/hematology lab
5. Blood bank technician

94. INFLAMMATORY BOWEL DISEASE

I. WHEN TO SUSPECT/ RECOGNIZE?

a) Introduction:

Inflammatory bowel disease (IBD) represents a group of idiopathic chronic inflammatory

intestinal conditions. The two main disease categories included are Crohn’s disease (CD) and
ulcerative colitis (UC), with both overlapping and distinct clinical and pathological features. In
addition the spectrum also comprises two categories ; IBD unclassified and indeterminate colitis.
The pathogenesis of IBD is still under investigation. The most simplified view is that intestinal
injury results due to aberrant immune response to commensal bacteria in a background of genetic
predisposition.
b) Case definition:

o Ulcerative colitis:
Ulcerative colitis is a chronic disorder of unknown etiology in which a part or the whole of the
mucosa of the colon becomes diffusely inflamed and ulcerated. Rectum is involved in a vast
majority of the cases.
o Crohn’s Disease:
A chronic granulomatous disease which can affect any part of GI tract in a discontinuous,
asymmetric manner. Unlike Ulcerative colitis which is a mucosal disease, Crohn’s disease is a
transmural disease.
o IBD unclassified:
Categorization is not possible after clinical, radiological, endoscopic and histological features
o Indeterminate colitis:
Categorization is not possible even after evaluation of resected specimen.

II. INCIDENCE OF THE CONDITION IN OUR COUNTRY

The epidemiological studies from this region are being made available it is clear that the
incidence and prevalence rates of IBD in Asia–Pacific region are low compared with Europe and
North America. They are however, increasing rapidly.
There are substantial variations in the incidence and prevalence rates of IBD in various ethnic
groups in Asia. The highest incidence rates are recorded from India, Japan and the Middle East
and there exists a genetic predisposition of South Asians (Indians, Pakistanis and Bangladeshis)
to ulcerative colitis (UC). In a study done in 2001 from Ludhiana in Punjab, the crude prevalence
rate was 44.3/105. The incidence was calculated after a second visit to the same area one year
later. The crude incidence rate was 6.02/105. The incidence rate of UC in India is higher than in
Asian countries like Japan (1.95/105) and Korea (1.23/105). There is no population-based study
on Crohn’s disease (CD) in India, however, the accepted perception is that the incidence of CD is
rapidly rising in India. The peak age of incidence of CD is the third decade of life, with a
decreasing incidence rate with age. The incidence rate in UC is quite stable between the third and
seventh decades.
III. DIFFERENTIAL DIAGNOSIS
The main differential diagnosis of Ulcerative colitis and Crohn’s disease are :

IV. PREVENTION AND COUNSELING

IBD is an autoimmune disease, and environmental factors which can trigger an episode have not
been identified, hence primary prevention strategy is not possible. There is a family history in
5% of IBD patients.
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA

There is no gold standard test available to make a diagnosis of IBD. A diagnosis of ulcerative
colitis or Crohn’s disease is made on the basis of compatible clinical history, examination,
imaging, endoscopy and histology findings.
a) Clinical Diagnosis:

History
The most important features are the chronic duration of symptoms and the frequent remissions
and relapses which characterize IBD and help in distinguishing from other infectious diseases
affecting the large and small bowel.
Ulcerative colitis
1. Diarrhea : Large bowel diarrhea which is daytime or nocturnal
2. LGI bleed : Blood may be mixed with stool and at times separate from the stools
3. Rectal symptoms: tenesmus, urgency , frequency of stools
4. Abdominal pain and fever in case of severe disease
5. Symptoms are limited to large bowel

Crohn’s disease(CD)
Symptoms depend upon the site of involvement. In CD , any part of bowel from esophagus to
anal canal may be involved .
Small Intestinal involvement / Ileocolonic involvement :
1. Abdominal Pain
2. Symptoms suggestive of recurrent partial intestinal obstruction may be present
3. Chronic diarrhea
4. Fever, anorexia, weight loss

Large bowel involvement :

1. Chronic diarrhea
2. Hematochezia
3. Peri anal disease
4. Fever, weight loss
5. Abdominal pain

Upper GI involvement
1. Dysphagia, odynophagia
2. Epigastric pain
3. Symptoms suggestive of gastric outlet obstruction

Extraintestinal manifestations (EIM) :Arthritis is the most common EIM and is observed in
15-20% of cases. Other extraintestinal complications include ankylosing spondylitis,
pyodermagangrenosum, erythema nodosum, iritis, uveitis, episcleritis, and primary sclerosing
cholangitis.
Complications include :
1. Hemorrhage: profuse bleeding from ulcers in UC. Bleeding is less common in CD. Massive
bleeding in CD is more often seen from ileal ulceration than colitis.
2. Strictures, bowel perforation and Intra-abdominal abscesses in CD.
3. Fistulas and perianal disease in CD
4. Colorectal cancer: Significantly increased risk of colon cancer in UC after 8 years of
diagnosis; the risk is lower in CD as compared to UC.
b) Investigations:

Primary and secondary care settings :

sts

care hospital before initiating therapy. This is so as to rule out intestinal tuberculosis which
closely mimics Crohn’s disease.
Referral Hospitals:

i ) Parasites
ii)Clostridium difficile(should be considered even in absence of antecedent antibiotics).

i) Haemoglobin , ESR , serum albumin , Human immunodeficiency virus (HIV)

ii) Perinuclear antineutrophil cytoplasmic antibody (p-ANCA) and anti-

Saccharomyces cerevisiae antibodies (ASCA): need not be done

iii) Celiac serology

An endoscopic examination is necessary a) to establish the diagnosis b) to assess severity of

disease c) to take targeted mucosal biopsies . In cases with severe activity , a full length
colonoscopy is not indicated as there is a high risk of perforation.
Ulcerative colitis: An ileocolonoscopy is indicated to establish the extent of disease Crohn’s
Disease: Endoscopic procedures required include : 1) ileocolonoscopy 2) UGI endoscopy (
especially in pediatric cases) 3)Capsule endoscopy/ double balloon enteroscopy if small bowel
involvement suspected.

Multiple mucosal biopsies should be taken from inflamed areas. Features suggestive of
ulcerative colitis include crypt architectural destruction, crypt abscesses, goblet cell depletion,
paneth cell metaplasia, basal plasmocytosis. In Crohn’s disease non caseating granulomas may
be seen in 30% of cases
1. Abdominal X ray: In severe UC or CD where perforation or toxic mega colon is suspected. In
CD, if intestinal obstruction is suspected.
2. Contrast enhanced computed tomography ( Enteroclysis/Enterography) : In cases with CD i)
to evaluate small intestinal involvement ii) to differentiate from intestinal tuberculosis
3. Barium meal follow through: If facilities for CT (enteroclysis) are not present.

extent and severity of the disease . The tables below show the classification for extent and
severity of UC and CD.

Table 1: Disease extent in Ulcerative colitis:

In addition , these investigations also help in
1) differentiating Ulcerative colitis from Crohn’s disease
2) Intestinal tuberculosis from Crohn’s disease as shown in the tables below.

Table 5 : Features for differentiating between ulcerative colitis (UC) and Crohn’s disease (CD)
(adapted from World Gastroenterology Organisation Global Guidelines June 2009)
IBD management should be based on:
UC vs. CD (although this is less important for early aspects of treatment)
Disease location and phenotype
Severity
The goals of treatment are to:
-free remissions (decreasing the frequency and severity of

recurrences and reliance on steroids)

ons hospitalization and surgery

Treatment include two phases

• Induction of remission
• Maintenance of remission

The figure below shows the drugs which are useful in induction and maintenance phase

Disease extent: Proctitis and Proctosigmoiditis

Inducing Remission
Proctitis : 5ASA suppositories ; Optimal dose : 1gm/day
Proctosigmoiditis : 5ASA enemas : 2-4 gm/ 42 If no response within 4 week
Use of topical glucocorticoids
If still no response :
Use of hydrocortisone rectal drip: 200mg/200ml/1-2 hrs

Oral 5 ASA in a dose of 1600-2400 mg daily may be used with or without topical therapy
If disease extent is left sided colitis/pancolitis, then the treatment may be planned as in the
table below:
A. For Induction of remission depending upon the severity of disease
ii) Referral criteria:
Criteria for surgery referral :

Standard Operating procedure

a. In Patient : Patients with severe disease not responding to oral steroids
b. Out Patient : Patients with mild to moderate disease or patients in remission on follow up
c. Day Care : Any patient requiring infliximab maintenance infusion

VI. WHO DOES WHAT? and TIMELINES

a. Doctor: Diagnose and strategise therapy
b. Nurse : Assist in administering drugs
c. Technician : Assist in endoscopy and imaging investigations

95. INTESTINAL OBSTRUCTION

WHEN TO SUSPECT/ RECOGNIZE?

Introduction
Intestinal obstruction is an important gastrointestinal emergency and a common cause of
hospitalization. Most of the patients with intestinal obstruction report to surgeons or surgical care
units. Some of them however report to physicians or medical emergency units. . Intestinal
obstruction carries a high risk of mortality and morbidity if surgical therapy is inappropriately
delayed because of misdiagnosis.
Case definition
Acute intestinal obstruction occurs when there is an interruption in the forward flow of intestinal
contents. This interruption can occur at any point along the length of the gastrointestinal tract.
The clinical presentation varies depending on the severity, duration, site and type of intestinal
obstruction..The classical clinical tetrad of presentation is colicky abdominal pain, nausea and
vomiting, abdominal distention, and progressive obstipation. There are two types of intestinal
obstruction-mechanical and adynamic.
Mechanical intestinal obstruction
Site of obstruction: The obstructive pathology may lie in the proximal small intestinal or distal
intestine including the colon. Grade and severity of the obstructing lesion: The intestinal
obstruction could be either complete or incomplete (partial). While in the partial intestinal
obstruction, the gas or liquid stool can pass through the point of narrowing, in complete intestinal
obstruction, the obstruction is complete and there is no passage of gas or the liquid stool beyond
the point of the obstruction. Partial obstruction is further classified as high grade or low grade
according to the severity of the narrowing. In general, surgical intervention is often required for
complete intestinal obstruction; partial intestinal obstruction can be treated using conservative
measures.The mechanical intestinal obstruction could remain uncomplicated or may get
complicated by vascular compromise, intestinal perforation and septicemia.
Adynamic intestinal obstruction
There are two types of adynamic intestinal obstruction - paralytic ileus and acute intestinal
pseudo-obstruction.
It is important to classify intestinal obstruction into above mentioned catagories asthe treatment
of intestinal obstruction will vary according to the site, severity and cause of the intestinal
obstruction. Therefore, following questions should be addressed while dealing with a patient
with intestinal obstruction:
1. Differentiation between complete mechanical obstruction, partial mechanical obstructionor
adynamic obstruction
2. The site of obstruction: Small bowel obstruction (proximal or distal) vs. large bowel
obstruction (colon/rectal)

Patho-physiology
In simple intestinal obstruction, the intestine is occluded at one point. Fluid and chyme
accumulate proximal to the site of intestinal obstruction. This leads to impairment in intestinal
water and electrolyte absorption and enhanced intestinal secretion resulting in volume depletion.
Stasis of intestinal contents predisposes to bacterial overgrowth (predominantly anaerobes) in the
segment proximal to obstruction. The bacterial overgrowth leads to bacterial fermentation and
increased production ofgas. Accumulation of liquid and gas in the intestine leads to intestinal
dilatation which induces localinflammation and neuro-endocrine reflexes that initially increase
enteric propulsiveactivity to attempt to overcome the obstruction. Intestinal motilitygradually
decreases as intestinal muscle becomes fatigued.Intestinal dilatation graduallycompromises
vascular perfusion because of increasing intraluminalpressure and intramural tension. Forward
arterial flow is severely compromisedwhen the intraluminal pressure reaches the diastolic
pressure,and ceases when the intraluminal pressure reaches the systolic pressure.
Venousobstruction causes increased intraluminal fluid transudation and intramuraledema.
Almost 80% of blood flow to the intestine goes to the mucosa, therefore intestinal mucosa is
highly sensitive to ischemia as it is perfused by end arteries and has a high rate of metabolic
activity.
In closed-loop obstruction, anintestinal segment is occluded at two points.Common forms of
closed loops include an incarcerated hernia, in whicha loop of the intestine is compressed at both
ends within a hernial sac, and volvulus,in which a loop of intestine is mechanically compressed
at both ends because of a twist in the supporting mesentery. If the ileocecal valve is competent,
anobstructive lesionin the coloncauses a closed loopdue to a pathologic mechanical obstruction
at the distal end and a physiologic occlusion at theileocecal valve proximally. If the ileocecal
valve is incompetent, the obstructive lesionin the colon produces a simpleobstruction as the
colon is decompressed by way of the small intestine. Aclosed loop of intestine rapidly dilates
because of the lack of a proximaland a distal outlet for the accumulated gas and liquid. The
mucosa consequently develops ischemia rapidly. Extrinsic compression that
strangulatesmesenteric vessels (e.g. at a point of volvulus or at the neck of a hernialsack)
exacerbates the ischemia and rapidly produces intestinalgangrene or necrosis and perforation.
INCIDENCE OF THE CONDITION IN OUR COUNTRY
The most common (75%) cause of small intestinal obstruction is post-operative adhesions The
rate of adhesive small intestinal obstruction development is highest in the first few postoperative
years following the index surgery, particularly after colorectal surgery, but the risk remains life-
long. The risk of recurrent intestinal obstruction from adhesions after 10 years of the index
surgery varies widely from 15 to 50%. Although, post-operative intestinal obstruction recovers
mostly with conservative management, 25 to 66% of them may require exploratory laparotomy
and adhesinolysis. Although hernia was the second most important cause of intestinal
obstruction, there has been a marked decline of intestinal obstruction due to hernia from 40% in
the 1960s to 15%, presumably due to an increased rate of elective hernia repair. Other causes of
intestinal obstruction include intestinal tuberculosis, bands, and volvulus.
OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,
Clinical features of intestinal obstruction:
The clinical presentation varies depending on the severity, duration, andtype of intestinal
obstruction. The classical clinicaltetrad is colicky abdominal pain, nausea and vomiting,
abdominal distensionand progressive obstipation.
Differentiation between proximal vs distal intestinal obstruction
Proximal intestinal obstruction typically produces epigastricpain that occurs every 3 to 4
minutes, with frequent bilious vomiting. Distalintestinal obstruction typically produces peri-
umbilical pain that occurs every 15 to 20 minutes, with infrequent feculent emesis.Abdominal
distension is more marked in the distal obstruction as there is a large length of the intestine
proximal to the obstructive lesion, which can accumulate volumes of fluid and gas. Closed-loop
obstruction often presents with pain outof proportion to the abdominal signs because of
concurrent mesentericischemia. Inspection occasionally reveals visible peristalsis. Air-filled
intestinal loops produce abdominal tympany. Palpation reveals mild generalized abdominal
tenderness. Peritoneal signs, such as rebound tenderness and guarding, are typically absent,
unless intestinal necrosis or perforation supervenes. Intestinal sounds are initially high-pitched
(tinkling) and hyperactive, with audible rushes or borborygmi corresponding to paroxysms of
abdominal pain, but become progressively hypoactive and softer, and then disappear because of
intestinal fatigue. Patients with obstructive lesion in the rectum may give a history of spurious
diarrhoea, altered bowel habit and progressive constipation before presenting with large bowel
obstruction.
Features that suggest complications
The development of rigors, high fever, or systemic toxicity suggests thatthe obstruction may be
complicated by intestinal necrosis or perforation.Intussusception typically presents in infants
with episodic abdominal pain,currant jelly stools, and bilious vomiting.Physical examination
reveals an acutely ill, restless, and febrilepatient. Signs of intravascular volume depletion include
tachycardia, orthostatichypotension, dry mucous membranes, and poor skin turgor.
Jaundicesuggests possible gallstone ileus or malignant obstruction.
Features that suggest aetiology of intestinal obstruction
A good systemic and abdominal examination can provide important clues to the aetiology of the
intestinal obstruction. A history of previous abdominal surgery especially intestinal surgery can
point towards the most common cause of intestinal obstruction i.e. postoperative adhesive
intestinal obstruction. Other causes of intestinal obstruction such as abdominal scars, clinically
obvious external incarcerated hernia (femoral, inguinal, umbilical, or incisional), per-rectal
examination (fecal impaction, or a rectal mass), and digital examination of the stoma to rule out
stomal obstruction in patients with colostomy or ileostomy.Presence of hepatomegaly,
splenomegaly, a palpableabdominal mass, or periumbilical (Sister Mary Joseph nodule),
inguinal, and right supraclavicular (Virchow node) lymphadenopathy may suggest presence of a
malignant obstructive lesion in the intestine with systemic dissemination.
Evaluation at the time of acute obstruction
Plain upright abdominal radiograph
Plain upright abdominal X-ray film should be done for initial confirmation of intestinal
obstruction in patients presenting with clinical signs and symptoms of intestinal obstruction. It
can confirm intestinal obstruction in approximately 60%and its positive predictive value
approaches 80% in patients with high-grade intestinal obstruction.Presence of multiple air fluid
levels (> 3) in the erect film is an important sign pointing towards the diagnosis of intestinal
obstruction. At times when the patient is too sick a decubitus film also may help in detecting the
presence of air fluid levels. Large air fluid levels occurring more or less at the same level on the
radiograph are suggestive of paralytic ileus whereas air fluid levels at different levels are more
likely in a dynamic obstruction. Additionally, the abdominal film can show dilation of intestinal
loops (dilation >3 cm), and a transition zone between dilated and non dilatedintestinal segment.
The pattern of dilation can suggest the site of intestinal obstruction. While the supine abdominal
film in patients with small intestinal obstruction shows dilatation of multiple loops of small
intestine, with a paucity of air in the large intestine, the large intestinal obstruction shows
dilatation of the colon, with decompressed small intestine in the setting of a competent ileocecal
valve. It is important to assess the diameter of the distended caecum in such cases as dilatation
beyond 10 cm indicates impending caecal rupture. Air-filled loops of small intestine are
distinguished from those of large intestine by their more central abdominal location, by their
narrower calibre even when dilated, and by the presence of valvulaeconniventes that extend
across the entire luminal diameter as opposed to the colonic haustral folds that extend only
partially across the luminal diameter. Presence of free air under the diaphragms immediately
confirms intestinal perforation.Although this finding diminishes in significance if it is found on
an X-ray done in the early postoperative period following an abdominal surgery.
Limitation of abdominal radiograph: Plain abdominal film can appear normal in early
obstruction and in high gut obstruction (jejunal or duodenal obstruction) and thus may be
misleading.
Next step:
An abdominal CT scan,non contrast and contrast enhanced (both oral and intravenous contrast;
water-soluble contrast preferred) is appropriate for further evaluation of patients with suspected
intestinal obstruction in whom clinical examination and radiography do not yield a definitive
diagnosis. CT is very useful in a patient suspected to have intestinal obstruction and it can show
all that necessary information about the intestinal obstruction. The presence of a discrete
transition point helps guide operative planning.
CT findings in patients with intestinal obstruction include dilated loops of intestine proximal to
the site of obstruction, with distally decompressed intestine. In addition, CT can identify
emergent causes of intestinal obstruction, such as volvulus or intestinal strangulation.Although
CT is highly sensitive and specific for high-grade obstruction, its value diminishes in patients
with partial obstruction. In these patients, oral contrast material may be seen traversing the length
of the intestine to the rectum, with no discrete area of transition.
A C-loop of distended intestinal with radial mesenteric vessels with medial conversion is highly
suspicious for intestinal volvulus. Thickened intestinal walls and poor flow of contrast material
into a section of intestinal suggests ischemia, whereas pneumatosisintestinalis, free intra-
peritoneal air, and mesenteric fat stranding suggest necrosis and perforation. The CT can also
identify intussusceptions easily by picking up the intussusceptum in the intussuscepiens, as the
mesenteric fat and vasculature can be identified within the lumen of the intestine or a ‘double
target sign’ can be seen on cross-sectional imaging.
The American College of Radiology recommends non-contrast CT as the initial imaging
modality of choice.However, because most causes of small intestinal obstruction will have
systemic manifestations or fail to resolvenecessitating operative interventionthe additional
diagnostic value of CT compared with radiography is limited. Radiation exposure is also
significant. Therefore, in most patients, CT should be ordered when the diagnosis is in doubt,
when there is no surgical history or hernias to explain the etiology, or when there is a high index
of suspicion for complete or high-grade obstruction.The CT signs of strangulation include:a
thickened intestinal wall because of intestinal wall edema, inflammation, or intramural
hemorrhage; mural thumb-printing from intramural hemorrhage or edema;
pneumatosisintestinalis from intramural gas produced by bacteria; absence of enhancement with
intravenous contrast because of vascular hypoperfusion;hazy or streaky mesentery or ‘‘dirty’’ fat
from inflammatory infiltration, portal venous gas, target sign, and ascites.
Evaluation after resolution of an episode of intestinal obstruction with conservative
management
After the acute intestinal obstruction has resolved, the cause of intestinal obstruction should be
investigated and treated appropriately (medical or surgical) depending upon the diagnosis. The
basic principal of investigation is to find out site, cause, extent and etiology of the intestinal
obstructive disease.

enteroclysis

gical examination of the biopsies for pathological diagnosis

Evaluation after control of an episode of intestinal obstruction with surgery

Often, in patients with refractory adhesive intestinal obstruction, all that is required at
laparotomy is adhesiolysis to separate the adhesions and relieve the obstruction. In such cases
there is no need for any excision of intestine unless there is a strangulated gangrenous segment of
intestine. Whenever resection is warranted, the resected specimen should be evaluated both
histologically and microbiologically to determine the etiology. In some patients, inflammatory
lesions such as tuberculosis or Crohn’s disease, malignant lesions such as
adenocarcinomas/gastrointestinal stromal tumors or lymphomas, a specific treatment will be
required for the management of the disease postresection.
TREATMENT & REFERRAL CRITERIA
General measures
The principles in management of acute intestinal obstruction include correction of abnormalities
in the fluid and electrolyte imbalances, gastric decompression, and bowel rest, prevention of
infection, analgesics, and specific treatment for cause of obstruction.
Monitoring of clinical and hemodynamic status

Pulse, Blood pressure

Respiratory rate
Abdominal girth
Intestinal sound
Abdominal tenderness
Fluid and electrolyte balance

Intravenous fluid: Isotonic crystalloids

Arterial blood gas: Correction of acid base abnormalities
Correction of electrolyte imbalance, especially hypokalemia
Measurement of urine output
Symptomatic treatment
Oral administration of water-soluble contrast agent (Urograffin)(see below)*

Analgesics such as intravenous anti-cholinergics or NSAIDS

Anti-emetics: Metoclopromide, ondansetron
Antibiotics:

Antibiotics are used to treat intestinal overgrowth of bacteria and translocation across the
intestinal wall. The presence of fever and leukocytosis should prompt inclusion of antibiotics in
the initial treatment regimen. Antibiotics should have coverage against gram-negative organisms
and anaerobes, and the choice of a specific agent should be determined by local susceptibility
and availability.
Nutritional support:
o If intestinal obstruction is prolonged (for example ,in patients with post operative state)and the
patients cannot be fed enterally, they should be given total parenteral nutrition. Generally
speaking, a previously healthy adult can tolerate 5-7 days of fasting or bowel rest without any
significant clinical debility. Beyond this period appropriate parenteral nutritional support is
advisable.

Outcome following conservative management

Conservative management is successful in 40 to 70 percent of clinically stable patients, with a
higher success rate in those with partial intestinal obstruction.Although conservative
management is associated with shorter initial hospitalization, there is also a higher rate of
eventual recurrence. With conservative management, resolution generally occurs within 24 to 48
hours. Beyond this time frame, the risk of complications, including vascular compromise,
increases. If intestinal obstruction is not resolved with conservative management, surgical
evaluation is required.
Patients who develop adhesive intestinal obstructionof the small intestinein the postoperative
period(both early and late)constitute a special group of patients in whom a new form of
conservative intervention is indicated as outlined below.After the baseline abdominal
radiographs have documented intestinal obstruction, the next step is to administer 100 ml of
urograffin(water-soluble contrast agent) diluted in 400 ml of saline or drinking water orally or
through the nasogastric tubewhich has already been inserted as part of the conservative
management of intestinal obstruction. Thereafter, abdominal radiographs are obtained at 8-12 h
intervals till 24 hours of ingestion of urograffin.The appearance of contrast in the colon within 8-
24 h after its administration predicts resolution of small intestinal obstruction with a sensitivity
of 96% and specificity of 98%. Water soluble contrast agent administration is effective in
reducing the need for re-operation and shortening the hospital stay compared with conventional
‘drip-and-suck’ regimen. This simple therapeutic maneuver also has a diagnostic valueand can
delineate the level of obstruction in those patients in whom the contrast fails to reach the large
intestine in the stipulated time frame. In those patients in whom water soluble contrast agent does
not reach colon, the probability of need for surgery is higher. While administration of water
soluble contrast agent can occasionally be repeated, one should keep a close vigil on abdominal
signs and clinical status of the patient. This modality can also be used in other patients with
intestinal tuberculosis or Crohn’s disease who are likely to have a partialsmall intestinal
obstruction.
Indications for surgery
Although there are clinical features which allow a clinician to decide about the time of surgery
and also predict or suggest resolution of intestinal obstruction with conservative management in
the index patient, such a prediction is challenging at occasions. As such, presence of fever,
tachycardia, leukocytosis, or anion-gap acidosis, in the setting of abdominal imaging consistent
with obstruction constitutes a low threshold for laparotomy. Peritonitis remains an absolute
indication for exploration today as it did decades ago.There are clinical scenarios that are
considered somewhat exempt from an “early” operative approach in the absence of peritonitis.
These include small bowel obstruction in the early postoperative period (unless following
laparoscopic surgery), tuberculosis, Crohn’s disease, or carcinomatosis. Postoperative small
bowel obstruction occurs within 4–6 weeks of abdominal surgery with an estimated incidence of
1–4%. Caused by filmy adhesions in most open cases, up to 90% of these obstructions resolve
(dissolve or reform) with non-operative management within 7–14 days of the index operation.
The exception to this watchful waiting approach is postoperative obstruction following
laparoscopic surgery which warrants an early surgical approach more often than not. The cause
of obstruction will depend on the underlying operation, but it is likely that (amongst other
causes) intestine is incarcerated within a peritoneal defect caused by trocar placement. Clinical
situations such as, volvulus, obstructed hernia, large bowel obstruction with gross cecal
dilatation and instances where a closed loop obstruction is suspected should have a low threshold
for surgical intervention.
Patients with an intestinal obstruction that resolves after reduction of a hernia should be
scheduled for elective hernia repair, whereas immediate surgery is required in patients with an
irreducible or strangulated hernia. Stable patients with a history of abdominal malignancy or high
suspicion for malignancy should be thoroughly evaluated for optimal surgical planning.
Abdominal malignancy can be treated with primary resection and reconstruction or palliative
diversion, or placement of venting and feeding tubes. There is emerging evidence to suggest that
patients with colonic/rectal obstruction due to malignancies are best treated by emergency
surgical diversion/or resection (wherever feasible) rather than colonoscopic stenting.
Patients with post operative adhesive obstruction
Treatment of stable patients with intestinal obstruction and a history of abdominal surgery
present a challenge. Conservative management of a high-grade obstruction should be attempted
initially, using nasogastric suction and decompression, aggressive intravenous rehydration, and
antibiotics. Most show improvement in 48 hours. If not, then a therapeutic trial with water
soluble contrast agent (as described above) is warranted in the absence of peritoneal signs.
Specific measures
The cause of the intestinal obstruction should be treated appropriately.
a) Clinical Diagnosis: As above

b) Investigations: Haemogram, electrolytes, sugar, urea levels, chest and abdominal X rays

c) Treatment:

Standard Operating procedure

a. Inpatient: All patients suspected or confirmed to have intestinal obstruction should be admitted
and treated appropriately as described above.
b. Outpatient: Not applicable
c. Day Care: not applicable

d) Referral criteria:

Non availability of a surgeon,basic facilities as outlined above

A sick patient
Failed conservative management
Complete obstruction
Complicated obstruction
Perforation
Obstruction secondary to suspected malignancy
Obstruction in the setting of IBD
*Situation 2: At Super Specialty Facility in Metro location where higher-end technology is
available
a) Clinical Diagnosis:As above

b) Investigations:Hemogram, electrolytes, RFT, LFT, Blood gases, Serum lactate levels, X-ray:
chest/abdomen, CT scan, endoscopic facilities
c) Treatment:

Standard Operating procedure

a. Inpatient: as outlined above
b. Outpatient Not recommended;provide follow up and counseling after discharge
c. Day Care: Not recommended in the acute setting;

d) Referral criteria:None

WHO DOES WHAT? and TIMELINES

a. Doctor
b. Nurse
c. Technician

96. PANCREATIC CARCINOMA

I. WHEN TO SUSPECT/ RECOGNIZE?

a) Introduction:

The most common histological type of pancreatic cancer is ductal adenocarcinoma, which
accounts for over 90% of all tumors. Most pancreatic cancers are advanced at the time of
diagnosis.The overall 5-year survival rate is 4%. Because the 5-year survival of this condition is
so poor, incidence and mortality rates are virtually identical. At the time of diagnosis,
approximately 80% of all pancreatic cancers are advanced. The 5-year survival of operated
patients approaches 40% when performed at specialized medical institutions. Pancreatic cancer is
rare before the age of 45 years and 80% of cases occur in the 60–80 year age group.
b) Case definition:

For both situations of care (mentioned below*)

The three main symptoms of pancreatic cancer are pain, loss of weight, and jaundice. However,
signs and symptoms are non-specific.
Cases of pancreatic cancer are defined by image guided biopsy, surgical resection or intra-
operative biopsy, or suggestive imaging features with a progressive and compatible clinical
course on follow up.
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY

The incidence of pancreatic cancer in India hastraditionally been thought to be low (0.5-2.4 per
100,000 men and 0.2-1.8 per 100,000 women). However, this is likely to be a reflection of
under-recognition and under-reporting. The incidence of pancreatic cancer is higher in the urban
male populations of western and northern parts of India. Time trends show that the incidence is
increasing for both carcinoma of the pancreas and also peri-ampullary tumors.
The annual pancreatic cancer load of India in 2001 was approximately 14,230 patients: the
estimated current figure is approximately 17,000 and is likely to increase in the near future.
III. DIFFERENTIAL DIAGNOSIS

1) Chronic pancreatitis, including autoimmune pancreatitis.

2) Acute pancreatitis, including focal pancreatitis / pseudo-tumoral pancreatitis / groove

pancreatitis.

3) Metastasis to the pancreas from renal cell carcinoma, melanoma, breast cancer, colon cancer
e.t.c

IV. PREVENTION AND COUNSELING

No simple screening test is available for the general population.

The strongest etiological association of pancreatic cancer is with cigarette smoking. Hence health
education to reduce tobacco consumption should lower the risk of developing pancreatic
carcinoma.

Other high-risk groups include patients with chronic pancreatitis, adult onset diabetes of less than
two years’ duration, hereditary pancreatitis, familial pancreatic cancers, and certain familial
cancer syndromes. However, there are no screening or preventive guidelines for these higher risk
groups.

V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &

REFERRAL CRITERIA

INVESTIGATIONS,
The goals of investigations are:
(a) Establishing the diagnosis, and
(b) Assessing the tumor resectability

The following investigations can be used as indicated:

1) Abdominal ultrasound.

2) Computerized tomography (CT) scan.

3) Magnetic resonance (MR), including magnetic resonance cholangiopancreatography (MRCP).

4) Positron emission tomography (PET) - CT scan

5) Endosonography (EUS).

6) Laparoscopy with laparoscopic ultrasonography

Endoscopic retrograde cholangiopancreatography (ERCP) is now seldom used for the primary
diagnosis. However, it can be used to obtain intra-ductal tissue for diagnosis, when biliary
drainage is planned.
TREATMENT
(a) Curative treatment

Pancreaticoduodenectomy (with or without pylorus preservation) is the most appropriate

resectional procedure for tumors of the pancreatic head. Left sided resection (with splenectomy)
is appropriate for localized carcinomas of the body and tail of the pancreas. Involvement of the
splenic vein or artery is not in itself a contraindication to such resection.
(b) Neoadjuvant treatment

Neoadjuvant treatment is indicated for tumors considered borderline resectable. This category
includes the following:
(1) No distant metastases.
(2) Venous involvement of the SMV/portal vein demonstrating tumor abutment with or without
impingement and narrowing of the lumen, encasement of the SMV/portal vein but without
encasement of the nearby arteries, or short segment venous occlusion resulting from either tumor
thrombus or encasement but with suitable vessel proximal and distal to the area of vessel
involvement, allowing for safe resection and reconstruction.
(3) Gastroduodenal artery encasement up to the hepatic artery with either short segment
encasement or direct abutment of the hepatic artery, without extension to the celiac axis.
(4) Tumor abutment of the SMA not to exceed greater than 180 degrees of the circumference of
the vessel wall. Gemcitabine or gemcitabine-based combination therapy may be considered as
initial therapy prior to 5-FU-based chemoradiation.
(c) Palliative treatment

Palliative treatment is indicated for unresectable tumors, which are defined by the following
criteria, according to the tumor location:
Pancreatic head tumors:
1) Distant metastases
2) Greater than 180 degrees SMA encasement, any celiac abutment
3) Unreconstructible SMV/portal occlusion
4) Aortic invasion or encasement

Pancreatic body tumors:

1) Distant metastases
2) SMA or celiac encasement greater than 180 degrees
3) Unreconstructible SMV/portal occlusion
4) Aortic invasion
Pancreatic tail tumors:
1) Distant metastases
2) SMA or celiac encasement greater than 180 degrees

All tumors with metastases to lymph nodes beyond the field of resection should be considered
unresectable.
1. Surgical palliation
Surgery for palliative purpose is now rarely indicated. It may have some role in resource-limited
setting. It may also be indicated if the patient is found to be unresectable during laparotomy.
Duodenal and biliary bypass should be used during palliative surgery. The biliary bypass should
be constructed with the bile duct in preference to the gall bladder.
2. Medical palliation
2.1 Patients should have access to palliative care specialists. Pain relief should be achieved using
a progressive analgesic ladder.
2.2 Patients with pancreatic head tumors, who require relief of jaundice will need biliary
stenting. Endoscopic stent placement is preferable to trans-hepatic stenting. Both plastic and self-
expanding metal stents (SEMS) are effective in achieving biliary drainage but SEMS are
preferable for patients with longer life expectancy (more than 6 months). Currently, the choice
between these stents depends on clinical factors, local availability, and local expertise.
Plastic stents have been traditionally placed to relieve jaundice before surgery. However, covered
SEMS can also be placed without compromising the surgery and afford a faster relief of
jaundice.
2.3 Gastric outlet obstruction can be palliated with enteral SEMS.
2.4 Treatment of associated depression.
2.5 Pancreatic enzyme replacement for pancreatic insufficiency.
2.6 Low molecular weight heparin for prophylaxis of thromboembolic disease.
2.7 Gemcitabine is considered the standard front line chemotherapy for patients with metastatic
disease. Gemcitabine combinations have shown a favorable impact on time to progression or
survival for patients with good performance status.
Treatment in Situations where technology and resources are limited
a) Clinical Diagnosis:
b) Investigations:
1) Liver function tests.
2) CA 19.9 levels (CA 19-9 may be elevated in cases of benign biliary obstruction and does not
represent an appropriate baseline until the patient is decompressed. In addition, CA19-9 may be
undetectable in Lewis-a negative individuals).
3) Chest imaging.
4) Abdominal ultrasound.
5) CT or MRI scanning.
c) Treatment:
1) Nutritional build up and early referral for potentially resectable patients.
2) Symptom palliation for unresectable patients.
Standard Operating procedure
a. In Patient
b. Out Patient
c. Day Care

d) Referral criteria:
1) Suspected carcinoma pancreas, where the diagnosis cannot be established with the existing
resources.
2) Potentially resectable patients for further staging.
3) Potentially resectable patients for pancreaticoduodenectomy surgery to a high volume center.
4) Unresectable patients, with specialized palliation needs, like celiac plexus neurolysis, patient
controlled analgesia, stenting for relief of biliary obstruction e.t.c.
a) Clinical Diagnosis:
b) Investigations:
In addition to above:
1) PET-CT scan
2) Endoscopic ultrasound.
3) Laparoscopy and laparoscopic ultrasound.
4) Guided biopsy techniques for patients considered not suitable for surgical resection. If biopsy
is required in a resectable lesion, then EUS-directed FNA biopsy is preferable to a CT-guided
FNA because of lower risk of peritoneal seeding with the former. Biopsy proof of malignancy is
not required before surgical resection and a non-diagnostic biopsy should not delay surgical
resection when the clinical suspicion for pancreatic cancer is high.
c) Treatment:
In addition to above, super-specialty facilities should also have:
1) Facilities for assessment of resectability.
2) Increased therapeutic resources, including oncologic treatment.
3) Adequate surgical expertise for pancreatic resections.
4) Specialized services in histopathology, intensive care, and palliative care.
5) Facilities for the organization and conduct of local, national, and international trials.
Standard Operating procedure
a. In Patient
b. Out Patient
c. Day Care
VI. WHO DOES WHAT? and TIMELINES
a. Doctor Clinical evaluation, decides investigations, interprets the investigations, and generates
a treatment plan.
b. Nurse Ensures adequacy of palliative care, and carries out the treatment plan.
c. Technician Carries out the investigations planned.
General surgery
97. BLUNT ABDOMINAL TRAUMA

1. Name of the condition: Blunt abdominal trauma

2. When to suspect/ recognize?
a. Introduction: Blunt abdominal trauma (BAT) is an increasingly common problem
encountered in the emergency department. The usual causes of BAT include vehicular accident,
assault, falls, sports injuries and natural disasters.
b. Case definition: BAT is suspected in any patient involved in above situations and presents
with abdominal pain, distention or shock. It should be looked for in patients of polytrauma.
3. Incidence of the condition in our country: One study has reported 2.1% incidence of BAT
amongst all surgical patients admitted to a tertiary hospital during 1 year.
4. Differential diagnosis:Abdominal trauma forms adifferential diagnosis of any patient
presenting with acute abdomen.
5. Prevention and counseling: Use of appropriate safety measures during various activities
associated with BAT can significantly reduce its incidence.
6. Optimal diagnostic criteria, investigations, treatment and referral criteria:
a. Situation 1 At Secondary Hospital/ Non-metro situation: Optimal standard of treatment
in situations where resources are limited
I. Clinical diagnosis:This is based on
a. High level of suspicion of intra-abdominal injury
b. Presence of wounds/ bruising on the abdomen
c. Abdominal guarding/ tenderness
d. Presence of free gas/ fluid in the peritoneal cavity
e. Presence of fracture of lower ribs and/ or pelvis increases the likelihood of intra-abdominal
injury
f. Note should be made of altered mental state, drug or alcohol intoxication and distracting
injuries which may mask the features of BAT
g. Repeated examination increases the accuracy of diagnosis
II. Investigations:
a. All hemodynamically stable patients with suspected BAT should undergo Focused Abdominal
Sonography in Trauma (FAST)or Diagnostic Peritoneal Lavage (DPL)
b. Urgent laparotomy is indicated in patients with evidence of BAT who remain
hemodynamically unstable despite initial resuscitation
III. Treatment (Standard operating procedure):
a. Inpatient:
i. All patients should have initial cervical stabilization and resuscitation, if required
ii. Initial fluid resuscitation should be done with 2L warmed Ringer Lactate solution
infusedrapidly through 2 peripheral lines
iii. A nasogastric tube and a Foley catheter should be put
iv. Laparotomy should be done, if indicated on the basis of clinical features, FASTor DPL
v. Laparotomy should be done through a long midline incision
vi. Bleeding should be controlled by clamping/ packing till definitive control is possible
vii. Hollow viscus should be repaired
viii. In case the intra-abdominal injuries are extensive, patient is very sick and OT facilities/
surgeon’s experience is suboptimal, Damage Control Surgery may be done. Definitive surgery
should be done subsequently under improved circumstances or at a higher center.
b. Outpatient: Not indicated
c. Day care: Not indicated
IV. Referral criteria: After Damage Control Surgery if the local facilities are inadequate.

1. Clinical diagnosis: Same as 6a

2. Investigations:
a. Same as 6a
b. CECT abdomen is preferred investigation in all hemodynamically stable patients with BAT
c. Angiography and angioembolization may be considered in hemodynamically stable patients
with solid organ injury who are suitable for non-operative management
3. Treatment (Standard operating procedure):
a. Inpatient:
i. Same as 6a
ii. In case the intra-abdominal injuries are extensive, patient is very sick and surgeon’s
experience is suboptimal, Damage Control Surgery may be done. Definitive surgery should be
done subsequently under improved circumstances
iii. Angiography and angioembolization may be considered in hemodynamically stable patients
with solid organ injury who are suitable for non-operative management
b. Outpatient: Not indicated
c. Day care: Not indicated
4. Referral criteria: Not indicated
7. Who does what and timelines:
a. Doctor: Does initial evaluation, subsequent monitoring, decision regarding investigations and
therapeutic intervention.
b. Nurse: Assists in resuscitation, monitoring, investigation and treatment.
c. Technician: Assists in resuscitation, investigation and treatment.
8. Further reading/ references
a. Udeani J, Steinberg SR. Blunt abdominal trauma. URL:
http://emedicine.medscape.com/article/433404-print
b. Joint theatre Trauma System Clinical Practice Guideline: Blunt abdominal trauma. URL:
http://www.usaisr.amedd.army.mil/cpgs/Blunt%20Abdominal%20Trauma%2030%20Jun%2010.
pdf
c. M. Swarnkar, P. Singh & S. Dwivedi : Pattern Of Trauma In Central India: An
Epidemiological Study With Special Reference To Mode Of Injury. The Internet Journal of
Epidemiology. 2010 Volume 9 Number 1

98. CHOLECYSTECTOMY

INTRODUCTION:
Cholecystectomy is one of the commonest elective surgical procedure performed in India. Most
are performed to address symptoms related to biliary colic from cholelithiasis, to treat
complications of gallstones (eg, acute cholecystitis, biliary pancreatitis), or as incidental
cholecystectomies performed during other open abdominal procedures. Currently, most
cholecystectomies are done using the laparoscopic technique in cities; however, the open
technique is required in places where facilities or trained staff are not available.
DEFINITION:
Cholecystectomy implies the surgical resection the gall bladder.
INDIAN INCIDENCE
In India, the incidence of gall stones is around six percent in the total population. It is 10 per cent
in women and three per cent in men. In elderly people it may go up to 20 percent.
INDICATIONS:
Asymptomatic patients
Cholecystectomy is not indicated in most patients with asymptomatic stones because only 2-3%
of these patients go on to become symptomatic per year. To properly determine the indications
for elective cholecystectomy, the risk of the operation (taking into account the age and comorbid
factors of the individual patient) must be weighed against the risk of complications and death
without operation.
The widespread use of diagnostic abdominal ultrasonography has led to the increasing detection
of clinically unsuspected gallstones. This, in turn, has given rise to a great deal of controversy
regarding the optimal management of asymptomatic (silent) gallstones.
Patients who are immunocompromised, are awaiting organ allotransplantation, or have sickle
cell disease are at higher risk of developing complications and should be treated irrespective of
the presence or absence of symptoms.
Additional reasons to consider prophylactic cholecystectomy include the following:

prevalence of gallbladder cancer

cified (porcelain) gallbladder

developing cholelithiasis is increased during rapid weight loss. Routine prophylactic
cholecystectomy prior to gastric bypass (RYGB) is controversial, but cholecystectomy should
clearly precede or be performed at the time of RYGB in patients with a history of gallbladder
pathology.

Symptomatic gallstone disease

Biliary colic with sonographically identifiable stones is the most common indication for elective
cholecystectomy.
Acute cholecystitis, when diagnosed within 72 hours from the onset of symptoms, can and
usually should be treated by surgery. Once 72 hours pass after the onset of symptoms,
inflammatory changes in the surrounding tissues are widely believed to render dissection planes
more difficult. Interval cholecystectomy after 4-6 weeks or percutaneous cholecystostomy are
other options.
Biliary dyskinesia should be considered in patients who present with biliary colic in the absence
of gallstones, and a cholecystokinin–diisopropyl iminodiacetic acid (CCK-DISIDA) scanning
should be obtained. The finding of a gallbladder ejection fraction <35% at 20 minutes is
considered abnormal and constitutes another indication for cholecystectomy.

Complex gallbladder disease

Gallstone pancreatitis
Cholecystectomy can be safely performed during the same hospitalization after the clinical signs
of mild to moderate biliary pancreatitis have resolved. Patients diagnosed with gallstone
pancreatitis should first undergo imaging to rule out the presence of choledocholithiasis.
Cholecystectomy should be delayed in cases of acute moderate to severe biliary pancreatitis (5
Ranson criteria).
Choledocholithiasis
The following treatment options are available for patients found to have choledocholithiasis:
Preoperative ERCP with sphincterotomy
Postoperative ERCP with sphincterotomy
Laparoscopic intraoperative cholangiogram with laparoscopic common bile duct (CBD)
exploration
Open CBD exploration and T-tube placement
Mirizzi syndrome
P.L. Mirizzi described an unusual presentation of gallstones that, when lodged in either the cystic
duct or the Hartmann pouch of the gallbladder, externally compressed the common hepatic duct,
causing symptoms of obstructive jaundice. Although an initial trial of dissection may be
performed by an experienced laparoscopic biliary surgeon, one must be prepared for conversion
and for biliary reconstruction.
Endoscopic stone fragmentation at ERCP, with papillotomy and stenting, is a viable alternative
to operative surgery to treat Mirizzi syndrome in the acute setting.[24 ]Subsequent
cholecystectomy may be performed.[25 ]
Cholecystoduodenal fistula
Patients with cholecystoduodenal fistula leading to gallstone ileus should undergo exploratory
laparotomy and removal of the stone, followed by exploration of the remainder of the
gastrointestinal tract for additional stones. The fistula may be addressed at the time of the initial
procedure but is probably better addressed at a second operation (3-4 wk postoperatively) after
inflammation has subsided.[25 ]
Cholecystenteric fistula does not represent an absolute contraindication to laparoscopic surgery,
although it does require careful visualization of the anatomy and good laparoscopic suturing
skills.
Acalculous cholecystitis
A greater proportion of patients with acalculous cholecystitis are too ill to undergo surgery. In
these situations, percutaneous cholecystostomy guided by CT or ultrasonography is advised.
Ninety percent of these patients demonstrate clinical improvement. Once the patient has
recovered, the cholecystostomy tube can be removed, usually at 6 weeks, without sequelae.
Interval cholecystectomy is not necessary.[27 ]
Incidental gallbladder cancer
Gallbladder cancer may be an incidental finding at cholecystectomy, with an incidence ranging
from 0.3-5.0%.
Uncertainty of diagnosis, uncertainty of the degree of tumor spread, or postoperative
identification of cancer on pathological examination of a routine cholecystectomy specimen
should engender early reoperation.
Before reoperation, distant metastases should be excluded by a detailed clinical examination
including a per-rectal/per-vaginal examination, examination for supraclavicular lymph nodes,
and CT/MRI of the chest and abdomen.
Special situations
Children
Cholecystectomy is a safe and effective treatment for most children diagnosed with biliary
disease (BD).
Cirrhosis
Cholecystectomy in safe in patients with Child class cirrhosis.
Diabetes mellitus
The presence of diabetes mellitus, in and of itself, does not confer sufficient risk to warrant
prophylactic cholecystectomy in asymptomatic individuals.
However, consider that acute cholecystitis in a patient with diabetes is associated with a
significantly higher frequency of infectious complications such as sepsis.
Pregnancy
The treatment of biliary colic or uncomplicated cholecystitis in a pregnant patient is conservative
management followed by elective cholecystectomy. Using antibiotics, analgesics, and
antiemetics help most pregnant women avoid surgical intervention. Surgery is generally
indicated for patients with recurrent acute cholecystitis who have failed maximal medical
therapy.
Classically, the second trimester is considered the safest time for surgery. This is because of the
findings of increased risk for spontaneous abortion and teratogenesis during the first trimester,
and the increased risk for premature labor and difficulties with visualization in the third
trimester.
Pregnancy was formerly considered to be an absolute contraindication to the laparoscopic
approach because of concern for potential trocar injury to the uterus and the unknown effects of
pneumoperitoneum to the fetal circulation. However, this has not been borne out in the literature,
and cholecystectomy is now considered safe.
Recommendations for pregnant patients who undergo laparoscopic cholecystectomy include
placing them in the left lateral recumbent position to shift the weight of the gravid uterus off the
vena cava and maintenance of insufflation pressures between 10 and 12 mm Hg. In addition,
maternal PaCO 2 monitoring must be performed by measuring either arterial blood gases or end-
tidal CO 2 , but arterial PaCO 2 may be more accurate.
Other recommendations include avoiding rapid changes in intraperitoneal pressures, avoiding
rapid changes in patient position, and using open technique for the umbilical port placement.

INVESTIGATIONS:
aemogram
Liver Function Tests
Blood sugar
Serum creatinine
Bleeding time, clotting time and prothrombin time
Xray chest
ECG
USG abdomen
In patients with dilated common bile duct or raised liver functions, MRCP or ERCP may be
indicated based on availability. Alternatively, an on table cholangiogram or CBD exploration
may be done during surgery. Patient can be referred to another centre in case of non availability
of expertise or experience.

OPERATIVE TECHNIQUES:
Principles of surgery remain the same regardless of whether it is being done by open or
laparoscopic technique.

omy in the calots triangle showing either the continuity between cystic
duct and gall bladder or junction between cytic duct and common bile duct.
 er.

REFERRAL CRITERIA:

bladder cancer.

possible.

WHO DOES WHAT?

Doctor:
a) Surgeon: diagnosis & work up

Pre operative planning

Operative procedure
Post operative follow up
b) Anesthetist: PAC, anesthesia, post op ICU management

NURSE:

TECHNICIAN:
99. CIRCUMSION

INTRODUCTION:
Religious male circumcision is considered a commandment from God in Judaism widely
practiced in Islam and customary in Christian churches in Africa. Virtually all the current policy
statements from specialty societies and medical organizations do not recommend routine
neonatal circumcision
The opponents to circumcision consider it a violation of human rights
CASE DEFINITION:
The words “circumcision” is derived from the Latin circum (meaning “around”) and coedre
(meaning “to cut”). Male circumcision is the removal of some or the entire foreskin (prepuce)
from the penis
MEDICAL INDICATIONS:
– true phimosis caused by BXO (Balanitis xerotica obliterans)

– inability to retract prepuce for intercourse

bnormally tight frenulum

INCIDENCE:
Proportion of males circumcised worldwide vary from one sixth to a third
Circumcision is most prevalent in the Muslim countries of the world
In India too, it is nearly 100% among Muslims 15
PREVENTION AND COUNSELLING:
Physiological adhesion between the foreskin and glans penis may persist until 6 years of age and
be mistaken for phimosis. Forcible retraction of the skin is not recommended in physiological
phimosis.
At 4-5 years of age, topical corticosteroid cream may be used for 6 weeks if phimosis continues
to exist.
Circumcision – is done if it is

Carcinoma penis should be ruled out. When confined to prepuce, circumcision may be adequate
treatment but regular follow up is necessary
Similarly chancre which may present as phimosis should be ruled out
Balanitis xerotica obliterans – normal foreskin becomes thickened and does not retract
Has increased susceptibility to carcinoma and hence requires early treatment
Treatment is circumcision
OPTIMAL DIAGNOSTIC CRITERIA:
Phimosis is diagnosed by inability to retract the prepucial skin
SITUATION 1:
i.PHIMOSIS: clinical features

ii. PARAPHIMOSIS: clinical features

Retracted prepuce cannot be pulled forward; forms a tight ring and acts as constriction. Venous
congestion increases with swelling of glans and can result in ulceration and gangrene of the glans
iii. History of diabetes with recurrent attacks of balanophosthitits
iv. History of bleeding and short duration of lack of retractibility would suggest carcinoma
v. History of STD; sexual history to r/o chancre

DIFFERENTIAL DIAGNOSIS:
1. Chancre
2. Cancer
3. Meatal stenosis (masked by prepuce)

INVESTIGATION:
Simple phimosis is a clinical diagnosis and requires no investigation for confirmation
Routine investigation before surgery such as
Blood sugar
Haemogram
Urine r/m
X Ray and ECG may be done as per anaesthetic indication
Biopsy of underlying lesion if any
USG of the abdomen and pelvis to evaluate the entire urinary tract in cases of UTI
TREATMENT:
Medical treatment in children 5-6 years with congenital phimosis – topical steroid cream
Surgical treatment – circumcision
PROCEDURE:
In infant:
Applying a clamp (or bone forcepts) across the prepuce distal to the glans with blind division of
the foreskin is to be condemned
Perform a proper circumcision under direct vision as in an adult
ANAESTHESIA –
GA – in children, infants and neonates
Dorsal penile nerve block, Ring block and / or EMLA (lidocaine/prilocaine) topical cream may
be used in adults Razmus et al reported that newborns circumcised with the dorsal block and ring
block in combination with oral cucrose had lowest pain scores
Wg et al found EMLA cream in addition to local anaesthetic effectively reduces the sharp pain
induced by needle puncture
In adults frenular stretch must to avoid bleeding from frenular artery
Histopathology: should be done when there is suspicion of malignancy or other associated
conditions
POST OP:
Analgesic
Antibiotic: perioperative dose
Abstinence for 4-6 weeks in adults
The patient should be reviewed 5-7 days post op
Retract and clean any skin covering the glans to prevent adhesion
COMPLICATINS OF CIRCUMCISION:

– if insufficient skin is removed in a child during the first sugery

SOP: Day care

REFERAL CRITERIA:
The patient should be referred to a higher centre for treatment of associated conditions if any,
such as malignancy
Patient with bleeding disorders and co morbidities may be safely operated in a higher centre

SITUATION 2:
DIAGNOSIS: Clinical as in situation 1
INVESTIGATIONS: as in situation 1
HbA1C
Coagulation profile if bleeding disorder is suspected

TREATMENT:
As in situation 1
Additional procedures:
Devices are available for infant circumcision – Plastibell, Gomco clamp, or Mogen clamp used
together with a restraining device
1. Frenulum may need to be broken or crushed and cut from the corona near the urethra to ensure
that the glans can be freely and completely exposed

SOP: Day care

WHO DOES WHAT? AND TIMELINES
a. Doctors:
xamination

b. Nurse:

c. Technician:

rgeon
100. COLECTOMY

INTRODUCTION:
Sir William Arbuthnot was one of the early proponents of the usefulness of total colectomies.
Colectomy is commonly performed for the treatment of colon cancer.
DEFINITION:
Colectomy implies the surgical resection of any extent of the large intestine (colon).
Based on the segment of colon removed colectomies are termed as
1. Right hemicolectomy.
2. Extended right hemicolectomy
3. Transverse colectomy
4. V resection
5. Left hemicolectomy
6. Extended left hemicolectomy
7. Sigmoidectomy
8. Proctosigmoidectomy
9. Total colectomy
10. Total proctocolectomy
11. Subtotal colectomy

INDIAN INCIDENCE: not documented

DIFFERENTIAL DIAGNOSIS:

Inflammatory bowel disease-ulcerative colitis, Crohn’s disease

wer gastro intestinal bleeding

PREVENTION:
In familiar situations like FAP & HNPCC early colectomy is advised.
It is important to understand the carcinogenesis in colorectal cancer & the associated molecular
events.
ENVIRONMENTAL FACTORS also pay an important role, particularly dietary factors &
estrogen replacement.
Association between hyperplastic polyposis & colorectal cancer & adenomas called sporadic
MIS tumuors
Colorectal cancers: are Sporadic in 75% cases & Genetic in 25% (younger age at diagnosis)
Positive Familial history is present in 15%-20%.
HNPCC (5%)-80% risk
FAP(less than 1%)-100% risk of development of CRC – prophylactic total
colectomy/proctocolectomy
COUNSELLING:
GENETIC COUNSELLING
PREDISPOSITION SHOULD BE COUNSELLED & SCREENED FOR COLON CANCER.
Screening colonoscopy and polypectomy – reduces colon cancer mortality.
1. OPTIMAL DIAGNOSTIC CRITERIA:
Situation 1
Clinical Diagnosis
Anatomical locations and clinical manifestations of colon cancer

INVESTIGATIONS:
Haemogram
Colonoscopy – investigation of choice
- Biopsy & HPE

- Brush cytology if biopsy is not possible

-ray abdomen – if patient presents with features of large bowel obstruction

- When colonoscopy is contra indicated or not available

- Findings – constant irregular filling defect
- Detects associated lesions
- Small ulcerative lesions can be diagnosed

inal ultrasound – if available

– if available is used in large palpable abdominal masses
= To determine local invasion
– when evidence of hydronephrosis on USG/ CT in left sided tumours

TREATMENT:
1. Pre op evaluation of staging, respectability, patient’s operative risks are mandatory.
2. Accurate localization of tumour – of particular importance.
a. Sometimes known cancer may not be apparent on serosal aspect.
b. Localization by tattooing during colonoscopy, Barium enema.
c. Pre op CT, USG assessment of iver metastasis should be done

PRE OP PREPARATION:
Mechanical bowel preparation
Prophylactic antibiotics
Blood grouping and cross matching
Thromboembolism prophylaxis
OPERATIVE TECHNIQUES:
Resection should follow
Standard oncological principles:

argins(5 cm) determined by area supplied by the primary feeder

artery

– harvesting of minimum 12 nodes

y strongly influences prognosis & therapy

Ro – absence of residual tumour, margins free histologically

R1 – no gross residual tumour but margins histologically positive
R2 – residual gross disease remains unresected

RADIAL MARGIN:
T4 lesions are a complex group & should be considered separate from other T groups
Radial tumour free margins should be resected. Radial margin should be histologically free of
disease for resection to be curative.
Specimen labeling, marking are important for a good pathological report
R1 & R2 resection – incomplete resection for cure affects curability though TNM stage remains
same
LATERAL CIRCUMFERENTIAL MARGIN:
In addition to radial, proximal & distal margins, circumferential margins should also be
pathologically assessed. Positive margins are associated with increased rate of local and distal
failure.
Disease free survival and mortality significantly related to margin involvement after TME
ADJUVANT Ro stage:
Adjuvant therapies require complete resection
A case is not Ro if it is
LYMPHADENECTOMY:
Should be radical (up to the level of origin of primary feeding artery)
Apical nodes positive for disease may have prognostic significance in addition to number of
positive lymph nodes
ENBLOC RESECTION of adherent tumours : En bloc removal of adjacent organs locally
invaded by cancer colon can achieve survival rates similar to patients with tumour that do not
invade an adjacent organ, provided negatgive resection margins are achieved.
PERFORATION OF TUMOUR SHOULD BE AVOIDED (SAGES GUIDELINE)
Inadvertent full thickness perforation of rectum would probably classify tumour as T4 and
resection as R1
Perforation at the site of cancer, as opposed to an area remote from the tumour has a greater
impact on survival & local recurrence.
Inadvertent local perforation predisposes to local recurrence and warrants post-operative
radiotherapy.
INTRAOPERATIVE SPILLAGE:
HAS AN INDEPENDENTT EFFECT ON PROGNOSIS
Adjuvant radiotherapy may be considered to decrease rates of local recurrence
NO TOUCH TECHNIQUE:
Value inconclusive
SURGICAL PROCEDURES:
Anatomical Resection of Colon Cancer
Colectomy may be performed by the
i) Conventional open technique

REFERRAL CRITERIA:
Patients suspected of colon cancer & biopsy proven should be referred to a higher centre for
further evaluation and treatment when
1) Adequate surgical facilities are not available / surgeon does not have sufficient experience in
colon cancer surgery.

2) Competent pathologist to report on malignant lesions as per standard oncological guidelines is

not available.

3) For adjuvant / neo-adjuvant radio and chemo therapy

TREATMENT:
Patient requiring colectomy for biopsy proven cancer are best referred to a super specialty centre
In view of the need for multi modality treatment.
SITUATION 2:
All investigations as in situation 1
 – 6 mm polyps may be picked up effectively

– fetal glycoprotein

- Increased pre op CEA in node positive Ca – indication for chemotherapy

– if single photon emission is studied, such as technetium or thallium

-PET – useful in evaluation of recurrent colorectal cancer

-Differentiates post op changes from recurrent / residual disease

-Useful diagnostic tool but prohibitive cost
-PET – fusion tests provide the most powerful integrated images

R MEDICINE IMAGING:

-Using 131I, 111In, 99mTc bound to monoclonal antibodies, leucocytes & erythrocytes.
TREATMENT:
As outlined in situation 1.
Laparoscopic resection is gaining popularity. However it is not freely available & performed as
per protocols.
SPECIAL CONSIDERATIONS
1. Synchronous malignancies or polyps

Patients with synchronous malignancies should be considered for subtotal colectomy depending
on the distance between lesions
Colonic cancer with multiple adenomatous polyps – subtotal colectomy (Due to increased risk of
metachronous lesion and to facilitate surveillance of the remaining colon)
Factors that influence the decision to perform prophylactic subtotal colectomy
-number
-location
-size of accompanying polyps
-age
-compliance of patient
2. Cancer is a polyp

Complete endoscopic removal of polyp with cancer in situ – no further treatment

Histoplathology shows invasive carcinoma:
Ensure that endoscopic polypectomy was complete
Specimen was submitted with proper orientation to the pathologist for histopathology
Carcinoma at margin of resection requires formal resection
Carcinoma with free margins – a. thorough pathological review,
b. identification of adverse histological features
i. poor differentiation,
ii lymphatic or venous invasion
iii invasion into the stock of the polyp – formal
resection
It is difficult to locate the previous polypectomy site during surgery
Even if polyp is not removed it may be soft and difficult to palpate through the colon wall
Endoscopic distance (from anal verge or dentate line) misleading
Polypectomy site should be videotaped for later review and marked with vital dye that can be
seen serosally at the time of surgery
3. Obstructing Cancers- 2% of colorectal cancers

Partial obstruction – Gentle bowel preparation over several days-Elective surgery

Total obstruction
- Rt colon cancers – Rt Hemi colectomy – immediate ileocolostomy

- Lt colon cancers

1) Endoscopic decompression by laser passed beyond the obstructed

Segment – This allows mechanical preparation and elective resection.
- This is possible only when the narrowed lumen can be traversed by the endoscope.

- It is not possible when obstruction is complete

2) Primary resection and immediate anastamosis with on-table colonic

washout with or without proximal colostomy.

3) Primary resection with colostomy. Anastamosis at second stage.
4) Subtotal colectomy with primary anastamosis
5) Decompressive colostomy followed by formal colonic resection
4. Adjacent organ involvement- 10%

Locally advanced tumours are potentially curable with multi organ resection.-Do not necessarily
Portend a dismal prognosis.
-A non metastasizing variant of colon cancer grows to a large size without spreading to regional
nodes
-Separation of adhesions adjacent to a malignancy can lead to dissemination of tumour cells. -
Enbloc resection of these tumours, depending on location can lead to five year survivals of 70%
Hepatic metastases – 10% at the time of exploration.
-Solitary metastasis amenable to –wedge resection with clear margins can be removed
concomitantly.
-Formal hepatic lobectomy done as a second stage procedure.
5. Ovarian metastasis – 7% at the time of colon resection

Oophorectomy: at the time of colorectal surgery

Indications
i) Large ovarian metastasis (Krukenbergt’s tumour) which are symptomatic (prevents second
surgery for the metastasis, benefit of preventing primary ovarian cancer)
ii) Direct ovarian involvement
iii) Post menopausal women – prophylactic oophorectomy
6. Inadvertent Perforation

-Predisposes to local recurrence

-Warrants post op radiotherapy
Follow up
Aim: Early detection of recurrence or metachronous lesion
History
Physical examination
Faecal occult blood

Tumour
markers (CEA) - monthly – 3 years, 3 monthly-next 2 years
Colonoscopy – first colonoscopy within 6-12 months of surgery, yearly-next 2 years, 2-3 yearly
thereafter.
CXR
CT abdomen and pelvis – if primary loco regionally advanced
-LFT ↑
-CEA ↑
80-90% of recurrence of colon cancers occurs in the first two years.
SOP
All patients should be admitted when a colectomy is planned
WHO DOES WHAT?
Doctor:
c) Surgeon: diagnosis & work up
Pre operative planning
Operative procedure
Post operative follow up
d) Radiotherapist : radiotherapy – neoadjuvant & adjuvant
e) Medical oncologist : Chemotherapy
f) Anesthetist: PAC, anesthesia, post op ICU management

NURSE:
ng of colostomy when required by some nurse

TECHNICIAN:

101. FISTULA IN ANO

WHEN TO SUSPECT/RECOGNIZE?
When a patient presents with a discharging opening gin the perianal region, on e should suspect a
fistula in ano
INTRODUCTION:
A fistula is an abnormal communication between two epithelial surfaces.
DEFINTION:
By definition a fistula in ano is a communication between the anal canal and skin by a tract
which may be straight and simple or complex with ramifications or a horse shoe tract involving
the right and / or left halves. The discharge may be pus, fecal matter, flatus or serosanguinous.
Fistula are classified as low or high
Based upon their relationship to the anal sphincter complex, anal fistulas are categorized into:
1. Intersphincteric
2. Trans sphincteric
3. Supra sphincteric
4. Extra sphincteric

Treatment options are based upon these classifications

INCIDENCE:
Indian incidence is not documented
DIFFERENTIAL DIAGNOSIS:
Furunculosis
Crohn’s disease
Pilonidal sinus
Tuberculosis
Actimycosis
Lymphogranuloma venereum
Granuloma inguinale
Perianal abcess
PREVENTION:
Adequate drainage of anorectal abscesses may prevent fistula formation
Predisposing causes
1. Crohn’s disease
2. Malignancy
3. Chlamydia

In the presence of a complex, recurrent, non healing fistula these should be suspected.
COUSELLING:
Surgical treatment alone offers permanent cure. So patients should be counseled for early surgey
when it is a simple fistula so that it does not become complex.
OPTIMAL DIAGNOSTIC CRITERIA:
SITUATION 1:
CLINICAL DIAGNOSIS:
Patients with anal fistula commonly present with complaints of

ng

The presentation may be acute when there is acute perianal sepsis

A chronic anal fistula presents with periodic exacerbation and pus discharging openings around
the anus per rectal exam and proctoscopy should be done to visualize both the internal and
external openings. This may be adequate for a straight low tract.

INVESTIGATIONS:
Fistulogram may be done when branching is suspected, in recurrent fistulae and when internal
opening is not appreciable.
Examination under anesthesia
Probe test, caution may cause now internal opening
Injection technique is useful in delineating the tract
Biopsy when specific cause is anticipated
Barium enema – when co existing disease is suspected
Blood sugar – to r/o diabetes mellitus
Complete blood count
Urine r/m
X ray chest – to rule out TB

TREATMENT:
Simple low fistulae can be managed in a secondary hospital where a surgeon is available

SURGICAL PROCEDURES:
Surgical options are dictated by the type of fistula. Aim is to drain the septic focus and remove
the fistula with minimal injury to the sphincter complex
Fistulotomy
Fistulectomy
Seton
Combination of the above:
Fistulotomy (of superficial position), with seton division (of the cephalad position)
Staged procedures may be required in high anal fistulae
Fistula presenting as perianal abscess would require drainage, analgesics and antibiotics followed
subsequently by a definitive procedure
Fistulotomy and curettage / Fistulectomy – low anal fistula
Trans sphincteric fistula that involve =<30 percent of sphincteric muscle – sphincteromy without
risk of incontinence
High Trans sphincteric fistulas – seton placement
REFERRAL CRITERIA:
Complex/recurrent/high anal fistulae may need referral to a higher centre for adequate
investigation and management. Colostomy and staged procedure may be required.
Co existing conditions like rectal cancers, Crohn’s disease, TB fistulae, HIV infection require
referral
SOP:
In patient
SITUATION 2:
Clinical diagnosis as in situation 1
INVESTIGATION:
All investigations as in situation 1
Additional investigations:
MRI, MR Fistulogram in complex, high, trans sphincteric, supra and extrasphincteric fistulae
Colonoscopy – associated ulcerative colitis, carcinoma, TB etc
HIV test in suspected cases
Biopsy when multiple openings are present, malignancy or specific cause is suspected
prothrombin time
HbA1C in cases of diabetes mellitus
TREATMENT: as in situation 1
Colostomy – when significant sphincter involvement is present, or non healing ulcer Multiple
procedures – complex fistula with multiple tracts
SOP:
Day Care – Low fistulae – subcutaneous / submucous fistula
All others – should be admitted
WHO DOES WHAT?
Doctor:
Clinical examination
Diagnosis
Planning surgery
Post op care
Anesthesia
Nurse:
Siting of colostomy when required, by stoma nurse
Care of stoma
Dressing of the wound
Pre & post operative care
Assisting during surgery
Technician:
Pre op equipment and drugs to be checked and kept ready
Assist anesthetist in the OT
Assist the surgeon, positioning of the patient

102. HAEMORRHOIDS
When to suspect / recognize?
When a patient presents with an h/o passing fresh blood per rectum
INTRODUCTION:
Three haemorrhoidal cushions are found in the left lateral, right anterior and right posterior
positions of the anal canal. Bleeding results when these cushions are engorged and subjected to
raised intra abdominal pressure while straining during defecation.
DEFINITION:
Haemorrhoids are cushions of submucosal tissue containing venules, arterioles and smooth
muscle fibers located in the anal canal
Treatment is indicated only if they become symptomatic due to venous engorgement of the
haemorrhoidal plexus
INCIDENCE:
Haemorrhoids is a common condition but the exact incidence in our country is not documented
DIFFERENTIAL DIAGNOSIS:

PREVENTION AND COUNSELLING:

Excessive straining, increased intra abdominal pressure and hard stools increase venous
engorgement of haemoohoidal plexus. Avoidance of these would prevent the development of
haemoorhoids
OPTIMAL DIAGNOSTIC CRITERIA:
Symptoms:
EXAMINATION:
DIRECT VISUALISATION: thrombosed/prolapsed haemorrhoids, external haemorrhoids &
skin tags be visualized.
DIGITAL RECTAL EXAMINATION:
Thrombosed haemorrhoids, as well as other associated conditions such as anal cancer, BPH may
be felt per rectum.
PROCTOSCOPY:
Internal haemorrhoids occur in 3, 7 & 11 “o” clock positions. These are visualized during
prctoscopy. Haemorrhoids are classified into 4 graes by descent
Grade Presentation
1. Bleeding
2. Protrusion below the anal verge while straining with spontaneous reduction
3. Protrusion regressing with manual reduction
4. Irreducible protrusions

Based on their location, haemorrhoids can be classified into

External – located distal to dentate line, covered by anoderm, painful, arise from inferior
haemorrhoidal plexus
Internal – located prominal to dentate line, covered by insensuate anorectal mucosa, painless,
may prolapsed or bleed
Interno – external – features of both

INVESTIGATIONS:
Hb
Peripheral smear
TLC, DLC, ESR
Blood grouping and Rh typing
USG abdomen

TREATMENT:
MEDICAL:

chronic blood loss

SURGICAL:
I. Minor Outpatient procedures:
1. Sclerotherapy – for grade 1 & II haemorrhoids and bleeding haemorrhoids
2 to 5 ml of 5% phenol in almond oil injected around pedicle in the submucosa aseptically
2. Banding – gr II & III haemorrhoids by modified Barron’s band applicator above the dentate
line
II. In patient
GR III & IV haemorrhoids
1. Haemorrhoidectomy
– MORGAN operation

– FERGUSON operation

2. Excision of thrombosed pile mass:

ANESTHESIA: GA/Spinal/Caudal block

REFERRAL CRITERIA:
Patients who opt for stapled haemorrhoidopexy
Patients with portal hypertension
Patients with bleeding disorders
Patients with co-morbidities that may require ICU care
SOP
Outpatient / day care procedures: Minor procedures for Grade I & II
In Patient: Operative procedures for Grade III & IV
Situation 2:
CLINICAL DIAGNOSIS – Same as in situation 1
INVESTIGATIONS – As in situation 1
+
Colonoscopy – to r/o other conditions (malignancy) and co-existing when required
Coagulation profile
TREATMENT
As in situation 1 &
Outpatient procedures:
1. Photocoagulation – 1&II degree haemorrhoids

Infrared coagulation probe applied to the apex of each haemorrhoid to coagulate the underlying
venous plexus
In-patient procedures:
1. Stapled haemorrhoidectomy: for grade III haemorrhoids. May be done as a day care procedure
or as an in-patient

SOP:
In-patient
Day care procedure – depending on the education and awareness of the patient
WHO DOES WHAT? AND TIMELINES
a. Doctor
b. Nurse

c. Technician

103. HERNIA
I. Introduction

A hernia is an area of weakness or disruption of the fibromuscular tissue of body wall. Often
hernia is also defined as an actual anatomical weakness or defect. Strictly it is defined as “an
abnormal protrusion of a viscus or a part of viscous through an opening – artificial or natural
with a sac covering it.
II. Incidence

75% of the abdominal hernias are groin hernia.

