Sei sulla pagina 1di 217


Page 1 of 217


King Fahad Medical City –Ryadh - Saudi Arabia

He was kind enough to share them with his residents. They describe the important
points-anesthetic concerns- in most common anesthesia topics, to help you prepare for
the vaiva/case scenario exam.I hope that you will find them helpful in your exam as well
as in your clinical works as it was for me.


B:breathing/respiaratory system

C:circulation/heart condition.


M:metabolic concerns..lytes/glucose/ABG..etc.

G:gastrointestinal system.
THA Page 2 of 217
 Usually elderly Pt
 If a revision   blood loss and it takes longer Epidural or GA
 Look for the cause of arthritis  # due to CV disease (syncope) avascular necrosis
due steroids, infarction (sickle cell disease)
 Spinal Vs GA  less risk of PE with spinal and  blood loss
A, B, C  look under elderly, and other co-existing diseases
 Consider Autologus blood donation
 Lab: ECG, CBC….. depend on the co-existing diseases
 If suspect a difficult A/W  GA, due to position
 Intra-op: risk of PE (cement, BM, fat) consider art-line in Pt with CV disease
 Post-op: need to anticoagulated, pain epidural or PCA
 DDx of circulatory collapse intra-op: PE, MI, total spinal, anaphylaxis
Thalassemia Page 3 of 217
 Ethnic: Mediterranean, African-American, middle east and Asian
 -thalassemia
o major (homozygote) (Cooley’s anemia) severe, need treatment
o intermediate (hetro)
o minor (hetro)
o manifest after 1st year of life, when Hb F disappears.
 -thalassemia
o 4 genes for the -chain synthesis
o 1 gene deletion silent carrier.
o 2 genes deletion mild microcytic anemia.
o 3 genes deletion severe hemolytic anemia.
o 4 genes deletion hydrps fetalis
  GI absorption of iron and with multi-Tx  iron overload
hemochromatosis .
 treatment :
o Tx and folate in mild form
o Multi Tx and iron chelating agent in the severe form
o Splenectomy
The Myotonias Page 4 of 217
 delayed relaxation of skeletal muscle after voluntary contraction,
 myotonic contracture is not relieved by regional, NDMR, or deep GA.
 Relaxation may be induced by infiltration of the muscle with local anesthetic.
 caused by genetic abnormalities that produce defects in sodium or chloride
channels or proteins which alter ion channel function in muscle cells
 giving drugs that Na influx into the cell and delay return of membrane
excitability,like quinine, tocainide, or mexilitene, may relax myotonic
Myotonic Dystrophy (Steinert's Disease)
 is the most common form of the myotonias and the most severe.
 AD inherited disorder (1 in 8000), S/S during the 2nd and 3rd decades of life.
 clinical features associated with myotonic dystrophy: muscle degeneration,
cataracts, premature balding, DM, thyroid dysfunction, adrenal insufficiency,
gonadal atrophy, cardiac conduction abnormalities.
 Cardiac abnormalities LV diastolic dysfunction, cardiac failure is rare.
o AV block , A.fib, or flutter, ventricular dysrhythmias.
o 1st -degree AV block may actually precede the onset of clinical symptoms
o Sudden death may be a result of the abrupt onset of 3rd -degree AV block.
Thoracic trauma: Page 5 of 217
 ACLS, and in addition to other injuries
 Heart and major vessels
 Chest wall  flail chest > 3 ribs# need intubation with PEEP
 Esophageal
 Diaphragm  initially no S/S  then CXR diagnostic
 Lung parenchyma  contusion
 Tracheal, bronchial injury with blunt trauma Pt may have stridor,
wheezing, dyspnea S: subQ emphysema, pneumomediastinum, air leak, loss
of expiratory volume
 Due to association with other injury, mainly c-spine  DLT is difficult to insert
so consider other option
 If chest tube drain >1L initially or >200ml/h  open
 When putting a C-line  have it in the same side of the chest injury
 Always be careful with PPV which can worse the hemodynamic with
tamponade, and convert a pneumo to a tension pneumo
 Complication of chest injury empyema, recurrent pneumo, persistence air
leak, BPF
TOF Page 6 of 217
 Most common cyanotic CHD, F=M
 VSD, RVH, overriding aorta, RVOTO(sub, valvular, supra)
 70% have bicuspid aortic valve, 10% LAD from RCA
 CXR:  pul vascular marking, Rt aortic arch, ECG: RAD, RVH
 Tet spells: hypercyanotic attaches peak 2-6 m, by age 6y  ferq & severity
 Initiated by feeding, crying, defecation
 Any thing that  PVR or  SVR  tet spells (PO2, PCO2, acidosis)  Rt
to Lt shunt
 S/S: clubbing, cyanosis, polycythemia
 Pre-op: avoid dehydration, and don’t upset them
 Hemodynamic goals:
o Preload 
o R/R slow and sinus
o cont 
o SVR 
o PVR 
A N/A
TOF, obst Page 7 of 217
 Corrected TOF, not  risk, and no special precautions
 May have a residual or recur VSD, or  pul outflow tract obstruction
 All TOF need Echo for that reason
 12-ECG  may have arrhythmias, or conduction abnormality after the repair
 So for residual defect manage as TOF
 hemodynamic Goals:
o preload 
o R/R  slightly  maintain sinus
o Cont  maintain, or slightly 
o Afterload maintain, avoid sudden  in SVR
 No spinal
 early epidural is desirable, may  PVR
 Consider art-line
Tonsillectomy and Adenoidectomy Page 8 of 217
 Peds considerations
 Indication: recurrent tonsillitis, OSA, abscess
 A tonsils size(0-+4(75%)), A/W obstruction wheezing , stridor
 B OSA with snoring,  O2 sat, cor pulmonale, chest retraction and  RR
 C  CHD need Abx prophylaxis, Rt heart failure ECG, CXR, Echo
 D over counter meds may contain ASA
 Induction  normal
 Intra-op avoid NSAID’s , give zofran and decadron
 Post-op:
o N&V, dehydration, pain, bleeding  see other card
o Pul edema  due to relief of the obstruction  frothy pink secretion in
the ETT,  sat, wheezing,  RR
o DDx  anaphylaxis , CHF, volume overload, ARDS, aspiration
o Mx supportive  ETT, PPV with PEEP, O2 , diuretics
o Usually subsided with in 24 hrs
Transplanted heart Page 9 of 217
 High risk of infection mainly cholecystitis
 The efferent denervation is permanent, while some may retain afferent
 The response to exercise in normal heart is by  HR, in a transplanted heart it’s
by  SV, with little and delayed  in HR
 They are preload dependent
 ECG may shows both donor and recipient P waves
 No vagal input No bradycardia
 But they response to stress(hypoxia, PCO2) by  HR but it’s delayed
 Premature CAD, with in 3 yrs, mainly without angina, if they have Aff pain
 The main symptom is dyspnea
C altered response to stress, and drugs, CAD, maintain preload
D atropine and pancuronium No effect, Neostgmine  may slow HR,
Norepi  -effect, Adenosine  effect, in addition to the side effect of
immunosuppressant drugs, may need stress dose steroids, and Abx coverage
M adrenal suppression, glucose intolerance
Heme anemia, thrombocytopenia
Trauma in pregnancy Page 10 of 217
 Closed head injury is the major cause of death
 Other risks:
o Uterine rupture
o Placenta Abruption
o Fetal injury
o Spleen and liver rupture
 GSW, stabbing
 Same rule of nines apply to pregnant Pt
 With inhalation injury CO poisoning  the fetus has a higher affinity to CO
than the mother
 Apply the same ATLS, maintain LUD
 Have fetal US done, and continue FHR monitor
TURP-TURB: Page 11 of 217
 Distilled H2O hemolysis not used any more
 Sorbitol converted to fructose hyperglycemia, and to lactate acidosis, also
well cause osmotic diuresis and dehydration
 Glycine(inhibitory neurotransmitter) transit blindness ammonia 
TURP Syndrome:( water intoxication syndrome)
 S/S mild (restlessness, nausea, SOB, or dizziness) to severe (seizures, coma, HTN,
bradycardia, or CV collapse).
 In the awake patient: a classic triad of symptoms  in both SBP and DBP
associated with an  in pulse pressure, HR, and mental status changes.
 Volume overload  Lt heart failure pul edema
 CNS S/S due to both the type of irrigation and the severity of  in serum Na
 Management:
o ABC, 100% O2, intubate
o Notify the surgeon to terminate the procedure
o Consider DDx: over-sedation hypercarbia, hypoxia,
Anaphylactic reaction if CV collapse, diabetic coma
o 12 leads ECG, and invasive monitoring art line, CVP
Tylenol overdose Page 12 of 217
 A single dose of 10-15g can produce liver injury, 25g fulminant hepatic failure
 Ingestion even a lower dose with alcohol   the chance of hepatic failure
 Tylenol normally detoxified by conjugation to glutathione, but with overdose
 glutathione depleted metabolized by P-450 to a toxic compound
 First few hr after N&V, RUQ pain with or without obtundation
 After 24h symptom disappear and Pt looks well
 24-72h  liver failure appear, with possible ATN, and cardiotoxicity
 Poor prognosis with  Phos, coaglupathy, encephalopathy and acidosis
  bilirubin correlate with  survival
 Management:
o Mucomyst, with best result if given 12-20h after ingestion
o Roughly 150mg/kg over 15min, then 50mg/kg over 4h then 100mg/kg
over 16h
o Look at the nomogram
Ulcerative Colitis Page 13 of 217
A may have Ankylosing spondylitis  difficult A/W, with S/S bowel
obstruction  RSI
B  possible restrictive lung disease with ank-spond
C AR, hypovolemia
D steroids (stress dose)
M  electrolytes imbalance, K , metabolic acidosis,  albumin, adrenal
G  obstruction, perforation
Upper Ext nerve injury: Page 14 of 217
  sensation over the 4th and 5th fingers
 Muscle wasting, unable to grip a paper between fingers
 Loss of skin sensation over the lateral 3 ½ of the palm of the hand
 Weakness of wrist flexion, when making a fist  the index and middle
finger remain straight, also loss of thumb flexion
 If the injury at the axilla  unable to extend the forearm (triceps)
 If in the spiral groove  wrist drop
 Loss of arm flexion (biceps), loss of sensation over the lateral aspect of the
Axillary N
 Loss of skin sensation over the lower ½ of the deltoid muscle, with
weakness of arm abduction
URTI Page 15 of 217
 Need to distinguish from allergic rhinitis
  incidence of croup, bronchospasm, and laryngospasm
 If emergency or urgent surgery proceed, and anticipate the above problems
 If elective, and < 1yr  postponed
 If elective, >1 yr   temp  postponed
 Elective > 1yr  normal temp  P/E  purulent secretion, LRTI  postponed
 = = = =  clear  proceed to surgery
 How long to postponed for, if too long, the child may end up with another episode
of URTI, So 2-4 wks is reasonable
Uterine Rupture Page 16 of 217
 Risk see box 37-1 chestnut
 Mainly fetal distress and bleeding
A & B  onst
C hypovolemic shock, hypotension
Heme bleeding, anemia
 See abruption card
 Basically same management they come for stat C/S due fetal distress
VAE: Page 17 of 217
 When the surgical field > 5cm above the Rt atrium.
 40-50% in the sitting position, if known PFO, avoid sitting position
 Dx. By TEE the most sensitive then pericardial doppler, placed in the Rt
sternal border 3rd to 6th intercostal space, which detect 0.25ml of air
 Miller all Pt going for in sitting position need to have CVP
 Mx: 100% O2
Notify the surgeon, flood the surgical field with saline gauze
Wax the bone edges
Compress the jugular vein
Head down
Aspirate through the CVP
D/C N2O, and PEEP which may cause paradoxical embolism
von Willebrand's Disease Page 18 of 217
 AD, 3types I, II, III(very rare), group O blood have 20-30% less vWF
 Prolonged bleeding time, N PT and PTT
 I (70-80%) vWF, IIA also function abnormal, IIB they have
thrombocytopenia which aggravated by giving DDAVP (C/I).
 Pregnancy  vWF
 Rx  DDAVP 0.3ug/kg 1hr prior to surgery.
 DDAVP may cause fibrinolysis by releasing t-PA so consider giving TXA
 Cryo have vWF , recombinant Vwf.
 Hematology consult, Possible HIV +
 Do gentle intubation, avoid blind suctioning, avoid Regional anesthesia
VSD Page 19 of 217
 Rare in adult , with S/S depend on the size, and PVR, the larger, and the lower
PVR  more severe symptom
 small asymptomatic, load pansystolic murmur Lt sternal border, with normal
 mod also asymptomatic, with biventricular enlargement on CXR
 large when pul blood flow > systemic, S/S early as 4 wks, Lt Rt change to
Rt Lt  cyanosis
 hemodynamic goals:
o Preload 
o R/R N and sinus
o Cont slight 
o Afterload 
o PVR
 Pre-op Abx prophylaxis
A N/A
B pul edema
C shunt, CHF, low forward CO
White Cell–Related Transfusion Reactions Page 20 of 217
Febrile Reactions:
 antibodies to the HLAs after multiple Tx, 1% of all RBC transfusions.
 the patient experiences a temp  of more than 1°C within 4 hrs of a blood Tx and
defervesces within 48 hours.may also develop chills, respiratory distress, anxiety,
headache, myalgias, nausea, and a nonproductive cough.
 Febrile reactions can be treated with acetaminophen
 should be distinguished from a hemolytic transfusion reaction (direct Coombs test)
Graft-versus-Host Disease (GVHD)
 the donor lymphocytes may become engrafted, proliferate, and establish an
immune response against the recipient.
 Patients at risk for GVHD include organ transplant recipients, neonates who have
undergone a blood-exchange Tx, and patients immunocompromised by many other
disease processes. GVHD typically progresses rapidly to pancytopenia, and the
fatality rate is very high
 Also when a genetic relationship exists between the donor and the recipient
 GVHD has been reported with the transfusion of whole blood, packed RBCs,
granulocytes, platelets, and fresh, not frozen, plasma. It has not occurred following
transfusion of FFP, cryoprecipitate, or frozen RBCs
Wilms tumor Page 21 of 217
A delayed G. emptying  RSI
B lung mets, chemo, and radiotherapy effect
C HTN, severe if both kidneys involved  CHF,  renin secretion
D chemo
R hyperaldosternism(2nd) K
H severe anemia, low PLT, acquired vWD possible need F VIII concentrate
M art,and central line
Lab X-match, Lytes CBC
other upper body IV access
Potential intra-op problem IVC obstruction  CO
Tumor in the IVC  embolic phenomena
Post-op  ICU backup
mazen m a z e n

h o m e o f f i c e ,
AAA Elective Page 22 of 217
 Long procedure, large fluid shift, and high risk of blood loss
A N/A
B potential COPD
Renal border line function
 In the pre-op evaluation: concentrate on cardiac function with detailed H/P and
work up
 Lab: CBC-D, BUN, creat, Lytes, Mg, ECG, CXR, PFT, ABG, Echo if available
 Consider optimizing any medical condition pre-op by meds, consultation, and
further evaluation.
 X-match for at least 6 U of blood, have FFP ready
 Consider Epidural to do it as a combined technique
 Have the cell saver in the room, IV worming device, with blood set
 Lines: Big 14G peripheral IV, Art line, CVP/PAC, bear hugger
 Monitors: standard + 5 leads ECG, Foley, temp, art-line, CVP/PAC, TEE
 Induction: routine, modify on cardiac status
 Before induction have inotrops and vasodilators ready to go
Abruptio placenta Page 23 of 217
 Risk  with cocaine abuse, smoking, trauma, previous abruption,  age
 Most common cause of DIC, risk ante-postpartum hemorrhage, fetal hypoxia
 The bleeding could be concealed, and can have 2500ml of blood
 DDx placenta previa, uterine rupture
A obst
B obst
C hypovolemic shock,
Heme anemia, coaglupathy  DIC
R ARF from both shock, and DIC
Fetus  Demise, hypoxia,
 Depend on the severity, usually partial managed conservative with bed rest
 ABC, RSI, GI prophylaxis, induction with Ketamine, LUD
 Lab CBC, Lytes, BUN, creat, PT, PTT, fibrinogen, D-dimer , X-match
 Monitor  Art line, CVP/PAC, fetal monitoring , large IV
 Synto may not work  atony consider ergot, hemoabt(PGF2), may end up
need hysterectomy
Achondroplasia: Page 24 of 217
A potential difficult A/W, foramen Magnum Stenosis Avoid neck
extension , OSA
B Kyphoscoliosis  Restrictive lung disease
C Cor-pulmonale, pul HTN
CNS hydrocephalus, possible  ICP, central sleep apnea
 Lab CXR, C-spine, CT, MRI base of the skull, PFT, ECG, Echo, in
addition to the regular blood work
Acromegaly Page 25 of 217
 99% from pituitary adenoma
A large tongue , epiglottis, large nose  difficult intubation and mask fitting
Need FOI, possible vocal cord paralysis, and subglottic stenosis  smaller
ETT, and potential post-op A/W obstruction
C HTN, Cardiomegaly, cardiomyopathy, arrhythmias, CHF, hemodynamic
instability (ECG, CXR, Echo)
D  steroids for other pituitary problems
N  neuropathy (document), adenoma effect ? pressure  vision
M DM, hyperthyroid,
Position  nerve compression
Monitors  art line
ACT Page 26 of 217
 Mainly for depression, possible difficult to obtain an accurate medical history
 C/I: Pheo, pregnancy, recent CVA and MI, SOL with  ICP, and long bone #
 The main effect is on the CVS:
o Initial PSN effect with hypotension and bradycardia, even arrest
o Followed by intense SNS activation with HTN, tachycardia, arrhythmias
and  ICP and IOP
 Review the old anesthetic record for the dose, and any problems may had
 Also review all Pt med (TCA, MAOI)  avoid indirect sympathomimetics, also
be careful when direct acting drugs  exaggerated response
 Monitors  standard CAS monitors, consider invasive monitoring in sick Pt
 Pt with pacemaker or AICD not C/I have the magnet in the room, know what is
the program
Acute liver dysfunction Page 27 of 217
  M&M
 Postponed if not an emergency
 History of alcohol, drugs, exposure to toxins at work
A  LOC
B hypoxia, hyperventilation, V/Q mismatch
D altered drug metabolism
M lytes abnormalities
Renal impairment
CNS  encephalopathy
Heme coags abnormalities
 Avoid sedation pre-op
 Correct coags pre-op
 Intra-op avoid hypoxemia, and hypotension both  hepatic blood flow
Acute pericarditis, and effusion Page 28 of 217
 Most common cause is viral infection
 Post-MI  Dressler Syndrome
 S/S diffuse chest pain, with diffuse ST-elevation in ECG pericardial leads,
with sinus tachy, chest exam  friction rub.
 Consider Echo, if suspected effusion or tamponade
 Normal pericardial fluid 20-30 ml,
o In chronic effusion the pericardium can accommodate up to 1000
ml, without S/S of tamponade
o But in acute effusion as low as 200 ml can give symptoms
Adrenal Insufficiency (Addison disease): Page 29 of 217
 Need 90% destruction of the adrenal gland to produce symptoms
 primary (Addison's disease) is idiopathic adrenal insufficiency due to
autoimmune destruction. causes both a gluco and a mineralocorticoid
 Hashimoto's thyroiditis in association with autoimmune adrenal insufficiency
is termed Schmidt's syndrome.
 Other: bacterial or fungal infections, metastatic cancer, sepsis and
 Secondary: anterior pituitary fails to secrete sufficient quantities of ACTH.
from tumor, infection, surgical ablation, or radiation therapy.( less severe S/S,
aldosterone is maintained
 S/S Wt loss, muscle weakness, BP, abd/back pain due bleeding, N&V,
hyperpigmenation in primary only
 Dx by ACTH stim test
Adult with repaired CHD Page 30 of 217
 Type of CHD,
 When, What, and Where, (Repair)
 Understand the physiology of the repair
 Residue, Sequelae, and the complication of the repair.
 Follow up with cardiologist, recent Echo, if not ask for one
 Discuss the case with a college who knows more about CHD(peds cardiac
 The Need for SBE prophylaxis
 High risk for arrhythmia (pads on) for pacing, cardioversion, or shock
 Have inotrops support ready.
 In case of shunt  be meticulous about air in the IV, use saline instead of
air for epidurals.
 In case of pulmonary HTN have NO in the room
AI Page 31 of 217
 Well tolerated in pregnancy
 hemodynamic Goals:
o preload maintain, LUD
o R/R  slightly  maintain sinus
o Cont  maintain, avoid cardiodepressant
o Afterlaod 
 Epidural is good
Airway foreign body Page 32 of 217
 Emergency and potential life threatening
 In addition to peds consideration
 Brief H/P AMPLE, depend on the Severity of the symptoms and
hypoxemia may consider CXR( most are radiolucent), but may see
 Do inhalation induction with Sevo, Avoid PPV, minimal support if needed
 Assess the eye for depth (see later)
 The dilemma  Full stomach Vs need of maintaining spontaneous
 Once the eye in stage III  do direct laryngoscopy  Lidocaine spray
 May give IV bolus of propofol upon the removal of the foreign body
 Consider a dose of decadron , and racemic Epi
Airway laser surgery: Page 33 of 217
 Risk for both the patient and OR personal
 Knew what is the indication papiloma, stenosis, neoplasm  PFT, flow volume
loop, CT
 The airway is shared with the surgeon close communication
 Eyeglasses and laser mask, Pt eyes closed, covered with wet gauzes, and metal
shields, cover the exposed skin with wet towels
 Consider glyco pre-med
 Use laser-metal ETT, and fill the cuff with NS with methylene blue
 Avoid N2O, use the lowest FiO2 possible < 40%, other Jet ventilation
 Pt need to be completely paralyzed
 In case of airway fire remove ETT, have 60 cc syringe filled with NS ready,
after controlling the fire asses the airway damage, and ongoing fire, avoid high
Fi02 initially till you make sure that there is no ongoing fire direct
laryngoscope, bronchoscope with possible lavage and CXR, reintubate with new
ETT, keep intubated, Abx, and steroids ICU post-op
 CO2 laser only 0.01 mm penetration less bleeding and edema post-op
 With Nd-YAG laser deeper penetration, and risk of air embolism
 The metal-ETT are bigger than the PVC tubes so use one size smaller
Equations Page 34 of 217
alveolar gas equation:

Shunt equation

ventilation–perfusion ratio (VQI),is determined as follows:

Amniotic fluid embolism Page 35 of 217
 Catastrophic event with high mortality rate 86%
A  LOC, obst
B hypoxia, pul edema
C cardiopul collapse, RV failure
D  D/C synto
Heme  DIC, hemorrhage
CNS seizure
 ABC, 100% O2, Large IV,LUD, Lab as abruption, last thing to do CPB (case
 If Pt survive  ICU
Amphetamines Page 36 of 217
 For management same as cocaine
A&B obst
C HTN arrhythmias, tachycardia
D  MAC with acute intoxication, while chronic  MAC
CNS seizure
Obst  risk of abruption
 R. anesthesia  severe hypotension, with possible arrest

  serotonin and dopamine level
C HTN arrhythmia
MSK rhabdomyolysis
M+R lytes abnormality, ARF
Fetus toxicity
Amyloidosis: Page 37 of 217
 Extracellular deposition of amyloid type protein
A macrogolssia, tracheal stenosis (smaller ETT)
B pul edema from CHF
C arrhythmias, restrictive myopathy, CHF, autonomic dysfunction
Renal CRF, nephritic syndrome
Heme Factor X deficiency
 Lab/DI: CBC, lytes, BUN, Creat, CXR, PFT/ flow volume loop, ABG,
ECG, ECHO, coags
 Monitoring: CAS, Art-line, CVP/PAC, TEE
 Avoid Regional if coagulopathic
 The main goal intra-op is to maintain U/O, avoid any nephro-toxic drugs
 Have an ICU backup
Amyotrophic Lateral Sclerosis (ALS) Page 38 of 217
 Degenerative disease of the CNS with involvement of both UMN and LMN
 S/S Asymmetric weakness,  reflex, fasciculation and muscle atrophy
A bulbar involvement  Aspiration  mod RSI
B respiratory failure
D Sux C/I,  sensitivity to NDMR,
M abnormal glucose and Ca metabolism, with thyroid dysfunction
 Do Regional technique better
 If GA: Mod RSI, ICU post-op
Anesthesia for organ donation: Page 39 of 217
Condition Cause
Hypotension Hypovolemia (DI; hemorrhage) Neurogenic shock

Hypoxemia Neurogenic pul edema, Pul contusion, Pneumonia

Gastric aspiration, Fluid overload

Hypothermia Hypothalamic infarction, Exposure

Dysrhythmia Intracranial injury or herniation, Hypothermia

(especially bradycardia) Hypoxia, Electrolyte abnormality
Myocardial contusion, ischemia
 Avoid vasopressors  may cause visceral ischemia
 Consider using low dose Dopamine if needed
 They are atropine resistance
 Consider use NDMR due to somatic spinal reflex
 No need for GA, for  BP consider use vasodilators
Anesthesia For The Geriatric Patient Page 40 of 217
  physiological reserve of all organs
 Common diseases with aging are Sleep apnea, COPD, CAD, HTN,
arrhythmias, DM, arthritis, Alzheimer
A  stiff neck
B CC, CV, V/Q mismatch,  response to hypoxia and hypercarbia
C diastolic dysfunction, HTN, CAD, arrhythmias, CHF
D  Vd, with  both hepatic and renal clearance,  MAC,  sensitivity to
narcotics and sedatives
M DM,  Na,  heat production with more prone to hypothermia
GI/hep  gastric empting,  hepatic mass and blood flow
Renal   GFR, Na losing ,  drugs clearance, risk of volume overload
CNS Alzheimer, dementia, stiff ligament  difficult epidural/spinal
heme anemia
 Always IV wormer, bear hugger, and consider invasive monitoring
Aneurysm Page 41 of 217
 F>M, usually present with SAH
 Aneurismal SAH classification by Hunt & Hess and WFNS to estimate the
surgical risk and outcome
 WFNS Grade GCS Scale* Motor Deficit
 I 15 Absent
 II 13–14 Absent
 III 13–14 Present
 IV 7–12 Present or absent
 V 3–6 Present or absent
B pul edema
C HTN, ECG changes ST, T, QT, U  role out IHD
M lytes disturbance, SIADH, DI, pituitary dysfunction
 Classic S/S: headache, N&V, photophobia, LOC
 Lab: CBC, Lytes, BUN, Creat, CXR, ECG, review CT/MRI, X-match
 Induction as Supratentorial
 May need controlled hypotension, unless they do temporary clipping
Ankylosing spondylitis Page 42 of 217
 M>F, 20-30 y.o, -ve rheumatoid factor, HLA-B27 is +ve in 90% of Pts
 S/S: back pain and stiffness improve with exercise, lumber disc
degeneration, sacroilitis
A; Spines: limitation in the movement of all the spines, with  risk of C5-C7 #,
possible difficult intubation , TMJ involvement, Cricoarytenoid involvement
B: restrictive lung disease,  chest wall compliance and  VC, consider PFT
C: Aortitis with AI, CHF due to cardiomyopathy, dysrhythmias secondary to
cardiac conduction system involvement.
Renal  risk of RF
Drugs: anti-inflammatory drugs
Better to extubate awake
Intervertebral ligament calcification, difficult to perform neuraxial block by
midline approach, ? C/I if pt have peripheral neuropathy.
Aortic Regurgitation Page 43 of 217
 Chronic: rheumatic disease, hypertensive and atherosclerotic diseases, cystic medial
necrosis with or without other features of Marfan's syndrome, connective tissue diseases
including Reiter's syndrome and ankylosing spondylitis, luetic (syphilitic) aortitis,
 Acute: infective endocarditis, nonpenetrating trauma, ascending aortic aneurysm dissection
 Chronic: LV volume overload LV dilationLVH eccentric hypertrophy
 LVEDV but LVEDP still normal over time  LVEDP
 Acute: severe AR LV volume overload, but without time for LV dilation,HR is the only
comp mechanism to maintain forward CO, LVEDP and LAP  rapidly, with pul congestion.
History: chronic AR usually remain asymptomatic for years. Early symptoms include a
sensation pounding in the chest, palpitations, or head pounding. Exertional dyspnea may be the
first manifestation of LV decompensation, with later development of orthopnea and PND.
 Symptoms of more advanced disease include angina pectoris, which may be nocturnal, and
eventually symptoms of right-sided CHF with ascites and peripheral edema.
 Prognosis worsens with the onset of symptoms; mortality rate is estimated to be more than
10% per year among patients with severe AR and angina pectoris and more than 20% per
year among patients with symptoms of CHF.
 Acute severe AR Patients typically exhibit symptoms referable to the underlying disease,
including fever with infective endocarditis, and chest or back pain with aortic dissection.
Aortic Stenosis Page 44 of 217
 Valvular AS should be distinguished from nonvalvular forms of LV outflow obstruction, including
congenital supravalvular stenosis and subvalvular membrane, ridge or tunnel stenosis, and dynamic
subvalvular LV outflow obstruction in HOCM
 The normal AVA is 2.5-3.5 cm2. AS is not usually of hemodynamic significance until the valve
area is  to 25% of normal. mild 1.5 to 3.0 cm2, moderate 1.0 to 1.5 cm2, severe <1.0 cm2. With
normal CO, severe AS mean transvalvular pressure gradient 50 mm Hg.
 Transvalvular gradients are affected by flow, so patients may have low gradients despite severe AS
if there is LV systolic dysfunction.
 therapeutic decisions typically are based on the presence of symptoms in the setting of significant
aortic stenosis, categorization of disease as mild, moderate, or severe is of lesser clinical
Etiology congenital (bicuspid), rheumatic, or senile degenerative (calcific) in origin.
History long latent period >30 yrs
 The three classic symptoms associated with aortic stenosis are dyspnea, angina pectoris, and
syncope. (life expectancy < 5 yrs)
 Dyspnea due to in LVDP, LA, and pulmonary venous pressures.
 Angina occurs without CAD resulting from  O2 demand from  LV mass and  intracavitary
pressures in the setting of a fixed blood supply and from  coronary flow due to progressive
outflow obstruction.
 Syncope may be caused by peripheral vasodilation with exertion, with  in peripheral oxygen
requirement in the setting of a fixed CO.
Appendectomy Page 45 of 217
 In older Pt consider other and possible catastrophic problem (AAA)
A full stomach (RSI)
C dehydration, with  intravascular volume
GI Vomiting, full stomach
M Lytes abnormalities, acid base disturbance
Other could be septic
Lab CBC-D, lytes, BUN, Creat, ABG
Pain PCA

 For rectal Ca, with possible bowel obstruction
 Usually in elderly with other co morbidities
 With bowel prep  fluid deficit  hypotension upon induction
A RSI (b. obstruction)
C hypovolemia, elderly
Position lithotomy, jackknife
Monitors CAS, art line, temp, foley
Pain PCA, epidural
Arnold chiari malformation Page 46 of 217
 It’s one of the chiari malformation it’s type II
 associated with myelomeningocele
 present for posterior fossa decompression and repair of myelomeningocele and
insertion of shunt
 on of the main issue is position during induction due to myelomeningocele,
may put a donut where the defect is in the hall, if big may have to the induction
in lateral position then turn prone
A potential difficult airway, due to hydrocephalus  awake intubation
B vocal cords paralysis trach, resp depression due to post fossa compression
C bradycardia
CNS  the defects, and CN palsy
 position as above

AS Page 47 of 217
 Mild  well tolerated
 Mod/severe not well tolerated
 hemodynamic Goals:
o preload maintain, LUD, treat hypovolemia aggressively
o R/R  slightly  maintain sinus  treat arrhythmia aggressively
o Cont  maintain, avoid cardiodepressant
o Afterlaod , avoid sudden  in SVR
 Need are-line, CVP/PAC risk of arrhythmia with insertion, to maintain
PCWP =18
 GA opioids, mix kitamine/STP
 Have the crash cart in the room, pads on the Pt
 3 types: ostium secundum @ foramen ovale
Asthma: Page 48 of 217
 H/P: how bad is the asthma? Severity? Frequency? Any hospital or ICU admission
in the past, if yes when was the last one, how he/she manage the asthma at home,
or need ER visit, Exam: V/S, A/E , wheezing
 Review PFT results pre-post bronchodilators, and optimize pre-op
 If Pt is steroids (PO) dependent asthma consider steroids coverage peri-op
 Pre-med -agonist, Anticholenergics,
 Induction: IV Lidocaine, avoid STP, intubate deep, may consider LMA
 Maintenance: avoid any histamine releasing drugs,
 Emergence: consider extubate deep, IV Lidocaine pre-extubation
 Consider regional anesthesia to avoid intubation
Autonomic hyperreflexia: Page 49 of 217
 Post spinal cord injury above T-7  70-75%, following the resolution of
spinal shock, 2-3 weeks after injury
 Stimulation below the level of transection Severe HTN with bradycardia
A potential difficult A/W, unstable C-spine, aspiration risk (FOI), (RSI)
B  respiratory reserve and volumes, risk of aspiration, pneumonia, PE,
respiratory failure  PFT, ABG,  post-op vent (ICU)
C hyperreflexia, orthostatic hypotension, assess the volume status. ECG,
D (Sux C/I), have anti-HTN ready (Niprid) N. stimulator  show resistance
N deficit
 Neuraxial  best is a good choice but may be difficult to assess the level of
the block too high, or too low
 Hyper-reflexia may happen post-op due to bladder or rectal distension.
 Sequelae  CV collapse, arrhythmias, pul edema, stroke, seizure, death
AVM: Page 50 of 217
 M>F, 10-40yrs
 S/S parenchymal hemorrhage, SAH, Sz, motor/sens deficit
 In Peds  Vein of Galen AVM  hydrocephalus + high output cardiac failure
A  LOC
B aspiration during Sz
CNS Sz,  LOC,  ICP
 Pt may have (NPPB) normal perfusion pressure breakthrough  cerebral
hyperperfusion with normal CPP
o Rx: diuretics, hypervent, mild hypothermia, N-low MAP, high dose STP
 The rest of management like Aneurysm
 High risk of bleeding  blood in the room
Airway laser surgery: Page 51 of 217
 Risk for both the patient and OR personal
 Knew what is the indication papiloma, stenosis, neoplasm  PFT, flow
volume loop, CT
 The airway is shared with the surgeon close communication
 Eyeglasses, Pt eyes closed, covered with wet gauzes, and metal shields
 Consider glyco pre-med
 Use laser-metal ETT, and fill the cuff with NS with methylene blue
 Avoid N2O, use the lowest FiO2 possible, other Jet ventilation
 Pt need to be completely paralyzed
 In case of airway fire remove ETT, have 60 cc syringe filled with NS
ready, after controlling the fire asses the airway damage direct
laryngoscope, bronchoscope with possible lavage and CXR, reintubate with
new ETT consider ICU post-op
Delta rhythm (0–3 Hz) Deep sleep, deep anesthesia, or pathologic states (e.g.,
brain tumors, hypoxia, metabolic encephalopathy)
Theta rhythm (4–7 Hz) Sleep and anesthesia in adults, hyperventilation in
awake children and young adults
Alpha rhythm (8–13 Hz) Resting, awake adult with eyes closed; predominantly
seen in occipital leads
Beta rhythm (>13 Hz) Mental activity, light anesthesia
Hyponatremia < 130 Page 53 of 217
  or  in serum Na   &  in ECV & PV, so it’s result from excess or deficit of water
 total body Na regulated by aldosterone and ANP, where serum [Na] by ADH
 S/S depend on the rate and severity of  of Na: loss of apatite, N&V, cramps, weakness,
LOC, coma and seizure
 Acute CNS S/S is due to cerebral edema
 What is the serum osmolality see figure
 Cerebral salt wasting syndrome, mediated by BNP, independent of SIADH, risk head
trauma, tumor, SAH, and infection
 SIADH  see other card
 Rx < 120 with 3% NS @ 1-2 ml/kg/hr to  serum Na 1-2 mEq/l/hr only for few hrs, not
more than 25 mEq/l/48 hrs
 Rapid correction  abrupt brain dehydration central pontine myelinolysis mild (transient
behavioral disturbances or seizures) to severe (including pseudobulbar palsy and
quadriparesis).Within 3 to 4 weeks of the clinical onset of the syndrome, areas of
demyelination are apparent on MRI, risk factors (alcoholism, poor nutritional status, liver
disease, burns, and hypokalemia) , cerebral hemorrhage and CHF
 Once serum Na > 120 fluid restriction is enough , Also treat the underlying causes
To calculate the net water loss necessary to  [Na+] in hyponatremia, use the following equation:
Current [Na+] × current TBW = desired [Na+] × desired TBW TBW= 0.6x wt
1. Isolation of each lung to prevent contamination of a healthy lung
a. Infection (abscess, infected cyst) b. Massive hemorrhage
2. Control of distribution of ventilation to only one lung
a. Bronchopleural fistula b. Bronchopleural cutaneous fistula
c. Unilateral cyst or bullae d. Major bronchial disruption or trauma
3. Unilateral lung lavage
4. Video-assisted thoracoscopic surgery
1. Surgical exposure—high priority
a. Thoracic aortic aneurysm
b. Pneumonectomy
c. Upper lobectomy
2. Surgical exposure—low priority
a. Esophageal surgery
b. Middle and lower lobectomy
c. Thoracoscopy under general anesthesia
Omphalocele and Gastroschisis Page 55 of 217
o Impaired blood supply to the herniated organs, and intestinal obstruction
o Major intravascular fluid shift and dehydration full-strength balanced salt
o Hypothermia and hypoglycemia
A possible difficult airway  Beckwith-Wiedemann syndrome consists of
mental retardation, hypoglycemia, congenital heart disease, a large tongue, and
an omphalocele.
B respiratory failure
C CHD in 20% of infants with omphalocele.
Induction: NG  aspirate gastric content then RSI , need large IV , possible
central, and arterial line
Post-op keep intubated
Stroke & TIA: Page 56 of 217
 Hemorrhagic or ischemic
 Etiology: Atherosclerosis, embolic  MI, A.fib, VHD, post-op  CEA,
trauma, severe HTN
A  LOC, loss of A/W reflux (RSI)
B hypoventilation
C HTN, CAD, VHD, A.fib, arrhythmias  ECG, Echo
D anti-PLT, ASA, coumadin
N   LOC