15 % males and 5% females will develop groin hernia.
Femoral hernia incidence is 17%.
Incidence of Umbilical hernia is 8.5%.
Others type of hernias are seen in 1.5%.
These figures exclude incisional hernias which can form after any surgery through abdominal
wall or lumbar area.
III. Differential Diagnosis
a. Hydrocele – Infantile, Encysted, Large vaginal and bilocular – absence of cough impulse,
getting above the swelling and transillumination. The swelling is not reducible.
b. Undescended testis – the corresponding half of the scrotum is empty and underdeveloped.
c. Femoral Hernia- the sac is below and laterals to the pubic tubercle.
d. Lipoma of cord – the localized swelling moves with pulling of the spermatic cord. Cough
impulse is absent and the swelling can not be reduced.
e. Groin abscess- May mimic small strangulated hernia. Signs of acute inflammation are present.
Cough impulse is absent and it can not be reduced.

IV. Prevention and Counseling

No specific preventive measures except in incisional hernia where various factor can lead to
development of incisional hernia.
All patients having hernia other than direct inguinal hernia or hernia with wide neck are
counseled to undergo surgery at the earliest convenience to prevent any chance of complications
like obstruction and strangulation etc.
V. Optimal diagnostic criteria, Investigations, Treatment and referral criteria ( Situation 1
)

a) CLINICAL DIAGNOSIS

A swelling in groin or abdominal wall exhibiting cough impulse and showing sign of reducibility
is clinically diagnosed as hernia. The clinical spectrum includes :-

and para-umblical hernia- in umbilical and para-umblical area.

 sion in groin area.

In congenital hernia the inguino-scrotal swelling is present since birth or during childhood .
b) INVESTIGATIONS

In most of the cases practically no investigations are required to confirm the diagnosis of hernia.
Clinical diagnosis is enough. Ultrasound of whole abdomen may be done in cases of hernia to
rule out other abdominal pathology .
c) TREATMENT

i. In-Patient – Principles of Hernia surgery include reduction of hernia , excision of the sac and
repair of wall. Repair may be done by suture or mesh.

o Congenital inguinal hernia is treated by herniotomy alone.

o Direct and indirect inguinal hernia is treated by herniorrhaphy or hernioplasty using a mesh by
various techniques.

o Epigastric hernia with small defect may be treated by suture repair using double breasting
technique . When the defect is large , hernioplasty using a mesh may be done.

o Umblical and Para-umblical hernia – approach is same as for epigastric hernia.

o Femoral hernia – Same principles of hernia repair are applied by High, Low or inguinal
approach depending upon the case and expertise of surgeon.

o Incisional hernia – An anatomical repair or mesh repair may be considered depending upon
individual case and expertise of the surgeon.

ii. Out-patient – None

iii. Day-care – In appropriate situation and setting viz local anesthesia, small size hernia , patient
residing within approachable distance etc . day care practice may be considered.
d) REFERRAL CRITERIA

Referral can be considered from situation 1 in hernia only if the patient has associated severe co-
morbidities requiring special care.
Optimal diagnostic criteria, Investigations, Treatment and referral criteria (Situation 2)
a) CLINICAL DIAGNOSIS

Same as situation 1.
b) INVESTIGATIONS

Same as situation 1.
c) TREATMENT

i. In-patient – Same as for situation 1. In addition, patient can be offered laparoscopic repair ,
particularly in bilateral and recurrent hernia after informed patient consent provided that the
infrastructure, equipment and expertise is available.
ii. Out-patient – None

iii. Day-care – Same as situation 1.

d) REFERRAL CRITERIA

None
VI. Who does what ? and timelines
a. Doctor
-operative care and follow up.
b. Nurse
 -operative care, operative assistance, post-operative care, administration of treatment
instructed by the doctor and monitoring as instructed.
c. Technician

104. HYDROCELE

I. Introduction

Hydrocele is collection of fluid between two layers of tunica vaginalis of testis. It can be
congenital or acquired which is further of two types i.e. primary or secondary.
II. Incidence

Hydrocele is quite a common condition with little high incidence in zones or areas affected by
filariasis. Those present since birth are called congenital hydrocele where the processus vaginalis
is essentially patent. Secondary hydrocele is most commonly due to tuberculosis, malignancy or
chronic infection.
III. Differential Diagnosis

Primary hydrocele in adults has to be differentiated from

a. Inguinal Hernia- One can not get above swelling and transillumination is absent (except
congenital hernia ).
b. Epididymal cyst – The testis is palpable separately.
c. Spermatocele – The testis is palpable separately.
d. Testicular tumor - The consistency is firm to hard, Testicular sensation and fluctuations are
absent and transillumination can not be elicited.

IV. Prevention and Counseling

There are no specific preventive measures for both congenital and adult hydrocele except that
wherever filariasis is endemic or prevalent, anti filarial prophylaxis may be taken or whenever
the person suffers from it, prompt and proper treatment should be taken.
V. Optimal diagnostic criteria, Investigations, Treatment and referral criteria ( Situation 1
)
a) CLINICAL DIAGNOSIS

For primary hydrocele in adults, 3 classical signs i.e. can get above the swelling, presence of
fluctuations and transillumination are diagnostic of hydrocele. Secondary hydrocele is generally
very small and soft and signs of primary pathology may be present. In congenital variety,
classical history of no scrotal swelling in morning and full blown swelling in the evening
coupled with above signs is diagnostic.
b) INVESTIGATIONS

In most of the cases practically no investigations are required to confirm the diagnosis of primary
hydrocele and congenital hydrocele. At the most, ultrasound may be done to find out testicular
morphology . For secondary hydrocele , complete battery of investigation consisting of
ultrasound, FNAC, CT scan and investigations for tuberculosis and tumor markers etc will be
required depending upon the possible primary pathology.
This battery is unlikely to be available in situation 1; hence referral to higher centre would be
advisable.
c) TREATMENT

i. In-Patient – Congenital hydrocele is treated surgically by herniotomy through inguinal

approach.

Adult hydrocele (primary) is treated by eversion or excision or plication depending upon size of
hydrocele and thickness of the sac. Since hematoma is a very common complication , hence
perfect hemostasis must be achieved in this surgery.
ii. Out-patient – None.
iii. Day-care – For congenital hydrocele , overnight stay is routine. For adult hydrocele , in
appropriate setting , the operative procedure can be considered on day care basis if surgery has
been done under local anesthesia.

d) REFERRAL CRITERIA

Referral may be considered in secondary hydrocele if the primary cause turns out to be testicular
malignancy.
Optimal diagnostic criteria, Investigations, Treatment and referral criteria (Situation 2)
a) CLINICAL DIAGNOSIS

Same as situation 1.
b) INVESTIGATIONS

Same as situation 1.
c) TREATMENT
i. In-patient – Same as situation 1.
ii. Out-patient – None
iii. Day-care – All the surgical options mentioned for congenital and primary variety of adult
hydrocele can be considered on day care basis in situation 2 .

d) REFERRAL CRITERIA

None
VI. Who Does What? and Timelines
a. Doctor
-operative care and follow up.
b. Nurse
-operative care, operative assistance, post-operative care, administration of treatment
instructed by the doctor and monitoring as instructed.
c. Technician

105. PAROTID NEOPLASM

1. Name of the condition: Parotid neoplasm

2. When to suspect/ recognize?
a. Introduction: Parotid gland is the commonest site of salivary gland neoplasms.
b. Case definition: Neoplasms of parotid gland may be benign or malignant.
3. Incidence of the condition in our country: Not reported
4. Differential diagnosis: Skin, soft tissue and lymph node swellings form an important
differential diagnosis of parotid neoplasm.
5. Prevention and counseling: Parotid lesions should be investigated and treated early to
prevent morbidity of facial nerve injury and mortality due to advanced parotid malignancy.
6. Optimal diagnostic criteria, investigations, treatment and referral criteria

I. Clinical diagnosis:
a. Painless, slow growing swelling in front of or below the ear. Occasionally, there may be a
bulge in the tonsillar region if deep lobe is involved. Presence of pain or facial paralysis may
suggest malignancy.
II. Investigations:
a. Fine Needle Aspiration Cytology is necessary to confirm the diagnosis and as a prelude to
radical parotidectomy.
III. Treatment (Standard operating procedure)
a. Inpatient:
i. Superficial parotidectomy is the treatment of choice for benign neoplasms located in the
superficial lobe of parotid.
ii. Isolated deep parotidectomy or total parotidectomy with preservation of facial nerve is
indicated for benign neoplasms located in the deep lobe of parotid.
iii. For malignant neoplasms of the parotid gland total parotidectomy with excision of adjacent
involved structures, facial nerve and ipsilateral neck dissection, if required, should be done.
b. Outpatient: Not indicated
c. Day care: Not indicated
IV. Referral criteria: Patient should be referred to a higher center if frozen section or nerve
grafting of the facial nerve are anticipated.

I. Clinical diagnosis:
a. Painless, slow growing swelling in front of or below the ear. Occasionally, there may be a
bulge in the tonsillar region if deep lobe is involved. Presence of pain or facial paralysis may
suggest malignancy.
II. Investigations:
a. Fine Needle Aspiration Cytology is necessary to confirm the diagnosis and as a prelude to
radical parotidectomy.
b. CECT/ MRI should be done to evaluate the nature of lesion, involvement of adjacent
structures and presence of significant lymphadenopathy.
III. Treatment (Standard operating procedure)
a. Inpatient:
i. Superficial parotidectomy is the treatment of choice for benign neoplasms located in the
superficial lobe of parotid.
ii. Isolated deep parotidectomy or total parotidectomy with preservation of facial nerve is
indicated for benign neoplasms located in the deep lobe of parotid.
iii. For malignant neoplasms of the parotid gland total parotidectomy with excision of adjacent
involved structures, facial nerve and ipsilateral neck dissection, if required, should be done.
iv. Ipsilateral neck dissection is indicated in the presence of significant lymphadenopathy.
v. Frozen section biopsy is indicated if operative findings are suspicious of malignancy, even if it
was not suspected preoperatively.
vi. Nerve grafting should be done when facial nerve needs excision.
b. Outpatient: Not indicated
c. Day care: Not indicated
IV. Referral criteria: Not indicated
7. Who does what and timelines:
a. Doctor: Clinical evaluation, treatment planning and execution.
b. Nurse: Assisting in evaluation and treatment.
c. Technician: Assisting in investigations and operation.
8. Further reading/ references:
a. Day TA, Deveikis J, Gillespie MB, Joe JK, Ogertmen B, Osguthorpe JD et al. Salivary gland
neoplasms. Current Treatment Options in Oncology 2004, 5:11–26
b. Meyers MN, Ferris RL (Eds.). Salivary gland disorders. Springer Verlag Berlin 2007.

106. PEPTIC ULCER PERFORATION

INTRODUCTION:
Lau and Leow have indicated that perforated peptic ulcer was clinically recognized by 1799, but
the first successful surgical management of gastric ulcer was by Ludwig Heusner in Germany in
1892. In 1894, Henry Percy Dean from London was the first surgeon to report successful repair
of a perforated duodenal ulcer. Wangensteen et al reported that in a patient with perforation but
without evidence of pneumoperitoneum, one can safely assume that perforation has sealed off on
its own. They advocated a nonoperative approach for such patients. However, they too supported
operative treatment in patients with perforated ulcer and evidence of pneumoperitoneum.
Berne and Donovan emphasized the use of a water-soluble upper GI study to demonstrate
spontaneous sealing of the perforation. They demonstrated that as many as 40% of perforated
peptic ulcers had no evidence of leak on upper GI contrast studies. Berne and Donovan
concluded that these patients can be observed safely as long as peritonitis does not develop.
Mortality rates were 6% and 3% in the operative and nonoperative groups, respectively.
Donovan et al proposed dividing patients based on their Helicobacter pylori infection status and
recommended nonoperative treatment in all patients except those without H pylori infection and
those in whom prior treatment of H pylori infection had failed.
Despite strong arguments favoring nonoperative treatment of patients with perforated PUD,
delaying the initiation of surgery more than 12 hours after presentation was demonstrated to
worsen the outcome. Therefore, when definitely indicated, a laparotomy should be performed as
soon as possible.
INDIAN INCIDENCE
There are no statistics available on this topic.
SYMPTOMS

reading of pain to rest of abdomen

SIGNS
Tachycardia
Fever
Pallor
Reduced abdominal wall movements

COMPLICATIONS
INVESTIGATIONS
• Haemogram
• Liver Function Tests
• Blood sugar
• Serum creatinine
• Bleeding time, clotting time and prothrombin time
• Xray chest
• ECG
• USG abdomen

MANAGEMENT
Resuscitation
Fluid resuscitation should be initiated as soon as the diagnosis of peptic ulcer disease (PUD) is
made. Essential steps include insertion of a nasogastric tube to decompress the stomach and a
Foley catheter to monitor urine output. Intravenous infusion of fluids is begun, and broad-
spectrum antibiotics are administered. In select cases, insertion of a central venous line or a
Swan-Ganz catheter may be necessary for accurate fluid resuscitation and monitoring. As soon
as the patient has been adequately resuscitated, emergent exploratory laparotomy should be
performed.
Conservative Treatment
Wangensteen et al reported that in a patient with perforation but without evidence of
pneumoperitoneum, one can safely assume that perforation has sealed off on its own. They
advocated a nonoperative approach for such patients. However, they too supported operative
treatment in patients with perforated ulcer and evidence of pneumoperitoneum.
Berne and Donovan emphasized the use of a water-soluble upper GI study to demonstrate
spontaneous sealing of the perforation. They demonstrated that as many as 40% of perforated
peptic ulcers had no evidence of leak on upper GI contrast studies. Berne and Donovan
concluded that these patients can be observed safely as long as peritonitis does not develop.
Mortality rates were 6% and 3% in the operative and nonoperative groups, respectively.
Donovan et al proposed dividing patients based on their Helicobacter pylori infection status and
recommended nonoperative treatment in all patients except those without H pylori infection and
those in whom prior treatment of H pylori infection had failed. Despite strong arguments
favoring nonoperative treatment of patients with perforated PUD, delaying the initiation of
surgery more than 12 hours after presentation was demonstrated to worsen the outcome.
Therefore, when definitely indicated, a laparotomy should be performed as soon as possible
Surgical Treatment
The appropriate surgical procedure depends on the location and nature of the ulcer. Many
authorities recommend simple oversewing of the ulcer, with treatment of the underlying H pylori
infection or cessation of nonsteroidal anti-inflammatory drugs (NSAIDs) for bleeding PUD.
Additional surgical options for refractory or complicated PUD include vagotomy and
pyloroplasty, vagotomy and antrectomy with gastroduodenal reconstruction (Billroth I) or
gastrojejunal reconstruction (Billroth II), or a highly selective vagotomy.
The patient is placed in the supine position. A midline incision provides the most expeditious
entry into the abdominal cavity. The incision can be extended to the symphysis pubis if
necessary.
Once the abdomen is entered, the stomach and duodenum are carefully examined to determine
the site of perforation. If the anterior surfaces of the stomach and duodenum show no
abnormalities, the gastrocolic ligament is serially divided between clamps to allow entrance into
the lesser sac and inspection of the posterior surface of the stomach.
The choice of operative procedure depends on variables such as the presence of shock, the
presence of life-threatening comorbid conditions, the degree of contamination of the upper
abdomen, the amount and duration of perforation, and whether the patient has a history of, or
currently has intraoperative evidence of, chronic peptic ulceration.
In the presence of life-threatening comorbid conditions and severe intra-abdominal
contamination, the safest technique for an acute anterior duodenal perforation is a simple closure
with a Graham patch, using omentum. Several full-thickness simple sutures are placed across the
perforation, using 2-0 or 3-0 silk sutures. A segment of omentum is placed over the perforation.
The silk sutures are secured.
If contamination of the upper abdomen is minimal and the patient is stable, a definitive ulcer
procedure can be performed. For a perforated duodenal ulcer, this may include a highly selective
vagotomy, a truncal vagotomy and pyloroplasty, or vagotomy and antrectomy.
For a perforated gastric ulcer, the procedure performed depends on the patient's condition. If the
patient is moribund, the ulcer is best excised by grasping it with multiple Allis clamps and using
a linear stapler. Alternatively, the ulcer can be excised with electrocautery; the defect is
approximated with a 2-layer closure with inner continuous 3-0 absorbable sutures and outer
interrupted Lambert sutures using 2-0 or 3-0 silk sutures.
In a stable patient, the ulcer is excised and sent for frozen section analysis to exclude
malignancy. For a benign gastric ulcer, a distal gastrectomy with either a Billroth I
gastroduodenostomy or a Billroth II gastroduodenostomy is performed.
Post Operative Care & Complications The nasogastric tube can be discontinued on
postoperative day 2 or 3, depending on the return of GI function, and diet can be slowly
advanced. Patients who are found to have H pylori infection should receive the appropriate
antibiotic regimen. Patients with high serum gastrin levels should undergo an evaluation for
Zollinger-Ellison syndrome. Patients should undergo upper endoscopy to evaluate the area of
ulcer and healing of the perforation site 4-6 weeks after surgery.
Surgical complications include pneumonia (30%), wound infection, abdominal abscess (15%),
cardiac problems (especially in those >70 y), diarrhea (30% after vagotomy), and dumping
syndromes (10% after vagotomy and drainage procedures).
REFERRAL CRITERIA:

systemic illnesses.

rence of perforation few days after surgery may need ICU care, parenteral
nutrition, investigations for gastrinoma and further surgery.

MEDICOLEGAL:

WHO DOES WHAT?

Doctor:
g) Surgeon: diagnosis & work up

Pre operative planning

Operative procedure
Post operative follow up
h) Anesthetist: PAC, anesthesia, post op ICU management

NURSE:
TECHNICIAN:

107. SKIN AND SOFT TISSUE LESIONS

1. Name of the condition: Skin and subcutaneous lesions

2. When to suspect/ recognize?
a. Introduction: There are a large number of skin and subcutaneous lesions, both benign and
malignant. The aim of the surgeon is to identify those which are malignant or carry malignant
potential and institute appropriate treatment.
b. Case definition: All lesions identified clinically as occurring in skin or subcutaneous tissue.
3. Incidence of the condition in our country: The condition is very common. However, the
exact incidence is not reported.
V. Clinical diagnosis: Based on clinical features specific for each lesion.
VI. Investigations:
a. FNAC
b. Incision biopsy (for larger lesions)
c. Excision biopsy (for smaller lesions)
VII. Treatment (Standard operating procedure)
a. Inpatient: Not indicated
b. Outpatient/ Day care: These lesions can be treated on day care or outpatient basis. All lesions
do not need treatment.
i. Confirm diagnosis by investigations
ii. Excise the lesion under LA with appropriate margin.
iii. For large lesions or in children general anesthesia may be used.
iv. Skin is closed by primary suturing/ grafting.
VIII. Referral criteria: Not indicated.

b. Situation 2 At Superspecialty Facility in Metro location where higher end technology is

available: Same as “a”
V. Clinical diagnosis
VI. Investigations
VII. Treatment (Standard operating procedure)
a. Inpatient
b. Outpatient
c. Day care
VIII. Referral criteria
7. Who does what and timelines
a. Doctor: Clinical diagnosis, investigations and treatment
b. Nurse: Assisting the surgeon in investigations and treatment
c. Technician: Assisting in investigations and treatment
8. Further reading/ references:
a. Luba MC, Bangs SA, Mohler AM, Stulberg DL. Common benign skin tumors. AmFamPhy
2003. 67(4):729-738.
b. Skin lesions. URL info.wirral.nhs.uk/document_uploads/evidence.../SkinLesions.pdf

108. SMALL BOWEL PERFORATIONS

I. Introduction

Small perforation is breach in seromuscular continuity of small intestine ie from D-J junction to
ileocaecal junction. It can be single or multiple and of varying sizes depending on nature and
stage of pathology causing it. It may even be associated with gangrenous segment of variable
length of small intestine.
II. Incidence of the condition in our country

In India, the commonest cause of small bowel perforation is enteric fever and tuberculosis.
Rapidly increasing incidence of vehicular trauma contributes to another category of perforation
called traumatic perforation. Penetrating injury caused by knife, gunshot etc also adds to the
etiology of these perforations. Rarely these perforations can be associated with long standing
small intestinal volvulus or near the site of band compressing the gut causing ischemia and
perforation. Iatrogenic perforations too can occur during conduct of various other abdominal
operations and even gynecological operations.
III. Differential diagnosis

The common conditions that should be considered in any patient presenting with features of
peritonitis (apart from small bowel perforations):-
1. Acute Pancreatitis
2. Duodenal perforation
3. Appendicular perforation with peritonitis
4. Mesenteric vascular ischemia
IV. Prevention and counseling

Timely medical advice and treatment for conditions like enteric fever and tuberculosis. In case of
injury whether blunt or penetrating, seek hospitalization without any delay. Using of seat belts
during travel (wherever possible) is also a good preventive step
V. Optimal diagnostic criteria, Investigations, Treatment & Referral Criteria( Situation 1)

a. Clinical diagnosis
ory of
fever, trauma, abdominal pain, vomiting, distension of tummy, inability to pass flatus and feces
of variable duration depending on type and duration of pathology.
d but rarely
may be localized also. Hippcratic facies will be present. The patient may be in shock (
hypovolemic or septic) or may even be having septicemia at the time of presentation.
b. Investigations
-ray abdomen in erect posture shows gas under one or both domes of diaphragm

-ray provides some doubt

c. Treatment ( Standard operating procedure )

i. In Patient

for surgery which essentially consists of

mosis depending on condition of the

patient, condition of the bowel, location and multiplicity of pathology.( If single perforation with
healthy bowel and condition of the patient is not bad , primary closure; otherwise ileostomy. In
the event of multiple perforations with healthy bowel and good condition of the patient ,
resection and anastomosis ; otherwise ileostomy is advised . Once a while exteriorization may be
considered if the condition of bowel and patient demands this procedure )

Postoperative
Care in ward and involves
- I/V fluids, antibiotics, pain killers and monitoring
- Oral allowance after bowel movements
- Stitch removal at appropriate time
ii. Outpatient None
iii. Day Care None
d. Referral criteria

available either at diagnostic level or treatment level or at the level of post-operative care, then
the case must be referred to higher centre.

Optimal diagnostic criteria, Investigations, Treatment & Referral Criteria (Situation 2)

a. Clinical diagnosis

b. Investigations
agnostic laparoscopy if any equivocality is
involved despite already mentioned investigations.
c. Treatment (Standard operating procedures )
i. In Patient

ities and infrastructure available

-operative care of the patient in HDU or ICU if the patient is unstable .

ii. Out patient – None
iii. Day care – None
d. Referral criteria – None from situation 2

VI. Who does what and Timeliness?

a. Doctor
-operative care and follow up.
b. Nurse
-operative care, operative assistance, post-operative care, administration of treatment
instructed by the doctor and monitoring as instructed.
c. Technician

109. VARICOSE VEINS SURGERY

INTRODUCTION:
The description of varicose veins as a clinical entity can be traced back as early as the fifth
century BC. Forefathers of medicine including Hippocrates and Galen described the disease and
treatment modalities, which are still used today. Throughout the centuries, surgical treatments
have evolved from large, open surgeries to minimally invasive approaches. Varicose veins
represent a significant clinical problem and are not just a “cosmetic” issue because of their
unsightly nature. The problem arises from the fact that varicose veins actually represent
underlying chronic venous insufficiency with ensuing venous hypertension. This venous
hypertension leads to a broad spectrum of clinical manifestations, ranging from symptoms to
cutaneous findings like varicose veins, reticular veins, telangiectasias, swelling, skin
discoloration, and ulcerations.
DEFINITION:
When veins become abnormally thick, full of twists and turns, or enlarged, they are called
varicose veins. Generally, the veins in the legs and thighs have a tendency to become varicosed.
INDIAN INCIDENCE
In India, the incidence of varicose veins is reportedly less than in the Western countries. This
could be genuinely less or underreported as culturally the society does not permit exposure of
legs and therefore it may not be bothering many people.
INDICATIONS:
Surgical removal or obliteration of varicose veins is often for cosmetic reasons alone.
Noncosmetic indications include symptomatic varicosities (e.g., pain, fatigability, heaviness,
recurrent superficial thrombophlebitis, bleeding), or for the treatment of venous hypertension
after skin or subcutaneous tissue changes, such as lipodermatosclerosis, atrophie blanche,
ulceration, or hyperpigmentation, have developed.
Conservative treatment with stockings and external compression is an acceptable alternative to
surgery, but worsening cutaneous findings or symptoms despite these measure usually warrant
intervention. Nonetheless, a patient's desire for surgical management over conservative treatment
or for cosmetic purposes alone are both reasonable relative indications for surgery.
TESTS FOR REFLUX
Trendelenburg test: This physical examination technique distinguish patients with reflux at the
SFJ from those with incompetent deep venous valves. The leg is elevated until the congested
superficial veins have all collapsed. Direct pressure is used to occlude the GSV just below the
SFJ. The patient stands with the occlusion still in place. If the distal superficial varicosities
remains empty or fills very slowly, the principal entry point of high pressure into the superficial
system is at the SFJ. Rapid filling despite manual occlusion means that some other reflux
pathway is involved.
Doppler auscultation: A Doppler transducer is positioned along the axis of a vein with the
probe at an angle of 45° to the skin. When the distal vein is compressed, audible forward flow
exists. If the valves are competent, no audible backward flow is heard with the release of
compression. If the valves are incompetent, an audible backflow exists. These compression-
decompression maneuvers are repeated while gradually ascending the limb to a level at which
the reflux can no longer be appreciated.
Venous refilling time (VRT): This is a physiologic test, again using plethysmography. The VRT
is the time necessary for the lower leg to become infused with blood after the calf-muscle pump
has emptied the lower leg as thoroughly as possible. In healthy subjects, venous refilling is
greater than 120 seconds. In patients with mild and asymptomatic venous insufficiency, VRT is
between 40 and 120 seconds. In patients with significant venous insufficiency, VRT is
abnormally fast at 20-40 seconds. Such patients often complain of nocturnal leg cramps, restless
legs, leg soreness, burning leg pain, and premature leg fatigue. A VRT of less than 20 seconds is
markedly abnormal, and is nearly always symptomatic. If the VRT is less than 10 seconds,
venous ulcerations are likely.
Duplex US with color-flow imaging (sometimes called triplex ultrasound): This is a special type
of 2-dimensional ultrasound that uses Doppler-flow information to add color for blood flow in
the image. Vessels in the blood are colored red for flow in one direction and blue for flow in the
other, with a graduated color scale to reflect the speed of the flow. Venous valvular reflux is
defined as regurgitant flow with Valsalva that lasts great than 2 seconds.
INVESTIGATIONS:

RELEVANT ANATOMY
The greater saphenous vein (GSV) originates on the medial foot as part of the venous arch and
receives tributaries from deep veins of the foot as it courses upward along the anterior aspect of
the medial malleolus. From the ankle, the GSV continues along the anteromedial aspect of the
calf to the knee and into the thigh, where it is found more medially. From the upper calf to the
groin, the GSV is usually contained within an envelope of thin fascia. Visualization of this
fascial envelope is an important way of identifying the GSV with duplex ultrasound. This fascial
envelope often prevents the GSV from becoming significantly dilated, even when large volumes
of reflux pass along its entire length. A normal GSV is typically 3-4 mm in diameter in the mid
thigh. Along its course, a variable number of named perforating veins may connect the GSV to
the deep system at the femoral, posterior tibial, gastrocnemius, and soleal veins. The Cockett
perforators, between the ankle and the knee, are a special group of perforating veins. Rather than
directly connecting the superficial to deep venous systems, they connect the subfascial deep
system with the posterior arch vein, which then empties into the GSV.
Besides perforating veins, the GSV has numerous superficial tributaries as it passes through the
thigh. The most important of these are the posteromedial and anterolateral thigh veins, found at
the level of the mid thigh, and the anterior and posterior accessory saphenous veins at the level of
the canal of Hunter in the upper thigh, where a perforating vein often connects the GSV to the
femoral vein. Just below the SFJ, the GSV receives several additional important tributary veins.
These include the lateral and medial femoral cutaneous branches, the external circumflex iliac
vein, the superficial epigastric vein, and the internal pudendal vein. These tributaries are
frequently involved in the reflux that leads to the appearance of surface varicose veins on the
lower thigh or upper calf.
The termination point of the GSV into the common femoral vein is called the saphenofemoral
junction in the English literature but is known as the crosse (i.e., shepherd's crook) in the French
medical literature. The terminal valve of the GSV is located within the junction itself. In most
cases, at least one additional subterminal valve is present within the first few centimeters of the
GSV. Most patients have a single subterminal valve that can be readily identified approximately
1 cm distal to the junctional valve.
Reflux at or near the SFJ does not always come through the terminal valve of the GSV, nor does
it always involve the entire trunk of the GSV. Reflux can enter the GSV below the subterminal
valve or even immediately below the junction, passing through a failed subterminal valve to
mimic true SFJ incompetence. Reflux can also pass directly into any of the other veins that join
the GSV at that level, or it may pass a few centimeters along the GSV and then abandon the GSV
for another branch vessel.
When a perforating vein is the primary site of reflux, dilatation of the vessel proceeds both
proximally and distally. When dilatation reaches the most proximal portion of the vein, the
saphenofemoral or saphenopopliteal junction is often recruited as a secondary point of reflux.
Although most large varices are tributaries off of an incompetent GSV or SSV, failed perforating
veins or connecting veins can also give rise to independent varices in the greater saphenous
distribution without involving the saphenous system itself. Identifying the originating point and
the primary pathway of reflux in the thigh is often difficult, which is why duplex ultrasound has
become so helpful in varicose vein workup.
OPERATIVE TECHNIQUES:
1. Safenofemoral ligation with long saphenous vein removal for long saphenous vein
varicosities. Surgical removal of the GSV has evolved from large open incisions to less invasive
stripping. Original methods of stripping used different devices and variations of techniques. The
Mayo stripper was an extraluminal ring that cut the tributaries as it was passes along the vein.
The Babcock device was an intraluminal stripper with an acorn-shaped head that pleated up the
vein as it pulled the vessel loose from its attachments. The Keller device was an internal wire
used to pull the vein through itself, as is done today with perforation-invagination (PIN)
strippers.

Currently, the technique of PIN stripping begins with a 2- to 3-cm incision made at the groin
crease. The femoral vein and SFJ are exposed with dissection and all tributaries of the SFJ must
be identified and flush-ligated to minimize the incidence of reflux recurrence.
After ligation and division of the junction, the stripping instrument (usually a stiff but flexible
length of wire or plastic) is passed into the GSV at the groin and threaded through the
incompetent vein distally to the level of the upper calf. The stripper is brought out through a
small incision (5 mm or smaller) approximately 1 cm from the tibial tuberosity at the knee. An
inverting head is attached to the stripper at the groin and is secured to the proximal end of the
vein. The vessel is then inverted into itself, tearing away from each tributary and perforator as
the stripper is pulled downward through the leg and out through the incision in the upper calf. If
desired, a long epinephrine-soaked gauze or ligature may be secured to the stripper before
invagination, allowing hemostatic packing to be pulled into place after stripping is complete.
An older technique of stripping to the ankle (rather than to just the knee) has fallen into disfavor
because of a high incidence of complications, including damage to the saphenous nerve, which is
closely associated with the vein below the knee
2. Subfacial ligation with below knee removal of long saphenous vein for below knee
varicosities associated with incompetent perforators.

3. Removal of the short saphenous vein is complicated by variable local anatomy and risk of
injury to the popliteal vein and peroneal nerve. The saphenopopliteal junction must be located by
duplex examination before beginning the dissection, and adequate direct visualization of the
junction is essential. After ligation and division of the junction, the stripping instrument (often a
more rigid stripper that facilitates navigation) is passed downward into the distal calf, where it is
brought out through a small incision (2-4 mm). The stripper is secured to the proximal end of the
vein, which is invaginated into itself as it is pulled downward from knee to ankle and withdrawn
from below.

4. Stab phlebectomy (or ambulatory phlebectomy)

Performed by Galen as early as the second century, this procedure came back into modern favor
during the 1960s and has increased in popularity ever since. This procedure is extremely useful
for the treatment of residual vein clusters after saphenectomy and for removal of nontruncal
tributaries when the saphenous vein is competent. Ambulatory phlebectomy is a treatment for
superficial varicose veins. The procedure involves the removal of the varicose veins through
small 2–3 mm incisions in the skin overlying the veins. The procedure may be performed in
hospital or outpatient settings. The procedure may be performed with tumescent local anesthesia,
such as with lignocaine.
A microincision is made over the vessel using a tiny blade or a large needle, a phlebectomy hook
is introduced into the microincision, and the vein is delivered through the incision. With traction,
as long a segment as possible is pulled out of the body until the vein breaks or cannot be pulled
any further. Another microincision is made and the process is begun again and repeated along the
entire length of the vein to be extracted. Short segments of veins can be removed through tiny
incisions without ligatures, and skin closure is not necessary.
NEWER METHODS
1. Endovenous laser

2. Radiofrequency ablation

3. Sclerotherapy

4. Cutaneous electrodesiccation

5. Subfascial endoscopic perforating vein surgery

POST SURGERY INSTRUCTIONS
After treatment of large varicose veins by any method, a 30- to 40-mm Hg gradient compression
stocking is applied and patients are instructed to maintain or increase their normal activity levels.
Most practitioners also recommend the use of gradient compression stockings even after
treatment of spider veins and smaller tributary veins.
Activity is particularly important after treatment by any technique because all modalities of
treatment for varicose disease have the potential to increase the risk of DVT. Activity is a strong
protective factor against venous stasis. Activity is so important that most venous specialists will
not treat a patient who is unable to remain active following treatment.
COMPLICATIONS
A correct diagnosis of superficial venous insufficiency is essential. Veins should be treated only
if they are incompetent and if a normal collateral pathway exits. Removal of a saphenous vein
with a competent termination will not aid in the management of nontruncal tributary varices.
In the setting of deep system obstruction, varicosities are hemodynamically helpful because they
provide a bypass pathway for venous return. Hemodynamically helpful varices must not be
removed or sclerosed. Ablation of these varicosities will cause rapid onset of pain and swelling
of the extremity, eventually followed by the development of new varicose bypass pathways.
The most annoying minor complications of any venous surgery are dysesthesias from injury to
the sural nerve or the saphenous nerve. Subcutaneous hematoma is a common complication,
regardless of treatment technique used. It is easily managed with warm compress, NSAIDS, or
aspiration if necessary.

WHO DOES WHAT?

Doctor:
i) Surgeon: diagnosis & work up

Pre operative planning

Operative procedure
Post operative follow up
j) Anesthetist: PAC, anesthesia
NURSE:

TECHNICIAN:
Orthopedics
123. THE INFECTION OF BONES AND JOINTS
The common infection of bones and joints are mainly due to phylogenic organisms, tuberculosis
or rarely brucellosis.
1. When to suspect/recognize
A. Introduction
The common infection of bones and joints are mainly due to pyogenic organisms. It usually
occurs in small children in the metaphysical regions of long bones, usually to a focus of infection
elsewhere in the body through hematogenous/ lymphatic. The offending organisms are
staphylococcus commonly: other organisms are less common like streptococcus, Ecoli etc.
The bacteria get lodged in the metaphysis where they continue to grow, block small vessels
which causes necrosis of bone. Pus focus rapidly which may transverse laterally under the
periostenum, form an abscess or may even burst on the surface. This is the tone when treatment
should be started aggressively lest it should get converted into chronic osteomyelitus.
B. Definition

Osteomyelitus is an acute or chronic inflammatory process. Within bone, bone marrow and
surrounding soft tissue that develops. Secondary to infection with bacterial organisms (and rarely
fungi).
ii) Incidence of the condition in our country
It is very common condition in our country
iii) Differential diagnosis
- Cellulitis
- Ewing’s Sarcoma
- Osteosarcoma
- Arthritis

iv) Prevention and counseling – early diagnosis and treatment

Can prevent considerable morbidity.
v) Optimal diagnoster criteria, investigation, treatment and Referral criteria.
Situation 1:- At secondary hospital/Non-Metro situation: limited technology and resources.
a. Clinical Diagnosis
Signs of acute inflammation
High temperature
Rapid pulse
Extreme degree of pain (Rest/movement)
Local tenderness
b. Investigation

Complete hemogram, culture and sensitivity of aspirated material, ZN staining, Gram’s staining.

c. Treatment
- Rest – The limb of the patient to be put on rest
- Antibiotic – broad specters antibiotic to be started
sensitivity
- Out patient – if abscess is present regardless of the stage of disease effective drainage is to be
done.
- Day Care – Multiple drill holes, rectangular window, thorough Debridement
- In patient – Immobilization, saucerisation, IV antibiotic, sequestrectomy
- Referral Criteria – No improvement in patients, general condition, deterioration of patients,
conditions and other associated complications
Situation 2:- Super specialty facility in metro location where higher end technology is available.
a. Clinical Diagnosis – Signs of acute inflammation, high temperature, rapid pulse, extreme
degree of pain, Local tenderness
b. Investigations:- Complete hemogram, Blood Culture, culture and sensitivity of aspirated
material, ZN staining, Gram’s staining
 Bone scan
CT Scan
ELISA against different antigens of organisms and antibody detection in serum
Histopathological study
i) FNAC
ii) Open Biopsy
MRI
Radioisotope labeled Leukocyte scanning
PET scanning
c. Treatment
- Rest – The limb of the patient to be put on rest
- Antibiotic –
- Out patient – if abscess is present regardless of the stage of disease effective drainage is to be
done.
- Day Care – Multiple drill holes, rectangular window, thorough debridement
- In patient – Immobilization, saucerisation, IV antibiotic, sequestrectomy
- Referral Criteria – No improvement in patients, general condition, deterioration of patients,
conditions and other associated complications

Who does what:-

Doctor:- Early diagnosis and treatment
The diagnosis and treatment is to be started as early as possible. Delaying the treatment can only
increase the severity of the disease. Sometimes patient need to be referred.
Nurse:- Patient care
The patient need to be hospitalized in the early stages of the disease to avoid chronicity of the
disease for proper patient care.
Technician:- Investigation
In doubtful cases proper investigation to be done in quick time and in a proper way to avoid
contamination of the samples.

124. OSTEOARTICULAR TUBERCULOSIS

INTRODUCTION
For purposes of description osteoarticular tuberculosis can be discussed under the following
heads:
• Tuberculosis of joints
• Bone tuberculosis
• Spine tuberculosis
Infection of a joint or bone with Mycobacterium tuberculosis is almost always secondary to a
primary focus, in the lymphatic glands or lungs or mesentery, from where it disseminates by
hematogenous route. Malnutrition or any debilitating disease, poor environment increase the
incidence of the disease. Patients with immunodeficiency disease or HIV infection are more
prone to develop tuberculosis.
Involvement of any bone or joint in the body can be affected by tuberculosis. Case definition the
lesion in the joint can be:
i. Extra-articular
ii. Intra-articular: It can originate in the bone (osseous lesion) or in the synovium (synovial
disease).
Vertebral body involvement with tuberculosis is the most common and is nearly equal to
tuberculosis of all other regions put together.
There may be a history of trauma, under the effect of which a small hematoma may form
resulting in vascular stasis in that area. The hematoma may become a nidus for the tubercle
bacilli to settle down and form a tubercolosis follicle with caseation, epitheloid cells, gaint cells
and fibrosis at the periphery.
The lesion in the bone is essentially a lytic lesion which is evident radiologically, unlike in
pyogenic infection which is characterized by intense sclerotic activity. As the tuberculous lesions
heal, sclerosis takes place. At certain sites like the short long bones and in hand and feet or the
clavicle, there is intense sclerotic activity by layer of subperiosteal bone and is characteritic of a
tuberculous lesion. The tuberculous pus formed in the medullary canal may travel distally or
laterally thus lifting the periosteum, may form an abscess and even burst giving rise to a
tuberculous sinus. Multifocal tuberculous is somewhat common and is occasionally. The
response to a tuberculous lesion is exudative and may form a cold abscess, which is nothing but a
collection of necrotic material caseous tissue and the exudative reaction. These cold abscesses
than track through the fascial planes or the neurovascular bundles and may present at a distant
site. Since the abscess is away from the area of inflammatory activity, it has no signs of
inflammation in the skin overlying the abscess. A superficial abscess may burst and result into a
sinus or an ulcer.
Granulation tissue is almost always present in the tuberculous lesion. Ischemic necrosis of bone
due to endarteritis and thromboembolic phenomenon in bone lead to formation of sequestra,
which in osseous tuberculosis happen to be small. Isolated large sequestrate in osteroarticular
tuberculosis are rare.
Incidence of condition in our country
It is an extremely common condition in our country and is seen in all strata of society.
Differential Diagnosis
It can mimic almost any condition seen in bone like chronic osteomyelitis, osteoid osteoma,
fibrous dysphasia, malignant/benign tremors.
Prevention and Counseling
In case of pain, swelling, night cries fever an orthopedics surgeon may be consulted.
Referral criteria
In case of the symptom like swelling discharging sinuses, paraplegia or the disease not
responding to standard anti tubercular drugs the patient may be referred to a higher centre.
Situation 2:- Clinical Diagnosis
The tuberculosis of the joints mainly involves big joints. The common differential diagnosis
includes pauciarticular juvenile chronic arthritis and septic arthritis. The involvement of joint
may be osseous or synovial but if not treated, one would infect the other. Tuberculous synovitis
leads to effusion in the joint and synovial membrane becomes edematous. At this stage the joint
would look swollen and movements may be present or limited due to muscle spasm. The
radiological picture may show an increased joint space.
Later on, the granulation tissue may extend from the periphery on to the articular cartilage or in
the subchondral region in the form of a pannus thus eroding it. Once the articular cartilage is
eroded there is tremendous muscle spasm and all movements are restricted. Because of the
destruction of the articular cartilage the joint space on X-ray looks diminished.
When the lesion is osseous it involves the subchondral bone which also leads to erosion of the
cartilage. The lesion may start from the epiphysis in children or may be metaphyseal in origin.
When the disease begins to heal, fibrosis occurs across the joint leading to a fibrous ankylosis. At
this stage the movements of the joint are restricted and may be painful. There is considerable
muscle spasm which may produce a deformity at the joint. Prolonged muscle spasm may lead to
subluxation or dislocation of the joint causing further deformity and shortening. If sinus has
formed, secondary infection may be superimposed on the tuberculous infection. Fibrous
ankylosis may be converted into bony ankylosis either due to complete healing or new bone
formation due to superadded pyogenic infection. There are no movements in the joint after bony
ankylosis and it is also painless. Radiologically, in bony ankylosis the trabeculae are seen to be
crossing the joint line.
CLINICAL FEATURES
It is characteristically insidious in onset, and starts as monoarticular or mono-osseous
involvement. The child complains of pain in the joint, aggravated by movement, and often wakes
‘up at night because muscle spasm gets reduced and causes pain. It is classically called as “night
cries”. Low- grade fever, loss of weight and appetite are some of the symptoms of generalized
toxemia usually seen. Joint movements are painful and elicit muscle spasm on attempted
movement. In later stages when the cartilage gets eroded, all movements get restricted. Muscle
atrophy around the joint is a predominant feature and occurs early. Sometimes an abscess forms
which bursts to form a sinus. It may get secondarily infected and may alter the radiological
picture.
INVESTIGATIONS
i) Blood
A low hemoglobin, relative lymphocytosis and raised erythrocyte sedimentation rate (ESR) are
often found in the active stage of the disease. The ESR is often used as a guide in monitoring the
progress of the disease during treatment, though some people do not consider it a reliable
investigation.
ii) Mantoux Test
A positive Mantoux test is seen in patients with active tuberculous lesion. A negative test may
rarely be seen in severe or disseminated disease or in an immunocompromised patient.
iii) Radiographic Examination
It can be diagnostic in view of the typical radiological appearance of the tuberculous lesions. In
early stage of the joint disease, capsular markings may become prominent. The earliest sign is
widespread osteoporosis around a joint. Lytic lesion and periosteal reaction are seen, although
latter is much more prominent in pyogenic infection.
In case of joints, small bone erosions occur near the capsular reflection. Joint space decreases
due to cartilage erosion and lytic lesions are seen in the epiphyseal area. The radiological signs
of a healing lesion are absence of rarefaction and bony ankylosis.
iv) Smear and Culture
Tuberculous pus, joint aspirate, granulation tissue, sputum etc. may be examined by smear and
culture for tuberculous bacilli.
The culture and sensitivity tests for various anti fuberculosis drugs also help in giving
appropriate chemotherapy in resistant cases or cases of multi-drug resistant tuberculosis; which
are seen quite frequently in today’s clinical practice.
FNAC (Fine Needle Aspiration Cytology)
Occasionally, even the most modern methods of imaging may not help the clinician to reach to a
final diagnosis, and therefore FNAC or biopsy may be undertaken to obtain tissue diagnosis.
FNAC is now available for the cytological diagnosis of vertebral tuberculosis. ‘Biopsy is a safe
and a quick diagnostic procedure with high accuracy in the hands of trained cytopathologists. It
recommended that it should be practiced in all diagnostic centres of our country, even for
suspected vertebral tuberculosis.
BIOPSY
Biopsy may have to be done in cases where there is doubt about the diagnosis, particularly in the
early stages of the disease. Biopsy from the bone or synovium can provide an early diagnosis for
timely starting the treatment and preventing damage to the joint. Biopsy from a cystic lesion in
bone or from synovium is more likely to be positive.
Investigations should also be done to find out the primary focus of the disease. An X-ray of the
chest should always be done. Some other investigations may include: sputum smear examination
and culture, routine urine examination for isolation of tubercie bacilli and an intravenous
pyelogram for ruling out pulmonary and genitourinary lesions, respectively.
TREATMENT
The patient’s response to treatment is variable as anywhere else in the body and is dependent
upon the host resistance, severity of infection, and the stage of the disease when the diagnosis is
first made and treatment started. Eradication of the disease and preservation of function are
important both in osseous and joint diseases. In case of joints, joint mobility and stability are also
the early goals to be achieved. It is possible only if treatment is started early, i.e. when the
disease is limited only to synovium. In case the articular cartilage is eroded the joint becomes
unsalvageable in terms of function, mobility and stability. In such a situation the aim of
treatment is to achieve a sound bony ankylosis which is painless and gives stability, although the
patient will not have movements at that joint.
GENERAL MEASURES
Good nutrition consisting of a high-calorie and high-protein diet is essential to build up the
resistance. General rest and local rest to the specific bone and joint are essential parts of the
treatment. Local rest can be provided by means of splints or plaster casts. However, in cases
where the articular surface is not involved a judicious blend of rest and mobilization exercises
have to be resorted for restoration of function.

CHEMOTHERAPY
Most of osteoarticular lesions would respond to antituberculous drugs if the therapy is started
early.
However, in case of persistently draining sinuses which are secondarily infected, suitable broad
spectrum antibiotics have to be given. About 15% of patients do not respond to chemotherapy
alone if the lesion contains much caseation and sequestra. In such situations excision of the
diseased focus not only removes the diseased toxic material but also increases vascularity and
allows the anti-tuberculosis drugs to reach the site of the lesion.
A standard drug regimen is given which includes rifampicin, pyrazinamide, ethambutol,
isoniazid, and in some cases even streptomycin. The latter is useful because it kills the rapidly
multiplying extracellular tubercle bacilli in the lungs for the initial six months. After two
clinically and radiologically, pyrazinamide is stopped and isoniazed, rifampicin and ethambutol
are continued for one year. In some cases therapy may be required for 18 months for complete
healing of the lesion. In case the infection is suspected to be with multidrug resistant ofloxacin,
capreomycin, kanamycin, etc. may have to be given.
SURGICAL TREATMENT
Surgical treatment is an adjunct to the anti-tuberculosis drug therapy. It cannot be a substitute for
the prolonged course of the drug therapy. Surgical treatment has become safe with the advent of
powerful anti-tuberculosis drugs and one is no longer scared of a flare up of the lesion. However,
a trail of conservative treatment must be given before surgical treatment is undertaken. The
indications for surgery are specific and are as follows:
Doubtful diagnosis requiring excision of the focus or curettage of the lesion.

latter from getting eroded.

involved.

The surgical procedures generally perfomed in children are:

The general principle of surgery in tuberculosis demands that the abscess should be completed
evacuated. In case of an osseous lesion, all sequestra, granulation tissue and caseous material
should be removed till new bleeding bone is encountered, so that the antibiotics may reach the
site of lesion better. The cavities so produced should be packed with autogenous bone grafts.
Avoid dead spaces to prevent hematoma formation and close the wound primarily with or
without suction.
Tuberculosis can involve any bone or joint of the body but in children it has a special
predilection for the hip and knee joints commonly, and for ankle and elbow joints rarely.
Tuberculosis of spine with or without paraplegia is extremely common. Long bones are rarely
involved but the short long bone involvement is somewhat common.
Referral Criteria
No need to refer anywhere since the patient is already in a tertiary care hospital.
Who does What
Doctor – Diagnosis, chemo therapy advice and surgery
Nurse – General care like nutrition advise, care of the wounds.
Technician – Radiographic examination microbiological examination.

125. NAME OF CONDITION: Tuberculosis of Spine

I. WHEN TO SUSPECT/ RECOGNIZE?

Introduction: India is classified as a country with a high burden and the least prospects of a
favourable time trend of the disease. The average prevalence of all forms of tuberculosis in India
is estimated to be 5 per thousand. Skeletal tuberculosis is found in 1 to 3 % of these cases. Spine
might be involved in upto 50% of these cases. Neurological complications and progressive
deformity are the dreaded complications of tuberculosis of spine. It is imperative to diagonose
this condition early and initiate early medical treatment while recognising and treating patients
requiring surgical interventions for optimal outcomes.
Case definition:
For both situations of care (mentioned below*)
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY. The average prevalence of all
forms of tuberculosis in India is estimated to be 5 per thousand Skeletal system involvement
occurs in 1% to 3% of the patients and up to 50% of these affected patients have TB of the spine

III. DIFFERENTIAL DIAGNOSIS

Tumours of spine
Traumatic conditions
Other infectious afflictions of spine like brucella, pyogenic .
IV. PREVENTION AND COUNSELING
Prevention would entail measures as for other forms of tuberculosis. Osteoarticular tuberculosis
is always secondary, so primary infection should be treated effectively for sufficient time. Once
diagnosed, close follow up, regular anti tubercular treatment and aggressive surgical approach
may prevent dreaded complications
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,

TREATMENT & REFERRAL CRITERIA

Clinical Diagnosis: The presentation depends on the following:
Stage of disease
Affected site
Presence of complications
Back pain is the earliest and most common symptom. Any back pain not responding to
conservative treatment for more than 6 weeks and/or accompanied by constitutional symptoms
should be investigated further
Neurologic abnormalities occur in 50% of cases and can include paraplegia, paresis, impaired
sensation, nerve root pain.
Patients with cervical spine disease can present with dysphagia or stridor.Symptoms can also
include torticollis, hoarseness, and neurologic deficits.
The examination should include the following:
Assessment of spinal deformity
Inspection of skin, with attention to detection of sinuses and subcutaneous mass indicating cold
abscess
Meticulous neurologic examination
a) Investigations:
The erythrocyte sedimentation rate (ESR) is elevated. IgM for mycobacterium tuberculosis can
be done.HIV status should be confirmed. Microbiology studies can be used to confirm diagnosis.
Aspirates of cold abscees can be obtained to stain for acid-fast bacilli (AFB).
The following are radiographic changes characteristic of spinal tuberculosis
o Paradiscal involvement with decreased disc space
o Increased anterior wedging
o Collapse of vertebral body
o Enlarged psoas shadow with or without calcification
o Fusiform paravertebral shadows suggest abscess formation.
b) Treatment: .
Goals of management in active tuberculosis
Eradication/ Control of Disease
Decompression of spinal cord
Prevention of progressive deformity and later neurological complications
Early mobilization of the patient.
• Treatment options
Chemotherapy alone (long course is preferred)
Surgery with Chemotherapy
Antero-Lateral Decompression
Antero-Lateral Decompression + post fusion
Antero-Lateral Decompression + strut grafting+post fusion
Ant. Decompression + strut grafting+posterior instrumentation
Ant. Decompression + strut grafting + instrumentation
Standard Operating procedure
a. In Patient

In patients without deficit,chemotherapy alone is sufficient if the risk of progressive deformity is

not there. Inpatient care might be needed initially for patients who are undergoing treatment to
ensure rest and monitor response to ATT.
A close watch on development of neurological symptoms is to be kept and at signs of
deterioration, the patient may be referred.
b. Out Patient
Patients on ATT are to be followed closely for progression of deformity and deterioration of
neurological deficit
c. Day Care
Patients needing drainage of cold abscess may be kept in day care.
c) Referral criteria:
Failure to respond to conservative treatment
Deformity/risk of progresion
Recurrence of the disease
Doubtful diagonosis
Severe neurologic symptoms
Progressive neurologic symptoms inspite of ATT
Unsuccessful nonoperative treatment
Instability with spinal deformity,
Spinal tumour syndrome.
*Situation 2: At Super Specialty Facility in Metro location where higher-end technology is
available
a) Clinical Diagnosis: As described above in situation 1
b) Investigations:
Routine blood investigation,Tb-PCR, In MDR Tb-culture and sensitivity
MRI is the most effective imaging study for demonstrating neural compression. MRI is standard
for evaluating disk-space infection and osteomyelitis of the spine and is most effective for
demonstrating the extension of disease into soft tissues and the spread of tuberculous debris
under the anterior and posterior longitudinal ligaments.
CT scanning provides much better bony detail of irregular lytic lesions, sclerosis, disk collapse,
and disruption of bone circumference. CT guided biopsy maybe done in case of doubtful
diagonoses.
c) Treatment:
Standard Operating procedure
a. In Patient
Tuberculosis spine with no neurological deficit
Chemotherapy alone is sufficient if there is no risk of progressive deformity
Efforts should be made to identify patients who are at risk of developing kyphosis in active
disease. Growing children with dorsal and dorsolumbar caries with more than 3 body
involvement or in which there is destruction more than 1.5 times the vertebral body height are at
risk of kyphosis.
Indications of surgery
Failure to respond to conservative treatment
Deformity/risk of progresion
Recurrence of the disease
Doubtful diagonosis
Tuberculosis spine with neurological deficit
Middle path regime
In patients with mild deficit trial of chemotherapy can be done, however a close observation is
must
Indications for surgery for management of tuberculosis with deficit
Severe neurologic symptoms
Progressive neurologic symptoms
Unsuccessful nonoperative treatment
Instability with spinal deformity,
Spinal tumour syndrome.
Operative treatment of tuberculosis spine
trol of disease and adequate
decompression but there might be progression of kyphotic deformity

providing structural support and by its osteogenic potential, the graft may prevent progression of
kyphosis.

deformity as a consequence of fracture of the graft, slippage of the graft out of its bed, resorption
of the graft,or subsidence of the graft into the cancellous vertebral bodies. Anterior grafting
procedure should be accompanied by instrumentation either anterior or posterior.

early fusion and rapid mobilisation of the patient.

impregnated titanium mesh.

intensive care facilities should be available.

exhausted its reserve.
b. Out Patient
Regular follow up of operated patients as well as patients on conservative treatment. At each
follow-up detailed neurological examination should be performed and serial x rays should be
taken and deformity progression should be noted.
Regular biochemical investigations for monitoring ATT
c. Day Care
For drainage of cold abscesses when needed.
d) Referral criteria: Not applicable
VI. WHO DOES WHAT? and TIMELINES
a. Doctor
Clinical diagnoses
Investigations
Clinical decision making
Surgical procedure
Maintenance of record and follow up
b. Nurse
Councelliung
Surgical assistance
c. Technician
Investigations
Helps in surgery
Orthosis

126.DEGENERATIVE CERVICAL SPODYLOLYSIS

Clinical Diagnoses
Degenerative cervical spodylolysis may present as axial neck pain,cervical
radiculopathy,cervical myelopathy or a combination of these.
Patient complaints should be carefully correlated with physical examination and imaging results
for correct diagnosis and appropriate management
All differential diagonoses like peripheral neuropathy, motor neuron disease, amyotrophic lateral
sclerosis, multiple sclerosis, CVA, syringomyelia, tumors: intrinsic to spinal cord or extrinsic
must be ruled out.
Indications and Timing of surgery
There is a definite role of conservative management in neck pain and radiculopathy with minor
sensory symptoms.
Patients with very mild and subtle signs of myelopathy can be managed conservatively but close
observation and regular follow up is must.
Once moderate signs and symptoms of myelopathy develop patients are less likely to improve on
their own and surgical intervention is required.
Manipulation and traction are not recommended in myelopathy because of potential risk of
aggravating neurological deficit
Indications for surgery in degenerative disease of cervical spine
– Cervical spondylotic myelopathy
– Radiculopathy with a significant motor deficit
– Radicular pain not responding to conservative treatment
– Intractable Neck pain due to pseudarthrosis

Choice of Surgical approach

The decision of which surgical approach is to be used should be based on:
1. Source of spinal cord compression
2. Number of vertebral segments involved

3. Cervical alignment

4. Coexisting neck pain

5. Comorbidities

6. Previous surgeries

7. Surgical skill and facilities.

Primary focal ventral pathology causing cord compression is best treated by anterior approach.
Primary posterior compression related to facet hypertrophy and ligamentum flavum should be
tackled by posterior approach
In multisegmental pathology(>3 levels)
In presence of lordotic spine either posterior approach or anterior approach should be considered.
In presence of kyphotic spine anterior approach is to be considered. Only posterior approach is
contraindicated. Supplemental posterior procedure may be needed in multilevel corpectomy
Anterior approach
Anterior plating improves the rate of fusion, reduces the length and type of postoperative
immobilization, reduces the prevalence of graft-related complications, and leads to less
postoperative kyphosis, particularly in patients undergoing two or more levels of anterior
cervical discectomy and fusion
Autograft is superior to allograft in terms of fusion rates,duration to fuse and graft collapse.
Long-term results will be needed before use of structural supports such as metallic cages or
synthetic spacers in conjunction with local autograft or allograft can be unequivocally
recommended..
Corpectomy may be preferable to multilevel ACDF especially in higher risk patients such as
diabetics, smokers and revision cases.
In revision cases when a contralateral anterior approach is contemplated, preoperative
laryngoscopy should be done to rule out subclinical vocal cord paresis on the previously treated
side. 21
Cervical arthroplasty
A promising new technology that may improve patient outcome following anterior cervical
decompression. Possible indications are:
1. Monosegmental radiculopathy with mild spondylosis

2. Myelopathy due to single level disc herniation in absence of facet joint or posterior disease.

Posterior approach
Indicated in multisegmental pathology in a lordotic spine or posterior pathology.
Only laminectomy without fusion is contraindicated as it might lead to sequalae such as
segmental instability, kyphosis, swan neck deformity, perineural adhesions etc.
Laminoplasty or laminectomy with instrumented posterior fusion is the procedure of choice for
cervical spondylotic myelopathy.
Significant preoperative neck pain is a relative contraindication to laminoplasty and laminectomy
with fusion may be preferred.
The keyhole foraminotomy technique can be used for patients with unilateral radicular findings
caused by a lateral or foraminal soft cervical disc herniation or foraminal stenosis
CSM is a disease of elderly and associated with significant postoperative morbidity and
mortality. Patient and his/her attendants must be counselled regarding postop complications and
possible requirement of ventilatory support.

127. DISTAL HUMERUS FRACTURES IN ADULTS

1. INCIDENCE:

2. CLASSIFICATION:
AO Classification is the easiest to follow and contemplate on management:
1.3.A – Extraarticular
A.1 – Avulsion Fragment
A.2 – Simple Fracture
A.3 – Comminuted
1.3.B – Partly Articular
B.1 – Lateral Condyle Fracture – Saggital Plane
B.2 – Medial Condyle Fracture – Sagittal Plane
B.3 – Fracture in Frontal Plane.
1.3.C – Articular Fracture
C.1 – Articular Simple Metaphyseal Simple
C.2 – Articular Simple Metaphyseal Multifragmentary
C.3 – Articular Multifragmentary
3. Diagnosis:

History – Accident / Fall on Hand sustaining injury to Elbow.

Pain around elbow joint which increases on movement
Examination – Swelling, Deformity, Bruising, Tenderness, Crepitus, Instability.
Check for any signs of Compartment Pressure
Check for Distal Pulses & Neurological deficits, of Ulnar, Radial and Median Nerves
4. Investigations:

X Ray – Elbow AP / Lateral View

Traction View
Special Tests – CT Scan – To delinate the fracture & plan Surgery especially in Intraarticular
fractures
Compartment Pressure Monitoring in suspicious cases
Ultrasound Doppler Study – to rule out vascular injury
Angiogram – If vascular injury is suspected
MRI – rarely needed
5. Treatment:
Initial Management – Splint the Limb with elevation & Ice Packs applc’n along with Anti-
Oedema measures.
Proper Management –
a) Conservative – In Medically unfit patients – Cast / Bag of Bones Treatment
b) Surgical – External Fixator – in Open Fractures
Open Reduction & Internal Fixation (ORIF)
- 3.5mm LCDCP
- LCP – Anatomical Plates

Total Elbow Arthroplasty – In cases with extreme intraarticular comminution

6. Complications:

minence

7. When to Refer :
– “Life before Limb”
– for Vascular repair
In cases with Neurological Injury – for Immediate / Delayed Nerve repair.

Comments:
The common deficiency
(a) The writing style is not consistent. Radial head fracture is given as 33% of elbow region
while distal radius as 1/6 of fracture (not known) of what?
(b) Imaging – just mentioned AP, Lateral and sometime oblique. Why and for what a particular
special x-ray is needed?
(c) Complication has been clubbed as most common to least common, early or late in one list.
This will not help.
(d) When to refer – Generally written type B & C to higher center. Can we make such guidelines
in the issue.
The outcome of treatment depends on –
a) Training of the surgeon. b) Infrastructure – operating theatre & available instrumentation .We
need to define what all we should have in primary health center, secondary and tertiary care
centre. If we refer all type B & C fracture for all fractures than how the patients in Village,
Tehsil, District will be treated as we do not have any networking of referral centers (they are all
concentrated in the cities. Summarily the objective of the guidelines should be well stated. Is it to
stop small centers in cities to stop operating the particular type of fractures and force them to
refer or to make a national policy for the overall effective management of the orthopaedic
patients?
128. UPPER LIMB FRACTURES
129. Fracture of both bones forearm in adults
INCIDENCE:
1% of all fractures
CLASSIFICATION:
AO CLASSIFICATION:
TYPE A FRACTURE: simple fracture
- simple fracture of ulna and radius is intact
- simple fracture of radius and ulna is intact
- simple fracture of both radius and ulna

TYPE B FRACTURE: wedge fracture

- wedge fracture of ulna and radius intact
-wedge fracture of radius and ulna intact
-wedge fracture of both radius and ulna

TYPE C FRACTURE: complex fracture

- ulna complex fracture and radius simple fracture
- radius complex fracute and ulna simple fracture
- complex fracture of both radius and ulna

HISTORY:
Fall on an outstretched hand or direct impact.
DIAGNOSIS:
of the forearm

INVESTIGATIONS:
in diagnosis and to rule out injuries of joint above and below.
Other investigations such as BLOOD ROUTINE, CHEST RADIOGRAPHS, ECG and
ECHOCARDIOGRAPHY performed for working up the patient for surgery.

rule out any injury to nerves.

TREATMENT: Mostly operative
NON OPERATIVE (in undisplaced fractures which are stable): If operative treatment is
contraindicated because of the patient's poor general condition
1. Closed Reduction and Cast Immobilization
2. Functional Bracing for 6 weeks
OPERATIVE:
EXTERNAL FIXATORS- In case of open fractures with severe soft tissue damage and in
maintaining length in fractures with severe bone loss. Later change into definitive fixation.
INTRAMEDULLARY NAILING- the anatomical reduction cannot be as accurate as can be
achieved with plating. Plating of fractures of both bones is ideal either in LCDCP or LCP in
osteoporotic fractures.
PLATING- Most commonly used and permits accurate reduction of fracture.
COMPLICATIONS:
yndrome

-ulnar synostosis

FRACTURES THAT NEED TO BE REFERRED TO HIGHER CENTRES:

Comments:
The common deficiency
(e) The writing style is not consistent. Radial head fracture is given as 33% of elbow region
while distal radius as 1/6 of fracture (not known) of what?
f) Imaging – just mentioned AP, Lateral and sometime oblique. Why and for what a particular
special x-ray is needed?
(g) Complication has been clubbed as most common to least common, early or late in one list.
This will not help.
(h) When to refer – Generally written type B & C to higher center. Can we make such guidelines
in the issue. The outcome of treatment depends on –
c) Training of the surgeon.
d) Infrastructure – operating theatre & available instrumentation

We need to define what all we should have in primary health center, secondary and tertiary care
centre. If we refer all type B & C fracture for all fractures than how the patients in Village,
Tehsil, District will be treated as we do not have any networking of referral centers (they are all
concentrated in the cities.
Summarily the objective of the guidelines should be well stated. Is it to stop small centers in
cities to stop operating the particular type of fractures and force them to refer or to make a
national policy for the overall effective management of the orthopaedic patients?

130. FRACTURE OF SHAFT OF THE HUMERUS

INCIDENCE:
Fractures of the humeral shaft account for roughly 3% of all fractures.
CLASSIFICATION:
AO classification
Bone = humerus = 1
Segment = diaphysis = 2
Groups = A/B/C where
A: Simple fracture
B: Wedge fracture
C: Complex fracture
Subgroups:
A1: Simple fracture, spiral
A2: Simple fracture, oblique (≥30deg)
A3: Simple fracture, transverse (<30deg)
B1: Wedge fracture, spiral wedge
B2: Wedge fracture, bending wedge
B3: Wedge fracture, fragmented wedge
C1: Complex fracture, spiral
C2: Complex fracture, segmental
C3: Complex fracture, irregular
HISTORY:
Fall from a height or a direct impact as in vehicular accidents.
DIAGNOSIS:

ficit over the base of the thumb on the

dorsal aspect indicates an associated injury of the radial nerve.

fractures.
d elbow joints are not uncommon.
-rays (AP and lateral) of the entire humerus including the shoulder and elbow joint should be
taken to confirm the diagnosis.

COMPLICATIONS:
Nerve injury - Radial nerve palsy (upto 10%) is the most important complication.
 Vascular injury - Injuries to the brachial artery have been reported in association with humeral
shaft fractures. A careful assessment of the peripheral circulation is essential in all humeral
fractures.

Non-union - In general, spiral or oblique fractures heal better than the transverse or segmental
fracture. Soft tissue interposition, excessive fracture mobility and infection are important factors
responsible for non-union of a humeral shaft fracture.

Joint stiffness - A proper rehabilitation programme is essential to prevent joint stiffness

following injury.

Malunion - This may be functionally inconsequential; arm musculature and shoulder, elbow,
and trunk range of motion can compensate for angular, rotational, and shortening deformities.

INVESTIGATIONS:

elbow joints on each view. ,

ion in cases of severely displaced or

comminuted fracture patterns.

pathologic fracture is suspected.

MANAGEMENT:
CONSERVATIVE:
90%) will heal with nonsurgical management.

bayonet apposition are acceptable and will not compromise function or appearance.
 ency traction by the weight of the cast and arm to effect
fracture reduction.

o Indications include displaced midshaft humeral fractures with shortening, particularly spiral or
oblique patterns. Transverse or short oblique fractures represent relative contraindications
because of the potential for distraction and healing complications.

o The patient must remain upright or semi upright most of the time with the cast in a dependent
position for effectiveness.

o It is frequently exchanged for functional bracing 1 to 2 weeks after injury.

o More than 90% union is reported

OPERATIVE:

o Multiple trauma
o Inadequate closed reduction or unacceptable malunion
o Pathologic fracture
o Associated vascular injury
o Floating elbow
o Segmental fracture
o Intraarticular extension
o Bilateral humeral fractures
o Open fracture
o Neurologic loss following penetrating trauma
o Radial nerve palsy after fracture manipulation (controversial)
o Nonunion

Open reduction and internal fixation

The fracture site is exposed, fragments reduced and fixed with a compression plate (DCP,
LCDCP, LCP) and screws, with an anterolateral approach or upper two thirds fracture and
posterior approach for lower thirds fracture
Interlocking intramedullary nail

An ‘antegrade’ or a ‘retrograde’ nail is introduced into the medullary cavity of the humerus after
closed reduction of the fracture. The nail is then locked proximally and distally to achieve
rotational stability. This requires image intensification and is comparable to plating.
External fixation

This method of treatment may be used in open or multiple fractures. Percutaneous pins are
threaded into the bone and then held together by an external frame.
Patients with associated neurovascular injury or in unstable fractures where facilities are not
available for ideal internal fixation should be referred to higher centre.
Comments:
The common deficiency
(i) The writing style is not consistent. Radial head fracture is given as 33% of elbow region while
distal radius as 1/6 of fracture (not known) of what?
(j) Imaging – just mentioned AP, Lateral and sometime oblique. Why and for what a particular
special x-ray is needed?
(k) Complication has been clubbed as most common to least common, early or late in one list.
This will not help.
(l) When to refer – Generally written type B & C to higher center. Can we make such guidelines
in the issue.

The outcome of treatment depends on –

e) Training of the surgeon.
f) Infrastructure – operating theatre & available instrumentation

We need to define what all we should have in primary health center, secondary and tertiary care
centre. If we refer all type B & C fracture for all fractures than how the patients in Village,
Tehsil, District will be treated as we do not have any networking of referral centers (they are all
concentrated in the cities.
Summarily the objective of the guidelines should be well stated. Is it to stop small centers in
cities to stop operating the particular type of fractures and force them to refer or to make a
national policy for the overall effective management of the orthopaedic patients? 32
131. RADIAL HEAD FRACTURE
INTRODUCTION-
Radial head fractures account for almost 33% of fractures of the elbow region. Radial head plays
an important role in providing smooth movements of forearm (Pronation and Supination) and the
elbow joint (flexion and extension at radiocapitullar joint).
CLASSIFICATION-
Mason`s classification- most widely followed
1- undisplaced or minimally displaced fracture. Displacement < 2mm
2- displaced fracture. Displacement > 2mm
3- communited fracture
4- fracture with dislocation of elbow
HISTORY-
Fall on an outstretched hand with a valgus strain.
DIAGNOSIS-
A) CLINICAL FEATURES -
-Pain and swelling over elbow region
-On examination- tenderness over the radial head with restriction of forearm and elbow
movements
B) IMAGING TECHNIQUES –
X-RAY - AP, LATERAL, OBLIQUE VIEWS.
CT – rarely a CT and an MRI may be necessary to study the fragments and the stability of the
joint
MANAGEMENT-
A. (MASON TYPE 1) CONSERVATIVE TREATMENT– MAY BE DONE IF THERE IS NO
RESTRICTION OF RANGE OF MOTION WITH AS ABOVE ELBOW PLASTER SLAB FOR
2 WEEKS.
B. SURGERY-
1) IN ISOLATED RADIAL HEAD FRACTURES TREATED WITH OPEN REDUCTION &
INTERNAL FIXATION WITH SCREWS. (MASON TYPE 2)
2) PROSTHETIC REPLACEMENT- IS USED TO PRVENT PROXIMAL MIGATION OF
THE RADIUS. (MASON TYPE 3 & 4 ) EVEN RADIAL EXCISION GIVES FAIRLY GOOD
RESULTS.

3) RADIAL HEAD EXCISION-MAY BE USEFUL FOR OLDER PATIENTS WITH

COMPLEX ISOLATED FRACTURES. LEVEL OF EXCISION IS PROXIMAL TO
ANNULAR LIGAMENT THROUGH LATERAL KOCHER APPROACH.

COMPLICATIONS
ated to improperly placed hardware or loss of fixation. Late excision of the radial
head may be necessary after other soft tissues have healed.
- treat with radial nerve splint. If it doesn’t recover, Jones
tendon transfer is to be done.
- loss of extension common. No massaging is to be done.

ESSEX – LOPRESTI LESION

• Defined as longitudinal disruption of forearm interosseous ligament, usually combined with
radial head fx and/or dislocation plus distal radioulnar joint injury
• Difficult to diagnose
• Treatment requires restoring stability of both elbow and DRUJ components of injury.
• Radial head excision in this injury will result in disabling proximal migration of the radius.

WHEN DO YOU REFER IT TO HIGHER CENTRE?

1. Essex Lopresti lesion
2. When the patient comes late
3. In Type 2 fractures when facilities are not available for fixation

Comments --- The common deficiency

(m) The writing style is not consistent. Radial head fracture is given as 33% of elbow region
while distal radius as 1/6 of fracture (not known) of what?
(n) Imaging – just mentioned AP, Lateral and sometime oblique. Why and for what a particular
special x-ray is needed?
(o) Complication has been clubbed as most common to least common, early or late in one list.
This will not help.
p) When to refer – Generally written type B & C to higher center. Can we make such guidelines
in the issue.

The outcome of treatment depends on –

g) Training of the surgeon.
h) Infrastructure – operating theatre & available instrumentation

We need to define what all we should have in primary health center, secondary and tertiary care
centre. If we refer all type B & C fracture for all fractures than how the patients in Village,
Tehsil, District will be treated as we do not have any networking of referral centers (they are all
concentrated in the cities.
Summarily the objective of the guidelines should be well stated. Is it to stop small centers in
cities to stop operating the particular type of fractures and force them to refer or to make a
national policy for the overall effective management of the orthopaedic patients?

132. HAND INJURIES

Carpal Injuries
Scaphoid Fracture
Introduction: Fracture of the carpal scaphoid bone is the most common fracture of the carpus,
and frequently diagnosis is delayed.
Incidence & classification: Scaphoid fracture accounts for about 50-80% of carpal injuries. It is
most common in young men. It is caused by a fall on the outstretched palm, resulting in severe
hyperextension and slight radial deviation of the wrist. Herbert’s classification is most
commonly used for scaphoid fracture:
A (Acute, Stable): A1 Tubercle
A2 Nondisplaced fracture of the waist
B (Acute, Unstable): B1 Oblique, distal third
B2 Displaced or mobile, waist
B3 Proximal pole
B4 Fracture Dislocation
B5 Comminuted
C (Delayed Union)
D (Established nonunion): D1 Fibrous
D2 Sclerotic
Diagnosis & Investigations: Clinical evaluation + X-rays (PA, Lateral, scaphoid view, clenched
fist view), MRI, CT, bone scan may be used to diagnose occult scaphoid fractures
Complications: Delayed union, malunion, nonunion, osteonecrosis, CRPS
Management:
1. Tuberosity fractures and Nondisplaced distal third fractures: Conservative with scaphoid cast
for 6-8 weeks
2. Other Non-displaced fractures: Conservative or Percutaneous fixation
3. Displaced but reducible fractures: Percutaneous fixation
4. Irreducible displaced fractures: ORIF

Reasons for referral to higher centre: Lack of expertise, lack of infrastructure, Fracture
dislocations
Other carpal injuries: Triquetrum, trapezium, lunate are commonest after scaphoid fracture.
Trapezoid, capitate, pisiform and hamate are relatively rare fractures. Specialized views or CT
scan may be required for their diagnosis. Undisplaced fractures are treated conservatively;
however displaced fractures may require ORIF. Complications can be osteonecrosis, missed
dislocations, osteoarthritis, CRPS etc.

Hand Fractures:
Metacarpal and phalangeal fractures are common, comprising 10% of all fractures. There is a
high degree of variation in mechanism of injury accounting for broad spectrum of patterns of
fractures in hand.
Incidence & classification: Distal phalanx fractures are most common of all hand fractures
(45%) followed by metacarpal fractures (30%), proximal phalanx (15%) and middle phalanx
(10%). These fractures can be classified in various ways:
1. Location of fracture e.g. head, shaft, base
2. Open vs. closed
3. Displaced vs. Undisplaced
4. Extraarticular vs. Intraarticular
5. Stable vs. Unstable
6. Fracture pattern : transverse, comminuted, spiral, split

Diagnosis & Investigations: Clinical evaluation + X-rays (PA, latéral and oblique radiographs).
CT may be required to assess the intraarticular fractures.
Complications: Delayed union, malunion, nonunion, CRPS, stiffness and loss of motion,
infection, post-traumatic osteoarthritis etc.
Management:
Metacarpal fractures:
Metacarpal head: Undisplaced stable fractures can be treated conservatively with MCP joint
immobilized at >70 degrees. Displaced fractures usually require ORIF with k-wires or mini-
plates
Metacarpal neck: Stable fractures: Conservative
Unstable fractures: CRIF or ORIF (K-wires, mini-plates)
Metacarpal Shaft: Stable fractures: Conservative
Unstable fractures: CRIF or ORIF (K-wires, mini plates)
Metacarpal Base: Undisplaced: Conservative
Displaced: CRIF or ORIF
Proximal and middle phalanx
Intraarticular fractures: ORIF is preferred. For comminuted fractures, ligamentotaxis with
external fixators or specialized reconstruction techniques can be used.
Extraarticular fractures: Stable fractures: Conservative
Unstable fractures: CRIF or ORIF (K-wires, mini plates)
Distal Phalanx
Intraarticular fracture (Mallet finger) : Extension block pinning for bony mallet finger,
Extension splinting for soft mallet finger
Extraarticular fractures: Usually treated as soft tissue injury. If displaced widely, CRIF is
recommended.
Reasons for referral to higher centre: Lack of expertise, lack of infrastructure, Fracture
dislocations
Tendon Injuries
Extensor Tendon Injuries are usually treated with primary repair Flexor tendon injuries are
treated according to zone of injuries:
Zone 1: Direct Repair, tenodesis or arthrodesis in some cases
Zone 2: Need expertise, primary repair or delayed grafting
Zone 3: primary repair
Zone 4: primary repair
Zone 5: primary repair
Complication include stiffness, rupture of the graft or repair site, bowstringing etc. referral
should be made in case of lack of expertise or infrastruacture.
Comments:
The common deficiency
(q) The writing style is not consistent. Radial head fracture is given as 33% of elbow region
while distal radius as 1/6 of fracture (not known) of what?
(r) Imaging – just mentioned AP, Lateral and sometime oblique. Why and for what a particular
special x-ray is needed?
(s) Complication has been clubbed as most common to least common, early or late in one list.
This will not help.
(t) When to refer – Generally written type B & C to higher center. Can we make such guidelines
in the issue.

The outcome of treatment depends on –

i) Training of the surgeon.
j) Infrastructure – operating theatre & available instrumentation
We need to define what all we should have in primary health center, secondary and tertiary care
centre. If we refer all type B & C fracture for all fractures than how the patients in Village,
Tehsil, District will be treated as we do not have any networking of referral centers (they are all
concentrated in the cities.
Summarily the objective of the guidelines should be well stated. Is it to stop small centers in
cities to stop operating the particular type of fractures and force them to refer or to make a
national policy for the overall effective management of the orthopaedic patients?

133. LONG LIMB TRAUMA

Fracture Neck of Femur (Intra-capsular)
Fracture neck of femur is still the unresolved fracture as evident by the number of procedures
available and practiced, thus none is universally applicable and the surgeon has to select one
which would be ideal in a given situation. The treatment varies with the age of the patient, the
level of the fracture and the displacement of the fragments. Also the duration of the fracture is a
major deciding factor. If union of the fracture is not likely to be achieved then what alternative
method should be adopted which will suit the patient, keeping in mind his age, life style,
profession and economic status. Majority of our patients are not covered by health insurances,
hence all the expenditure has to be born by the patient himself. It is therefore desirable on the
part of treating orthopaedic surgeon to choose a method which these patients can afford.
Fracture neck femur is commonly seen in old people but in our country quite a good number of
patients are young adults. It is infrequent in children.
Fracture neck femur whether intra-capsular or extra-capsular can be diagnosed and differentiated
by clinical examination and confirmed by the roentgenograms. Any underlying pathologic
condition like metastasis or osteoporosis if present can also be identified on roentgenograms.
Fracture neck femur intra-capsular can be divided as per the following classifications:
(A) Garden Classification

-displaced.
acement but still has some
contact between the two fragments.
(B) According to the site of fracture
Usually caused by trivial fall in the elderly due to presence of osteoporosis, however metastasis
from malignancies can also lead to the pathologic fractures.
The aim of treatment is to achieve union of the fracture and a durable hip joint afterwards.
Principles of management include:
a. Osteosynthesis
i. Screws, Moore’s Pins etc
ii. DHS, Blade Plate

iii. Internal Fixation + Fibular Grafting

iv. Muscle pedicle Graft + Internal Fixation

b. Osteotomy
i. Pauwels valgus osteotomy

ii. Mcmurray’s osteotomy

c. Arthroplasty
i. Hemiarthroplasty

ii. Total Hip Replacement

iii. Excision Arthroplasty

The following points should be considered.

1. Age of the patient: Based on the age the following groups should be made.
a. 1-16 years before the closure of the upper femoral epiphysis

b. 16-50 years young adults

c. 50-60 years middle age group

d. Above 60 years (old age)

2. Site of fracture:
a. Sub-capital

b. Transcervical
c. Basicervical
3. Displacement of fragments:
a. Undisplaced fractures

b. Displaced fractures
4. Duration of fracture:
a. 1-21 days – Fresh

b. More than 21 days – Neglected fracure

Management: Primary health centre level: The doctor on duty should recognise the features
of fracture and disloction. Only first aid including the splintage and intravenous drip should be
given. In open fractures Tetanus toxoid can be given. There is no need to waste time in
preparation of medico-legal formalities. The injured should be referred to the higher centre
earliest feasible causing no further harm.
Community health centre and Civil hospital level: (Non Metro Hospital)
1. Investigations: X-rays of the pelvis including both hip and knee joint and of other areas if
required, General Investigations and specific if required according to the status of the health of
the patient.

2. Treatment:

FRESH FRACTURE
Age 1-16 years when growth plate is intact:
The implant used for internal fixation either should not cross the epiphyseal plate or the implant
causing least possible damage should be used.
Sub-capital and transcervical fractures should be fixed with multiple Kirschner (K) wires or
Moore’s pins after closed reduction in valgus.
Basicervical fractures can be fixed either by K wires, Moore’s pins or cancellous/cannulated lag
screws. When screws are used they should not cross the preferably epiphyseal plate.
Age 16-50 years
Sub-capital fractures:
Undisplaced: Internal fixation with 2-3 cancellous/cannulated lag screws
Displaced: Closed reduction and fixation with Lag screws. Valgus osteotomy and fixation with
double angled blade plate can also be done to convert shearing forces into compression forces.
Transcervical fractures:
Undisplaced: Internal fixation with 2-3 cancellous/cannulated lag screws
Displaced: Closed reduction and fixation with Lag screws. Valgus osteotomy and fixation with
double angled blade plate can also be done to convert shearing forces into compression forces. If
closed reduction fails open reduction is done followed by any of the above procedures.
Basicervical fractures:
Undisplaced: Internal fixation with Dynamic Hip Screw (DHS)
Displaced: Closed reduction and fixation with Lag screws or DHS. If closed reduction fails then
open reduction and internal fixation (ORIF) with lag screws or DHS.
Age 50-60 years:
Sub-capital fractures:
Undisplaced: Internal fixation with 2-3 cancellous/cannulated lag screws
Displaced: Closed reduction and fixation with Lag screws. Valgus osteotomy and fixation with
double angled blade plate can also be done to convert shearing forces into compression forces.
Arthroplasty including hemi or excision may be done according to the need and requirement of
the patient.
If closed reduction fails open reduction and fixation with any of the methods described above
may be done or hemi/excision arthroplasty may be offered according to the need and requirement
of the patient.
Transcervical fractures:
Undisplaced: Internal fixation with 2-3 cancellous/cannulated lag screws
Displaced: Closed reduction and fixation with Lag screws. Valgus osteotomy and fixation with
double angled blade plate can also be done to convert shearing forces into compression forces.
Arthroplasty including hemi or excision may be done according to the need and requirement of
the patient. If closed reduction fails open reduction and fixation with any of the methods
described above may be done or hemi/excision arthroplasty may be offered.
Basicervical fractures:
Undisplaced: Internal fixation with Dynamic Hip Screw (DHS) 43
Displaced: Closed reduction and fixation with Lag screws or DHS. If closed reduction fails then
open reduction and internal fixation (ORIF) with lag screws or DHS. Hemi/excision arthroplasty
may be offered.
Physiologic Age above 60 years:
Sub-capital fractures:
Undisplaced: Internal fixation with 2-3 cancellous/cannulated lag screws. Arthroplasty including
hemi or excision may be done according to the need and requirement of the patient.
Displaced: Arthroplasty including hemi or excision may be done according to the need and
requirement of the patient.
Transcervical fractures:
Undisplaced: Internal fixation with 2-3 cancellous/cannulated lag screws. Arthroplasty including
hemi or excision may be done according to the need and requirement of the patient.
Displaced: Arthroplasty including hemi or excision may be done according to the need and
requirement of the patient.
Basicervical fractures:
Undisplaced: Internal fixation with Dynamic Hip Screw (DHS)
Displaced: Arthroplasty including hemi or excision may be done according to the need and
requirement of the patient.
3. Referral Criteria for Metro hospital
a. Polytrauma patient.

b. Patient with co-morbid conditions requiring multiple speciality care.

c. Patients requiring Joint replacement.

d. Non unions / Neglected fractures ie fractures more than 3 weeks duration.

e. Pathological fractures.
f. Suspected HIV positive cases.

g. Fractures associated with any condition requiring higher investigations like CT Scan, MRI etc.

Metro hospital level:

1. Investigations: X-rays of the pelvis including both hips and knee and of other areas if
required, General Investigations and specific if required according to the presence of any co-
morbidity. Special investigations like MRI/CT scan if required.

2. Treatment: All the treatment as in situation 1

Treatment for the referred patients in the form of multispecialty approach.

FRACTURE MORE THAN 3 WEEKS DURATION
Osteosynthesis in such fractures has a high failure rate. Internal fixation has to be combined with
some type of bone graft or osteotomy particularly in young patients in whom it is desirable to
preserve the patient’s own femoral head. In patients above the physiologic age of 60 years
arthroplasty is the preferred treatment whether unipolar, bipolar, total hip or excision is as per the
affordability and requirement of the lifestyle of the patient and condition of the hip joint
(Osteoarthrosis).
Age 1-16 years:
Mc Murray’s osteotomy and POP one and a half spica may be tried.
Abduction osteotomy and internal fixation with angled paediatric blade plate. Care should be
taken not to damage the epiphyseal plate. If the gap between the fragments is more than 1 cm
free fibula with a screw may be tried but the chances of damage to the epiphyseal plate are very
high leading to limb length discrepancy and deformity of head later on.
Age 16-55 years:
In this age group patients own hip should be joint should be preserved. Osteosynthesis is carried
out aiming at union of fracture and obtaining a durable hip joint. The results of various
procedures depend upon the changes which have already taken place at the site of fracture with
passage of time. These changes are:
a) Fracture surfaces get smoothened out.
b) There is progressive absorption of the neck of femur resulting in increase in the gap between
the fragments and decrease in the size of the proximal fragment.
c) The head of the femur may start showing signs of avascular necrosis.
A good quality X-ray of pelvis including both hip joints in as identical position as possible
should be taken. CT scan or MRI of pelvis can be extremely useful in accurately measuring the
gap between the fragments and the size of the proximal fragment. Sometimes the absorption of
the proximal fragment is more marked in the centre than the periphery giving it the shape of a
cup or moon. This may not be clearly seen on routine. AP view X-ray of the hip and can be
better appreciated on CT scan or MRI. Avascular necrosis of the head of the femur may be seen
earlier on MRI / CT scan than on plain X-ray of the hip.
Based on these changes the fracture can be allocated to one of the following 3 stages.
Stage I
a) Fracture surfaces are still irregular (Fresh)
b) The size of proximal fragment is 2.5 cm or more
c) Gap between the fragments is 1 cm or less
d) Head of the femur is viable. There is no sign of avascular necrosis on
X-ray picture or MRI or CT Scan.
Stage II
a) Fracture surfaces are smoothened out
b) The size of the proximal fragment is 2.5 cm or more
c) The gap between the fragments is more than 1 cm but less than 2.5 cm
d) The head of the femur is viable.
If either of the feature a or c is present it is allocated to stage II.
Stage III
a) Fracture surfaces are smoothened out
b) The size of the proximal fragment is less than 2.5 cms
c) The gap between the fragments is more than 2.5 cms
d) The head of the femur shows signs of avascular necrosis
If any of the feature b, c or d is present the fracture is allocated to stage III. Treatment
Stage I: In this stage the success rate of various procedures aimed at osteosynthesis is very high.
The procedures which are useful are:
1. Closed reduction and internal fixation with one screw and double fibular graft or 2 screws and
one fibular graft. If the neck of the femur is narrow then one screw and one fibular graft may be
given.
2. Closed/open reduction Vascularised fibular graft along with screw/k-wire
3. Closed reduction or open reduction and bone muscle pedicle graft based on quadratus femoris
or sartorius or tensor fascia femoris can be used.
4. Abduction osteotomy and osteosynthesis with double angled blade plate. This procedure is
particularly useful when the fracture is situated more near the base and length of proximal
fragment is 3.5 cms or more.
5. McMurrays osteotomy with one and half POP hip spica. Stage II: In this stage when the
fracture surfaces are smoothened out (as in case of established nonunion) and the gap between
the fragments is more than 1 cm various methods of osteosyntehsis which have given good
results are
1. Closed reduction and internal fixation with one screw and double fibular graft or 2 screws and
1 fibular graft.
2. Open reduction, freshening of fracture surfaces and internal fixation with 2 screws and one
free fibular graft.
3. Closed/open reduction Vascularised fibular graft along with screw/k-wire
4. Open reduction and internal fixation with multiple screws and bone muscle pedicle graft based
on quadratus femoris or sartorius or tensor fascia femoris.
5. Other methods of treatment which can be useful (although they will not achieve union of
fracture but improve the function of hip) are
a. McMurrays osteotomy
b. Osteotomy with internal fixation
c. Bachelor's or Girdlestone procedure
Stage III: In this stage when the size of the proximal is less 2.5 cms, it cannot give good hold to
the implant as well as the graft or there is a gap of more than 2.5 cm between the fragments or
femoral head is showing signs of avascular necrosis, chances of union are less. Osteosynthesis is
likely to have very high failure rate. The treatment options available are
1. Total hip arthroplasty - - if the patient can afford and his life style permits. It may preferably
be non-cemented or may be cemented.
2. Bipolar or hemi arthroplasty
3. McMurray's osteotomy
4. Subtrochantric osteotomy with internal fixation
5. Excision hip Girdlestone's or Bachelor's procedure
6. Patient may be left alone if the patient is poor and cannot afford treatment or is unfit for
surgery. He can start walking with the support of a walker or crutches. Later on he can walk with
the support of stick or even without than in about 3-4 months time. They are often able to squat
or sit in cross legged position (Budha position).
After the age of 55 years
1. Replacement arthroplasty : if the patient can afford or his life style permits. It may be total hip
replacement or bipolar or hemi-arthroplasty. 2. Osteosynthesis if the patient wants it and is
prepared to wait for 5 - 7 months for independent walking. This should be carried out only in
stage I and stage II.
3. Excision hip (Girdlestone procedure or Bachelor's procedure)
4. Osteotomy with internal fixation
5. Leave him alone.
There are rough guidelines to help the orthopaedic surgeon to manage fracture neck of femur in
different age groups and fracture at different levels of neck for fresh as well as neglected cases.
The decision regarding the choice of operative procedure rests with the surgeon depending upon
the patient's requirements, his life style, profession and financial position. It also depends upon
the training of the Orthopaedic surgeon and facilities available to him. Use of free fibular
graft/vascularised fibula in addition to internal fixation with screws particularly where there is
posterior comminution improve the chances of union and may be carried out in such cases. If the
reduction of the fracture is less than anatomical but otherwise satisfactory addition of free fibular
graft can improve the chances of union.
If the patient is suffering from a generalized disease like diabetes mellitus, congestive heart
failure, chronic kidney or liver disease, malignancy etc., or is taking steroids adversely affecting
the chances of union of fracture, replacement arthroplasty may be a better option even in
younger.

135. Trochanteric fractures (Extra-capsular fracture neck femur)

Hip fractures in the elderly are frequent, and their number is increasing fast. The
intertrochanteric and the subtrochanteric fractures pose a number of management dilemmas
depending on the fractures configuration and status of the bones. A number of different treatment
modalities for management of these fractures have been proposed and tried with varying results
for both intertrochanteric and subtrochanteric fractures of proximal femur.
Intertrochanteric hip fractures account for approximately half of the hip fractures in the elderly;
out of this more than 50% fractures are unstable. Unstable pattern occur more commonly with
increased age and with low bone mineral density. The fracture commonly occurs through bone
affected by osteoporosis. The presence of osteoporosis in intertrochanteric fractures is important
because fixation of the proximal fragment depends entirely on the quality of cancellous bone
present, Unstable intertrochanteric fractures are those in which comminution of posteromedial
buttress exceeds a simple lesser trochanteric fragment or those with subtrochanteric extension.
The results of unstable fractures are less reliable and have a high rate of failure - 8%-25%.
The goal of treatment of any intertrochanteric fracture in the elderly is to restore mobility safely
and efficiently while minimizing the risk of medical complications and technical failure and to
restore the patient to preoperative status. Unstable intertrochanteric fractures are technically
much more challenging than stable fractures; a stable reduction of an intertrochanteric fracture
requires providing medial and posterior cortical contact between the major proximal and distal
fragment to resist varus and posterior displacing forces. Hence Surgeons must understand
implant options available and should strive to achieve accurate realignment and proper implant
placement.
Subtrochanteric fractures occur 'between lesser trochanter and a point 5 cm distally and are seen
as independent entities or as an extension of intertrochanteric fractures. The common problem
for these fractures has been malunion, delayed union or non-union. Many newer designs of
implants bas been designed for fixation of subtrochanteric fractures. The newer implants were
designed to avoid bending, breakage of plates and nails, the loosening of screws and inadequate
fixation. After the failure of A O angled blade plate many implants were designed like dynamic
hip compression screw, dynamic condylar screw, modifications of axial compression screw
devices like Medoff's device.
Most of the hip fractures in the elderly results from simple fall from standing. This is mainly
because elderly people are unable to dissipate energy as compared to the young person, and
diminished ambulatory speed. Their protective responses are also diminished because of slow
reaction time, weakness, disorientation and the side effect of medication. Elderly people also
lack shock absorbers such as pad of fat or muscles over the trochanteric region and finally
diminished bone strength because of osteopaenia allows fractures to occur with trivial fall.
Trochanteric fractures can be classified as:
Management: Primary health centre level:
The doctor on duty should recognise the features of fracture and disloction. Only first aid
including the splintage and intravenous drip should be given. In open fractures Tetanus toxoid
can be given. There is no need to waste time in preparation of medico-legal formalities. The
injured should be referred to the higher centre earliest feasible causing no further harm.
Non Metro Hospital (CHC and Civil Hospital level):
1. Investigations: X-rays of the pelvis including both hips and knee joint and of other areas if
required, General Investigations and specific if required according to the status of the health of
the patient.

2. Treatment:

Closed reduction and DHS is the standard modality for most of the Trochanteric fractures. If
closed reduction fails open reduction can be done. In unstable Trochanteric fractures Proximal
Femoral Nail (PFN), Intramedullary Hip Screw can also be done depending upon the facilities
and the expertise of the operating surgeon. Where there is comminution at the site of entry for
the DHS, Dynamic Condylar Screw (DCS) may be used.
For subtrochanteric fractures a DCS is the implant of choice after closed or open reduction.
Other modalities like PFN, Angled blade plate, Reconstruction nail or Modified Kuntscher’s nail
may also be used as per the preference of the surgeon.
3. Referral Criteria for Metro hospital
a. Polytrauma patient.

b. Patient with co-morbid conditions requiring multiple speciality care.

c. Patients requiring Joint replacement.

d. Non unions / Neglected fractures ie fractures more than 3 weeks duration.

e. Pathological fractures.

f. Suspected HIV positive cases.

g. Fractures associated with any condition requiring higher investigations like CT Scan, MRI etc

Metro hospital level

1. Investigations: X-rays of the pelvis including both hips and knee and of other areas if
required, General Investigations and specific if required according to the presence of any co-
morbidity. Special investigations like MRI/CT scan if required.

2. Treatment: All the treatment as in CHC/Civil hospital level along with multidisciplinary
approach as required for other co-morbid conditions of the patient. In very osteoporotic patients
cement augmentation along with DHS should be done to decrease chances of cut through. In few
selected ones with either osteoarthritis of hip joint or in those patients in whom union is
suspected we can go for arthroplasty.

Since lots of co-morbidities are common in geriatric population, a thorough preoperative medical
evaluation is necessary. The detailed preoperative work up directly affects the timing of surgery
and the operative procedure. Majority of these fractures should be treated operatively for ease of
nursing care, rapid mobilisation, decreased mortality, decreased hospitalization and restoration of
function. The operative treatment should be considered urgently, but not as an emergency
procedure.
The optimal time for surgical intervention appears to be after the patient is evaluated medically
and any transient medical ailment corrected i.e. electrolyte and fluid imbalance. However it
should not be delayed more than 48-72 hours unless intervention significantly decreases the
operative risk.
Also most of these patients are osteoporotic and have a high chance of getting fracture in the
opposite side, so anti osteoporotic treatment should be started in all of these patients and so is the
early mobilization as osteoporosis will increase if they stay in bed waiting for the union to occur.

136. FRACTURE SHAFT OF FEMUR

Fractures of the shaft of the femur are the result of high-energy trauma and therefore can be both
life-threatening injuries and causes of severe permanent disability. Isolated injuries can occur
with repetitive stress and may occur in the presence metabolic bone diseases, metastatic disease,
or primary bone tumors.
The femur is very vascular and fractures can result in significant blood loss into the thigh. Up to
40% of isolated fractures may require transfusion, as such injuries can result in loss of up to 3
units of blood. This factor is significant, especially in elderly patients who have less cardiac
reserve.
Most femoral diaphyseal fractures are treated surgically with intramedullary nails or plate
fixation. The goal of treatment is reliable anatomic stabilization, allowing mobilization as soon
as possible. Surgical stabilization is also important for early extremity function, allowing both
hip and knee motion and strengthening. Injuries and fractures of the femoral shaft may have
significant short- and long-term effects on the hip and knee joints if alignment is not restored.
The 3 types of femoral shaft fractures are as follows:
ype I - Spiral or transverse (most common)
- Comminuted
- Open

Primary health centre level: The doctor on duty should recognise the features of fracture and
disloction. Only first aid including the splintage and intravenous drip should be given. In open
fractures Tetanus toxoid can be given. There is no need to waste time in preparation of medico-
legal formalities. The injured should be referred to the higher centre earliest feasible causing no
further harm.
Non-Metro Hospital( CHC and Civil Hospital level):
1. Investigations: X-rays of the part including hip and knee and of other areas if required, x-ray
of pelvis with both hips is must. General Investigations and specific if required according to the
status of the health of the patient.

2. Treatment: Conservative management of fractures in children in spica cast or with skeletal

traction, Kuntscher’s nail for isthmic fractures, Interlocking Nailing in comminuted fractures,
Plating for lower third fractures, Plating of shaft femur fracture in children.

Referral Criteria
a. Polytrauma patient.
b. Patient with co-morbid conditions requiring multiple speciality care.

c. Non unions / Neglected fractures.

d. Pathological fractures.

e. Open fractures requiring Plastic surgery or with Large gaps due to bone loss

f. Non unions / Neglected fractures and failed osteosynthesis.

g. Fractures associated with neurovascular injuries/Suspected Fat Embolism.

h. Suspected HIV positive cases.

i. Fractures associated with any condition requiring higher investigations like CT scan, MRI etc.

Metro Hospital -Higher referral centre:

1. Investigations: X-rays of the part and of other areas if required, x-ray of pelvis with both hips
is must. General Investigations and specific if required according to the presence of any co-
morbidity. Special investigations like MRI/CT scan or angiography if required.

2. Treatment: All the treatment given at situation 1, Closed/Open Interlocking Nailing,

DCS/Distal femoral Nail or Plate for Supracondylar/Intercondylar fractures, External
fixator/Enders/solid undreamed Nail for open fractures, Fibular grafting with plating and
cancellous bone grafts for non unions, Illizarovs Ring Fixator, Rail road fixator for gap defects,
Plastic/Vascular surgeon assistance.

137. FRACTURE OF TIBIA/FIBULA

1. Introduction /description

Lower leg fractures include fractures of the tibia and fibula. Of these two bones, the tibia is the
main weight bearing bone. Fractures of the tibia generally are associated with fibula fracture,
because the force is transmitted along the interosseous membrane to the fibula.
The skin and subcutaneous tissue are very thin over the anterior and medial tibia and as a result
of this; a significant number of fractures to the lower leg are open. Even in closed fractures, the
thin, soft tissue can become compromised. In contrast, the fibula is well covered by soft tissue.
Fractures of the tibia can involve the tibial plateau, tubercle, shaft, and plafond.
2. Incidence:
Fractures of the tibia are the most common long bone fractures. The most common fracture of
the lower limb occurs at the tibial diaphysis. Isolated mid-shaft or proximal fibula fractures are
uncommon.
3. Mode of injury

Tibial plateau fractures occur from axial loading with valgus or varus forces, such as in a fall
from a height or collision with the bumper of a car. The lateral tibial plateau is fractured more
frequently than the medial plateau.
Tibial tubercle fractures usually occur during jumping activities.
Mechanisms of injury for tibia-fibula fractures can be divided into 2 categories:
-energy injuries such as ground levels falls and athletic injuries and in osteoporotic
patients

-energy injuries such as motor vehicle injuries(esp motor cycle accidents, pedestrians
struck by motor vehicles, and gunshot wounds

Tibial plafond fractures refer to fractures involving the weight-bearing surface of the distal tibia.
This type of injury usually results from high-energy axial loading but may result from lower-
energy rotation forces.
4. Clinical presentation:

Patient may complain of severe pain, swelling and bruising down the broken leg, deformity of
bones and inability to ambulate with tibia fracture. Tibial plateau fractures often present with a
knee effusion. Approximately 20% of tibial plateau fractures are associated with ligamentous
injuries.
Limb loss may occur as a result of severe soft-tissue trauma, neurovascular compromise,
popliteal artery injury, compartment syndrome, or infection such as gangrene or osteomyelitis.
Popliteal artery injury is a particularly serious injury that threatens the limb.
5. MANAGEMENT:
5.1 Primary health centre level:
The doctor on duty should recognise the features of fracture and disloction. Only first aid
including the splintage and intravenous drip should be given. In open fractures Tetanus toxoid
can be given. There is no need to waste time in preparation of medico-legal formalities. The
injured should be referred to the higher centre earliest feasible causing no further harm.
5.2 CHC and Civil Hospital level:

Trauma patient should be managed by addressing airway, breathing, and circulation. Check and
document neurovascular status. Apply sterile dressing to open wounds. Apply gentle traction to
reduce gross deformities; splint the extremity. After first aid, pain management and splintage,
PRICE therapy (Protection, rest/immobilise the limb, ice therapy, compression and elevation)
should be started.
Investigations: Perform radiographs of the knee, tibia/fibula, and ankle as indicated and of other
areas if required, General Investigations and specific if required according to the status of the
health of the patient. In patients with tibial plateau fractures and tibial plafond fractures,
computed tomography can help further evaluate the extent of the fracture. In tibial plateau
fractures, radiographs may underestimate the degree of articular depression when compared with
computed tomography. This is important because articular depression of greater than 3 mm may
be considered for surgery.
Treatment: soft tissue envelope is the most important component in the evaluation and
subsequent care of tibial fractures. Compartment syndrome can develop in fractures of the lower
leg. Signs of compartment syndrome include crescendo symptoms- (5 P’s) puffiness/oedema,
pain out of proportion with passive stretch of involved muscles, paresthesias, and pallor, and a
very late finding is pulselessness and paralysis. Increased compartment pressure is present during
compartment syndrome; therefore, external palpation frequently aids in the diagnosis. However,
a soft extremity on palpation does not rule out compartment syndrome.
Compartment syndrome must be treated promptly with an emergency surgical fasciotomy
Open fractures must be diagnosed and treated appropriately. Tetanus vaccination should be
updated, and appropriate antibiotics should be given in a timely manner. This should involve
antistaphylococcal coverage and consideration of an aminoglycoside for 61
more severe wounds. Adequate wound debridement and wound care. Fractures with tissue at risk
for opening should be protected to prevent further morbidity. External fixator should be applied
in non comminuited fractures.
All simple both bone leg fractures, minimally displaced fractures in children / adults should be
managed with closed reduction and above knee cast. In displaced fractures closed reduction and
interlock nailing in shaft fractures should be done, Plating should be done for lower third
fractures. Post closed reduction (pop cast) or open reduction and fixation adequate limb elevation
is required and patient is encouraged to do passive exercises to avoid edema of limb, deep vein
thrombosis and to aid in adequate wound healing.
Tibial plateau fracture : Immobilize un-displaced fractures and keep the patient non-
weightbearing for 3 months.
Tibial tubercle fracture- For un-displaced fractures, immobilize the knee.
Isolated midshaft or proximal fibula fracture- Immobilization in a long leg cast generally is not
required. Recommend a few days without weight-bearing activity until swelling resolves,
followed by weight-bearing activity as tolerated. In some case, immobilization in above knee
cast is done
Some of the complications that may arise in treatment are:
articularly in oblique and
spiral fractures

fragment is imperfect

ult of severity of the fracture, poor blood supply to one fragment, and
sometimes distraction of the bone fragments

associated joint, soft tissue, or vascular injury

a fibular neck fracture or the pressure of a splint,

Referral Criteria for higher centre (Medical College / Tertiary centre)
a. Open fractures requiring Plastic surgery or with Large gaps due to bone loss.

b. Comminuted fractures, Fractures requiring Interlocking Nail, proximal intra-articular

fractures, distal pilon fractures, open fractures

c. Polytrauma patient.

d. Patient with co-morbid conditions requiring multiple speciality care.

e. Non unions / Neglected fractures and failed osteosynthesis.

f. Pathological fractures.

g. Fractures associated with neurovascular injuries/Suspected Fat Embolism.

h. Suspected HIV positive cases

5.3 Metro Hospital or Higher centre level

At Medical College / Tertiary centre the goal of management of these include in addition to
situation 1.
3. Investigations: computer tomography of concerned joint, colour Doppler studies of limb and
CT- angiography if required.

4. Treatment: All Closed/Open (upto 3A as per gustilio Anderson classification) should

managed with iterlocking Nailing. All proximal tibial intra-articular fractures esp. depressed
fractures should be internally fixed with LCP/LCDCP. Distal pilon fractures should be operated
and internally fixed with plating.

Open fractures should be managed by cupious washing of wound, wound debridement and
application of External fixator/Enders/nails. In fractures with bone loss various options available
are;
-tiblisation of fibula and fixation with plating/ k-wires
- Illizarovs Ring Fixator and Rail road fixator for gap defects and limb lengthening.
-in case of smaller gaps, compression at fracture site and ORIF with plate/nail with cancellous
bone grafts
Vascular surgeon assistance (vessel repair or grafting) and plastic surgeon assistance (flap or
skin grating) in case of vessel injury and skin or soft tissue loss respectively should be taken. 63

138. PROTOCOL FOR THE MANAGEMENT OF PELVIC FRACTURE

I. WHEN TO SUSPECT/ RECOGNIZE?

a) Introduction:

Pelvic fracture are predominantly (10% -20%) present in blunt multiple trauma and represent a
significant source of morbidity and mortality. Major forces are required to fracture the normal
pelvis. Pelvic ring disruptions, more than any other fracture of the body, can lead to severe
complications, including massive bleeding and organ injuries. Exsanguinating hemorrhage is the
most dreaded acute complication of pelvic fracture. In addition, because of its function as a bony
basin for different organs, the cauda equina and essential nerves for the lower limbs, serious
injuries of those structures significantly increases the total trauma impact of the multiply injured
patient with pelvic injury. The unstable untreated pelvis enforces immobility and does not allow
appropriate positioning of those patients with chest and brain injuries for their necessary
intensive care.
History suggestive of pelvic fracture
-motorcycle collision
-car vs. pedestrian
-fall from more than 15ft height
-lateral impact injuries
-MVC with vehicle incompatibility (i.e., car/motorcycle, pedestrian/motor vehicle)
-Crushing injury (e.g., falling tree, wall)
-Gun shot and projectile related
b) Case definition:
For both situations of care (mentioned below*)
A patient having injury of the pelvic ring, a break in the continuity of fibro-osseous ring. For
management purpose these injuries are classified into subgroups.
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY
Accidents in India are definitely on an increase. The exact number of pelvic fractures in our
country is not known. But, indirect estimates point to a very high incidence.
As per the data from the National Crime Records Bureau,467537 persons died due to injury and
violence in 2009.Injury and violence deaths increased from 246277 in 1998 to 467537 by 2009
(NCRB, 1998 & 2009 a, b ). During the same period the non fatal injuries also increased
correspondingly to 1,070,302 in 2009.Injury deaths are only tip of the iceberg. For every death, it
is estimated that nearly 30-50 persons are hospitalized and 50-100 are likely to receive
emergency care.
The data from the recently completed million death study by the Registrar General of India
indicates that injuries contributed for 10 % of deaths and was the leading cause in younger age
groups (RGI,2009).Of urban population deaths leading causes were RTI’s (47%),suicides (34%)
and assault (10%).Leading causes of injuries were falls (27%),RTI’s(27%) and burns (7.3%) (G
Gururaj)
From above figures it can be estimated that the number is quit high.
III. DIFFERENTIAL DIAGNOSIS

In all cases of trauma, especially in cases with a history suggestive of pelvic injuries should be
actively looked for pelvic fracture or dislocation after initial resuscitation (ABC’s).
IV. PREVENTION AND COUNSELING

Accidents don’t just happen; they are caused. Majority (>90 %) of them are directly or indirectly
due to human error, natural (< 10 % ) causes account for very few deaths. All the causes should
be identified by epidemiological methods. Since accidents are multifactorial, they call for an
intersectoral approach to both prevention and care of the injured.
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,

TREATMENT & REFERRAL CRITERIA

*Situation 1: At Secondary Hospital/ Non-Metro situation: Optimal Standards of
Treatment in Situations where technology and resources are limited
a) Clinical Diagnosis:
After assessment ABC’s
Gross inspection (open wounds, deformities)
-Extensive echymosis and soft tissue swelling
-Disruption of the subcutaneous fat along with echymotic skin and potentially deep fascia
(Morelle-Levelle lesion)
-open wounds around the pelvis
Perineal laceration or puncture wound
Presacral laceration.
Deformities
Disturbed relationship of ASIS, iliac crest,
Limb length discrepancies
Instability
Comprehensive neurovascular assessment
Urogenital and rectal examination
b) Investigations:
Chest, pelvic and cervical spine radiograph
Focused abdominal ultrasonography for trauma (FAST),
Diagnostic peritoneal lavage (DPL)
Dependent on specific injuries
-- CT of head, ECG, retrograde urethrogram etc
CT Pelvis with 3D reconstruction
c) Treatment:
The primary objective in the initial care of the multiply injured patient is survival with normal
cognitive functions. The first hour after admission to the emergency room is most critical in
terms of survival and reduction of morbidity. Multiply injured patients should have immediate
evaluation of their vital organ functions, resuscitation, focused and rapid diagnostic procedures,
and appropriate surgical treatment, including damage control followed by stabilization of their
vital organ functions in the intensive care units (ICU), as per ATLS Protocol (Reference ATLS)
Algorithm for management of haemorrhagic shock in pelvic fracture
STABLE HAEMODYNAMIC STATUS
ICU-intensive care unit
NO
YES
Consider surgical bleeding control or repeat angiography
ICU
Standard Operating procedure
Pelvic binder / pneumatic antishock garment,
Pelvic external fixator / C-clamp
Skeletal traction in Type –C injuries
a. In Patient ) all patient of pelvic injuries are high energy trauma
b. Out Patient ) they need in patient treatment for at least 24 hrs
c. Day Care ) to exclude other serious injuries.

d) Referral criteria: Depending upon the resources at the centre patients are referred timely
preferably after an attempt at stabilizing the patient .Sometimes only few minutes are there for
decision to operate for control of bleeding, (damage control and than referral).

Excessive requirement for blood,

Polytrauma with additional injuries
If adequate OT facilities are not available
For arterial bleeding ,angiography requirement
*Situation 2: At Super Specialty Facility in Metro location where higher-end technology is
available
e) Clinical Diagnosis:

Same as situation 1
b) Investigations:
Blood gas analysis
Chest, pelvic and cervical spine radiograph
Focused abdominal ultrasonography for trauma (FAST),
Diagnostic peritoneal lavage (DPL)
Dependent on specific injuries
-- CT of head, ECG, ECHO, retrograde urethrogram etc
-- CT pelvis with 3D reconstruction
-- CT abdomen
-- Angiography
f) Treatment:
Same as situation 1
Once the patient is stable than the definite management of pelvic fracture is undertaken usually
after 5th day and before end of 2nd week.

Secondary survey & assessment of pelvic fracture

(stability and personality)
In Secondary “regeneration “period (i.e., 2-10 days)
Once the patient is haemodynamically stabilized detailed assessment of the personality of the
fracture and stability should be determined. To asses this
Secondary diagnostic procedures are undertaken
AP, inlet, outlet and Judet view of pelvis
CT scan (with contrast), fluoroscopy and stress view
3D CT, MRI, bone scan, U/S, Angiography
Once this is determined definitive pelvic fracture management is done depending upon the
type of injury as described below in flow charts.
Indications for ORIF of unstable pelvic disruptions (type C)
ANTERIOR (symphysis or remi)
-to improve pelvic stability in association with laprotomy acutely (no faecal contamination or
suprapubic tube) or simplified fracture management (acute or semi acute phase)
- Remi fracture associated with lesion of femoral artery or nerve
-bone protruding into perineum (tilt # in female)
-asso. Ant acetabular fracture that require ORIF
POSTERIOR
-Inadequate reduction of posterior SI complex, esp. SI jt dislocation > 1 cm displacement or
>30* ext rotation
-open fracture with a posterior wound (rarely for perineal wound)
-associated posterior acetabular fracture that requires ORIF
Standard Operating procedure
a. In Patient ) all patient of pelvic injuries are high energy trauma
b. Out Patient ) they need in patient treatment for at least 24 hrs
c. Day Care ) to exclude other serious injuries.

g) Referral criteria: not applicable for tertiary centre unless some facilities are missing.

VI. WHO DOES WHAT? and TIMELINES

a. Doctor
--Monitors and supervises the treatement and performes any
procedures on urgent basis, coordinates with other departments
-- Arranges interhospital transfer in time
b. Nurse
Carry out all the treatment and maintains the formulary (drugs and consumables and equipment)
c. Technician
Helps in resuscitation, transport , immobilization etc.

139. SPINAL INJURY

I. WHEN TO SUSPECT/ RECOGNIZE?

d) Introduction:

With an estimated annual incidence of 300 per crore population, approximately 40,000 new
spine injury cases are added every year in India. 40% of these are complete lesions i.e. tetra or
paraplegia. The socio economic impact of spinal injuries is huge with 85% of victims being male
in the age group of 15 to 35 years. Management of patients who have sustained spinal cord injury
requires careful assessment and management. Inadequate assessment and management of these
injuries may lead to worsening of existing spinal cord injury or the production of a new cord
injury.
b) Case definition: For both situations of care (mentioned below*)
Spinal cord injury (SCI) is an insult to the spinal cord resulting in a change, either temporary or
permanent, in its normal motor, sensory, or autonomic function.
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY:

In the absence of a national spinal cord injury registry in India, the exact incidence is not known.
Approximately 30 cases per million population. Approximately 40% of these will be complete.
Majority of the cases are due to road side accidents or fall from height.
III. DIFFERENTIAL DIAGNOSIS:
All trauma patients should be assumed to have a spinal injury and treated as such till a detailed
clinical examination and radiological investigations has been performed. Potential spinal cord
injury should be suspected in following situations:
a. Altered mental status.

b. Evidence of intoxication.

c. Associated head injury, extremity fracture

d. Focal neurological deficit.

e. Spinal pain or tenderness

f. Mechanism of injury e.g fall from height, fall on head, whiplash injuries, high energy injuries

IV. PREVENTION AND COUNSELING :

All trauma patients should be assumed to have a spinal injury and treated as such, until this can
be confidently excluded. Full spinal immobilisation should be employed including a collar,
spinal board and blocks. Tape can be used to secure the head to the blocks. This should be done
as soon as physically possible and prior to moving the patient to a site of definitive care.
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,
TREATMENT & REFERRAL CRITERIA
*Situation 1: At Secondary Hospital/ Non-Metro situation: Optimal Standards of
Treatment in Situations where technology and resources are limited
a) Clinical Diagnosis:

After the ABC have been taken care of, the patient is gently log rolled and whole of the spine is
palpated for tenderness or a palpable step-off deformity. Neurogenic 79

shock, incontinence of bowel, bladder and penile erection indicate severe spine injury. A careful
and detailed neurological examination is then performed and meticulously documented.
Frankel’s grades : Spinal Cord Injury is most commonly graded using Frankel’s grades (A to E).
A; Complete motor and sensory loss
B: Sensation only present below lesion
C: Sensations present and motor function is present but useless
D: Motor useful but not normal
E: No neurological deficit. After the motor and sensory examination, presence of sacral sparing
may be noted by voluntary rectal sphincter tone and toe flexor contractions. Presence of sacral
sparing indicates a better neurological prognosis.
Although spinal shock is over by 24 hours, rarely it may be prolonged. A positive
bulbocavernous reflex or a positive anal wink indicates the end of spinal shock. If no motor or
sensory function can be documented at this stage, a complete spinal cord injury is present.
b) Investigations:
All patients with suspected spinal injury should have radiographic evaluation.
1. Initial screening can be done by conventional antero-posterior and lateral x-rays. The cervical
spine radiographs must include the C7-T1 junction to be considered adequate

2. Additional Open-mouth views should be done to evaluate odontoid injury.

3. Whole spine should be evaluated with a patient of spinal injury.

d. The patient should be referred for advanced diagnostic modalities only when the patient is
stable:
CT Scan: CT scan cervical spine in all cases of head injuries or intoxication at the same time as
the brain CT. CT should be done when plain X-Ray is inadequate particularly upper cervical
spine injuries and C7-T1 junction.
MRI: MRI is essential for evaluating injury to the soft tissues and ligaments, discs, intrinsic cord
damage (oedema, hematoma, or contusion) and Para vertebral soft tissues. MRI is particularly
useful in scenarios such as central cord syndrome where plain radiographs will not show any
fractures or dislocations. If possible MRI should be done before the cervical traction is applied.
In patients with pre-injury morbidities such as Ankylosing Spondylitis, CT and MRI should be
done to rule out occult instability even if x-rays are normal.
b) Treatment:

Standard Operating procedure

a. In Patient
1. Once the patient with a potential spinal injury reaches the emergency, the patient should be
transferred off the backboard onto a firm padded surface while maintaining spinal alignment. A
baseline skin assessment can be performed at the time of shifting the patient from spine board to
hospital bed.
2. Adequate number of personnel should be employed for logrolling during patient repositioning,
turning and transfers.
3. Secure ABC
a. Airway: If intubation is required rapid sequence intubation with manual inline stabilisation
should be done. Awake fibreoptic intubation is ideal in a cooperative patient and if facilities are
available.
b. Prevent and treat hypotension
i. Look for other causes of hypotension such as abdominal, chest and pelvic injury
ii Look for Neurogenic shock i.e. hypotension with bradycardia in cervical spine and high
thoracic injuries.
b. Monitor and regulate temperature
4. Perform a baseline neurological assessment on any patient with suspected spinal injury.
Determine a neurological level and the completeness of injury (as described above). Perform
serial examinations as indicated to detect neurological deterioration or improvement. The
neurological examination should be done as per an objective system such as ASIA scoring
system and documented properly. Perform serial examinations as indicated e.g. after each
intervention to detect neurological deterioration or improvement
5. Once initial resuscitation is done, complete a comprehensive tertiary trauma survey in the
patient with potential or confirmed spinal cord injury.
6. In the patient with acute spinal cord injury, particularly higher cervical injury, assess and
document early and frequently any evidence of traumatic brain injury (TBI) in the form of loss of
consciousness and posttraumatic amnesia
7. Screen for thoracic and intra-abdominal injury in all patients with spinal cord injury.
8. No clinical evidence exists to definitively recommend the use of any neuroprotective
pharmacologic agent, including steroids, in the treatment of acute spinal cord injury to improve
functional recovery. However high dose methyl-prednislone may be used as per NASCIS III
recommendations (Methylprednisolone: Bolus dose of 30 mg/kg of body weight over 15
minutes, followed by a 45-minute pause, and then a 23-hour continuous infusion of 5.4 mg/kg/hr,
If patient presents between 3 and 8 h, give the above steroid infusion for total of 48 h) if the
patient presents within 8 hours of injury. The risk of complications such as such as higher
infection and sepsis rates, respiratory complications and gastrointestinal hemorrhage should be
kept in mind while administering steroids.
9. Genitourinary Tract :
i. Place an indwelling urinary catheter as part of the initial patient assessment unless
contraindicated
ii. Leave indwelling urinary catheters in place at least until the patient is haemodynamically
stable
iii. CIC should be taught to patient or the relatives as soon as the patient is stable
10. Gastrointestinal Tract
Initiate stress ulcer prophylaxis.
Evaluate swallowing function prior to oral feeding in any acute SCI patient
11. Measures to prevent bed sores:
i) Assess areas at risk for skin breakdown frequently.

ii) Place the patient on a pressure-reduction mattress or a mattress overlay depending on the
patient's condition.

iii) Use a pressure-reducing cushion when the patient is mobilized out of bed to a sitting position.

iv) Reposition to provide pressure relief or turn at least every 2 hours while maintaining spinal
precautions.
v) Keep the area under the patient clean and dry and avoid temperature elevation.

vi) Assess nutritional status on admission and regularly thereafter.

vii) Inspect the skin under pressure garments and splints.

viii) Educate the patient and family on the importance of vigilance and early intervention in
maintaining skin integrity.

b. Out Patient care

A secondary hospital is expected to provide outpatient care to the spinal cord injury patients who
may be referred back from specialized centers after definitive treatment. This may be in form of
i. physiotherapy for passive mobilisation of all joints and active exercises for muscles
ii. Teaching of clean intermittent cathetrisation
iii. Counselling of the patient and attendants
iv. Care of bed sores
c. Day Care

Day care might be needed for situations like debridement of bed sores.
c) Referral criteria:

1. The patient should be hemodynamically stable and fully resuscitated at the time of referral
2. All the patients who need surgery (indications discussed in the next section) need to be
referred to a specialized tertiary care centre.
3. The decision of need for surgery can only be made by an experienced spinal surgeon either
orthopedic or neurosurgeon. In absence of these all patients with proven or suspected spine
injury should be referred to a higher center.
4. It is desirable to have a two way communication with higher center while referring a patient.
*Situation 2: At Super Specialty Facility in Metro location where higher-end technology is
available
h) Clinical Diagnosis: As described above (in situation 1)

i) Investigations:

Radiographic evaluation of patients with spinal injury.

1.Initial screening can be done by conventional antero-posterior and lateral x-rays.
2. Additional Open-mouth views should be done to evaluate odontoid injury.
3. Special views like swimmer’s view and oblique views can be done to see junctional areas
4. CT scan of the whole spine should be done if in presence of clinical suspicion but fractures
cannot be demonstrated on x rays or if junctional areas are not visualised.
5. MRI should be done to evaluate ligamentous injury, spinal cord injury.
In patients with pre-injury morbidities such as AS,DISH, stiff spine CT and MRI should be done
to rule out occult instability even if x-rays are normal.
6. Whole spine should be evaluated with a patient of spinal injury.
j) Treatment:

Standard Operating procedure

a. In Patient

1. Once the patient with a potential spinal injury reaches the emergency , the patient should be
transferred off the backboard onto a firm padded surface while maintaining spinal alignment. A
baseline skin assessment can be performed at the time of shifting the patient from spine board to
hospital bed. Adequate number of personnel should be employed for logrolling during patient
repositioning, turning and transfers.
2. Secure ABC
a. Airway: If intubation is required rapid sequence intubation with manual inline stabilisation
should be done. Awake fibreoptic intubation is ideal in a cooperative patient and if facilities are
available.
b.Prevent and treat hypotension
i. Look for other causes of hypotension such as abdominal, chest and pelvic injury
ii Look for Neurogenic shock i.e. hypotension with bradycardia in cervical spine and high
thoracic injuries.
c. Monitor and regulate temperature.
3. Perform a baseline neurological assessment on any patient with suspected spinal injury .
Determine a neurological level and the completeness of injury. Perform serial examinations as
indicated to detect neurological deterioration or improvement. The neurological examination
should be done as per an objective system such as ASIA scoring system and documented
properly. Perform serial examinations as indicated e.g. after each intervention to detect
neurological deterioration or improvement. ASIA score is very elaborate, one can follow TLISS/
TCLISS (as recommended by STSG)

4. No clinical evidence exists to definitively recommend the use of any neuroprotective

pharmacologic agent, including steroids, in the treatment of acute spinal cord injury to improve
functional recovery. However high dose methyl-prednislone may be used as per NASCIS III
recommendations (Methylprednisolone: Bolus dose of 30 mg/kg of body weight over 15
minutes, followed by a 45-minute pause, and then a 23-hour continuous infusion of 5.4 mg/kg/hr,
If patient presents between 3 and 8 h, give the above steroid infusion for total of 48 h) if the
patient presents within 8 hours of injury. The risk of complications such as such as higher
infection and sepsis rates, respiratory complications and gastrointestinal hemorrhage should be
kept in mind while administering steroids, It is basically a treatment option,not standard care.

5. Once initial resuscitation is done, complete a comprehensive tertiary trauma survey in the
patient with potential or confirmed spinal cord injury.
6. In the patient with acute spinal cord injury, particularly higher cervical injury, assess and
document early and frequently any evidence of traumatic brain injury (TBI) in the form of loss of
consciousness and posttraumatic amnesia

7. Screen for thoracic and intra-abdominal injury in all patients with spinal cord injury.

8. Perform early stabilization of extraspinal fractures. Perform this surgery as early as possible to
facilitate early rehabilitation and concomitantly with any required spinal stabilization if the
patient is medically stable.
9. Surgical treatment
a. Perform a closed or open reduction as soon as permissible on patients with bilateral cervical
facet dislocation in the setting of an incomplete spinal cord injury
b. Consider early spinal stabilization where indicated
c. Consider early surgical spinal canal decompression direct or indirect in the setting of a
deteriorating spinal cord injury as a practice option that may improve neurologic recovery,
although there is no compelling evidence that it will.
The following algorithms may be followed as a guide to help in decision making in operative
treatment of spine injuries. These algorithms are meant as a guide and the treatment plan for each
patient needs to be individualised
i) Upper cervical injuries
a) Occipital condyle fractures:
Type III injuries require surgical stabilisation if associated with craniocervical instability

b) Atlas fractures
Surgical stabilisation if:
• neurologic symptoms,

• instability is more than 5 mm on dynamic radiographs

• significant pain is present with the evidence of nonunion.

The surgical procedure is stabilization of C1-C2 or occiput-C2

c) Odontoid factures:
10. Adjunctive measures:

c. Assess areas at risk for skin breakdown frequently.

d. Place the patient on a pressure-reduction mattress or a mattress overlay depending on the

patient's condition.

e. Use a pressure-reducing cushion when the patient is mobilized out of bed to a sitting position.

f. Reposition to provide pressure relief or turn at least every 2 hours while maintaining spinal
precautions.

g. Keep the area under the patient clean and dry and avoid temperature elevation.

h. Assess nutritional status on admission and regularly thereafter.

i. Inspect the skin under pressure garments and splints.

j. Educate the patient and family on the importance of vigilance and early intervention in
maintaining skin integrity.
11. Genitourinary Tract
Place an indwelling urinary catheter as part of the initial patient assessment unless
contraindicated
Leave indwelling urinary catheters in place at least until the patient is haemodynamically stable
CIC should be taught to patient or the relatives as soon as the patient is stable
12. Gastrointestinal Tract
laxis.

spinal cord injury, halo fixation, cervical spine surgery, prolonged intubation, tracheostomy.
b. Out Patient

Out patient care is needed for non surgically treated patients on ambulatory care andSurgically
treated patients. This will entail:
Prescription of appropriate orthoses
Physiotherapy services
Counselling: social, psychological,vocational
c. Day Care

k) Referral criteria:

Surgically treated patients may be referred back to secondary hospitals for physiotherapy, and
care of back, bladder and bowel.
VI. WHO DOES WHAT? and TIMELINES
a. Doctor

Primary assessment and resuscitation

Clinical diagonosis
Ordering and interpretation of investigations
Clinical decision making
Surgical procedures
b. Nurse

Primary resuscitation can be performed by a nurse

Prevention of bed sores
Maintenance of inventory(drugs,consumables etc.)
Operating room assistance
c. Technician

Pre trauma technicians do primary immobilization and do safe transport to hospitals

Primary resuscitation can be performed by technicians
Appropriate radiological investigations
Physiotherapy
ANNEXURE 2
AO classification of thoracolumbar fractures

- injury patterns of the vertebral body

disruption either anteriorly or posteriorly

140. THE NEUROLOGICAL DISORDERS:

POLIOMYELITIS AND CEREBRAL PALSY.
Standard treatment guidelines for Poliomyelitis
1. Introduction/Definition/Description

Poliomyelitis is an acute viral infection caused by polioviruses (three antigenic types I, II, and
III). The poliovirus is an enterovirus. All three viruses can cause paralysis; however it occurs
most commonly by type I followed by type III and very rarely by type II.
2. Incidence of the condition

Due to intensive pulse polio immunization along with routine immunization has reduced its
incidence to negligible and it almost near eradication in our country. But there are still a
reasonable number of patients of residual paresis who need some sort of surgical correction
either for proper fitting of orthosis or for the proper use of the extremity.
3. Differential diagnosis

The cases of cerebral palsy, myopathies and the neuropathies like motor neuron disease, Gullain-
Barre syndrome etc need to be differentiated from poliomyelitis.
4. Clinical features

Three types of cases occur: Inapparent infections (95% cases), non-paralytic infections (about
5%) and paralytic cases 0.5% cases. The acute attack can cause death in 2-10% of case. The
non-paralytic infection is manifested by fever, sore throat, headache, nausea, vomiting, diarrhea
and rigidity of the neck and back lasting for 2-10 days. The paralytic attack is manifested by
acute flaccid paralysis of the muscles of the limb or the trunk and face followed by maximum
recovery within 6 months. Broadly and conventionally these are acute attack and the residual
paresis and paralysis.
5. Management
5.1 Primary Health centre level: No surgical treatment is expected at this level. Only referral to
higher centre. One should recognize the features of flaccid or lower motor neuron level disorder
and its residual effects.
5.2 CHC and Civil Hospital level:
The acute poliomyelitis is managed by pediatricians and the orthopedics management include
only the splintage of the extremity in the functional and proper resting position till the phase of
convalescence.
For residual motor weakness: The goal of the treatment at the non metro clinic or small hospital
is: Evaluation of the motor weakness by muscle power charting by Medical Research Council
(MRC) grading system (Grade 0 to5). X-rays of the affected area as per the requirement.
Following can be done at this level: Prescription of orthosis/calipers and its fitting;
-corrective cast application; -Simple corrective procedures like-
tenotomy for the tight tendo-achillis; lengthening of tendon etc -arrangement of polio corrective
surgery camps ( but the team of surgeons from teaching Medical Institute/College should
evaluate the cases and supervise the surgeries).
-Additionally at the district level hospital the patients can provided the orthosis and walking aids
(like sticks, crutches, walkers etc), and wheel chair/tricycles from the district level charitable
agencies (Governmental/Non-governmental).
-They can be issued the disability certificates for their financial benefits for various schemes run
by the Government.
Criteria for referral: The cases who need investigations like nerve conduction studies and
electromyographies. Those who need tendon transfers, correction of deformity at multiple joints
and in different planes. Any case where the non metro level surgeon is in doubt in decision
making of the type of surgery should be referred.
5.3 Situation 3 At the metro or the medical college level hospital the goal of management of
these cases include: In addition to the situation 1- If required the elctromyographic studies, nerve
conduction studies.
Then all surgeries for the correction of deformity -by tendon transfer (dynamic)
-the osteotomies/tenodesis,
-tendon lengthening, -tenotomies, capsulotomies and arthrodesis as per the indication and after
the careful evaluation of the individual. The goal of the treatment is focused on the independent
walking (for lower limb) or the proper use of the upper extremity with/without orthosis.
The lower extremity should be with planti-grade foot with no or minimal residual deformity at
various joints and the limb should be suitable for fitting of the orthosis/calipers.
The upper extremity should be made for the independent usage with/without support.
Various common surgical procedures include:
Tendo-achillis lengthening-for equinus correction,
Jone’s Teno-suspension- for dropped first metatarsal and sub-luxed
1st metatraso-phalangeal joint,
Tibialis posterior tendon transfer- for foot drop,
Dorsal bony wedge resection (Japa’s) and Steindler’ release for cavus foot deformity correction,
Osteotomy for deformity correction (e.g. supra-condylar osteotomy),
Tendon lengthening/tenotomies and capsulotomies-for contracture release,
Tripple arthrodesis for talipes equino-varus correction in mature feet etc. 104

All the surgeries should be performed by the experienced surgeon and standard text book on the
subject should be available in the operation theatre for the reference. References:
1. WHO. The initiative for global eradication of poliomyelitis- a guide to clinicians. Geneva:
WHO; 1994.

2. GOI, Evaluation of Pulse polio Immunization India1996-97.New Delhi:

MOH and FW; 1997.

3. Warner WC, Jr. Paralytic disorders. In:Campbell’s Operative

Orthopaedics. Eleventh Eds; 2008.pp.1401-98.

4. Turek SL. Orthopaedics-Principles and Their Application. 4th Eds. In:
Orthopaedics Neurology. 1998. Pp.464-595. 106
141. STANDARD TREATMENT GUIDELINES FOR CEREBRAL PALSY
1.Definition: Cerebral palsy is defined as the non-progressive motor impairment (motor
neurological deficit) due to the insult to the developing brain; affecting the movements and
posture, however, no sensory impairment.
The involvement of the brain most commonly occurs between the time of conception and the age
2 years (the time of major motor development). After 8 years of the age, the development of the
immature brain is almost complete; its affection is just like adults. This is very common disorder
in the child hood and its incidence is on rise.
2. Types: As per the time of affection of the brain this is categorized as prenatal, perinatal and
post natal. Most common is prenatal and only less than 10% cases are affected during the
delivery time i.e. perinatal.
3.Management
For the management, the complete and proper evaluation of the individual as whole and the
affected part is mandatory. Some times in the situation of spasticity it is difficult to judge the
muscle power and the treatment can be worsening rather than improving the functions and there
can also be recurrence of the deformity. Therefore, whenever in doubt, the peripheral surgeon
can refer the patient to the medical institute or to the metro hospital for the treatment after
evaluation. These patients apart from motor power evaluation may require the gait analysis; MRI
of the brain and electromyography. The treatment of the some rare types of cerebral palsy is
really difficult and very much demanding even at the level of the medical institute or the metro
hospital. At the metro hospital the team approach involving the peaediatrician, the orthopedic
surgeon, psychiatrist, physiotherapist and psycho-social workers is required for the better
outcome in such patients.
3.1 Situation 1
No surgical intervention is expected at this level. One should refer the patient to the higher
centre.
3.2 CHC/Civil Hospital level: At the non-metro hospital only simple surgeries like tendo-
achillis tenotomy and adductor tenotomy for equines and the scissoring gait respectively can be
tried and that too if the operating surgeon has the confidence and has reasonable experience.
Otherwise it is better to refer the patient.
3.3 The goal of the treatment at the non metro clinic or small hospital is: Evaluation of the motor
weakness by muscle power charting by Medical Research Council (MRC) grading system
(Grade 0 to5).
Following can be done at this level: -Prescription of orthosis/calipers and its fitting;
-corrective cast application;
-Simple corrective procedures like- tenotmy for the tight tendo-achillis; lengthening of tendon
and adductor tenotomy etc.
3.4-Arrangement of camps for providing orthosis and walking aids -Additionally at the district
level hospital the patients can be provided the walking aids (like sticks, crutches, walkers etc),
and wheel chair from the district level charitable agencies (Governmental/Non-governmental).
They can be issued the disability certificates for their financial benefits from various schemes run
by the Government.
Criteria for referral: The cases that need special investigations like nerve conduction studies,
electromyographies and MRI/CT scans. Those who need tendon transfers, correction of
deformity at multiple joints and in different planes; and need care of multiple specialists under
one roof. Any case where the non metro level surgeon is in doubt in decision making of the type
of surgery should be referred.
3.2Situation 2
At the metro or the medical college level hospital the goal of management of these cases include:
In addition to the situation 1- If required the elctromyographic studies, nerve conduction
studies, MRI and CT scan of brain as per indication.. The non surgical treatment like botulinum
injection can be given to relieve the spasticity.
Then all surgeries for the correction of deformity
-by tendon transfer
-the osteotomies/tenodesis,
-tendon lengthening,
-tenotomies, capsulotomies and arthrodesis as per the indication and after the careful evaluation
of the individual. The goal of the treatment is focused on the independent walking (for lower
limb) or the proper use of the upper extremity with/without orthosis. The lower extremity should
be with planti-grade foot with no or minimal residual deformity at various joints and the limb
should suitable for fitting of the orthosis/calipers and if feasible for independent walking. The
upper extremity should be made suitable for fitting of orthosis and for the use in daily day to day
routine like self eating, bathing; cleansing after toilet etc.
Various common surgical procedures include:
Tendo-achillis lengthening-for equinus correction,
Adductor tenotomy – to correct scissoring gait
Split tibialis anterior transfer for inversion foot
Tibialis posterior tendon transfer- for foot drop,
Egger’s operation/Fractional release of hamstrings (Tendon lengthening/tenotomies and
capsulotomies)-for knee contracture release,
Tripple arthrodesis for talipes equino-varus correction in mature feet. Flexor pronator release
and transfer of flexor carpi ulnaris to the wrist dorsiflexors for contracture of flexor and
pronator muscle group. Sever’s and Fairbank operation and derotation osteotomy of
humerus- for internal rotation contracture at shoulder etc
All the surgeries should be performed by the experienced surgeon and standard text book on the
subject should be available in the operation theatre for the reference.

143. ANKYLOSING SPONDYLITIS

I. WHEN TO SUSPECT / RECOGNIZE?
a. Introduction:

A form of spondyloarthritis, is a chronic, inflammatory arthritis and autoimmune disease. It

mainly affects joints in the spine and the sacroiliac joint in the pelvis, and can cause eventual
fusion of the spine.
b. Case Definition:

The typical patient is a young male, aged 20–40, however the condition also presents in females.
The condition is known to be hereditary. Symptoms of the disease first appear, on average, at age
23 years. These first symptoms are typically chronic pain and stiffness in the middle part of the
spine or sometimes the entire spine, often with pain referred to one or other buttock or the back
of thigh from the sacroiliac joint.
II. INCIDENCE OF CONDITION IN OUR COUNTRY
Three men are diagnosed with AS for every one woman; the overall prevalence is 0.25%. Many
rheumatologists believe the number of women with AS is underdiagnosed, as most women tend
to experience milder symptoms.
III. DIFFERENTIAL DIAGNOSIS

Differential diagnosis of Ankylosing Spondylitis include

1. Rheumatoid Arthritis
2. Other Spondylo arhtropathies

IV. PREVENTION AND COUNSELLING

As no direct cause for the disease has been identified the preventive measures could not be
established.
Patient needs to be counselled regarding the chronic nature of the disease and need for regular
treatment, possible complications and possible treatment options and chances of improvement.
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA

* SITUATION 1: At Secondary Hospital / Non Metro situation : Optimal standards of

Treatment in situations where technology and resources are limited
a. Clinical diagnosis: chronic pain and stiffness in the middle part of the spine or sometimes the
entire spine, often with pain referred to one or other buttock or the back of thigh from the
sacroiliac joint. Post inactivity stiffness and morning stiffness. In 40% of cases, ankylosing
spondylitis is associated with an inflammation of the eye (iritis and uveitis), causing redness, eye
pain, vision loss, floaters and photophobia. This is thought to be due to the association these two
conditions have with inheritance of HLA-B27. Other common symptoms are generalized fatigue
and sometimes nausea.
b. Investigations:
1. X Ray
2. CT Scan
3. MRI
4. Complete Blood Picture
5. ESR
6. CRP
7. Liver function test
8. Renal function test
9. HLA B27

c. In a patient complaining of back pain of more than 12 weeks duration:

1. Morning stiffness of > 30 minutes
2. Improvement in back pain with exercise but not with rest.
3. Awakening because of back pain during the second half of the night only .
4. Alternating buttock pain.
5. Peripheral assymetrical large joint involvement.
6. Plain X Ray showing features of sacroilitis.
7. Absence of RA factor.