 Avoid swinging in BP, and hyperglycemia
 With chronic HTN the cerebral autoregulation curve shifted to the Rt
Bioterrorism Page 57 of 217
 Use of nerve gases which are a potent Ach.esterase inhibitor and cause a
cholinergic crisis
 A mass casualty with both physical trauma and gas intoxication
 Healthy soldiers Vs civilian with different age groups and other co-
 The amount, duration and the rout of exposure are the major determine of
the clinical course of intoxication
 Exposure to vapor gives respiratory symptoms (SOB, wheezing,
bronchorrhea) with rapid cardiopulmonary collapse (muscarinic effect)
 Where dermal exposure slow, and gradual S/S local muscle twitches
and fasciculation (nicotinic effect) then resp failure, also carry more risk
to the health care personal with direct contact
 All the nerve gases causes irreversible inhibition to AchE in both central
and peripheral NS
 The key point in the management is to give the antidote ASAP, and protect
the health care personal
BKA Page 58 of 217
 For PVD, DM, gangrene, trauma, tumor
 Most of the Pt with major co-morbidities e.g. CAD, PVD, DM, COPD,
CVA, Sepsis, CRF,
 H/P standard + depend on the co-morbidities
 Lab also as above
 Options: GA Vs spinal/epidural may  the incidence of phantom limb
pain, but look for C/I
 monitors standard + depend on the above co-morbidities
 Position  risk of ischemic necrosis (pads)
 EBL 250 ml
 The use of tourniquet  bleeding, but be aware of risk thrombus
embolization PE
 Post-op pain(epidural, nerve block, PCA), DVT (S/C heparin), MI, CVA,
infection, bleeding
BPF and Empyema Page 59 of 217
 Causes: after pulmonary resection for carcinoma, traumatic rupture of a
bronchus or bulla ( barotrauma or PEEP), penetrating chest wound, or
spontaneous drainage into the bronchial tree of an empyema cavity or lung
 PPV contamination of the healthy lung, loss of air with  alveolar
ventilation and CO2 retention, and potential tension Pneumothorax
 In case of empyema with BPF drain the empyema under LA with chest tube
under suction, then do a CXR, then may fix the BPF under GA
 GA options ( the main target is to avoid PPV)
o Awake intubation with DLT
o Gas induction and maintaining spontaneous ventilation
 Keep FiO2 always 1, and avoid N2O
 For non-surgical management: DLT and resting the affected lung, or use of
 Keep a high index of suspicion for tension Pneumothorax
Brain death Page 60 of 217
―irreversible cessation of all function of the entire brain, including the cortex
and brain stem, determined in accordance with accepted medical standards‖


o No spontaneous movement
o Unresponsive to external stimuli
o Absent respiratory reflex (apnea test)
o Absent cranial nerve reflexes (Gag or cough reflex to suction)
o Pupillary light reflex ( no pupil constriction)
o Corneal reflex ( no blinking with corneal touch)
o Oculocephalic reflex ( doll’s eyes)
o Oculovestibular reflex (cold caloric test)
o Atropine resistance
o Electroencephalography
Brain metabolism and physiology: Page 61 of 217
 In adult:O2 3.5 ml/100g/min& 5.5 mg/100g/min of glucose, peds 5.5 ml O2
 the autoregulation is abolished by trauma and hypoxia
 CSF from the choroids plexus and absorbed by the arachnoid villi, volume
100-150 ml, rate of production and absorption 0.3-0.4 ml/min, with 
production by Lasix and acetazolamide
 Enf  production and  resistance to absorption, Iso 0/  resistance
 ICP N= 10 mmHg,  ICP   CPP, and herniation
 All volatile agents  CBF with return to baseline in 3 hrs, with  CMRO2
 All volatile agents and kitamine cause cerebral vasodilation, except N2O
 N2O cause  CBF w/out dilation, and no change in CMRO2
 All IV drugs cause  CBF and  CMRO2
Bronchiectasis: Page 62 of 217
 Localized irreversible dilation of bronchus
 May have COPD, and restrictive component
 And may associated with other condition so look of other underlying disease:
aspergillosis, HIV, R. arthritis
 If Pt present to OR with active pul infection postponed Sx, and give Abx therapy
 Lab: PFT, ABG, CXR pneumonia
 Pt may present with hymoptysis  required arterial embolization, or resection of
the affected segment
 Consider DLT to isolate the affect lung
 Need pre-op Abx
Carcinoid Tumors Page 63 of 217
 GI is the most common source, 50% appendix, 25% in the ileum(the source of
metastatic tumors), also from the lung,
 hormones secreted by nonmetastatic tumors reach the liver by portal vein and are
usually inactivated there. once metastases to the liver, the hormones secreted by
the hepatic metastases may have direct access to the systemic circulation, to
produce the S/S of the carcinoid syndrome
 Could be a manifestation of MEN I,
 Release Serotonin, Histamine, Kinins
 Symptoms: cutaneous flushing, abd pain, V, diarrhea, HTN, hypotension,
bronchospasm, and hyperglycemia
A N/A, Gentle induction, avoid sux, STP
B bronchospasm, endobronchial tumor obstruction
C Rt side disease  myocardial fibrosis  TR, PR, consider CVP, art line
sympathomimetic drugs can trigger mediator release from carcinoid tumors
D Give antihistamines, avoid drugs that can cause histamine release
octreotide 10-100 ug IV
M Dehydration due to diarrhea, and vasoconstriction , hyperglycemia
Cardiac herniation Page 64 of 217
 An emergency and life threatening with mortality 50%
 With pneumonectomy, in the 1st few hrs or few days later
 Pathophysiology:
o twisting of the SVC (SVC syndrome),
o twisting IVC (cardiovascular collapse),
o twisting distal trachea (wheezing),
o twisting pulmonary veins (pulmonary edema),
o pericardial constriction of the heart (myocardial ischemia and
ventricular arrhythmia)
 Risks:
o Events that  intrapleural pressure in the (ventilated) hemithorax or
that  intrapleural pressure in the surgical (empty) hemithorax may
predispose the patient to cardiac herniation.
o Placing the patient with the empty hemithorax in a dependent
o Use of high levels of pressure and volume during mechanical
ventilation of the remaining lung can push the heart into the empty
hemithorax. And coughing
Cardiac Risk* Stratification for Noncardiac Surgical Procedures Page 65 of 217
High (Reported cardiac risk often greater than 5%)
· Emergent major operations, particularly in the elderly
· Aortic and other major vascular surgery
· Peripheral vascular surgery
· Anticipated prolonged surgical procedures associated with large fluid
shifts and/or blood loss
Intermediate (Reported cardiac risk generally less than 5%)
· Carotid endarterectomy
· Head and neck surgery
· Intraperitoneal and intrathoracic surgery
· Orthopedic surgery
· Prostate surgery
Low† (Reported cardiac risk generally less than 1%)
· Endoscopic procedures · Superficial procedure
· Cataract surgery · Breast surgery
*Combined incidence of cardiac death and nonfatal myocardial infarction.
†Do not generally require further preoperative cardiac testing.
 Pre-op: H/P
 Lab: CBC, Lytes, BUN, creat, Glucose, ECG, PFT if needed
A N/A
B possible smoker COPD
C CAD, HTN (need to well controlled pre-op)
CNS neurological deficit
 Regional (deep, superficial cervical plexus) Vs GA same out come
 Induction: anticipate fluctuation of BP
 Maintenance: Iso neuro-protection, Keep BP 20% higher, monitor blood
glucose, LA infiltration over the carotid sinus, give heparin 100u/kg
 Monitors: standard+ 5leads ECG, Art-line, in cardiac Pt consider TEE,
Emergence: early to assess for nay neuro deficit
 Post-op potential problems: new neuro deficit back to OR or Angio,
hemodynamic instability mainly HTN, bleeding with hematoma formation which
may compromise the Airway  Back to the OR, 100% O2 have difficult airway
Canadian Cardiovascular Society Functional Classification of Angina Pectoris Page 67 of 217
Class Definition Specific Activity Scale
I Ordinary physical activity, (eg, walking and climbing stairs) does not cause
angina; angina occurs with strenuous, rapid, or prolonged exertion at work or
recreation. Ability to ski, play basketball, light jog (5 mph), or shovel snow
without angina
II Slight limitation of ordinary activity; angina occurs on walking or climbing
stairs rapidly; walking uphill; walking or stair climbing after meals, in cold, in wind,
or under emotional stress; or only during the few hours after awakening; when
walking > 2 blocks on level ground; or when climbing more than 1 flight of stairs at a
normal pace and in normal conditions. Ability to garden, rake, roller skate, walk
at 4 mph on level ground, and have sexual intercourse without stopping
III Marked limitation of ordinary physical activity; angina occurs on walking 1 to
2 blocks on level ground or climbing 1 flight of stairs at a normal pace in normal
conditions. Ability to shower or dress without stopping, walk 2.5 mph, bowl, make
a bed, and play golf
IV Inability to perform any physical activity without discomfort; anginal
symptoms may be present at rest. Inability to perform activities requiring 2 or
fewer metabolic equivalents (METs) without angina
Cesarean Section Page 68 of 217
 Depend if elective/urgent Vs stat
 Always have the room ready: Anesthesia machine checked, A/W equipment
ready, Emergency drugs ready
 Always ask for blood for any bleeding case
 Enough time to evaluate Pt, H/P as routine obstetric Hx, and anesthetic Hx with
physical exam mainly the A/W, chest, edema …..+ review lab, obstetric
 Obtain informed consent from the Pt for neuroaxial block, with risk/benefit
discussion, if not C/I for the block.
 Pre-meds  GI, other if indicated e.g. asthma, anxiety, endocarditis, steroids
 IV  at least 1.5 -2.0 L of fluids
 O2, Pre-block V/S
 If using hyperbaric L.A lie the Pt down very quickly + LUD, repeat BP
 Inform the Pt that if she feel sick to tell me right way (BP)
 Examine the block by asking the surgeon to use a teeth forceps
 As soon as the baby out give synto 5 U then 20 U in the bag
 For spinal: 10.5 mg marcaine hyperbaric, 20 ug fentanyl, 150 ug epimorph
CHF: Page 69 of 217
 Causes: IHD, VHD, CHD, Cardiomyopathy, HTN, pul HTN
 Hallmark: CO,  VEDP, SVR, metabolic acidosis
 Could be Sys Vs Dias, Rt or Lt
 S/S: SOBOE, orthopnea, PND,  exercise tolerance
 P/E: crackles,S3 gallop,  JVP, hepatosplenomegaly, ascites, peripheral edema
 Rx that proven to improve outcome: ACEI, -blocker, spironlactone
 Rx that improve symptom: Dig, and loop diuretics
 Other antiarrhythmics, anticoag, vasodilators
 Other modality: biventricular pacing, AICD
 Assess using NYHA functional capacity
I  no limitation with normal activity, and no symptom
II  slight limitation with normal activity, symptomatic
III  marked limitation with normal activity, comfortable at rest, les the normal
activity produce symptom
VI  severe limitation, symptomatic at rest
 Pre-op: postponed if decompensated, Cardiology consult to optimize
 Workup: CBC, Lytes, Chem, 12-ECG, CXR, review Echo
Lab and Clinical Criteria for Estimating Hepatic Reserve (Child-PughPage 70 of 217
Serum bilirubin
mg/100 mL <2.0 2.0–3.0 >3.0

Serum albumin
g/100 mL >3.5 3.0–3.5 <3.0

Ascites None Easily controlled Not easily controlled

Encephalopathy None Minimal Advanced

Nutrition Excellent Good Poor

Prothrombin time
(sec > control) 1–4 4–6 >6

Surgical risk mortality rate 5% 10% 50%

Chronic constrictive pericarditis Page 71 of 217
 It resemble tamponade in impede diasolic pressure,  venous pressure, and 
stroke volume
 Causes: idiopathic, CRF, radiation, R. arthritis, and post-heart
 S/S: arrhythmias A.fib and flutter, kussmaul sign exaggerationin  CVP with
inspiration, pulsus paradoxes but less than tamponade
 CXR: calcification over the pericardium.
 ECG:  voltage of QRS, inverted T-waves
 Rx  surgical pericardiotomy
 Anesthesia Mx
o Preload  maintain, and avoid , since they’re preload dependent
o Cont maintain, avoid cardio-depressant drugs
o Rate: avoid sudden  HR
o Afterload maintain, avoid sudden drop in SVR, since limited CO
o Avoid all histamine releasing drugs
o Art-line, PAC, CVP at least
Clinical Predictors of Increased Perioperative Cardiovascular Risk (Myocardial
Page 72 of 217
Infarction, Heart Failure, Death)
 Unstable coronary syndromes
· Acute or recent myocardial infarction* with evidence of important
ischemic risk by clinical symptoms or noninvasive study
· Unstable or severe† angina (Canadian class III or IV)‡
 Decompensated heart failure
 Significant arrhythmias
· High-grade atrioventricular block
· Symptomatic ventricular arrhythmias in the presence of underlying heart disease
· Supraventricular arrhythmias with uncontrolled ventricular rate
 Severe valvular disease
 Mild angina pectoris (Canadian class I or II)
 Previous myocardial infarction by history or pathological Q waves
 Compensated or prior heart failure
 Diabetes mellitus (particularly insulin-dependent)
 Renal insufficiency
Coarctation of the Aorta Page 73 of 217
 If corrected no special precautions
 Arm-leg different < 20mmHg good outcome
 Uncorrected high risk of LV failure, aortic rupture or dissection, endocarditis
 High mortality rate,  risk of offspring CHD
 Risk of having bicuspid aortic valve, aneurysm of circle of Willis
 Measure Rt Vs Lt side BP, and upper Vs lower BP
 Need Echo and 12-ECG
 hemodynamic Goals:
o preload 
o R/R  slightly  maintain sinus
o Cont  maintain, avoid cardiodepressant
o Afterload maintain, avoid sudden  in SVR
 Avoid Regional GA is better tolerated for C/S
 Monitors  Art-line, CVP,
 Ephedrine and dopamine are the best choice since they have choronotropic
Cocaine abuse Page 74 of 217
 Affect three main neurotransmitters Norepi, Serotonin and dopamine
 Can present like PIH with HTN, edema, proteinuria
B aspiration, bronchspasm, pneumothorax, pneumomediasinum
C MI, HTN, arrhythmias
Renal  ARF
Heme thrombocytopenia, DIC, anemia
Hepatic failure, rupture
CNS seizure, ICH, SAH, CVA
fetus  UP blood flow, cross placenta
 The main problem is severe HTN with induction, So consider NTG, hydralazin
with induction, avoid pure -blockers alone may get unopposed -effect, with
 risk of coronary vasospasm
 Regional OK, be aware of severe hypotension with spinal,and ephedrine is not
a good choice(not work) Neo better
Coma/LOC Page 75 of 217
 Management:
o Monitors
o Give thiamine 100 mg IV, Dextrose 50g IV
o Lab: ABG, ECG, chemostrip, lytes, BUN, creat, CBC-D, LFT,
coagulation profile, urine analysis, blood/urine for toxicology and
drugs level
 DDx:
o CNS pathology: tumor, trauma, seizure disorder, aneurysm, AVM
o Infection: meningitis, encephalitis, sepsis
o Metabolic: hypoglycemia, DKA, HONKC, uremia, hepatic
encephalopathy , acidosis
o Respiratory: hypoxia, hypercarbia
o Overdose: EtOH, drugs(opioids, TCA, Cocaine, Tylenol,…..)
 H/P AMPLE, VS, Neuro GCS, lateralization, pupils,
Myasthenic Syndrome Myasthenia Gravis
Manifestations Proximal limb weakness Extraocular, bulbar and
(arms > legs) facial muscle weakness
Exercise improves with strength Fatigue with exercise
Muscle pain common Muscle pain uncommon
Reflexes absent or Reflexes normal

Gender Male > female Female > male

pathology Small cell carcinoma of the lung Thymoma

Response to Sensitive to Sux and NDMR Resistant to Sux

muscle relaxants Sensitive to NDMR

Poor response to Good response to

anticholinesterases anticholinesterases
Congenital Diaphragmatic Hernia Page 77 of 217
95% Lt side
neonatal and premature consideration
A insert NGT , keep suction
B hypoplastic lung  RDS,  risk of pneumothorax with PPV, keep Airway
pressure < 20-30 cmH2O, and avoid lung expansion after hernia repair, neonate
could be on NO or ECMO, N2O is C/I, keep 100% O2
C  15% CHD
R renal abnormality
N neuro abnormality

Congenital lobar emphysema

o LUL most common
o Emergency and potential life threatening
A ?
B resp failure, ball valve  avoid PPV, cyanosis, N2O C/I, 100% O2
C mediastinal shift  hemodynamic instability , 20% CHD
Lab X-match
Induction gas induction, with spontaneous breathing
COPD Page 78 of 217
A  airway reactivity   bronchospasm
B  risk of hypoxia, hypercarbia, bronchospasm, and PPC: atelectasis, pneumonia,
respiratory failure, smoking
C cor pulmonale, RV failure, pul HTN
D avoid STP,  sensitivity to resp depressant drugs
Heme polycythemia
  PPC with: FEV1/FVC < 70%, FEF25-75 <50%, FVC< 75%, with respiratory
failure more likely if FEV1 <50%, PaCO2 > 50
 H/P: smoking, wheezing, coughing, sputum amount and color, exercise tolerance,
home O2, A/E bilaterally, wheezing, crackles,  JVP, peripheral edema, cyanosis
 With smoking  risk of CAD
 Lab: CXR, ABG, PFT, ECG, CBC-D, lytes, BUN, creat
 For PFT do pre and post bronchodilators
 Optimize the Pt pre-op: smoking cessation, bronchodilators(-agonist, steroids,
anticholenergic) , consider Abx therapy
 Pt may need O2 supplement pre-op if PaO2<60, cor pulmonale, Hct >55
Coronary Artery Disease— Myocardial Infarction Page 79 of 217
Anatomic Site Leads ECG Changes Coronary Artery
Inferior II, III, aVF Q, ST, T Right
Lateral I, aVL, V5–V6 Q, ST, T Left circumflex
Anterior I, aVL, V1–V4 Q, ST, T Left
Anteroseptal V1–V4 Q, ST, T LAD