Any 2 out of first four criteria strongly indicate presence of Ankylosing Spondylitis even in the
absence of xray and lab investigations.
d. Treatment:

Standard Operating Procedure

i. In Patient :
1. Surgery
a. Joint Replacement for hip and knee.

ii. Out Patient :

1. NSAIDS: First line therapy to relieve symptoms.
2. DMARDs such as cyclosporin, methotrexate, sulfasalazine, and corticosteroids, used to reduce
the immune system response through immunosuppression;
DMARDs are useful only for peripheral arthritis & not for axial skeleton involvement.
iii. Physical Therapy – Patients to be encouraged to undertake active and passive range of motion
exercises for all joints to maintain and prevent the progression of loss of mobility. Deep
breathing exercises (Pranayaam) should be promoted to improve chest function.

iv. Day Care

1. Injectable medications

d. Referral criteria:

For further evaluation and management of cases not responding to conventional therapy.
* SITUATION 2: At Super Specialty facility in Metro Location where higher end
technology is available
a. Clinical diagnosis:

As in situation 1
b. Investigations:

As in situation 1
c. Treatment:

Standard Operating Procedure

i. In Patient : as in situation 1. Others include
1. Corrective surgeries for spinal deformity
ii. Out Patient : As in situation 1. In addition to that
1. TNFα blockers (antagonists) such as etanercept, infliximab, golimumab and adalimumab (also
known as biologics), are indicated for the treatment of and are effective immunosuppressants in
AS as in other autoimmune diseases.
iii. Day Care: As in situation 1
d. Referral criteria:
VI. WHO DOES WHAT? AND TIMELINES
a. Doctor

Early diagnosis and appropriate treatment. Counsel the patient for prevention of deformities and
dietary advice.
b. Nurse

counseling the patient. Injectable treatment

c. Technician

Appropriate bracing manufacturing and application of braces

Physiotherapy

145. GOUTY ARTHRITIS

I. WHEN TO SUSPECT / RECOGNIZE?

a. Introduction:

Gout characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot,
swollen joint. The metatarsal-phalangeal joint at the base of the big toe is the most commonly
affected (approximately 50% of cases). However, it may also present as tophi, kidney stones, or
urate nephropathy. It is caused by elevated levels of uric acid in the blood which crystallize and
are deposited in joints, tendons, and surrounding tissues.
b. Case Definition:

Affluent males are the usual victims. It very rarely affects pre-menopausal women & such a
patient should be viewed with suspicion if a diagnosis of gout is made.
Gout can present in a number of ways, although the most usual is a recurrent attack of acute
inflammatory arthritis. The metatarsal-phalangeal joint at the base of the big toe is affected most
often, accounting for half of cases. Other joints, such as the heels, knees, wrists and fingers, may
also be affected. Joint pain usually begins over 2–4 hours and during the night. Other symptoms
that may occur along with the joint pain include fatigue and a high fever.
Long-standing elevated uric acid levels (hyperuricemia) may result in other symptomatology,
including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead
to chronic arthritis due to bone erosion. Elevated levels of uric acid may also lead to crystals
precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.
II. INCIDENCE OF CONDITION IN OUR COUNTRY

Gout affects around 1–2% of the Western population at some point in their lifetimes, and is
becoming more common. A number of factors have been found to influence rates of gout,
including age, race, and the season of the year. In men over the age of 30 and women over the
age of 50, prevalence is 2%
III. DIFFERENTIAL DIAGNOSIS

Differential diagnosis of Gout include

3. Septic Arthritis
4. Pseudo Gout
5. Rheumatoid Arthritis

IV. PREVENTION AND COUNSELLING

Both Dietary and lifestyle changes can decrease uric acid levels.
i. reducing intake of food such as meat and seafood,

ii. consuming adequate vitamin C,

iii. limiting alcohol and fructose consumption

iv. avoiding obesity.

v. Coffee, but not tea, consumption is associated with a lower risk of gout.
OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA
* SITUATION 1: At Secondary Hospital / Non Metro situation : Optimal standards of
Treatment in situations where technology and resources are limited
a. Clinical diagnosis:

Usual presentation is acute inflammatory arthritis—a red, tender, hot, swollen joint. The
metatarsal-phalangeal joint at the base of the big toe is the most commonly affected
(approximately 50% of cases). However, it may also present as tophi, kidney stones, or urate
nephropathy. It is caused by elevated levels of uric acid in the blood which crystallize and are
deposited in joints, tendons, and surrounding tissues.
Investigations:
1. X Ray
2. Serum Uric Acid Level (Suggestive; to be confirmed by 3 below)
3. MSU crystals in Synovial fluid and tophi (Essential for diagnosis)
4. Complete Blood Picture
5. ESR
6. CRP
7. Renal function test

a. Treatment:

Standard Operating Procedure

ii. In Patient :
1. Surgery
a. Excision of symptomatic tophi

vi. Out Patient :

3. Acute Attack
a. NSIADS
b. Colchicine
c. Steroids

4. Chronic (No role in acute attack)

a. Allopurinol
b. Febuxostat
c. Probenacid
5. Physical Therapy
vii. Day Care
1. Injectable medications
2. Intra articular Steroid Injection

e. Referral criteria:

For further evaluation and management of cases not responding to conventional therapy.
* SITUATION 2: At Super Specialty facility in Metro Location where higher end
technology is available
e. Clinical diagnosis:

As in situation 1
f. Investigations:

As in situation 1
g. Treatment:

Standard Operating Procedure

iv. In Patient : as in situation 1.

v. Out Patient : As in situation 1.

vi. Day Care: As in situation 1

h. Referral criteria:
VIII. WHO DOES WHAT? AND TIMELINES
a. Doctor

Early diagnosis and appropriate treatment. Counsel the patient for prevention and dietary advice.
b. Nurse

counseling the patient. Injectable treatment

c. Technician

Appropriate bracing
Physiotherapy

146. OSTEOARTHRITIS
I. WHEN TO SUSPECT / RECOGNIZE?

a. Introduction:

Osteoarthritis (OA) also known as degenerative arthritis or degenerative joint disease is a group
of mechanical abnormalities involving degradation of joints, including articular cartilage and
subchondral bone. A variety of causes—hereditary, developmental, metabolic, and mechanical—
may initiate processes leading to loss of cartilage, When bone surfaces become less well
protected by cartilage, bone may be exposed and damaged. As a result of decreased movement
secondary to pain, regional muscles may atrophy, and ligaments may become more lax.
b. Case Definition:

Osteoarthritis can be classified into either primary or secondary depending on whether or not
there is an identifiable underlying cause.
Primary osteoarthritis is a chronic degenerative disorder related to aging. A number of studies
have shown that there is a greater prevalence of the disease among siblings and especially
identical twins, indicating a hereditary basis. Up to 60% of OA cases are thought to result from
genetic factors
Secondary Osteoarthritis is caused by other factors such as

arthritis (e.g. costochondritis, gout, and rheumatoid arthritis). In gout, uric acid crystals cause the
cartilage to degenerate at a faster pace.

factor.
-alignment of extremities.

II. INCIDENCE OF CONDITION IN OUR COUNTRY Osteoarthritis affects nearly 27

million people in the United States, accounting for 25% of visits to primary care physicians, and
half of all NSAID prescriptions. It is estimated that 80% of the population have radiographic
evidence of OA by age 65, although only 60% of those will have symptoms.
III. PREVENTION AND COUNSELLING

Life style modification , weight control, regular exercise

Patient needs to be counselled regarding the nature of the disease and need for treatment,
possible treatment options and chances of improvement.
IV. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA

* SITUATION 1: At Secondary Hospital / Non Metro situation : Optimal standards of

Treatment in situations where technology and resources are limited
a. Clinical diagnosis:

The main symptom is pain, causing loss of ability and often stiffness. "Pain" is generally
described as a sharp ache, or a burning sensation in the associated muscles and tendons. OA can
cause a crackling noise (called "crepitus") when the affected joint is moved. It commonly affects
the hands, feet, spine, and the large weight bearing joints, such as the hips and knees, although in
theory, any joint in the body can be affected. As OA progresses, the affected joints appear larger,
are stiff and painful, and usually feel better with gentle use but worse with excessive or
prolonged use. In smaller joints, such as at the fingers, hard bony enlargements, called
Heberden's nodes (on the distal interphalangeal joints) and/or Bouchard's nodes (on the proximal
interphalangeal joints), may form, and though they are not necessarily painful, they do limit the
movement of the fingers significantly. OA at the toes leads to the formation of bunions,
rendering them red or swollen.
b. Investigations:
1. X Ray - Particularly standing xrays for knees in which eccentric joint space reduction is the
diagnostic crieterion as compared to inflammatory where there is concentric space reduction.
c. Treatment:

Standard Operating Procedure

iii. In Patient :
1. Surgery
a. Arthroscopy joint debridement
b. Joint Replacement
ii. Out Patient :
6. Life style modification
7. Physical therapy
8. Analgesics
a. Oral
b. Topical
9. Steroids
a. Systemic
b. Intra articular
10. Glucosamine (controversial)

iii Day Care

1. Injectable medications
2. Intra articular Steroid injection
3. Intra articular hyaluronic acid injection

f. Referral criteria:

For further evaluation and management of cases not responding to conventional therapy.
* SITUATION 2: At Super Specialty facility in Metro Location where higher end
technology is available
i. Clinical diagnosis:

As in situation 1
j. Investigations:

As in situation 1 .
k. Treatment:

Standard Operating Procedure

vii. In Patient : as in situation 1.

viii. Out Patient : As in situation 1.

ix. Day Care: As in situation 1

l. Referral criteria:

X. WHO DOES WHAT? AND TIMELINES

a. Doctor

Early diagnosis and appropriate treatment. Counsel the patient for prevention and dietary advice.
b. Nurse

counseling the patient. Injectable treatment

c. Technician
Appropriate bracing manufacturing and application of braces
Physiotherapy

147. OSTEOMALACIA
I. WHEN TO SUSPECT / RECOGNIZE?

a. Introduction:

Osteomalacia is a generalized bone condition in which there is inadequate mineralization of the

bone. Many of the effects of the disease overlap with the more common osteoporosis, but the two
diseases are significantly different. There are two main causes of osteomalacia: (1) insufficient
calcium absorption from the intestine because of lack of dietary calcium or a deficiency of or
resistance to the action of vitamin D; and (2) Phosphate deficiency caused by increased renal
losses
b. Case Definition:

Osteomalacia is the softening of the bones due to defective bone mineralization secondary to
inadequate amounts of available phosphorus and calcium. It may show signs as diffuse body
pains, muscle weakness, and fragility of the bones. The most common cause of the disease is a
deficiency in vitamin D, which is normally obtained from the diet and/or sunlight exposure
II. INCIDENCE OF CONDITION IN OUR COUNTRY

In the US and Europe, more than 40% of the adult population older than age 50 are vitamin D
deficient, this being the most prominent cause of osteomalacia. http://bestpractice.bmj.com/best-
practice/monograph/517/resources/references.html - ref-4In developing countries vitamin D
deficiency leading to clinical rickets is described in 60% of infants. In the Middle East, a high
prevalence of rickets and osteomalacia has been described in Muslim women and their infants,
perhaps due to increased clothing coverage of the skin.
III. DIFFERENTIAL DIAGNOSIS

Differential diagnosis of osteomalacia include

Osteoporosis
Pagets disease
IV. PREVENTION AND COUNSELLING

Ensuring adequate sunlight exposure and dietary intake of fortified foods containing vitamin D,
calcium, and phosphorus may help avoid osteomalacia
It is recommended that maintenance dosing in adults <50 years age should be 400-800
International Units (IU) of vitamin D daily, and that adults ≥50 years age should get 800-1000
IU of vitamin D daily. Adults should also take 1.2 g of elemental calcium in the diet or as a
supplement.
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA

* SITUATION 1: At Secondary Hospital / Non Metro situation : Optimal standards of

Treatment in situations where technology and resources are limited
a. Clinical diagnosis:

Osteomalacia in adults starts insidiously as aches and pains in the lumbar (lower back) region
and thighs, spreading later to the arms and ribs. The pain is symmetrical, non-radiating and is
accompanied by sensitivity in the involved bones. Proximal muscles are weak, and there is
difficulty in climbing up stairs and getting up from a squatting position.
Physical signs include deformities like triradiate pelvis and lordosis. The patient has a typical
"waddling" gait. However, those physical signs may derive from a previous osteomalacial state,
since bones do not regain their original shape after they become deformed. May present as
pathological fracture.
b. Investigations:

Serum Calcium
Serum Phosphate
Alkaline Phosphatase
Serum urea creatinine
24 Hr urinary calcium
X rays of the deformed part
c. Treatment: Nutritional osteomalacia responds well to administration of 10,000 IU weekly of
vitamin D for four to six weeks. Osteomalacia due to malabsorption may require treatment by
injection or daily oral dosing of significant amounts of vitamin D
Standard Operating Procedure
i. In Patient : For corrective surgery

ii. Out Patient : supplementation and bracing

iii. Day Care: Injectable form of Vit D

d. Referral criteria:

For evaluation and management of cases not responding to conventional therapy.

* SITUATION 2: At Super Specialty facility in Metro Location where higher end
technology is available
m. Clinical diagnosis:

As in situation 1
n. Investigations:

As in situation 1 . Others are

1,25 – dihydroxy- Vit D level
Parathormone level
DXA
Bone Biopsy with double tetracycline labelling
Technitium Bone scan
o. Treatment:

Standard Operating Procedure

i. In Patient : as in situation 1
UV-B radiation Tanning beds and other UV-B radiation devices have been used to treat vitamin
D deficiency in the elderly and in malabsorptive disorders.
ii. Out Patient : As in situation 1

iii. Day Care: As in situation 1

p. Referral criteria:

VI. WHO DOES WHAT? AND TIMELINES

a. Doctor

Early diagnosis and appropriate treatment. Counsel the patient for prevention and dietary advice.
b. Nurse

Counselling the patient

c. Technician

Appropriate bracing manufacturing and application

Physiotherapy

148. OSTEOPOROSIS
I. WHEN TO SUSPECT / RECOGNIZE?

a. Introduction:

Osteoporosis is a disease of bones that leads to an increased risk of fracture. In osteoporosis the
bone mineral density (BMD) is reduced, bone microarchitecture is deteriorating, and the amount
and variety of proteins in bone is altered.
b. Case Definition:

Osteoporosis is defined by the World Health Organization (WHO) as a bone mineral density that
is 2.5 standard deviations or more below the mean peak bone mass (average of young, healthy
adults) as measured by DXA; the term "established osteoporosis" includes the presence of a
fragility fracture. The disease may be classified as primary type 1, primary type 2, or secondary.
The form of osteoporosis most common in women after menopause is referred to as primary type
1 or postmenopausal osteoporosis. Primary type 2 osteoporosis or senile osteoporosis occurs
after age 75 and is seen in both females and males at a ratio of 2:1. Finally, secondary
osteoporosis may arise at any age and affects men and women equally. This form of osteoporosis
results from chronic predisposing medical problems or disease
II. INCIDENCE OF CONDITION IN OUR COUNTRY

The exact incidence of osteoporosis in India is not known .However ,according to one
study,approximately 6-7 crores of Indian population is suffering from osteopenia / osteoporosis
III. DIFFERENTIAL DIAGNOSIS

Differential diagnosis of Osteoporosis include

6. Multiple myeloma
7. Osteomalacia
8. Chronic kidney disease
9. Primary hyperparathyroidism
10. Metastatic bone malignancy
11. Vertebral deformities
IV. PREVENTION AND COUNSELLING
a. Risk factors for Osteoporosis includes following
i. Prior fragility fracture
ii. Female gender
iii. White ancestry
iv. Old age
v. Low BMI
vi. Loss of height
vii. Sec amenorrhoea
viii. Primary hypogonadism
ix. Smoking
x. Excessive alcohol use
xi. Prolonged immobilizatioin
xii. Low calcium intake
xiii. Vit D defficiency
xiv. Glucocorticoid excess
xv. Corticosteroid use
xvi. Hyperthyroidism
xvii. Heparin use
xviii. Anticonvulsant use
xix. Weight loss
b. Prevention

Change in life style, diet, exercise. Amongst the various risk factors for osteoporosis modifiable
risk factors can be modified to prevent development of osteoporosis. Medications to prevent
development of osteoporosis.
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA

* SITUATION 1: At Secondary Hospital / Non Metro situation : Optimal standards of

Treatment in situations where technology and resources are limited
a. Clinical diagnosis:

Osteoporosis itself doesn’t have any symptom.

Symptoms develop once the fragility fracture occurs. Symptoms develop according to the site of
fracture. Pain may or may not be there due to osteoporotic fracture. Vertebral compression
fracture at times may present with neural symptoms.
b. Investigations:
1. Plain X-ray of spine
2. Dual energy X ray absorptiometry (DXA) BMD
3. Renal function test
4. Calcium
5. Albumin
6. Phosphorus
7. Urinary calcium level
c. Treatment:

Standard Operating Procedure

iv. In Patient :
1. Surgery
a. Vertebroplasty
b. Open surgical spinal stabilization
ii. Out Patient : supplementation and bracing
11. Pain control
a. Bed rest
b. Analgesics
c. Brace
12. Antiresorptive agents
a. Bisphosphonates
b. Estrogen analogs
c. Raloxifen
d. Calcitonin
13. Bone anabolic agent
e. Teriparatide
f. Calcium salts
g. Sodium fluoride
14. Nutrition
h. Calcium
i. Vitamin D
j. Vitamin K
15. Exercise
k. Aerobics
l. Weight bearing
m. Resistance exercise
16. Orthosis
n. Spinal orthoses
17. Long term Osteoporosis prophylaxis
iv. Day Care: Injectable medication
g. Referral criteria:

For further evaluation and management of cases not responding to conventional therapy.
* SITUATION 2: At Super Specialty facility in Metro Location where higher end
technology is available
q. Clinical diagnosis:

As in situation 1
r. Investigations:

As in situation 1 . Others are

1. QCT (quantitative computer tomography)

2. Quantitative Ultrasound

3. Biochemical markers of bone resorption (increased urinary excretion of C- telopeptides)

4. Vit D level

5. Testosterone level

6. Urinary free cortisol

7. Serum protein electrophoresis

s. Treatment:
Standard Operating Procedure
i. In Patient : as in situation 1. In addition to that
1. Surgery
a. Vertebroplasty
b. Kyphoplasty

ii. Out Patient : As in situation 1. In addition to that

1. Other agents
a. RANKL inhibitors
b. Strontium ranelate
iii. Day Care: As in situation 1
t. Referral criteria:
XII. WHO DOES WHAT? AND TIMELINES
a. Doctor

Early diagnosis and appropriate treatment. Counsel the patient for prevention and dietary advice.
b. Nurse

counseling the patient

c. Technician

Appropriate bracing manufacturing and application of braces

Physiotherapy

149. RHEUMATOID ARTHRITIS

I. WHEN TO SUSPECT / RECOGNIZE?

a. Introduction:

Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder that may affect many
tissues and organs, but principally attacks synovial joints. The process produces an inflammatory
response of the synovium (synovitis) secondary to hyperplasia of synovial cells, excess synovial
fluid, and the development of pannus in the synovium. The pathology of the disease process
often leads to the destruction of articular cartilage and ankylosis of the joints. Rheumatoid
arthritis can also produce diffuse inflammation in the lungs, pericardium, pleura, and sclera, and
also nodular lesions, most common in subcutaneous tissue. Although the cause of rheumatoid
arthritis is unknown, autoimmunity plays a pivotal role in both its chronicity and progression,
and RA is considered a systemic autoimmune disease.
b. Case Definition:

Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder that may affect many
tissues and organs, but principally attacks synovial joints. It can be a disabling and painful
condition, which can lead to substantial loss of function and mobility if not adequately treated. It
is a clinical diagnosis made on the basis of symptoms, physical exam, radiographs (X-rays) and
labs, although the American College of Rheumatology (ACR) and the European League Against
Rheumatism (EULAR) publish diagnostic guidelines
These new classification criteria overruled the "old" ACR criteria of 1987 and are adapted for
early RA diagnosis. The "new" classification criteria establish a point value between 0 and 10.
Every patient with a point total of 6 or higher is unequivocally classified as an RA patient,
provided he has synovitis in at least one joint and given that there is no other diagnosis better
explaining the synovitis. Four areas are covered in the diagnosis:
1. joint involvement, designating the metacarpophalangeal joints, proximal interphalangeal
joints, the interphalangeal joint of the thumb, second through third metatarsophalangeal joint and
wrist as small joints, and elbows, hip joints and knees as large joints:
a. Involvement of 1 large joint gives 0 points
b. Involvement of 2-10 large joints gives 1 point
c. Involvement of 1-3 small joints (with or without involvement of large joints) gives 2 points
d. Involvement of4-10 small joints (with or without involvement of large joints) gives 3 points
e. Involvement of more than 10 joints (with involvement of at least 1 small joint) gives 5 points
2. serological parameters – including the rheumatoid factor as well as ACPA – "ACPA" stands
for "anti-citrullinated protein antibody":
a. Negative RF and negative ACPA gives 0 points
b. Low-positive RF or low-positive ACPA gives 2 points
c. High-positive RF or high-positive ACPA gives 3 points
3. acute phase reactants: 1 point for elevated erythrocyte sedimentation rate, ESR, or elevated
CRP value (c-reactive protein)
4. duration of arthritis: 1 point for symptoms lasting six weeks or longer
II. INCIDENCE OF CONDITION IN OUR COUNTRY

About 1% of the world's population is afflicted by rheumatoid arthritis, women three times more
often than men. Onset is most frequent between the ages of 40 and 50, but people of any age can
be affected. The incidence of RA is in the region of 3 cases per 10,000 population per annum. It
is up to three times more common in smokers than non-smokers, particularly in men, heavy
smokers, and those who are rheumatoid factor positive. First-degree relatives prevalence rate is
2–3% and disease genetic concordance in monozygotic twins is approximately 15–20%.
III. DIFFERENTIAL DIAGNOSIS

Differential diagnosis of Rheumatoid Arthritis include

12. Crystal induced arthritis
13. Osteoarthritis
14. SLE
15. Psoriatic Arthritis
16. Lyme Disease
17. Reactive Arthritis

IV. PREVENTION AND COUNSELLING

As no direct cause for the disease has been identified the preventive measures could not be
established. Patient needs to be counselled regarding the chronic nature of the disease and need
for regular treatment, possible complications and possible treatment options and chances of
improvement.
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA
* SITUATION 1: At Secondary Hospital / Non Metro situation : Optimal standards of
Treatment in situations where technology and resources are limited
a. Clinical diagnosis:

Rheumatoid arthritis typically manifests with signs of inflammation, with the affected joints
being swollen, warm, painful and stiff, particularly early in the morning on waking or following
prolonged inactivity. Increased stiffness early in the morning is often a prominent feature of the
disease and typically lasts for more than an hour.
For diagnosis and management of other body system involvement by RA Physician needs to be
consulted.
Clinical diagnosis can be made as per the guidelines given by ACR & EULAR.
b. Investigations:
1. X Ray
2. Complete Blood Picture
3. ESR
4. CRP
5. Liver function test
6. Renal function test
7. Rheumatoid Factor (RA)
8. Anti-citrullinated protein antibodies (ACPAs) or anti-CCP

c. Treatment:

Standard Operating Procedure

v. In Patient :
1. Surgery
a. Arthroscopy Synovectomy in early stage
b. Joint Replacement in late stages

ii. Out Patient : supplementation and bracing

18. Disease modifying anti-rheumatic drugs (DMARDs)
a. First Line DMARDs:
i. Methotrexate
ii. Hydroxychloroquine
iii. Sulfasalazine
iv. Leflunomide

b. Second Line
i. Azathioprine
ii. cyclosporin (cyclosporine A)
iii. D-penicillamine

iv. gold salts (Oral & Parenteral)

v. minocycline

19. Anti-inflammatory agents and analgesics

a. Anti-inflammatory agents include:
i. glucocorticoids

ii. Non-steroidal anti-inflammatory drug (NSAIDs, most also act as analgesics)

b. Analgesics include:
i. Paracetamol

ii. Opiates

iii. Diproqualone

iv. Lidocaine topical

20. Bed rest during acute flare ups
21. Physiotherapy

iii Day Care

1. Injectable medications
2. Intra articular Steroid injection
h. Referral criteria:

For further evaluation and management of cases not responding to conventional therapy. *
SITUATION 2: At Super Specialty facility in Metro Location where higher end technology
is available
u. Clinical diagnosis:

As in situation 1
v. Investigations:

As in situation 1 . Others are

1. Anti-MCV assay (antibodies against mutated citrullinated Vimentin).

2. point-of-care test (POCT) for the early detection of RA has been developed. This assay
combines the detection of rheumatoid factor and anti-MCV for diagnosis of rheumatoid arthritis
and shows a sensitivity of 72% and specificity of 99.7%

w. Treatment:

Standard Operating Procedure

iv. In Patient : as in situation 1.

v. Out Patient : As in situation 1. In addition to that

1. Biological agents (biologics) include:
a. tumor necrosis factor alpha (TNFα) blockers – etanercept (Enbrel), infliximab (Remicade),
adalimumab (Humira), certolizumab pegol (Cimzia), golimumab (Simponi)
b. Interleukin 1 (IL-1) blockers – anakinra (Kineret)
c. monoclonal antibodies against B cells – rituximab (Rituxan)
d. T cell costimulation blocker – abatacept (Orencia)
e. Interleukin 6 (IL-6) blockers – tocilizumab (an anti-IL-6 receptor antibody) (RoActemra,
Actemra)
vi. Day Care: As in situation 1
a. Referral criteria: Window of opportunity DMARDs exists within 4 to 6 months of the onset
of disease. Early diagnosis & institution of right therapy is thus crucial.

VI. WHO DOES WHAT? AND TIMELINES

b. Doctor Early diagnosis and appropriate treatment. Counsel the patient for prevention and
dietary advice.
c. Nurse

counseling the patient. Injectable treatment

d. Technician

Appropriate bracing manufacturing and application of braces

Physiotherapy

150. RICKETS
I. WHEN TO SUSPECT / RECOGNIZE?

a. Introduction:

Rickets is a softening of bones in children due to deficiency or impaired metabolism of vitamin

D, phosphorus or calcium,http://en.wikipedia.org/wiki/Rickets - cite_note-0 potentially leading
to fractures and deformity. Rickets is among the most frequent childhood diseases in many
developing countries. The predominant cause is a vitamin D deficiency, but lack of adequate
calcium in the diet may also lead to rickets (cases of severe diarrhea and vomiting may be the
cause of the deficiency). Although it can occur in adults, the majority of cases occur in children
suffering from severe malnutrition
b. Case Definition:

The primary cause of rickets is a vitamin D deficiency. Vitamin D is required for proper calcium
absorption from the gut. Sunlight, especially ultraviolet light, lets human skin cells convert
Vitamin D from an inactive to active state. In the absence of vitamin D, dietary calcium is not
properly absorbed, resulting in hypocalcaemia, leading to skeletal and dental deformities and
neuromuscular symptoms
Types:

o Type I
o Type II

II. INCIDENCE OF CONDITION IN OUR COUNTRY

In developed countries, rickets is a rare diseasehttp://en.wikipedia.org/wiki/Rickets - cite_note-6

(incidence of less than 1 in 200,000). Children ages 6 months to 24 months are at highest risk,
because their bones are rapidly growing.Mother’s milk gives adequate calcium and vitamin-D so
nutritional rickets develops once breast feeding is stopped. Renal or vitamin-D resistant rickets
develops in children of 5-8 years of age.
III. DIFFERENTIAL DIAGNOSIS

Differential diagnosis of reickets include

Hypophosphatasia
Metaphyseal dysplasia
Blounts disease
IV. PREVENTION AND COUNSELLING

A sufficient amount of ultraviolet B light in sunlight each day and adequate supplies of calcium
and phosphorus in the diet can prevent rickets. Recommendations are for 400 international units
(IU) of vitamin D a day for infants and children.
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA
* SITUATION 1: At Secondary Hospital / Non Metro situation : Optimal standards of
Treatment in situations where technology and resources are limited
a. Clinical diagnosis:

Signs and symptoms of rickets include:

baby syndrome" or "slinky baby", increased tendency for fractures

o Genu varum, Genu Valgum, Cranial, spinal, and pelvic deformities

is due to metaphysial cartilage hyperplasia.

b. Investigations:

Alkaline Phosphatase
Serum Calcium
Serum Phosphorus
X rays of the deformed part
c. Treatment:

The goals of treatment are to relieve symptoms and correct the cause of the condition.
Replacing calcium, phosphorus, and vitamin D, Exposure to moderate amounts of sunlight is
encouraged. Positioning or bracing may be used to reduce or prevent deformities. Skeletal
deformities may require corrective surgery later on.
Standard Operating Procedure
i. In Patient : For corrective surgery

ii. Out Patient : supplementation and bracing

iii. Day Care: Injectable form of Vit D

d. Referral criteria:

Vitamin D resistant Rickets

Hypophosphatemic Rieckets
* SITUATION 2: At Super Specialty facility in Metro Location where higher end
technology is available
x. Clinical diagnosis:

As in situation 1
y. Investigations:

As in situation 1 . Others are

25 hydroxy – Vit D level
1,25 – dihydroxy- Vit D level
24 hours urinary Ca and Phosphorus levels
z. Treatment:

Standard Operating Procedure

i. In Patient : as in situation 1 and Recombinant Growth hormone therapy for
Hypophosphatemic rickets

ii. Out Patient : As in situation 1

iii. Day Care: As in situation 1

aa. Referral criteria:

VI. WHO DOES WHAT? AND TIMELINES

a. Doctor
Early diagnosis and appropriate treatment. Counsel the patient for prevention and dietary advice.
b. Nurse

Counselling the patient

c. Technician

Appropriate bracing manufacturing and application

Physiotherapy
Pediatrics
152. PROTOCOL FOR DENGUE FEVER IN CHILDREN

1 Introduction
Dengue has a wide spectrum of clinical presentations, often with unpredictable clinical evolution
and outcome. Reported case fatality rates are approximately 1%, but in India, Indonesia and
Myanmar, focal outbreaks away from the urban areas have reported case-fatality rates of 3-5%.
2 Classification and Case definition
The Newer WHO Classification of Dengue is practical from the management perspective and
involves 2 categories- Dengue and Severe Dengue [including both the previously classified
categories Dengue Shock Syndrome and Dengue Haemorrhagic fever]1
2.1 Case definition of Dengue fever (DF) (1,2):
Dengue fever is an acute febrile illness with one or more of the following:- Headache, retrorbital
pain, myalgia, arthralgia, rash, hemorrhagic manifestations, and leukopenia and lab confirmation
by ELISA.
2.2 Case Definition of Severe Dengue
Severe dengue should be considered if the patient is from an area of dengue risk presenting with
fever of 2–7 days plus any of the following features:
• There is evidence of plasma leakage, such as: – high or progressively rising haematocrit;
– pleural effusions or ascites;
– circulatory compromise or shock (tachycardia, cold and clammy extremities, capillary refill
time greater than three seconds, weak or undetectable pulse, narrow pulse pressure or, in late
shock, unrecordable blood pressure).
• There is significant bleeding.
• There is an altered level of consciousness (lethargy or restlessness, coma, convulsions).
• There is severe gastrointestinal involvement (persistent vomiting, increasing or
intense abdominal pain, jaundice).
• There is severe organ impairment (acute liver failure, acute renal failure, encephalopathy or
encephalitis, ARDS or other unusual manifestations. )
2.3 Warning Signs in Dengue Fever *
• Abdominal pain or tenderness
• Persistent vomiting
• Clinical fluid accumulation
• Mucosal bleed
• Lethargy, restlessness
• Liver enlargement >2 cm
• Laboratory: increase in HCT concurrent with rapid decrease in platelet count
*(requiring strict observation and medical intervention)
3 Differential diagnosis
3.1 Conditions that mimic the febrile phase of dengue infection

ella,

3.2 Conditions that mimic the critical phase of dengue infection

4 Investigations
4.1 Situation 1
4.1.1 Diagnostic Methods

4.1.2 Supportive Tests

-Hemoglobin, haematocrit, White Cell Count, Platelet count.

The presence of giant platelets and clumps is indicative of good platelet function

5 Treatment
5.1 Situation 1
5.1.1 Out Patient Management
Simple Dengue Fever with no warning signs, adequate oral intake and clinically well.
Home Care Advice
• Adequate rest
• Adequate fluid intake - Milk, fruit juice, electrolyte solution (ORS) and barley/rice water.
• Paracetamol [ Acetylsalicylic acid, Mefenemic acid, ibuprofen or other non-steroidal anti-
inflammatory agents (NSAIDs) and steroids to be avoided.]
• Tepid sponging
• To look for mosquito breeding places in and around the home and eliminate them
• Antibiotics are not necessary.
To observe for the following Danger signs and report immediately for hospital admission
• Bleeding:
- red spots or patches on the skin
- bleeding from nose or gums
- vomiting blood
- black-coloured stools
- heavy menstruation/vaginal bleeding
• Frequent vomiting
• Severe abdominal pain
• Drowsiness, mental confusion or seizures
• Pale, cold or clammy hands and feet
• Difficulty in breathing

Out -patient laboratory monitoring- as indicated

• Haematocrit
• White cell count
• Platelet count

5.1.2 Admission Criteria to Secondary Centre

mstances (living far from a health facility without reliable means of

transport).

5.1.3 Admission Criteria to Tertiary Centre directly from OPD

 fever is present with other co-morbidities

5.1.4 Management

dextrose at maintenance. Give only isotonic solutions.[ see annexure 1] Start with 5 ml/kg/hour
for 1–2 hours, then reduce by 2ml/kg/hour every 2 hours till 2ml/kg/hr provided there is clinical
improvement and haematocrit is appropriately improving. IV fluids are usually required for 1-2
days.
ocrit after 2 hours. If the haematocrit remains
the same, continue with the same rate for another 2–4 hours and reassess. If the vital
signs/haematocrit is worsening increase the fluid rate and refer immediately.
al fluid therapy usually 24-48 hrs, titrated to adequate
urine output.

5.1.5 Tests for Monitoring:

Frequent recording of vital signs and investigation are essential for evaluating the results of
treatment.
ration should be recorded every hour (or more
often) until stable subsequently 2 hourly.

volume of its administration in order to evaluate the adequacy of fluid replacement.

-ray, ultrasound abdomen, electrolytes 12-24 hrly as when clinically indicated
5.1.6 Referral Criteria
Warning signs and signs of Severe dengue.

-morbid conditions
5.2 Situation 2
4.2.1 Diagnostic Tests
As in situation 1 in addition the following tests may be useful –

4.2.2 Supportive Tests

As in Situation1 and in addition-

5.2.1 Admission Criteria

Same as in Situation 1 in addition

referred.
5.2.2 Pre requisites for management
• Paediatric Intensive care facilities should be available.

5.2.3 Management:
–
7 ml/kg/hour for 1–2 hours, then reduce to 3–5 ml/kg/hr for 2–4 hours, and then reduce to 2–3
ml/kg/hr or less according to the clinical response.
rises only minimally, continue with the same rate (2–3 ml/kg/hr) for another 2–4 hours. If the
vital signs are worsening and haematocrit is rising rapidly, increase the rate to 5–10 ml/kg/hour
for 1–2 hours. Reassess the clinical status, repeat the haematocrit and review fluid infusion rates
accordingly.

output of about 0.5 ml/kg/hr. Intravenous fluids are usually needed for only 24–48 hours. Reduce
intravenous fluids gradually when the rate of plasma leakage decreases towards the end of the
critical phase. This is indicated by urine output and/or oral fluid intake that is/are adequate, or
haematocrit decreasing below the baseline value in a stable patient.

risk is over.
- antipyretics, empirical antibiotics as clinically indicated.

5.2.4 Monitoring as follows-

hourly vital signs and peripheral perfusion. (Until the patient is out of the critical phase), urine
output (hourly).

children in shock who are fluid unresponsive. Arterial blood gas monitoring as clinically
indicated. Infusion pump will help in precise regulation of fluid input.

first 6 hours , decreasing frequency as patient improves ), Platelet counts 12 hourly blood
glucose, and other organ functions (such as renal profile, liver profile, coagulation profile, as
indicated).

-ray –Effusions, pulmonary edema

5.2.5 Treatment of Shock- See flow chart 1

5.2.6 Treatment of haemorrhagic complications

• A drop in haematocrit with no clinical improvement despite adequate fluid administration

indicates significant internal bleeding. Internal bleeding is difficult to recognize in the presence
of haemo-concentration. First correct the component of shock according to standard guidelines
with early use of packed cell transfusion. Component transfusion is indicated in cases with
significant clinical bleeding.

• The results of hematological tests (PT, APTT) may be studied to document the severity of DIC
Transfusion of cryoprecipitate and or fresh frozen plasma should be considered in cases of DIC
with bleeds.

• Indications for platelet transfusion

• Shock, acidosis with rapidly declining platelets ( greatest risk of DIC)

• Significant mucosal bleeds (harbinger of intracranial hemorrhage)
• Platelet count < 20,000 cu mm in the acute phase
• Need for invasive procedures such as central lines maintain platelet count > 50,000 cu mm
• A low platelet count is less significant after recovery from shock and may not need to be
transfused.

5.2.7 Treatment of Fluid overload

Fluid overload with large pleural effusions and ascites is a common cause of acute respiratory
distress and failure in severe dengue. Other causes of respiratory distress include acute
pulmonary oedema, severe metabolic acidosis from severe shock, and Acute Respiratory Distress
Syndrome (ARDS)
5.2.7.1 Prevention of fluid overload
• When the following signs are present, resuscitation intravenous fluids should be discontinued
or reduced to the minimum rate necessary to maintain euglycaemia:

– signs of cessation of plasma leakage;

– stable blood pressure, pulse and peripheral perfusion;
– haematocrit decreases in the presence of a good pulse volume;
– afebrile for more than 24–48 days (without the use of antipyretics);
– resolving bowel/abdominal symptoms;
– improving urine output.
• Aim for a minimum acceptable urine output [ 0.5ml/kg/hr] to titrate fluids.
• Maintain intravascular volume by using colloids and maintaining oncotic pressure.

5.2.7.2 The action plan for the treatment of fluid overload is as follows:
ely.

and peritoneal cavities to return to the intravascular compartment resulting ion dieresis.

5.2.7.3 If the patient has stable haemodynamic status and is out of the critical phase (more
than 24–48 hours of defervescence)
• Stop intravenous fluids but continue close monitoring.
• If necessary, give oral or intravenous furosemide 0.1–0.5 mg/kg/dose once or twice daily, or a
continuous infusion of furosemide 0.1 mg/kg/hour. Monitor serum potassium and correct the
ensuing hypokalaemia.

5.2.7.4 If the patient has stable haemodynamic status but is still within the critical phase,
reduce the intravenous fluid accordingly.
• Avoid diuretics during the plasma leakage phase.
• Patients who remain in shock with low or normal haematocrit levels but show signs of fluid
overload may have occult haemorrhage. Further infusion of large volumes of intravenous fluids
will lead only to a poor outcome. If the patient remains in shock and the haematocrit is elevated,
repeated small boluses of a colloid solution may help.

5.2.8 Other Complications of Dengue

-infection

Should be managed under standard ICU protocols

5.2.9 Supportive Care and Adjuvant Therapy
This may include:
h a preference to continuous veno-venous haemodialysis
(CVVH), or peritoneal dialysis if the former unavailable;
-threatening
hypotension in dengue shock and during induction for intubation, while correction of
intravascular volume is being vigorously carried out;

or encephalitis; cardiac abnormalities, such as conduction abnormalities, may occur.

5.3 Criteria for discharge:

6 Annexure
6.1 Immediate replacement of plasma loss/ Issotonic solutions: (1,2)
This should be done with any of the following solutions;

ractory shock, colloids such as Plasma , plasma substitutes (6%

hetastarch/dextran/ / 5% albumin /) may be preferred

restoration of fluid volume and a fall in haematocrit, suggesting the possibility of occult blood
loss.

hyperglycemia and osmotic diuresis, delaying correction of hypovolaemia. Secondly, dextrose is

rapidly metabolized resulting in a hypotonic solution that is inappropriate for shock correction.
6.2 Recognition of Shock
The following clinical signs should indicate the presence of shock
Tachycardia , Low pulse volume
Capillary Refill time > 2 sec
Narrow pulse pressure
Blood pressure less than the 3rd centile for age
Cold clammy peripheries
Altered sensorium
Poor urine output [ <0.5ml/kg/hr consistently ]
Tachypnoea
Metabolic acidosis
6.3 Choice of Vasoactive agents/ post resuscitation fluid removal (8)
-
0.2mcg/kg/min
-10mcg/kg/min
-0.75mcg/kg/min (no loading dose)
 -3mcg/kg/min,
furosemide infusion 3- 5mg/kg/day, titrate to urine output of 3-5 ml/kg/hr. Cease infusion and
infuse fluid if hypoperfusion occurs.
modynamics unstable: Ventilation vital (high risk of
mortality), can consider peritoneal dialysis if 24 hour experienced nursing and medical staff
available in PICU

6.4 Good Clinical Practice

output provide the most objective
guides to fluid replacement and prevention of fluid overload.
–fluid resuscitate with 10-20ml/Kg of isotonic fluids over 30-60 minutes. Consider in
severe shock
fluid rate downwards to avoid overload
-1ml/kg/hr).

ing fluid should be used for fluid resuscitation,

separately. Start enteral feeds early.

. If possible, aim for
platelets > 50,000/cu mm prior to central line insertion.

conversely, low platelet counts in the recovering, stable patient may not be an indication for
transfusions.

Flow Chart 1-Volume replacement flow chart for a patient with Severe Dengue and a >20%
increase in haematocrit. [No Shock]
153. EMPYEMA THORACIS

INTRODUCTION :
Empyema thoracis is a disease of historical importance with modern menace. It results into
significant morbidity ; affects precious growing period of a child, parental working days &
possible negligence of other family members & also incurs formidable burden on scarce
resources if treated improperly or inadequately. Traditionally empyema is being managed
empirically. However, with the widespread availability of radioimaging techniques , fibrinolytic
agents, safe & effective surgical procedures ( open or thoracoscopy ) the recent data is leading to
more focused management guidelines though optimal management is still controversial (22).
CASE DEFINITION :
‘Empyema’ is a term derived from the Greek verb ‘empyein’ ( to suppurate ) & literally refers to
frank pus in the pleural space. It could be localised or free collection of purulent material in
pleural space as a result of combination of inoculation of bacteria & culture medium of pleural
fluid. It is an advanced parapneumonic effusion. Pleural space infection is a continuum but
classically has been divided into three stages :
Stage 1 or Exudative or Acute phase ( lasts upto 3 days ) : The inflammatory process associated
with the underlying pneumonia leads to accumulation of clear fluid with no or low PMN
invasion ,ph >7.3, normal glucose & LDH levels : termed as ‘ simple ‘ parapneumonic effusion .
Stage 2 or Fibrinopurulent or Transitional phase ( 3 to 21 days ): There is deposition of fibrin in
the pleural space leading to septations & formation of loculations.There is increase in white cell
count , ph < 7.3, glucose < 40mgs.,LDH >3 times the normal. This is termed as ‘complicated ‘
parapnumonic effusion. Eventually when it becomes overt or frank pus which is termed as an ‘
empyema’.The presence of septations (fibrinous strands in pleural fluid )doesn’t necessarily
mean fluid doesn’t flow freely, although separate loculations will not communicate with each
other.
Stage 3 or Organisational or Chronic phase (> 3 wks . duration ): Fibroblasts infiltrate the pleural
space & thin intrapleural membranes are reorganised to become thick & non elastic – the ‘peel’
or ‘rind’. These solid fibrous or leather like peels may prevent lung re-expansion ( “trapped
lung” ), impair lung function & create a persistent pleural space with potential for infection.At
this stage spontaneous healing may occur or a chronic empyema may develop.
Further complications which may occur are : bronchopleural fistula , lung abscess, pneumatocele
formation, empyema necessitans : perforation through chest wall, fibrothorax etc…
Video-assisted thoracoscopic surgery (VATS ) is a key hole or minimal access surgical
approach. It achieves debridement of fibrinous pyogenic material, breakdown of loculations, and
drainage of pus from the pleural cavity under direct vision. It leaves three small scars.
Mini-thoracotomy achieves debridement and evacuation in a similar manner to VATS but it is an
open procedure leaving a small linear scar along the rib line.
Decortication involves an open posterolateral thoracotomy and excision of the thick fibrous
pleural rind with evacuation of pyogenic material. It is a longer and more complicated procedure
leaving a larger linear scar along the rib line.
INCIDENCE OF CONDITION :
Empyema thoracis constitutes 5-10 % cases seen by a paediatrician in our country(23). The
reported rate of empyema thoracis complicating community acquired pneumonia is said to be
27% in children(21). The prevalence of small parapneumonic effusions is difficult to estimate
(and often undetected )& they are unlikely to be reported in case series. However cases non
secondary to infection viz.. heart disease, malignancy, connective tissue disorders, trauma etc.
are largely dependent on the referral base & case mix in the particular hospital (5,6,7,8).
DIFFERENTIAL DIAGNOSIS:
Empyema secondary to bacterial infection eg.. staph./streptococci,Mycobacteria, Anarobes etc..
Neoplasm
Massive consolidation
Chylous collection
Haemothorax
Lung abscess
PREVENTION & COUNSELING :
Though complete prevention of empyema may not be possible due to factors such as variance in
microbial virulence & host’s immunological idiosyncracies etc.. but following measures will be
very beneficial………
* Adequate management of pneumonia ie early recognition, proper selection , duration& mode
of delivery of antibiotics according to regional sensitivity pattern & prompt referral facilities to
higher centers.
*Prevention of pneumonia :
Ensuring widespread vaccination program for predisposing conditions such as
measles,Hib,Pneumococcal, chickenpox etc. because significant fall in incidence of empyema
has been reported in vaccinated as compared to non vaccinated zones (21).
Since Staph aureus is the most common organism responsible in our country improving hygienic
conditions especially during hot & humid conditions of the year ie April to August will bring
down in general incidence & severity of staph infections.
Improvement in nutritional status as PEM is known predisposing factor for all infective illnesses
& their complications.
Improvement in dental/oral hygiene as it is a welknown predisposing factor for development of
aspiration pneumonia.
Patients with immunodeficient conditions, tuberculosis, musculoskeletal/neurological illnesses,
CHD, Diabetes, Renal disease etc..must remain under high index of suspicion as classical
clinical presentation may be absent in such situations.
SITUATION 1 :
At Secondary hospital / Non metro situation : Optimal standards of Treatment in
Situations where technology& resources are limited.
Clinical Diagnosis*
Acute , recurrent or chronic presentations are common.
If a child with pneumonia remains pyrexial or unwell 48 hrs. after the start of the treatment
possibility of parapneumonic effusion or empyema should be suspected.
Constitutional signs / symptoms viz.. lassitude, poor appetite, pallor, intermittent fever, easy
fatigability, sick look with dull percussion note & decreased breath sounds on auscultation in the
setting of partially treated pneumonia, PUO, Disseminated infections e g.. Pyoderma / otitis
media /arthritis/Osteomylitis / Serosal infections etc..
Febrile response may be blunted in immunocompromised patients.
*Physical findings & presentation may vary depending on type organism & duration of illness.
*Inflammation of pleural space may present with abdominal pain &vomiting.
INVESTIGATIONS :
1) Chest X-ray : Posteroanterior ( PA ) view
2) Ultrasound chest :Sensitive for confirmation of pleural fluid , for guided diagnostic tapping &
insertion of chest drainage tube.
3) Pleural fluid exam:
Colour, Odour, Gram staining, AFB, Bacterial culture, cytology.
Biochemistry: Ph, Sugar, LDH, Proteins.
4 ) Blood & sputum culture : if feasible
TREATMENT :
Conservative Management : Antibiotics ± Intercostal Dranaige Tube (ICD)
If effusion is simple & small in quantity : can be managed with antibiotics alone .But very close
observation is necessary for development of enlarging size &/or compromise of respiratory
function when prompt ICD placement is necessary.
Repeated thoracentesis has no role. If effusion is complicated or frank pus : Antibiotics + ICD
Surgical management : Only if adequately trained personnel & blood banking facilities are
available then limited thoracotomy in a situation where there is no satisfactory response
(persistent fever, incomplete lung expansion ,loculations on ultrasound etc..)ie.. in stage 2 or
fibrinopurulent phase.
Standard operating procedure ( SOP )
All the patients of parapneumonic effusion or empyema should be admitted in hospital i e.. no
out patient or day care management to be done.
Pediatric surgeon or General surgeon familiar with basic thoracic surgery along with
paediatrician or respiratory physician should manage these cases.
They should be monitored closely & carefully by frequent clinical assessment & room air
saturation by pulse oximeter whenever child is in resp. distress.
Diagnostic imaging, microbiology, pleural fluid analysis should be carried out promptly.
Conservative management to be started swiftly & supported by antipyretics, analgesia, oxygen ,
if necessary.
Empirical antitubercular therapy should be avoided as far as possible.
Antibiotics :
Intravenous antibiotics for 10 to 14 days for community acquired pneumonia covering Gram
positive cocci & anaerobes to be started empirically pending preferably c & s report. Broad
spectrum coverage should be started for hospital acquired pneumonia as well as empyema
following surgery, trauma & aspiration. Oral antibiotics should be continued at discharge for 1-4
wks. or longer depending on disease state.
Chest drainage tube(ICD) insertion:
Chest drains should be inserted by adequately trained personnel to reduce the risk of
complications. Preferably procedure should be done in operation room or isolated / treatment
room on ward. However , if need arises it can be done as a bed side procedure as well.
A suitable assistant and trained nurse must be available.
Routine measurement of the platelet count and clotting studies are only recommended in patients
with known risk factors.
Where possible, any coagulopathy or platelet defect should be corrected before chest drain
insertion.
Ultrasound should be used to guide thoracocentesis or drain placement.
If general anaesthesia is not being used, intravenous sedation should only be given by those
trained in the use of conscious sedation, airway management and resuscitation of children, using
full monitoring equipment. .
Local anaesthesia, 2% xylocaine Or .25% bupivacaine, can also be used .
Large bore surgical drains should be inserted at the optimum site suggested by ultrasound, but
preferentially placed in the mid axillary line through the ‘‘safety triangle’’.
Substantial force should never be used to insert a drain. Trocar usage preferably should be
avoided & should it be needed ,due to circumstances, great care is mandatory to have a guard or
control on it while inserting.
Chest tube should be secured well with non absorbable suture & appropriate dressing.
A chest radiograph should be performed after insertion of a chest drain.All chest tubes should be
connected to a unidirectional flow drainage system (such as an underwater seal bottle) which
must be kept below the level of the patient’s chest at all times.
A bubbling chest drain should never be clamped.
A clamped drain should be immediately unclamped and medical advice sought if a patient
complains of breathlessness or chest pain.
The drain should be clamped for 1 hour once 10 ml/kg are initially removed.
Patients with chest drains should be managed on wards by staff trained in chest drain
management. When there is a sudden cessation of fluid draining, the drain must be checked for
obstruction (blockage or kinking) by flushing.
The drain should be removed once there is clinical resolution.
A drain that cannot be unblocked should be removed and replaced by new catheter if significant
pleural fluid remains.
Surgical management :
Proper planning & ensuring availability of all the trained & experienced personnel ie ..surgeon,
anaesthesiologist ,OT technician & nursing staff and also smooth supply of oxygen,blood
,medicines etc..is very important .
Limited thoracotomy with or without rib resection by 5-7cms total incision on either side of
chest tube ,if already in situ.
To ensure complete lung expansion at the end of the procedure with minimal air leak.
If necrotic lung tissue is present then excision of the segment is to be done.
Send debrided tissue or ‘gubbin ‘ for histopathological examination.
ICD removal after complete lung expansion ,minimal or no drainage ,afebrile state & no air leak
X ray chest to be done before ICD tube removal
Good analgesia ( oral &/or suppositories ) & early ambulation to hasten the recovery should be
practiced regularly.
Antibiotics for 1-2wks. after the discharge are usually sufficient except in situation of
complications.
Follow- up :
Till complete resolution of disease process & near complete lung expansion on x- ray chest.
Evaluation of underlying condition, if any.
Referral criteria
If no satisfactory response to conservative management by 5-7 days.
Initial presentation as stage 2 or 3 of an empyema Suspecting underlying immunodeficiency
condition or empyema associated with non pneumonic pathologies which also require
specialist’s attention.
Development of complications eg Persistent air leak.
Non availability of trained personnel at given time.
Situation 2
At Super Speciality Facility in Metro location where higher end technology is available
Clinical diagnosis*
If a child with pneumonia remains pyrexial or unwell 48 hrs. after the start of the treatment
possibility of parapneumonic effusion or empyema should be suspected.
Constitutional s/s viz.. lassitude, poor appetite, pallor, intermittent fever, easy fatigability, sick
look with dull percussion note & decreased breath sounds on auscultation in the setting of
partially treated pneumonia, PUO, Disseminated infections e g.. Pyoderma / otitis media
/arthritis/Osteomylitis / Serosal infections etc..
Patients inadequately treated or responded to previous therapy.
Complications of an empyema eg.. BPF, lung abscess, empyema necessitans etc.
Patients with underlying conditions such as liver abscess, pancreatitis ,trauma , surgical or
endoscopic procedure done etc with respiratory signs & symptoms.
Response may be blunted ‘absent fever’ in immunocompromised patients.
*Acute , recurrent or chronic presentations are common.
*Physical findings & presentation may vary depending on type of organism & duration of
illness.
*Inflammation of pleural space may present with abdominal pain &vomiting
Investigations
Diagnostic imaging Posteroanterior or anteroposterior radiographs should be taken; there is no
role for a routine lateral radiograph.
Ultrasound may be used to confirm the presence of a pleural fluid collection, septations, to guide
thoracocentesis or drain placement.
Chest CT scans should not be performed routinely. It should be done once surgery is
contemplated to know pleural peel thickness, loculations & their details such as
number,position,size etc.; parenchymal pathology,guide for port placement if VATS is being
planned .
Diagnostic microbiology
Blood cultures should be performed in all patients with parapneumonic effusion.
When available, sputum should be sent for bacterial culture.
Diagnostic analysis of pleural fluid
Pleural fluid must be sent for microbiological analysis including Gram stain and bacterial
culture.
Aspirated pleural fluid should be sent for differential cell count.
Tuberculosis and malignancy must be excluded in the presence of pleural lymphocytosis.
If there is any indication the effusion is not secondary to infection, consider an initial small
volume diagnostic tap for cytological analysis, avoiding general anaesthesia/sedation whenever
possible.
Biochemical analysis of pleural fluid : Ph, LDH, sugar, & proteins
Diagnostic bronchoscopy
There is no indication for bronchoscopy and it is not routinely recommended. Considered only
when bronchoalveolar lavage is necessary or suspected foreign body or assessing bronchial
mucosal status for safe closure of br. stump when major pulmonary resection is also planned
alongwith decortication .
Treatment
Conservative management (antibiotics ± simple drainage)
Effusions which are enlarging and/or compromising respiratory function should not be managed
by antibiotics alone.
Give consideration to early active treatment as conservative treatment results in prolonged
duration of illness and hospital stay.
If a child has significant pleural infection, a drain should be inserted at the outset and repeated
taps are not recommended.
Antibiotics
All cases should be treated with intravenous antibiotics and must include cover for Gram positive
cocci eg..Staph Aureous, Streptococci & Anarobes.
Broader spectrum cover is required for hospital acquired infections, as well as those secondary to
surgery, trauma, and aspiration.
Where possible, antibiotic choice should be guided by microbiology results.
Oral antibiotics should be given at discharge for 1–4 weeks, but longer if there is residual
disease.
Chest drains
Chest drains should be inserted by adequately trained personnel to reduce the risk of
complications.
A suitable assistant and trained nurse must be available.
Routine measurement of the platelet count and clotting studies are only recommended in patients
with known risk factors.
Where possible, any coagulopathy or platelet defect should be corrected before chest drain
insertion.
Ultrasound should be used to guide thoracocentesis or drain placement, when available.
If general anaesthesia is not being used, intravenous sedation should only be given by those
trained in the use of
conscious sedation, airway management and resuscitation of children, using full monitoring
equipment. Large bore surgical drains should be inserted at the optimum site suggested by
ultrasound. The usual site for ICD insertion should be in the mid axillary line in the 5th
intercostal space which is in the ‘safe triangle.’
Substantial force should never be used to insert a drain. Trocar usage preferably should be
avoided & should it be needed ,due to circumstances, great care is mandatory to have a guard or
control on it while inserting.
Chest radiograph should be performed after insertion of a chest drain.
All chest tubes should be connected to a unidirectional flow drainage system (such as an
underwater seal bottle) which must be kept below the level of the patient’s chest at all times.
Appropriately trained nursing staff must supervise the use of chest drain suction.
A bubbling chest drain should never be clamped.
A clamped drain should be immediately unclamped and medical advice sought if a patient
complains of breathlessness or chest pain.
Patients with chest drains should be managed on specialist wards by staff trained in chest drain
management.
When there is a sudden cessation of fluid draining, the drain must be checked for obstruction
(blockage or kinking) by milking / flushing. If it can not be unblocked in presence of significant
pleural infection then it should be reinserted.
The drain should be removed once there is clinical resolution & / or lung expansion on x-ray.
Intrapleural fibrinolytics
Intrapleural fibrinolytics are said to shorten hospital stay and may be used for any stage 2
empyema .
There is no evidence that any of the three fibrinolytics ( Streptokinase, Urokinase, Alteplase ) are
more effective than the others, but only urokinase has been studied in a randomised controlled
trial .
Urokinase should be given twice daily for 3 days (6 doses in total) using 40 000 units in 40 ml
0.9% saline for children weighing 10 kg or above, and 10 000 units in 10 ml 0.9% saline for
children weighing under 10 kg.
Surgery
Patients should be considered for surgical treatment if they have persisting sepsis in association
with a persistent pleural collection, despite chest tube drainage and antibiotics.
Failure of chest tube drainage, antibiotics, and fibrinolytics would necessiiate surgical
intervention.However, a pediatric surgeon should be involved early in the management of
empyema thoracis.
If requisite skill & facilities are available then VATS debridement is preferable over open
surgical procedure in stage 2 & select stage 3 empyema cases.
Organised empyema in a symptomatic child may require formal thoracotomy and decortication.
Other management
Antipyretics should be given.
Analgesia is important to keep the child comfortable, particularly in the presence of a chest
drain.
Early mobilisation , chest physiotherapy and exercise is recommended.
Secondary scoliosis noted on the chest radiograph is common but transient; no specific treatment
is required but resolution must be confirmed.
Standard operating procedure ( SOP )
All the patients of parapneumonic effusion or empyema should be admitted in hospital i e.. no
out patient or day care management to be done.
Pediatric surgeon or a surgeon well trained in pediatric thoracic surgery along with paediatrician
or respiratory physician should manage these cases.
CECT( Contrast Enhanced Cat Scan ) should be done if surgery is contemplated.
There are no evidence based criteria to guide the decision on when a child should proceed to
surgery, and consequently there is little consensus on the role of medical versus surgical
management (1)
Intrapleural fibrinolytics
Intrapleural fibrinolytics shorten hospital stay and are recommended for any complicated
parapneumonic effusion (thick fluid with loculations) or empyema (overt pus).
There is no evidence that any of the three fibrinolytics(streptokinase,urokinase &tPA ) are more
effective than the others, but only urokinase has been studied in a randomised controlled trial in
children so is recommended(10 to 16)
Surgery:
The decision to involve a pediatric surgeon early in the decision making process should be
encouraged and referral should not automatically mean surgery is inevitable .(1)
Available procedures are: VATS, Mini thoracotomy & Decortication.
A chest drain(s) is left after each procedure for further drainage of fluid/pus.
A persistent radiological abnormality in a symptom-free well child is not an indication for
surgery.
Role of surgical management in complex empyema
(A) Organised empyema with a thick fibrous peel
Organised empyema in a symptomatic child may require formal thoracotomy and decortication.
The surgical management of an organised empyema, in which a thick fibrous peel is restricting
lung expansion and causing chronic sepsis with fever, requires a formal thoracotomy with
excision of the pleural rinds (decortication) to achieve proper lung re-expansion. However, if the
child is asymptomatic, surgery is not necessarily indicated.(18 )
(C) Bronchopleural fistula and pyopneumothorax
Different approaches have been advocated for a bronchopleural fistula related to an empyema.
Most fistulae are peripheral and the majority resolve with continued chest drainage and
antibiotics provided the lung shows satisfactory lung expansion.
However, at times they are slow and difficult to resolve, and it has been said that conservative
management and open thoracostomies result in protracted recovery and morbidity. A more
radical approach is partial decortication and muscle flap surgery to bring a blood supply to the
necrotic area and help with healing the fistula. This can either be done as a staged procedure or a
more aggressive one stage approach (19, 20)
Follow up
Children should be followed up after discharge until they have recovered completely and their
chest radiograph has returned to near normal.
Underlying diagnosis—for example, immunodeficiency –may need to be considered in selected
situations.
open chest tube care in select patients till tube is in situ
For monitoring of ATT
Referral to tertiary speciality centre
Non availability of skilled & experienced personnel or infrastructure necessary for
management of complex situations eg. BPF, major lung resections or Thoracoscopic procedure
or need of PICU facilities etc..
When respiratory paediatrician is needed to be involved early in the care of patients requiring
chest tube drainage for a pleural infection & in critically ill child.
Who does what ? & Time lines :
Doctor : Pediatric Surgeon :
Does all the interventional procedures & involved in decision making regarding overall
management with paediatrician.
Pediatrician (Respiratory ) : Along with surgeon involved in conservative management & post
operative care & preop. preparation
General Surgeon : Does interventions In situation 1 only & in situation 2 maybe involved in
assisting pediatric surgeon.
Anaesthesiologist : Anaesthesia & pain management
Junior doctor : Assisting in surgery, ICD care ,dressings & day to day ward management
b ) OT Technician : Helping anaesthesiologist & surgeon in OT & if required on ward bedside
interventions.
C ) Nursing Staff : Care & organisation of instrument trolly, medications & ICD care, suction
etc. & day to day nursing care.
Time line :
Radiological clearance takes few wks. to many months.
If an empyema fails to respond in 3-5 days of conservative treatment then surgical intervention
should be considered to reduce morbidity.
Dwelling time for fibrinolytics is 1-4 hours.
There is no specific / precise time period for spontaneous closure or need for surgical
intervention in BPF patients.
Antibiotics are needed for 4-8 wks. ( Intravenous 2-3 wks. & oral 1-4wks.)
ATT is required for 6-9 mths duration.
154. INGUINAL HERNIA IN CHILDREN
Dr.Sanjay Rao
Dr.Vinay C
Dr. Zameer K
Consultant Pediatric Surgeons,
Narayana Hrudayalaya,
Bangalore
a) WHEN TO SUSPECT/ RECOGNIZE?

Inguinal hernia is suspected in any child with a swelling in the inguinoscrotal region.
a. Introduction:

Inguinal hernia repair is one of the most common pediatric operations performed. Most hernias
that present at birth or in childhood are indirect inguinal hernias. All pediatric inguinal hernias
require operative treatment to prevent the development of complications, such as inguinal hernia
incarceration or strangulation.
b. Case definition:

Inguinal hernia is a type of ventral hernia that occurs when an intra-abdominal structures, such as
bowel or omentum, protrude through the open processus vaginalis through the inguinal canal.
b) INCIDENCE OF THE CONDITION IN OUR COUNTRY

Although the exact incidence of indirect inguinal hernia in infants and children is unknown, the
reported incidence ranges from 1-5%. Sixty percent of hernias occur on the right side. Premature
infants are at increased risk for inguinal hernia, with incidence rates of 2% in females and 7-30%
in males.
Inguinal hernias are much more common in males than in females. The male-to-female ratio is
estimated to be 4-8:1.
Premature infants are at an increased risk for inguinal hernia, with the incidence ranging from 7-
30%. Moreover, the associated risk of incarceration is more than 60% in this population.
c) DIFFERENTIAL DIAGNOSIS
Congenital Hydrocoele
Inguinal adenitis Femoral adenitis Psoas abscess Saphenous varix Retractile testis Varicocele
Testicular tumor Undescended testis
d) PREVENTION AND COUNSELING :

A high index of suspicion is required-especially in the high risk population of premature babies.
If a child has developed a unilateral hernia, there is a potential risk of developing a hernia on the
opposite side-this risk is higher in premature babies and infant girls. These families need to be
counseled about signs and symptoms of these recurrences.
e) OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,

TREATMENT & REFERRAL CRITERIA

Diagnostic criteria: diagnosis is clinical.
1. History of a soft swelling in inguinal region. Gets larger when child cries, may disappear
completely when the child is quietly lying down.
2. Examination: Soft, reducible mass in the inguinal area is diagnostic. Even in the absence of
the mass at examination, a strong history is adequate for diagnosis.

Investigations:
No imaging studies are required. General tests towards anaesthesia fitness may be required (
haemoglobin, urine analysis).
Referral Criteria:
A strong clinical history and physical findings of inguinal hernia are indications for referral for
surgery.
HISTORY
The child with an inguinal hernia presents with a bulge at the internal or external ring or within
the scrotum. The parents typically provide the history of a visible swelling or bulge, commonly
intermittent, in the inguinoscrotal region in boys and inguinolabial region in girls.
Usually, a simple inguinal hernia in an infant is painless.
The bulge commonly occurs after crying or straining and often resolves during the night while
the baby is sleeping. 39
If the family provides a history of a painful bulge in the inguinal region, one must suspect the
presence of an incarcerated inguinal hernia. Patients with an incarcerated hernia generally
present with a tender firm mass in the inguinal canal or scrotum. The child may be fussy,
unwilling to feed, and inconsolably crying. The skin overlying the bulge may be edematous,
erythematous, and discolored. EXAMINATION
Physical examination of a child with an inguinal hernia typically reveals a palpable smooth mass
originating from the external ring lateral to the pubic tubercle. The mass may only be noticeable
after coughing or performing a Valsalva maneuver and it should be reduced easily. Occasionally,
the examining physician may feel the loops of intestine within the hernia sac. In girls, feeling the
ovary in the hernia sac is not unusual; it is not infrequently confused with a lymph node in the
groin region. In boys, palpation of both testicles is important to rule out an undescended or
retractile testicle.
Hernia and hydrocele: Transillumination has been advocated as a means of distinguishing
between the presence of a sac filled with fluid in the scrotum (hydrocele) and the presence of
bowel in the scrotal sac. However, in cases of inguinal hernia incarceration, transillumination
may not be beneficial because any viscera that are distended and fluid-filled in the scrotum of a
young infant may also transilluminate.
INVESTIGATIONS
No laboratory studies are needed in the assessment of a patient with a suspected inguinal hernia
and/or hydrocele.
Ultrasonography: Its routine use is unnecessary. It is indicated when presentation and
examination suggest a diagnosis other than hernia or hydrocele. An enlarged inguinal lymph
node can mimic an incarcerated inguinal hernia.
Laparoscopy: Diagnostic laparoscopy may rarely be required for determining the presence of an
inguinal hernia. It is used only in the following: a) assessment of contralateral hernia when one is
being operated upon, and b) recurrent hernia after previous surgery.
TREATMENT
Congenital hernias are treated surgically with herniotomy. Surgical treatment can be either open
or laparoscopic. Inguinal hernias do not spontaneously heal and must be surgically repaired
because of the ever-present risk of incarceration. Repair is usually planned as an elective
procedure as soon as possible after diagnosis. If hernia is irreducible, ie cannot be easily pushed
back into the abdomen, child needs to be admitted and a manual reduction tried by an
experienced pediatric surgeon. If successful, the operation is performed after 24-48 hours to
allow local oedema to settle down.
If reduction is unsuccessful, or if there is clinical evidence of inflammation (as evidenced by
pain, redness, edema of skin on hernia) emergency exploration and hernia repair is necessary.
Hydroceles without hernia in neonates: This is the only exception in which surgical treatment
may be delayed. Repair of hydroceles in neonates without the presence of hernia is typically
delayed for 12 months because the connection with the peritoneal cavity (via the processus
vaginalis) may be very small and may have already closed or be in the process of closing. If the
hydorcoele persists after this observation period, operative repair is indicated and appropriate.
Postpone the operation in the event of upper respiratory tract infection,otitis media, or significant
rash in the groin.
FOLLOW UP
No specific limitations are indicated once the diagnosis of an inguinal hernia has been
established; however, following operative repair, avoidance of major physical activity for 1 week
is recommended. After that time, the patient is allowed to participate in physical activities (eg,
sports, swimming, running).
Children younger than 5 years are likely to recover extremely quickly from surgery; they are
typically capable of returning to their normal level of activities within 24-48 hours of surgery.
*Situation 1: At Secondary Hospital/ Non-Metro situation: Optimal Standards of
Treatment in Situations where technology and resources are limited
a. Clinical Diagnosis:

Similar generic diagnostic criteria apply. A typical history and physical finding are adequate for
diagnosis.
b. Investigations:
a. Investigations are not required other than for anaesthetic purposes.
b. Rarely, ultrasonography and diagnostic laparoscopy may be indicated

c. Treatment:
a. Inguinal hernia: Treatment is surgery -herniotomy operation that aims at ligating the patent
processus vaginalis at the internal ring after reduction of contents into the abdomen
b. Congenital hydrocoele: Treatment is deferred until the 2nd birthday as there is a 80% chance
of spontaneous closure. Surgery is indicated if hydrocoele persists beyond the 2nd year and if it
is rapidly growing is size.
c. All hernia and hydrocoele repairs in infants and children MUST be performed by a qualified
pediatric surgeon.

Standard Operating procedure

a. In Patient : inpatient care is indicated if:
I. h/o incarceration or obstructions
II. neonate awaiting hernia repair
b. Out Patient
i. Outpatient care is adequate for diagnosis and follow up in most children
ii. Clinical evaluation usually sufficient to diagnose
c. Day Care
i. most hernia operations in children are done as day care procedures

d. Referral criteria:

A child with a hernia needs referral to a higher centre if:

1. neonatal age and anaesthesia facilities are inadequate
2. ex-premature baby who had prolonged ventilation
3. recurrent inguinal hernia
4. inguinal hernia with complications (incarceration, obstruction)
5. associated major morbidity-such as cardiac anomalies, lung disease, renal disease, ascites

*Situation 2: At Super Specialty Facility in Metro location where higher-end technology is

available
Clinical Diagnosis:
ation1
 Investigations:

Treatment:

a. principles of treatment are same as above

Standard Operating procedure

i. criteria same as above

ii. all babies under 1 year of age need inpatient care after surgery-as there is an increased risk of
apnoea in this subgroup.
iii. All children with comorbid problems-cardiac, respiratory or others, need inpatient care after
surgery

b Out Patient

c. Day Care

problems can be treated as day care procedures

No further referrals
f) WHO DOES WHAT? and TIMELINES
a. Doctor makes a clinical diagnosis, counsels the family and plans surgery- a pediatric surgeon
performs the surgery
b. Nurse: assists surgeon in care of child during pre, intra and post operative course of the baby
c. Technician: assists medical and nursing teams in care of child during intra and post-operative
periods.

155. NEONATAL CHOLESTASIS

I. WHEN TO SUSPECT/ RECOGNIZE?

Introduction:
Neonatal cholestatis is a pathological condition in the newborn where in bile flow from the liver
is reduced. Neonatal Cholestasis Syndrome (NCS) includes a wide spectrum of clinical
conditions ranging from congenital malformations of the hepatobiliary tree, infections, inborn
errors of metabolism to some of the recently identified clinical conditions with or without genetic
predilection. Most of these disorders have linkage with insults during antenatal, natal and
postnatal periods. NCS has largely remained ignored in our country.
Case definition:
Neonatal cholestasis refers to conjugated hyperbilirubinemia >1.5 – 2 mg% and/or direct
component of more than 20% of total bilirubin in a newborn/ infant with passage of high
coloured urine with or without clay stools.
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY

NCS constitutes 30% of referrals with hepatobiliary disorders in India. The average age of
presentation to a specialized center is 3.5 months (range birth to 15 months) with a consequent
delay of 3 months in referral (medical and surgical centers).
Based on consensus conference by paediatric gastroenterology, out of 1008 cases analysed in our
country
-47%, metabolic-4%, others-2%)
-34%, Choledochal cyst-4%)

In neonatal hepatitis-
III. DIFFERENTIAL DIAGNOSIS
A. CAUSES OF EXTRA HEPATIC OBSTRUCTION

B. HEPATOCELLULAR
1. INFECTIVE

2. METABOLIC

inemia
3. MISCELLANEOUS

4. IDIOPATHIC
C. PAUCITY OF INTRAHEPATIC DUCTS
Syndromic - Alagille's syndrome, Byler's, Aagene's

Non - Syndromic - a 1AT deficiency, Idiopathic, Familial

IV. PREVENTION AND COUNSELING

A high index of suspicion is necessary. Mothers must be informed about the need to seek
medical attention if jaundice persists beyond two weeks of birth and / or baby passes pale stools
and high coloured urine. If the previous sibling has had liver disease antenatal counselling and
referral for further evaluation may be necessary.
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,

TREATMENT & REFERRAL CRITERIA

a. Diagnostic criteria:
1. Clinical: Neonate with jaundice persistent beyond 2 weeks, dark colour urine and/or pale stool
2. Screening Biochemistry: Serum bilirubin direct and indirect
Any child that meets with the clinical and /or biochemical criteria needs investigation, treatment
and referral.
Typical presentation:

weeks of age.

feeds well.

in the early weeks.

Clinical examinations:
Clinical evaluation-
1. Sick baby : Sepsis/UTI/Congenital infections/metabolic disorders.