Electrolyte Disturbances
Ca2+ Ca2+ K+ K+
Rate <100 <100 <100 <100
Rhythm Regular Regular Regular Regular
PR interval Normal Normal/  Normal Normal
QT interval   T flat/U wave T peaked QT 
Craniosynostosis: Page 80 of 217
 May associated with other syndrome  Crouzon’s syndrome  (MH)
 Main issues: difficult A/W, massive blood loss, VAE, ICP
A possible difficult A/W  maxillary hypoplasia, large tongue, micrognethia
Awake FOI, multi masks and blads
B  tracheal stenosis, tracheomalacia, OSA
D  Avoid ketamine and sux
M  lytes abnormality
N  ICP, seizure disorder, mental retardation
 Have a big IV access, blood in the OR
 If only one suture  short procedure, if > 1 , long with risk of bleeding 
so need art line, CVP, IV wormer , bear hugger, Foley cath
 If involve below the orbit  A/W swelling  keep intubated post-op (ICU)
till the swelling subsided
Creutzfeldt - Jakob disease Page 81 of 217
 human spongiform encephalopathies.
 The other two diseases in this group are kuru and Gerstmann-Straussler syndrome.
Pathologically, these disorders are characterized by vacuolation of brain tissue and neuronal
loss. caused by an unusual infectious agent—a prion. A prion is a small proteinaceous
infectious agent. Prions are resistant to alcohol, formalin, ionizing radiation, proteases, and
nucleases, but can be inactivated by heat (autoclaving), phenol, detergents, and extremes of
 incubation time is long (years)
 The typical clinical characteristics include subacute dementia, myoclonus, and EEG
Management of Anesthesia
 Because of the transmissibility of the disease, appropriate precautions should be taken to
protect other patients and health care providers.
A prone to aspirate gastric impaired swallowing function and decreased activity of laryngeal
C autonomic dysfunction  abnormal CV responses to anesthesia and vasoactive drugs.
DBecause lower motor neuron dysfunction  succinylcholine should be avoided.
Crohn's Disease Page 82 of 217
A RSI for S/S of bowel obstruction
B N/A
C hypovolemia
D Steroids (stress dose), immunosuppressant
G obstruction, fatty liver, cirrhosis, perforation
R amyloidosis
Heme chronic anemia, iron def, vit B12, folate
M hypovolemia, K,  3rd space loss,  albumin   free fraction of drugs
MSK arthritis with  ROM
Cushing Syndrome :( Glucocorticoid Excess) Page 83 of 217
 Cortisol function: 1- maintain BP by converting Norepi  epi, 2- anti-
inflammatory, 3- Na retention, and K excretion, 4- hyperglycemia by 
gluconeogenesis, and  glucose uptake by the cells
 Exogenous therapy (most common) > 21 days
 Bilateral adrenal hyperplasia due to ACTH from pituitary adenoma or non-
endocrine tumor (lung, kidney, pancreas)
A possible difficult A/W, mucosa easily traumatize
C HTN, volume overload
D steroids (stress dose), avoid etomidate, titrate NDMR
N  emotional, psycosis
M  DM, K, met alk, Addison crisis
MSK osteopenia, muscle wasting
Immun  infection
Post bilateral adrenalectomy may need mineralocorticoid replacement in day 5,
give 0.05–0.1 mg·day–1 of fludrocortisone
CV diseases in pregnancy Page 84 of 217
 Lt  Rt shunt e.g. ASD, VSD, PDA are well tolerated in pregnancy
 The main keys in management for anesthesia are
o Avoid air bubble in the IV
o For epidural insertion use saline instead of air both due to risk of
paradoxical air embolism
o Pain   catecholamine   SVR  shunt  RV failure
o So early epidural is desirable
o Slowly titrate the epidural, and avoid spinal  sudden SVR  convert
the shunt to Rt Lt
o Give O2 all the time
CVP Waveform Components Page 85 of 217


a wave End-diastole Atrial contraction

c wave Early systole Isovolumic ventricular contraction,

tricuspid motion toward right atrium

v wave Late systole Systolic filling of atrium

h wave Mid- to late diastole Diastolic plateau

x descent Mid-systole Atrial relaxation, descent of the

base, systolic collapse

y descent Early diastole Early ventricular filling, diastolic

Cyanide toxicity Page 86 of 217
 By preventing oxidative phosphorylation cellular hypoxia anaerobic
 S/S lactic acidosis, tachyphylaxis to SNP,  SvO2, Sz
 100% O2
 Thiosulfate 150 mg/kg IV administered over 15 minutes (acts as a sulfur
donor to convert cyanide to thiocyanate)
 If severe, with deteriorating hemodynamics and metabolic acidosis  slow
IV administration of sodium nitrate, 5 mg/kg. ( converts Hb to
methemoglobin, which acts as an antidote by converting cyanide to
 hydroxocobalamin (vitamin B12a) which binds cyanide to form
cyanocobalamin (vitamin B12) can be administered (25 mg/hour IV to a
maximum of 100 mg)
Cystic fibrosis: Page 87 of 217
 A disease of the exocrine glands: salivary, sweet, GI, pul
 Rx: chest physio, Abx, bronchodilator, GI enzyme
A sinusitis  avoid nasal intubation with active nasal infection.
B pneumonia, mixed obstructive/restrictive disease, bronchiectasis
C cor-pulmonale
GI cholelithiasis, pancreatic insufficiency, hepatic dysfunction
Heme bleeding disorder
 Lab: CBC-D, lytes, BUN, creat, coags, CXR, PFT, ECG, Echo if needed
 Monitors: CAS, art-line
 Suction the airway before extubation
 Consider regional block for post-op pain control
 Encourage chest physio post-op
Deliberate Hypotension: Page 88 of 217
 Mainly used to  blood loss: aneurysm, AVM, spine Sx, major head and neck
 The main C/I are: uncontrolled HTN, severe anemia, TIA’s angina, heart failure,
resp failure, acidosis, hypoxia, Renal insuff
 Ass intravascular volume pre-op, and expand it if necessary.
 Have a target MAP based on awake MAP e.g. 70% of the awake MAP
 Monitors: Art-line, CVP, SSEP or EEG in brain and spine Sx
 Choices:
o SNP: rapid on/off, risks:  pul shunt,  ICP, cyanide and thiocyanate toxicity,
and rebound HTN, also it’s inhibit PLT aggregation, do not exceed
10ug/kg/min for 10 min, or > 1mg/kg in 2hrs, or 0.5mg/kg in 24hrs, Rx of
toxicity: IV thiosulfate, if abnormal renal functionhydroxocobalamin
o NTG: less potent, no cyanide problem, but  shunt,
o Isoflurane: easy titration,  CMRO2,
o Other: Trimethaphan, Esmolol and Labetalol, Prostaglandin E1, Nicardipine
Diabetes Insipidus Page 89 of 217
 from inadequate secretion of ADH (central DI)
 or resistance on the part of the renal tubules to ADH (nephrogenic DI)
 Failure to secrete adequate amounts of ADH results in polydipsia,
hypernatremia, and a high output of poorly concentrated urine.
 due to destruction of the pituitary gland by intracranial trauma, infiltrating
lesions, or surgery.
 depends on the extent of the hormonal deficiency. During surgery, the
patient with complete DI receives an iv infusion of aqueous ADH (100–200
mU·h–1) combined with administration of an isotonic crystalloid solution.
The serum sodium and plasma osmolality are measured on a regular basis,
and therapeutic changes are made accordingly.
 ADH also may be given intramuscularly (as vasopressin tannate in oil).
 DDAVP administered intranasally has prolonged antidiuretic activity (12–
24 hours) and is associated with a low incidence of pressor effects.
 As a consequence of the large outpouring of ADH in response to surgical
stress, patients with a residually functioning gland usually do not need
A stiff joint syndrome ―prayer sign,‖,  mobility of the AO joint. difficult
intubation, FOI, RSI  full stomach
B N/A
C CAD, PVD, cardiomyopathy , silent MI, autonomic neuropathy,  risk of
post-op MI
D metformin associated with lactic acidosis in hypotension, hypoxia
GI delayed gastric emptying, full stomach
M hypo, hyperglycemia, lytes abnormalities, DKA, hyperosmolar coma
Renal  renal function
CNS neuropathy (positioning), CVA
 Pre-op: lab: ECG, Lytes, FBS, BUN, creat
 D/C OHA in AM, consider insulin/D5% infusion peri-op for long cases
 Document neuropathy pre-op for positioning and regional anesthesia
 monitoring intra-op, includes 5-leads ECG, Art-line, frequent ABG, or
chemosrip for glucose, and in PARR
 unless it’s an emergency Sx, postponed DKA, and hyperosmoalr coma
Diabetic Ketoacidosis Page 91 of 217
 Accumulation of acetoacetate and -hydroxybutyrate
 ketone bodies are organic acids metabolic acidosis with an unmeasured AG.
 Provoked by intercurrent illness, trauma, or cessation of insulin therapy.
 the degree of hyperglycemia does not correlate with the severity of the acidosis.
 Blood sugar levels are often in the 300–500 mg·dl–1 range.
 leukocytosis, abdominal pain, GI ileus, and mildly  amylase levels are all
common in DKA, Pt may Dx as acute abdomen.
 Regular insulin 10 units iv bolus followed by an insulin infusion nominally at
(blood glucose/150) units·h–1
 Isotonic iv fluids as guided by V/S and urine OP; anticipate 4–10 l deficit
 When urine >0.5 ml·kg–1·h–1, give KCl 10–40 mEq·h–1 (with continuous ECG)
 When glucose  to 250 mg·dl–1, add dextrose 5% at 100 ml·h–1
 Consider sodium bicarbonate to correct pH <7.1
 When glucose levels  below 250 mg·dl–1, glucose should be added to the iv
fluid while insulin therapy continues.
 K replacement is a key concern in patients with DKA, Because of the diuresis,
the total body potassium stores are reduced.
DIC Page 92 of 217

Dilated Cardiomyopathy
 myocardial contractility systolic dysfunction CO ventricular filling pressure
 Dilatation of both ventricles MR, TR.
 Causes: the most common is IHD and alcohol
 Other causes:
o Direct:
 Toxic :Alcohol, Anthracyclines, Catecholamines, Cobalt, Phenothiazines, Radiation,
Uremia, Adriamycin.
 Infectious:Protozoan (Chagas' disease) Viral (coxsackievirus, other enteroviruses,
 Metabolic :Starvation, Thiamine deficiency (beriberi)
 Genetic, Idiopathic
o Indirect
 Ischemic
 Large-vessel coronary disease (postinfarction cardiomyopathy)
 Small-vessel coronary disease
 Global ischemia (cardiac surgery)
 Anemia, TTP, Hypersensitivity, Idiopathic myocarditis
Down syndrome: Page 93 of 217
 Highly associated with CHD 50%, cyanotic 8%(mainly TOF)
A C1-2 subluxation, subglottic stenosis, large tongue  difficult intubation, avoid
neck extension
C CHD, TOF, CHF, Tet spells, Rt Lt shunt ( be meticulous about air in the IV)
M hypothyroidism, hypothermia

ECT during pregnancy

 Obstetric consideration
  Risk of abortion and premature labor, also  risk of bleeding
 Minimize the amount of drugs as much as possible
 Use only the drugs that are known to be safe(STP, Sux, NDMR, Opioids,
Ketamine, Etomidate)
 Have an obstetric consultation
 Beyond the 1st trimester do GA with ETT, RSI, with maintaining LUD
 Have FHR monitor
Delta rhythm (0–3 Hz)  Deep sleep, deep anesthesia, or pathologic states (e.g.,
brain tumors, hypoxia, metabolic encephalopathy)
Theta rhythm (4–7 Hz)  Sleep and anesthesia in adults, hyperventilation in
awake children and young adults
Alpha rhythm (8–13 Hz)  Resting, awake adult with eyes closed;
predominantly seen in occipital leads
Beta rhythm (>13 Hz)  Mental activity, light anesthesia

Effect of anesthesia is depend on the dose.

@ low dose  frequency
@ moderate dose  frequency and  amplitude
@ high dose  silent

compare to SEP, EEG records the spontaneous brain activity with higher
amplitude, while the SEP have a smaller amplitude in response to a specific
Ehlers-danlos Syndrome: Page 95 of 217
 CTD, abnormal metabolism of type III collagen
A avoid A/W traumatization
B spontaneous Pneumothorax, Avoid high airway pressure
C MR, Arrhythmias, consider SBE prophylaxis
Heme bleeding disorder with normal coags profile
 Anticipated problem  bleeding
 Obstetric  premature labor & bleeding
 Avoid Regional Anesthesia
Eisenmenger Syndrome Page 96 of 217
 Chronic Lt Rt shunt changes to Rt Lt
 Pregnancy  S/S due to  SVR
 hypoxia IUGR, demise
 high rish of thromboembolic event mainly post partum
 Hemodynamic Goals:
o preload maintain, avoid AC compression  LUD
o R/R  maintain normal sinus
o Cont  maintain, avoid cardiodepressant
o Afterload maintain, avoid sudden  in SVR
o PVR  avoid  by hypoxia, acidosis,  PCO2
 Consider inhaled NO, O2 all the time, with pulse oxi
 Monitors  Art-line, PAC/CVP
 For the 1st stage  single shot spinal opioids
 2nd stage may consider slow titrating epidural
 Be aware that they could be anticoagulated
 For C/S crash cart in the room, with pads on the Pt
 Epidural have better outcome than GA careful titrate LA
Electric shock and lightning strike Page 97 of 217
 Electric shock
o Direct effect of the current
o Conversion of electric to heat energy
 Factors determine the nature and severity: magnitude of energy delivered,
resistance to current, type of current, current pathway, and duration of
o Bone and skin have a high resistance
o Blood vessels, muscle, nerve have a low resistance
o The skin resistance can be  by moist  and convert a low voltage to a
life threatening shock
o Alternating current is more dangerous than a direct current
o Transthoracic (hand-hand) are more dangerous than vertical ones
o VF more common with alternating, while asystole more with direct
o Respiratory arrest due to CNS effect (medulla), tetanic contraction of
resp muscles, and prolonged paralysis
o Consider C-spine precaution, and other injuries
o Potential burn to the face  early intubation
Cardiac Conditions Associated With Endocarditis Page 98 of 217
Endocarditis prophylaxis recommended
High-risk category
 Prosthetic cardiac valves, including bioprosthetic and homograft valves
 Previous bacterial endocarditis
 Complex cyanotic CHD (eg, single ventricle states, TGA, TOF)
 Surgically constructed systemic pulmonary shunts or conduits
Moderate-risk category
 Most other congenital cardiac malformations (other than above and below)
 Acquired valvar dysfunction (eg, rheumatic heart disease)
 Hypertrophic cardiomyopathy
 Mitral valve prolapse with valvar regurgitation and/or thickened leaflets
Endocarditis prophylaxis not recommended
Negligible-risk category (no greater risk than the general population)
 Isolated secundum atrial septal defect
 Surgical repair of ASD, VSD, or PDA (without residua beyond 6 mo)
 Previous coronary artery bypass graft surgery
 Mitral valve prolapse without valvar regurgitation
 Physiologic, functional, or innocent heart murmurs
Endocarditis Prophylaxis Page 99 of 217
 Dental, oral, esophageal, and respiratory
o Adult: Ampicillin 2g IV 30 min pre-op
o Peds: Ampicillin 50mg/kg within 30 min of starting
o Allergy to Amp  Clindamycin 600 mg , Peds 20mg/kg
o High risk: Amp & Gent
 Adult 2g/ 1.5/kg max 120mg
 Peds 50mg/kg & 1.5 kg
 Allergy to Amp Vanco and Gent, 1g for adult and
20mg/kg for peds
o Moderate risk: Amp alone
 Same as above dose
 Allergy to Amp Vanco also the same dose
Epidermolysis Bullosa Page 100 of 217
 inherited or acquired
 loss of intercellular bridges and separation of the skin layers intradermal
fluids accumulation and bulla formation.
 3 types
o simplex benign
o junctional rarely survive beyond early childhood
o dystrophic.
 Systemic manifestations and Anesthetic considerations:
o A very fragile m.m bledding & bulla formation with fixation of
the tongue difficult intubation
use a lot of lubricant on the ETT, and avoid suctioning
o skin: very fragile avoid tapes for IV and ETT, avoid tourniquet, BP
cuff must be pad with cotton
o GI: esophageal stricture malnutrition anemia, cardiomyopathy
o CVS: cardiomyopathy and MVP
o Lytes: loss of albumin hypovolemia and electrolytes imbalance
o Associated diseases: D.M, hypercoagulation, porphyria cutanea tarda,
multiple myoloma
Epiglottitis Page 101 of 217
 an emergency and life threatening condition
 1-7 y.o, most common pathogen is H. influenzae, with  incidence due to vaccine
 The main conflict is difficult airway with risk of aspiration
 Other DDx is retropharyngeal abscess
 Rapid onset within 24h, high grade fever, and the kid is sitting foreword, mouth
opening and drooling, inspiratory stridor, with toxic appearance
 Need to managed in the OR, keep the kid with the parents, and do a gas induction
without starting an IV, in the presence of the ENT surgeon in the room, and the
difficult airway cart in the room
 Do a gas induction with Sevo, and maintain spontaneous ventilation
 Use a smaller ETT, and have different sizes ready
 After Intubation keep sedated and transfer to ICU, and need to be kept intubated
for 24-72h, with Abx therapy
 After intubation risk of pul edema
 NO NO NO muscle relaxant
 Give atropine
Epilepsy: Page 102 of 217
H/P: why(pathology: head injury, tumor, CVA, bleeding), frequency, type, last
aepisode, S/S of  ICP
Meds: what, dose, to be taken in AM
A N/A
B possible frequent aspiration
C tuberous sclerosis, drugs effect (cardiotoxicity)
D  resistance to NDMR with phenytoin, enzyme induction with pentobarb,
hepatic toxicity with carbamazepine, other: aplastic anemia, avoid any drugs that
may  seizure threshold.
Epilepsy surgery Page 103 of 217
 Hx  type generalized, focal, absence, with, or without Aura
 Review all meds, mainly anticonvulsant   metabolism of NDMR
 Discuss with the surgeon the anesthetic plan GA Vs sedation with LA
 May need awake test with speech mapping
 In case of sedation use a judicious amount of sedation, O2 by NP, and
keep communication with Pt all the time
 In case of A/W obstruction D/C sedation gtt, 100% O2 LMA, ETT
 In addition to the standard CAS monitoring, if an Art-line needed have in
the same side of the lesion e.g. Rt temporal Rt radial art line
 Avoid any pre-med that may change the seizure threshold, also avoid any
long acting anticonvulsant
Ethylene Glycol poisoning Page 104 of 217
 Found in: detergent, antifreeze, polish
 The toxic metabolite Glycolic acid is responsible for the metabolic acidosis
with anion gap, and osmolar gap
 S/S depend on when they present and at which stage:
o Stage I (30min-12hr) CNS with hallucination, coma, Sz, tetany
o II (12-24hr) Cardioresp HTN, tachycardia, pul edema
o III (24-72hr) Renal flank pain, Ca oxalate in the urine
 Management:
o Lab: CBC-D, Lytes, BUN, creat, EG level, ABG, Osmolality, CXR,
o Monitors: ECG, art-line, pulse oxi, Foley cath
o ECG QT, Lytes Ca
o Gastric lavage
o Depend on the serum level of EG whether to give EtOH or not or to
start HD
Familial Periodic Paralysis Page 105 of 217
 Two forms: hyperkalemic, and hypokalemic, both AD inherited diseases.
 intermittent, acute episodes of skeletal muscle weakness. Attach may last hours
or days.
Hyperkalemic Periodic Paralysis.
 evidence of myotonia as well as episodes of muscle weakness.
 caused by a sodium channel mutation.
 Episodes of weakness lasting several hours can occur: during rest after exercise,
infusions of KCl, metabolic acidosis, or hypothermia.
 The weakness may be so severe as to produce respiratory distress.
 hyperkalemia is often transient, occurring only at the onset of weakness.
 K levels measured during the episode of weakness may be N or even 
 Treatment consists of a low-K diet and the administration of thiazide diuretics.
 Consider glucose containing solution pre-op during fasting.
Hypokalemic Periodic Paralysis.
 More common. caused by a calcium channel mutation.
Fat Embolus Syndrome Page 106 of 217
 associated with multiple traumatic injuries and surgery for long bone #
 Risk factors include:male sex, age (20–30 years), hypovolemic shock,
intramedullary instrumentation, rheumatoid arthritis,
 The incidence of FES in isolated long bone fractures is 3–4%, and the
mortality rate ranging from 10 to 20%.
 Axillary/subconjunctival petechiae
 Hypoxemia (PaO2 < 60 mm Hg; FIO2 < 0.4)
 CNS depression (disproportionate to hypoxemia)
 Pulmonary edema
 Tachycardia (>110 beats·min–1)
 Hyperthermia
 Retinal fat emboli
 Urinary fat globules
  platelets/hematocrit (unexplained)
Flow volume loop Page 107 of 217
Fluids Page 108 of 217
 Blood volume
o Preterm 100 ml/kg
o Newborn 85 ml/kg
o Up to 2y 75 ml/kg
o 2-puberty 70 ml/kg
 Maintenance use the rule 4-2-1, add the deficit using the same rule from NPO
and replace it 50% in the first hr, and the rest in the nest 2 hrs
 Glucose requirement for neonate 4-6 mg/kg/min
 D10W 100mg/ml of glucose
 Dehydration
o Based on body wt in infant 5% mild, 10% mod, 15% severe
o >15 kg 3% mild, 6% mod, 9% severe
 Clinical signs
Mild mod severe
Urine   anuria
Mucosa slight dry Dry parched
Fontanel N sunken marked sunken
Eye N sunken marked sunken
Gestationl diabetes Page 109 of 217
  maternal/fetal M/M,  risk of C/S
 In addition to obstetric consideration
A Stiff joint syndrome difficult A/W
C hypovolemia, ANS dysfunction hypotension with R.anesthesia
D insulin
M hypoglycemia, DKA, HNKC
CNS ANS dysfunction,
R renal dysfunction
Fetus/neonate  hypoglycemia, hypothermia,  bili, lethargy
Lab: CBC-D, Lytes, BUN, Creat, ECG, ABG (PRN)
Pre-med GI,
Review White classification for DM its according to the severity
Guillian barre’ Syndrome Page 110 of 217
 Widespread inflammatory demyelination of peripheral and ANS
 It’s ascending in nature, LMN involvement ? caused by viral infection GI, flu
A full stomach, difficult intubation if TMJ involvement
B respiratory involvement
C arrhythmia, autonomic dysfunction
D NO Sux, (K),  sensitivity to NDMR
GI bowel obstruction
CNS  demyelination
 Pre-op: PFT, ABG, CXR, ECG, CBC, Lytes
 Before induction have an art-line in place, unpredictable response to intubation
and induction, consider CVP, have N. stimulator in place
 Post-op: continue mech vent (ICU)
 In Pt with previous disease assess for residual neuropathy, and do PFT
 In pregnancy  premature labor, epidural OK, avoid Spinal  severe
Head and spinal cord injury Page 111 of 217
 15% of CO to the brain, with CBF of 50ml/100g/min
 Pathophysiology:
 TBI primary injury is due to hematoma, contusion, or DAI, the secondary is
an exacerbation of neuronal damage from change in CBF, and systemic factors
e.g. BP, hypoxia, severe  PCO2, anemia,  temp, Sz
 Hypotension is the most important factor  poor prognosis
 The effect of  ICP   CPP, and herniation
 The Autorgulation of CBF is disrupted, but PCO2 reactivity is preserved with 
in magnitude, it’s very important to maintain SBP > 90
  ICP  maintain O2, adequate cerebral drain head up, adequate pain/sedation,
PCO2 30, mannitol .25-1g/k, hypothermia
 Anesthesia goals:
o Optimize CPP, avoid ischemia, avoid drugs/tech  ICP, avoid CMRO2
 Exam: GCS, pupils, brainstem reflex, focal/lateralization neuro signs
 Lab: CT-head, CBC, Coags, Lytes, toxicology screen
 Induction: RSI, use lido, sux , inline stabilization.
 Monitors: routine, art line, CVP, ICP, temp
Name Calculation Units
CI CO/BSA l·min–1·m–2
SVR (MAP-CVP/CO) X 80 dyne-cm·s–5
PVR (MPAP-PCWP/CO) X 80 dyne-cm·s–5
Stroke index SI CI/heart rate cc·beat–1·m–2

Left ventricular stroke work index :LVSWI SI X (MAP-PCWP) X 0.0136


Right ventricular stroke work index :RVSWI SI X (MPAP-CVP) X 0.0136

Hemophilia Page 113 of 217
 A deficient or functionally defective Factor VIII:C. (85%)
 B (Christmas disease)  deficiency or abnormality of Factors IX(14%)
 C  deficiency or abnormality of Factor XI (1%)
 Both hemophilia A and B are sex-linked recessive disorders, which therefore
occur almost exclusively in males. Hemophilia C is an AR disorder that
occurs almost exclusively in Ashkenazi Jews
 Normal concentration of vWF, direct relation between the severity of
bleeding and the plasma concentration of the factors
 CNS bleed is the major cause of death.
 Lab:  PTT, with N PT, with normal BT, Hematology consult
 Rx factors concentrate VIII, IX and XI, may give Cryo if needed, VIII t1/2
is 12 hrs, IX is 24 hrs, also DDAVP  factors release from the endothelium
 With time type A may develop inhibitors to factor VIII:C , and the dose of
factor VIII:C need to be  , Possible HIV +
 Do gentle intubation, avoid blind suctioning, avoid Regional anesthesia
Hepatitis B,C, Page 114 of 217
 Depends on the activity and the stage, with  Post-op M&M
 Risk of transmission to OR personal (use needle-less system)
A RSI for GI bleeding,
B hypoxemia due to shunt, restrictive lung disease, Pul HTN
C hyperdynamic circulation, CHF
D altered drug pharmacokinetics
Heme anemia, PLT, coagulation defect
M  albumin, lytes abnormality, hypoglycemia, acidosis
Renal hepatorenal syndrome
GI portal HTN, ascites, upper GI bleed
CNS encephalopathy
 Correct coagulation pre-op (FFP, Cryo, PLT, Vit K)
 Consider paracentesis pre-op if respiratory compromise
 Have an ICU consult and back-up bed
 Lab: CBC-D, BUN, creat, lytes, coags(PT, PTT, fibrinogen), CXR, PFT, ECG,
Echo, LFT, ABG
HIV Page 115 of 217
 The main considerations are the disease process, side effect of antiviral drugs,
and health care personal safety
A N/A
B PCP, TB, hypoxia, ARDS like,
C accelerated CAD, pericarditis, myocarditis, pul HTN, endocarditis, autonomic
D drugs related side effect neuropathy, pancreatitis, lactic acidosis, and the
protease inhibitor may interact with cytochrome P-450 either by induction or
inhibition which can  sensitivity to BNZ
GI esophagitis, diarrhea
Heme leukopenia, anemia, ITP
Endo DM, adrenal insufficiency
CNS demyeliantion neropathy like gullian barre’ syndrome
R+ Lytes CRF from sepsis, dehydration, drugs
 Possible substance abuse cocaine, heroin, opioids , other infection HCV,
HOCM Page 116 of 217
 With pregnancy  HR and contractility with  SVR  worsen the
 -blockers is the treatment of choice
 Synto  no bolus, give slowly
 hemodynamic Goals:
o preload , LUD
o R/R   maintain sinus, treat arrhythmia aggressively
o Cont  , avoid  contractility (kitamine)
o Afterload , avoid sudden  in SVR
 Neo is the drug of choice if BP
 Epidural  very slow titration
 With GA risk of CHF
HTN Page 117 of 217
 Essential or secondary.
 With secondary look for the underlying cause: cushing, pheo, ….
 Postponed if DBP > 110
 Continue -blockers, and 2-agonist peri-op
A N/A
B N/A
C CHF, LVH, PVD, HTN, with labile BP
M  intravascular volume
R renal impairment
CNS TIA, CVA, Rt shift of auto regulation curve
 Hydrate pre-induction
 Consider Art-line depend on Pt status and the procedure
 Lab ECG, CBC, Lytes, BUN, creat
Hydrocephalus: Page 118 of 217
 Etiology:
o Trauma/hemorrhage  IVH
o Congenital Arnold-chiari malformation
o Neoplastic tumor
o Post-inflammatory sbscess, meningitis
 Pt may come for VP, VA, or LP shunt.
A impaired A/W reflex  aspiration RSI
B impaired resp drive  ABG
C Cushing reflex (brady, HTN)
D avoid ketamine and sux
N   ICP,  LOC
 The rest of management as  ICP card
Hyperosmolar Nonketotic Coma Page 119 of 217
 In type II (NIDDM)
 elderly patient with minimal or mild diabetes may present with remarkably
high blood glucose levels and profound dehydration.
 enough endogenous insulin activity to prevent ketosis; even with blood
sugar concentrations of 1000 mg·dl–1, they are not in ketoacidosis.
 it is the combination of an impaired thirst response and mild renal
insufficiency that allows the hyperglycemia to develop.
 The marked hyperosmolarity may lead to coma and seizures,
 with the increased plasma viscosity producing a tendency to intravascular
 responds quickly to rehydration and small doses of insulin.
 One to 2 L of NS, or equivalent, infused over 1–2 hrs if there are no
cardiovascular contraindications.
 Insulin, by bolus or infusion, should be administered.
 Consider NaHCO3 if severe acidosis
 With rapid correction of the hyperosmolarity, cerebral edema is a risk, and
recovery of mental acuity may be delayed after the blood glucose level and
circulating volume have been normalized.
Hyperparathyroidism Page 120 of 217
 Primary benign parathyroid adenoma (90% of cases) or hyperplasia (9%) and
very rarely to a parathyroid carcinoma, or as part of a (MEN) syndrome.
 most Pt are hypercalcemic, most are asymptomatic at the time of diagnosis.
 occurring during pregnancy is associated with a high maternal and fetal
morbidity rate (50%), The placenta allows the fetus to concentrate Ca,
promoting fetal hypercalcemia and leading to hypoparathyroidism in the
 Pregnant women with primary hyperparathyroidism should be treated with
 Secondary in parathyroid function as a result of conditions that produce
hypocalcemia or hyperphosphatemia.e.g. CRF, malabsorption
 Tertiary  development of hypercalcemia in a patient who has had prolonged
secondary hyperparathyroidism that has caused adenomatous changes in the
parathyroid gland and PTH production to become autonomous.
 Surgery is the treatment of choice for the patient with symptomatic disease.
Hyperthyroidism Page 121 of 217
 most common etiology is the multinodular diffuse goiter of Graves' disease.
between the ages of 20 and 40 years and is predominant in women
A potential difficult if large goiter
B N/A
C hyperdynamic, HTN
D Avoid ketamin, and pancuronium
M  Ca
Heme anemia, PLT
 Consider giving -blockers peri-op, to  HR, and  the conversion of T4 to T3
Hypertrophic Cardiomyopathy Page 122 of 217
 AD, Peak 5th decade of life, F>M, HTN is a common cause, Could associated with LVOFO
or without
 Sport  sudden death, Good EF due to hypercontractile state, MR is common
 Could be dynamic obstruction by the anterior leaflet of the MV during systole systolic
anterior motion (SAM).
 Angina, Syncope, Arrhythmia,CHF
 A.fib systemic embolism
 Atrial kick very important A.fib not well tolerated
 CXR Cardiomegaly
 -blockers 1st choice by  HR and contractility  outflow obstruction.
 CCB is other choice.
 CHF is difficult to treat digoxin  contractility  obstruction, diuretics
hypovolemia  obstruction.
Hyponatremia < 130 Page 123 of 217
  or  in serum Na   &  in ECV & PV, so it’s result from excess or deficit of water
 total body Na regulated by aldosterone and ANP, where serum [Na] by ADH
 S/S depend on the rate and severity of  of Na: loss of apatite, N&V, cramps, weakness,
LOC, coma and seizure
 Acute CNS S/S is due to cerebral edema
 What is the serum osmolality see figure
 Cerebral salt wasting syndrome, mediated by BNP, independent of SIADH, risk head
trauma, tumor, SAH, and infection
 SIADH  see other card
 Rx < 120 with 3% NS @ 1-2 ml/kg/hr to  serum Na 1-2 mEq/l/hr only for few hrs, not
more than 25 mEq/l/48 hrs
 Rapid correction  abrupt brain dehydration central pontine myelinolysis mild
(transient behavioral disturbances or seizures) to severe (including pseudobulbar palsy and
quadriparesis).Within 3 to 4 weeks of the clinical onset of the syndrome, areas of
demyelination are apparent on MRI, risk factors (alcoholism, poor nutritional status, liver
disease, burns, and hypokalemia) , cerebral hemorrhage and CHF
 Once serum Na > 120 fluid restriction is enough , Also treat the underlying causes
To calculate the net water loss necessary to  [Na+] in hyponatremia, use the following
Current [Na+] × current TBW = desired [Na+] × desired TBW TBW= 0.6x wt
Hypoparathyroidism Page 124 of 217
 underproduction of PTH or resistance of the end-organ tissues to PTH results in
 normally: hypocalcemia PTH and 1,25(OH)2D synthesis  Ca2+
mobilization from bone, GI absorption, and renal tubule reclamation.
 most common cause of acquired PTH deficiency is inadvertent removal of the
parathyroid glands during thyroid or parathyroid surgery.
 Other : 131I therapy for thyroid disease, neck trauma, granulomatous disease, or
an infiltrating process (malignancy or amyloidosis).
 Idiopathic is rare and may occur as an isolated disease or as part of an
autoimmune polyglandular process (hypothyroidism, adrenal insufficiency).
 Pseudohypoparathyroidism is an inherited disorder in which parathyroid gland
function is normal but the end-organ response to the PTH is deficient.
 Affected patients have hypocalcemia and hyperphosphatemia.
 They are characterized by mental retardation, a short stature, obesity, and
shortened metacarpals.
 Chvostek's sign is a contracture of the facial muscle produced by tapping the
facial nerve as it passes through the parotid gland.
Hypotension Page 125 of 217

Preload: Contractility:
 Hypovolemia  Ischemia
 Venodilation (spinal)  Valve dysfunction
 Tamponade  CHF
 Tension Pneumothorax  Drugs

 Too fast and too slow Afterload:
 Arrhythmias  Drugs
 Anaphylaxis
Other (may affect any component):  Sympathectomy
 Electrolytes imbalance  Hyperthermia
 Acid-base  sepsis
 Hypoxia & hypercarbia
Hypothyroidism Page 126 of 217
 Hashimoto’s thyroiditis may associated with other autoimmune disease e.g.
SLE, RA, DM, hypoparathyroidism, Addison’s disease.
 May associated with amyloidosis.
A goiter  altered A/W anatomy, with possible A/W obstruction
B OSA, hypoventilation,  response to PCO2 and PO2,  sensitivity to
narcotics, pul edema
C bradycardia, CHF, heart block, hypotension, edema
GI  gastric emptying  aspiration
M Na, possible SIADH, hypothermia, possible Addison’s disease
 postponed if severe hypothyroid Pt until at least partially treated.
 The management of hypothyroid patients with symptomatic CAD has been
a subject of particular controversy. In symptomatic patients or unstable
patients with cardiac ischemia, thyroid replacement should probably be
delayed until after coronary revascularization.
 Maintain normal body temperature.
 Consider adrenal insufficiency when intra-op hypotension not responding
to fluids and inotrops.
 ICP: Page 127 of 217
 Normal ICP < 10 mmHg, to convert to cmH2O X by 1.32
A   LOC, aspiration risk
B  resp failure
C arrhythmias, hemodynamic instability, MI  (ECG, Echo)
D  avoid sux
N   ICP,  LOC, risk of herniation
M  DI, SIADH, cerebral salt wasting
Monitors: routine, artline, ICP, CVP
Mx: 1- hyperventilate PaCO2 25-30 good only for 6 hrs
2- diuretics mannitol 0.25- 1.0 g/kg over 10 min, Lasix 0.5-1.0 mg/kg
3- Steroids  need 6-24 hrs to work
4- head elevation
5- Barbiturate
6- CSF drain
 Avoid neck twisting obstruction of IJ, avoid hyperglycemia
 Maintain CPP, MAP > 60, avoid PEEP if possible
IHD Page 128 of 217
 Apart from atherosclerotic disease, other causes are: collagen vascular disease,
sickle cell disease, pheo, PIH, cocaine abuse
 Avoid ergot, synto OK
 Need continues sat and ECG monitor
 Epidural is good prevent  catecholamine and hyperventilation which 
PCO2  coronary vasospasm
 Neo is a better choice
 Epidural best for C/S
Immediate Hemolytic Transfusion Reactions Page 129 of 217
 Catastrophic and life threatening with mortality 20-60%
 Hemolysis of the donor RBC  ARF, DIC, death
 Intravascular and extravascular (RES)
 Antibodies anti-A,B, Kell, Kidd, Lewis, and anti-Duffy
 Ag-Ab complex  activate Hageman factor(XII) kinin bradykinin  
capillary permeability, also complement  histamine , serotonin
 S/S: fever, chills, N&V, diarrhea, rigor, flushing, hypotension, tachy, chest and
abdominal pain
 Under GA most of S/S are masked only hypotension, tachycardia,  bleeding,
 Management: (keep index of suspicion)
o Stop Tx, re-check blood,
o 3 main objectives:
 Maintain BP  volume, inotrops
 Preserve renal function diuretics, alk the urine (NaHCO3)
 Prevent DIC  no specific therapy, maintain BP, prevent stasis
o Blood sample should be collected in EDTA tubes for re-X match, direct
coombs test ( for definitive diagnosis)
1. Isolation of each lung to prevent contamination of a healthy lung
a. Infection (abscess, infected cyst) b. Massive hemorrhage
2. Control of distribution of ventilation to only one lung
a. Bronchopleural fistula b. Bronchopleural cutaneous fistula
c. Unilateral cyst or bullae d. Major bronchial disruption or trauma
3. Unilateral lung lavage
4. Video-assisted thoracoscopic surgery
1. Surgical exposure—high priority
a. Thoracic aortic aneurysm
b. Pneumonectomy
c. Upper lobectomy
2. Surgical exposure—low priority
a. Esophageal surgery
b. Middle and lower lobectomy
c. Thoracoscopy under general anesthesia
Infratentorial Intracranial Tumors Page 131 of 217
 Those tumors produce a mass effect on the brain stem, and  ICP by obst hydro
A CN involvement +  LOC  unprotected A/W RSI
B Resp depression
C brady, HTN, arrhythmias ST-changes , prolonged QT
Position sitting  risk of VAE , CV instability in elderly, risk SC compression
Prone  see other card
 Monitors as Supratentorial tumors
 Induction also the same
 Post-op:
o need for continuous CV monitoring 24-48 hrs
o HTN is a common problem post-op, need to treated aggressively  other
wise  intracranial bleeding and edema
o Manipulation of CN IX, X, XII  loss pharyngeal sensation  may need
to keep intubated
ITP Page 132 of 217
 More common in young female, characterize by thrombocytopenia with
petechiae, where major cause of mortality is intracranial bleed
 The main ttt is steroid, if not working  splenectomy
 Consider DDx: TTP, drug induced thrombocytopenia, Connective T disease,
HIV, other in preg  PIH, DIC, essential thrombocytopenia
 The main issues with Anesthesia Are
o A avoid traumatize the airway
o Avoid Regional
o Risk of bleeding  PLT Tx
 In Preg  antibodies cress the placenta  affect the fetus  CNS bleed  C/S