2. Dysmorphism : Downs syndrome/ alagilles syndrome.

3. Examination of eye and fundus must be done-

4. Chronic Cholestatis – Pruritis/ irritability/xanthomas

5. Failure to thrive.

*Situation 1: At Secondary Hospital/ Non-Metro situation: Optimal Standards of

Treatment in Situations where technology and resources are limited
e. Clinical Diagnosis:
2. Jaundiced child
3. Dark urine
4. Pale stool
5. Hepatomegaly ± splenomegaly

f. Investigations:

a. LFT
b. RFT
c. PT/INR
d. RBS

g. Treatment:

Standard Operating procedure

4. Resuscitation if required,
5. Correction of Hypoglycemia
6. Administration of Vitamin K (0.3mg/kg parenteral)
7. Initiation of antibiotics: if there is clinical or laboratory evidence of infection or sepsis

a. In Patient : Child needs admission if

1. there is clinical evidence of dehydration

2. clinical ± laboratory evidence of hypoglycemia
sepsis or coagulopathy.
3. failure to thrive
b. Out Patient : Baby who is clinically well, feeding well and has no evidence of
hypoglycemia or coagulopathy can be investigated as an outpatient
c. Day Care : No role of day care admission.

h. Referral criteria: ( All workup at this level must be completed by 48 hours)

1. Any child with neonatal cholestasis syndrome who is > 2 weeks of age

2. Clinically unwell, poor feeding, poor weight gain

3. Evidence of coagulopathy, hypoglycemia or sepsis

*Situation 2: At Super Specialty Facility in Metro location where higher-end technology is

available
Clinical Diagnosis:
Investigations: Urgent Investigations

Standard LFT are usually abnormal with modestly raised levels of AST, ALT, and alkaline
phosphatase. GGT is raised in all cases of cholestasis except in one of the bile acid synthetic
defects. Serum albumin does not fall till late. None of the biochemical tests are of deciding value
and at best reflect the degree of damage to liver.
Tests directed towards infective and metabolic causes :
Blood Tests
• TORCH, VDRL, Hepatitis B/C, HIV
• T4, TSH
• Serum cortisol
• α l AT levels and phenotype
• Galactose 1 Phosphate Uridyl transferase (to r/o galactosemia)
• Urinary succinyl acetone (to r/o tyrosinemia)
• Cholesterol, triglycerides
• S. iron and ferritin levels (to r/o neonatal hemachromatosis)
Radiology
Role of USG
USG can exclude choledochal cyst, any focal lesions, dilated CBD, anomalies of viscera or
portal hypertension.
Role of Hida Scan
Hepatobiliary scintigraphy, after a 5 day priming with phenobarbitone,is useful. Excretion of the
radio-tracer into the gut rules out biliary atresia. However, the converse is not true and absence
of gut excretion of radiotracer requires further evaluation.
Role of Liver Biopsy
Liver biopsy is useful in the charecterisation of NCS in some cases. Coagulopathy and ascitis are
contraindications for percutaneous liver biopsy.
TREATMENT
On suspicion of cholestatic liver disease, vitamin-K is started along with supplementation of
other fat soluble vitamins (A,D,E,)
Treatable Causes
Medical

Galactosemia
Surgical
3. Biliary Atresia
4. Choledochal cyst
5. Spontaneous perforation of bile ducts
6. Inspissation of bile ducts

SUPPORTIVE CARE
Nutrition
- 125% RDA

-2-3 gm/kg/day in infants (0.5gm/kg/day in hepatic encephalopathy)

then 10,000 IU monthly till cholestasis resolves. Avoid hyper- vitaminosis as it can enhance
fibrosis.

-nosis and
then monthly till cholestasis resolves. If the child has rickets give a dose of 60,000 IU.

ion (50-200 mg/day) is required to avoid neuro-muscular

degeneration, retinal pigmentation and hemolytic anemia.

Perform prothombin time (PT) monthly. Administer injectable vitamin K if PT is prolonged.

-5) times RDA)

Pruritis
For control of pruritis following agents have been tried :-
1. Phenobarbitone-5mg/kg/day

2. Rifampicin- 1Omg/kg/day
3. Ursodeoxycholic acid-10-20 mg/kg/day

4. Cholestyramine-4- 8gm/kg/day

5. Terfenadine l-3mg/kg/day

6. Carbamazepine

Liver Transplantation
This may remain the only option for infants with decompensated liver disease (ascites and /or
encephalopathy) or failed portoenterostomy.

Standard Operating procedure

In Patient only: May require ICU monitoring

Referral criteria:
Referral criteria for a specialist centre:
Any case of neonatal cholestasis as defined by above parameters with deranged liver function
tests to be referred to tertiary centre for further management.
Child needs to be referred to a specialist pediatric liver unit if,
1. Evidence of progressive liver failure
2. Evidence of complications such as portal
hypertension, SBP, Respiratory distress, pathological
fractures.
3. Failure of Kasai operation
Evidence of liver cirrhosis in biopsy
Jaundice not cleared by 2 months after surgery
4. Considerations for liver transplant
Situation 2:
Referred cases from secondary centres or any newborn with evidence of cholestatis with
deranged liver function tests.
Investigation:
Subsequent investigation (if initial workup negative)
& phenotype
- P uridyl transferase

Bone marrow aspiration/skin biopsy/muscle biopsy/ serum lactate / pyruvate / ammonia, very
long chain fatty acid, urinary organic acids, urinary bile acids, auto immune screen / sweat
chloride test.
Treatment:
 italisation treatment is mandatory.

Medical:
Neonatal hepatitis:
2. Bacterial Sepsis/ UTI : antibiotics
3. Malaria : antimalarial
4. Toxoplasmosis & syphilis : specific antibiotics
5. CMV : ganciclovir
6. Herpes : acyclovir
7. Metabolic:
8. Galactosemia : stop lactose milk
9. Fructosemia : withdrawal of fructose containing item
10. Hypothyroidism : Thyroxine

Chronic cholestatis:
nutritional status
ergy (125%RDA)
-3 gm/kg

Phenobarbitone / Rifampicin/ UDCA/ Cholestyramine/ Terfenadine/ Carbamazepine

Surgical
VI. WHO DOES WHAT? and TIMELINES
Doctor :

Nurse

Technician

156. Urinary tract infection and vesico ureteric reflux

When to suspect and recognise

h) Introduction

Urinary tract infection (UTI) is a common condition affecting children and vesico ureteric reflux
(VUR) is one common cause of recurrent UTI. UTI in the presence of infection results in kidney
damage and one of the common causes of chronic renal failure in adult hood . UTI and VUR
need prompt recognition to reduce morbidity and mortality in children.
( B) Case definition.
Vesico ureteric reflux may be primary due to short intramural course of ureters or it may be
secondary to posterior urethral valves, Ureteroceles. Neurogenic bladder
or it may be a part of duplex system of the kidney.
II . Incidence of the condition in our country
The exact incidence in our country is not known But from published data it is the risk of
developing UTI before the age of 14 years is approximately 1% in boys and 3-5% in girls The
incidence varies with age. During the first year of life, the male to female ratio is 3-5:1. Beyond
1-2 years, there is female preponderance with male to female ratio of 1:10. The incidence of
VUR in children with UTI is approximately 30 to 50 % in the siblings of the index case shows an
incidence of 20 to 30 %.
III . Differential diagnosis of VUR
I. Obstructive Mega ureters,

II. Ureteroceles,

III. Uretral valves,

IV. PUJ obstructions

V. Ureteric stenosis,

VI. Neurogenic bladder,

VII. Posterior urethral valves with reflux

VIII. Stones in the bladder and ureter.

IV. Prevention and counselling

VUR is congenital disease either primary or secondary to congenital outlet obstructions. As such
prevention is not possible.
Presence of pelviureteric dilatation on antenatal scans needs evaluation soon after birth.
However UTI secondary to VUR can be prevented by prophylactic antibiotic therapy,
Periodical cultures and recognising infective episodes and treating them aggressively.
Mothers must be counselled on the need for long term chemo prophylaxis and have the urine
culture done every febrile episode of the child with VUR. Early recognition can prevent damage
and scarring to the kidney ,
As regards the parents can be counselled that Grade I to III is likely to disappear spontaneously
in most cases within a period of two to three years. However spontaneous disappearance Gr IV
and Gr V is likely to be less but can be given a chance of Chemo prophylaxis and observation for
a period of two to three years.
Break through infections and fresh scars and structural abnormalities will be an indication for
surgical intervention.
V. Optimal diagnostic criteria , investigations treatment and referral criteria.
Situation 1. At secondary hospital / Non metro situation – optimal standards of treatment in
situations where technology and resources are limited.
A. Clinical diagnosis
High degree of suspicion of VUR in all UTI patients.
Febrile episodes with anorexia , vomiting and shivering
Recurrent fever/ PUO
Recurrent vomiting
Failure to thrive.
Voiding dysfunction and dysuria
b. Investigations
Urine Routine and microscopy
Urine culture and sensitivity (MSSU)
Blood urea and serum creatinine
Ultra sonogram
Micturiting cysto urethrogram if expertise is available
C. Treatment:
If the urine culture is positive
c. Day care: No role for day-care

d. Out patient : UTI treated with appropriate oral antibiotics

e. Inpatient: UTI treated by appropriate antibiotics intravenously : Sick child

Based on culture and sensitivity report child needs admission . Appropriate antibiotics are chosen
and administered for a period of 7 to 10 days intravenously.
It should be followed by oral chemo prophylaxis till the reflux subsides with periodical
monitoring of the urine culture especially during febrile episodes.
In metro hospitals for the VUR no surgical intervention is done .
Ultrasonogram done shows some structural abnormalities , should be investigated further with
Intravenous urogram and sent to higher centres for intervention.
Referral criteria
11. All cases of UTI who have not been evaluated with MCU should be referred to higher centre
for further evaluation and plan of management.
12. All patients with VUR should be referred to higher centres for Radionuclide studies to see
the differential renal function and asses the renal damage.

Lower grades of reflux with recurrent UTI and evidence of development of new scars and
anatomical abnormalities need to be referred to higher centres for management.
( B) All cases of Gr IV and Gr V VUR should be referred to centres doing major paediatric
surgical work as they do not undergo spontaneous resolution and require surgical or endoscopic
management. .
Situation 2
At super specialty at metro location where higher end technology is available
Investigations.
Routine urine examination and culture and sensitivity
Blood urea creatinine
Ultrasonogram
DMSA scan
IVU in selected cases to exclude upper urinary tract lesions
Bladder function Urodynamics studied in selected cases
Other investigations such as Plasma rennin activity and Genetic studies may be required in some
cases.
Absolute indications for surgery
i. Anatomic abnormalities of the bladder and VU junction

j. Unresolving VU reflux

k. Progressive renal injury

l. Break through Pyelonephritis inspite of appropriate antibiotic prophylaxis

m. Failure of renal and somatic growth

n. Non compliance in medical management of the drug regime

Treatment
Primary treatment
Treatment of UTI with appropriate drug with appropriate dosage and period of time.
Spontaneous resolution for most of the minor VUR and to a small extent Major VUR It happens
over period of time which is usually 3 years.
Children need long term chemoprophylaxis & surveillance ( BP monitoring ), Somatic growth
monitoring , renal function tests , urine analysis and Periodical cultures
Periodical assessment of renal condition with Ultra sonogram and Nuclear scans and MCU
Surgical treatment:
Type of surgery
Open surgery :- Reimplantation of ureters
Average stay 7 to 10 days
Has a success rate of 98 %
Child may need readmission for removal of stents if used for splinting the reimplanted ureters
Alternative management
There is a role for alternate procedures in select patients like
1.Circumcision
2.Endoscopic injection therapy
3 Diversion procedures like Ureterostomy and vesicostomy.
Long term management will include surveillance of the child and addressing bladder dysfunction
if present.
Referals
Even in Metro cities there are several levels of care. Surgical and endoscopic procedures should
be done in institutions with proper cystoscopes for different age groups including the neonates. C
arm facilities and monitors to see the endoscopic procedures are necessary. Anaesthetist trained
in paediatric anaesthesia is essential.
Who does what and timelines

- Ray technician to monitor C Arm

Further Reading and references

Consensus statement of management of Urinary tract infections
Indian Paediatric nephrology group Ind Paeditrics 2001:38:106-1155
Progress in Paediatric urology Edited bY Minu bajpai. Volume 6
Vesico ureteric reflux
 Methods of giving Phototherapy
Baby fulfills the criteria for phototherapy

months whichever is earlier)

nventional
phototherapy overhead or a double surface phototherapy can be given

position of the baby to be changed frequently

ould be a 5-8 cm space between it and the lamp cover to
prevent over heating
-475 nm
 aintained

10% wt loss )
r is not a guide to hyperbilirubinemia in infants on phototherapy ,hence bilirubin
should be monitored every 12 hrs

phototherapy for feeding

Exchange transfusion

Choice of blood:

In Rh hemolytic disease, blood is prepared before delivery, type O Rh negative crossed

matched against mother. If the blood is obtained after delivery to be crossed against baby OR
ABO group of baby and Rh negative blood
ABO incompatibility: O Rh negative or Rh compatible with the baby and mother, crossed
matched against mother and infant and have low
titer of anti A or anti B antibodies Usually type O cells are used with AB plasma to ensure that
no anti A or anti B antibodies
Volume for Exchange transfusion involves double volume of the infants blood that is 80
ml/ kg x 2 = 160 ml/kg ( in preterm neonates blood volume = 100 ml/kg)
Technique :

Procedure done under servocontrolled warmer and cardiac and blood pressure monitoring,
for resuscitation should be readily available an assistant to record
volumes of blood, observe and check the vitals

e, Umbilical vein cannulated , position of the

catheter to be checked by X –ray

-1 ½ hrs, Photo therapy to be

continued after the procedure

- 3ml

- 1500 gms - 5 ml

-2000 gms -10 ml

-3500 gms - 15 ml

-20 ml

158. NEONATAL INTESTINAL OBSTRUCTION

. WHEN TO SUSPECT/ RECOGNIZE?
a. Introduction:

Neonatal Intestinal Obstruction (NIO) is a common condition affecting neonates and requires
prompt recognition and appropriate specialist treatment to save these babies and to reduce
avoidable morbidity & mortality
b. Case definition:

Intestinal Obstruction in a new born child caused by intrinsic or extrinsic factors involving the
stomach / duodenum / jejunum / ileum / any part of the colon.
INCIDENCE OF THE CONDITION IN OUR COUNTRY
The Exact incidence of the condition in our population is difficult to ascertain.
However it may be approximately assessed to be 14 per 1,000 live births

DIFFERENTIAL DIAGNOSIS
a. Gastric Outlet Obstruction - Pyloric / Antral web / Hypertrophic Pyloric Stenosis
b. Malrotation
c. Duodenal Atresia
d. Jejuno-ileal Atresia
e. Meconium Ileus
f. Colonic Atresia
g. Hirschprung’s Disease
h. Meconium Plug Syndrome
i. Necrotising Enterocolitis (NEC)
j. Medical conditions mimicking Neonatal intestinal obstruction like Neonatal Sepsis with
ileus, Hypothyroidism etc.
k. Other rare conditions like intestinal duplications, intra-abdominal cysts, congenital
bands etc.

PREVENTION AND COUNSELING

As this is often a congenital disease, prevention is impossible.
 However, the obstetricians at all levels need to have a high index of suspicion about the
possibility of a GI obstruction when polyhydramnios is detected on antenatal scans
When a fetus is suspected to have NIO, the counseling can be done to have a discussion
with the obstetrician, the pediatrician & the pediatric surgeon and to plan the delivery to
be done at a place where neonatal surgery is safely feasible

16. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,

TREATMENT & REFERRAL CRITERIA

*Situation 1: At Secondary Hospital/ Non-Metro situation: Optimal Standards of
Treatment in Situations where technology and resources are limited
Clinical Diagnosis: Any child with any of the following criteria should be suspected to have
NIO
10. Bilious Vomiting (green colour)
11. Abdominal distention
12. Visible peristalsis
13. Not passed meconium beyond 48 hours after birth (72 hours in preterm babies)
14. Passing abnormal stool (pellets / mucus / mucus plug)
15. Feed intolerance
16. Upper or Lower Gastrointestinal Bleeding.
Persistent Non-bilious vomiting
Investigations:
a. Plain X-Ray Abdomen (preferably erect)
b. Air contrast X-Ray - A naso-gastric tube is inserted prior to shifting the baby for the X-Ray.
About 20 cc of Room air is insufflated through the naso-gastric tube and the X-Ray is taken.
(This is to highlight the stomach, duodenum and the proximal jejunum and to rule out
obstruction at this level.). Make sure the insufflated air is aspirated out immediately after the X-
Ray is taken and the NG tube is left for drainage
c. Ultrasonography, if indicated.

Treatment:
Standard Operating procedure
10. Day Care - No role for treatment on day care basis
11. Out Patient - No role for treatment on out-patient basis
12. In Patient -
Gastric Deompression
Place a No. 8 infant feeding tube through the nasogastric route. In very small babies,
oro-gastric tube can be utilised if the nostrils are small. The baby should be kept nil orally.
Ensure that the tube is correctly placed in the stomach and that it is patent.
Gently aspirate the tube hourly and connect to continuos drainage.
Maintain accurate chart to monitor the colour and volume of the aspirates
i. Temperature Maintenance
Keep the child warm using an incubator / warmer and keeping the room ambient
temperature high. A room warmer can be used in winter seasons
Intravenous Fluids to maintain Hydration / glucose levels.
The choice of IV fluids in the first 48 hours is 10% Dextrose @ 80 ml/ kg / day.
After 48 hours of birth, the IV fluid of choice would be Isolyte P to be run @ 100 - 120
ml / kg / day (the rate will vary as per the gestation of the baby and other factors as
determined by the pediatrician).
The fluid should be infused using ‘Burette’ / ‘Pediatric Drip Chamber set’ in order to
avoid over or under infusion. Microdrip sets with ‘dosiflow’ regulators may be used if these
are not available.
I.V. Antibiotics. Broad spectrum antibiotics to cover gram positive, gram negative and
anerobic bacteria should be used. Some of the suggested combinations are:
1. Ampicilin / Gentamicin / Metronidazole
2. Cefotaxime / Amikacin / Metronidazole
3. Co-Amoxiclav / Amikacin / Metronidazole
4. The choice of the antibiotic will vary on a lot of factors and can be suitably chosen by the
treating clinician .
ii. Preferable Investigations
1. Serum glucose / Electrolytes
2. BUN / Serum Creatinine
3. Hemoglobin & Blood Counts
4. Blood culture
5. Ultrasonography of the Abdomen
b) Referral criteria:
a. Ideally, all cases of neonatal intestinal obstruction should be transferred to hospitals with level
2 / 3 Neonatal intensive care facilities.
b. However, in situations where a qualified pediatric surgeon is available, these children can be
handled provided the hospital has the following facilities
i. Neonatal nursery with the availability of full-time trained neonatal / pediatric nurses
ii. Round the clock availability of Pediatrician
iii. Warming system for the baby - Radiant warmer/ Incubator etc/
iv. Operation Theatre well equipped with Monitors for ECG / Pulse Oximetry / Baby warming
systems and other facilities for operating on a small baby
v. A Well Trained Anesthesiologist with adequate exposure to neonatal anesthesia
vi. Facilities for post-operative monitoring of the baby - warmer, multi-system monitor,
resuscitation equipment etc.
c. Mode of transportation & Precautions during transfer”
i. Keep the child warm using clean blankets/ thermocol boxes, cotton padding etc, Keep the NGT
open & connect to continuous drainage. Strictly Avoid oral / NGT feeds
ii. Maintain the patency of IV line by flushing it before transportation and run fluids at the pre-
determined rate if the travel is expected to last more than a few hours
iii. It is preferable to have a trained paramedical / medical supervision during transportation . The
person should preferably be trained in basic neonatal care / neonatal resuscitation methods,
handling medical equipment like those required for airway maintenance / suction etc.
iv. *Situation 2: At Super Specialty Facility in Metro location where higher-end technology
is available
a) Clinical Diagnosis: Same as earlier

b) Investigations:
a. Blood:
i. CBC / CRP / Blood Culture
ii. S. Electrolytes / BUN / Creatinine
iii. Arterial Blood Gas
iv. Blood Grouping & Rh typing /
v. Serum Bilirubin
vi. Other blood tests as deemed necessary by the neonatologist.
b. Imaging: (Depending on the working diagnosis)
i. Plain X-Ray of Abdomen in all cases
ii. Air contrast X-Ray - if upper GI obstruction is suspected.
iii. Upper G.I. barium study - if upper GI obstruction is suspected.
iv. Contrast (Gastrograffin preferably) Enema - if lower GI obstruction is suspected.
v. Ultrasonography of Abdomen / Pelvis
vi. CT scanning / MRI - in rare instances
c. Additional Screening for Associated anomalies may be required in select cases
i. 2-D Echocardiography
ii. Renal Ultrasonography
iii. Chromosomal & Metabolic screening
iv. Any other as indicated

c) Treatment: Standard Operating procedure

a. Out Patient - no role
b. Day Care - No role
c. In Patient:
i. Initial resuscitation / Stabilisation
ii. IV Fluids / Antibiotics as indicated earlier
iii. Pre-operative Preparation - This will by and large depend on the condition of the baby
and if any pre-existing morbidity is present and will be handled by the neonatologist.
iv. Operative plan - This will depend on the diagnosis made about the level of obstruction.
The possibilities include

1. Simple laparotomy + Ladd’s procedure / release of bands / Pyloromyotomy etc.

2. Laparotomy + Resection anastomosis
3. Laparotomy + Resection + Ileostomy / colostomy
4. Laparotomy + pull-thorough
5. One stage pull-through for Hirschprung’s Disease
6. Laparotomy + Other procedures as per variations in the operative findings.
i. Post-operative Care - This will again have to be tailored to suit the child’s condition and
requirements. The probable supportive measures will include:
1. IV Fluids with possible transfusion of blood products like Packed Cells / Plasma / etc.
2. IV Antibiotics- as suggested earlier and as dictated by various factors influencing the
decision making process.
3. Inotropic Support - Dopamine / Dobutamine / Noradrenaline
4. Ventilatory Support
5. Parenteral Nutrition
6. Advanced Support like peritoneal dialysis
7. Vascular access
ii. Some children may also require Additional Surgery like:
1. Re-look laparotomy
2. Definitive surgery
3. Explorations for complications like anastomotic leak, adhesive obstruction / dehiscence
4. Ilesotomy / colostomy closure
iii. Other events during hospitalisation complicating the clinical course during
hospitalisation = like renal failure, nutritional support, colostomy / ileostomy care etc.
iv. Maternal support during hospitalisation including rooming in while feeding is initiated

d) Referral criteria:
a. Even within the metro cities, as there are several levels of hospital care available, we
recommend that new born babies with surgical problem should be handled by only those
hospitals with reasonably good neonatal care (level 2 & 3) facilities with the availability of
qualified Pediatric Surgeon and an experienced pediatric anesthetist.
b. However, depending on the nature of the disease and the general condition of the baby,
decision may be taken to handle the baby in centres with less than optimal facilities in Metro
cities if there is a genuinely good cause to believe that good surgical and post-operative care can
be extended to the child without much detriment to the baby
c. In any situation, after the initial resuscitation, if the general condition of the baby is poor or
if there is a possible necessity of ventilatory support or specialised treatment, it will be necessary
to shift the baby to a higher centre where such facilities are available, ensuring safe
transportation of the baby

17. WHO DOES WHAT? and TIMELINES

a. Doctor
i. Pediatrician:
1.Initial assessment and day to day care of the baby,
2.Early involvement of a pediatric surgeon and regular co-ordination with him/ her
3.taking appropriate decisions & involving the various specialists as indicated
ii. Resident / Registrar
1.Periodic assessment of the patient and regular reporting to the specialists
2.Carry out the orders of the Pediatrician / Pediatric Surgeon in charge of the patient
3.To ensure that all the orders are properly carried out by the nursing and other
paramendical personnel
4.Blood sampling and vascular access
iii. Pediatric Surgeon
1.Prompt assessment of the baby on referral and to formulate an appropriate plan of
action
2.Co-ordinating with the anesthetist and the other Operation Theatre personnel for the
proposed surgery
3.Performing the appropriate surgery and to make reasonable efforts for a smooth post-
operative recovery.
4.Post-operative care & Daily assessment with regard to the post-operative recovery
5.Vascular access
6.Take decisions with regard to the daily progress and further interventions as and when
indicated
iv. Anesthetist
1.Suitable pre-operative preparation
2.Appropriate anesthetic care and smooth post-operative recovery
3.Co-ordination with the other clinicians involved in the care of the child
v. Neonatologist
1.Initial assessment and day to day care of the baby,
2.Early involvement of a pediatric surgeon and regular co-ordination with him/ her
3.Taking appropriate decisions & involving the various specialists as indicated
4.Other specialist interventions AS AND WHEN NEEDED like :
a.Vascular access
b.Umbilical Venous / Arterial cannulation
c.Peritoneal dialysis
d.Enteral / Parenteral nutrition
a. Nurse
i. Nursing care of the baby
ii.Following all the instructions of the attending doctors
iii.Close co-ordination with all the departments
iv.Maintaining the records of the children upto date
a. Emergency Room
i. Ward
ii. Neonatal Intensive Care Unit
iii. Operation Theatre
iv. Post-operative Recovery
a. Technician

159. PROTOCOL FOR NEONATAL SEIZURES

Neonatal Seizures
(Seizure protocol adapted from: Sankar JM, Agarwal R, Deorari A, Paul VK. AIIMS Protocol on
management of neonatal seizures. Available at:
http://www.newbornwhocc.org/pdf/Seizures_2010_270810.pdf)
a) WHEN TO SUSPECT/ RECOGNIZE?

a) Introduction:

Neonatal seizures (NS) are the most frequent and distinctive clinical manifestation of
neurological dysfunction in the newborn infant. Infants with NS are at high risk of neonatal death
or neurological impairment and epilepsy disorders in later life. Though, mortality due to NS has
decreased over the years from 40% to about 20%, the prevalence of long-term neurodevelopment
sequelae has largely remained unchanged at around 30%.2 Improper and inadequate
management of seizures could be one of the major reasons behind this phenomenon.
b) Case definition and classification:

A seizure is defined clinically as a paroxysmal alteration in neurologic function, i.e. motor,

behavior and/or autonomic function.
Four types of NS have been identified- subtle, clonic, tonic and myoclonic. Myoclonic seizures
carry the worst prognosis in terms of neuro-developmental outcome and seizure recurrence.
Focal clonic seizures have the best prognosis.

b) INCIDENCE OF THE CONDITION IN OUR COUNTRY

The incidence of NS is 2.8 per 1000 in infants with birth weights of more than 2500 g; it is
higher in preterm low birth weight neonates – as high as 57.5 per 1000 in very low birth weight
infants.
c) DIFFERENTIAL DIAGNOSIS

The most common causes of seizures as per the recently published studies from the country are
hypoxic ischemic encephalopathy, metabolic disturbances (hypoglycemia and hypocalcemia),
and meningitis.
HIE secondary to perinatal asphyxia is the commonest cause of NS. Most seizures due to HIE
(about 50-65%) start within the first 12 hrs of life while the rest manifest by 24-48 hours of age.
Common metabolic causes of seizures include hypoglycemia, hypocalcemia, and
hypomagnesemia. Meningitis should be excluded in all neonates with seizures.
Meningoencephalitis secondary to intrauterine infections (TORCH group, syphilis) may also
present as seizures in the neonatal period. Seizures due to subarachnoid, intraparenchymal or
subdural hemorrhage occur more often in term neonates, while seizures secondary to
intraventricular hemorrhage (IVH) occur in preterm infants. Cerebral dysgenesis and neuronal
migration disorders are rare causes of seizures in the neonatal period.
a) PREVENTION AND COUNSELING

Good obstetric and neonatal care would go a long way in prevention of neonatal seizures.
Screening and management of polycythemia and hypoglycemia can prevent seizure occurrence
due to these reasons. Avoiding animal mlk feeding by exclusive breastfeeding may reduce
seizures due to late onset hypocalcemia.
b) OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS,

TREATMENT & REFERRAL CRITERIA

Approach and diagnosis

Detailed approach to an infant with neonatal seizures1, 4-6

1. History

Seizure history: A complete description of the seizure should be obtained from the
parents/attendant. History of associated eye movements, restraint of episode by passive flexion
of the affected limb, change in color of skin (mottling or cyanosis), autonomic phenomena, and
whether the infant was conscious or sleeping at the time of seizure should be elicited. The day of
life on which the seizures occurred may provide an important clue to its diagnosis. While
seizures occurring on day 0-3 might be related to perinatal asphyxia, intracranial hemorrhage,
and metabolic causes, those occurring on day 4-7 may be due to sepsis, meningitis, metabolic
causes, and developmental defects.
Antenatal history: History suggestive of intrauterine infection, maternal diabetes, and narcotic
addiction should be elicited in the antenatal history. A history of sudden increase in fetal
movements may be suggestive of intrauterine convulsions.
Perinatal history: Perinatal asphyxia is the commonest cause of neonatal seizures and a detailed
history including history of fetal distress, decreased fetal movements, instrumental delivery, need
for resuscitation in the labor room, Apgar scores, and abnormal cord pH (<7) and base deficit
(>10 mEq/L) should be obtained. Use of a pudendal block for mid-cavity forceps may be
associated with accidental injection of the local anesthetic into the fetal scalp.
Family history: History of consanguinity in parents, family history of seizures or mental
retardation and early fetal/neonatal deaths would be suggestive of inborn errors of metabolism.
History of seizures in either parent or sib(s) in the neonatal period may suggest benign familial
neonatal convulsions (BFNC).
2. Examination

Vital signs: Heart rate, respiration, blood pressure, capillary refill time and temperature should
be recorded in all infants.
General examination: Gestation, birth-weight, and weight for age should be recorded as they
may provide important clues to the etiology – for example, seizures in a term ‘well baby’ may be
due to subarachnoid hemorrhage while seizures in a large for date baby may be secondary to
hypoglycemia. The neonate should also be examined for the presence of any obvious
malformations or dysmorphic features.
CNS examination: Presence of a bulging anterior fontanel may be suggestive of meningitis or
intracranial hemorrhage. A detailed neurological examination should include assessment of
consciousness (alert/drowsy/comatose), tone (hypotonia or hypertonia), and fundus examination
for chorioretinitis.
Systemic examination: Presence of hepatosplenomegaly or an abnormal urine odor may be
suggestive of IEM. The skin should be examined for the presence of any neuro-cutaneous
markers. Presence of hypopigmented macules or ash-leaf spot would be suggestive of tuberous
sclerosis.
3. Investigations

Essential investigations: Investigations that should be considered in all neonates with seizures
include blood sugar, serum electrolytes (Na, Ca, Mg), cerebrospinal fluid (CSF) examination,
cranial ultrasound (US), and electroencephalography (EEG). CSF examination should be done in
all cases as seizures may be the first sign of meningitis. It should not be omitted even if another
etiology such as hypoglycemia is present because meningitis can often coexist. CSF study may
be withheld temporarily if severe cardio-respiratory compromise is present or even omitted in
infants with severe birth asphyxia (documented abnormal cord pH/base excess and onset within
12-24 hrs). An arterial blood gas (ABG) may have to be performed if IEM is strongly
suspected.One should carry out all these investigations even if one or more investigations are
positive, as multiple etiologies may coexist, e.g. sepsis, meningitis and hypoglycemia.
Imaging: Neurosonography is an excellent tool for detection of intraventricular and parenchymal
hemorrhage but is unable to detect SAH and subdural hemorrhage. It should be done in all
infants with seizures. CT scan should be done in all infants where an etiology is not available
after the first line of investigations. It can be diagnostic in subarachnoid hemorrhage and
developmental malformations. Magnetic resonance imaging (MRI) is indicated only if
investigations do not reveal any etiology and seizures are resistant to usual anti-epileptic therapy.
It can be diagnostic in cerebral dysgenesis, lissencephaly, and other neuronal migration
disorders.
Electroencephalogram (EEG): EEG has both diagnostic and prognostic role in seizures. It
should be done in all neonates who need anticonvulsant therapy. Ictal EEG may be useful for the
diagnosis of suspected seizures and also for diagnosis of seizures in muscle-relaxed infants. It
should be done as soon as the neonate is stable enough to be transported for EEG, preferably
within first week. EEG should be performed for at least one hour.9 Inter-ictal EEG is useful for
long-term prognosis of neonates with seizures. A background abnormality in both term and
preterm neonates indicates a high risk for neurological sequelae. These changes include burst-
suppression pattern, low voltage invariant pattern and electro-cerebral inactivity.
Management

Detailed approach to an infant with neonatal seizures1, 4-6

1. Initial medical management:

The first step in successful management of seizures is to nurse the baby in thermoneutral
environment and to ensure airway, breathing, and circulation (TABC). Oxygen should be started,
IV access should be secured, and blood should be collected for glucose and other investigations.
A brief relevant history should be obtained and quick clinical examination should be performed.
All this should not require more than 2-5 minutes.
2. Correction of hypoglycemia and hypocalcemia:
If glucostix shows hypoglycemia or if there is no facility to test blood sugar immediately, 2
ml/kg of 10% dextrose should be given as a bolus injection followed by a continuous infusion of
6-8 mg/kg/min.
If hypoglycemia has been treated or excluded as a cause of convulsions, the neonate should
receive 2 ml/kg of 10% calcium gluconate IV over 10 minutes under strict cardiac monitoring. If
ionized calcium levels are suggestive of hypocalcemia, the newborn should receive calcium
gluconate at 8 ml/kg/d for 3 days. If seizures continue despite correction of hypocalcemia, 0.25
ml/kg of 50% magnesium sulfate should be given intramuscularly (IM).
3. Anti-epileptic drug therapy (AED)1
Anti-epileptic drugs (AED) should be considered in the presence of even a single clinical seizure
since clinical observations tend to grossly underestimate electrical seizures (diagnosed by EEG)
and facilities for continuous EEG monitoring are not universally available. If aEEG is being
used, eliminating all electrical seizure activity should be the goal of AED therapy.1 AED should
be given if seizures persist even after correction of hypoglycemia/ hypocalcemia (Figure 1).
3.1 Phenobarbitone (Pb)
It is the drug of choice in neonatal seizures. The dose is 20 mg/kg/IV slowly over 20 minutes
(not faster than 1 mg/kg/min). If seizures persist after completion of this loading dose, additional
doses of phenobarbitone 10 mg/kg may be used every 20-30 minutes until a total dose of 40
mg/kg has been given. The maintenance dose of Pb is 3-5 mg/kg/day in 1-2 divided doses,
started 12 hours after the loading dose.
3.2 Phenytoin
Phenytoin is indicated if the maximal dose of phenobarbitone (40 mg/kg) fails to resolve seizures
or earlier, if adverse effects like respiratory depression, hypotension or bradycardia ensue with
phenobarbitone. The dose is 20 mg/kg IV at a rate of not more than 1 mg/kg/min under cardiac
monitoring. Phenytoin should be diluted in normal saline as it is incompatible with dextrose
solution. A repeat dose of 10 mg/kg may be tried in refractory seizures. The maintenance dose is
3-5 mg/kg/d (maximum of 8 mg/kg/d) in 2-4 divided doses. Oral suspension has very erratic
absorption from gut in neonates, so it should be avoided. Thus only IV route is preferred in
neonates and it should preferably be discontinued before discharge.
3.3 Benzodiazepines
This group of drugs may be required in up to 15-20% of neonatal seizures. The commonly used
benzodiazepines are lorazepam and midazolam. Diazepam is generally avoided in neonates due
to its short duration of action, narrow therapeutic index, and because of the presence of sodium
benzoate as a preservative. Lorazepam is preferred over diazepam as it has a longer duration of
action and results in less adverse effects (sedation and cardiovascular effects). Midazolam is
faster acting than lorazepam and may be administered as an infusion. It causes less respiratory
depression and sedation than lorazepam. However, when used as continuous infusion, the infant
has to be monitored for respiratory depression, apnea, and bradycardia (equipment for
resuscitation and assisted ventilation should be available at the bedside of all neonates given
multiple doses of AED).
The doses of these drugs are given below:
Lorazepam: 0.05 mg/kg IV bolus over 2-5 minutes; may be repeated
Midazolam: 0.15 mg/kg IV bolus followed by infusion of 0.1 to 0.4 mg/kg/hour.
According to Volpe, the expected response of neonatal clinical seizures to anticonvulsants is
40% to the initial 20-mg/kg loading dose of phenobarbitone, 70% to a total of 40 mg/kg of Pb,
85% to a 20-mg/kg of phenytoin, and 95% to 100% to 0.05 to 0.1 mg/kg lorazepam.1
3.4 Antiepileptic drugs for seizures refractory to above treatment
In exceptional circumstances when the seizures are refractory to the first-line AEDs, the
following second-line drugs might be tried.
10.6 Maintenance anti-epileptic therapy
Principles of AED used in older children and adults are applicable to neonates also.
Monotherapy is the most appropriate strategy to control seizures. Attempts should be made to
stop all anti-epileptic drugs and wean the baby to only phenobarbitone at 3-5 mg/kg/day. If
seizures are uncontrolled or if clinical toxicity appears, a second AED may be added. The choice
may vary from phenytoin, carbamezepine, and valproic acid.
10.7 When to discontinue AED
This is highly individualized and no specific guidelines are available. We follow an adaptation of
the protocol recommended by Volpe.1 We usually try to discontinue all medication at discharge
if clinical examination is normal, irrespective of etiology and EEG. If neurological examination
is persistently abnormal at discharge, AED is continued and the baby is reassessed at one month.
If the baby is normal on examination and seizure free at 1 month, phenobarbitone is discontinued
over 2 weeks. If neurological assessment is not normal, an EEG is obtained. If EEG is not
overtly paroxysmal, phenobarbitone is tapered and stopped. If EEG is overtly abnormal, the
infant is reassessed in the same manner at 3 months and then 3 monthly till 1 year of age (Figure
2). The goal is to discontinue phenobarbitone as early as possible.
1. Volpe JJ. Neurology of the newborn. 5th ed. Philadelphia: Saunders Elsevier, 2008. Chapter 5,
Neonatal Seizures;p.203-44.

Tekgul H, Gauvreau K, Soul J, Murphy L, Robertson R, Stewart J, et al. The current etiologic
profile and neurodevelopmental outcome of seizures in term newborn infants. Pediatrics

Figure 1 Acute management of neonatal seizures

160. UNDESCENDED TESTIS IN CHILDREN
l) WHEN TO SUSPECT/ RECOGNIZE?
.
h. Introduction :

Diagnosis and management of the undescended testicle is required by 1 year of age as per current
recommendation.
i. Case definition:

Cryptorchidism is the absence of one or both testes from the scrotum. It is the most common
birth defect involving the male genitalia.
INCIDENCE OF THE CONDITION IN OUR COUNTRY
The incidence of cryptorchidism is 1% to 4% in full-term newborns and in up to 45% of preterm
male babies.However, a large number of these will descend spontaneously by 6 months of age.
m) DIFFERENTIAL DIAGNOSIS

n) PREVENTION AND COUNSELING

If a newborn boy has been found to have an undescended testis, the family needs to be counseled
about the need for review at 6 months and the possibility of surgery.
In case of pain and swelling in the groin, there is a possibility of torsion and emergency
intervention is necessary.
o) OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA

History and Physical Examination

It is important to note if the testes were ever palpable in the scrotum at the time of birth or within
the first year of life.
Classification is based on testicular location, either along the normal line of descent (abdomen,
inguinal canal, external ring, pre-scrotal, upper scrotal) or in an ectopic position (usually in the
superficial inguinal pouch or perineal) It is important to document associated findings such as
hernia, hydrocele, penile size, and meatal position.
Check the size, location, and texture of the contralateral descended testis. Assess testicular
mobility, size, consistency, and spermatic cord tension.
The key to distinguishing a retractile from an undescended testis is success of delivery and
stability of the testis within the scrotum. The retractile testis will remain intrascrotal after
overstretching of the cremaster muscle, whereas a low cryptorchid testis will return to its
undescended position after being released. If there is any question, a follow-up examination is
indicated.
Imaging and Laboratory Tests
Routinely no imaging studies are needed. Ultrasound (US), computed tomography (CT) scans
and magnetic resonance imaging (MRI) imaging studies are optional in select cases.
Basic investigations (such as hemoglobin and urinalysis) will be required for anesthetic workup.
TREATMENT
Surgery
Surgery is planned between the 6th to the 12th month of age by a trained pediatric surgeon.
Palpable testis
Standard open inguinal orchidopexy is done.
Nonpalpable testis
Exploration for a non-palpable testis is usually performed with laparoscopy. Once the testes is
located by laparoscopy, it may be brought down into the scrotum in a single or two stage
procedure.
FOLLOW UP
Children are usually followed up as per the following time table:
10. 1 week after surgery
11. 3 months after surgery
12. Annually thereafter till puberty
13. Testicular self examination is taught to the boy at puberty

*Situation 1: At Secondary Hospital/ Non-Metro situation: Optimal Standards of

Treatment in Situations where technology and resources are limited
r. Clinical Diagnosis:

history and physical examination

s. Investigations:

a. tests for anesthesia- Hemoglobin, urinanalysis

t. Treatment:

-12months of age
- standard open orchidopexy
-palpable testis-laparoscopic assisted orchidopexy-either as single stage or two-stage
Standard Operating procedure
a. In Patient: Child needs inpatient care if there are other co-morbidities that increase anesthesia
risk
b. Out Patient: Children are evaluated and worked up as outpatients, followup too is done in the
outpatient department
c. Day Care: Most orchidopexy operations are done as day case procedures. Children require
inpatient admission if pain control is inadequate post operatively and if there are co-morbid
conditions that require monitoring in the post op period.

u. Referral criteria:

Child with undescended testis referred to higher centre if:

1.adequate anaesthesia facilities unavailable locally
2.intersex anomaly is suspected- as when there is:
1. severe hypospadias with unilateral non palpable testis
2. bilateral nonpalpable testis with or without hypospadias
3.child dysmorphic and a syndrome suspected

*Situation 2: At Super Specialty Facility in Metro location where higher-end technology is

available
Clinical Diagnosis: as above

Investigations:
a. for location of testis- not routinely required
b. for intersex anomalies;
i. Karyotyping,
ii. Ultrasonography of abdomen and pelvis
iii. genitography
iv. genitoscopy
v.laparoscopy
vi. hormonal assessment
c. for syndromes:
i. genetics consultation
ii. karytyping
iii. developmental assessment

Treatment: as above
– as per DSD protocol

Standard Operating procedure

a. In Patient
b. Out Patient
c. Day Care

Referral criteria:
No further referral needed
p) WHO DOES WHAT? and TIMELINES
q)
a. Doctor makes a clinical diagnosis, counsels the family and plans surgery- a pediatric surgeon
performs the surgery

b. Nurse: assists surgeon in care of child during pre, intra and post operative course of the baby

c. Technician: assists medical and nursing teams in care of child during intra and post-operative
periods.
Urology:
161. HAEMATURIA
Introduction:-
Hematuria is the presence of red-blood cells (RBC) in urine.
• It may be categorized as gross (visible to naked eye) or microscopic (detected in urine
microscopy). The recommended definition of microscopic hematuria is three or more red blood
cells per high-power field on microscopic evaluation of urinary sediment from two of three
properly collected urinalysis specimens.

• It may arise from any part of the urinary tract, from glomerulus to meatal tip and may be
characterized as initial, terminal or total, which points to the approximate site of origin (distal to
external sphincter, proximal urethra-bladder neck, and bladder and upper tracts, respectively).

• Severity of hematuria bears no relation with the etiology, therefore, its presence must be
considered serious unless proven otherwise.

Prevalence:-
The prevalence of asymptomatic microscopic hematuria varies from 0.19 percent to as high as 21
percent any varies widely with different age groups.
Differential diagnosis
Hematuria is a manifestation of a Etiologies
myriad of varied clinical diagnoses
ranging from exercise-induced to
cancer-related. The differential
diagnosis can be classified on the
basis of site of origin as shown
below: Origin
Glomerular Acute glomerulonephritis, lupus
nephritis, benign familial hematuria,
Berger’s disease, Goodpasture’s
disease, exercise hematuria.
Renal Polycystic kidney disease, Medullary
sponge kidney, papillary necrosis,
 renal infarct, lymphoma, multiple
myeloma, amyloidosis, inflammation
and infections, vascular malformation
Urologic Neoplasia, calculi, benign Prostatic
hyperplasia, urethral stricture,
endometriosis, diverticulitis,
infection, foreign body, GUTB
Adjacent organ Abdominal aortic aneurysm,
appendicitis, infiltrating malignancy
Hematologic Congenital and acquired
coagulopathy, therapeutic
anticoagulation, sickle-cell disease
and trait, sickle-cell thalassaemia,
sickle-cell Hemoglobin-C disease
Fictitious Vaginal bleed
False hematuria Food pigments, drug metabolites,
malingering
162. URINARY AND MALE GENITAL TRACT INFECTIONS
Introduction
Infections of the urinary tract pose a serious health problem, also because of their frequent
occurrence.
Clinical and experimental evidence support that the ascent of micro-organisms within the urethra
is the most commom pathway leading to urinary tract infections, especially for organisms of
enteric origin (I.e Escherichia coli and other Enterobacteriaeae). This is a logical explanation for
the greater frequency of UTIs in women than in men and the increased risk of infection
following bladder catherisation or instrumentation.
Classification of Urinary and Male Genital Tract Infections
For practical clinical reasons, urinary tract infections (UTIs) and male genital tract infections are
classified according to entities with predominating clinical symptoms: (I) uncomplicated lower
UTI (cystitis); (2) uncomplicated pyelonephritis; (3) complicated UTI with or without
pyelonephritis; (4) Urosepsis; (5) urethritis; and (6) prostatitis, epididymitis, orchitis.
Definitions
the definitions of bacteriuria and pyuria are as follows:
Significant bacteriuria in adults:

e uncomplicated pyelonephritis in female;

urine in men (or in catheter, urine specimen in women) with complicated UTI.

In a suprapubic bladder puncture specimen any count of bacteria is relevant.

Asymptomatic bacteriuria (ABU)
ABU is defined as two positive urine cultures taken more that 24h apart with 105
uropathogens/ml of the same bacterial strain.
Pyuria
The requirement for pyuria is 10 white blood cells per high power field in the resuspended
sediment of a centrifuged aliquot of urine or per mm3 in unspun urine. For the routine, a dipstick
method can also be used, including leukocyte esterase test, or nitrite reaction. 9
Table 1. Classification of prostatitis according to NIDDK/NIH
 -10 days. Tetracyclines and
fluroquinolones should not be used due to effects on teeth and cartilage.
be recommended afterwards.

The underlying disorded must be managed if

permanent cure is to be expected. In order to avoid inducing resistant strains, treatment should be
guided by urine culture whenever possible.

Patient with UTI may develop sepsis. Early signs of systemic inflammatory response (fever or
hypothermia, tachycardia, tachypnea, hypotension,oliguria, leukopenia) should be recognized as
the first signs of possible multiorgan failure. In conjunction with appropriate antibiotic therapy,
life supporting therapy in collaboration with an intensive care specialist may be necessary. Any
obstruction in the urinary tract needs to be drained.
Follow-up of patients with UTI
for follow-up after uncomplicated UTI and pyelonephritis in women, a urinanalysis by dipstick is
enough for routine use.
In women who will have recurrence within 2 weeks, repeated urinary culture with antimicrobial
testing and evaluation of the urinary tract is recommended.
In the elderly, newly developed recurrent UTI may warrant a full evaluation of the urinary tract.
In men with UTI, a urologic evaluation should be done when the patient is in adolescence, in
cases with recurrent infection and in all causes with pyelonephritis. Also patients with prostatitis,
epididymitis and orchitis should follow these recommendations.
In children, investigations are indicated after two episodes of UTI in girls and one episode in
boys. Recommended investigations are ultrasonography of the urinary tract supplemented by
voiding cystourethrography.
Urethritis
Symptomatic urethritis is characterized by dysuria and purulent discharge
Diagnosis
The Gram stain of secretion or urethral smear showing more than 5 leukocytes per high power
field (HPF) (1,000) and eventually gonococci located intracellularly as Gram-negative diplococci
indicate a pyogenic urethritis. A positive leukocyteesterase test or more than 10 leukocytes per
high-power field (400) in the first voiding urine specimen are diagnostic.
Therapy
The following guidelines for therapy comply with the recommendations of the Centre for
Disease Control and Prevention (1998).
For the treatment of gonorrhea the following antimicrobials can be recommended:
Cefixime 400 mg orally Ciprofloxacin 500 mg orally
As a single dose as a single dose
Cefriaxone 250 mg i.m. Ofloxacin 400 mg orally as
As a single dose single dose
(i.m. with local anaesthetic)
As gonorrhea is frequently accompanied by chalamydial infection, an antichlamydial active
therapy should be added. The following treatment has been successfully applied in C.
trachomatis infections :
First choice Second choice
Azithromycin Erythromycin
1 g (=4 caps.@250 mg) orally 500 mg orally 4 times daily for 7 days
as single dose
Doxycycline Ofloxacin
10 mg 2 times daily orally for 7 days 200 mg orally for 7 days
if therapy fails, one should consider infections by T. vaginalis and / or Mycoplasma, which can
be treated with a combination of metronidazole (2 g orally as single dose) and erythromycin (4
times daily 500 orally for 7 days).
Prostatitis, Epididymitis and Orchitis
Prostatitis
Treatment
g. Acute bacterial prostatitis can be a serious infection and parenteral administration of high
doses of bactericidal antibiotic such as aminoglycosides and a penicillin derivative or a 3rd
generation cephalosporin are required until defervescence and normalization of infection
parameters. In less severe cases a fluoroquinolone may be given orally for at least 10 days.

h. In chronic bacterial prostatitis and chronic inflammatory pelvic pain syndrome, a

fluoroquinolone or trimethorpim should be given orally for 2 weeks after the initial
diagnosis. Then the patient should be reassessed and antibiotics only continued if pretreatment
cultures were positive or if the patient reports positive effect of the treatment. A total treatment
period of 4-6 weeks is recommended.

Epididymitis, Orchitis
The majority of cases of epididymitis are due to common urinary pathogens. Bladder outlet
obstruction and urogenital malformations are risk factors for this type of infection.
Treatment
Prior to antimicrobial therapy a urethral swab and midstream urine should be obtained for
microbiological investigation. Fluoroquinolones, preferably those which react well against C.
trachomatis (e.g. ofloxacin, levofloxacin) should be first choice drugs because of their broad
antibacterial spectra and their
Table 4. Recommendations for perioperative antibacterial prophylaxis in urology
BLI = B- Lactamase inhibitor, ESWL- extracorporeal shock-wave lithotripsy. 10,20,30 = 1st,
2nd, 3rd generation respectively.
11. Fluroquinolone with sufficient renal excretion

Favorable penetration into the tissues of the urogenital tract. In case C. trachomatis has been
detected as etiologic agent, treatment could also be continued with doxycycline 200 mg/day for a
total treatment period of at least 2 weeks. Macrolides may be alternative agents. In case of C
.trachomatis infection, the sexual partner should be treated as well.
Antibiotics and α Blockers in combination
Urodynamic studies have shown increase urethral closing pressure in patients with chronic
prostatitis. A combination treatment of α blockers and antibiotics is reported to have a higher
cure rate than antibiotics alone in inflammatory CPPS. This is a treatment option favored by
many urologists.
In general, surgery should be avoided in the treatment of prostatitis patients except for drainage
of prostatic abscesses.
Perioperative Antibacterial Prophylaxis in Urological Surgery
The main aim of antimicrobial prophylaxis in urology is to prevent symptomatic / febrile
genitourinary infections, such as acute pyelonephritis, prostatitis, edpididymitis and urosepsis as
well as serious wound infections.
Antibiotic prophylaxis is recommended only for a maximum of 24 hours after surgery in most
situations. More rampant use leads to antibiotic resistance and places an additional economic
burden. Prophylaxis does not substitute for poor surgical asepsis.

163. UROLITHIASIS AND URETERIC COLIC

When to suspect /recognize
Introduction:-
American urological association (AUA) has been the frontrunner in formulating guidelines for
Urolithiasis since 1991. Since then, editions of guidelines have been published with the 2005
guidelines on staghorn calculus being the latest (1) The European association of urology(EAU)
has published similar guidelines since 2000. The latest updates have been published in 2010(2).
The significant differences in the socioeconomic and disease pattern (mode of presentation, stone
bulk, health care delivery facilities) for urolithiasis in India make it imperative to formulate our
own guidelines.
We have reviewed the literature for drafting the guidelines. The recommendations drawn are
largely based on the AUA/EAU guidelines with modifications recommended where appropriate.
Indian references have been cited, particularly so, if they are prospective randomized studies
and/or metanalysis. Recommendations have been given when adequate literature support is
available. The referral criteria are noted when appropriate.
Case definition
The index patients are defined as follows:-
Ureteral stones
A non pregnant adult patient with unilateral ureteral calculi (no renal stones) and normal
functioning contralateral kidney, the body habitus, anatomy and medical condition should not
preclude the application of any of the available treatment options (2)
Staghorn calculi
A staghorn calculi is defined as a stone with central body and at least one calyceal branch. A
partial staghorn calculus fills part of the collecting system. A complete staghorn fills all the
calyces and the renal pelvis.
Index patient (staghorn calculi):-
Adult with a staghorn stone (non Cystine, non uric acid) who has two functioning kidneys
(functioning both kidneys) or a solitary kidney with normal function. The patients overall
medical condition, body habitus and anatomy should permit any of the available intervention (1).
Non staghorn calculi
Any pelvic and /or calyceal calculi which do not fit in the definition of staghorn calculi (2).
Incidence in our country
Although a few studies have been reported for a small group of subjects in screening
camps. The true incidence of urolithiasis in India is still not known. It is commonly seen in
western states, hypothetically, attributable to high salinity of water .The presentation of a patient
with urolithiasis differs in India. Large stone bulk on presentation is commonly seen in India.
What should be the optimal?
Renal stones
Investigations:-
Imaging is absolutely imperative if, the patient has a solitary kidney or a history of fever. If the
diagnosis of stone is in doubt then imaging is mandatory. (2) Execratory urography has been
the gold standard in the work up for urolithiasis. Non contrast computerized
tomography(NCCT) scan is quick and safe, contrast free alternative to excretory urography.
Randomized studies have shown that non contrast helical CT has similar or superior results to
excretory urography in acute flank pain(3) Contrast media should not be given or should be
avoided when there is a elevated creatinine level, pregnancy or lactation(4)(5) Additional
information can be gained by contrast enhanced CT scan(CTU), however at the moment there is
no level 1 evidence to suggest that CTU is superior to IVU in the work up of urolithisis. .(6).
X-ray KUB and ultrasound is used by few clinicians as a measure of preoperative investigations,
however this cannot be considered as a standard. These investigations help to plan access and
predict the possible success rates.
Recommendation:-Excretory urography is the gold standard in work up for urolithiasis and is
mandatory in solitary kidney, history of fever and when the diagnosis is in doubt.
NCCT is the investigation of choice in acute flank pain due to stone.
Analysis of stone composition
Stone analysis is desirable in recurrent stone formers. The preferred analytical procedures
are:- (2)
1) X ray crystallography.
2) Infrared spectroscopy. The other methods of stone analysis are:-
1) Radiographic characteristics of the stone.
2) Microscopic examination of the urinary sediments to detect crystals.
3) Urine Ph (alkaline in infection stones and acidic in uric acid stones.
4) Urine culture.
Special investigations which are ordered on case to case merit are renal scintigraphy, antegrade,
retrograde contrast study.
Indications for intervention
The indication for stone removal depends on the size, site and shape of the calculus. The
likelihood of spontaneous passage, presence of obstruction should be assessed.
The indications for intervention are:-
1) When the stone diameter is more than 7 mm (because of low rate of spontaneous passage).
2) When adequate pain relief is not achieved.
3) When there is stone obstruction associated with infection.
4) Pyonephrosis.
5) Obstruction in single kidney.
6) Bilateral obstruction.
Recommendation:-For1, 2 stone removal with or without prior decompression(depending on the
clinical situation) is recommended ,in situation ,3,4,5,6 emergency deobstruction of the
collecting system is recommended.
The choice of decompression can be with ureteric stents, percutaneous nephrostomy depending
on surgeon preference, expertise and the level of obstruction (7) (8) (9) (10)
Treatment (including standard operating procedure)
I) Extracorporeal shock wave lithotripsy(ESWL)
The success of lithotripsy depends on the body habitus, location of the stone, efficacy of the
lithotripter, stone bulk. The contraindications for ESWL for renal stones include pregnancy,
bleeding disorders, uncontrolled urinary tract infections, morbid obesity, aortic aneurysms
close to F1(2)
i) Role of stents
Routine use of stents is not recommended for ESWL for renal stones. (11)
ii) Location of stones
The stone clearance is lower for stones in the lower calyx as compared to anywhere else in the
kidney. Various studies have attempted to show the correlation of geometry of the lower calyx to
predict the clearance of stone in this location. However the calyceal stone burden is the most
important factor in predicting the clearance.
Although there is no critical size, 20 mm should be considered the upper limit for stones in
the lower calyx to be recommended for ESWL. The EAU guidelines recommend ESWL as the
treatment of choice for renal stones less than 20mm2(300mm2) (2). A multicentre trial has
compared ESWL and Flexible ureteroscopy for lower calyceal stones. It failed to show any
difference in the clearance rates (12)
iii) Total stone burden
It is recommended that stones smaller than 20mm2 to be treated with ESWL , while for
larger stones more than 20mm2(300mm2), PCNL should be considered the treatment of
choice.(2)
iv) Composition and hardness of stone
The composition of the stone is an important factor for predicting the success rates of renal
calculi. Specific stone compositions have different clearance rates because of the varying
fragility of stones. Cystine stones are harder to fragment, hence cystine stones larger than 15mm
should not be treated with ESWL.PCNL would be a good option in these patients(2)
The measurement of stone density with NCCT helps in predicting success rates of ESWL.
Stones with greater than 1000 Hounsfield units (HU) show poor results with
ESWL.(13)(14)
v) ESWL-procedural standard operating protocol
Simultaneous fluoroscopy and ultrasound monitoring is desirable.(2) The acoustic coupling
between shock head and the skin should be optimal. Ultrasound gel is the best available gel. The
ultrasound gel should be applied straight from the container rather than by hand.(15)(16). Level 4
evidence is available to suggest that proper analgesia results in limited movement and respiratory
excursions. Better fragmentation can be achieved with starting the fragmentation at lower
energy setting and then ramping up the power(17) . the manufacturers recommendation
regarding the number of shocks and frequency should be followed.The optimal shock wave
frequency is 1.0 Hz(18) It is important to limit the number of shocks and the power, due to
concerns regarding damage to the kidney.
In case of infected stones, antibiotics should be given according to urine culture sensitivity,
the same should be continued after surgery for 4 days (2) Clinical experience suggests that stones
in the ureter rather than the kidney should be treated with shorter intervals between sessions.
vi) Complications
The complications which are likely to be encountered and which should be counseled to the
patient prior to surgery are:-
5. Pain

6. Hydronephrosis

7. Fever

8. Urosepsis
Recommendations:-
It is recommended that stones smaller than 20mm2 to be treated with ESWL. Routine use of
stents is not recommended for ESWL for renal stones.The contraindications for ESWL for renal
stones include pregnancy, bleeding disorders, uncontrolled urinary tract infections, morbid
obesity, aortic aneurysms close to F1. Antibiotics should be given according to urine culture
sensitivity, the same should be continued after surgery for 4 days. The physicians should refer to
the manufacturer recommendation regarding the decision of number, frequency and power of
shocks.
II)Percutaneous Nephrolithotomy
Technically most of the renal stones can be managed with a percutaneous nephrolithotomy.
However the usual indications for PCNL are larger than 20mm2, staghorn, partial staghorn
calculi and stones in patients with chronic kidney disease.
Standard operating protocol
General anaesthesia is preferable, although studies have demonstrated the utility of regional
anaesthesia (19) PCNL has been performed traditionally in a prone position however it can
technically also be performed in supine position, the advantage of this (supine position) approach
is that the retrograde access is easier in supine position, anesthetist has a better control over the
airway and simultaneous ureteric and renal stones can be managed without changing the
position.(20)(21) The access to the collecting system can be gained either ultrasound guided or
fluoroscopy guided depending on the availability of instruments and expertise. The
advantage of ultrasound guided access is the potential to avoid major visceral injuries.(22) The
access site should be the posterior calyx. The tract should be the shortest possible tract from
the skin to the desired calyx traversing the papilla. Depending on the stone configuration a
calyx should be selected (Supracostal, infracostal or subcostal) so that maximum stone bulk can
be cleared minimum number of tracts. (23) Renal tract dilatation either balloon, amplatz or
metallic dilators are a matter of surgeon preference and availability (2). In lower polar stones
ESWL, PCNL and flexible ureterorenoscopy are competing procedures with different success
rates and complications (12)(24).In complicated cases or when secondary intervention is
required a nephrostomy tube which serves the dual purpose of tamponade and a conduit
for second look is placed.
In uncomplicated cases, tubeless percutaneous nephrolithotomy with or without application of
tissue sealants is a safe alternative (25) (26)
i) Complications
The patients should be counseled regarding the complications which are likely to be
encountered such as life threatening bleeding with a possible need for angioembolisation or even
nephrectomy. It may be associated with infective complications leading to urosepsis. The
patients should be counseled regarding the possibility of residual calculi and the
consequences thereof. The procedure becomes challenging in complex stones, although the
complications are not specific to them. Such cases should be identified and managed by
experienced surgeons.
Recommendations
Technically, most of the renal stones can be managed with a percutaneous nephrolithotomy.
However the uasual indications for PCNL are larger than 20mm2, staghorn, partial
staghorn calculi and stones in patients with chronic kidney disease. The access to the
collecting system can be gained either ultrasound guided or fluoroscopy guided depending on
the availability of instruments and expertise. Renal tract dilatation either balloon, amplatz or
metallic dilators are a matter of surgeon preference and availability. In complicated cases or
when secondary intervention is required a nephrostomy tube which serves the dual
purpose of tamponade and a conduit for second look is placed. In uncomplicated cases,
tubeless percutaneous nephrolithotomy with or without application of tissue sealants is a safe
alternative.
III) Flexible ureterorenoscopy
Flexible ureteroscopy offers a good treatment option for calculi less than 20mm in size. Due
to improved technology and development in accessories and optics the role of flexible
ureteroscopy is likely to be expanded in the future. The procedure wherein flexible ureteroscopy
is used in the kidney is called as retrograde intrarenal surgery (RIRS). Flexible URS is not
recommended as a first line of treatment for renal calculi. It has been demonstrated as a
effective way of treating stones which are refractory to ESWL. It has also been seen useful
when simultaneously used with PCNL, in this way it reduces the number of tracts during the
procedure
It is recommended that sterile urine should be documented prior to intervention. (27)(28)
Standard technique for flexible ureteroscopy
• Fluoroscopy equipment is advisable in all cases
• Preoperative imaging helps to determine the size and location of the stone.
• The use of safety wire is recommended (0.035 floppy tip) .
• The ureteroscope can be introduced over a guide wire (back loaded) or they may be advanced
through a ureteral access sheath.
• Stone extraction blindly without endoscopic vision should not be done
• Small stones can be extracted with baskets of forceps.
• Intracorporeal lithotripsy can be performed with holmium laser. The other alternatives are
ballistic, ultrasonic or electrohydraulic lithotripsy. (2). The holmium Yag laser is the preferred
modality for flexible ureteroscopy
• The stenting after an uncomplicated flexible ureteroscopy is optional. The indications for
stenting after completion of URS are ureteral stricture, ureteral injury, solitary kidney, renal
insufficiency, large stone burden residual stones.
Accessories and instrumentation
A 365 micron laser fiber is suited for ureteral stones. The 200 micron fiber preserves tip
deflection. Holmium laser is the preferred energy source for flexible ureteroscopy. Nitinol
baskets preserve tip deflection, in addition the tipless design reduces the mucosal injury, hence
they are more suited for flexible ureteroscopy.Access sheaths have been used by various
workers. The size of the available access sheaths ranges from 9-16Fr, they have a hydrophilic
coating. Generally they are introduced over a wire. The advantages of access sheath are reducing
the operating time particularly in large stone burden. Another theoretical advantage is, it helps in
maintaining a low pressure in the pelvicalyceal system.(31)
Recommendations:-
Flexible ureteroscopy offers a good treatment option for calculi less than 20mm in size.
Flexible URS is not recommended as a first line of treatment for renal calculi. It has been
demonstrated as a effective way of treating stones which are refractory to ESWL. Stenting
after a uncomplicated ureteroscopy is optional.It is mandatory that sterile urine should be
documented prior to intervention.
Staghorn calculi:-
A retrospective study with 200 patients has shown that renal deterioration occurs in 28% of
patients with staghorn calculi treated conservatively. This emphasizes the fact that staghorn
stones should be aggressively managed surgically(32) PCNL should be the recommended
modality as clearance rates are greater than 3 times that of ESWL.(33)
The following are the treatment options in staghorn calculi:-
1) Percutaneous nephrolithotomy should be the first treatment utilized for most patients.
(level2)
2) ESWL should not be used as the preferred treatment modality for staghorn stones.
3) Open surgery should be recommended only if the stones are not expected to be removed
in a reasonable number of stages.
4) Nephrectomy should be considered in non functioning kidneys. (1)
Recommendations:-
PCNL is the first choice for staghorn calculi. Open surgery is desirable in the situation when
expertise is not available wherein the stone can be cleared in reasonable number of stages and
tracts. Nephrectomy should be considered for non functioning kidneys.
Management of ureteric calculi and ureteric colic
The most common cause for ureteric colic is ureteric calculus. The priority in these patients
should be relief of pain. The subsequent management of patients with ureteric colic would be
determined by the level of obstruction and the stone size.
i) Agents recommended for relieving pain
It is recommended that pain should be relieved with diclofenac whenever possible. A
alternative drug might be used if pain persists. Further more it has been shown that the resistive
index significantly reduces if diclofenac is administered.. Level 4 evidence suggests that
hydromorphine might be helpful, however there is a significant risk of vomiting (34) (35)
(36) Diclofenac can affect renal function in patients with already reduced function. There is
however no effect if the kidneys are functioning normally. (37)
ii) Agents for preventing episodes of renal colic
Diclofenac sodium is recommended for the purpose. Studies indicate that the incidence of
recurrent renal colic decreases with administration of diclofenac sodium. (38) When the pain is
unremitting the treating urologist should think of alternative measures such as drainage by
stenting or percutaneous nephrostomy or even removal of the stone.
iii) Medical expulsive therapy (MET)
The beneficial effect of these drugs is attributed to ureteral smooth muscle relaxation mediated
through inhibition of calcium channel pumps or alpha receptor blockade. The prerequisite for
this approach is that the patient should be comfortable this approach. And there should not be
any immediate indication for stone removal.. Studies indicate that alpha blockers facilitate
ureteral passage ,while nifedipine provides marginal benefit. Alpha blockers are
recommended for MET(2)
Ureteric calculi
Guidelines for Index patients
• Patients with bacteriuria should be treated with appropriate antibiotics
• Blind basketing without visualization endoscopically should not be performed.
• Patients with newly diagnosed stones less than 6 mm and well controlled symptoms, should be
advised MET
• Patients who opt for Medical expulsion therapy should have well controlled pain, no evidence
of sepsis, and adequate functional reserve, such patients should be periodically observed for
stone position and assessment of hydronephrosis.
• Stone removal is recommended in persistent obstruction, failure of stone progression. or
increasing or unremitting colic.
• Patient should be informed about the available treatment options.
• Both ESWL/ flexible URS are the preferred treatment options for upper ureteric calculi less
than 1cm in size. For larger stones Antegrade ESWL/PCNL/laproscopic removal are
recommended depending on expertise and instruments available
• URS is the preferred modality for distal and midureteric calculus.

Recommendations:-
Alpha blockers are recommended for MET. It is recommended that pain should be relieved
with diclofenac whenever possible. Patients with newly diagnosed stones less than 6 mm and
well controlled symptoms, should be advised MET .Patients who opt for Medical expulsion
therapy should have well controlled pain, no evidence of sepsis, and adequate functional reserve,
such patients should be periodically observed for stone position and assessment of
hydronephrosis. Both ESWL/ flexible URS are the preferred treatment options for upper ureteric
calculi less than 1cm in size. For larger stones antegrade ESWL/PCNL/laproscopic removal are
recommended depending on clinical situation expertise and instruments available. URS is the
preferred modality for distal and midureteric calculus
Treatment of calculi in special situations
Calyceal diverticular stones
Once symptomatic all these stones require treatment. ESWL, PCNL, laparoscopy and
observation remain the treatment options which can be offered to the patient. As the
drainage of the calyx in concern is at times questionable ESWL has rather poor results.
Sometimes the combination this treatment modality is recommended (39).
Anomalous kidneys
These group of patients include those patients with stones in ectopic, horseshoe or kidneys with
fusion anomalies. The approach to managing these stones should be individualized. The factors
to be taken into consideration are the stone bulk, the location of the stone, the vascular and the
anatomy of the pelvicalyceal system. Ultrasound helps in gaining access in ectopic kidney apart
from being a diagnostic tool. CT is pivotal in deciding the management and choosing the
method of treatment in anomalous kidney..
CT will also give the attenuation values and be a deciding factor in deciding ESWL or flexible
ureteroscopy. Flexible ureteroscopy will be useful tool in stones small burden stones in size with
the availability of smaller flexible ureteroscopes, and access sheaths. However the surgeon
should consider complete “on table” clearance in these patients as the drainage is likely to be
impaired. USG guided approach for ectopic kidneys should be done by surgeons well versed
with it. Laparoscopic assisted PCNL has shown good clearance rates with minimal morbidity and
less likely hood of ancillary procedures. Although adequate fragmentation can be achieved with
ESWL, the drainage of fragments might be impaired due to the anatomical abnormalities. The
choice of ESWL as a treatment option should be done prudently.(40)
Pediatric urolithisis Although the treatment modalities used are same in children as in adults.
Specific points should be noted in children. The indications for ESWL are similar to those in
adults. Stones in Children with a diameter of less than 20mm are ideal cases. The success
rates decreases as stone burden increases. Larger stones should be treated with PCNL (2).
They are as follows:-
1) Children have a tendency to pass larger fragments.
2) Ultrasound should be the modality for localization of stone when ESWL is the
modality chosen.
3) Smaller instruments should be used for endourologic manipulations(2)
Role of open surgery in the current era
In a developing country such as India, the cost factor plays a major role, which is mostly borne
by the patient or a health care delivery mechanism, A study from India by Sinha et al , which
although is a retrospective data and has a small sample size suggests that PCNL is less costly and
as effective as open surgery. However randomized level 1 evidence by Al Kohlany et al
comparing open surgery with PCNL suggests that PCNL offers equivalent clearance as open
pyelolithotomy, with less morbidity, short hospital stay.and less renal damage. The trade off in
a Indian clinical scenario will be to offer the best cost effective alternative
available.(41)(42)(43)
Nephrolithiassis –metabolic work up
See recommendation in section on- Nephrolithiassis –metabolic work up .
Who does what/ and timeline
Doctor
The treating doctor ideally should be an Urologist or a surgeon trained in Urology. He is
responsible for the initial workup of the patient and subsequent management of the patient. He is
responsible for counseling the patient regarding the success rates, complications and possible
outcome of any given procedure. All possible treatment options in a given clinical situation
should be discussed with the patient. The patient on discharge should be given instructions for
follow up and measures (dietary and pharmacologic) to prevent stone recurrence.
Nursing and technical staff:-The nursing staff should be trained in the aspect of maintenance and
use of endourologic equipment, considering the fragility and cost of these equipments. The
responsibility of sterilization of these equipment lies with these personnel .The technical/nursing
staff prepares the trolley and assists the surgeon during the procedure.
Referral criteria:-
The criterion for referral remains, lack of appropriate infrastructure and expertise at primary
level.
The indications for referral to tertiary care centre in managing stones disease are:-
!)Complex calculi ( multiple stones , staghorn calculi, stones with CKD, stones with obstructive
uropathy) where in the opinion of the treating physician , the patient needs nephrolurological
care and advanced surgical and medical care from a infrastructure standpoint
2) Special situations such as pediatric urolithiasis, stones in ectopic kidney.
Annexure 1
Indications and selection of modality for treating calculi in a index patient
It depends on the stone size location, stone composition and BMI of the patient
The following are the guidelines to be followed 34
1) Stone less than 1cm in the kidney -ESWL
2) Stone more than 1cm and less than 2cm in the kidney , -Flexi URS/ESWL/PCNL
3) Any stone more than 2cm in the kidney-PCNL
4) All staghorn and partial staghorn-PCNL
5Non progressive more than 6mm stone in the mid and lower ureter-semirigid URS.
6) Stones less than 1cm in upper ureter-ESWL
7) stones larger than 1cm in upper ureter-PCNL/ESWL/Flexi URS
Annexure 1
Resources required for one patient/procedure (units)
Human resources
ESWL
i. Urologist-1

j. Technician-1
k. Anesthetist-1

PCNL
12. Urologist-1

13. Surgical assistant-1

14. Technician/Nurse-2

15. Anesthetist-1

Flexible ureteroscopy
1) Urologist-1
a) Surgical assistant-1

3) Technician/Nurse-2
4) Anesthetist-1
Investigations:- As detailed in previous section
Drugs and consumables
List of consumables for PCNL
Normal saline 1000ml-(n=4)
5% Dextrose 1000ml-(n=2)
Normal saline -3000ml-(n=3)
Iv set – (n=1)
Injection Fortwin – (n=1)
Injection Metoclopromide-(n=4)
Injection Tramadol 50 mg –(n=4)
Injection ranitidine-50 mg-(n=4)
Foley catheter 16 fr-(n=1)
Urobag-(n=2)
Irrigation set-(n=1)
Phosphate enema-(n=1)
Injection glycopylorrate-(n=1)
Antibiotic according to clinical situation
List of consumables for ureteroscopy
Normal saline 1000ml-(n=4)
5% Dextrose 1000ml-(n=4)
Normal saline -3000ml-(n=3)
Iv set – (n=1)
Injection Fortwin – (n=1)
Injection Metoclopromide-(n=4)
Injection Tramadol 50 mg –(n=4)
Injection ranitidine-50 mg-(n=4)
Foley cathter 16 fr-(n=1)
Urobag-(n=1)
Irrigation set-(n=1)
Phosphate enema-(n=1)
Injection glycopylorrate-(n=1) 42
Antibiotic according to clinical situation
Equipment
Trolley preparation for PCNL
Tray with cover-2
Legging-2
Towel clips-5
Towel -2
Surgeon gown -3
Gloves -3
Hole towel-2
Artery forcep-2
Needle holder-1
Number 11 knife-1
Sponge holder -1
Scissor-1
Knife holder-1
Thread-1
20cc syringe-2
10 cc synringe-1
Bowl-1
Xylocaine jelly-2
Cystoscope sheath (19 Fr/20 Fr)
Telecope-30 degree
Light cable with cord 1 in number 43
Open end ureteric cathter-1 in number
Nephroscope -24-26 Fr (depending on availability)
Suction pipe-1
Stone holding forcep-1
Spanner -1
Ultrasound probe (optional)
Puncture needle-1
Metal rod/Telescopic metal dilators (till 24 Fr)-1
J tip guide wire/ glidewire-1
Teflon dilator with Upto 14 Fr-1
Ampatz dilator set-1
Amplatz sheath (size depends on surgeon preference)
Nephrostomy catheter (Nelaton preferable)
Trolley preparation for URS
Trolley with cover-1
Legging-2
Hole towel-1
Gown with napkin-1
Gloves-3
Towel clip-2
Sponge holder-1
Bowl-1
Scissors-1
Ureteric cathter-1
Ureteric dilator set-1
Irrigation tube-1
Cystoscope sheath with bridge-1
Telescope-30 degree-1
Guide wire 0.035/glide wire-1 each
Ureteroscope (depends on surgeon preference)-1 45
164. Benign Hyperplasia Of Prostate (BPH)
General comments:
Clinical guideline are supposed to be reflections of the best currently available evidence. They
have 2 parts –
a. A systematic review of the best available evidence and the strength of that evidence.
I. The methodology of systematic review is important. This should be clearly stated. All relevant
studies should be studied. If Indian studies are available, then they should be included. The
evidence should then be ranked using a standard system e.g. levels of evidence - Oxford Centre
for Evidence-based Medicine [1]. If necessary relevant focused questions can be framed in order
to exactly define the purview of the exercise.
b. Recommendations for practice based on that evidence. These should be graded according to
the level of available evidence.