 It’s: thrombocytopenia, fever, renal dysfunction, hemolysis, CNS involvement
Sz, and jaundice
 ttt  Tx plasma, plasmaphoresis, IVIG, steroids
 also the same issues as ITP regarding anesthesia
Kidney Tx Page 133 of 217
 Of course for CRF
A RSI for possible gastroparesis
B pul edema if volume overloaded
C hyper/hypovolemia, pericardial effusion, pericarditis, arrhythmias
D altered drugs pharmacokinetics
G Gastroparesis
M  K, secondary hyperparathyroidism with  Ca and  phos
Heme PLT dysfunction secondary to uremia
 Lab CBC-D, CXR, ECG, Lytes, BUN, creat, X-match
 monitorsCAS, Art-line, foley, CVP
 Goals  maximize the renal perfusion at the time of graft reperfusion by
maintaining a high BP,  intravascular volume, and diuresis with lasix, and
 Possible problem Bleeding
 Post-op pain  epidural, PCA
Lower Ext nerve inury: Page 134 of 217
Lumbosacral trunk:
 Foot drop, with loss of ankle dorsiflexion
 L5 dermatome loss of sensation lateral leg
 In obstetric  with prolonged labor and difficult vaginal delivery
 Weakness of hip adduction and internal rotation
Peroneal N
 With prolonged lithotomy position
 At the knee level (injury) foot drop, with no sensory deficit
Femoral N:
 Due to pelvic Sx, prolonged hip flexion, abduction, external rotation during
the 2nd stage of labor, as well as lithotomy position
 Walking OK, but unable to claim stairs, with loss of the patellar reflex
Meralgia paresthetica(Lateral femoral cutaneous nerve)
 tingling, numbness, burning sensation over the lateral thigh
 resolve spontaneous after giving birth
Ludwig's Angina Page 135 of 217
 An emergency and life threatening situation
 generalized septic cellulitis of the submandibular region
 occurs after dental extraction, especially of the second or third mandibular molars
 it’s bilateral, involves 3 fascial spaces: submandibular, submental, and sublingual
 Early S/S: chills, fever, drooling of saliva, inability to open the mouth, and
difficulty in speaking.
 hemolytic streptococci, aerobic and anaerobic, including gas-forming bacteria
 The infectious process may spread into the thorax, causing empyema, pericarditis,
pericardial effusion, and pulmonary infiltrates, Pneumothorax, necrotizing fasciitis
 Review the CT/MRI, CXR for Pneumothorax
A difficult, difficult A/W
B hypoxia, pneumonia, effusion, empyema
C dehydration, pericardial effusion, pericarditis
 Have the ENT surgeon in the room, scrubbed, and the neck is prepped, and the
difficult airway cart in the room, consider a reinforced and small size ETT
 Awake FOI, give glycopyrolate, other option is inhalation induction
 Post-op keep intubated  to ICU until swelling subsided
Lung volumes and Page 136 of 217
Page 137 of 217
TABLE 30–7. Underestimation of Left Ventricular End-Diastolic Pressure


Decreased left ventricular

Mean LAP<LVEDP Increased end-diastolic a wave

Mitral valve closure prior to end-

Aortic regurgitation LAP a wave<LVEDP

Bidirectional runoff for pulmonary

Pulmonic regurgitation PADP<LVEDP
artery flow

Right bundle branch block PADP<LVEDP Delayed pulmonic valve opening

Decreased pulmonary Obstruction of pulmonary blood

vascular bed flow
Magnesium Page 138 of 217
 mainly intracellular, 50% in bone, 25% muscle, and < 1% in the serum.
 protein-bound (30%), chelated (15%), and ionized (55%)
 Magnesium is necessary for enzymatic reactions involving DNA and protein
synthesis. As a primary regulator or cofactor in many enzyme systems, magnesium
is important for the regulation of the Na–K pump, Ca-ATPase enzymes, adenyl
cyclase, proton pumps, and slow Ca channels.
 The distal tubule of the kidney is the major site of magnesium regulation.
 clinical features of Mg, like Ca neuronal irritability and tetany.
 can aggravate digoxin toxicity and CHF.
 S/S: weakness, lethargy, muscle spasms, paresthesias, and depression. When
severe  seizures, confusion, and coma.
 CV coronary artery spasm, CHF, dysrhythmias, and hypotension.
 is associated with K, Na, phos, and Ca.
 Rarely resulting from inadequate dietary intake, most commonly caused by
inadequate GI absorption, excessive Mg losses, or failure of renal Mg
conservation. Excessive Mg loss is associated with prolonged nasogastric
suctioning, GI or biliary fistulas, and intestinal drains
Magnesium Page 139 of 217
 Mainly intracellular, distal tubule is the major site of magnesium regulation
 Rarely from inadequate dietary intake, most commonly caused by
inadequate GI absorption, excessive Mg losses, or failure of renal Mg
conservation. Excessive Mg loss is associated with prolonged NGT,
gastrointestinal or biliary fistulas, and intestinal drains.
A N/A B N/A C arrhythmias, CHF, BP, coronary artery spasm.
M may associated with other electrolytes abnormality
Rx stop NGT, give Mg
 Most common cause is iatrogenic, other Addison’s disease, lithium, hypothy
 S/S depend on Mg level  Hypotension Deep tendon hyporeflexia
Somnolence Respiratory insufficiency, deep tendon areflexia Heart
block, respiratory paralysis Cardiac arrest
 Rx D/C Mg, IV CaCl, diuretics, dialysis
Marfan syndrome: Page 140 of 217
 AD,  length of long bone
A TMJ laxity  dislocation with intubation
B scoliosis, kyphoscoliosis, Pectus excavatum, restrictive lung defect
spontaneous Pneumothorax careful with PPV
C cystic media necrosis, aortic dissection, AR, MVP, MR, arrhythmia,
aneurysm  Avoid sudden  in contractility, -blockers and volatiles are
good, need endocarditis prophylaxis
Other lens dislocation, retinal detachment
Position careful
Neuraxial potential difficult, may need a bigger dose and volume of LA
Lab Echo, CT-chest and angio all for dissection, valve, tamponade,
CXR pneumo, ABG, CBC, lytes, BUN, creat, PFT
Masseter Muscle Rigidity Page 141 of 217
 most common in children and young adults. peak age incidence at 8–12 yrs of age.
 Characteristically, anesthesia is induced by inhalation with halothane or sevo, after
sucx is given. Snapping of the jaw or rigidity on opening of the jaw is seen.
 this rigidity can be overcome with effort and usually abates within 2–3 minutes.
 A peripheral nerve stimulator usually reveals flaccid paralysis.
 However, increased tone of other muscles also may be noted.
 Repeat doses of succinylcholine do not relieve the problem.
 Tachycardia and dysrhythmias are not infrequent.
 (if the anesthetic is continued with a triggering agent), the initial signs of MH
appear in 20 minutes or more.
 If the anesthetic is discontinued, the patient usually recovers uneventfully.
However, within 4–12 hours, myoglobinuria occurs and CK elevation is detected.
 Muscle biopsy with caffeine–halothane contracture testing has shown that approx
50% of Pt who experience MMR are also susceptible to MH.
 DDx of MMR are: (1) myotonic syndrome, (2) TMJ dysfunction, (3) underdosing
with Sux, (4) not allowing sufficient time for Sux to act before intubation, (5)
increased resting tension after succinylcholine in the presence of fever or elevated
plasma epinephrine.
Maxillofacial trauma Page 142 of 217
 Lower 1/3  mandible (30% in the body of the mandible)
 Middle 1/3  maxilla, zygomatic, orbital, nasal  LeForte I, II, III
 Upper 1/3 frontal and cranium ( CNS)
 100% O2, and clear the A/W from foreign bodies, blood, # teeth (count), if
there is bleeding apply pressure, nasal packing, and consider a close
reduction for a #
 In case of tongue injury  laceration edema/swelling  difficult
 In case of mid and upper facial injury avoid nasal intubation  Bleeding,
and possible basal skull #
Laryngeal injury
 S/S hoarseness, stridor, sub-Q emphysema with crepitus  void blind
 After intubation with direct vision bypass the injury and make sure that the
cuff is beyond the injury
Trismus after facial injury  due to muscle spasm  relived by GA
Meconium Aspiration: Page 143 of 217
 Risk of PPHTN.
  risk with post-term pregnancy
 The new recommendation it does not matter thin or thick meconium
 If there is meconium suction the hypopharynx
 Apply NALS
 If not vigorous (HR < 100, resp depression)  ETT suction, 100% O2
 If vigorous  no need for ETT or tracheal suctioning
MH acute crisis Page 144 of 217
Manifestations :
 Hypercarbia, Tachycardia, Tachypnea, Temp  (1°C–2°C increase every 5
minutes), HTN, Cardiac dysrhythmias, Acidosis, Arterial hypoxemia,
Hyperkalemia, Skeletal muscle activity, Myoglobinuria
 DDx: pheo, thyroid storm, carcinoid
 Call for help
 Discontinue inhaled anesthetics and succinylcholine
 Hyperventilate the lungs with 100% O2
 Administer dantrolene (2.5 mg/kg iv) with repeated doses (up to a maximum of 10
mg/kg iv) based on Paco2, heart rate, and body temperature (each ampule of 20 mg
is mixed with 50 ml of distilled water)
 If Dantrolene is not available, give procainamide IV 1mg/kg up to 15mg/kg
 Treat persistent acidosis with sodium bicarbonate (1–2 mEq/kg iv)
 Control body temperature (gastric lavage, external ice packs until 38°C)
 Replace anesthetic circuit and canister
 Monitor with capnography and arterial blood gases
 Be prepared to treat hyperkalemia and cardiac dysrhythmias
Mineralocorticoid Physiology Page 145 of 217
 Aldosterone is a major regulator of extracellular volume and K homeostasis
through the resorption of Na and the secretion of K.
  Renal perfusion pressure+ sympathetic stimulation+ Na, and
hypovolemia  renin from juxtaglomerular Renin splits
angiotensinogen to angiotensin I ACE in the lung Angiotensin II
 Other stimuli that aldosterone includeK and, to a limited degree, Na,
PGE, and ACTH.
 So  aldosterone  K and Na and HTN, while  is the opposite
Mineralocorticoid Insufficiency:
 Common in CRF, and DM, Pt usually on fludrocortisone 0.05-0.1 mg/d
C hypovolemia, heart block due to K,
M K, Na, and metabolic acidosis (hyperchloremic)
D Avoid Sux, and NSAID   PGE  Renin  exacerbation
Mitral Regurgitation Page 146 of 217
 Chronic regurgitation caused by abnormal leaflet anatomy can be due to congenital or
rheumatic disease, myxomatous degeneration(MVP), CTD, infective endocarditis and LV
 CTD associated with MR include SLE, rh arthritis, ank spondylitis, and scleroderma.
 Valvular involvement in CTD is variable; about 50% of patients with SLE have detectable
MR, and approximately 25% have significant regurgitation.
 Acute severe MR is caused by infective endocarditis which result in chordae tendineae,
acute MI with papillary muscle rupture or retraction usually from RCA, or prosthetic valve
dysfunction. Almost always associated with MS.
 Long latent period 30-40 yrs. LA volume overload LV volume overload with  foreword
LV SV, Eccentric hypertrophy of the LV, Regurgitation fraction > 0.6 associated with
severe MR, PAWP giant V wave, In acute MR there is sudden  in LAP pul edema.
 Patients with chronic MR remain asymptomatic for an extended period.
 Later, patients develop symptoms of fatigue and exertional dyspnea, followed by more overt
symptoms of CHF, including orthopnea and paroxysmal dyspnea.
 When CHF develops rapid deterioration with 5 yrs mortality rate 50%
Physical Findings
Mitral Stenosis Page 147 of 217
 normal MVA 4.0 to 6.0 cm2, Symp(exercise or tachycardia) 2.0 to 2.5 cm2; rest < 1.5 cm2.
mild gradient < 5 mm Hg and VA >1.5 cm . Severe gradient > 10 mmHg, and valve area
< 1 cm2. MS in adults is predominantly of rheumatic origin. F>M.
 The MV is the most common site of rheumatic valve disease. Long latent period > 20 yrs.
 Obstruction to LV inflow  LA dilation and HTN and resultant pul venous HTN
interstitial edema  work of breathing dysponea, and predispose to supraventricular
 Pul arteriolar and capillary vasoconstriction protect against pul edema, although  PVR
exacerbates pul arterial and RV HTN and causes RVH.
 Pul HTN can be severe late in the course of MS, with eventual RV systolic dysfunction.
 Acute decompensation occur due to stress e.g. sepsis, pregnancy, A fib, PE which can
lead to pul edema
 Stasis of the blood in the LA thrombi A fib systemic emboli.
 Early fatigue or dyspnea precipitated by events with associated tachycardia, including
strenuous physical exercise, emotional stress, fever, pregnancy, or surgery.
MR Page 148 of 217
 Well tolerated in pregnancy
  risk of A.fib with systemic embolization due to hypercoaglable state in
 hemodynamic Goals:
o preload maintain, LUD, avoid overload
o R/R  slightly  maintain sinus, aggressively treat arrhythmia
o Cont  maintain, avoid cardiodepressant
o Afterlaod 
o PVR avoid pain, hypoxia,  PCO2
 If mild no need for aggressive monitoring, but if severe then art-line, CVP/PAC
 MVP manage as MR
MS Page 149 of 217
 Not well tolerated, with  risk of pul edema.
 Arrhythmias are not tolerated at all, and needs to treated very aggressively with
-blockers, Digoxin, over even cardioversion, then lasix
  mortality during labor/post-partum
 Mild is usually tolerated ok
 But mod/severe  pregnancy worsen NYHA by 1-2 classes
 Need invasive hemodynamic monitoring art-line, PAC, O2 all the time
 In the 2nd stage avoid explosive effort  valsalva  VR pul edema
 Avoid overzealous hydration  pul edema
 Tachycardia  -blockers
 hemodynamic Goals:
o preload maintain, LUD, avoid overhydration
o R/R  slow and sinus
o Cont  maintain, avoid cardiodepressant
o Afterlaod maintain, avoid sudden  in SVR
o PVR avoid  by pain, hypoxia, PCO2
 Neo is the best choice in case of hypotension
Mucopolysaccharoidosis: Page 150 of 217
I H Hurler
I H/S Hurler/Scheie
I S Scheie
II Hunter
III Sanfilippo
IV Morquio

A Coarse facial features, macrogolssia, short neck  difficult A/W

B Restrictive defect
C CAD, VHD, AR, Cardiomyopathy
GI hepatosplenomegaly
MSK joint stiffness, AO instability, odontoid hypoplasia, kyphoscoliosis,
 Routine lab + Echo, CXR
Multiple Sclerosis Page 151 of 217
 demyelination in the brain and spinal cord, F>M
 symptoms depend on the sites: visual disturbances, nystagmus, limb weakness and
paresthesias, The legs are affected more than the arms.
 Bowel retention and urinary incontinence are frequent complaints.
 Involvement of the brain stem can produce diplopia, trigeminal neuralgia, cardiac
dysrhythmias, and autonomic dysfunction, while alterations in ventilation can lead
to hypoxemia, apnea, and respiratory failure.
 As is typical in many immune disorders, pregnancy is associated with an
improvement in symptoms, but relapse frequently occurs in the first three
postpartum months.
 treatment Corticosteroids, immunosuppressants (azathioprine, methotrexate,
cyclophosphamide, and cyclosporine)
 Symptoms exacerbation with stress (emotional, surgical)  temp, infections
Management of Anesthesia
 Possible exacerbation post-op
 Document neurological symptoms pre-op, re-exam post-op
 the patient should be advised that surgery and anesthesia could produce a relapse
despite a well managed anesthetic
Murmurs Page 152 of 217
 Innocent murmurs: soft, systolic and not radiated, may vary with position, not
characteristic of any lesions
 Noninnocent murmurs: all diastolic murmurs, all pansystolic, continues, late
systolic and transmitted murmurs
 For innocent murmurs no need for surgical delay, and no need for prophylaxis
 Not noninnocent one’s if heard in the pre-op delay, and further investigation
Midsystolic Page 153 of 217
 flow across aortic or pulmonic valve (e.g., secondary to AR or ASD)
Aortic valve leaflet sclerosis (e.g., in elderly patients)
Aortic or pulmonic outflow obstruction (valvular, subvalvular, supravalvular)
Dilatation of aortic root or proximal pulmonary artery
Papillary muscle dysfunction
Late Systolic
MVP, Papillary muscle dysfunction
Early Diastolic
Aortic or pulmonic valve insufficiency
 flow across nonstenotic AV valve (e.g., secondary to MR or ASD)
MS (with sinus rhythm)
Continuous Murmurs
Muscular dystrophy Page 154 of 217

 7 main types with progressive and variable rate in losing of muscle function.
Duchenne’s muscular dystrophy
 The most common, and the most severe form.
 Due to lack of protein Dystrophin.
 Painless degeneration of the skeletal muscle.
 X-linked trait (boys)
 S/S 2-5 yrs old.
 In the wheelchair by age of 12.
 The affected muscle may become enlarged, due to fatty infiltration.
 Death by 15-25.
 Secondary to CHF and pneumonia.
 Serum CK reflect the progression of the disease, with 30-300 folds above
normal, later with complete degeneration the level well .
 Smooth muscle involvement  GI hypomotility and gastroparesis.
o myocardial degeneration loss of R-wave in the lateral leads
o  contractility dilated cardiomyopathy, and arrhythmias
MVP: Page 155 of 217
 More common in young female than in male
 May associated with other disease e.g. marfan syndrome, connective tissue
 Risk of endocarditis, stroke, arrhythmias, sudden death
 If associated with MR or CHF, Pt could be on ACEI, -blockers, Diuretics,
antiarrhythmics, anticoagulants
 P/E  late systolic click, if MR  late systolic murmur
A N/A unless associated with other disease
B if CHF  plu edema, ? scoliosis  restrictive lung defect
C CHF, Arrhythmias, Endocarditis prophylaxis
D avoid histamine releasing drugs, and ketamine
CNS Stroke, anxious Pt may benefit from pre-op meds
Hemodynamic goals
Preload maintain
Contractility avoid 
R & R  sinus, little fast
Afterload avoid , better 
Myasthenia Gravis Page 156 of 217
Osserman and Genkins classification:
• Class I—ocular symptoms only
• Class IA—ocular S’s with EMG evidence of peripheral muscle involvement
• Class IIA—mild generalized symptoms
• Class IIB—more severe and rapidly progressive symptoms
• Class III—acute, presenting in weeks to months with severe bulbar symptoms
• Class IV—late in the course of the disease with severe bulbar symptoms and marked
generalized weakness
 autoimmune disease with anti-acetylcholine receptor antibodies, F>M
 Abnormal thymus glands 75% of pts(85% show hyperplasia; 15% thymoma).
75% of pts either go into remission or are improved post-op
 Medical ttt: anticholinesterase, steroids, other immunosuppressant (azathioprine,
cyclophosphamide, cyclosporine)and plasmapheresis.
 underdosage  ―myasthenic crisis‖ whereas overdosage will produce a
―cholinergic crisis.‖ Excessive doses of cholinesterase inhibitors produce
abdominal cramping, vomiting, diarrhea, salivation, bradycardia, and skeletal
muscle weakness that mimics the weakness of myasthenia , to differentiate
Myasthenic Syndrome (Lambert-Eaton Syndrome) Page 157 of 217
 Associated with small cell ca of the lung
 IgG antibodies against Ca channel in the presynaptic membrane   Ach
release in response to nerve stimulator
 M>F, age 50-70
 Mainly proximal muscle weakness
B rarely respiratory failure
C autonomic dysfunction  orthostatic hypotension
D sensitive to both Sux and NDMR, Pt could be on diaminopyridine  Sz
 Keep high index of suspicion in a Pt with Lung Ca
 Consider Art-line
Page 158 of 217
NALS Page 159 of 217
 Exam table goes trend for drainage and reverse trend to  PO2
 Avoid hypothermia   VO2  metabolic acidosis
 Assess for choanal atersia  usually cyanotic and resp depression at rest, pink
when crying
 If Apgar score < 8 with not resp depression give O2 by ―blow by‖
 So If not breathing or cyanotic suction the A/W, warmth, dry, tactile
stimulation by rubbing the back, flicking the soles of the foot, give O2  not
breathing or HR < 100 PPV with initial P 30-40 cmH2O for 4-5 sec to open
the alveoli, the vent @ rate 40-60 min  if HR > 100, and Pink ongoing care, if
HR < 60 PPV and start Chest compression for 30 sec  if still HR < 60 five
Epi  ….. Bicarb………..
 For vent I:E = 1:1, @ 40-60 min, after the 1st breath the P 20-30 cm H2O
 For chest compression to vent 3:1  1,5:0.5 sec  90:30 pre minute
 Chest compression using two thumbs just below a line drown between two
nipples to compress the AP diameter by 1/3 to ½
 Intubation can be considered at any time
 If Vent without ETT for > 2-3 min  decompress the stomach
Necrotizing fasciitis Page 160 of 217
 Emergency and life threatening with high mortality rate
 Possible underlying disease: DM, alcoholism, malnutrition, renal and CV
 Septic shock, possible under resuscitated
A full stomach  RSI
B ARDS, respiratory failure, pul edema
C septic shock with  SVR,  CO
M lactic acidosis, lytes abnormalities
 Lab and Mx as septic shock
 Post-op  ICU
Neonatal Considerations: Page 161 of 217
In addition to the pediatrics considerations
Metabolic risk of hypoglycemia S/S: apnea, convulsion
Glucose infusion @ 4-8 mg/kg/min
 hyperglycemia  cerebral hemorrhage, glucosuria H2O and
lytes depletion
Physiological jaundice  alter drugs pharmacokinetics, and  free
bili kernicterus, which  by hypoxia, acidosis, hypothermia
Renal  Na loss, immature renal function
CNS fragile cerebral vessels  risk of IVH  by hypoxia, hypercarbia,
Na, fluctuation in BP, low Hb, rapid administration od NHCO3
Eye ROP maintain O2 sat 90-95% or PO2 50-70
Peri-op nerve injury: Page 162 of 217
 Symptoms: pain, paresthesia, motor weakness, where, when did it start
 Presence of risk factors or conditions that may have neuropathy as a
symptoms: DM, Obesity, R Arthritis, PVD, smoking, alcohol,
 Drugs that may cause neuropathies  chemo, anti-virals
 Review anesthetic records, OR note for documentation of padding, position
 A block done or not if yes any symptom at the time of the block pain or
paresthesias with injection
 If the surgical procedure done in the same side  ? surgical complication
or prolonged use of a tourniquet, also BP cuff may cause injury
 V/S, complete neurological exam, and mainly examining the affected side
sensory, motor, reflex, and looking for any pressure demarcation
 Also assess for nerve or dermatomal distribution
Obtain a Neurology consult for further evaluation and need for nerve
conduction study, and possible MRI
 Sensory only F/U in 2wks, motor  further evaluation
Neuraxial Anesthesia and anticoagulation Page 163 of 217
 IV heparin e.g. vascular Sx  delay IV heparin 1hr post catheter
placement, and catheter removal 2-4 hr after the last dose or one hr before
the next dose
 S.C heparin also delay catheter placement 2-4 hrs, or delay the heparin 1 hr
post catheter placement
 LMWH: needle placement 10-12hrs after the last dose of LMWH, if Pt
receiving a higher dose 1mg/kg  delay 24hr
 Post-op 1st dose of LMWH delay 24 hr, and may keep the catheter until
next AM, give LMWH 2hrs later
 Anti-PLT: plavix ?? no data, but better at least 10 days before needle
placement, NSAID are OK
 Pt on oral med (Warfarin)  stop 5 days per-op INR= 1.4 is OK
Neurofibromatosis Page 164 of 217
 AD, café-au-lait spots >6, with > 1.5 in diameter, with CNS vascular and
skin involvement, and short stature
 Could be a part of MEN IIB
A difficult intubation, due to laryngeal or tracheal compression
B restrictive lung defect, interstitial lung disease, possible mediastinal mass
C HTN due to renovascular, Pheo, coarctation, Wilm’s tumor
CNS Astrocytoma, meningioma (ICP), spinal cord tumor, Sz disorder
M diffuse endocrine disorder as well as carcinoid tumor
MSK  Kyphoscoliosis
 Regional Anesthesia  could be difficult, Avoid if there is spinal cord
 Lab CBC, Lytes, BUN, creat, ECG, Echo, CXR, PFT with F/V loop
Neuroleptic Malignant Syndrome (NMS) Page 165 of 217
 S/S include fever, rhabdomyolysis, tachycardia, hypertension, agitation, muscle
rigidity, and acidosis, mental changes, and stupor, hypoxia, acidosis, CK, and
 The mortality rate is unknown, but may be as high as 20%. Dantrolene is an
effective therapeutic modality in many cases of NMS.
 there are significant differences between the two. MH is acute, whereas NMS
often occurs after longer term drug exposure.
 Phenothiazines and haloperidol or any of the newer potent antipsychotic agents
alone or in combination are usually triggering agents for NMS
 Sudden withdrawal of drugs used for Parkinson's disease may also trigger NMS
 (ECT) with Sux does not appear to trigger the syndrome.
 does not seem to be inherited, .
 possible due to dopamine depletion in the CNS by psychoactive agents.
 bromocriptine, a dopamine agonist, is often useful in treatment of NMS
  with dehydration, rapid titration of triggering drugs, and psychomotor agitation
 Other DDx: CNS diseases  meningitis, tumor,
Non-obstetrical surgery during pregnancy Page 166 of 217
 Obstetric consideration
  Risk of abortion and premature labor
 Minimize the amount of drugs as much as possible
 Use only the drugs that are known to be safe(STP, Sux, NDMR, Opioids,
Ketamine, Etomidate)
 If urgent Sx consider delay to the 2nd trimester
 Have an obstetric consultation
 For GA < 16 wks have FHM pre, and post op, for >16 wks have it intra-op
for abdominal procedure consider a transvagainal monitor
 FHR variability present @25-27 wks
 Maintain normal maternal BP, Oxygenation, acid-base status, avoid
aortocaval compression
 For pelvic and lower limb and upper limb consider regional technique
 For laparoscopic procedures max peritoneal inflation pressure 8-12 mm Hg
 For spinal or epidural give a fluid bolus before
 Always give reflux prophylaxis, and do RSI, with maintaining LUD
Obesity Page 167 of 217
A difficult intubation
B OSA, pickwickian syndrome, restrictive defect, with  FRC and Pul HTN
C HTN, CAD, pul HTN with cor-pulmonale, RV and LV dysfunction
GI GERD,  gastric acidity, fatty liver with liver dysfunction
D calculate the drug dosage according to the lean body mass
 H/P evidence of OSA, and RV/LV dysfunction  snoring, orhtopnea,
PND, EXAM RV/LV failure
 LAB CBC-D, Lytes, BUN, Creat, ABG, PFT, ECG,LFT, and consider
 Difficult IV access, and regional anesthesia
Obstetric considerations: Page 168 of 217
 Physiological and anatomical changes
A difficult A/W, Full stomach, ,RSI
B easy desat   FRC,  VO2
C hyperdynamic state, Aortocaval compression   BP,  UP blood flow
D   MAC,  cholinesterase,  albumin  Free F of drugs, placental drug
GI/Hepatic  full stomach,  gastric empting,  liver enzyme
Omphalocele and Gastroschisis Page 169 of 217
o Impaired blood supply to the herniated organs, and intestinal obstruction
o Major intravascular fluid shift and dehydration full-strength balanced salt
o Hypothermia and hypoglycemia
A possible difficult airway  Beckwith-Wiedemann syndrome consists of
mental retardation, hypoglycemia, congenital heart disease, a large tongue, and
an omphalocele.
B respiratory failure
C CHD in 20% of infants with omphalocele.
Induction: NG  aspirate gastric content then RSI , need large IV , possible
central, and arterial line
Post-op keep intubated
M  intravascular volume, with lytes abnormality
Organophosphate poisoning Page 170 of 217
 Bind to acetylcholinestrase enzyme
 S/S: Nicotinic: muscle weakness, fasciculation
Muscarinic: DUMBELS syndrome
D diaphoresis, diarrhea
U urination
M miosis
B bradycardia, bronchorrhea, bronchospasm
E Emisis
L lacremation
S salivation
A salivation, aspiration
B Respiratory failure, , bronchorrhea, bronchospasm
C hypotension, bradycardia, shock, arrhythmias, QT(poor prognosis)
D Avoid aminoglycosids ABx
M lytes abnormalities, acidosis, dehydration
GI N&V, diarrhea
Osteogenesis Imperfecta: Page 171 of 217
 A connective tissue disorder with 4 subtypes
 Multiple #, short stature, blue sclera
A deformity of the base of the skull, vertebral # Awake FOI
B kyphoscoliosis  restrictive lung defect
C Cor-pulmonale
Heme impaired PLT function
Other hemolytic anemia’s: Page 172 of 217
 Membrane defect  abnormal shape RBC hemolysis
 May have a hemolytic crisis which can triggered by infection and folate
 May come for splenectomy

G6PD Deficiency:
 RBC enzyme defect
 Can have a hemolytic crisis if exposed to some food and drugs: Fava beans,
PNC, Tyhlenol, antimalarial drugs, methylene blue, ASA in large dose
 Usually happened 2-5 day after ingestion
 May have DIC
Oxygen Delivery and Oxygen Consumption Page 173 of 217
Oxygen Delivery.
 Oxygen delivery is a function of arterial oxygen content (Cao2) and cardiac output.
Cao2 is expressed as the number of milliliters of oxygen contained in 100 ml of
blood and is calculated as follows:
Cao2 = (Hgb × 1.34 × Sao2) + (0.003 × Pao2)
DO2 = CO × Cao2

Oxygen Consumption.
 O2 consumption = CO x (CaO2-CvO2)