This standard treatment guideline on BPH does not state the methodology used to arrive at the
recommendations. The levels of evidence are not mentioned. There is no grading of the
recommendations. The document is without any references to back up the claims.
The authors should be clearly mentioned in the published version ( we understand this is not
desirable in a document for peer review). A conflict of interest declarations should be included in
the final document.
Use of the term benign hyperplasia of the prostate (BPH) – BPH is a histological diagnosis. It
symptoms come under the umbrella of lower urinary tract symptoms. While BPH occurs in the
vast majority of elderly men, it can be difficult or impossible to directly attribute the symptoms
of the patient to BPH.
Introduction
Line 17 – 20 : ”However, a significant proportion, particularly in rural areas tend to disregard
symptoms till complications develop and this segment requires a more proactive and
individualized approach.” – There is no evidence that the rural population disregard symptoms
more than the urban people. The lack of access to effective health care in rural areas will make a
proactive and individualized approach difficult. It is important for guidelines to be applicable to
the entire populations of the country.
Evaluation of BPH
1. Symptom assessment – Need to state the complete term International Prostatic Symptom
Score before using the abbreviation IPSS.

Mandatory diagnostic tests

2. PSA measurement – Need to state the complete term. There is no evidence that prostate
specific antigen measurement has any role in the routine management
of BPH. The role of PSA screening for prostate cancer is controversial. Metaanalysis of the
recent evidence showed screening to have no significant impact on either overall mortality or
death from prostate cancer with significant overdiagnosis and overtreatment and is unlikely to
save lives. It cannot be recommended in India. A patient anxious about prostate cancer should be
explained about the benefits and risks of PSA screening and about the available evidence. He
should be then in a position to make an informed choice.
3. Abdominal ultrasound evaluation –Upper tract imaging is not required for routine evaluation
of BPH. The estimation of prostate size by abdominal ultrasound is also unreliable. Ultrasound
evaluation should be restricted to the bladder and post void residual urine as an optional test.
4. Uroflowmetry – This is not mandatory even in developed countries. The equipment is
specialized, expensive (Indian makes cost Rs. 50000/- approx., foreign equipment – 1.5 – 2.5
lacs/ - approx.) and require regular maintenance and calibration. It cannot be mandatory and
should be an optional test.

Optional diagnostic tests

2. Blood urea – Blood urea estimation is superfluous when creatinine is being measured. It is not
as accurate indicator of renal function as creatinine. Unnecessary.
3. Urine Cytology – Urinary cytology is a specialized test with low sensitivity. In absence of
microscopic haematuria, it is unlikely to be useful.
6. Urethrography – An uroflowmerty is a non invasive test which can indicate a possible urethral
stricture. An urethrography is invasive and will require prior urine culture sensitivity before its
performance.
Uroflowmetry and ultrasound abdomen can be added as optional tests.
Treatment options
2. a. “Dose titration is not essential for Alfuzosin and Tamsulosin ” should read - Dose titration
is not required for extended release Alfuzosin and Tamsulosin.
“Hypotensive episodes are least seen with use of Alfuzosin” – The vasodilatory effects of
Alfuzosina nd Tamsulosin are similar. There are no statistical differences between the two in this
regard [4].
b. 5 Alpha reductase inhibitors: “Reduction of blood loss during TURP is evident only after
long term use of 5 ARI’s.” - The evidence is very weak and not enough for a
recommendation[5,6,7,8].
c. Combination therapy: “Concominant use of Alpha adrenergic blockers and 5Alpha reductase
inhibitors is appropriate therapy for patients with LUTS due to BPH, particularly if response has
been insufficient with either drug.” - Combination
therapy is necessary in those who are at risk of progression (moderate to severe LUTS, enlarged
prostates, and reduced Qmax) . Response is not a criterion for combination therapy [9].
3. Indications for surgery

“Patients presenting with chronic low pressure require catheterization and urodynamic
evaluation” – Catheterization is not required unless the patient has acute on chronic retention,
overflow incontinence or obstructive uropathy with raised creatinine.
4. Minimally invasive procedures

TUNA and intraprostatic stents – Cannot be recommended based on current evidence.

5. Surgical (endoscopic and open) procedures • “Open prostatectomy is still an acceptable
procedure for glands exceeding 100 gms in wt.” – Any gland over 60 gms can be managed with
open prostatectomy if TURP is not available.
f) “Follow-up with IPSS, DRE & PSA recommended every 3 to 6 months initially and annually
thereafter.” – Three monthly follow up is not required after surgery. PSA is certainly not needed.

Conclusions: Very poorly written clinical practice guideline. It is unfit for use in its present
form. Needs extensive revision.
165. RENAL CELL CARCINOMA (RCC)
Renal cell carcinoma (RCC), which accounts for 2% to 3% of all adult malignant neoplasms, is
the most lethal of the urologic cancers. The mortality rate of RCC is as much as twice that of
bladder cancer1,2. There is no epidemiological data available from Indian subcontinent.
However, the disease is fairly prevalent in our country.
In 2010, an estimated 58,240 Americans were diagnosed with renal malignancies and 13,040
deaths were estimated3. In 2008, there were an estimated 88,400 new cases and 39,300 kidney
cancer–related deaths from RCC in Europe4.
Surgical excision remains the only curative treatment as this tumor is remarkably resistant to
radiotherapy and chemotherapy.
Presentation –
Incidental: detected on imaging (CT / ultrasound) performed for other indication

Symptomatic: local / metastatic / paraneoplastic

-reducing varicocoele / pathological fracture

Workup –
Any mass lesion detected on ultrasound needs further imaging.
b) CT / MRI abdomen & pelvis/ MR Urography – both without and with contrast (if renal
functions permissible). MRI specifically indicated if disease is infiltrating adjacent organs or
IVC thrombus (triphasic multiplanar CT or high resolution color Doppler ultrasound optional for
the latter).
c) Blood investigations – Hemogram, kidney functions, alkaline phosphatase (ALP), calcium,
albumin, lactate dehydrogenase (LDH)
d) Chest X-ray – in all cases. Further imaging (CT scan) required only if clinically indicated or
primary tumor locally advanced or lymph-nodes enlarged

e) Bone scan – only if clinically indicated (bone pain, raised ALP) or primary tumor locally
advanced or lymph-nodes enlarged.

f) PET CT – not routinely recommended in the workup for RCC. Has good specificity but low
sensitivity in the evaluation of metastatic disease. Currently, it may be considered in case of
equivocal findings on conventional imaging, where detection of metastatic disease will influence
management decision.

g) Biopsy / FNAC – not required in most cases. Acceptable in the following indications:
h) Considering inflammatory mass / lymphoma / metastasis, vague Radiology, multiple masses,
associated significant lymphadenopathy

i) Considering non-surgical therapy (e.g. cryotherapy, systemic therapy in case of metastatic

disease) / active surveillance (small renal masses) / watchful waiting

Staging (American Joint Committee on Cancer, TNM staging system for renal cancer, 7th ed,
2010) –
Stage wise treatment –
In addition to clinical stage, patient’s performance status (ECOG5) should be taken into
consideration before deciding the treatment options.
Stage I
Preferred – nephron-sparing surgery if technically feasible
Optional – radical nephrectomy*
Others
9. Active surveillance
10. Ablative therapies (cryotherapy, radiofrequency ablation, microwave thermotherapy, high
frequency focussed ultrasound, etc.)

Adrenalectomy / lymphadenectomy: not indicated, unless grossly involved intraoperatively

(staging changed)
* In patients with early stage RCC radical nephrectomy is justified when NSS is technically not
feasible / the patient understands the other option (NSS) and opts for RN.
Stage II
Preferred – radical nephrectomy
Optional (imperative setting**) – nephron-sparing surgery
Adrenalectomy / lymphadenectomy: not indicated
** Imperative indications of NSS: solitary kidney, compromised function or reserve of
contralateral kidney (chronic renal insufficiency, severe diabetes mellitus, severe hypertension),
bilateral synchronous tumors, familial RCC
Stage III
Preferred – radical nephrectomy, with tumor thrombectomy (if present)
Lymphadenectomy – may be performed for better staging. LND in patients with high-risk
disease improves stage assessment and may prolong survival6,7. A mere sampling of the renal
hilar lymph nodes is insufficient for pathologic staging. For right sided tumor, paracaval and
interaortocaval lymph nodes and for left sided tumor para-aortic and interaortocaval lymph nodes
should be removed from the crus of the diaphragm to the common iliac artery. If disease is
confirmed within the interaortocaval nodes, a complete retroperitoneal LND is recommended to
define the full extent of metastatic lymph node involvement8.
Adrenalectomy: not required unless direct invasion or tumor nodule (stage changed)
Stage IV
16. Nephrectomy with adjacent organ excision

17. Metastasectomy (if solitary metastasis)

18. Adrenalectomy

19. Cyto-reductive nephrectomy

Patients of stage IV disease are candidates for adjuvant systemic therapy (vide infra).
Socio-economic and facility issues –
Advanced –
• staging tools

• surgical facility

• follow up facility

• socio-economic support

may not be available everywhere.

Centers which intend to treat RCC must be equipped with facility for histopathology / CECT /
Blood transfusion.
If above facilities not available / locally advanced disease / patient wants NSS → ref. to higher
center.
Follow up protocol after definitive local treatment –
Risk grouping (UCLA integrated staging system)9:
Indications:
l. Metastatic RCC with resectable disease (cytoreductive nephrectomy and metastatectomy
should be done whenever feasible)

m. Non-resectable Locally advanced / metastatic RCC

Agents–

Targeted therapy in the form of tyrosine kinase

inhibitors (1-4) and m-TOR inhibitors (5-6) have become first line systemic treatment for
management of metastatic RCC. A substantial improvement in progression-free survival and
overall survival has been achieved in large randomized controlled trials, when compared to
Interferon-α. These agents have also been found to be effective in non-clear cell RCC, which are
typically resistant to cytokines and interferons. Sarcomatoid variant is associated with poor
prognosis, and a modest response with doxorubicin & gemcitabine is observed.
Limitations –
• high cost and limited availability

• significant side-effects

• efficacy

Note : Targetted therapy for metastatic RCC/ locally advanced RCC should be decided by
Urologist and given in supervision of a Urologist.

166. BLADDER CANCER

I. WHEN TO SUSPECT / RECOGNIZE?
a) Introduction / b) Case definition: Bladder carcinoma is the most common malignancy of the
urinary tract and is the 9th most common cancer diagnosis worldwide. At the initial diagnosis of
bladder cancer, 70% of cases are diagnosed as non-muscle-invasive bladder cancer (NMIBC)
and approximately 30% as muscle-invasive disease. [1, 2]
Non-muscle-invasive bladder cancer: Bladder cancer that does not involve the muscularis
propria.
Invasive bladder cancer: Bladder cancer that histologically invades the muscularis propria.

– Tobacco consumption
– Occupational exposure to chemicals
– Radiation therapy
– Chronic urinary tract infection
– Bladder schistosomiasis
– Chemotherapy – Cyclophosphamide
• Active and passive tobacco smoking continues to be the main risk factor, while exposure-
related incidence is decreasing.
II. INCIDENCE OF THE CONDITION IN OUR COUNTRY: Exact incidence is unknown.
The recent trends indicate increasing incidence of bladder cancer. This may be partially
attributed due to better detection and improved health care. Expected to be of same incidence as
the western world.
III DIFFERENTIAL DIAGNOSIS:
20. Chronic cystitis
21. Tuberculous cystitis
22. Bladder calculi
23. Interstitial cystitis
24. Radiation cystitis
25. Eosinophilic cystitis

IV. PREVENTION AND COUNSELING:

11. Mass education about bladder cancer and its relationship with tobacco use
12. Anti-tobacco campaign
13. Careful history about smoking, occupational exposure to risk factors and storage LUTS
14. Detailed evaluation of all patients with gross hematuria and elderly patients (>40 years) with
microscopic hematuria and associated risk factors like smoking
15. All patients with hematuria should undergo full urological evaluation
16. Prompt referral of men with advanced bladder cancer to higher centers for further evaluation

V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &

REFERRAL CRITERIA
Diagnostic criteria:
1. History of gross painless hematuria
2. History of severe storage LUTS – may be due to CIS
3. Recurrent cystitis in elderly
4. Positive cytology
5. Cystoscopic examination and imaging studies showing tumour(s) in the bladder.
Diagnosis –The diagnosis mainly depends on the cystoscopic examination of the bladder,
biopsy, and urine cytology. The initial therapy for bladder tumours is complete macroscopic
transurethral resection of bladder tumours (TURBT) including a part of underlying muscle [7].
Cold cup biopsies should be discouraged.
A second TURBT should be considered [8]:
1. If there is suspicion that the initial resection was incomplete
2. When multiple or large tumours are present
3. When pathologist reported no muscle in the specimen
4. When a high grade tumour (pT1G3) was detected.
The management algorithm is based on the diagnosis of invasion of muscularis propria or not.
Routine bladder mapping biopsies are not indicated except in
1. Patients with positive urine cytology with normal looking mucosa in cystoscopy
2. Biopsy of the apical prostatic urethra when there is a bladder neck tumour or when
abnormalities of prostatic urethra are visible.
Carcinoma in situ (CIS) is diagnosed based on the histology of bladder mucosal biopsies.
Fluorescent cystoscopy is recommended in these cases [9].
Investigations:
4. Urine cytology: Cytology is useful when a high-grade malignancy or CIS is present. It is used
to predict high grade tumour before TUR. However, urinary cytology often is negative in the
presence of low-grade cancer.
5. Ultrasonography (USG): Transabdominal USG permits characterization of renal masses,
detection of hydronephrosis and visualization of intraluminal masses in the bladder. It can be as
accurate as IVU for diagnosis of upper urinary tract obstruction [10]. The USG is thus a useful
tool for investigation in patients with haematuria to detect obstruction; it cannot however exclude
the presence of upper tract tumours.
6. Pelvic examination (Bimanual examination) under anaesthesia: Helpful in assessment of local
staging in muscle invasive bladder cancer and advanced cases. Not of much value in superficial
bladder cancers. Should be done along with TURBT.[11]
7. Cystoscopy & TURBT: Cystoscopy should describe all macroscopic features of the tumour
(site, size, number and appearance) and mucosal abnormalities. A bladder diagram is
recommended. The gold standard in establishing the diagnosis of bladder tumour is TURBT.
8. Intravenous Urography (IVU): Intravenous urography (IVU) is used to detect filling defects in
the calyces, renal pelvis and ureters, and hydronephrosis. Acceptable for staging of muscle
invasive bladder cancer when CT Urography is not readily available [12].
9. CT Urography (CTU): CTU is mainly recommended for histologically proven muscle invasive
bladder cancers for staging. It is not useful for making a diagnosis of muscle invasive bladder
cancer. Pre TURBT CTU is indicated in select group of patients in whom it would significantly
alter the management. Especially in muscle invasive tumours of the bladder and in upper tract
tumours, CT urography gives more information than IVU does (including status of lymph nodes
and neighbouring organs) [12].
10. MRI – abdomen and pelvis/ MR Urography: Optimal investigation for staging in muscle
invasive bladder cancer Recommended only when there is definite contraindication for CT
urography or IVU like contrast allergy and renal failure.
11. Serum alkaline phosphatase – if elevated indicates metastatic bone disease.
12. Bone scan –Indicated in patients with raised alkaline phosphatase and with bone pain.
13. CT scan of chest is recommended for optimal staging in muscle invasive bladder cancer; if
not available chest X-ray is acceptable.

Staging of bladder cancer:

Based on Tumour Node Metastasis (TNM) classification of carcinoma bladder (2010) [13].
• T - primary tumour
• TX Primary tumour cannot be assessed
• T0 No evidence of primary tumour
• Ta Non-invasive papillary carcinoma
• Tis Carcinoma in situ. ‘flat tumour’
• T1 Tumour invades subepithelial connective tissue
• T2 Tumour invades muscle
• T2a Tumour invades superficial muscle (inner half)
• T2b Tumour invades deep muscle (outer half)
• T3 Tumour invades perivesical tissue
• T3a Macroscopically
• T3b Microscopically (extravesical mass)
• T4 Tumour invades any of the following: Prostate, uterus, vagina, pelvic wall, abdominal wall
• T4a Tumour invades prostate, uterus or vagina
• T4b Tumour invades pelvic wall or abdominal wall
• N - regional lymph nodes
• NX Regional lymph nodes cannot be assessed
• N0 No regional lymph node metastasis
• N1 Metastasis in a single lymph node in the true pelvis (hypogastric, obturator, external iliac or
presacral)
• N2 Metastasis in a multiple lymph nodes in the true pelvis (hypogastric, obturator, external
iliac or presacral)
• N3 Metastasis in a common iliac lymph node(s)
• M - distant metastasis
• MX Distant metastasis cannot be assessed
• M0 No distant metastasis
• M1 Distant metastasis

Characteristics of Stages Ta, T1, and Tis

Stage Ta tumours are confined to the urothelium, have a papillary configuration of their
exophytic part, and do not penetrate from the urothelium into the lamina propria or detrusor
muscle.
Stage T1 tumours originate from the urothelium but penetrate the basement membrane which
separates the urothelium from the deeper layers. T1 tumours invade into the lamina propria, but
are not so deep that they reach the detrusor muscle.
Carcinoma in situ (Tis) is a high-grade (anaplastic) carcinoma confined to the urothelium, but
with a flat non-papillary configuration. Unlike a papillary tumour, Tis appears as reddened and
velvety mucosa and is slightly elevated but sometimes not visible. Tis can be local or diffuse.
Three types of Tis are distinguishable;

s (with a history of papillary tumours);

Characteristics of grade [14]:
1973 WHO Classification
Apart from their architecture, the individual cells show different degrees of anaplasia:
Grade 1: well differentiated tumour
Grade 2: moderately differentiated tumour
Grade 3: poorly differentiated tumour
2004 WHO Classification
A new classification system was initially proposed by the WHO/ISUP in 1998 and updated by
the WHO in 2004. For non-invasive urothelial neoplasias, the categories are:
• Flat lesions
• Hyperplasia (flat lesion without atypia or papillary)
• Reactive atypia (flat lesion with atypia)
• Atypia of unknown significance
• Urothelial dysplasia
• Urothelial carcinoma in situ (CIS)
• Papillary lesions
• Urothelial papilloma (a completely benign lesion)
• Papillary urothelial neoplasm of low malignant potential
• (PUNLMP)
• Low-grade papillary urothelial carcinoma
• High-grade papillary urothelial carcinoma

The 2004 WHO grading system defines Tis as a non-papillary, i.e. a flat, lesion in which the
surface epithelium contains cells that are cytologically malignant. Papillary tumours are
classified as either papillary urothelial neoplasms of low malignant potential (PUNLMP) or as
urothelial carcinomas, with the latter being subdivided into two grades: low grade and high
grade. The intermediate group (G2) has been eliminated; this group was the subject of
controversy in the 1973 WHO classification. Use of the 2004 WHO classification is advocated,
as this should result in less diagnostic variability among pathologists.
Predicting recurrence and progression of tumours [15,16]:
TaT1 tumours
The pattern of recurrence and progression depends on the following clinical and pathological
factors:
1. Number of tumours
2. Tumour size
3. Prior recurrence rate
4. T-category
5. Pesence of concurrent CIS
6. Tumour grade.
CIS
No prognostic factors are well established. Retrospective studies suggest the following:
1. Concurrent CIS with T1 tumours have worser prognosis than primary CIS and secondary CIS
[17, 18]
2. Responders to BCG have better prognosis than those non-responders. [19]
Treatment: Treatment strategy varies according to the stage and grade of bladder cancer.
Non-muscle invasive bladder cancer (superficial bladder cancer) NMIBC:
The standard initial therapy for Ta and T1 papillary bladder tumours is complete TURBT.
Tumours less than 1cm in size can be resected enbloc. Larger tumours should be resected in
fractions, which include the exophytic part, the underlying bladder wall and the edges of
resection area. Complete and correct TUR is essential to achieve a good prognosis [20].
Prognostic Factors and Adjuvant Treatment
TaT1 papillary tumours
Recommendations for Low Risk Tumours
Patients with a single, small, low grade Ta tumour without CIS, who are at low risk for both
recurrence and progression, should receive:
1. A complete TUR.
2. An immediate single post-operative instillation with a chemotherapeutic agent (drug optional
– Mitomycin C preferred). [21]
3. No further treatment is recommended prior to recurrence.
Recommendations for High Risk Tumours
Patients with TaT1 high grade tumours with or without CIS and those with CIS alone are at high
risk of progression. Treatment should consist of:
1. Complete TUR of papillary tumours followed by an immediate post-operative instillation with
a chemotherapeutic agent (drug optional – Mitomycin C preferred).[21]
2. A second TUR after 4–6 weeks.[9]
3. Adjuvant intravesical immunotherapy with BCG (full dose or reduced dose in case of side
effects). Maintenance therapy for at least 1 year (monthly once) is necessary [22,23] although the
optimal maintenance scheme has not yet been determined.
4. Immediate cystectomy may be offered to patients at highest risk of tumour of progression
(Patients with multiple tumours, large tumours (> 3 cm), and highly recurrent tumours (> 1
recurrence/year), stage T1 tumours with high grade tumours, and CIS).
5. In patients with BCG failure, cystectomy is recommended. [24]
Recommendations for Intermediate Risk Tumours
In the remaining intermediate risk patients, adjuvant intravesical therapy is necessary but no
consensus exists regarding the optimal drug and the most appropriate scheme. BCG is more
effective than chemotherapy in both reducing recurrence and progression. The major issue in the
management of intermediate risk tumours is to prevent recurrence and progression, of which
recurrence is clinically the most frequent. Treatment should include:
1. Complete TUR followed by an immediate postoperative instillation with a chemotherapeutic
agent (drug optional).
2. A second TUR after 4–6 weeks when the initial resection was incomplete.
3i. Adjuvant intravesical chemotherapy (drug optional), schedule: optional although the duration
of treatment should not exceed 1 year. (Or)
3ii. Adjuvant intravesical immunotherapy with BCG (full dose or reduced dose in case of side
effects). Maintenance therapy for at least 1 year (monthly once) is necessary although the
optimal maintenance schedule has not yet been determined.
Carcinoma in situ
CIS have a high risk of progression to muscle invasive disease which exceeds 50% in some
studies. BCG intravesical immunotherapy (induction and maintenance) is superior to intravesical
chemotherapy in increasing the complete response rate and the overall percent of patients
remaining tumour free. Moreover, BCG reduces the risk of 63
progression as compared to either intravesical chemotherapy or a different immunotherapy [25].
Early radical cystectomy at the time of diagnosis provides excellent disease-free survival, but
over-treatment occurs in up to 50% of patients.
Recommendations for the treatment of CIS
1. In concurrent CIS, the initial strategy (TUR, early intravesical instillation, a second TUR) is
based on the features of the papillary tumour.
2. Intravesical BCG immunotherapy including at least 1 year maintenance.
3. After the 6 week induction course, a second course of 6 weekly BCG instillations or
maintenance cycles consisting of 3 weekly instillations may be considered in non-responders
since about 40-60% of these patients will respond to additional treatment with BCG. [23]
4. In BCG non-responders at 6 months, radical cystectomy is recommended. [26].
Muscle invasive bladder cancer:
Neo-adjuvant chemotherapy:
Neo-adjuvant cisplatin-containing combination chemotherapy improves overall survival by 5-7%
at 5 years [27]. It should be considered irrespective of the type of definitive treatment. Neo-
adjuvant chemotherapy is not recommended in patients with performance status (PS) > 2 and
impaired renal function [28].
Radical Surgery and Urinary Diversion
Cystectomy is the preferred curative treatment for localized muscle invasive bladder cancer [29].
Radical cystectomy includes removal of regional lymph nodes, the extent of which has not been
sufficiently defined [30]. A delay in cystectomy increases the risk of progression and cancer-
specific death [31]. No pre-operative radiotherapy should be administered. Radical cystectomy in
both sexes must not include the removal of the entire urethra in all cases, which may then serve
as outlet for an orthotopic bladder substitution. If no bladder substitution is attached, the urethra
must be checked regularly. Terminal ileum and colon are the intestinal segments of choice for
urinary diversion. The type of urinary diversion does not affect oncological outcome.
Contraindications for orthotopic bladder substitution [32]:
1. Positive margins at the level of urethral dissection
2. Positive margins anywhere on the bladder specimen (in both sexes), if the primary tumour is
located at the bladder neck or in the urethra (in women), or if tumour extensively infiltrates the
prostate.
Pre-operative bowel preparation is not mandatory.
Before cystectomy, the patient should be counselled adequately regarding all possible
alternatives, and the final decision should be based on a consensus between patient and surgeon.
For patients with inoperable locally advanced tumours (T4b), primary radical cystectomy is a
palliative option and not recommended as a curative treatment.
Neoadjuvant Radiotherapy in Muscle-Invasive Bladder Cancer [33]
Pre-operative radiotherapy does not increase the survival for operable muscle invasive bladder
cancer.
Bladder-Sparing Treatments
Radical TURBT
Radical TURBT is not recommended except in a rare situation when patient not willing for open
surgery or unfit for radical cystectomy [34].
External beam radiotherapy [35, 36]
External beam radiotherapy alone should only be considered as a therapeutic option when the
patient is unfit for cystectomy or a multimodality bladder-preserving approach
Radiotherapy can also be used to stop bleeding from the tumour when local control cannot be
achieved by transurethral manipulation because of extensive local tumour growth.
Chemotherapy [37,38]
Although cisplatin-based chemotherapy, as primary therapy for locally advanced tumours in
highly selected patients, has led to complete and partial local responses, the long-term success
rate is low.
Multimodality treatment [39,40]
There are comparable long-term survival rates in cases of multimodality treatment success.
Delay in surgical therapy can compromise survival rates.
Adjuvant Chemotherapy [41]
Adjuvant chemotherapy is advised within clinical trials, but not for routine use.
Metastatic Disease [42 -47]
Urothelial carcinoma is a chemosensitive tumour. Performance status (PS) and the presence or
absence of visceral metastases are independent prognostic factors for survival.
These factors are at least as important as the type of chemotherapy administered. Cisplatin-
containing combination chemotherapy is able to achieve a median survival of up to 14 months,
with long-term disease-free survival reported in about 15% of patients with nodal disease and
good PS. Single-agent chemotherapy provides low response
rates of usually short duration. Post-chemotherapy surgery after a partial or complete response
may contribute to long-term disease-free survival. Prognostic factors should guide the treatment
selection.
NOTE : All chemotherapeutic drugs/ targeted therapy should be decided and administered in
consultation with a Urologist.
First-line treatment for “fit” patients:
Use cisplatin-containing combination chemotherapy with GC, MVAC, preferably with GCSF, or
HD-MVAC with GCSF.
Carboplatin and non-platinum combination chemotherapy is not recommended.
First-line treatment in patients ineligible (‘unfit”) for cisplatin:
Use carboplatin combination chemotherapy or single agents.
For cisplatin-ineligible patients (‘unfit’) with either PS 2 or impaired renal function, or with poor
prognostic factors, first-line treatment is carboplatin-containing combination chemotherapy,
preferably with gemcitabine/carboplatin.
Second-line treatment:
In patients progressing after platinum-based combination chemotherapy for metastatic disease
vinflunine should be offered, which has the highest level of evidence to date, or clinical trials of
other treatments.
Follow-up for non-muscle invasive bladder tumours [48, 49]
Patients with non-muscle invasive bladder tumours need to be regularly followed up because of
the risk of recurrence and progression; however, the frequency and duration of cystoscopies
should reflect the individual patient’s degree of risk.
The result of the first cystoscopy after TUR at 3 months is a very important prognostic factor for
recurrence and for progression. The first cystoscopy should thus always be
performed at 3 months after TUR in all patients with non-muscle invasive bladder tumour.
Recommendations for follow-up cystoscopy
Patients with tumours at low risk of recurrence and progression should have a cystoscopy at 3
months. If negative, the following cystoscopy is advised at 9 months and consequently yearly for
5 years.
Patients with tumours at high risk of progression should have a cystoscopy and urinary cytology
at 3 months. If negative, the following cystoscopies and cytologies should be repeated every 3
months for a period of 2 years, every 4 months in the third year,
every 6 months thereafter until 5 years, and yearly thereafter. A yearly evaluation of the upper
tract by IVU or retrograde pyelogram is recommended.
Patients with intermediate-risk of progression (about one-third of all patients) should have an in-
between follow-up scheme using cystoscopy and cytology, adapted according to personal and
subjective factors.
Patients with Tis should be followed up for life due to the high risk of recurrence and
progression, both within the bladder and extravesically. Urine cytology together with cystoscopy
(and bladder biopsies in cytology positive cases) is essential for monitoring of treatment efficacy.
The follow-up schedule is the same as for patients with high-risk tumours.
Follow up for muscle invasive bladder cancer [50]
Follow-up is based on the stage of initial tumour after cystectomy. At every visit, the following
should be performed:
History, Physical examination, Serum chemistries and chest radiograph annually for pT1 disease;
semiannual evaluation for patients with pT2 disease; and quarterly evaluation for patients with
pT3 disease. For the last group, semiannual CT scan is recommended.
Bone scan only when indicated or symptomatic. IVU can be done for upper tract surveillance
when CT scan is not readily available.
After 5 years of follow-up, stop oncological surveillance and continue with functional
surveillance.
Referral criteria:

without palpable pelvic mass suggestive of bladder

cancer

*Situation 1: At Secondary Hospital / Non-Metro Situation: Optimal Standards Of Treatment In

Situations Where Technology And Resources Are Limited.
a) Clinical diagnosis: Careful evaluation of patients with gross painless hematuria, Pelvic
examination for bladder masses, not useful in non-muscle invasive bladder cancers.
b) Investigations: Urine microscopy for hematuria, urine cytology for malignant urothelial cells.
Ultrasound of abdomen and pelvis - to localize the cause of hematuria like renal and bladder
tumours. Cystoscopy in all cases of gross hematuria and those with bothersome severe storage
LUTS and positive microscopic hematuria.
c) Treatment: According to the stage of the disease.
Standard operating procedure:
j) Inpatient:
k) Outpatient:
l) Daycare:

Referral criteria:
Patients with gross painless hematuria known to have bladder tumour
Positive urine dipstick or microscopic hematuria
Positive urine cytology
*Situation 2: At super specialty facility in metro location where higher end technology is
available.
a) Clinical diagnosis: Evaluation of gross hematuria, positive microscopic hematuria and
positive urine cytology. Pelvic examination – to look for bladder masses.
b) Investigations: All the possible investigations mentioned.
c) Treatment: According to the stage of the disease and the treatment options selected by the
patient after counseling.
Standard operating procedure
a) Inpatient
b) Outpatient
c) Daycare

Referral Criteria:
For diagnosis and staging – CT Urography, molecular urinary markers.
Evaluation of metastatic disease – bone scan if required.
VI. WHO DOES WHAT? AND TIMELINES
n. Doctor – clinical diagnosis, treatment, follow-up
o. Nurse – counseling, preoperative preparation, essential post-operative care, stoma care and
follow-up
p. Technician – Investigations and preoperative preparation.

167. PROSTATE CANCER

I. WHEN TO SUSPECT / RECOGNIZE?

most important medical problems facing the male population.[1]Prostate cancer is the 2nd most
common cause of cancer death in men. Affects 4% of men in undeveloped countries & 15% of
men in developed countries [2]

– 11 fold when two

or more first line relatives has PCa[3]

II. INCIDENCE OF THE CONDITION IN OUR COUNTRY: Exact incidence is unknown.

Expected to be of same incidence as the western world.
III DIFFERENTIAL DIAGNOSIS:
m) Benign prostatic hyperplasia
n) Granulomatous Prostatitis
o) Transitional cell carcinoma of prostate
p) Chronic prostatitis
q) Prostatic calculi

IV. PREVENTION AND COUNSELING:

d) Mass education about prostate cancer
e) Opportunistic screening for prostate cancer with serum PSA
f) Counseling about serum PSA and its implications
g) Chemoprevention of prostate cancer
h) Recognizing bladder outflow obstruction and other complications in men due to prostate
cancer
i) Thorough examination in elderly men who are at risk
j) Prompt referral of men with suspicion of prostate cancer to higher centres for further
evaluation

V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &

REFERRAL CRITERIA
Diagnostic criteria: Screening & Early detection of prostate cancer
Population or mass screening is defined as the examination of asymptomatic men (at risk). It
usually takes place as part of a trial or study and is initiated by the screener. In contrast, early
detection or opportunistic screening comprises individual case findings, which are initiated by
the person being screened (patient) and/or his physician. The primary endpoint of both types of
screening has two aspects:
1. Reduction in mortality from PCa.
2. Quality-of-life adjusted gain in life years (QUALYs).
Screening for prostate cancer has conflicting results.
Based on the results of two large, randomised trials [4,5], it is accepted that at present
widespread mass screening for PCa is not appropriate. Rather, early detection (opportunistic
screening) should be offered to the well-informed man. Hence
• Early PSA testing should be a shared decision between patient and physician
• PSA testing & DRE – offered to men >40 years of age & expected life expectancy of atleast 10
years

Diagnosis –The main diagnostic tools to obtain evidence of PCa include digitial rectal
examination (DRE), serum concentration of PSA and transrectal ultrasonography (TRUS).
Investigations:
1. DRE: Most prostate cancers are located in the peripheral zone of the prostate and may be
detected by DRE when the volume is about 0.2 mL or larger. A suspect DRE is an absolute
indication for prostate biopsy. In about 18% of all patients, PCa is detected by a suspect DRE
alone, irrespective of the PSA level [6]
2. Serum PSA(Prostate-specific antigen) is organ-specific but not cancer-specific. Thus, serum
levels may be elevated in the presence of benign prostatic hypertrophy (BPH), prostatitis and
other non-malignant conditions. The level of PSA as an independent variable is a better predictor
of cancer than suspicious findings on DRE or TRUS [7]. The level of PSA is a continuous
parameter: the higher the value, the more likely is the existence of PCa. This means there is no
universally accepted cut-off or upper limit.[8] As yet, there is no long-term data to help
determine the optimal PSA threshold value for detecting non-palpable, but clinically significant,
PCa. Modifications to improve the specificity of PSA in early detection of Ca.P
a. PSA density
b. PSA density of transition zone
c. Age specific PSA
d. PSA molecular forms – PCA3
e. Free / Total PSA ratio (at PSA 4-10ng/ml) <0.10 – 56% biopsy positive
f. PSA doubling time (PSADT)
g. PSA velocity
h. When in doubt, repeat PSA under standardised conditions
3. Transrectal ultrasound of prostate (TRUS) guided biopsy of prostate. Gray-scale TRUS does
not detect areas of PCa with adequate reliability. It is therefore not useful to replace systematic
biopsies with targeted biopsies of suspect areas.
However, additional biopsies of suspect areas may be useful. Transrectal ultrasonography
(TRUS) guided biopsy under antibiotic cover with periprostatic nerve block– minimum 10 core
laterally and posteriorly directed biopsy is recommended (>12 not significantly more
conclusive). [9]The indications for a repeat biopsy (including TZ biopsy) [10] are:
a. Rising and/or persistent PSA, suspicious DRE;
b. Atypical small acinar proliferation (ASAP).
c. Extensive High-grade prostatic intraepithelial neoplasia (PIN)
Complications of biopsy – infection, sepsis < 1%, clot retention, acute urinary retention, bleeding
from rectum, hematuria, hemospermia (the last 3 are mostly self limiting).
d. Pathology of prostate cancer:
i. The Gleason score is the sum of the most dominant and second most dominant (in terms of
volume) Gleason grade.
ii. A diagnosis of Gleason score 4 or lower should not be given on prostate biopsies
iii. Gleason score system is the single strongest prognostic factor for clinical behaviour and
treatment response.
4. TRUS is also useful for staging of prostate cancer, however remains inadequate. [11]
5. MRI – abdomen and pelvis/ MR Urography [12] (risk stratification)
a. Local staging (T-staging)
b. MRI demonstrates higher accuracy for the assessment of uni- or bilobar disease (T2),
Extracapsular extension (ECE) and Seminal vesicle invasion (SVI) (T3), as well as the invasion
of adjacent structures (T4).
c. Lymph node status (N-staging) is only important when potentially curative treatment is
planned.
6. Pelvic lymph node dissection remains the only reliable staging method in clinically localized
PCa. [13]
7. Bone scan - Skeletal metastasis (M-staging) is best assessed by bone scan. This may not be
indicated in asymptomatic patients if the serum PSA level is less than 20 ng/mL (risk
stratification) in the presence of well or moderately differentiated tumours.[14]
8. Serum alkaline phosphatase – if elevated, indicates metastatic bone disease.
9. Transurethral resection of prostate- In those men who come with bladder outflow obstruction
in an unsuspected fashion and biopsy report may reveal carcinoma of prostate.

Staging of prostate cancer: Based on Tumour Node Metastasis (TNM) classification of

carcinoma prostate [15].
• T - primary tumour
• TX Primary tumour cannot be assessed
• T0 No evidence of primary tumour
• T1 Clinically inapparenttumour not palpable or visible by imaging
• T1a Tumour incidental histological finding in 5% or less of tissue resected
• T1b Tumour incidental histological finding in more than 5% of tissue resected
• T1c Tumour identified by needle biopsy (e.g. because of elevated prostate-specific antigen
[PSA] level)
• T2 Tumour confined within the prostate1
• T2a Tumour involves one half of one lobe or less
• T2b Tumour involves more than half of one lobe, but not both lobes
• T2c Tumour involves both lobes
• T3 Tumour extends through the prostatic capsule
• T3a Extracapsular extension (unilateral or bilateral) including microscopic bladder neck
involvement.
• T3b Tumour invades seminal vesicle(s)
• T4 Tumour is fixed or invades adjacent structures other than seminal vesicles: external
sphincter, rectum, levator muscles, and/or pelvic wall
• N - regional lymph nodes
• NX Regional lymph nodes cannot be assessed
• N0 No regional lymph node metastasis
• N1 Regional lymph node metastasis
• M - distant metastasis
• MX Distant metastasis cannot be assessed
• M0 No distant metastasis
• M1 Distant metastasis
• M1a Non-regional lymph node(s)
• M1b Bone(s)
• M1c Other site(s)

• Group I T1a-c N0 M0 PSA < 10 Gleason < 6

• T2a N0 M0 PSA < 10 Gleason < 6
• Group IIA T1a-c N0 M0 PSA < 20 Gleason 7
• T1a-c N0 M0 PSA > 10 < 20 Gleason < 6
• T2a, b N0 M0 PSA < 20 Gleason < 7
• Group IIb T2c N0 M0 Any PSA Any Gleason
• T1-2 N0 M0 PSA > 20 Any Gleason
• T1-2 N0 M0 Any PSA Gleason > 8
• Group III T3a, b N0 M0 Any PSA Any Gleason
• Group IV T4 N0 M0 Any PSA Any Gleason
• Any T N1 M0 Any PSA Any Gleason
• Any T Any N M0 Any PSA Any Gleason
– (Note: When either PSA or Gleason is not available, grouping should be determined by cT
category and whichever of either PSA of Gleason is available. When neither is available
prognostic grouping is not possible, use stage grouping)
Treatment: Treatment of prostate cancer depends on the stage of the disease and prognostic
information available.
Deferred treatment (Watchful waiting & Active surveillance) [16- 20]

Make difference between active survillience and watchful waiting

Indications:
• In presumed localisedPCa (Nx-N0, M0):
– Stage T1a: well and moderately differentiated tumours. In younger patients with a life
expectancy of > 10 years, re-evaluation with PSA, TRUS and biopsies of the prostatic remnant is
recommended
– Stage T1b-T2b: well & moderately differentiated tumours. In asymptomatic patients with a
life expectancy of < 10 years
– Inclusion criteria for active surveillance with the lowest risk of cancer progression are:
• PSA < 10 ng/ml, biopsy Gleason score < 6, < 2 positive biopsies, < 50% cancer per biopsy,
cT1c-2a
• In presumed localisedPCa (Nx-N0, M0):
– Stage T1b-T2b patients who are well informed and have well-differentiated (or Gleason 2-4)
PCa and a life expectancy of 10-15 years.
– All patients not willing to accept side-effects of active treatment.
– Well-informed, asymptomatic patients with high PSA levels for whom cure is unlikely.
• In locally advanced disease (stage T3-T4):
– Asymptomatic patients with well- or moderately differentiated cancer, PCa and a short life
expectancy
– PSA < 50 ng/mL and PSA doubling time > 12 months
• In metastatic disease (M1):
– A very rare patient without any symptoms and the possibility of close follow-up

The criteria for active surveillance have not reached a consensus stage yet. Every institution has
different parameters and that should be mentioned. Active surveillance is not the same as
watchful waiting.
2. Radical Prostatectomy [21,22]period between biopsy and surgery
• Indications
– In patients with low and intermediate risk localisedPCa (cT1a-T2b and Gleason score 2-7 and
PSA < 20) and a life expectancy > 10 years
• Optional
– Selected patients with low-volume high-risk localisedPCa (cT3a or Gleason score 8-10 or PSA
>20)
– Highly selected patients with very high-risk localisedPCa (cT3b-T4 N0 or any T N1) in the
context of multimodality treatment
• Recommendations
– Short-term (3 months) neoadjuvant therapy with gonadotrophin releasing-hormone analogues
is not recommended in the treatment of stage T1-T2 disease
– Nerve-sparing surgery may be attempted( offered) in pre-operatively potent patients with low
risk for extracapsular disease (T1c, Gleason score < 7 and PSA < 10 ng/mL or see Partin tables /
nomograms)
– Unilateral nerve-sparing procedures are an option in stage T2a disease
– Recommendation for Lymphadenectomy
– Extended PLND is recommended for all patients who have a greater than 2% chance of having
lymph node disease. (NCCN guidelines)

3. Definitive radiation therapy [23-28]

• In localised prostate cancer T1c-T2c N0 M0, 3D-CRT with or without IMRT is
recommended even for young patients who refuse surgical intervention. There is fairly strong
evidence that low-, intermediate- and high-risk patients benefit from dose escalation
• For patients in the high-risk group, short-term ADT prior to and during radiotherapy results
in increased overall survival, but three years of adjuvant ADT are better according to the results
of EORTC 22961
• Transperineal interstitial brachytherapy with permanent implants is an option for
• Patients with cT1-T2a, Gleason score < 7 (or 3 + 4), PSA < 10 ng/mL, prostate volume < 50
mL, without a previous TURP and with a good IPSS
• Immediate post-operative external irradiation after RP for
• Patients with pathological tumour stage T3 N0 M0 improves overall survival, biochemical and
clinical disease-free survival with the highest impact in cases of positive margins (R1)
• An alternative option is to give radiation at the time of biochemical failure, but before PSA
rises above 0.5 ng/mL
• In locally advanced prostate cancer T3-4 N0 M0, overall survival is improved by concomitant
and adjuvant hormonal therapy for a total duration of 3 years, with external beam irradiation for
patients with a WHO 0-2 performance status.
• For a subset of patients with T2c-T3 N0-x and a Gleason score of 2-6, short-term ADT before
and during radiotherapy may favourably influence overall survival
• In very high-risk prostate cancer, c-pN1 M0 with no severe co-morbidity, pelvic external
irradiation and immediate long-term adjuvant hormonal treatment improve overall survival,
disease-specific failure, metastatic failure and biochemical control

4. Experimental local treatment of prostate cancer[29-32]under invstigations

• Cyrosurgery:
– Patients with low-risk PCa (PSA < 10 ng/mL, < T2a, Gleason score < 6) or intermediate-risk
PCa (PSA > 10 ng/mL, or Gleason score > 7, or stage > 2b) represent potential candidates for
CSAP.
– Prostate size should be < 40 mL at the time of therapy.
– Long-term results are lacking, while 5-year biochemical progression free rates are inferior to
those achieved by RP in low risk patients. Patients must be informed accordingly.
• Cryosurgery - a possible alternative treatment for PCa in patients who are unfit for surgery or
with a life expectancy < 10 years.
• All other minimally invasive treatment options – such as HIFU microwave and electrosurgery –
are still experimental or investigational.
• Focal therapy of PCa is still in its infancy and cannot be recommended as a therapeutic
alternative outside clinical trials

r) Hormonal therapy[33-4]

Bone densitometry and bisphosphonates

17. In advanced PCa, androgen deprivation therapy (ADT)
18. delays progression,
19. prevents potentially catastrophic complications, and
20. palliates symptoms effectively, but does not prolong survival.
21. In advanced PCa, all forms of castration used as monotherapy (e.g. orchiectomy, LHRH and
DES) have equivalent efficacy.
22. Non-steroidal anti-androgen monotherapy (e.g. bicalutamide) is an alternative to castration in
patients with locally advanced disease.
23. In metastatic PCa, the addition of a non-steroidal anti-androgen to castration (CAB) results in
a small advantage in OS over castration alone, but is associated with increased adverse events,
reduced QoL, and high costs.
24. Intermittent ADT should no longer be regarded as experimental, even though long-term data
from prospective clinical trials are still awaited. ‘Minimal’ ADT should, however, continue to be
seen as experimental.
25. In advanced PCa, immediate ADT (given at diagnosis) significantly reduces disease
progression, as well as the complication rate due to progression itself, compared with deferred
ADT (delivered at symptomatic progression). However, the survival benefit is at best marginal
and not related to cancer-specific survival.
26. Bilateral orchiectomy might be the most cost-effective form of ADT, especially if initiated
after the occurrence of symptoms from metastatic disease.
Follow-up [47-50]
After treatment with curative intent
14. In asymptomatic patients, a disease-specific history & a serum PSA measurement
supplemented by DRE - recommended tests for routine follow-up. These should be performed at
3, 6 & 12 months after treatment, then every 6 months until 3 years, and then annually.
15. After radical prostatectomy, a serum PSA level of more than 0.2 ng/mL can be associated
with residual or recurrent disease.
16. After radiation therapy, a rising PSA level over 2 ng/mL above the nadir PSA, rather than a
specific threshold value, is the most reliable sign of persistent or recurrent disease.
17. Both a palpable nodule and a rising serum PSA level can be signs of local disease recurrence
18. Detection of local recurrence by TRUS and biopsy is only recommended if it will affect the
treatment plan.
19. In most cases TRUS and biopsy are not necessary before second-line therapy.
20. Metastasis may be detected by pelvic CT/MRI or bone scan. In asymptomatic patients, these
examinations may be omitted if the serum PSA level < 120 ng/mL.
21. Routine bone scans & other imaging studies are not recommended in asymptomatic patients.
If a patient has bone pain, a bone scan should be considered irrespective of the serum PSA level.

After hormonal therapy [51-53]

• Patients should first be evaluated at three & six months after the initiation of treatment. (one
month and 3 months after initiating treatment)
• As a minimum,
• serum PSA measurement
• digital rectal examination (DRE),
• serum testosterone and careful evaluation of symptoms in order to assess the treatment
response and the side-effects of the treatments given.
• Follow-up should be tailored for the individual patient, according to symptoms, prognostic
factors and the treatment given.
• In patients with stage M0 disease with a good treatment response, follow-up is scheduled every
six months, and should include as a minimum a disease-specific history, DRE and serum PSA
determination
• In patients with stage M1 disease with a good treatment response, follow-up is scheduled for
every three to six months.
• As a minimum, this should include a disease-specific history, DRE and serum PSA
determination, and is frequently supplemented with haemoglobin, serum creatinine and alkaline
phosphatase measurements.
• Patients (especially if M1b status) should be advised on the clinical signs that could suggest
spinal cord compression
• When disease progression occurs, or if the patient does not respond to the treatment given, the
follow-up needs to be individualised
• Routine imaging of stable patients is not recommended

Treatment of biochemical failure after treatment with curative intent [54- 61]
Presumed local failure after radical prostatectomy
• Patients with presumed local failure only may be candidates for salvage radiotherapy. At least
64 Gy given and preferably before PSA has risen above 0.5 ng/mL.
• Other patients are best offered a period of watchful waiting (active monitoring), with possible
hormonal therapy later on
• Presumed local failure after radiotherapy
• Selected patients may be candidates for salvage radical prostatectomy and patients should be
informed about the higher risk of complications, such as incontinence and erectile dysfunction.
• Salvage prostatectomy should only be performed in experienced centres. Other patients are best
offered a period of watchful waiting (active monitoring), with possible hormonal therapy later on
• Presumed distant failure
• There is some evidence that early hormonal therapy may be of benefit in +/- local failure,
delaying progression, and possibly achieving a survival benefit in comparison with delayed
therapy.
• Local therapy is not recommended except for palliative reasons

Castration refractory prostate cancer (CRPC or HRPC)-

• Definition:
– Serum castration levels of testosterone (testosterone < 50 ng/dL or < 1.7 nmol/L)
– Three consecutive rises of PSA, 1 week apart, resulting in two 50% increases over the nadir,
with a PSA > 2 ng/mL
– Anti-androgen withdrawal for at least 4 weeks*
– PSA progression, despite consecutive hormonal manipulations†
• * Either anti-androgen withdrawal or one secondary hormonal manipulation should have been
done in order to fulfil the criteria for CRPC.
• † Progression of osseous lesions: progression or appearance of two or more lesions on bone
scan or soft tissue lesions using RECIST (Response Evaluation Criteria in Solid Tumours) and
with nodes > 2 cm in diameter.

CRPC-
Recommendation of treatment after hormonal treatment
• It is recommended to stop anti-androgen therapy once PSA progression is documented
• Four to six weeks after discontinuation of flutamide or bicalutamide, an eventual anti-androgen
withdrawal effect is apparent
• No clear-cut recommendation can be made for the most effective drug for secondary hormonal
manipulations. Secondary hormonal manipulations possibilities
• Abiraterone and Cabazitaxel have shown to prolong survival in CRPC after docetaxel
chemotherapy. Sipuleucel T is prostate vaccine which is used and has been approved in the west
for CRPC which is minimally symptomatic or asymptomatic. Not yet available in India.

Recommendation of cytotoxic therapy

26. Ideally, patients with CRPC should be counselled, managed and treated in a multidisciplinary
team
27. In non-metastatic CRPC, cytotoxic therapy should only be considered in clinical trials
28. In patients with a PSA rise only, two consecutive increases of PSA serum levels above a
previous reference level should be documented
29. Prior to treatment, PSA serum levels should be > 2 ng/mL to assure correct interpretation of
therapeutic efficacy
30. Potential benefits of cytotoxic therapy and expected side-effects should be discussed with
each individual patient
31. In patients with metastatic CRPC, and who are candidates for cytotoxic therapy, docetaxel at
75 mg/m2 every 3 weeks has shown a significant survival benefit
32. In patients with symptomatic osseous metastases due to CRPC, either docetaxel or
mitoxantrone with prednisone or hydrocortisone are viable therapeutic options
33. Second-line docetaxel should be considered in previously responding patients to docetaxel.
34. Otherwise, treatment is tailored to the individual patient
35. Cabazitaxel should be considered as effective second-line treatment following docetaxel
36. Chemotherapeutic drugs/ targeted therapy for cancer prostate patients should be decided and
administered under supervision of a Urologist.

Recommendation of palliative management

• Patients with symptomatic and extensive osseous metastases cannot benefit from medical
treatment with regard to prolongation of life
• Management of these patients has to be directed at improvement of QoL and mainly pain
reduction
• Effective medical management with the highest efficacy and a low frequency of side-effects is
the major goal of therapy
• Bisphosphonates may be offered to patients with skeletal masses (mainly zoledronic acid has
been studied) to prevent osseous complications. However, the benefits must be balanced against
the toxicity of these agents, in particular jaw necrosis must be avoided
• Palliative treatments such as radionuclides, external beam radiotherapy, adequate use of
analgesics should be considered early in the management of painful osseous metastases
• Spinal surgery or decompressive radiotherapy are emergency surgeries which have to be
considered in patients with neurological symptoms might be an emergency

Denosumab is more efficacious in preventing skeletal related events than Zoledronic acid with
no need to adjust dose for mild to moderate renal dysfunction
Referral criteria for Urologist :

ed prostate cancer / metastases

*Situation 1: At Secondary Hospital / Non-Metro Situation: Optimal Standards Of
Treatment In Situations Where Technology And Resources Are Limited.
a) Clinical diagnosis:Hard, nodular, asymmetric prostatic enlargement in digital rectal
examination.
b) Investigations: Ultrasound of abdomen and pelvis (preferably by trans rectal ultrasound) – to
assess the size and echotexture of prostate and to assess the tumour factors.
c) Treatment:According to the stageof the disease.
Standard operating procedure:
Inpatient:
Outpatient
Daycare:

Referral criteria:
Men who come with LUTS with DRE showing hard nodular prostate
Localized prostate cancer
Men with advanced prostate cancer / metastases
*Situation 2: At super speciality facitlity in metro location where higher end technology is
available.
a) Clinical diagnosis; DRE and look for metastatic lesions.
b) Investigations: All the possible investigations mentioned.
c) Treatment:According to the stage of the disease and the treatment options selected by the
patient after counseling.
Standard operating procedure
a) Inpatient
b) Outpatient
c) Daycare
Referral Criteria:
For diagnosis and staging – TRUS guided biopsy of prostate (depending on centers of
excellence)
Evaluation of metastatic disease – bone scan
Extensive metastatic disease requiring advanced speciality care like radiopharmaceuticals, spine
decompression surgery and neurosurgery.
VI. WHO DOES WHAT? AND TIMELINES
q. Doctor – clinical diagnosis, treatment
r. Nurse – counseling, Preoperative preparation, essential post-operative care.
s. Technician – Investigations like serum PSA, bone scan and for administering treatment like
radiopahramaceuticals.

168. Testicular Swelling – Testicular Torsion

General comments:
Clinical guideline are supposed to be reflections of the best currently available evidence. They
have 2 parts –
c. A systematic review of the best available evidence and the strength of that evidence.
I. The methodology of systematic review is important. This should be clearly stated. All relevant
studies should be studied. If Indian studies are available, then they should be included. The
evidence should then be ranked using a standard system e.g. levels of evidence - Oxford Centre
for Evidence-based Medicine [1]. If necessary relevant focused questions can be framed in order
to exactly define the purview of the exercise.
d. Recommendations for practice based on that evidence. These should be graded according to
the level of available evidence.

The standard treatment guidelines for testicular torsion fail to mention if it is based on based on
current literature following a systematic review. If the literature on testicular torsion lacks well
designed studies that are amenable to a structured analysis, this should be mentioned. The
evidence for the statements made here should be mentioned. There is no grading of the
recommendations. If due to lack of sufficient high quality evidence this document will largely be
a consensus document, this should be mentioned.
Review
V. OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT &
REFERRAL CRITERIA
Diagnostic criteria:
7. Blue dot sign – testicular appendix torsion – Unlikely to be seen in dark skin. This should be
mentioned.

Investigation
The diagnosis of testicular torsion is mainly clinical as mentioned. In case of a strong suspicion
of torsion testes, waiting for a USG ( with or without Doppler) can result in significant delay and
loss of viability.
If at all a USG is to be included in the guideline, it should be accompanied by a rider that - in
case of a strong suspicion of torsion testes the USG cannot be performed within 30 minutes,
scrotal exploration is recommended. It should be emphasized that by no means should be time
between presentation to the surgeon and exploration in strongly suspected cases exceed 1
hour.Treatment
It is not necessary to lay down the steps of surgery. Guidelines are not cookbooks. It is enough to
recommend scrotal exploration and fixation of the contralateral testes. While fixation of the
testes with in a subdartos pouch is a good technique, it is by no means the only technique.
Concluding remarks
With the above alterations, it will be suitable for publication.
References:
• Center for evidence based medicine, Oxford, UK http://www.cebm.net/index.aspx?o=1025.
Accessed on 1st April, 2012.
 General medicine

169. PAIN
Why do we get pain?
When any part of the body is overused or injured or diseased, we feel pain. Pain is
thus, a warning to us of disease. So that we can rest that part and take necessary
corrective measures. It follows that not all pain is bad. It serves a purpose. It tells us
of the need for rest or indicates an underlying disease. Treating pain alone is not
enough. But if the pain is too much one can get relief from pain relieving drugs.
170. HEADACHE

171 ABDOMINAL PAIN

3.1 UPPER ABDOMINAL PAIN :
When to refer at once?
� All Acute abdominal pain when accompanied by
� vomiting and no passing of stools or flatus.
� On examination there is Stiffness of abdominal wall or distension and
severe pain.
This is likely to be an acute abdomen requiring surgery.
Refer to a surgical centre at the earliest.

172. CHEST PAIN

General measures –
� Daily mild exercise.
� Avoid smoking.
� Avoid fats in food.
� Weight reduction if overweight.
� Reducing mental tensions or physical strain.
are all essential steps that must go along with drug treatment.

173. Other pains

General Precautions
1. Do not use aspirin for abdominal pain or those with nausea and vomiting.
2. In most situations, one must ensure an early referral especially if it does not cure
within three days or if one of the above features are present.
3. Note – a lot of new painkillers available in the market offer little or no advantage
over paracetamol. All of them have much more side effects than paracetamol. Always
prefer paracetamol
174. FEVER
Fever is usually a symptom of an infection. It is in a sense a sign of the
body trying to overcome an infection. Since it causes discomfort, we treat fever but
the aim must be to find out what infection is causing the fever and to treat that.
Very often, fever subsides by itself in 3-4 days. These self-limiting fevers
are generally caused by viruses. All other fevers need treatment.
General guidelines
� Advice rest in bed as long as there is fever.
� Give plenty of fluids to drink-water, rice water, soup, buttermilk etc.
� Meals should be light. Avoid oily, spicy food. But do not starve the patient.
� Record the fever using a thermometer. If it is more than 37 o Celsius, there is
fever. If it more than 39.5o Celsius, then one must sponge the patient with tepid
water to lower the temperature and refer the patient if the fever does not come
down.
� If patient is uncomfortable or has bodyache or headache, give paracetamol
thrice a day.
� Undress the patient. Small children may be undressed completely.
6.2 FEVER WITHOUT ANY LOCAL SYMPTOMS
If the fever for only one or two days :
� Get a blood smear done for malaria
� Give paracetamol and if needed sponging to lower the fever.
� Treat with chloroquine as if it is malaria. (page 128)
� If smear turns out to be positive for Malaria
� give primaquine also. (page 129)
� If smear if negative repeat blood smear and look for other causes.
If the fever is of more than a week :
� If there are typical features of chills and shivering, followed by high fever
and then sweating; often has headache also, is probably malaria–treat as
malaria.
� Get a blood smear done: if it shows malarial parasites treat as advised
� If smear is negative or report is delayed more than one day or not available and
chloroquine has been given consider the following :
� If fever is persistent; patient is sick and worsening; has headache; sometimes
replies slowly and in a confused manner to questions, sometimes diarrhoea/
constipation is present : think of typhoid. refer to a centre which has
Widal test.
If no referral centres available then start presumptively for treatment with
antibiotics for typhoid while blood is sent for the Widal report or patient is
persuaded to go to higher centre. (See page 125)
� If there is loss of weight and appetite – it may be tuberculosis affecting an
organ other then lung- Sometimes esp. in children cough may not be present.
for tuberculosis, see page 151
� Consider filariasis. see page 139
� Consider abscess in hidden location – behind liver, in bone, beneath
tooth etc.
� Consider noninfectious causes – auto-immune disease, drug fevers, and
malignancy.
32
When to refer ?
� Refer all fevers where no diagnosis is established and if after one round of antibiotics
over three to five days there is no improvement of fever.
� Even before 5 days, one must refer if one sees that :
� Patient is drowsy or confused or incoherent or unconscious or has fits.
� If there is severe headache and vomiting.
� If the patient is very ill, too weak to eat or drink or is dehydrated and
needs admission.
� If child has rapid breathing (over 40 breaths/minute or above for 1
year old 50/minute for infants below 1 year old) or chest indrawing or
there is great difficulty in breathing.
� Significant Lymph node enlargement.

7. COUGH
Why do we cough ?
Most types of cough do not require drug treatment. Basically cough cleans the windpipe
throwing out irritating material, which may reach it from outside or is produced locally.
Therefore, cough is a friend not an enemy. Some of the cough is due to allergy due to
irritants. Some common irritants are smoke, dust particles, pollen grains, germs.
General guidelines
1. Try to avoid irritants. Do not suppress the cough.
2. Cold dry air worsens cough. Warm, humid air is beneficial. Simple steam inhalation
and lots of warm fluids provide the best relief. Few drugs are better than this.
3. In case there is plenty of sputum, encourage patient to cough voluntarily. The
sputum must come out.
Obstetrics and Gynecology
209. ANTE PARTUM HAEMORRHAGE

Definition: APH is defined as bleeding from or into the genital tract occurring from 24th week of
pregnancy and prior to the birth of the baby

Why it occurs? The causes of APH include placenta previa,abruption placenta,local causes and
unexplained causes. Local causes comprise vasa previa and cervical or vaginal causes.

Commonly it is due to:

Placenta previa

Abruptio placenta

It may also be due to: - Exaggerated show, - Trauma to cervix or vagina - Cervical ectropion, - Carcinoma
of cervix or polyps - Vasa previa

How to diagnose Placenta Previa?

Definition: The term placenta previa refers to a placenta that overlies or is proximate to the internal os of
the cervix. The placenta normally implants in the upper uterine segment. In placenta previa, the placenta
either totally or partially lies within the lower uterine segment.

Incidence: 1 in 300 pregnancies Maternal morbidity and mortality is high if it is not treated properly.
Perinatal morbidity and mortality also are primarily related to the complications of placenta previa,
because the hemorrhage is maternal.

Predisposing factors:

o Advancing maternal age

o Multiparty 13

o Multifetal gestations

o Prior caesarean delivery o Prior placenta previa

Differential Diagnosis: Abruptio placentae, other probable causes.

Optimal Diagnostic Criteria, investigations, treatment and referral criteria: Situation 1: At Secondary
Hospital/ Non-Metro situation: (Optimal Standards of Treatment in Situations where technology and
resources are limited)-

a) Clinical Diagnosis: It is on the basis of history, physical examination and investigations.

History: Nature of bleeding:

Painless, recurrent, bright red. Initial bleeding may

 not be profuse enough to cause death; but it is a warning sign and requires close monitoring or refer the
patient to higher centre. On physical examination: Patient might be in shock

 – Abdominal examination: Height of uterus proportionate to gestational age, presenting part may be felt
high up (not engaged).

– Malpresentations, malpositions usually present

. – Uterine contraction may or may not be present. Some degree of uterine irritability is present in about
20% of the cases.

– Fetal heart sound may or may not be present, depending upon theamount of blood loss.

If you suspect placenta previa, do not perform a vaginal examination without preparation. Per vaginal
examination should be done in theatre but without any anesthesia with all preparations of immediate
cesarean section.

b) Investigations:

Blood investigations (Full blood count, blood group and type)

 14 Ultrasound examination: Rules out types of placenta previa; fetal anomalies

, fetal parameters, presentation and position. Transabdominal ultrasonography (TAS)

: It should be with partially full bladder

. It is a simple, precise, and safe method to visualize the placenta

. TAS has an accuracy of 93-98%

. Four types of placenta praevia according to abdominal sonography

 Type I- Dips in to lower segment

Type II - Reaches lower border of uterus up to cervical os but not covering completely.

Type III- covers the internal os

Type IV - Covers the internal os, even on full dilatation of the cervix. At 18 weeks, 5-10% of placentas
are low lying. Most ‘migrate’ with development of the lower uterine segment.

False-positive results can occur secondary to focal uterine contractions or bladder distention.

Transvaginal ultrasonography (TVS):

Recent studies have shown that the transvaginal method is safer and more accurate than the
transabdominal method.
Transvaginal ultrasonography is also considered more accurate than transabdominal ultrasonography. –
Skilled person should only do.

– The os–placental edge distance on TVS after 35 weeks’ gestation is valuable in planning route of
delivery. When the placental edge lies > 20 mm away from the internal cervical os, women can be offered
a trial of labour with a high expectation of success. A distance of 20 to 0 mm away from the os is
associated with a higher CS rate, although vaginal delivery is still possible depending on the clinical
circumstances. – In general, any degree of overlap (> 0 mm) after 35 weeks is an indication for Caesarean
section as the route of delivery

c) Treatment : Assess the blood loss

 Resuscitate:

 15 Monitor BP

 Start IV Line

 Restore blood volume by infusing normal saline

 Explain the need of blood transfusion

The definitive treatment depends upon the duration of pregnancy, fetal and maternal status and extent of
hemorrhage: Type I and Type II anterior - vaginal delivery can be expected. Trial of vaginal delivery
can be given and caesarean is done if patient bleeds Type II -b, III & IV - Elective/emergency
caesarean section has to be done at the earliest.

210. CARDIAC DISEASE IN PREGNANCY

WHEN TO SUSPECT / RECOGNISE?

The physiological adaptations of normal pregnancy can induce symptoms and alter clinical findings that
may confound the diagnosis of heart disease. Heart disease should be suspected or diagnosed at booking
for antenatal women. Heart disease may be suspected when a pregnant lady presents with symptoms of
progressive dyspnea or orthopnea, nocturnal cough, hemoptysis, syncope or chest pain. When there are
clinical findings like cyanosis, clubbing, distended neck veins, systolic murmur of grade 3/6 or greater,
diastolic murmur, cardiomegaly, persistent arrhythmias, persistent split second sound, or pulmonary
hypertension.
Introduction: The incidence of heart disease in pregnancy is 1% and it is the third leading cause of death
in women of reproductive age group. Risk of maternal mortality ranges from 0 to 50% depending on the
cardiac condition.

Case definition: Rheumatic Heart Disease (RHD) remains an important cause of heart disease especially
in developing countries like India. A large number of women undergoing valve replacement surgeries on
oral anticoagulants warrant specialized care during pregnancy and childbirth. With advances in paediatric
cardiac surgery more women with congenital heart disease (CHD) are now surviving and reaching child
bearing age. Ischemic heart disease is also on the rise as a result of increase prevalence of obesity,
hypertension and diabetes in young adults and delayed child bearing. Maternal mortality is higher in
conditions that restrict an increase in pulmonary blood flow especially pulmonary hypertension and mitral
stenosis. The situation is at its worst 28 in Eisenmengers syndrome, where there is refractory hypoxaemia
when the mortality is 25 to 50 %. Other cardiac complications associated with pregnancy include
infective endocarditis, cardiac arrhythmias, development of cardiomyopathy. Fetal outcome in
pregnancies complicated by maternal RHD is usually good although there is an increased incidence of
growth restriction and preterm birth. The effects of maternal anticoagulant therapy with warfarin could
lead to abortions, stillbirths in 7%, warfarin embryopathy in 8%of live born infants. Warfarin exposure in
the 2nd and 3rd trimesters could lead to disharmonic growth of organs due to hemorrhage in the fetus and
deformation from scarring leading to corpus callosum agenesis, Dandy Walker malformation, cerebellar
midline atrophy, optic atrophy and blindness, microphthalmia, mental retardation and developmental
delay. Anticoagulation may be indicated in certain cardiac conditions such as mechanical heart valves,
atrial fibrillation and pulmonary hypertension. Fetal growth restriction and preterm birth are more
common in pregnancies complicated by CHD with restricted maternal cardiac output, especially poor in
cyanotic varieties when the fetal wastage rates may be as high as 40%. The etiology of CHD is
multifactorial and incidence is 0.8 %. Incidence of CHD in the offsprings of parents with CHD ranges
from 5 -10%. However, risk may be as high as 50% as in Marfan’s syndrome.

. PREVENTION AND COUNSELING

Women may be aware of their cardiac condition before falling pregnant. An assessment of the patient’s
clinical status and ventricular function are necessary to best predict the outcome of pregnancy. In more
than 50% of women it is first diagnosed during pregnancy.

A Cardiologist should be involved in initial assessment and followup. In some women, life threatening
cardiac abnormalities can be reversed by corrective surgery and subsequent pregnancy is less dangerous.

Women with conditions like pulmonary hypertension, severe left sided obstructive lesions, dilated
aortopathy(>4cm) and severe systemic ventricular dysfunction should be counseled for early termination
of pregnancy to avoid maternal mortality.

Concurrent medical problems like infections, anaemia should be aggressively treated.

Pneumococcal and influenza vaccines are recommended to avoid respiratory infections precipitating
cardiac failure. Cigarette smoking and illicit drug abuses are prohibited to prevent cardiorespiratory side
effects and infective endocarditis.
Women with cardiac disease should be counseled regarding the risk of maternal death, possible reduction
in maternal life expectancy, fetal issues, need for timely switch over of anticoagulant therapy, need for
frequent hospital attendance and possible admission, intense feto-maternal monitoring during labour.

DIFFERENTIAL DIAGNOSIS

Normal physiological changes of pregnancy

b) Anaemia

OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT & REFERRAL CRITERIA

.

Treatment:

Clinical diagnosis A clinical suspicion or recognition of cardiac disease based on history, clinical
symptoms and signs as explained above is made.

.Investigations Basic work up as in any pregnancy like complete blood counts, urine routine, blood
grouping Rhtyping, VDRL, serology, APTT, PT, INR, ultrasound for dating, aneuploidy screening,
anomaly scan. Fetal echocardiography when indicated depending upon the risk of transmission.
Nonivasive studies like electrocardiography, echocardiography and chest radiography with abdominal
shielding can be conducted during pregnancy to support the diagnosis. 34 If indicated, cardiac
catheterization can be performed with limited x-ray fluoroscopy by an interventional cardiologist.

Treatment Clinical Classification Schemes commonly used are that of NYHA and ACOG. These
classification systems are useful to clinicians to evaluate the functional capacity and to aid in counseling
the woman regarding advisability of conception or continuation of pregnancy

The management in most instances is by a multidisciplinary team involving: Obstetrician Cardiologist

Cardiac Anaesthetist Neonatologist Intensivists

Antenatal period Severe mitral stenosis is associated with a higher risk of pulmonary edema. Both beta
blockers and balloon mitral valvotomy are safe in pregnancy. Pulmonary edema should be treated in the
usual way with oxygen and diuretics.

Women with prosthetic heart valves on oral anticoagulants will need replacement with heparin in early
pregnancy between 6 to 12 weeks, to prevent embryopathy. Again warfarin should be discontinued and
replaced with heparin at 35-36 weeks to allow clearance of warfarin from the circulation. Heparin is
discontinued 4-6hrs before delivery and regional anesthesia to minimize risks of obstetric hemorrhage and
spinal hematoma. Intravenous heparin is restarted 6 hrs after vaginal delivery and 24 hours after a
caesarean section. Warfarin is usually started the night after delivery provided there are no bleeding
complications and heparin is continued until 35 an INR of 2 or more is achieved. In an emergency
situation VitK or fresh frozen plasma can be used to reverse warfarin anticoagulation and protamine
sulfate for heparin anticoagulation.

Labor and Delivery

Vaginal delivery is recommended unless there is an obstetric indication for cesarean section

. 1. Await spontaneous onset of labor and induction of labor should be very judiciously attempted to
minimize risk of intervention thereby hemorrhage and infections.

2. Careful fluid balance with central venous pressure monitoring may be necessary to manage conditions
like mitral stenosis and aortic stenosis optimally. Such monitoring is rarely indicated in women who have
remained in functional class1& 2

3. Avoid supine position. A semi recumbent position with lateral tilt is preferred.

4. Monitor vitals - pulse, respiration, BP, Oxygen saturation and intake output.

5. Epidural analgesia is administered by cardiac anaesthetist judiciously based on the cardiac

hemodynamics, as it causes hypotension.

6. Cut short 2nd stage of labor with outlet forceps or vacuum extractor to reduce maternal effort.

7. Infective endocarditis prophylaxis to be given with broad spectrum antibiotics.

8. Avoid methyl ergometrine which causes intense vasoconstriction, hypertension and heart failure.
Instead use syntocinon for delivery of placenta. Epidural anesthesia is preferred by most clinicians.
Hypotension can be very hazardous with pulmonary hypertension or aortic stenosis , when narcotic
conduction analgesia or general anesthesia may be preferable

Peripartum Cardiomyopathy

Risk factors include multiparity, multiple pregnancy, hypertension, increased age.

Diagnostic criteria a) Development of cardiac failure in the last month of pregnancy or within 5 months
after delivery. b) Absence of an identifiable cause for the cardiac failure. c) Absence of recognizable heart
disease prior to the last month of pregnancy d) LV systolic dysfunction shown on echo as ejection
fraction 2.7cm/sqm

Recommended treatment

a) Fluid and salt restriction, treatment of hypertension, routine exercise postpartum if stable. b) Drugs like
digoxin, beta blockers, diuretics, vasodilators may be used. c) In selected patients’ aldosterone
antagonists, inotropes, anticoagulation, implantable defibrillators, biventricular pacing, cardiac
transplantation may be the last resort. Prognosis and recurrence depends on the normalization of left
ventricular size within 6 months of delivery.

211. BLEEDING IN FIRST TERM OF PREGNANCY

Abortion
Definition: An abortion also called miscarriage is the loss of the pregnancy prior to viability
(before 22 weeks of pregnancy or less than 500 g).
Types
Therapeutic abortion,
Unsafe Abortion,
Threatened Abortion,
Incomplete abortion,
Complete Abortion,
Septic Abortion,
Missed Abortion
, Blighted ovum
Causes
- Chromosomal abnormalities
- Reproductive tract abnormalities (Myoma, uterine abnormality, cervical incompetence) -
Endocrinal abnormalities (thyroid diseases, lutheal phase defect)
- Infections (listeria, Chlamydia….) - Environnemental (stress, smoking) - Others (Unknown,
Trauma, Intoxication)

Signs and symptoms - General • History of amenorrhea • Vaginal bleeding • Abdominal

cramps/pain • Endo-uterine bleeding on speculum

- Specific • Threatening abortion: the cervix is closed • Inevitable abortion: the cervix is open and
the products of conception are still in utero • Incomplete abortion: the cervix is open and the
products of conception are not com pletelyevacuated • Complete abortion: the cervix is open and
the products of conception are not present • Missed abortion: the heart beat is absent • Blighted
Ovum: gestational sac present but absence of the embryo
Complications - Hypovolemic shock - Infection - Septic shock – Anaemia
Investigations - Pregnancy test positive - Ultrasound - Complete Blood Count, Blood Group - For
repeated Miscariage refer to a gynecologist for the following investigations: genetical,
Immunological profile, Infection Screening, Hysteroscopy, Endocrine
Management
Threatened Abortion
Bed rest and avoid Intercourse • Progesterone (Utrogestan) Oral 100mg tablet three times daily
for 1 month Or CLINICAL TREATMENT GUIDELINES - GYNECOLOGY AND
OBSTETRICS 9 Chapiter 1: OBSTETRIC/ Bleeding in first term of pregnancy • Progesterone
(Utrogestan) Vaginal 200mg twice daily for 1 month • Review every week until Symptoms
resolve or immediately if any complications
Inevitable abortion
Assess the general status of the patient • If unstable Ș Correct the hypovolemic shock then
proceed with surgical management (Manual Vacuum Aspiration (MVA), Electric aspiration,
Dilatation and Curettage (D & C)) • If stable: Discuss with the patient the following op tions: Ș
Expectant management (As for threatened abortion) Ș Medical Management: Give Misoprostol
400 mcg-800 mcg (2-4 tablets) every 6 hours per os and/or vaginal ■ S/E: Diarrhea, Pain due to
uterine contraction, Increase of temperature with shivering both are dose dependant and settle
 rapidly without treatment Ș Surgical treatment: Manual Vacuum Aspiration (MVA), Electric
aspiration, Dilatation and Curettage (D & C) • If blood group Rhesus: Give Immunoglobuline:
Anti-D 300 µg IM single dose
Incomplete abortion
Assess the general status of the patient: • If unstable Pregnancy Bleeding in 10 CLINICAL
TREATMENT GUIDELINES - GYNECOLOGY AND OBSTETRICS Chapiter 1:
OBSTETRIC/ Bleeding in first term of pregnancy Ș Correct the hypovolemic shock then proceed
with surgical management (Manual Vacuum Aspiration (MVA), Electric aspiration, Dilatation
and Curettage (D & C))
If stable: Discuss with the patient the following options: Ș Medical Management: Give
Misoprostol 400 mcg-800 mcg (2-4 tablets) every 6 hours per os and/or vaginal Ș Surgical:
Manual Vacuum Aspiration (MVA), Electric aspiration, Dilatation and Curettage (D & C) • If
blood group Rhesus–Give Immunoglobuline: Anti-D 300 µg IM single dose
Complete Abortion • Assess the general status of the patient • If unstable: correct the
hypovolemic shock. • If stable: Reassure the patient • If blood group Rhesus –ve give
Immunoglobuline: AntiD 300 µg IM single dose
Missed abortion and Blighted Ovum • Give Misoprostol 400 mcg-800 mcg (2-4 tablets) every 6
hours per os and/or vaginal Ș Posology ■ Cervical ripening prior to uterine instrumentation: 400
mcg, vaginal or per os 3 hours before the procedure ■ Missed abortion (< 12 weeks gestation):
800mcg every 24 hours vaginal or sublingual for 2 days ■ Missed abortion (12-22 week
gestation): 200mcg every 12 hours vaginal or sublingual for 2 days or 400mcg oral every four
hours until expulsion
• Surgical Management: Manual Vacuum Aspiration (MVA), Electric aspiration, Dilatation and
Curettage (D & C) • If blood group Rhesus–Give Immunoglobuline: Anti-D 300 µg IM single
dose
Septic abortion
Assess the general status of the patient • If unstable Ș Correct the hypovolemic and/or septic
shock then proceed with surgical management (Manual Vacuum Aspiration (MVA), Electric
aspiration, Dilatation and Curettage (D & C)) • If stable: Surgical Management
Antibiotics Post abortion:
Treatment of first choice Ș Ampicilline IV 1 g every 6 hours, Gentamycine 160 mg Once daily
and Metronidazole IV 500mg every 8 hours for 48 hrs. Ș Then give after 48hrs: Amoxycilline
500 mg PO TDS 5/7 ■ C/I: allergy to betalactamine Ș Metronidazole 500mg PO TDS 7/7 •
Alternative treatment –if allergic to B-lactamines Ș Erythromycine 500 mg PO TDS 7/7

212. Ectopic Pregnancy

Ntroduction

When implantation of the embryo occurs outside the uterine cavity is called ectopic pregnancy. Common
site of implantation is in the fallopian tube. The risk of death from an undiagnosed ectopic pregnancy is
greater than that of an induced abortion or delivery. Therefore slogan is “If you think ectopic then only
you can diagnose ectopic”. Earlier the diagnosis, better is the prognosis with conservation of the
reproductive capacity. Chances of a subsequent successful pregnancy are reduced in these women.

Risk factors for ectopic pregnancy

PID Endometriosis IUCD use Progesterone only contraceptive pill use Pregnancy after tubal
ligation, tubal surgery ovulation induction and assisted reproduction techniques

I Case definition: For both situations of care (mentioned below) Implantation of the embryo anywhere
else other than the endometrial lining of the uterine cavity is an ectopic pregnancy.

III. Differential diagnosis: Very early intrauterine pregnancy Heterotopic pregnancy 48 IV Optimal
diagnostic criteria, investigations, treatment

Clinical Diagnosis: Presentation could be diverse depends on whether rupture has occurred. The
reproductive age group woman may present with amenorrhoea, bleeding pv, pain abdomen, sometimes
with shock due to rupture.

Investigations: 1. A urine pregnancy test should be positive 2. Ultrasound –abdominal/ vaginal-

thickened echogenic endometrium, absent intrauterine gestational sac, sometimes a pseudosac, fluid in the
culde sac, occasionally haematosalpinx, adnexal mass or a tubal ring representing the gestational sac. 3.
Culdocentesis if ultrasound facility is not available 4. Blood grouping crossmatching and reservation 5.
Histopathological examination of the operative specimen to confirm diagnosis.

Special investigations: 1. Serum Beta hCG titres need estimation serially to facilitate expectant
management or medical manangement with Methotrexate. When Methotrexate is used: 1. Complete blood
count 2. Liver function test 3. Renal function test

c) Treatment: The standard aim of care is to control the bleeding and remove the ectopic pregnancy. Start
an IV line, arrange for blood transfusion, rush patient to the operating room. General anaesthesia, IV
antibiotic prophylaxis given and catherised. Abdomen entered through a transverse suprapubic inscision.
The affected tube is brought out and salpingectomy is performed. Strict haemostatsis secured. Peritoneal
cavity cleared of blood and blood products. Mops and instruments counted and abdomen closed in layers.
Blood transfused depending on the amount of loss and post op hemoglobin. 49 Inj Anti D
immunoglobulin given if the lady is Rh negative and husband Rh positive Patient should be advised to
report immediately in future pregnancies

When ruptured ectopic is diagnosed laparotomy may be done as in situation 1. When laparoscopy is
chosen- Salpingostomy or salpingectomy is peformed. Expectant management : Proportion of all ectopics
will not progress to tubal rupture, but will regress spontaneously and be slowly absorbed. Level of hCG
must fall and the woman becomes clinically well.

it is an option for clinically stable asymptomatic women with an ultrasound diagnosis of ectopic
pregnancy and a decreasing serum hCG, initially less than serum 1000 iu/l.(ref rcog greentop) Women
managed expectantly should be followed twice weekly with serial hCG measurements and weekly by
transvaginal examinations to ensure a rapidly decreasing hCG level (ideally less than 50% of its initial
level within seven days) and a reduction in the size of adnexal mass by seven days. Thereafter, weekly
hCG and transvaginal ultrasound examinations are advised until serum hCG levels are less than 20 iu/l .
On hcg monitoring if the level increases or plateaues ,active medical management is resorted to.

Medical management with Methotrexate –. (rcog greentop) The most widely used medical treatment at
present is intramuscular methotrexate given as a single dose calculated from patient body surface area.

Dose: A single dose of 1mg/kg body weight or 50mg/square metre body surface area of methotrexate
given intramuscularly in addition to leukovorum (folic acid antagonist) 0.1mg/kg IM. Methotrexate
should not exceed 4 doses. There is 70-95% efficiency in the treated cases. It takes 4-6 weeks for the
complete resolution of ectopic pregnancy with methotrexate. Methotrexate is also useful in the
management of persistent ectopic which is a complication of conservative surgical treatment and
incomplete removal of trophoblastic tissue.

Serum hCG levels are checked on days four and seven and a further dose is given if hCG levels have
failed to fall by more than 15% between day four and day seven. Large uncontrolled studies have reported
that about 14% of women will require more than one dose of methotrexate and less than 10% of women
treated with this regimen will require surgical intervention.

Can be considered for women with confirmed or high suspicion for ectopic pregnancy who are
hemodynamically stable with no evidence of rupture.

Absolute contraindications are breast feeding, immunodeficiency, alcoholism, blood dyscrasias, active
pulmonary disease ,peptic ulcer disease,hepatic renal or hematologic disorder. Gestation sac larger than
3.5 cm and embryonic cardiac motion are relative contraindications

Molar pregnancy
Definition: It is a trophoblastic disease characterised by abnormal proliferation of the
trophoblastic cells with vesicular chorionic villi transformation
Cause - Chromosomal abnormality
Types - Complete mole - Partial mole
Signs and symptoms - Amenorrhea - Vaginal bleeding - Expulsion of molar vesicles -
Exacerbated hyperemesis gravidarum - The uterus is soft and larger than the gestational age
associated to para uterine luteinic cysts
Complications - Choriocarcinoma - Invasive mole - Placenta site trophoblastic tumor -
Hypertensive disorders of pregnancy
Investigations - ß HCG rapidly increased - Ultrasound - Full Blood Count - Cross match and
Rhesus
Management - Resuscitation if necessary - Aspiration under Ultrasound guidance - Administer
Oxytocin after aspiration - Products of evacuation should be sent for Histology Examination -
Post molar surveillance: • Monitor levels of ß HCG every 48 hrs for the 1st week, then weekly till
ß HCG is normal for 3 weeks, then test every month for 6 months. - If ß HCG is persistently high
• More likely persistent trophoblastic diseases (Choriocarcinoma, Invasive mole and Placenta site
tumor…) which require chemotherapy • Test renal and liver function prior and during treatment •
Staging of the disease prior to treatment
 Recommendations - Immediate contraception during 1 year of post molar monitoring. - Review if
any Vaginal bleeding problem. - If blood group Rhesus negative(Rh-): Give Immuno globuline:
Anti-D 300 µg IM single dose - Consider prophylactic Chemotherapy in case of unreliable
patient for follow-up

. Placenta praevia
Definition: The placenta embeds itself in the lower pole of the uterus, partially or wholly
covering the internal os in front of the presenting part.
Risk factors - Prior placenta praevia - Large placental area (Multiple pregnancies…) - Advanced
maternal age and High parity - Deficient endometrium (uterine scar, curettage, endome tritis,
fibroids…) - Uterine malformations
Types Low lying, marginal, partial and complete placenta praevia
Signs and symptoms - Sudden onset of bright red fresh painless hemorrhage after 22 weeks of
gestation - Unusual irritability and tenderness - Often malpresentation of the fetus - Endo-uterine
cavity hemorrhage on speculum examination
Complications - Hemorrhagic shock - Fetal distress - Anemia Late Pregnancy Bleeding in in late
pregnancy and intra-partum period - Prematurity - Fetal death and/or maternal death
Investigations - Complete blood Count, blood group/Rhesus – Ultrasound
Management
During pregnancy
Asymptomatic : Bed rest Ș Follow up every 2 weeks Ș If complete placenta praevia ■ Admit for
fetal lung maturation ≥ 24 weeks of gestation ■ Program a Cesarean section at 37-38 weeks of
gestation Ș Iron supplements
Symptomatic : Obligatory admission, do FBC and Blood group crossmatch, blood coagulation
tests Ș Surveillance of fetal heart rate Ș Ultrasound Ș Term >34 weeks of gestation ■ If minimal
hemorrhage and no uterine contractions: Expectant management ■ If Uterine contractions º
Complete placenta praevia or malpresentation: perfom Cesarean section. º Partial or marginal
placenta preavia: Carefully perform amniotom for vaginal delivery if the head is engaged.
Term

ABRUPTIO PLACENTA

Definition: Abruptio placenta is the detachment of a normally located placenta from the uterus before the
fetus is delivered. It is an obstetric emergency.

Types: It can be classified as- Revealed (separation of placenta with blood visible outside

) Concealed (blood collects behind the separated placenta. Not visible outside)

 Mixed, (common type).

According to Sher clinical grading for placental separation

1. Grade 1: (Herald bleed) diagnosed retrospectively 1. Less than 100cc -150cc of uterine bleeding 2.
Uterus non-tender 3. No Fetal Distress
2. Grade 2 ; Classical features of abruption 1. Uterus tender 2. Fetal Distress 3. Concealed hemorrhage

3. Grade 3 1. Fetal death 2. Maternal shock 3. Extensive concealed hemorrhage 4. Coagulopathy

Causes: unknown

. But following are risk factors:

o Increased age and parity

o Preeclampsia/ Chronic hypertension

o Preterm ruptured membranes

o Multifetal gestation o Hydramnios

o Cigarette smoking o Thrombophilias

o Prior abruption o Uterine leiomyoma

o External trauma (Sudden jerk or assault over abdomen)

o Anaemia

o Short cord.

Complications: Complications include the following:

o Maternal blood loss leading to shock, disseminated intravascular coagulation [DIC], mult-iorgan
failure. o Fetal distress or death

o IUGR if chronic and mild.

o In Rh negative mothers, chances of feto-maternal transfusion and Rh sensitization.

o Prematurity Optimal diagnostic criteria, investigations, treatment & referral criteria for Abruptio
placentae are following:

Clinical Diagnosis: Detailed history, physical examination and investigations, will be done to confirm the
diagnosis.

b) Investigations: Blood count, Blood grouping and typing, cross match, Coagulogram for DIC screen.

c) Ultrasound: Evaluation of fetal presentation, size, fetal well-being and placental localization and
separation.

d) Treatment: Admit

 History & examinations Assess blood loss .It is always more than revealed
. Treatment for placental abruption varies depending on gestational age and the status of the mother and
fetus. Begin continuous external fetal monitoring for both the fetal heart rate and contractions. Obtain
intravenous access using 2 large-bore intravenous lines. Institute crystalloid fluid resuscitation for the
patient. Type and cross match blood. Begin a transfusion if the patient is hemodynamically unstable
after fluid resuscitation. Correct coagulopathy, if present Administer Rh immune globulin if the patient
is Rh-negative.

Management of coagulopathy

Indicators for prompt delivery:

Fetal distress (Non-reassuring fetal heart rate pattern).

b. Maternal hemodynamic instability.

c. DIC 24

d. Labor

e. Term

Vaginal delivery is acceptable as early as possible (generally preferred with DIC). If bleeding is heavy
(revealed or concealed) deliver as soon as possible. Patient has to be delivered within 8 hours by
Artificial rupture of membrane and Oxytocin 2.5units (not more than 5 units) in 500 cc of Dextrose. If
cervix is fully dilated deliver by forceps or vaccum extractor. If vaginal delivery is not imminent or fetus
is alive deliver by cesarean section. All precautions for the prophylaxis of third stage of labor. In every
case of abruptio placentae, be prepared for postpartum haemorrhage.

Uterine Rupture
Definition: Uterine rupture refers to a tear or separation of the uterine wall
Causes/Risk factors - Previous uterine scar - Malpresentation and Malposition - Misuse of
uterotonics - Placenta insertion anomalies - Multiparity - Retracted pelvis - Obstructed labour -
Uterine manoeuvers - Instrumental deliveries - Trial of labor after cesarian section – Unkown
Signs and Symptoms - Pre-rupture bandle ring sign - Sudden, severe abdominal pain (may
decrease after rupture) - Bleeding – intra-abdominal and / or vaginal - Cessation of uterine
contractions - Tender abdomen - Absent fetal heart activity Easily palpable fetal parts on the
abdomen - Rapid maternal pulse - Hypovolaemic shock most of the time - Abdominal distension
/ free fluid
Complications - Fetal demise - Bladder laceration - Uterine multi-laceration leading to
Hysterectomy - Maternal death
Investigations - Full blood Count and blood group crossmatch - Clotting profile - CTG
monitoring - Ultrasound in a stable patient (In cases of uterine dehis cence suspicion)
Management
Non-Phramaceutical • Call for assistance – Senior obstetrician, pediatrician and anaesthetist for
assistance • Administer oxygen via face mask 6L/min • Blood Group and cross match, Order 2-4
units of packed red cells and order complete blood picture • Ensure the woman remains with her
legs bent or in lithotomy to perfuse the brain • Insert 2 large intravenous access using 14-16
gauge cannulas with appropriate intravenous fluid, e.g. sodium chloride 0.9 % or Hartmann’s
solution and gelatin based colloid or Haemacel.
• Assess for clinical signs of shock e.g. cool, clammy, pale, rapid pulse, decreased blood pressure
• Inform the patient and family Surgical Management • Emergency laparotomy: Conservative or
hysterectomy and repair complications (Bladder or ureter tear…)

POSTPARTUM HEMORRHAGE (PPH)

Definition - Loss of more than 500 ml of blood from the genital tract in the first 24 hours after
vaginal delivery and more than 1000 ml after cesarean section. - Excessive vaginal bleeding
resulting in signs of hyovolemia (Hypotension, Tachycardia, oliguria, light headedness) - A 10%
decline in post partum hemoglobin concentration from antepartum levels
Types - Primary: Occurs within first 24 hrs - Secondary: After 24hrs to the end of puerperium
(42days after delivery)
Risk factors - Overdistension of the uterus (Polyhydramnios, Multiple pregnancies,
Macrosomia…) - Grand multiparity - Previous history of PPH - Ante-partum hemorrhage -
Myomatous uterus - Hypertensive disorders - Drug use (Mgso4, Salbutamol…)
Causes - Atonic uterus (70%) - Genital tract trauma (20%) - Retained placenta or placenta
fragment (10%) - Coagulopathy (1%)
Signs and Symptoms - Continuous vaginal bleeding - Signs of Hypovolemic shock (low BP,
rapid pulse, cold and clammy skin) - Signs of Anemia (Palor, tachycardia, sweeling)
Complications - Hypovolemic shock - Sheehan syndrome - Renal failure - Anemia – Death
Investigations - FBC - Blood group crossmatch - Blotting profile
Management - Principles • Resuscitation of the mother • Identification of the specific cause of
PPH • Call for help (Obstetrician, Anesthesist, midwife…) • Management is done following the
figure below

COMPLICATIONS DURING PREGNANCY

Hyperemesis gravidarum

Definition: Severe nausea and vomiting in early pregnancy requiring hospital admission and
rehydration
Causes/Pathogenesis - Hormonal: High levels of β Human chorionic gonadotrophin (β hCG),
progesterone and oestrogen like in multiple pregnancy and Hydatiforme mole. -
Mechanical: There is a fall in lower oesophageal pressure, decreased gastric peristalsis and
gastric emptying in pregnancy - Emotional: Various psychological, family conflicts, prior
hyperemesis and social factors are associated with hyperemesis - Infection (UTI) - Endocrine
disorders (Hyperthyroidism)
Signs and Symptoms - Weight loss - Nausea and Vomiting typically in Early Pregnancy -
Dehydration - Altered general status (Fast pulse, restlessness)
 Complications - Metabolic disorder (Hyponatraemia, Hypokalaemia, metabolic hypochloraemic
alkalosis, Ketonuria) that may lead to coma - Malory-Weiss Syndrome. - Neurological disorder
(Wernicke’s encephalopathy) - Depression - Cachexia - Pregnancy termination – Death
Investigations - Full Blood count - Blood for urea, electrolytes and serum creatinine - Urinalysis,
microurine and culture, Ketonuria - Liver function tests - Thyroid function tests - Obstetric
ultrasound
Management Non-pharmaceutical management • Nil per os for 24-48 hrs • Monitor diuresis each
4hrs for 24-48 hrs • Isolation • Monitor electrolytes for 24hrs
Pharmaceutical management • Intravenous rehydration: Alternate Ringers lactate with Normal
saline according to daily needs and severity. • B-1 (Thiamine) 100mg per day in intravenous
rehydration solution
And
Antiemetics First choice Ș Metoclopromide: IM 5-10 mg TDS till ceasing of vomitting.
Ș And always associate Pyridoxine hydrochloride: IV or PO 10-25 mg TDS
Alternative Treatment: Administer one of the following medicine Ș Chlopromazine: 12.5-25 mg
IM/IV/PO three times daily Ș H-1 blockers (Meclezine 20mg Tabs once daily or twice daily if
needed) Ș Ondansentron (Emitino) 4mg IV/PO two times daily Ș Domperidone (Motilium) PO
10mg three times daily or 60mg per rectal two times daily Ș Corticosteroids: Dexamethasone
4mg PO/IV two times daily.

ANEMIA IN PREGNANCY

Anemia is defined as a decrease in the oxygen carrying capacity of the blood due to decrease in amount of
RBCs or haemoglobin or both.

WHEN TO SUSPECT/ RECOGNIZE?

WHO - Hemoglobin -11gm/dl or less

-Mild 8-11 gm/dl

-Moderate 5-7 gm/dl –

Severe below 5 gm/dl

ICMR categories

 -Mild 10-10.9 gm/d

l -Moderate 7-10 gm/dl

-Severe below 7gm/d

l -Very severe(decompensated) below 4gm/dl RBC

Introduction:
Anemia is a major problem in women of child bearing age in developing countries with effects that may
be deleterious to mothers and fetuses.

In India, anemia is directly or indirectly responsible for 40 percent of maternal deaths due to
haemorrhage, cardiac failure ,infection & preeclampsia . India contributes to about 80 per cent of the
maternal deaths due to anemia in South Asia. There is 8 to 10-fold increase in MMR when the Hb falls
below 5 g/dl. Maternal anemia is associated with increased perinatal morbidity & mortality rates
consequent to IUGR, preterm births, low iron stores and cognitive & affective dysfunction in the infant.
India was the first developing country to take up a National Programme to prevent anemia among
pregnant women and children. The National Anemia Prophylaxis Programme of iron and folic acid
distribution to all pregnant women in India through the primary health care system was evolved and
implemented from 1972. In order to tackle this public health problem, a multipronged 12 x 12 initiative
has also been launched in the country. The initiative is targeted at all adolescents across the country with
the aim for achieving hemoglobin level of 12 gm% by the age of 12 years by 2012.

III.DIFFERENTIAL DIAGNOSIS Nutritional Hemorrhagic Hemoglobinopathies Bone marrow

disorder HIV Drug induced Tuberculosis Inherited disordersAnemia caused by inflammation,
malignancy, chronic diseases & autoimmune disorders

PTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT & REFERRAL CRITERIA

Complete medical history and Physical examination is very important.

Clinical Diagnosis

Symptoms: 1. Weakness 2. Easy fatiguability 3. Lassitude 4. Dizziness or vertigo especially when

standing 5. Headache 6. Irritability 7. Indigestion, loss of appetite 8. Breathlessness 9. Palpitations 10.
Generalized swelling 11. Symptoms due to cause of anemia like yellowing of skin & mucous membranes,
bleeding from rectum et

Signs: 1. Pallor 2. Icterus 3. Glossitis, stomatitis 4. Koilonychia 5. Tachycardia, systolic murmurs,

bounding pulse 6. Fine crepitations at lung bases 57 7. Splenomegaly 8. Hepatomegaly 9. Edema

b)Investigations: Hb% PCV Peripheral smear for immature cells, type of anemia and MP. Urine
routine and microscopy, Urine C/S if required Stool for Routine and microscopy USG abdomen

CBC with peripheral smear Reticulocyte count 61 Red cell indices LFT, RFT, LDH Coombs Test
Iron studies - serum iron - serum iron binding capacity - serum ferritin Hb electrophoresis Bone
marrow aspiration/ Biopsy

c) Treatment: Although there are several different forms of anemia, this health profile will only address
the three most common: iron-deficiency anemia, vitamin B12 anemia and folic acid deficiency.

Non-drug treatment

Awareness/ Education Improvement of dietary habits-diet rich in Vit C, protein and iron, cooking in
iron utensils, avoiding tea & coffee intake with meals & overcooking Food Fortification Social
services such as improvement of sanitation & personal hygiene for eradication of helminthiasis Annual
screening for those with risk factors Routine screening for anaemia & providing iron supplementation
for adolescent girls from school days

Iron rich foods: Pulses, cereals, jaggery, Beet root, Green leafy vegetables, nuts, meat, liver, poultry, Egg,
fish, legumes, dry beans, and dry fruits viz: dates, figs, apricots etc .

Drug treatment: Prophylaxis WHO recommendation

60mg elemental iron and 0.25mg folic acid daily 58 To be given for 6 months in countries with
prevalence 40%

Treatment of Iron deficiency has included: Oral iron Parenteral iron Blood transfusion

Oral Iron - First line therapy - 200mg FeSo4 (60mg elemental iron)2- 3 times daily in conjunction with
folic acid. - If patient is non-compliant to oral therapy or if there is gastritis, then reduce doses & give it
after meals or change over to ascorbic acid/ carbonyl iron or parenteral therapy. - Diagnostic reevaluation
if there is no significant clinical or haematological improvement within 3 weeks.

Parenteral Therapy

Indications: - Hb less than 7g/dl and pregnancy >30 weeks - Malabsorption Syndrome - Incapacitating
side effects with oral iron

Preparations: - Iron sucrose - Iron dextran 59 - Iron sorbitol citrate

Total iron deficit (mg) = Amount of iron deficit + amount of iron to replenish stores Amount of iron
deficit (mg) = (Hb target- Hb initial)gm/dl x Body wt (Kg) × 2.2 + Stores

Or ( 100-Hb initial)% x Body wt (Pounds) x 0.3 + Stores

Where

Stores (mg) = 50% of deficit or approx 1000mg Iron Sucrose Complex is considered to show a significant
improvement of Hb and iron stores in pregnant women. The target Hb may be taken as 11gm% for the
Indian population according to WHO guidelines.

Deworming necessary : - Albendazole 400 mg single dose - Mebendazole 500 mg single dose or 100 mg
twice daily for 3 days - Levamisole 2.5 mg/kg single dose, best if a second dose is repeated on next 2
consecutive days - Pyrantel 10 mg/kg single dose, best if dose is repeated on next 2 consecutive days - To
prevent recurrence, patients should be advised to use footwear, improve sanitation, and personal hygiene.
Malaria prophylaxis in endemic area to be treated.

Treatment of Folic Acid/ Vitamin B12 deficiency

Tab. Folic acid 5 mg daily

Prophylactic - all woman of reproductive age should be given 400mcg of folic acid daily.
Preventive daily or intermittent iron or iron+folic acid supplementation taken by women during
pregnancy reduces anaemia in mothers. There is evidence that taking iron or iron and 60 folic acid daily
or intermittently has a similar effect in reducing anaemia at term and improving haemoglobin
concentrations in the mother.

Vitamin B12 deficiency:

Oral preparation of Vitamin B12 (not very effective) In Moderate cases- 1000mcg of Parenteral
Cynocobalamine every month In Severe cases 1000mcg/day for 1 week, following by weekly for 1 month

d)Referral criteria: Hb less than 5 gm% in all trimesters, less than 7gm% if >36weeks Cases not
responding to treatment Associated with medical disorders eg:leukaemias/ other obstetric
complications Haemolysis or evidence of bone marrow suppression Other types of anemia(Sickle cell
anemia, Thalasemia) Level II USG to rule out fetal complication/ compromise by CVS/ Amniocentesis
. If any of the below suspected, as the below are common in pregnancy:

Maternal risks during Antenatal period: Poor weight gain, preeclampsia, eclampsia, placenta previa,
accidental haemorrhage, premature rupture of membranes, pre term labour, cardiac failure etc. - Maternal
risks during Intranatal period: Dysfunctional labour, accidental hemorrhage, shock, anesthesia risk,
cardiac failure, if signs of respiratory distress - Maternal risks during Postnatal period: Postnatal sepsis,
sub involution, embolism, PPH (primary, secondary).

Blood Transfusion Packed cells to be transfused. Indications - Hb < 7 gm/dl & POG > 36 weeks - Hb < 6
gm/dl & POG < 36 weeks - CHF due to anaemia(exchange transfusion) - Replenish blood loss due to
APH/PPH - Not responding to oral & parenteral therapy Diagnosis & management of sickle cell
disease, Haemoglobinopathies, Pancytopenia in cases not responsive to iron. Manage congestive cardiac
failure/ PIH / Placenta Previa if associated/ where indicated. Megaloblastic Anemia VitB 12 or Folic
Acid Supplementation

LABOUR MANAGEMENT: 62 Oxygen and other measures to deal with heart failure and PPH to be
kept ready. To cut short second stage by Outlet forceps/vacuum delivery of fetus. To routinely employ
active management of third stage of labour. LSCS only for Obstetric Indications

POSTPARTUM MANAGEMENT: Iron should be continued till the patient restores her normal clinical
& haematological state & for an additional 3 months for store replenishment. Dietary advice Effective
method of contraception as per WHO guidelines & should not conceive for atleast 2 years giving time
for iron stores to recover. Sterilization is preferred if the family is complete.

. Cervical incompetence
Definition: Painless cervical dilation and shortening leading to mid-tremister loss often repetitive
and caused by anatomical or dysfunctional cervical incompetence
Risk factors - Functional or structural defect of the cervix - Prior cervical trauma (e.g. Repeated
cervical dilata tion and curettage and other cervical sur gical proce dures) - Uterine anomalies
(congenital cervical hypoplasia or aplasia) - In utero diethylstilbestrol exposure
Signs and Symptoms - Recurrent mid trimester losses without contractions with a live fetus -
Cervical length < 25 mm prior to 27 weeks on ultrasound - Premature rupture of membranes
Complications - Habitual loss of the fetus - Premature Rupture of membranes - Prematurity -
Infection - Depression - Secondary infertility
Investigations - Transvaginal Ultrasonography (Cervical length, dilatation and funneling of the
membranes) - Urine analysis, Vaginal and cervical swab before cerclage
Management
Prophylactic cervical cerclage
gestation Ș Give Progesterone supplementation 100mg PO/ vaginal three times daily until 20
weeks of amenorrhea for prevention of uterine contraction • If Infection treat before doing
cerclage • Decerclage at 37 weeks or at anytime if infection or bleeding or contractions. •
Consider prophlylactic antibiotics Ampicilline 2g IV Single dose. O OR • Cefotaxime 1 g single
Dose.
Emergency cervical cerclage: gestation after 14-24 wks
• If no infection cerclage is done immediately by a gynecologist.
If Infection treat before doing cerclage • Give Progesterone supplementation 100mg PO or
vaginal three times daily to prevent uterine contractions. • Non-steroids anti-inflammatory drugs
(Diclofenac 100mg suppository twice daily for 3-5 days, Indomethacin 100mg suppository twice
daily for 3-5 days) • Decerclage at 37 weeks or at anytime if rupture of membranes, bleeding or
contractions. • Consider prophlylactic antibiotics Ampicilline 2g IV single dose. OR •
Cefotaxime IV 1g single dose

Mal-presentations and mal-positions

Definitions - Lie: refers to the relationship of the long axis of the fetus to that of the mother. It
may be longitudinal, transverse or oblique - Presentation: refers to the portion of the fetus that is
foremost or presenting in the birth canal. - Malpresentations: all presentations of the fetus other
than the vertex. - Position: reference point on the presenting part, and how it relates to the
maternal pelvis. Normal position is Occiput anterior position (OA): when the foetal oc ciput is
directed towards the mother’s symphyisis or anteriorly - Mal position: Occipital Posterior (OP).
When the fetal occiput is directed towards the mother’s sacrum or posteriorly
Types
- Malpresentations: • Brow • Face • Breech
Ș Complete (flexed) breech presentation occurs when both legs are flexed at the hips and the
knees Ș Frank (extended) breech presentation occurs when both legs are flexed at the hips and
extended at the knees Ș Footling breech presentation occurs when a leg is extended at the hip and
the knee
Transverse • Compound - Malpositions: • Occiput Posterior Position (OP): when the fetal occiput
is directed towards the mother’s spine or posteriorly • Intermediate positions (Bregma)
Causes - Defects of the power: Laxity of the abdominal muscles, exaggerated dextrorotation of
the uterus - Defects of passage: Contracted Pelvis, android pelvis, pelvic tumor, uterine anomaly
and placenta previa. - Defect of passenger: Preterm fetus, macrosomia, multiple pregnancy, poly
hydramnios, anacephaly and hydrocephaly, Intauterine fetal death
Diagnosis and Management
Brow presentation: Partial extension of the fetal head before fixation on the pelvic brim • On
vaginal examination Ș The anterior fontannel and the orbital notches are felt, the referral point is
the nasal apex. The chin is not felt
Management Ș Deliver by C/S
Face presentation:
Hyperextension of the fetal head • On vaginal examination Ș The face is palpable and the point of
reference is the chin. You should feel the mouth and be careful not to confuse it with breech
presentation. Ș It is necessary to distinguish the chin-anterior position from chin- posterior
position
Management Chin-anterior position ■ If the cervix is fully dilated: vaginal delivery ■ If there is
slow progress and no sign of obstruction, augment labor ■ If descent is unsatisfactory, perform a
C/S Ș Chin-posterior position ■ Deliver by C/S
Breech presentation
Occurs when the buttocks and/or the feet are the presenting part • On the abdominal examination
Ș The head is felt in the upper abdomen and the breech in the pelvic brim • On vaginal
examination Ș The buttocks and/or feet are felt, thick dark meconium is normal • Complications
Ș Entrapment of the after coming head Ș Nuchal arm
• Management
Consider external cephalic version at 37 weeks if all requirements are met (Adequate amniotic
fluid, Placenta in fundal position, No uterine anomalies, No previous uterine scar, availability of
theatre) Ș Ideally, every breech delivery should take place in a hospital with surgical capability. Ș
Determine most favorable mode of delivery
Contraindications to vaginal delivery are : Ș Unfavorable pelvis, primigravida, macrosomia,
severe prematurity, IUGR, placental insufficiency, footling breech, hyperextension of fetal head,
fetal anomalies, nuchal arm, PROM or non-progressive labor Note: Vaginal breech delivery is
safe and feasible by a skilled health provider
Compound presentation : Occurs when an arm prolapses alongside with the presenting part • On
Vaginal Examnation Ș Fingers/Arm is felt with the presenting part
Management Ș Replace the arm and if sucessful continue with viginal delivery Ș If Contracted
pelvis and/or cord prolapse: Do a C – section
Transverse Presentation::
: Longitudinal axis of the foetus does not coinside with that of the mother
During pregnancy:
Inspection: abdomen is broader from side to side Ș Palpation: the fundus feels empty and the
fundal level is lower than expected Ș Ultrasound confirms the diagnosis
During labor:
Ș On vaginal examination the scapular is felt as point of reference
Ș Ultrasound confirms the diagnosis
Complications Ș Arm prolapse Ș Infection Ș Umbilical cord prolapse Ș Uterine rupture Ș Fetal
and maternal death
Management: Ș Deliver by Cesarean section
Occiput Posterior position (OP): : the fetus lies with its occiput towards the mother’s spine and its
face towards the mother’s symphysis and abdomen. • On vaginal examination: Ș The anterior
fontanelle is palpated Ș Identify the sagittal suture which is mostly asymmetric Ș Dilation is often
asymmetric, you can feel the fetal ear and a persistent anterior cervical lip is common
Management
Spontaneous delivery is possible: Make sure uterine contractions are adequate and no fetal
distress Ș Manual Rotation Ș Vacuum extraction delivery Ș Cesarean delivery should always be
the backup method of delivery for any Occiput posterior presentation that cannot be safely
delivered vaginally

.Multiple gestation
Definition: More than one foetus in the uterus. Mostly twin pregnancy but others may be
encountered, triplets or plus Definition: More than one foetus in the uterus. Mostly twin
pregnancy but others may be encountered, triplets or plus
Causes/Risk factors - Use of fertility reproduction (in vitro fertilization, ovulation induction) -
Hereditary factors - Previous multiple pregnancy
Signs and Symptoms - Fundal height larger the gestational age - Two audible fetal heart beats -
Multiple fetal parts or more than two fetal poles - Exaggerated symptoms of Pregnancy
Complications - Increased risk of Miscarriage - Prematurity - Pregnancy induced Hypertension -
Intrauterine fetal growth retardation - Malpresentations - Pregnancy induced diabetes -
Polyhydramnios - Antepartum and post-partum hemorrhage - Fetal transfusion syndrome (Twin-
twin transfusion syndrome) - Placenta praevia - Premature rupture of membranes
Investigations - Ultrasound to determine chorionicity - Blood sugar – FBC
Management
Antenatal
Routine antenatal care • Hb check • Monitor for associated obstetric complications to determine:
presentation of first twin, detect anomalies, mode of delivery • Bed rest • Increase nutrition
Mode of delivery:
Elective Cesarean section if Ș Previous Uterine scar Ș The first Twin is not cephalic Ș More than
two fetuses • Vaginal Delivery if Ș The first Twin is cephalic • Otherwise do a Caesarean section
if Ș Retained second twin • For Vaginal Delivery Ș Perform abdominal and vaginal examination
and assess: membranes; if intact perform amniotomy Ș Look for evidence of fetal and maternal
distress and manage accordingly If assessment favorable then oxytocin and delivery Ș C/S if the
evolution is poor. • Third Stage Ș Look for and anticipate post partum hemorrhage.

Hypertension in pregnancy/Preeclampsia
Definition: -when high blood pressure is noted during pregnancy, it may be one of the following:
Gestational Hypertension: new onset BP elevation of systolic >140mmHg/ diastolic >90mmHg
on 2 occasions 6 hrs apart after 20 wks gestation in a previously normotensive woman
Preeclampsia - gestational hypertension and persistent proteinuria ≥ 1+ on dipstick urine
analysis or >300mg/24 hours occurring >20 weeks pregnancy in a previously normotensive, non
proteinuric woman. Oedema is not a defining sign of PE. Eclampsia - Generalized convulsions
occurring after the 20th week of pregnancy in a patient with underlying pre-ecclampsia
Complications If not recognized and managed appropriately, preeclampsia can result in
complications such as eclampsia, hypertensive encephalopathy, pulmonary edema, liver
haematoma/rupture, renal failure, ARDS, HELLP syndrome, disseminated intravascular
coagulation, cortical blindness.
Prediction
Roll over test at 28 -30 wks: increased blood pressure of 20mmHg when patient rolls over from
lateral to supine position means a positive test. The test has a high negative predictive value
although the positive predictive value is low.
If the facility for colour doppler is available it can be performed at 24-26 weeks: Persistence of
diastolic notching in uterine artery after second trimester can be predictive of preeclampsia
Prevention
Low dose Aspirin (50-100mg/d) may reduce the risk of PE by 15%. It can be started in high risk
at 20 weeks and has to be stopped at 34 weeks gestation.
Hospitalization: Mild – Hospitalization is advised although complete bed rest is not advisable.
Severe- Immediate hospitalization is recommended if BP ≥ 160/100 or alarm signs
Maternal Assessment: • Blood pressure measurement: At least 4 times a day, more often in severe
cases • Urine quantification (24 hour protein ) on admission, repeat not required • Blood tests:
Monitor kidney function, electrolytes, full blood count, transaminases, bilirubin twice a week in
mild preeclapsia and thrice a week in severe preeclampsia
Fetal Assessment: The following tests should be carried out at diagnosis: Cardiotocography
Ultrasound for fetal growth and amniotic fluid volume assessment Umbilical artery doppler
velocimetry
If the results of all fetal monitoring are normal, cardiotocography need not be repeated more than
weekly unless if there is deterioration in maternal condition, vaginal 89 bleeding, abdominal pain,
or reduced fetal movement. Repeat ultrasound for fetal growth, amniotic fluid volume assessment
or umbilical artery doppler velocimetry is also not required more than every 2 weeks. Diet should
be adequate in proteins; salt restriction is not advised in Preeclampsia.
Antihypertensive Therapy:
It can be initiated if DBP >100mmHg. Lower threshold may be considered if disease has arisen
before 28 wks. Aim is to keep DBP between 80–100 mmHg, and SBP less than 150 mmHg. In
mild PE, it reduces the occurrence of severe hypertension, but there is no benefit in terms of
maternal & fetal outcome. In severe hypertension therapy is mandatory to reduce the risk of
CVA. • Tab. Methydopa -250- 500 mg 3-4 times /day. • Tab. Labetalol-100-200 mg 2-3 /day.. •
Labetalol: IV regimen: 20 mg stat. If DBP>110 after 20 min, give 40mg; ↑ to 80 mg & then 80
mg to a total of 220mg. If no response, discuss with senior physicians and anaesthetists. • Use of
ACE inhibitors is contraindicated in pregnant woman • Nitroglycerine (NTG) drip may be useful
in hypertensive crisis: Dose - 50mg in 500ml 5%dextrose, start at 10ml/h, ↑ by 5ml every 10-15‘
till SBP ≈ 140mmHg
Anticonvulsants
Consider giving intravenous magnesium sulphate to women with severe pre-eclampsia who are in
a critical care setting if birth is planned within 24 hours.
Termination of Pregnancy:
fetal condition, risk factors and availability of neonatal intensive care. Severe PE: Terminate at
34 weeks. Induction before 34 weeks may be indicated if: severe hypertension develops
refractory to treatment maternal or fetal indications of worsening condition Corticosteroid for
Lung Maturity Two doses of betamethasone 12 mg IM 24 hours apart are recommended between
24- 36 weeks.
Intrapartum care In women with severe pre-eclampsia
Accurate recording of fluid balance (including delivery and postpartum blood loss, Intake/output
chart) and Maintenance crystalloid infusion - 85 ml/hour, or urinary 90 output in preceding hour
plus 30 ml. Diuretics and CVP monitoring may be required if pulmonary oedema is suspected. •
Measure blood pressure, hourly in women with mild or moderate hypertension and continually in
women with severe hypertension. Continue use of antihypertensive treatment during labour. • Do
not routinely limit the duration of the second stage of labour in women with stable mild or
moderate hypertension or if blood pressure is controlled within target ranges in women with
severe hypertension. Operative birth is recommended in the second stage of labour if severe
hypertension has not responded to initial treatment • Use of Methergine is contraindicated for
active management of 3rd stage.
Ceasarean Section n is indicated for severe IUGR/ primi remote from term with unfavorable
cervix, for fetal distress or other obstetric indications. Thrombo prophylaxis to be considered in
severe PIH.
Analgesia & Anesthesia Issues: • GA Risks: - Aspiration, laryngeal edema, difficult intubation,
pulmonary edema/ arrythmias precipitated by pressor response to intubation, neuro-muscular
blockade effect of mag sulf. • Continuous lumbar epidural preferred method of pain relief as well
as for cesarean section provided there is no coagulopathy and platelet count is > 50,000/cu mm. •
Need adequate pre-hydration of 1000 cc, Level should be advanced slowly to avoid low BP
Postpartum Care
Women with PE who did not require anti-hypertensives: Measure BP at least four times a day
while the woman is an inpatient, at least once between day 3 and day 5 after birth, and on
alternate days thereafter until normal. Ask about severe headache and epigastric pain each time
blood pressure is measured. Start antihypertensive treatment if blood pressure is ≥ 150/100
mmHg.
Women with PE who did not require anti-hypertensives: Measure BP at least four times a day
while the woman is an inpatient, at least once between day 3 and day 5 after birth, and on
alternate days thereafter until normal. Ask about severe headache and epigastric pain each time
blood pressure is measured. Start antihypertensive treatment if blood pressure is ≥ 150/100
mmHg.
Discharge the women when there are no symptoms of pre-eclampsia, BP is ≤ 149/99 mmHg, with
or without treatment, and blood test results are stable or improving. 91 All women who have had
pre-eclampsia should have a medical review 6–8 weeks after birth to detect those women who
still need antihypertensive treatment. Women who continue to have proteinuria (≥1+) a further
review is required after 3 months to assess kidney function. Specific investigations like aPLa,
LAC and thrombophilia screen may be needed.

Eclampsia
General Measures: • Do not leave patient alone • Call for help and inform consultants -
obstetrician & anesthetist on call • Prevent maternal injury: Place in semi-prone position,
guardrails on the bed, padded tongue blade b/w teeth. • Airway: Maintain patency, start oxygen
inhalation, suction of mouth secretions. • Breathing: Assess, Ventilate as required. • Circulation:
Left lateral tilt, If pulse, BP absent, initiate CPR, call ICU • After the seizure has ended, a 16- to
18-gauge IV line should be obtained for drawing specimens for laboratory studies and
administering fluids • Attach ECG, automatic BP monitors, pulse oximeter • Indwelling Urinary
catheter - Fluid input / output chart
Treatment and prophylaxis of seizures: Magnesium sulphate is the anticonvulsant drug of choice.
Loading Dose: 4 g IV over 10-15 minutes Prepared by adding 8 ml of 50% MgSO4 solution to 12
ml of N Saline/ 20 ml of 20% solution Maintainance Dose: 92 MgSO4 (50% solution) + 1ml
Lidocaine 2% given IM every 4 hrs into alternate buttock
Monitor the following parameters before giving a repeat dose - respiratory rate > 16
breaths/minute - urine output > 25 ml/hour, and - patellar reflexes are present • Remember to
subtract volume infused from total maintenance infusion volume (85 ml/hour) • A higher
maintenance dose may be required initially to prevent recurrent seizures - consultant must make
this decision • If seizure continues, or if seizures recur, give a second bolus of magnesium
sulphate: 2-4 g depending on weight of patient, over 5-10 minutes (2 g if < 70 kg and 4 g if > 70
kg) • If seizures continue despite a further bolus of Mg sulphate, Diazepam (10 mg IV) or
thiopentone (50 mg IV) can be given. Intubation may become necessary in such women. Further
seizures to be managed by IPPV & muscle relaxation.

Magnesium Toxicity: • If urine output < 100 ml in 4 hours withhold Magsulph and review overall
management with attention to fluid balance and blood loss • Absent patellar reflexes: Stop
MgSO4 infusion until reflexes return • Respiratory depression: Stop MgSO4 infusion, Give
oxygen via facemask and place in recovery position and Monitor closely • Respiratory arrest:
Stop MgSO4 infusion, Give Calcium gluconate (10 ml slow IV), Intubate and ventilate. • Cardiac
arrest: Commence CPR, Stop MgSO4 infusion, Give IV Calcium gluconate*, Intubate and
ventilate; If antenatal, immediate delivery
Other Anticonvulsant Drugs • Phenytoin - 20 mg/kg diluted in 100ml saline infused at maximum
rate of 50 mg/min IV over 15-20mts followed by 100mg IV 8 hrly. It may cause hypotension,
arrythmias, local phlebitis, and requires ECG monitoring • Diazepam - 10 mg IV at a rate of
1mg/min. It can cause maternal sedation, fetal respiratory depression, hypotonia and ↓ beat-to-
beat fetal heart variability
Treatment of Hypertension : 93 • Reduction of severe hypertension is mandatory to reduce the
risk of CVA & further seizures. • Insufficient evidence to recommend one antihypertensive in
preference to another and so the choice of which drug to use should depend on personal
preference and availability. • Labetalol (20mg IV ↑ to 40 and 80mg every 20’ to max. 220mg) It
may precipitate fetal distress, thereby necessitates continuous fetal heart rate monitoring. • NTG
drip (5µg/m iv infusion, ↑to max 100µg/m)
Fluid therapy: • Close monitoring of fluid intake and urine output is mandatory. Fluid therapy
should be limited to maintenance crystalloid (85ml/h or urine output in preceding hour plus
30ml) to avoid tissue overload, pulmonary edema & ARDS. Colloids remain in vascular tree and
unless used carefully can cause circulatory overload.
Antibiotics: Inj. Ampiciliin 500 mg x 6hrly IV to prevent infection
Associated Complications: HELLP syndrome (3%), Disseminated intravascular coagulation
(3%), renal failure (4%), ARDS (3%)
Differential Diagnosis - • Cerebral tumors, Cerebral venous thrombosis, Intracranial hemorrhage
• Drug overdoses, Electrolyte imbalance • Epilepsy, head trauma, Stroke (ischemic/ non-
ischemic)
Monitoring: • Record BP every 10 minutes. Reduce DBP to 90-100 mm Hg with antihypertensive
medication • Auscultate lungs for aspiration after convulsion ended • Monitor the neurologic
status, urine output, respirations, and fetal status
Laboratory workup: • CBC, RFT, LFT, Electrolytes, Glucose, PLT, Coagulation profile •
Urinalysis for proteinuria • Blood gases & Invasive PCWP monitoring may be necessary for
accurate fluid management in patients with pulmonary edema or anuria • USG abdomen may be
used to rule out abruptio placentae • CT scan/ MRI if focal neurological deficits or prolonged
coma
Delivery : • The definitive treatment of eclampsia is delivery. • Attempts to prolong pregnancy in
order to improve fetal maturity are unlikely to be of value. • However, it is inappropriate to
deliver an unstable mother even if there is fetal distress. • Once seizures are controlled, severe
hypertension treated, and hypoxia corrected, delivery can be expedited. • Vaginal delivery should
be considered but caesarean section is likely to be required in primigravidae remote from term
with an unfavourable cervix/ deteriorating maternal or fetal condition • After delivery, high
dependency care should be continued for a minimum of 24 hours.
During Post partum period : • Mag sulf for 24 hrs after delivery or after last fit whichever is later
• Continue Vital monitoring, antihypertensives, antibiotics • Counsel about next pregnancy
Can it be prevented? Vigilant ANC & a well-timed delivery may prevent eclampsia, and
Magnesium is routinely given to women with severe PE in the expectation that it prevents
progression to eclampsia, but fits which occur without warning may be impossible to prevent.

HIV in pregnancy

Definition: Transmission of HIV virus from the infected mother to child may occur during
pregnancy, labor, delivery, and breastfeeding
Risks of Transmission - High Viral load - Low CD 4 cell count - Prolonged labour - WHO
advanced clinical stage
Complication - Mother-to-child transmission
Investigations - Serologic test for HIV after counseling. - CD4 count, viral load, - Baseline tests
such as FBC, RFT, LFT tests. - Test for syphilis (VDRL) - Screen for opportunistic infections –
Ultrasonography
Management
PMTCT Protocol
HIV + pregnant women eligibles to ART Ș All pregnant women HIV positive from 14 weeks of
gestation without considering WHO clinical stage and without considering their CD4 count are
eligible to ART for life. Ș This treatment must start as soon as possible after 14 weeks Ș The
regimen : ■ Tenofovir 300mg + Lamivudine 300mg + Nevirapine 200mg (TDF + 3TC + NVP) ■
Women with renal failure will receive: Abacavir 300mg+ Lamivudine 150 mg +
Nevirapine 200mg: (ABC+ 3TC + NVP)
Pregnant women with CD4 > 350 who are starting treatment should be given regimen EFV (in
order to avoid NVP side effects. N: B Those already on treatment with NVP should continue the
same Regimen
The Regimen : ■ Tenofovir 300mg + Lamivudine 300mg + Efavirenz 600mg : (TDF + 3TC +
EFV)
HIV+ pregnant women previously exposed to single dose of NVP Ș The Regimen : ■ Tenofovir
300mg + Lamivudine 300mg +Lopinavir/Ritonavir (Kaletra) 250mg (TDF + 3TC + Lop/r)
HIV + pregnant women with renal failure. Ș The Regimen : ■ Abacavir 300mg+ Lamivudine 150
mg + Efavirenz 600mg: (ABC+ 3TC + EFV) • Women with renal failure and who had been
previously exposed to Single dose NVP will receive: Ș The Regimen: ■ Abacavir 300mg+
Lamivudine 150 mg +Lopinavir/Ritonavir (Kaletra) 250mg (ABC+ 3TC + Kaletra)
HIV + pregnant women with renal failure. Ș The Regimen : ■ Abacavir 300mg+ Lamivudine 150
mg + Efavirenz 600mg: (ABC+ 3TC + EFV) • Women with renal failure and who had been
previously exposed to Single dose NVP will receive: Ș The Regimen: ■ Abacavir 300mg+
Lamivudine 150 mg +Lopinavir/Ritonavir (Kaletra) 250mg (ABC+ 3TC + Kaletra) Ș Treat the
HIV + partner in serodiscordant couples regardless of the number of CD4 or the clinical stage. ■
With CD4 > 350 ART regimen to include EFV in order to avoid NVP side effects Ș If the woman
turns POSITIVE during breastfeeding period, she should start ARV triple therapy and the child
should continue daily Nevirapine (NVP) for 6 weeks from initiation of ARV to the mother.
Prophylaxis to HIV exposed infants ■ Breasfeeding and non-breastfeeding children: Daily
Nevirapine (NVP) syrup for 6 weeks.

Hepatitis B during pregnancy

Definition: Hepatitis B is a viral disease of liver with an incubation period of 6weeks -6months.
Transmission is by - Blood - Sexual intercource - Vertical transmission
Causes/Risk factors - Non-immune women with a history of: • Health care providers • Household
/ intimate contact with hepatitis B carrier • Sexual workers
Multiple sexual partners • Intravenous drug users • Tattoos / body piercing • Blood transfusion
recepients
Signs and Symptoms - Most of the time asymptomatic but symptomatic in 0.5% cases include: •
Jaundice, tiredness, dark urine • Liver cirrhosis and liver failure
Complications - Mother to child transmission during 1st trimester (10%), 3rd trimester (80-90%)
and highest during delivery - Low birth weight - Miscarriage, prematurity and stillbirth in acute
infection - Hepatocarcinoma in approximately 15-20%
Investigations - HBs Ag - HBeAg (the e antigen identifies a high infective status) - HBV viral
load (HBV DNA) provides an accurate reflection of infectivity (high risk carriers have high viral
loads) - Anti-HBe (anti-HBe or HBeAb positive status indicates the woman is at lower risk of
spreading HBV infection than HBeAg positive women) - Liver function test (repeat at 28 weeks)
- HBs Ag of partners
Management Intrapartum management • Caesarean section doesn’t reduce the incidence of
vertical transmission in positive women (HBsAg/HBeAg) • Avoid procedures that may inoculate
the baby, for example: Ș Fetal scalp electrodes Ș Fetal scalp blood sampling Ș Vigorous
aspiration of the baby Ș Instrumental modes of birth
At birth
Protective eyewear, gown / apron and gloves should be worn by the attending providers • Care of
the newborn baby Ș Standard precautions should be utilised when handling the baby Ș Delay
Konakion® (vitamin K1) injection and administer after the baby has been bathed to remove all
maternal blood Ș The baby should remain in the delivery room until transfer to the ward unless
transfer to the Neonatology is indicated Ș Give the baby Breast milk normally
Newborn Immunoglobulin and vaccination
Ș The Hepatitis B immunoglobulin (HBIG) and Hepatitis B vaccine (HB vaccine) should
preferably be given within 12 hours after birth to the baby of women who are: ■ HBsAg positive
■ HBeAg positive Note: Efficiency of the immunoglobulin and vaccine given within/less than
12hrs is greater than 90% Ș Dosage: ■ Give HBIG 100 units in an intramuscular injection (thigh)
within 12 hours of birth (must be within 48 hours as efficacy decreases markedly if delayed
beyond this time)
Recommendations - Blood for Hepatitis B status checking should be taken from the woman’s
partner and vaccination offered if the partner is non-immune - All babies born to HBsAg positive
women should be followed up according to the National Immunization Program. The baby’s
blood should be tested for HBsAg, antiHBc and anti-HBs - HBsAg positive women should be
followed up every 12 months to assess their liver function - Breast feeding is not contra-indicated
after treatment

Hepatitis c virus during pregnancy

Definition: Hepatitis C is a blood borne viral liver infection that can result in liver disease, such
as cirrhosis, liver failure and hepatocellular carcinoma The incubation period is six to ten weeks;
however, seroconversion may occur up to three months
Causes/Risk factors - Hepatitis C virus - Intravenous drug user (past or present) - Known
abnormal liver enzymes - Administration of blood products - History of organ transplant or
haemodialysis - Partner who is Hepatitis C positive
Signs and Symptoms - The initial acute hepatitis may not be diagnosed as symptoms are mild or
absent - Lethargy - Nausea - Right upper quadrant pain - Malaise - Headache – Jaundice
Complications - Cirrhosis - Hepatocellurar carcinoma
Investigation
- Clinical assessment for liver disease should include: • Full blood Count (routinely repeat at 28
weeks) • Liver function tests (including ALT, albumin and bilirubin) (repeat at 28 weeks
gestation) • Ac-anti HcVirus, Hepatitis C RNA PCR
Management
Antenatal screening
Routine screening for hepatitis C antibodies • If positive, repeat at 28 weeks

Management of women who are Hepatitis C antibody positive

Counselling
Advise testing for Hepatitis B, human immunodeficiency virus (HIV) and syphilis if not already
tested Ș Inform the woman early in the consultation of her HbsAg result. Ș If viral load for
hepatis C is low and no coinfection with HIV, rate of transmission is less than 5% Ș Co-infection
of hepatitis C and HIV increase the vertical tramsmission of hepatitis C
Intrapartum management
There is no evidence that caesarean section will reduce the risk of perinatal transmission Ș Avoid
procedures which may inoculate the baby, for example: ■ Fetal scalp electrodes ■ Fetal scalp
blood sampling ■ Vigorous aspiration of the baby ■ Instrumental modes of birth
At birth Ș Protective eyewear, gown / apron and gloves should be worn by the attending provider
• Care of the newborn baby Ș Standard precautions should be utilised when handling the baby Ș
Delay Konakion injection and administer after the baby has been bathed to remove all maternal
blood Ș The baby should remain in the delivery room until transfer to the ward unless transfer to
the nursery is indicated Ș Breastfeeding should be encouraged unless nipples are cracked and
bleeding (express and discard milk until healed)

Urinary tract infections (UTI) in pregnancy

Definition: Often-bacterial infection of the ureters, bladder and urethra. UTI occurs much more
frequently in women than in men especially during pregnancy. Most often UTI is asymptomatic
in pregnancy.
Types - Asymptomatic bacteruria affecting 4-7% of pregnant women - Acute cystitis - Acute
pyelonephritis
Causes/Risk factors - Most commonly Gram-negative bacteria (E.coli 60%, Klebsiella species,
Proteus species…) - Less commonly Gram-positive cocci (Staphylococcus species…) - Gravidity
(hormonal and urine stasis in urinary tract organ) - Catheterization, Colposcopy, Intravenous
urogram, Cystoscopy, sexual intercourse, vaginal infection and frequent non aseptic vaginal
exams
Signs and Symptoms - Often asymptomatic bacteriuria - Symptomatic: Fever, Increased urgency
(pollakiuria), Dysuria, lower abdominal pain, back pain, positive ureteral point (especially right
lower ureteral point), Pyuria
Complications - Acute and chronic pyelonephritis - Recurrence - Pre-term labor – Prematurity
Investigations - FBC - Urine analysis - Urine culture - Blood Culture - Renal functions test
Management
Pharmaceutical management • The treatment would be rational if the choice of antibiotics is
based on culture and sensitivity results.
First choice • Nitrofurantoin 100 mg P.O. QID for 5-7 days
Alternative • Amoxycilline tab 500mg TDS for 5-7 days
Recommendations - Patient education - Increase water intake - Frequent urine and stool analysis -
Patients on nitrofurantoin should be monitored for the renal function

. Pyelonephritis during pregnancy

Definition: Pyelonephritis during pregnancy most often, is a complication of non-treated
asymptomatic bacteriuria
Causes See UTI
Signs and Symptoms Headache, fever, chills, nausea and/or vomiting, flank pain and dysuria
Complications - Miscarriage - Preterm labour - Sepsis - Renal calculi - Ureteric obstruction -
Perinephric abcess - Chronic renal failure
Investigations - Urine analysis showing bacteruria and pyuria - Gram stain and urine culture of
midstream urine or urine obtained by through catheterization. - Leucocytosis with neutrophilia -
Blood culture
Management Admit for parenteral medication
First choice • Associate Ampicillin, 1gr IV TDS and Gentamycine, 80 mg IV BD until 48 hours
after the fever subsided and then Amoxycilin 500 mgPO TDS for 10-14 days (With precaution
for Gentamycine in relation with renal function)
Alternative • Cefotaxime, 1 gr IV TDS until 48 hours after the fever subsided and then continue
with Amoxycilin 500 mgPO TDS for 10-14 days
Recommendations - Repeat urine analysis because reccurency is high - Any pregnant woman
who has had two UTI attacks should under go renal Ultrasound. - Increase water intake

Chorioamnionitis
Definition: It is a bacterial infection of amniotic fluid and fetal membranes. It typically
complicates premature rupture of membranes and results from bacterial ascending into the uterus
from the vagina.
Causes/Risk factors - Genital tract infections: • Syphilis, gonorrhea, chlamydia • Group B
streptococcal infection through PPROM • E.Colli, Staphylococcus areus • Bacterial vaginosis •
Ureaplasma urealyticum, Mycoplasma hominis and trichomonas vaginalis - Urinary tract
Infection - Premature rupture of membranes - Prolonged labor with rupture of membranes -
Multiple vaginal exams
Signs and Symptoms - Fever more than 38oC - Tachycardia (maternal and fetal) - Foul-smelling
discharge - Uterine tenderness
Complications - Fetal distress - Stillbirth - Endometritis - Neonatal Infection - Septicemia, septic
shock
Investigations - Ultrasound - FBC/CRP - Vaginal swab - Urinalysis - Cervical cultures - Group B
Streptococcal Screening - Fluid leakage culture
Management
First choice • Ampicillin 2 gr IV 6hrly until delivery followed by 1g TDS for 5 days OR
Penicillin G5 MUI 6hrly PLUS Gentamycin 160 mg OD for 5 days
OR • Amoxicilline+ Clavulanic Acid 625mg IV TDS for 5 days
Alternative • Cefotaxime 1g IV 8 hourly for 5 days • Erythromycine oral 500mg TDS for 5 days •
Anaerobic coverage can by Metronidazole 500mg IV TDS for 5 days • Antipyretics and
hydrotherapy: paracetamol 500mg PO TDS and IV Fluids

Obstetrical treatment
Vaginal delivery is preferred • Antenatal corticosteroids are contraindicated in women with
chorioamnionitis • Conservative and tocolysis therapy are contraindicated

DIABETES AND PREGNANCY

Pre gestational diabetes: Women who present with keto acidosis or random plasma glucose levels
greater than 200mg/dl plus classical signs and symptoms such as polyphagia, polyuria or
polydipsia are labeled as pregestational diabetes. American Diabetes Association (2004) also
 recommends that pregnant women with fasting glucose levels of 126mg/dl or greater be
considered to have overt diabetes.
Gestational diabetes mellitus: Current practice is a 2 step testing, screening and diagnosis.
Universal screening is recommended in India as Asians are a high risk group for diabetes.
O’Sullivan 50 g glucose, 1 hour screening test cutoff ranges from 130mg/dl to 140 mg/dl. The
next step, diagnostic 3 hour 100gm GTT has atleast 2 different algorithms for diagnosis of GDM

Recently, a single step 75 gm oral glucose tolerance test is also being used wherein a 2 hr
plasma glucose level is measured after random administration of oral glucose.A plasma value >
140 mg% is diagnostic of GDM.It serves both as a screening &a diagnostic test. However, further
studies are required before it is put to routine use in India.

DIFFERENTIAL DIAGNOSIS: Glycosuria of pregnancy

PRECONCEPTIONAL CARE:

Preconception Counselling

All women of reproductive age with preexisting diabetes should be advised about the potential benefits of
prepregnancy planning. They should be offered education on the role of diet, appropriate body weight,
and exercise. The American Diabetes Association has defined optimal preconceptional glucose control
using insulin to include selfmonitored preprandial glucose levels of 70 to 100 mg/dL and postprandial
values _ 140 mg/dL and _ 120 mg/dL at 1 and 2 hours, respectively. A reasonable target for HbA1c in
prepregnancy counseling is to aim for 6%. An improvement in HbA1C levels can also be achieved by
switching to short acting modern analogue and by enrolling the prepregnant subject into education
programs that teach enhanced carbohydrate counting. Women with diabetes whose HbA1c is above 10%
should be strongly advised to avoid pregnancy. In prepregnancy counseling the current drug regime
should also be reviewed. Some hypoglycemic drugs and the newer long acting insulin analogues have not
been evaluated for safety in pregnancy and they should be replaced. Antihypertensives particularly ACE
inhibitors and angiotensin receptor antagonists should be discontinued prior to pregnancy. Finally, folate,
400 µg/d, is given periconceptionally and during early pregnancy to decrease the risk of neural-tube
defects. When pregnancy occurs without any prepregnancy counseling , then an urgent assessment of all
the previous factors should be undertaken as soon as possible at the antenatal clinic. Retinal & renal
assessments are mandatory in all cases

OPTIMAL DIAGNOSTIC CRITERIA, INVESTIGATIONS, TREATMENT AND REFERRAL

CRITERIA

Clinical diagnosis:As described in case definition. Women with risk factors for GDM should be carefully
screened like the obese, prior GDM, prior macrosomic infant, elderly mothers, multiple pregnancy, south
east Asians, Hispanics, African Americans, polycystic ovarian syndrome, family history of diabetes. Such
women at very high risk may benefit from early screening in the first trimester. If early screening is
normal, screening is repeated at 24 to 26 weeks.

Investigations:
Close monitoring of blood glucose, baseline& interval glycosylated haemoglobin levels andurine sugar &
ketones are helpful throughout pregnancy.Target blood glucose values are fasting 95mg%, 1 hour
140mg% & 2 hour 120mg%. If a patient is controlled on diet, blood sugar monitoring with capillary
blood glucose levels 4 times a day (FBS and PPBS thrice) are enough. Patients on pharmaceutical
therapy- in addition need preprandial & 3 am values. Other investigations required specially include
ultrasound for dating, aneuploidy screening , anomaly scanning, growth profile monitoring for fetal
weight, AFI and biophysical profile is necessary in poorly controlled diabetics. Non stress test by 32 to 34
weeks. Lack of USG and NST facilities warrant referral to higher centers.

Treatment:

Diet and exercise are instituted first. For many patients with GDM ,oral hypoglycemic or insulin therapy
may be avoided altogether with no increase in adverse perinatal outcomes on diet alone. For women of
normal weight, the American Diabetes Association recommends a caloric intake of 30 to 35 kcal/kg,
taken as three meals and three snacks daily. For underweight women, this is increased to 40 kcal/kg/d. For
those more than 120 percent above ideal weight, it is decreased to 24 kcal/kg/d. An ideal dietary
composition is 55 percent carbohydrate, 20 percent protein, and 25 percent fat with less than 10 percent as
saturated fat. Generally a diet containing with CHO restriction to 45-60% preferably complex high fiber
carbohydrates sources of known low Glycemic Index, lean proteins including oily fish, and a balance of
polyunsaturated and monounsaturated fats is recommended. Women with a high BMI might be advised to
restrict calorie intake with expert dietetic advice and consider suitable enhanced mild or moderate
exercise during the pregnancy. 1 to 2 miles walk at least 3 times a week is recommended.

Pharmacotherapy with insulin is instituted when diet and exercise therapy fail as evidenced by an
abnormality in more than half the self monitored glucose values or an abnormal value in those women
tested weekly

Recommended initial dose of Insulin is, 0.7-0.8 U/kg body wt in the 1st trimester 1.0 U/kg body wt in the
2nd trimester 1.2U/kg body wt in the 3rd trimester

ose is adjusted according to the response of hyperglycaemia to initial therapy. Of the calculated daily
dose, 2/3rds is given before breakfast, divided as 2/3rd NPH insulin and 1/3rd regular insulin, and the
remaining 1/3rd of the daily dose is given as 1/2 regular insulin before dinner and 1/2 NPH insulin at bed
time.

Self-monitoring of capillary glucose levels using a glucometer is recommended because this involves the
woman in her own care. The goals of glucose control recommended during pregnancy are Fasting _≤95
mg/dL, Premeal _≤100 mg/dL,1-hr postprandial ≤140 mg/dL, 2-hr postprandial _≤120 mg/dL and 0200–
0600 _≤60mg/dL.

Antenatal care- twice weekly visits required. Well controlled diabetics can deliver at 40 weeks

Poorly controlled non compliant patients on pharmacotherapy need antenatal testing for monitoring
macrosomia or growth restriction and timely planning of delivery when fetus is optimally mature with
lung maturity.
Women with pregestational diabetes with nephropathy, retinopathy may worsen and warrant earlier
delivery. Preeclampsia, and IUGR may set in.

Good glycaemic control during pregnancy can avoid ketosis and sepsis.

Diabetic ketoacidosis should be suspected when a pregnant diabetic mother presents with blood sugar
more than 200mg/dl, vomiting and dehydration with low serum bicarbonate and presence of acetone as it
could lead to fetal loss if not intensively managed in conjunction with a physician.

Preterm labor in diabetics can be managed with antenatal steroids &tocolysis.However,women with
insulin treated diabetes who are receiving steroids for fetal lung maturation should be closely monitored
andreceive additional insulin according to protocol.Also, betamimeticdrugs should not be used for
tocolysis in such women

Labor and delivery- Women with pregestational diabetes and GDM requiring pharmacotherapy are best
managed with IV fluids(100-150ml/hr),insulin drips and hourly glucose monitoring protocols to maintain
blood glucose values at around 70 100mg% during active labor. Women with very mild GDM may not
require insulin therapy but should have blood glucose assessment during labor.

It is important to considerably reduce or delete the dose of long-acting insulin given on the day of
delivery. Regular insulin should be used to meet most or all of the insulin needs of the mother at this time,
because insulin requirements typically drop markedly after delivery. During labor and after delivery, the
woman should be adequately hydrated intravenously and given glucose in sufficient amounts to maintain
normoglycemia. Capillary or plasma glucose levels should be checked frequently, and regular insulin
should be administered accordingly. It is not unusual for a woman to require virtually no insulin for the
first 24 hours or so postpartum and then for insulin requirements to fluctuate markedly during the next
few days. Infection must be promptly detected and treated.

When estimated fetal weight is above 4.5 kg, elective caesarean is planned to avoid shoulder dystocia and
birth trauma. In those where the EFW ranges between 4 to 4.5 kg, other obstetric factors should be
considered in decision making for caesarean section.Uncontrolled diabetes & presence of end organ
disease are other indications of caesarean section.

Preparedness for the management of neonatal problems is a must.

Post partum management-A 75 g GTT should be performed at 6 to 12 weeks postpartum and other
intervals thereafter for GDM mothers. Subsequently, testing can be done annually or triannually(ADA
recommendation).

Contraceptive advice needs to be given as per WHO recommendations.

Referral criteria:

When careful monitoring facilities are not available. For expert opinion regarding anomalies and
paediatric surgery and for fetal echocardiography. When there are comorbidities warranting
multidisciplinary input especially in pregestational diabetics and poorly controlled gestational diabetics.
When there is need for intensive neonatal care unit to manage problems in the newborn.
Situation 2: At Superspeciality Facility in Metro location where higher end technology is available. a)
Clinical diagnosis: As described in situation1.

) Investigations: As described in situation I.Fetal echocardiography & periodic doppler studiesif growth
retardation present. c) Treatment: As described in situation 1. A multidisciplinary team is involved early
in care and planned delivery is carried out in the presence of anomalies to facilitate optimal care in a
tertiary center with good nicu and paediatricsurgeons.An endocrinologist is necessary for the management
of DKA. d) Referral Criteria: Even in a metro situation not all centers will be equipped with the multiple
specialists, skilled hands and facilities. The decision to refer to a better facility should be taken if it
warrants to give the best care to the mother and the newborn.

RHESUS ISOIMMUNIZATION

Definition: Rhesus isoimmunization is the condition where incompatibility exists between the fetal and
maternal rhesus group such that an immune response occurs.

Causes/Risk Factors - Delivery - Abruption placenta - Miscarriage - Incomplete Hydatiforme mole -

Invasive procedures - Ectopic pregnancy - Other causes of bleeding during pregnancy

Complications - Repetitive miscarriage - Fetal anemia - Hydrops fetalis (Hydrops fetalis is defined as an
abnormal collection of fluid in two or more fetal body compartments, including ascites, pleural effusions,
pericar dial effusions, and skin oedema) - Intra uterine fetal death

Investigations - Antibody titers • Serial measurements of circulating antibody titers should be performed
every 2-4 weeks. - MCA (Middle Cerebral Artery) pulsatility index by Doppler ultrasound is diagnostic
for fetal anemia

- Invasive testing • If antibody titers continue to rise in the presence of an Rh (D)-positive fetus, invasive
testing may be required. Ș Amniocentesis Ș Fetal blood sampling for fetal hemoglobin

Management

Rhesus (anti-D) prophylaxis • 250IU Anti-rhesus Immunoglobulin: Give one dose at 28 weeks’ gestation
and again after delivery if the baby is Rh (D)-positive within 72 hrs. Ș Any bleeding or invasive
procedure after 12 wks, the mother should receive prophylactic dose of 250 UI and to repeat the dose
after 6 weeks if you have the indication.

Monitoring the pregnancy • Blood group (ABO and Rh status) and antibody status testing at booking and
again at 28-30 weeks’ gestation

Foetal surveillance and blood transfusion • Ultrasound examination to detect/rule out hydrops fetalis
(ascites, pleural effusions, pericardial effusions, or skin edema). • In case of anemia, blood transfusion
done from 22 weeks and repeated in case of fetal anemia unless fetal hydrops is already present.

Timing of delivery • In case of complications, delivery can be done at ≥34 weeks of gestation

Recommendation - Routine screening of all pregnant women for blood group and rhesus at the first ANC
PRETERM LABOR AND PRETERM PREMATURE RUPTURE OF MEMBRANES

Definition - Preterm labor is occurance of uterine contractions between 24 to 37 weeks of gestation. -

Preterm Premature Rupture of Membranes is rupture of the fetal membranes 1 hr or more prior to the
onset of labor prior to 37 weeks.

Causes/Risk factors - History of previous preterm birth - Adolescent age and advanced maternal age -
Maternal infections (Pyelonephritis, Genital tract infection, other systemic infections) - Increased uterine
size (Twins, Poly hydramnios) - Maternal Trauma - Uterine abnormalities (Myomas, Uterine
malformations) - Other pregnancy complications (Abruption Placentae, cervical incompetence) - Social
economic and stress factors

Signs and Symptoms - Pelvic and back pain - Uterine contractions - Sterile speculum examination to
confirm leaking of amniotic fluid - Increased Vaginal discharge - Muco-bloody discharge

Complications - Infection (chorioamnionitis, Neonatal sepsis, maternal septicemia) - Prematurity -

Neonatal respiratory distress syndrome - Neonatal mortality and morbidity

Investigations - Full blood count - Vaginal Swab for lab analysis - Urine analysis - Materanl and fetal
Screening for infections - Obstetric Ultrasound

Management

Preterm labor with intact membranes (< 34 weeks gestation) • Admit and assess (Term and Cervical
changes) • Cervix dilatation

Alternati

Β2 agonists infusion Ș Salbutamol IV 2.5mg in 500 mls of Ringers lactate and run 20-30 drops per
minute and monitor contractions and maternal heart rate OR Ș Terbutaline sulfate IV 0.1 mg in Glucose
5%. The recommended initial rate of infusion is 5 micrograms/minute increased by 2.5 micrograms/
minute at intervals of 20 minutes until contractions stop. Usually, a rate of up to 10 micrograms/minute is
sufficient.

• Do ECG for mother before installing intravenous treatment with Β2 agonists • Monitor maternal heart
rate (it should not go up 120/ min) • Dexamethasone 6mg IM 4 doses 12 hourly for lung maturity.
Delivery should be delayed for 24 to 48 hours • Cervix dilatation ≥ 4 cm: Tocolyse with Β2 agonists or
Nifedipine for 24hrs and administer Dexamethasone 12mg IM 2 doses 12 hourly. This will assist transfer
to a center with good neonatology facilities. Preterm labor with rupture of Membranes (< 34 weeks of
gestation) • Perform speculum examination to confirm diagnosis and take samples for laboratory
examination • Do not tocolyse • Antibiotherapy: Ș Erythromycine 500mg every 8hrs for 10 days.

Alternative

Ș Ampicilline 2g in flash, then Amoxycilline 500mgs TDS for 10 days. • Corticosteroids: Dexamethasone
6mg IM 4 doses 12 hourly for 48hrs. Preterm labor with rupture of Membranes and signs of infection
(fever, Tender abdomen, Foul smelling vaginal discharge and fetal distress) < 34 weeks of gestation •
Labor induction with Oxytocin, 5 IU in glucose 5% 500 ml or Cytotec based on Bishop Score. •
Antibiotherapy: Ampicilline IV 1g TDS plus Metronidazole IV 500mg TDS until delivery and then
continu with Amoxycilline tabs 500mg TDS and Metronidazole tabs 500mg TDS for 5 days.

Preterm labor with rupture of Membranes (> 34 weeks of gestation) • Labor induction with Oxytocin, 5
IU in glucose 5% 500 ml or Cytotec based on Bishop Score • Antibiotherapy: Ampicilline 2g single dose.
Or Erytrhromycine 500 mg TDS for 5 days in case of allergy to Penecillines

Recommendations - Neonates should be transferred to neonatology unit. - Do not tocolyse in cases of

rupture of membranes - Tocolysis only indicated for the administration of corticosteroids or in Utero
transfer. - In case of multiple pregnancy the dose of corticoster oids is not increased and it remains the
same as in singleton pregnancy - Next pregnancy is at high risk for preterm labor and should be
monitored closely - Do ECG for mother before installing intravenous treatment with Β2 agonists

LABOR DYSTOCIA

Definition: Dystocia of labor is defined as difficult labor or abnormally slow progress of labor.

Risk factors/ Causes - Uterine power (inadequate contractions, contraction ring of the uterus, myomas,
uterine scar) - Passage (abnormal pelvic anatomy) - Passenger (macrosomia, malposition, fetal anomalies)
- Mother condition (fatigue…) Signs and Symptoms - Lumbar and abnormal back pain due to ineffective
contractions - Dehydration - Anxiety - Failure of cervix to dilate despite good uterine contractions -
Oedema of the cervix and vulva - Failure of the fetal head to descend - Bandl’s ring - Foetal distress -
Arrested labor - Mother exhaustion

Complications - Foetal distress - Rupture of the uterus - Birth canal injuries (Cervical tears, vaginal and
perineal lacerations, Fistula)

- Foetal hypoxia / Asphyxia - Foetal death - PPH - Post partum endometritis - Maternal death
Investigations - Fetal monitoring with a partogram - Ultrasonography Management Non pharmaceutical
management • Evaluation of pelvis, passenger, uterine power, pain and psych • Fetal monitoring Active
management

CORD PRESENTATION AND PROLAPSE

Definitions Cord Prolapse: Where the umbilical cord lies in front of or beside the presenting part in the
presence of ruptured membranes. Cord Presentation: Where the umbilical cord lies in front of the
presenting part and the membranes are intact

Causes /Risk factors - Breech and other malpresentations e.g. shoulder presentation - Preterm labour + / -
low birth weight < 2500 g - Multiple gestation (usually the second born twin) - High head at onset of
labour + / - artificial rupture of the membranes - Grand multiparity - Abnormal placentation - Long cord -
Polyhydramnios - Obstetric manipulations such as external cephalic version
Signs and Symptoms - Feeling of a soft usually pulsatile structure on vaginal examination - Cord with
presenting part in the vagina or in the introitus.

Complications - Fetal distress - Infection - Fetal death

Management - Treat as an obstetric emergency and arrange for immediate medical assistance
(obstetrician, anaesthetist, neonatologist) - The mode of delivery will depend on whether a fetal heart is
present or absent and the stage of labour - Aim to maintain the fetal circulation by preventing /
minimising cord compression until birth occurs

Cord pulsating Determine stage of labour by vaginal examination • First stage of labour Ș Arrange
immediate delivery by caesarean section Ș Administer Oxygen Ș Ensure continuous fetal monitoring until
in theatre and commencing caesarean section or until after vaginal birth Ș The priority is to relieve
pressure on the cord while preparations are made for emergency caesarean section. Ș Positioning the
woman in the deep knee-chest position (also known as Trendelenburg) so that the pelvis and buttocks are
elevated. Elevate the foot of the bed where possible. Ș Using sterile gloves, the midwife / medical officer
should insert their fin gers into the vagina, identify and carefully elevate the presenting part to reduce the
amount of cord compression and keep fingers inside until delivery. Ș If the cord is protruding outside the
vagina, the attending clinician may attempt to push back the cord gently within the vagina Ș Avoid
excessive handling of the cord Ș Acute intravenous tocolysis using β2 agonists (Salbutamol or
Terbutaline) to relieve pressure on the cord may be an effective adjunct treatment

Second stage of labour Ș If the woman is in the second stage of labour and vaginal birth is imminent and
with the presenting part engaged, prepare for vacuum extraction Ș If vaginal delivery is not feasible, do
immediately a caesarean section

Cord not pulsating • Confirm fetal death with ultrasonograph and/or CTG • Allow labor to proceed as for
vaginal birth of fresh stillbirth

. CESAREAN SECTION

Definition: It is a surgical procedure in which incisions are made through a woman’s abdomen and uterus
to deliver the fetus

Indications - Fetal • Non reassuring fetal heart pattern • Malpresentations • Cord prolapse • Macrosomia,
Congenital anomalies, Multiple pregnancy

- Maternal-Fetal • Obstructed labor • Placental abruption • Placenta praevia (Complete) • Perimortem •

Maternal-fetal disproportion

- Maternal • More than 1 previous Cesarean delivery • Contracted/limited pelvic cavity • Obstructive
tumors • Active genital herpes virus • Elective ceserean section • Abdominal cerclage • Reconstructive
vaginal surgery, eg., fistula repair • Medical conditions, eg. Cardiac (relative), pulmo nary,
thrombocytopenia…

Complications - Urinary tract injury - Gastrointestinal injury - Lacerations - Hemorrhage and shock -
Anesthesic Complications - Post operative peritonitis - Endometritis - Deep Venous Thrombosis and
Pulmonary emboli - Uterine dehiscence in the next pregnacy - Abdominal adhesions - Intrauterine
synechia - Risk of uterine rupture for the next pregnancy

Management

Pre Operative Management • Anesthesia consultation • Monitoring vital signs • Nil per Os when elective
ceserean section • Intravenous: Ringer lactate or Normal Saline 500 ml • Antibiotics: Ampicilline 2g IV
bolus single dose (Cefotaxime 1g IV if allergic to penicillins) • Urinary bladder catheterization

Lab: Ș Complete blood count Ș blood type and screen Ș Clotting profile • Patient education and consent •
Signing of the consent form

Post operative Management

Monitoring of vital signs and fundal status every 4-8 hours for 24 hours • Uterus massages and report
extra lochia. • Monitor fluids intake and output every four hours for 24 hours. • Encourage early activity •
Give fluids and soft diet after 6 hours • Antibiotics if indicated give pain relief medication. • If infant cord
blood indicates Rh incompatibility, administer anti Rh Immunoglobulin.

Recommendations - Discuss contraception and infant feeding - Patient to start activity at an early stage
post surgery - Regional anesthesia is preferred than general anesthesia - Antibiotics are not routinely
recommended after cesarean section

INSTRUMENTAL VAGINAL DELIVERY

Definition: Operative vaginal delivery is extraction of baby with use of instruments (Vacuum).

Indications - Fetal • Fetal distress - Maternal • Delay in the second stage of labor • Maternal exhaustion

Complications - Failure of instrumental delivery - Fetal Complications • Shoulder dystocia • Sub

aponeurotic/ subgaleal hemorrhage • Facial nerve pulsy • Skull fracture and/or intracranial hemorrhage •
Cervical spine injury - Maternal complications • Pain at delivery and post partum • Traumatic injury
including anal sphincter and bladder damage • Postpartum hemorrhage - Guidelines for instrumental
delivery • Obstetrics prerequisite for instrument vaginal delivery Ș Empty the urinary bladder of the
patient Ș Full dilatation of cervix Engagement of fetal head Ș Favorable presentation (vertex, deflexed
vertex or face presentations). Vacuum extraction is contraindicated for face presentations

Recommendations - An obstetrician who has experience to do it should do instrumental delivery. -

Vaccum extraction is contraindicated before 34 weeks of gestation - Epidural analgesia increases the risk
of instrumental delivery - Instrumental delivery with high suspicion of failure should be done in theatre
ready for C-section. - Episiotomy is not routenly indicated with instrumental delivery - Inform the
paediatrician for fetus assessment after delivery
PERINEAL LACERATIONS

Definition: They are tears of the perineal tissue between the vagina and rectum

Grades - 1st degree injury to perineal skin - 2nd injury to perenium involving perennial muscles but not
the anal sphincter - 3rd degree involvement is of the anal sphincter - 4th degree involvement of the anal
sphincter and anal mucosa

Causes/Risk factors - Routine episiotomy - Assisted delivery - Prolonged secong stage of labor - In-
experience of service provider - Nulliparity - Macrosomia - Patient age

Complications –

Maternal • PPH • Anesthesia risk • Injury to bladder, uterus, bone, pelvic nerve damage, • Anal
incontinence • Infections • Dyspareunia

Management - Surgical repair of the tear - Repair of the external anal sphincter end to end and internal
inner sphincter should be repaired by interupted sutures - Repair of the 3rd and 4th perineal tear should be
done in theatre under general or regional anesthesia - Its recommended to repair perineal tears with vicryl
2-0 which causes less irritation and discomfort - Check the anal canal if it’s not closed during the repair -
Antibiotics and laxatives are recommended to be used after anal sphincter repair - Women with history of
anal sphincter injury in previous pregnancy who are symptomatic should be advised about elective
ceserean section

EPISIOTOMY

Definition: It is an incision in the perineal body at the time of delivery

Indications - To prevent a tear (episiotomy is easier to repair) - To relieve obstruction of the unyielding
perineum - Controversy over whether it is preferable to make a cut, or let the perineum tear as needed;
current evidence suggests letting perineum tear and then repair as needed

Types - Mid-line episiotomy - Mideal lateral episiotomy

Complications - Bleeding - Infection with suture disunion - Hematoma - Extension into anal musculature
or rectal mucosa causing fecal incontinence - Fistula formation – Dyspareunia

Management - Repair as in perineal tear (2nd Degree) - Post episiotomy hygiene education

POST TERM PREGNANCY

Definition: Pregnancy lasting beyond 42 or more than 294 days from the first day of the last menstrual
period (LMP)

Causes/Risk Factors - Error in dating - Primiparity - Prior post term pregnancy - Fetus of male sex -
Regularly heavy exercise - Investigations - Ultrasound - Diminished amniotic fluid - Placenta calcified -
Umbilical artery Doppler
Complications - Dysmaturity syndrome - Fetal macrosomia - Fetal distress /Meconium stained liquor -
Stillbirth - Complications of induction of labor

Management - Induction of labor if no contra indication - Cesarean section if failure of induction or fetal
distress

INDUCTION OF LABOUR

Definition: Stimulation of uterine contractions prior to the onset of spontaneous labor for vaginal delivery
after the age of viability Indications

Indications - Maternal medical conditions (diabetes, hypertensive disorders, renal diseases…) - Fetal
growth restriction - Isoimmunization - Chorioamnionitis if no contra indication - Post-term pregnancy -
Premature rupture of membranes - Intrauterine fetal death - Fetal malformations

Contra indications - Malpresentation and malposition and macrosomia - Prior uterine scar - Active genital
herpes infection and Condylomma - Fetal compromise - Complete placenta praevia - Multiple gestation -
Any contraindication to vaginal delivery - Complications - Hyperkinesia - Fetal distress - Uterine rupture
- Failure of induction Water intoxication and increased incidence of neonatal jaundice with excessive use
of oxytocin

Methods - Sweeping the membranes - Artificial rupture of membranes (ARM) - Prostaglandin E2

(PGE2), Misoprostol. - Intravenous Oxytocin infusion - Mechanical dilatation of the cervix (Using Foley
catheter)

Management

Misoprostol (Cytotec®) 50mcg PO or intravaginal every 3-6 hours up to 6 times • Continously Monitor
fetal heart rate by CTG after administration or Ș If no CTG ■ Monitor FHR every 15 minutes ■ Monitor
contractions every 30 minutes ■ Follow the Partogram as recommended for the active phase Ș Vaginal
examination before the next dose

Oxytocin (Favorable Bishop’s Score >6) • Oxytocin 5 IU in Ringers lactate or Normal Saline 500 ml •
Start with 8 drops/min then add 4 drops every 30 minutes, maximum 40 drops/min N:B: With a syringe
pump dilute 5 IU oxytocin in 500mls of Ringers or Normal Saline. Start with 12mls/Hr (equivalent to 4
drops/Minute) and increase by 4 drops/ minute until adequate uterine contractions without exceeding 60
mls/Hr

Artificial rupture of membranes (ARM) + Oxytocin • Oxytocin 5 IU in Ringers lactate or Normal Saline
500 ml • Start with 8 drops/min then add 4 drops every 30 minutes, maximum 40 drops/min N:B: With a
syringe pump dilute 5 IU oxytocin in 500mls of Ringers or Normal Saline. Start with 12mls/ Hr
(equivalent to 4 drops/Minute) and increase by 4 drops/minute until adequate uterine contractions without
exceeding 60 mls/Hr

Recommendations - Assess woman and review indication before commencing induction of labour -
Document cervical score - Ensure there is a documented plan for ongoing management - If not in labour
within 12 hours of the first dose of Misoprostol review the assessment of the patient - Counter-verify the
gestational age before induction for post-term pregnancy
NEONATAL RESUSCITATION

Definition: Neonatal Resuscitation is providing life support to the newborn when the need arises

Risk factors of compromised newborn - Maternal risk factors • Maternal Age >40 years or < 16 years •
Diabetes • Pregnancy induced hypertension or preeclampsia • Severe anemia • Renal disease • Infections •
Use of narcotics • Lack of antenatal care

Pregnancy and labor risk factors • Fetal distress • Antepartum Hemorrhage • Post term pregnancy •
Prolonged Premature rupture of membranes • Malposition and malpresentation • Thick meconium •
General anesthesia • Emergency cesarean section • Instrumental delivery

- Fetal risk factors • Multiple gestation • Prematurity • Post term • Intrauterine fetal growth restriction •
Meconium-stained liquor • Macrosomia • Congenital malformation • Oligohydramnios and
Polyhydramnios, Hydrops fetalis, Intrauterine infections and isoim munisation • Non reassuring fetal
heart rate

Signs and symptoms of a neonate requiring Neonatal resuscitation - Mucous, blood or meconium in
airway - No breathing seen or felt - No pulse felt at umbilical cord or no heart beat heard with sthetoscope
– APGAR

Complications - Cerebral palsy - Neonatal death

Pharmaceutical management (where necessary) • Adrenaline 0.01-0.03mg/kg IV, IM, ET • Naloxone 0.1
mg/kg IV, IM, SC, ET use it if narcotic use suspected or if narcotic analgesia was used during labor
(Avoid it if mothers long term opiates users) • Normal Saline 10cc/kg IV over 5-10 minutes • Dextrose
10% 2ml/kg • To treat the underlying cause after stabilization, and refer the infant to Neonatology Unit

POST PARTUM COMPLICATIONS

Post partum fever

Definition Post partum fever (PPF) or puerperal fever is defined as an oral temperature of ≥38°C in the
first 10 days post partum or ≥ 38.7°C during the first 24 hrs post partum.

Causes - Benign fever - Urogenital infection • Endometritis • UTI - Breast engorgement - Mastitis/Breast
abscess - Pneumonia - Wound infection (C/S, cervical, vaginal and perineal lacerartions, episiotomy,
uterine rupture)Thrombo phlebitis - Deep Venous Thrombophlebitis - Pulmonary Embolism (PE) - Septic
pelvic vein thrombosis - Pelvic abscess - Pelvi-peritonitis - Malaria - Other causes of fever

Risk factors - Labor for ≥ 6 hours after ruptured membrane - Multiple pelvic examinations -
Chorioamnionitis - Increased duration of active phase of labor - Retained placenta or membranes -
Urethral catheterisation - Previous UTI - Operative vaginal delivery - Nipple fissure - Long operative
duration - Anemia - Imminosuppressive therapy - Immunodeficiency disorder - Corticoid therapy –
Malnutrition
Signs and symptoms - Pelvic pain - Foul-smeeling lochia - Fever - Sweating, Tachypnoea, Tachycardia, -
Chills - Headache – Malaise

Complications - Puerperal sepsis – Peritonitis

Investigations - FBC, CRP - Urinary analysis with culture and sensitivity - Wound swab for culture and
sensitivity - Blood cultures - Cervical and uterine sample and sensitivity – Ultrasound

Managemen

Non-pharmaceutical management • Fluid management • Oxygen therapy if necessary

Pharmaceutical management • Antipyretics Ș Paracetamol PO 1g TDS or QID not more than 6g/day. •
Antibiotics

First choice treatment Ș Ampicillin 2g IV q6h for 3 days plus Gentamycin 160 mg OD for 5 days Plus
Metronidazole 500mg PO/IVq8h for 5 days

Alternative Ș If allergic to ampicillin; Erythromycine 500mg PO q8h plus gentamycin plus metronidazole
for 5 days Ș Cefotaxim 1-2 g IV q 8h for 3 days, plus metronidazole

Recommendations - Avoid early rupture of membranes - Avoid multiple vaginal examinations -

Antibiotherapy will be given according to culture and sensitivity - IV therapy is preferred in cases of high
fever

Deep vein thrombosis and pulmonary embolus (DVT&PE)

Definition: DVT is the formation of blood clots within the deep veins, most commonly in the lower
extremities or pelvis. PE is thrombosis or showers of emboli in the pulmonary vessels

Pregnancy associated causes - Vessel damage during pregnancy - Mechanical impedance of venous return
- Changes in local clotting factors

Risk factors - Advanced maternal age - Increased parity - Multiple gestation - Surgery (C/S, episiotomy,
lacerations ) - Prolonged immobility, as with bed rest - Dehydration - Prior DVT or PE - Lupus
anticoagulant - Pre-eclampsia

Signs and symptoms - Pain or tenderness, fever - With PE tachycardia, dyspnea and chest pain. Death
with massive PE - Asymmetric limb swelling, > 2 cm larger than opposite side - Warmth or erythema of
skin over area of thrombosis - Homans sign (calf pain with dorsiflexion of the foot)

Complications - Septic pelvic thrombophlebitis – Death

Investigations - Fool blood count, coagulation test (PTT, PT/ INR) Liver function, renal function -
Ultrasound - CT scan - Chest x-ry – Angiography

Management
Non-pharmaceutical management

Assess and admit. • Bed rest • Graduated elastic compression stocking should be applied. • Inferior vena
cava filter can be used to avoid pulmonary embolism

Pharmaceutical management

First Choice • Enoxaparin: 1mg/kg SC every 12 hours. For each day of treatment, assess Quick time and
prothrombin test. Treatment is of 10 days for the acute phase. ThenWarfarin 5mg-7.5mg loading dose and
then the maintainence dose will depend on weight and INR results for 6 weeks monitoring INR

Plus • Acetylsalicylic acid (aspirin): 75-100 mg daily to be continued up to 6 weeks post−partum •

Caution: ASA (Acetyl salicylic acid) is secreted in breast milk but not a contraindication!!

Alternative choice • Enoxaparin can be substituted with Heparin. • Heparine IV loading doses 80 Units/kg
and then 18 Units/kg/Hr until the end of acute phase (5-10 days). Continue with Heparine SC 17500 units
every 12 hours. Monitor regularly PTT

Recommendations - Avoid hormonal contraception. Risk increases with oes trogen containing
contraceptions - Avoid protracted bed rest, where appropriate - For the next pregnancy need for anti-
coagulation therapy throught pregnancy

.Puerperal psychosis

Definition: Puerperal psychosis is a depressive disorder accuring within 6 months after delivery

Causes/Risks factors - Previous depression - Family history of depression - History premenstrual syndrom
- Current history of abuse - Unwanted pregnancy - Alcohol or substance abuse - Vulnerability to
hormonal change - Environmental stressors

Signs and symptoms - Five signs of the following, most of the day, every day, for two weeks - Depressed
or irritable mood - Inability to enjoy (anhedonia) - Changes in sleep: (cannot sleep when the baby is
sleep) - Changes in appetite - Guilt - Thought of death

Complications - Suicide – Infanticide

Investigations - Thyroid test to rule out hypothyroidism - CT scan to rule out cerebral tumor

Management - Medication and psychotherapy

Recommendations - If any signs/symptoms of depression alert health facility - Encourage breastfeeding

GYNECOLOGY

INFERTILITY

Definition: Infertility is defined as failure to conceive after one year of regular, unprotected sexual
intercourse. It is divided into two categories: - Primary: The woman has never conceived in spite of
having regular unprotected sexual intercourse for at least 12 months - Secondary: The woman has
previously conceived but is subsequently unable to conceive for 12 months despite regular unprotected
sexual intercourse.

Causes/Risk Factors - Anovulatory infertility - Tubal factor (STIs, bilateral occlusion, PID) -
Endometriosis - Uterine factors (Congenital disorders, Synechia, Myomas, Chromosomal abnormality) -
Male factor (STIs, Obstructive disorder, endocrine disorders.) - Cervical mucus abnormalities - Other
causes: psychological, smoking, work environment, - Endocrine disorders (Hyperprolactinemia,
Hypothyroidism…) - Unexpalined infertility

Investigations - Ovulation • Serum progesterone in the mid luteal phase • Serum FSH and LH day 3 from
the cycle • Basal body temperature - Tubal patency • Hysterosalpingography • Dye test and Laparoscopy -
Uterus • Ultrasonography • Hysterosalpingography • Hysteroscopy - Male partner • Semenalysis •
Testicular biopsy • Sperm function test - Endocrine System • Hormones test: Thyroid, prolactine tests -
Endometrial biopsy - Vaginal swab, Urinalysis - Post coital test (Hühner test)

Management - Treatment depends on the cause and may include: • Counselling on sexual technique and
fertility awareness • Large antibiotherapy spectreum Ovulation induction: Clomiphene Citrate 50 mg OD
for 5days starting from 2-5 of menstrual cycle - Tubal surgery - Male partner treatment including Vas
surgery - Assisted reproduction :In Vitro Fertilization (IVF), Intracytoplasmic sperm injection (ICSI) –
Adoption

Recommendations - Hyperstimulation syndrome is one of the side effects of induction of ovulation and
should be treated by a Gynecologist. - Any patient receiving induction of ovulation should have tubal
patency test before - Folic acid supplementation is recommended for any patient seeking pregnancy -
Patients taking clomifene need careful supervision best done by a specialist. - Clomifen should not be
used for more than 6 mounths - Infertility concerns the couple, they should consult together for better
management - Smoking cession - Be aware of ethical and legal implications during treatment

PELVIC MASSES

Definition: An abnormal structure or growth in the pelvic cavity arising from: - Pelvic organs such as the
ovaries, fallopian tubes, uterus, cervix, lymph nodes, bladder, bowel, peritoneum and appendix -
Metastatic from extrapelvic structures such as stomach or breast The differential diagnosis for pelvic
masses includes: Normal or ectopic pregnancy, distended urinary bladder, uterine fibroids, pelvic abcess,
tubo-ovarian mass and ovarian cysts.

Risk Factors - Infertility - Family history of brest, ovarian or colon cancer - Pelvic surgery: Hematoma,
abcess - Diverticulitis/Appendicitis - Pelvic Inflammatory Diseases - Endometriosis - Congenital
anomalies like pelvic kidney – Smoking

Signs and Symptoms - History of pelvic pain, fever, purulent cervical and vaginal discharge - Heaviness -
Pelvic mass - Pelvic pain and fever may be associated - Abnormal uterine bleeding - Dyspareunia,
dysmenorhea, infertility, Amenorhea - Related signs from the etiology: hemorrhage - Bowel symptoms:
Constipation, intestinal obstruction - Decrease appetite, nausea and vomiting, weight loss can be
associated - Urinary symptoms: urgency, frequency and urine retention. - Cachexia with malignant
masses

Complications - Torsion - Compression - Rupture - Infertility - Degeneration of Myomas - Malignancy

transformation

Investigations - Pregnancy test - FBC, ESR, Blood sugar - Urinalyisis - Renal function - CA 125 - Pelvic
Ultrasound - Intravenous Urography (IVU) - HSG - Culdocentesis – Laparoscopy Plain Abdominal Xray
- CT Scan and MRI

Management - Laparotomy or Laparoscopy for etiologic treatment - Adjuvant treatment depending on the
cause • Hormones (Oral Contraceptive Pills) • NSAIDs • Radiotherapy and chemotherapy for malignant
disease

Recommendations - Combination Oral Contraceptive Pills decrease the risk of ovarian cancer - Any
pelvic mass should be well investigated before decision of surgery

DYSFUNCTIONAL UTERINE BLEEDING

INTRODUCTION

DUB affects 22 to 30% of women and accounts for 12% of gynaecological referrals. DUB is not one
condition of one etiology – it is a group of disorders characterized by dysfunction of any part of the
reproductive system – uterus, ovary, pituitary, hypothalamus, higher centers. In clinical practice, the
diagnosis of DUB is usually made by exclusion of organic disease of the genital tract or systemic organic
disease.
DEFINITION It is defined as abnormal uterine bleeding without any clinically detectable organic
pathology.

How to make diagnosis? History:

H/o Abnormal Uterine Bleeding: a) Excessive menses-duration of menstrual flow > 7 days or menstrual
blood loss > 80 ml b) Frequent menses-duration of menstrual cycle < 21 days c) Irregular / acyclical
uterine bleeding.

H/o Symptoms Suggestive Of: a) Pregnancy b) Dysmenorrhoea/ dyspareunia/ infertility may suggest
endometriosis and PID, fibroids, adenomyosis c) H/o contraceptive practice, HRT Symptoms suggestive
of hypothyroidism, bleeding disorders, other systemic illness e) Ingestion of drugs, like antiplatelet drugs
(aspirin, clopedrogel)

Examination:

A general examination for signs of anemia, thyroid disease or bleeding disorders.

2. Abdominal examination for masses.

3. All women with abnormal genital tract bleeding must have a speculum examination to visualize the
cervix, vagina and exclude any local cause.

4. Per vaginal examination – look for uterine enlargement (fibroids), tenderness/fixity (PID,
endometriosis), any adnexal mass.

INCIDENCE:

1. Pubertal or adolescent DUB – usually women less than 20 yrs, incidence – 4% 2. Reproductive
DUB – seen in women from 20 to 40 yrs, incidence – 57% 3. Perimenopausal DUB – women
aged above 40 yrs, incidence – 39% 4. Postmenopausal DUB – incidence around 10%

DIFFERENTIAL DIAGNOSIS:

1. Pregnancy related bleeding a) Abortions b) Ectopic pregnancy c) Guestational trophoblastic disease

2. Fibroid uterus

3. Endometrial cancer

4. Thyroid abnormalities 42

5. PID, Endometriosis.

6. Endometrial TB 7. PCOS

DIAGNOSIS: Clinical diagnosis is made by history and examination as explained above. Final diagnosis
is only made after investigations.
INVESTIGATIONS: a) Urine pregnancy test b) Complete blood count c) Platelet count, BT, CT, PT,
PTT especially in puberty menorrhagia not responding to treatment d) Thyroid profile e) LFT & RFT
only in strongly suspected cases f) USG – TAS/TVS: Ultrasound is the first-line diagnostic tool for
identifying structural abnormalities. g) Pap smear h) Sonohysterography i) Endometrial biopsy – by
Novac curette, By Pipelle aspirator Women with irregular menstrual bleeding should be investigated for
endometrial polyps and/or submucous fibroids. Clinicians should perform endometrial sampling based on
the methods available to them. An office endometrial biopsy should be obtained if possible in all women
presenting with abnormal uterine bleeding over 40 years of age or 43 weighing more than or equal to 90
kg to exclude endometrial cancer or atypical hyperplasia, treatment failure or ineffective medical
treatment D & C- mandatory in perimenopausal age group (>40 years) and is contraindicated in
unmarried girls, puberty menorrhagia. j) Hysteroscopy – with hysteroscopic guided biopsy sensitivity is
98%. Hysteroscopy should be used as a diagnostic tool only when ultrasound results are inconclusive, for
example, to determine the exact location of a fibroid or the exact nature of the abnormality. [A]
Hysteroscopically-directed biopsy is indicated for women with persistent erratic menstrual bleeding,
failed medical therapy or transvaginal saline sonography suggestive of focal intrauterine pathology such
as polyps or myomas. k) Laparoscopy – to exclude unsuspected pelvic pathology such as endometriosis,
PID/Ovarian tumor. The indication is urgent is associated with pelvic pain. l) Saline infusion sonography
should not be used as a first-line diagnostic tool. m) Magnetic resonance imaging (MRI) should not be
used as a first-line diagnostic tool.

TREATMENT:

General

1. Assurance and sympathetic handling of physiological or emotional problems

2. Normal routine activities

3. Correction of anemia by diet, haematinic and even by blood transfusion

4. Clinically evident systemic/endocrine abnormalities should be investigated and treated accordingly

Medical Management:

Non hormonal methods:

1. Anti fibrinolytic agents – oral/IV tranexemic acid – 500 mg-1gm twice or thrice daily till severe
bleeding. Effective in ovulatory DUB, iatrogenic menorrhagia secondary to insertion of IUCD, Von
Wilibrand’s disease 44

2. Prostaglandin synthetase inhibitors (NSAIDS) – Mefenamic acid – 250 mg – 500 mg – twice or thrice
daily, effective in ovular DUB 3. Ethamsylate – 250 – 500 mg TDS oral/IV 4. Anti tubercular treatment
when disease is confirmed Hormonal

Method: To stop acute episodes of bleeding and to regulate the cycles 1. Progestins a. Tab nonethisterone
20 – 30 mg/day in divided doses. It arrests bleeding in 24 – 48 hrs; later dose is tapered and continued in
cyclical fashion from 5 th day of withdrawal flow in subsequent cycles for 3 to 4 cycles. b. Similarly
Medroxy progesterone acetate (MPA) can also be used.

2. Cyclical therapy: In ovular bleeding:

1. OCP is given from 5th to 25th day of cycle for 3 consecutive cycles. In ovular bleeding where patients
wants pregnancy or in case of irregular shedding or ripening dydrogesterone 10 mg per day from 16th to
25th day. In anovular bleeding: a) MPA 10mg 5th to 25th day, NE 5mg 5th day to 25th day for 3
consecutive cycles b. DMPA – 150 mg I.m every three months useful in maintenance therapy in woman
who have difficulty with or cannot take OCPs. c. Ormeloxifene (Sevista) – 2 tab of 60 mg/week that is on
Sunday and Wednesday for 12 weeks, 1 tab of 60 mg on following Sunday or Wednesday for 12 weeks d.
Levonorgestrol – Releasing IUD(Mirena)

Surgical Management Hysterectomy – TAH/vaginal hysterectomy/laparoscopic hysterectomy.

Hysterectomy should not be used as a first-line treatment solely for HMB. Hysterectomy should be
considered only when:

• Other treatment options have failed, are contraindicated or are declined by the woman

• There is a wish for amenorrhoea

• The woman (who has been fully informed) requests it • The woman no longer wishes to retain her
uterus and fertility

conservative surgeries: like Endometrial destruction or ablation – hysteroscopic and non hysteroscopic
methods are available (TCRE, uterine thermal balloon ablation, radio frequency induced endometrial
ablation, etc.)

3. Pre-requisite for undergoing these procedures:

a) To exclude atypical endometrium

b) CIN, Ca cervix, Ca endometrium has to be ruled out

c) Not expecting 100% amenorrhea

d) Uterus size less than 12 weeks

e) No pelvic inflammatory disease

f) Completed family

g) If necessary patient should be ready to undergo hysterectomy

h) Ready for regular follow up

i) Surgically fit
j) Patient should know that its not effective contraception 4. Associated co morbid medical conditions in
which surgery is required: (Hysterectomy).

Ammenhorea

. Primary amenorrhoea

Definition: Absence of menses at 14 years of age without secondary sexual development or age 16 with
secondary sexual development

Causes /Risk factors - Hypothalamic –pituitary insuficience - Ovarian causes - Out flow tract/Anatomical
(e.g.vaginal agenesis/septum, imperforated hymen or Mulleriam ageneis) - Chromosomal (e.g. complete
endrogene insensitivity, gonadal dysgenesis”Turner syndrome”)

Signs and symptoms - Absence of menses at age 14 without secondary sexual development - Presence of
secondary sexual character development and absence of menses at age 16 - Absence or presence of pelvic
pain

Investigations - Progesterone challenge test - Hormonal profile (Serum FSH) - Pregnancy test -
Ultrasound - Thyroid test - Karyotyping - X ray of the skull (Sella Turcica: Pituitary) Pituitary tumor or
necrosis - CT scan

Management

- Etiologic treatment • Hormonal treatment (Oral Contraceptive Pills) • Surgical treatment Ș

Hymenotomy if imperforate hymen Ș Resection of vaginal septum Ș Tumor resection

Recommendations - Any patient with primary amenorrhea and high levels of serum FSH should have
karyotyping - In cases of androgen insenstivity syndrome (XYfemale), we should remove the testes cause
of the risk of malignancy

Secondary amenorrhoea

Definition: Cessation or stopping of menstruation for a period equivalent to a length of 3 consecutive

cycles or 6 months

Causes - Pregnancy and lactation - Menopause - Hyopthalamo-putuitary (Inflamamtory, neoplastic,

Traumatic) - Stress - Anxiety - Excessive loss of weight - Drugs (danazol, LHRH analogue like
decapeptyl) - Contraceptives - Chronic diseases - Multiple genetic disorders - Premature ovarian failure
(POF) - Polycystic ovarian syndrome (PCOS) - Traumatic curettage, Post partum infection (Asherman
syndrome)

Signs and symptoms - At least 3 consecutive cycles of absence of menses - History of curretage, post
partum infection - Galactorrhea - Premature monapause - Obesity – Headache - Visual defects - Polyuria,
Polydipsia
Investigations - Hormonal profile - Pregnancy test - Ultrasound - Thyroid test - X ray of the skull
(turcique selle: Pituitary) Pituitary tumor or necrosis - CT scan

Management - Etiologic treatment • Hormonal treatment - Surgical treatment • Tumor resection • Lysis of
intrauterine synechiae - Weight loss - Normalize the Body Mass Index (BMI)

Recommendations - Patients with premature ovarian failure should receive hormal replacement therapy -
Patients with premature ovarian failure should receive contraception if they are not desiring pregnancy -
IVF and assisted reproduction is an option if the patient is desiring pregnancy

Dysmenorrhea

Definition: Dysmenorrhea is characterized by: Pain occurring during menstruation

Primary dysmenorrheal

- In adolscence with absence of pelvic lesions after 6 months of menarche - 6 months after menarche with
the onset of ovular cycles. - It is suprapubic, tends to be worst on the first day of menstruation, and
improves thereafter. - Associated with increased frequency and amplitude of myometrial contractions
mediated by prostaglandins - Associated with GIT symptoms like vomiting and diarrhea

Causes - Excess secretion of prostaglandins - Immaturity of the Hypothalmo- Pituitary -ovarian axis
leading to anovulatory cycle - Outflow tract obstruction

Investigations - Ultrasound to exclude pelvic lesions - Hormonal profile

Management

First choice : • 80% respond to therapy with • NSAIDs started 24-48 hours before the onset of pain. Ș
Aspirine 300-600mgPO TDS start 1or 2 days before the menstruation Ș Mefenamic acid PO 500 mg TDS
or Ibuprofen PO 400 mg TDS / day for 3 days

Alternative • Combined oral estrogen-progestogen contraceptive continued 9-12 months leading to

anovulatory cycles if symptoms improve • Surgical treatment: Interruption of pelvic pathway

. Secondary dysmenorrheal

Later in reproductive life - Presence of pelvic lesion, such as uterine fibroids or endometrial polyps -
Pelvic lesions - Dyspareunia (pain with intercourse) - Pelvic/lower abdominal pain occurring before,
during, after menstruation - Pelvic/lower abdominal pain occurring on days 1 and 2 of the menstrual
cycle. - An endometrial polyp or submucous fibroids usually occurring at the beginning of menstruation
cause Pelvic/ lower abdominal pain

Investigations - FBC ESR or C-reactive protein - Vaginal swab, - Urinalysis - Ultrasound - Laparoscopy –
Hysteroscopy

Management - The underlying condition (surgery, endometriosis IUD) - NSAIDs: Aspirine 300-600mg
PO TDS start 1or 2 days before the menstruation
Recommendations - Health care providers should explain the physiologic of dysmennorrhea - Regular
exercise

Premenstrual syndrome Definition: Premenstrual syndrome (PMS) or premenstrual tension (PMT) is a

very common disorder affecting up to 95% of women. It occurs mostly the last week before menstruation
(premenstrual phase) resolving or markedly improving at menstruation

Risk factors - Hormone changes over a normal menstrual cycle ( excesses or deficiencies of estrogen
or progesterone) - Side effects caused by the progestogen component of cyclical Hormonal
Replacement Therapy - Excessive Serotonin and β-endorphins secretion - Exaggerated end-organ
response to the normal cyclical changes in ovarian hormones.

Signs and Symptoms - Most women will experience at least one of menstrually related symptoms -
Physical, Emotional and Behavioral changes - Anxiety - Irritability - Bloating/fluid retention - Social,
family, or occupational disruption - Backache - Violence - Headache - Aggression - Breast
tenderness/swelling - Fatigue and Clumsiness - Depression and Loss of concentration - Food craving
- Anorexia - Mood swings

Investigations - FBC - Thyroid function tests - FSH, LH to exclude climacteric symptoms. –

Ultrasound

Management - As there is no accepted etiology for PMS - Placebo response rarey - Treatement the
most severe symptoms first.

Non-hormonal therapy • Yoga • Hypnosis • Music therapy • Homeopathy • Acupuncture • Self-help

groups, etc.

Hormonal therapy • Progesterone supplements (suppositories, pessaries, injections, oral micronized)

Ș Duphaston 10mg tabs P.O Dose: 20mg Once daily 11th to 25th day of the menstrual cycle Ș
Utrogetan 100mg tabs P.O Dose: 200mg Once daily 16th to 25th day of the menstrual cycle Ș
Lutenyl 5mg tabs P.O Dose: 5mg once daily 16th to 25th day of the menstrual cycle • Combined oral
contraceptive pills (COCP) • Bromocriptine may be useful for cyclical breast symptoms • Danazol
Low doses of Danazol (100 mg daily) have been shown to be beneficial in treating breast symptoms
without causing cycle suppression or severe side effects • Estradiol 17β-Estradiol implants (50-100
mg pellet 6-monthly) or transdermal estradiol patch therapy (100- 200 µg patch, used continuously)
act by causing cycle suppression. • Mirena intrauterine system (IUS) as the progestogen component
of treatment, systemic absorption is minimized and the acceptability of the treatment increased. •
GnRH analogs in severe cases can bring prompt and welcome relief from symptoms, but are
expensive for longterm treatment.

Recommendations - Mannagement of severe postmenstrual syndrome should take place in a multi-

disciplinary team - Treatment has shown a strong placebo effect - Psychosocial and familial support
can be beneficial to the patient - Manage symptomatic premenstrual pain - High intake of dietary
supplement (Calcium, Vitamin B6 and Vitamine C) for an alternative therapy
CANCERS AND TUMORS

Cervical Cancer

Definition:

Cancer of cervix caused mainly by human papilloma virus (HPV). Most common female cancer in
developing countries and can be prevented by screening and vaccination against HPV.

Cause/Risk factors

- Infection with human papilloma virus

- Early age of first sexual intercourse - Multiple sexual partners (unprotected)

- Multiparity

- Smoking

- Age ≥35 to

Signs and Symptoms

- Very often asymptomatic in early stages

- Abnormal vaginal bleeding

- Post coital bleeding

- Exclude cervix cancer in any post menopausal bleeding

- Foul smelling vaginal discharge

- Symptoms of metasis

- Hydronephrosis and renal failure

- By speculum examination, lesions infiltrating the cervix

Complications
- Anemia

- Cachexia

- Pain

- Hematuria and dysuria

- Ureteral obstruction and renal failure

- Oedema of legs

- Bowel invasion: Diarrhea, Tenesmus,rectal bleeding

- Sepsis

– Metastasis

Investigations

- For invasive cancer, consider stages of cancer

- Speculum examination: Cervical lesion that easily bleeds on contact

- PAP smear - VIA - VILI - HPV/DNA testing

- Colposcopy

- Biopsy

- FBC

- ESR

- Reneral function

- Intavenous pyelography

- X-rays: CXR, skeletal X-rays, CT-scan

- MRI lymphatic metastasis

Staging

• Stage 0: Carcinoma in situ

• Stage Ia1: Stromal invasion 5 mm, or gross cervical lesion 4 cm

• Stage IIa: extending to upper 2/3 vagina

• Stage IIIa: Extending to lower 1/3 vagina

• Stage IIIb: Extending into parametrium to pelvic sidewall or hydronephrosis

• Stage IVa: extending to bladder/ bowel mucosa

• Stage IVb: distant metastasis

Management

Principle of treatment

• Provide general supportive care, e.g., correction of anemia

• Undertake examination under anesthesia for staging, biopsy

• Provide supportive treatment, surgery, and or radio therapy according to staging

General measures

• It is important to clinically assess the extent of disease prior to the onset of treatment.

• Surgery can be utilized in early stage- disease Ia1-IIa.

• Radiotherapy+/- chemotherapy can be utilized in all stages I-IV

Surgery

• Stage Ia1: Cold knife cone or LEEP cone in young patients, in old women hysterectomy.

• Stage Ib1, Ib2, IIa: radical hysterectomy with bilateral pelvic lymphadenectomy (Para aortic nodes
optional)

• Stage III and IV: Inoperable (radiotherapy)

Recommendations - HPV vaccine is more important for the prevention of cancer cervix - Cervical
cancer screening (HPV, pap smear, VIA, VILI, Coloposcopy, biopsy) - Treatment of precancerous
lesion (cryotherapy, LEEP, Cervical conisation) - Trearment of invasive cancer (radiotherapy,
surgery, chemotherapy) - Psychologic and financial support in advanced stage of cervical cancer

Breast Cancer

Definition

This is a malignant growth that begins in the tissue of the breast in which abnormal cells grow in an
uncontrolled way. This is the most common and the second killer in women after cervical cancer in
the world, but can also appear in men.

Causes/Risk factors

- Early onset menarche

- Late menopause
- Delayed first pregnancy (after 30 years of age)

– Nullparity

Family history (maternal or paternal) BRCA1 and BRCA2 genes

- History of breast biopsy

- Excessive alcohol consumption

- Use of Hormonal therapy for more than 4 years

- Smoking

– Obesity

Protective factors

- Breastfeeding for 12 months

- Multiparity

- Regular physical exercise

Signs and Symptoms

- Asymptomatic

- Lump in the breast

- Unilateral nipple discharge

- Change in breast size

- Nipple or skin retraction

- Local lymphadenopathy

- Skin changes-orange like appearance (peau d’orange)

- Nipple or skin ulceration

- Breast pain

- Symptoms of metastasis

Investigations

- Self examination or examination by a practitioner

- Full Blood Count

- Bilateral Mammography and /or ultrasound

- Renal and Hepatic profile

- Chest X- Ray

- Biopsy (Preferably Fine niddle aspiration)

Staging

• Tis: if in situ including Paget disease

• T for invasive: notes size and relation to skin and chest wall Ș T1 (≤2cm) Ș T2 (>2cm and ≤ 5cm) Ș
T3 (> 5cm) Ș T4 (with extension to chest or skin)

• Regional lymph nodes (N): Ș No denotes no regional nodal metastasis Ș Subtyped if sentinel node
RT-PCR+/- , or staining by immunohistochemistry +/- ■ N1 denotes movable ipsilateral axillary
nodal metastases ■ N2 denotes fixed axillary lymph nodes, or enlarged internal mammary

• Distant metastasis (M) • Presence or absence (M1)

Stage grouping

• Stage 0: Tis, NO, MO

• Stage I: T1, NO, MO

• Stage IIa: Ș T0, N1, MO Ș T1, N1, M0 CLINICAL TREATMENT GUIDELINES -

GYNECOLOGY AND OBSTETRICS 153 Chapiter 1: OBSTETRIC/ Bleeding in first Chapiter 2:
GYNECOLOGY/ Cancers and Tumors Chapiter 1: OBSTETRIC/Diabetes in pregnancy term of
pregnancy Ș T2, N0, M0

• Stage IIb: ■ T2, N1, M0 ■ T3, N0, MO

• Stage IIIa: Ș T0, N2, M0 Ș T1, 1,N2, MO Ș T2, N2, MO Ș T3, N1, M0 Ș T3, N2, M0

• Stage IIIb: Ș T4, N0, MO Ș T4, N1, MO Ș T4, N2, MO

• Stage IIIc: Ș Any T, N3 Ș Stage IV: Ș Any T, any N, M1

Management

Depend on the stage of the diseases –

Stage 0 (Cancer in situ):

• Young women: conservative surgery only (lumpec

• Advanced age: Mastectomy only - Early stage: stage I and II

• Surgery: Modified radical mastectomy and lymphadenectomy (advanced age)

Ș Simple mastectomy or wide local lumbectomy (Young age)

• Hormonal therapy: Tamoxifen 20mg orally daily for 5 years: may cause retinal damage

Chemotherapy Ș Cyclophosphamide 30mg/kg IV single dose Ș Fluoruracil 300-1000mg /m2 IV, this
may be given every 4 weeks depending on the response of the patient Ș Paclitaxel 6mg /ml in
combination with Cisplatin 1mg /ml

Late cancer: stage III and IV: wide spread distance (metastasis)

• Hormonal therapy: Tamoxifen 20mg orally daily for 5 years: may cause retinal damage

• Chemotherapy: Ș Cyclophosphamide 30mg/kg IV single dose Ș Fluoruracil 300-1000mg /m2 IV,

this may be given every 4 weeks depending on the response of the patient Ș Paclitaxel 6mg /ml in
combination with Cisplatin 1mg /ml

Recommendation - Auto palpation once per month to exclude any breast mass - Regular clinical
checkup and mammography at least every 2 years

Endometrium cancer

Definition: Endometrium cancer is a growth of abnormal cells in the lining of the uterus, it usually
occurs in postmenopausal women (age peak: 40 to 55 years). The lifetime risk of developing the
cancer is 1.1%, while the lifetime of dying is 0.4%, reflecting the good prognosis with early diagnosis

Risk factors

- Post menopause

- Atypical hyperplasia of endometrium

- Excessive endogenous oestrogens (nullipartiy, obesity, early puberty, late menopause)

- Treatment with unopposed oestrogen

- Treatment with tamoxifen

- Family history of endometrium cancer

Obesity

- Hypertension

– Diabete

Stages –

Stage I: Disease confined to the body of uterus

- Stage Ia: Carcinoma confined to the endometrium

- Stage Ib: Myometrial invasion less than 50% - Stage Ic: Myometrial invasion more than 50%

- Stage II: Cervix involved

- Stage IIa: Endocervical gland involvement only

- Stage IIb: Cervical stromal invesion but does not extend beyond the uterus

- Stage III: Spread to serosa of uterus, peritoneal cavity, or lymph nodes

Stage IIIa: Carcinoma involving seros of the uterus or adnexae, positive ascites, or positive peritoneal
washings - Stage IIIb: Vaginal involvement either direct or metastatic

- Stage IIIc: Para-aortic or pelvic node involvement

- Stage IV: Local or distant metastases

- Stage IV a: Carcinoma involving the mucosa of the bladder or rectum - Stage IVb: Distant
metastases or involvement of other abdominal or unguinal lymph nodes

Signs and Symptoms

- Peri or post

-menopausal vaginal bleeding

- Postmenopausal vaginal discharge (pyometra)

- Symptoms of metastasis

Complications

- Metastasis to myometrium

- Hemetogenic and lymphathic metastasis

Investigations

- Transvaginal Ultrasound

- Hysteroscopy

- Endometrial biopsy

- CT-scan

- Investigations for metastasis

Management

Surgery
ophorectomy (TAH-BSO): stage I

• Radical hysterectomy: stage II

• Radical surgery with maximal debulk followed by radiotherapy: stage III Radical radiotherapy + or
not hormonal and or Chemotherapy: stage IV

Radiotherapy

• Most patient with early disease receive a combination of surgery and radiotherapy after
histopathology findings

• Patients treated with surgery alone are limited to those where the carcinoma is endometrioid type
confined to less than 50% of the mymetrial thickness

Hormonal therapy

• Progestogens are the most commom used form of hormonal therapy in endometrial cancer

Chemotherapy The use of chemetharapy is uncommon but should be considered in fit patient with
systemic disease Medicines used are:

• Epirubicin and Doxorubicin (anthracycline) and Cyplatin OR

• Carboplatin (platinum medicines) daily use limited by patient advanced age and poor performance
status. Cisplatinum 50mg/m2 IV, Adriamycin 45mg /m2 IV D1 followed by Paclitaxel 160mg/m2
repeat every 21 days OR Carboplatin and Paclitaxel as for ovarian canc

Recommendations

- Patient education e.g familial endometrial cancer

- Address if postmenaupausal bleeding

- Early reproductive period parity

- Avoid obesity

- Address if hypertensive and/or diabetic

- Consult before taking unopposed oestrogens and tamoxifen

. Ovarian cancer

Definition: Ovarian cancer is the leading cause of death of among all gyneacologic cancer
worldwide. More than 90% of ovarian cancers are epithelial origin from the surface (coelomic)
epithelium. It is the most common gynecological cancer.

Classification
- Epithelial Ovarian Cancer

- Germ Cell Ovarian Cancer

- Sex cord Stromal tumour

- Metastatic ovarian cancer from stomac (Krukenberg cancer)

Risk Factors

- Postmenaupaussal women but the cancer is considered in Women above 40 years old

- Family history of 2 or more affected first degree relatives (mother and sister)

- The family risk associated with predisposition to breast and ovarian cancer is inherited in an
autosomal dominant by a gene (BRCA1) located on Chromosome 17

- Abnormal ovarian development as in Turner’s syndrome - Nulliparity - Ovulatory stimulant drugs

Stages

Stage I: Disease confined to the ovaries (25% of presentations)

- Stage Ia: Involving only one ovary

- Stage Ib: Involving both ovaries

- Stage Ic: Positive cytology or ascites or breaching the capsule of either ovary

- Stage II: Confined to pelvis (5-10% presentations)

- Stage III: Confined to peritoneal cavity (45% presentations)

- Stage IIIa: Micronodular disease outside the pelvis

- Stage IIIb: Macroscopic tumor deposits 2 cm or retroperitoneal node involvement

- Stage IV: Distant metastases (20% of presentations)

Signs and Symptoms

- Most are asymptomatic

- Lower abdominal pain

- Pelvic mass

- Menstrual disturbances (e.g.menorrhagia)

- Gastro intestinal signs

- Pressure symptoms (Dyspareunia, urinary frequency, constipation)

- Ascites and any other signs related to metastasis

Complications

- Spread of the cancer to other organs (metastases)

- Severe loss of weight

- Ascites

- Intestinal occlusion

– Death

Investigations

- Abdominal ultrasound

- Intravenous urogram

- Ascitic tap for cytology –

Laparotomy/laparoscopy for biopsy and histology

- CT-scan and/or MRI

- CA-125

- Chest x-ray, FBC, liver function, renal function

Management Surgery is the principal treatment

• Laparatomy with large debulking if possible

• Washings from peritoneal cavity or any ascitis for cytology

• Where possible, a total abdominal hyterectomy, bilateral salpingo-oophorectomy and infracolic

omentectomy. The retroperitoneal lymph nodes are biopsied in women with clinically less than stage
IIIc. Chemotherapy is given to all patients after surgery, the overall response rate is 70-80%

• Carboplatin AUC 5-7 IV and Paclitaxel 175mg /m2 iv 21 day cycles for 3 -6 cycles or,

• Cisplatin 75mg/m2 iv and Paclitaxel 135 mg/m2 iv infusion over 24hrs (neurotoxic) or,

• Carboplatin and Cyclophosphamide 750mg /m2 IV

Recommendations

- Manage pelvic pain and/or abdomno-pelvic mass especially associated with vaginal bleeding

- Perform annual pelvic examination and pelvic ultrasound in reproductive and advanced age
Encourage oral contraceptive for high risk women of cancer of the ovary

- Consider prophylactic bilateral laparoscopic oophorectomy in women that don’t desire fertility with
a risk of cancer of the ovary.

- CA 125 is good test for follow up of patients with cancer of ovary but its not good for screening

MENOPAUSE

Definition: The menopause is the cessation of menstruation for at least 12 months in a female and
physiologically occurs at the age of 45 to 55 years.

Causes

- Age

- Primary ovarian failure

- Radiation and drugs

- Surgery

- Sheehan syndrome

Signs and Symptoms

- “Hot flushes “(i.e.; a sudden, unanticipated, and often unpleasant wave of body heat that can range
from mild to intense )

- Night sweats

- Palpitations

- Headaches

- Insomnia, tiredness

- Cessation of menses

- Vaginal atrophy and dryness

- Loss of libido, painful intercourse

- Bladder irritability, incontinence, UTIs

- Skin changes: dryness, thinning, loss of head hair, increase or loss of body hair

- Mood swings, emotional change

- Lack of concentration, failing memory

– Osteoporosis

Investigations - Hormonal profile (Serum FSH >15IU/litre) - Bone densitometry

Complications - Pathological fractures - Cardiovascular diseases

Management - Explain the process to the patient and reassure her - Suggest lifestyle adjustments -
Symptomatic treatment - Use hormone replacement therapy • Tibolone 2.5 mg tabs one tab/dayfor 30
days to be installed after 12 months of last menstruation • Estrogen (oral, patch or gel) plus
progesterone if the woman still has her uterus - Indication of hormonal replacement therapy: •
Treatment of menopausal symptoms like hot flashes • Prevention of osteoporosis - Side effects of
hormonal treatment increase the risk of breast cancer and DVT

PELVIC INFLAMMATORY DISEASES (PID)

Definition: PID is infection, usually sexually transmitted disease often including any combination of
inflammatory disorders involving uterus, fallopian tubes, ligaments of the uterus, and sometimes
ovary

Causes Pathogens (Neisseria gonorrhea, Chlamydia trachomatis, anaerobies, mycoplasma hominis,

Gardnerella vaginalis . . . )

Risk factors - Age < 20 represent 75 % - Earlier age at first sexual intercourse - Multiple sexual
partners - History of STIs - Induced abortion - IUD - HSG - Post partum and post abortum
endometritis

Signs and Symptoms - Asymptomatic - Fever - Lower abdominal tenderness, - Cervical-uterine-

adnexal excitation tenderness - Abnormal vaginal discharge - Abnormal genital bleeding –
Dyspareunia

Complications - Infertility - Ectopic pregnancy - Perihepatitis ( Fitz-Hugh-Curtis syndrome ) - Pelvic

abscess - Tubo-ovarian abscess - Pelviperitonitis – Death

Complications - Infertility - Ectopic pregnancy - Perihepatitis ( Fitz-Hugh-Curtis syndrome ) - Pelvic

abscess - Tubo-ovarian abscess - Pelviperitonitis – Death

Management

Chronic PID

First line treatment Ș Ceftriaxone, 1 g IM single plus Doxycyclline, 100 mg P.O. BID for 10-14 days
plus Ș Metronidazole, 500mg P.O. TDS for 10-14 days

Acute PID

Admit the patient • First line treatment

Ș Ampicillin, 500 – 1000 mg I.V. QID followed by 500 mg QID plus Gentamicin, 160 mg IM.
Injection plus Metronidazole, 500 mg IV TID followed by 500 mg P.O.TID For 10-14 days
Alternative treatment Ș Cefixime 800 mg PO single dose plus Doxycycline PO 100 mg BD plus
metronidazole 500 mg PO TDS for 10-14 days Ș Cefixime 800 mg PO single dose plus
Azithromycine single plus metronidazole 500 mg PO TDS for 10-14 days Ș Ceftriaxone, 1 g/day, IV
Plus Gentamicin, 160 mg, OD IM plus Metronidazole, 500mg

Surgical treatment Ș Laparatomy/Laparoscopy and drainage of abscess, salpingo-oopherectomy, Ș

Colpotomy Ș Hysterectomy with or without salpingo-oophorectomy

VAGINAL DISCHARGE SYNDROMES

. Bacterial vaginosis (BV)

Definition: Bacterial vaginosis (BV) is a clinical syndrome characterized by the presence of

malodorous vaginal discharge, with or without vaginal pruritus.

Cause - Bacterial infections (polymicrobial)

Signs and symptoms - Asymptomatic - Unpleasant fishy smelling vaginal discharges - External
genital irritation - Dysuria. – Dyspareunia

Complications - Premature rapture of membrane - Chorioamnionitis - Preterm delivery - Postpartum

endometritis - Post cesarean wound infection - Risk factor for HIV, HSV, Syphilis, Chlamydia
Gonococcal acquisition and transmission

Investigations - Amine (“fishy”) odor before or after addition of 10% KOH solution. - Vaginal pH
(pH ≥ 4.5) (unreliable if blood is present) - Homogeneous, smooth, non-inflammatory discharge -
Presence of clue cells (epithelial cells coated with bacteria) on microscopic examination. - Gram stain
of vaginal secretions - Screen for STDs

Management

First line treatment • Metronidazole, 500 mg P.O. BID for 7 days Or 2g P.O. single dose

Alternative treatment • Metronidazole 0.75% gel 5gm intravaginally QID for 5 days or • Clindamycin
2% cream 5 gm intra-vaginally once daily for 7 days, OR Clindamycine 300 mg P.O. BID for 7 days
OR • Tinidazole 2 gr PO single dose

In Pregnancy • Metronidazole, 250 mg P.O. TID for 7 days; after first trimester OR • Clindamycin,
300 mg P.O. BID for 7 days.

Recomandations - Avoid alcohol during treatment with oral metronidazole and for 24 hours
thereafter, due to possible disulfiram-type reaction. - Avoid use of Clindamycin cream in association
with latex condoms.

Sex Partners Routine treatment of male partners(s) with metronidazole does not prevent recurrence of
Bacterial vaginosis. For recurrent BV without evidence of other STD, recommend use of condoms,
and avoid douching.

Mucopurulent cervicitis
Definition: Mucopurulent cervicitis (MPC) is inflammation of the cervix

Causes - Infection with Neisseria gonorrhoeae or Chlamidia tra chomatis - Candida species - Genital
herpes or other organisms associated with bacterial vaginosis

Signs and symptoms - Vaginal discharge - Dyspareunia - Post-coital or intermenstrual bleeding -

Itching and irritation of external genitals - Lower back pain

Investigations - Vaginal swab - Colposcopy - Sample for pap smear - Lab test for Gonnorrhea and
Chlamydia

Complications - Parinatal transmission of STDs - Assending spread of infection - Salpingitis or

endometritis - For pregnant woman it may cause: - Chorioamnionitis - Premature rupture of
membrane - Postpartum infection

Management - The management depends on the cause

Trichomonal vaginitis

Definition: Trichomonal vaginitis is an inflammation of vagina and vulva.

Cause - Trichomonas vaginalis.

Signs and symptoms - Dysuria - Foul-smelling, frothy vaginal discharge that is most noticeable
several days after a menstrual period. - Vaginal itching and pain - Redness of vaginal lips and vagina

Complications - Premature birth - Low birth weight

Investigations - Microscopic examination of a saline wet mouted preparation - Litimus test for the pH
of vaginal secretion and whiff test

Management

First line treatment • Metronidazole, 500 mg P.O. BID for 7 days • Metronidazole gel, 0.75%, one full
applicator (5 g) intravaginally, once a day for 5 days • Clindamycin cream, 2%, one full applicator (5
g) intravaginally at bedtime for 7 days

Alternative treatment • Clindamycin 300 mg orally twice a day for 7 days or • Tinidazole 2 gr single
dose (when recurrentTrichomonal vaginitis) • Metronidazole 2 gr Po in single dose

In Pregnancy • Metronidazole, 2gm P.O single dose regimen.

Recommendations - Advise sexual abstention until symptoms improve and partner(s) treated - Avoid
alcohol during treatment with oral metronidazole and for 24 hours thereafter, due to possible
disulfiram-type reaction. - Repeated treatment failure: metronidazole 500 mg P.O. BID for 10-14
days. - Metronidazole gel is not effective for the treatment of Tvaginalis. - Consider metronidazole
resistance if patient is persistently infested after multiple treatment courses. - Tinidazole appears to be
effective against metronidazole resistant T. Vaginalis: dose is 2 gm once P.O.

Vulvo-vaginal candidiasis

Definition: Vulvo-vaginal candidiasis is a fungal inflammation of the vagina and vulva.

Causes - Fungus (candida albicans and non-albicans)

Signs and symptoms - Pruritis vulvae, - Whitish curd-like vaginal discharge - Vulval irritation -
Dyspareunia - Dysuria.

Invetigations - Potassium hydroxide test, - Lab swabs for culture - Random Blood sugar

Management

First line treatment • Vaginal Ș Nystatin, pessaris 100,000 IU per vaginum, x 4/ day for 14 days. Or •
Oral Ș Ketokonazole 200 mg BID for 5 days

Alternative treatment • Clotrimazole pessaries 100mg in vagina for 6 days or 200mg/day for 3 days.
Or • Miconazole pessaries 200 mg/day at bedtime for three days OR 100mg/day for 7 days or 2%
cream 5 gm intravaginal for 7 days.

Chronic Vulvo Vaginal Candidiasis First line treatment • Ketaconazole, 400 mg /day OR 200 mg BID
for 5-10 days. Then 100 mg/day for 6 mounths as prophylaxis. Alternative • Fluconazole, 150 mg
P.O. single dose, then 100 mg Ketoconazole /day for 6 mounths prophylaxis.