Oxygen extraction Ratio

ER= O2 consumption / O2 delivery
ER= [ CO x (CaO2-CvO2)] / CO x CaO2 = CaO2 – CvO2/CaO2
Pancreatitis:( acute, chronic) Page 174 of 217
 Associated with: chronic alcohol abuse, blunt abdominal trauma, gallstone,
perforated PUD
 Lab   amylase
 DDx  cholecystitis , MI, Pneumonia
 Chronic mainly with alcoholism, CF, old blunt trauma
A RSI, for GI ileus
C  hypovolemia, hypotension
D narcotic tolerant, malnourished   albumin   free fraction of drugs 
careful titration
M   Ca, acidosis, DM, acute alcohol withdrawal
Renal ARF  due to dehydration
CNS encephalopathy
Heme anemia, DIC
 Consider art-line , CVP
 Post-op ICU, pain management
Parkinson's Disease Page 175 of 217
 degenerative disease of the CNS caused by loss of dopaminergic fibers in the
basal ganglia of the brain.(substantia nigra)
 clinical features are resting tremor, cogwheel rigidity of the extremities,
bradykinesia, shuffling gait, stooped posture, and facial immobility.
A laryngospasm, muscle rigidity before giving MR difficult vent consider RSI
B frequent aspiration,  VC, COPD
C arrhythmias due to L-dopa, autonomic dysfunction,  intravascular volume
D L-dopa(sinemet) Levodopa+ a peripheral dopamine decarboxylase inhibitor
carbidopa to  systemic side effect give in AM t1/2 6-12, avoid Maxran,
Demerol, alfenta, droperidol, sux may use for RSI, K one case report
Post-op: In the postoperative period, patients with Parkinson's disease are more
susceptible to the development of mental confusion and even hallucinations.
PDPH Page 176 of 217
 In a supine position very mild, sitting  severe fronto-occipital headache
 May associated with cranial N symptoms: diplopia, tinnitus, N&V
 DDx: meningitis, migraine
 Review anesthetic Record for Neuraxial procedure, type and size of needle
for spinal, and wet tab documentation, and any other complications
 Review past-medical Hx neurological Hx (headache)
 Headache: character, severity, aggravating and relieving factors (position),
associated symptoms, and the location of the headache
 Exam: V/S include Temp, meningeal signs (meningismus, photophobia,
fever), Neuro Exam looking for any sensory or motor deficit
 Rx: bed rest, hydration, caffeine 300mg PO q8-12hrs, Tylenol, and
NSAID’s if not working or severe headache  Epidural blood patch
Peri-tonsilar abscess
Emergency and potential life threatening
A airway obstruction, with trismus , possible full stomach, do a gas induction
with no muscle relaxant , gentle intubation avoid rupture the abscess
Pheochromocytoma Page 177 of 217
 In normal medulla, norepinephrine account for only 20% of the secretion,
where it is greater in a Pt with pheochromocytoma.
 halothane and histamine-releasing drugs, can exacerbate the life-threatening
cardiovascular effects of the catecholamines secreted by these tumors.
 Most (85–90%) are solitary tumors localized to a single adrenal gland,
 usually the right, 10% of adults and 25% of children have bilateral tumors.
 extra-adrenal sites (10%) along the paravertebral sympathetic chain.
 95% in the abdomen, a small % located in thorax, urinary bladder, or neck.
 Malignant spread of highly vascular tumors in approximately 10% of cases.
 In about 5% of cases, this tumor is inherited as a familial AD trait.
 It may be part of the polyglandular syndrome as MEN Type IIA or IIB.
 Type IIA includes: medullary carcinoma of the thyroid, parathyroid
hyperplasia, pheochromocytoma;
 Type IIB consists of: medullary carcinoma of the thyroid,
pheochromocytoma, neuromas of the oral mucosa.
 may also arise in association with von Recklinghausen's neurofibromatosis
 or von Hippel-Lindau disease (retinal and cerebellar angiomatosis).
Phosphate Page 178 of 217
 distributed in similar concentrations throughout intracellular and
extracellular fluid.90% in bone, 10% is intracellular, and <1%, in the ECF.
 free ion (55%), complexed ion (33%), and in a protein-bound form (12%).
 Control of phos concentration by altered renal excretion and redistribution
within the body compartments.
 Absorption occurs in the duodenum and jejunum and is largely unregulated.
Phos reabsorption in the kidney is primarily regulated by PTH, dietary
intake, and insulin-like growth factor.
 Phos provide the primary energy bond in ATP and creatine phosphate.
Therefore, severe phosphate depletion results in cellular energy depletion.
 Phos is an essential element of second-messenger systems, including cAMP
and phosphoinositides, and a major component of nucleic acids,
phospholipids, and cell membranes.
 As part of 2,3-DPG, phos is important for off-loading oxygen from the
hemoglobin molecule.
Physiological changes in pregnancy: Page 179 of 217
A venous engorgement, edema,  by PIH, URTI and fluid overload, easy nasal
B FRC, TLC, ERV,  IRV, TV, minute vent, and O2 consumption,  shunt
from 5% to 14 %, shift of O2-Hgb curve to the Rt with P50 30mmHg
C  CO, Normal BP due  SVR,  plasma volume
Pierre Robin Syndrome:
A difficult A/W due to micrognathia, glossoptosis, cleft palate
B obstruction pul edema, Aspiration
C CHF, pul HTN, cor pulmonale, associated CHD
CNS Sz due to hypoxic brain injury
 Do awake FOI, have ENT surgeon in the room for possible trach
 A/W obstruction improve with age
 Extubate awake only
PIH and HELLP Page 180 of 217
 In addition to the changes in pregnancy
A  airway edema, difficult intubation difficult A/W cart in the room
B pul edema, more after delivery
C CHF,  BP,  volume,  oncotic pressure
D Mg, other meds, could be on ASA
M  Mg,  albumin
Heme anemia, hemolysis, thrombocytopenia ,  fibrinogen
CNS  LOC, headache, blurred vision, seizure, bleeding , edema
Renal  GFR, oliguria, ARF
GI/Hepatic  RUQ pain, liver rupture
 Rx start Mg bolus 4g then infusion @ 1-3 g/h, consider other anti-HTN meds
e.g. labetolol, SNP, NTG, hydralazine, (ACEI are C/I due to fetal effect)
 Monitor Mg level avoid Mg toxicity, consider early epidural  help  BP,
improve UP blood flow (if PLT are OK)
 Monitors: art line, fetal monitoring, CVP/PAC
 Before giving any fluid bolus look for evidence of CHF
 Lab: CBC-D, Lytes, BUN, Creat, Mg, PT, PTT, fibrinogen, LFT, BT
Pituitary Tumors, and transsphenoidal approach Page 181 of 217
 Ant regulated by the hypothalamus secret 7 hormones
 Post ADH, Oxytocin
 Tumors could be non-functioning, or hyper secreting
 The non-functional  mass effect  headache impaired vision, N&V, CN palsy,
and  ICP, or pan-hypopitutarism
 hyper secreting could be a MEN I, usually small, the most common is adenoma
secreting prolactin , then GH, then ACTH, other effect hyperthyroid, DM
 pituitary apoplexy  due to sudden hemorrhage  neuro deficit and  pituitary
function  Mx  steroids and surgical decompression
 May not develop DI until after starting steroids therapy
 Monitors routine with art-line for acromegaly, CVP if head-op position
 Lab  CBC, lytes, ABG, CXR, ECG, lateral neck XR
 Critical structures internal carotid artery, cavernous sinuses, CN III, IV, V, VI
A possible difficult intubation
C HTN, Cardiomegaly, cardiomyopathy
D hormone replacement, stress dose steroid,
Placenta previa Page 182 of 217
 Risks: previous C/S, previa
 Painless vaginal bleeding in the 2nd-3rd trimester
 Risk of abruption and IUGR
 Avoid vaginal exam and tocolytic therapy
A and B  obst
C hypovolemia, shock
D avoid tocolytic
Heme DIC rare, most are dilutional thrombocytopenia
lab as in abruption
shock as in abruption
GA Vs spinal/epidural depend wither if the placenta is anterior or >1 C/S with 
risk of accreta  GA, if posterior may consider spinal/epidural if the Pt is stable
Porphyrias Page 183 of 217
 A group of inborn error of metabolism, with defect in heme synthesis
 Complete deficiency of enzymes is incompatible with life
 Deficiency of one enzyme will lead to accumulation of one or more
intermediates molecules which will give the clinical manifestation of Porphyria.
 The rate-limiting step in heme synthesis is the conjugation of succinyl-CoA
with glycine to form D-aminolevulinic acid ALA (the enzyme is aminolevulinic
acid synthetase).
 generally manifest after puberty. Inheritance is an AD pattern,
 but congenital erythropoietic porphyria is inherited as an AR pattern.
 A functional classification for the anesthesiologist is based on a division of the
porphyrias into:
o Inducible: acute symptoms are precipitated on drug exposure, which are:
 Acute intermittent Porphyria
 variegate Porphyria ( 80% photosensitive)
 hereditary coproporphyria
o noninducible forms.
Post-op Stridor: Page 184 of 217
 Emergency, and life threatening
 Proceed immediately to the PARR
 Review the V/S, and quick AMPLE history , 100% O2, and Call for help,
do jaw thrust, apply oral A/W, apply CPAP, suction the A/W
 DDx: 1-Laryngeospasm, 2-laryngeal edema due to volume overload or
Trendelenburg position intra-op,3- VC paralysis due to neck or thoracic Sx,
or residual NM blockade, 4- A/W foreign body (secretion, blood, vomit
Post-op Altered LOC/Agitation: Page 185 of 217
 With  LOC could be life threatening, agitation potential harm to him self
and nurses
 Proceed immediately to the PARR
 ABC, restrain the Pt if needed, 100% O2. obtain new V/S
 Review anesthetic chart/ talk to the anesthetist who did the case, review the
old chart
 DDx:
o Psychological response to emergence
o Co-existing mental/psychological problem (post-traumatic stress)
o Intra-op re-call
o Residual anesthetics, NMB Agents, Ketamine.
o Drugs/alcohol withdrawal
o Withdrawal of anti-psychotic, seizure, Parkinson meds
o Surgical pain, bladder distention
o A/W obstruction  with hypoxia and hypercarbia
o Other metabolic abnormalities  Na, Ca, hypoglycemia
o CNS: hypoperfusion, CVA, Sz, postictal
Post-op hepatic dysfunction Page 186 of 217
 Classify as pre, intra and post hepatic
 The main S/S is jaundice
 Need repeat measurement of bili, AST/ALT, and ALP
 Most likely multifactorial
 One of the main factors could be intra-op hepatic hypoxemia
 Steps:
1) Review all meds given to the Pt without any exclusion peri-op, includes
intra-op use of vasopressors  splanchnic vasoconstriction  B flow
2) Look for source of infection
3) Blood Tx bili load  in Pt with co-existing liver dysfunction
4) Look for hematoma hyperbilirubinemia
5) Role out hemolysis  Hb,  retics
6) Review anesthetic and PARR records for any evidence of hypoxemia,
hypotension, hypovent, hypovolemia
7) Look for extra-hepatic source of liver dysfunction CHF, resp failure, PE,
8) Could be benign post-op intrahepatic cholestasis
Post-tonsillectomy bleeding Page 187 of 217
Emergency and potential life threatening
Go immediately to see the Pt
OR emerg meds , airway equipment double setup X2 suction , X2 scops
A  full stomach, possible difficult airway use ketamine for induction, RSI
B  hypoxia
C hemorrhagic shock, resuscitate the Pt
H possible bleeding disorder.
Lab CBC, lytes, PT, PTT, X-match
Pre-op Cardiac evaluation: Page 188 of 217
 See other card for clinical predictors
 See other card for stratification for noncardiac surgical procedure
 See the algorithm
 Recent MI wait 4-6 wks for elective surgery
 Lab evaluation
o Resting LV function is not a predictor for ischemic event
o 12 leads ECG
o Exercise or pharma stress test for Pt with intermediate risk, or when Pt
is unreliable
o Angio for Pt suspected or known CAD
 Pre-op therapy
o CABG for high risk Pt, with possibility to improve outcome
o PCA: no controlled trial for PCA vs medical therapy, If Pt had PCA,
with balloon dilation only, wait only for one week for elective
procedure, if stent 4-6 wks with minimum 2 wks, for anti-PLT therapy
o Medical: -blokers
 Anesthetic consideration
o No technique is superior
Preterm labor Page 189 of 217
 Between 20-37 wks
  fetal M&M
 Pt may given tocolytic therapy if there is no C/I
 -agonist: Ritodrine and terbutaline
o For short term only to allow time for lung maturity after steroids
o The effect persist to 60-90 min after D/C, need at least 10 min D/C
before giving anesthetic
o S/E: hyperglycemia, tachycardia, with possible arrhythmia, pul edema,
myocardial ischemia, hypotension, cerebral vasospasm, fetal
tachycardia, rebound hypoglycemia
o Avoid overzealous hydration which may  risk of pul edema, and
hyperventilation  K
o Lidocaine IV may prevent arrhythmia
 MgSO4
o See PIH for S/E, less severe than -agonist
o Risk of hypotension with spinal/epidural
o  sensitivity to NDMR
Prone position Page 190 of 217
 Difficult access to the A/W
 Difficult resuscitation
 Difficult to add invasive monitoring art-line, CVP, TEE
 Pressure injury to eyes, nose, iliac crest, knees, toes, breast, genitalia
 Brachial plexus injury
  CI, SV,  Venus return  due to pressure on the abdomen vena caval
pressure  epidural vein engorgement
Protein C and Protein S Deficiency Page 191 of 217
 Congenital  AD, or Acquired due to hepatic dysfunction, vit K deficiency,
and DIC, post-op, hemodialysis, postpartum
  risk of thrombo-embolic phenomena post-op
A N/A
B  PE, with possible Pul HTN,
C IHD (MI, angina), Peripheral vascular disease
D on coumadin  stop pre-op and start heparin
G bowel ischemia
R renal vein and artery thrombosis.
CNS sagital sinus thrombosis  stroke, TIA’s
 for neuraxial anesthesia look in the ASRA guidelines
 may give FFP to  protein C level.
Antithrombin III deficiency
  risk of thrombo-embolic phenomena
 Resistance to heparin, may give Antithrombin III concentrate, or FFP
Pul HTN Page 192 of 217
 The pulmonary vessels are more reactive compared to Eisenmenger
 High mortality rate
 Hemodynamic Goals:
o preload maintain, LUD
o R/R  maintain normal and sinus
o Cont  maintain, avoid cardiodepressant
o Afterlaod maintain, avoid sudden  in SVR
o PVR  Avoid any thing that  PVR  pain, hypoxia, acidosis, PCO2
 O2 all the time, Art-line,
 Consider: NO, prostacycline, CCB, NTG to  PVR
 PAC  risk/benefit
 No spinal, epidural slowly titrate
 GA same problem as in Eisenmenger
 Post-op ICU
Pulmonary embolism Page 193 of 217
 Associated with hyper-coagulation state (protein C and S deficiency ),
trauma, prolonged bed rest
 High M&M
 Pathophysiology:
o Pulmonary arteries obstruction   dead space ventilation 
hypoxemia , hypercarbia
o  PVR, Bronchospasm
o RV dysfunction and arrhythmias
 Pt may present to the OR for emergency surgery, insertion of IVC filter or
surgical embolectomy
 Also Pt may present with previous history of PE, and now anticoagulated
 have a hematology consult (Q: risk/benefit of holding meds pre-op) also
discuss with the surgeon regarding continuing the anticoagulation med peri-
 Have PT, PTT, and PLT count (HIT)
 Better to avoid Neuraxial technique in those Pt
 If diagnosis is in doubt  Spiral CT, V/Q scan, Echo
Pulmonary HTN Page 194 of 217
 @ rest mean of 25, with exercise > 30
 Primary (idiopathic) F:M 3:1, age 20-40
 Secondary:
o pul disease: asthma, COPD, restrictive lung disease, cystic fibrosis,
o heart disease: MS, AS, ASD, VSD
o collagen vascular disease
o thromboembolic disease: PE, sickle cell
 S/S  SOBOE, easy fatigue wheezing, graham steel murmur
 Lab: CXR, ECG(RVH, RAD, Rt atrial enlargement), Echo, ABG, PFT, NO
test to if responsive or not (Viagra)
 Cardiology consult and ICU
 Monitors: CAS, 5 leads EGC, art-line, CVP, PAC???, TEE, ECG look for
acute strain pattern in leads II, III and aVF
 Options RA Vs GA, better RA
 Have NO ready, and inotropic support (milrinon, dobutamine) SNP, NTG
 Keep 100 O2 all time
 Avoid things  PVR ( hypoxia, acidosis, hypothermia,  PCO2)
Pyloric stenosis Page 195 of 217
 M>F
 Not a surgical emergency, S/S appear 2-6wks
 With the consideration of neonate
A full stomach RSI
B compensated resp acidosis  hypoventilation
C hypovolemia  shock
M hypochloremic metabolic alkalosis, dehydration
 Pre op assess the level hydration skin turgor, anterior fontanel, moist tongue,
urine OP, V/S
 Check lytes Na >132, Cl>88, K > 3.2,
 Give K, if + urine OP
 Induction give atropine, insert NGT, or OGT to empty the stomach (no
guaranteed) and pre-oxygenate
 RSI with cricoid pressure
 Maintenance  need to be paralyzed  if not risk of mucosal perforation
 Infiltrate Marcaine with epi, give Tylenol 15mg/kg PR for pain control
Restrictive Cardiomyopathy Page 196 of 217
 Causes:
o Toxic :Methysergide, Anorectic agents, Radiation
o Infectious: viral myocarditis
o Infiltration: endomyocardial fibrosis
o Genetic
o Idiopathic
o Infiltration
 Sarcoid, Hemochromatosis, Amyloidosis ,Glycogen storage
 Impaired diastolic filling
 Have the same clinical picture of constrictive pericarditis
 Except that the LV is more affected than RV
 Management of anesthesia:
o As Tamponade
Restrictive lung disease Page 197 of 217
 The main feature is  lung compliance with  TLC, normal FEV1/FVC,
and  VC  N 70ml/kg,  as low as 15ml/kg, and possible
hyperventilation with  PCO2
 Could be acute Vs chronic, where the acute component could be reversible
 Causes:
o intrinsic lung disease ( edema, pneumonia, aspiration, ARDS,
fibrosis due to drugs, or idiopathic, and plural diseases)
o Neuromuscular diseases: spinal cord transection, Guillian barre,
muscular dystrophy, myasthenia, and myasthenic syndrome
o MSK scoliosis, sternal deformity
o Extrinsic: obesity, pregnancy, ascites
 S/S SOBOE,  exercise tolerance, cough, breathing pattern Vt, RR
 With severe disease Pt may have pul HTN, with S/S of Rt heart failure
 Pre-op: determine the severity by H/P and Lab, and treat the possible acute
reversible component
 A VC < 15ml/kg with  PCO2  high risk
 Lab: CBC-D, lytes, BUN, creat, CXR, ABG, PFT, ECG, Echo
Rheumatoid arthritis Page 198 of 217
 F> M, Age 30-50
 The hands and wrists are involved first, particularly the metacarpophalangeal and proximal
interphalangeal joints.
 A:C-spine: atlantoaxial subluxation, The degree of cord compression does not correlate
well with the patient's symptoms, and asymptomatic patients may have a high degree of
spinal canal stenosis., TMJ involvement, Cricoarytenoid arthritis which may cause pain,
horseness, dyspnea, stridor and airway edema.
So be caution with intubation and consider Fiberoptic intubation, and risk of post-
extubation stridor.
 B: pleural effusions, pulmonary nodules, interstitial lung disease, obstructive lung disease,
restrictive lung disease. more common due to costochondral involvement
 Several of the antirheumatic drugs cause pulmonary dysfunction as well
 V/Q mismatch and hypoxia
Consider PFT and possible post-op ICU bed
 C: Pericarditis in 30%, chronic constrictive pericarditis or pericardial tamponade
myocarditis, coronary arteritis
 dysrhythmias secondary to development of rheumatoid nodules in the cardiac
conduction system
 aortitis, producing aortic root dilation and aortic insufficiency, Valve fibrosis
Risk of RBC Tx Page 199 of 217
 Citrate Intoxication
o CPDA citrateionized calcium.
o Signs hypotension, narrow pulse pressure, VEDP, and CVP
o ECG changes: prolonged Q-T interval, widened QRS, and flattened T waves.
o The hypocalcemia is directly related to the rate and volume of blood Tx.
o Citrate is metabolized efficiently by the liver, Impaired liver function or
perfusion will lower the rate threshold for developing citrate intoxication.
o Treatment: CaCl
 Acid–Base Changes  ? metabolic acidosis
 2,3-DPG left shift of the O2–Hgb dissociation curve
 Hyperkalemia with rapid Tx   by acidosis, hypovolemia, and hypothermia
o ECG  peaked T waves, a prolonged PR interval, and a widened QRS.
o If ECG changes are observed the transfusion should be stopped and
intravenous calcium should be administered. Bicarbonate, dextrose, and
insulin may also be appropriate according to the severity of the episode
 Volume Overload
 Hypothermia   CO, left shift of O2-Hgb, acidosis, coags
 Microaggregate Delivery
Sarcoidosis: Page 200 of 217
 More common in African-American, F:M 2:1
A distorted anatomy with possible A/W obstruction  difficult A/W FOI
B restrictive lung disease with pulmonary fibrosis
C Arrhythmias, heart block, CHF
D on Steroid and immunosuppressant (stress dose)
GI liver involvement
CNS SOL, neuropathy, Sz
Lab/DI CBC-D, Lytes, BUN, creat, ABG, CXR, PFT, ECG, LFT
 Consider ICU backup if bad PFT
SARS: Page 201 of 217
 Not contagious until Pt become symptomatic with in 4-6 days(2-10)
 Transmission by close contact, and in a contact with resp secretion
S/S and Lab:
 Fever, chills, headache, myalgia (nonspecific)
 Nonproductive cough, with SOB, other N&V, diarrhea
 Radiological evidence of pneumonia within 7-10 days of symptoms onset
 Lab: lymphopenia,  PLT,  PTT and Liver enzymes and  CK
 SARS serum Antibodies positive
 SARS CoV isolation in cell culture
 PCR positive for SARS CoV RNA
 Suspected Pt should be in resp isolation room ASAP if history contact with
Pt with SARS or been in an epidemic area
 During Pt transfer have a surgical mask over the Pt
 Do CXR, pulse oxi, blood C/S, CBC-D, sputum for gram stain and C/S
 Test for other respiratory pathogens inf A, B, RSV, pneumococcal
Scleroderma Page 202 of 217
 Progressive systemic sclerosis:Inflammation, Vascular sclerosis, Fibrosis of skin and
 Tissue edema
 Some Pts have CREST syndrome, C: calcinosis, R: Raynaud’s phenomenon, E:
esophageal hypomotality, S: scleroderma, T: Telengectesia
 F>M, Age 20-40
 Pregnancy  the progression of the disease in 50% of the Pt.

A: flexion contracture difficult airway due to limited mouth opening,  motility,  LOS
tone GERD need RSI
B: A major cause of M&M, Chronic aspiration, Diffuse lung fibrosis restrictive lung
disease,  diffusion capacity
C: risk of IHD, fibrosis of the conductive system arrhythmia, cardiomyopathy CHF,
systemic and pulmonary HTN, pericarditis effusion  tamponade, with systemic HTN
 intravascular volume hypotension , Raynaud’s phenomenon in 70% risk of ischemia
with art-line
CNS: peripheral and cranial nerve neuropathy
o Eye: conjunctivitis and corneal abrasion
Scoliosis Sx Page 203 of 217
 Need two stage Sx, 1st anterior approach to release the anterior spinal artery, and
diskectomy, the 2nd stage to posterior  instrumentation
 The scoliosis could be secondary to muscular disease ( muscular dystrophy)
A Reflux RSI
B Restrictive lung disease,  risk of PPC (pneumonia, atelectasis)
C myopathy, arrhythmias
D avoid Sux
Heme consider autologus blood donation pre-op
 Consult (ICU, Heme), talk to the Pt regarding awake test
 Lab:CBC-D, Lytes, BUN, creat, X-match, CXR, PFT, ABG, ECG, Echo if needed
 OR: blood in the OR, bear hugger, Art-line, IV wormer
 Position: prone check all pressure points, and frequent checking
 May consider deliberate hypotension if there is no C/I, with that HR will , so
consider -blockers
 SSEP: if  latency by 10% or amp by 60%   BP, ask the surgeon to stop
 Volatiles have the least effect on SSEP  See SSEP card
 Post-op: pain, PPC, ICU
SEP Page 204 of 217
 Any injury will cause  in latency &  amplitude
 SSEP  50% in amp to surgical maneuver  significant
 Cortical ( SSEP, VEP) are more vulnerable to anesthetic drug effect
 brain stem/subcortical (SSEP, BAEP) are more resistance
key points:
 maintain a constant anesthetic level, and avoid any sudden changes
or a bolus doses of any drugs
 maintain and control other factors that may affect the SEP like
temp, BP, PaO2 and PaCO2
Effect of inhalational agents:
 SSEP  all  lat/amp, except enf /, N2O 0/
 VEP  all lat/ amp
 BAEP  alt/0 amp
Effect of IV drugs:
 All drugs  lat/ amp except ketamine and etomidate /, with 0/
effect on the VEP and no effect on BAEP at regular doses
Septic shock: Page 205 of 217
A LOC, full stomach
B resp failure, ARDS, pul edema
C low or high output failure, SVR,
D Abx, APC, steroids, inotrops, vasopressors
Met lactic acidosis, base deficit, K, lytes disturbance, adrenal insufficiency
Renal ATN, ARF
Heme thrombocytopenia, DIC
 ECG, Sat, Art-line, CVP/PAC, frequent ABG,
 Lab: CXR, ABG, ECG, CBC-D, Blood C/S, sputum, and urine, lytes, BUN,
creat, LFT, PT, PTT, Fibrinogen, D-dimer, ACTH stim test, if suspecting a
source of infection do further investigation e.g. TEE or TTE for ? edocarditis,
abdominal  CT…..
 Early goal directed therapy( CVP 8-12, MAP >65, Urine>0.5ml/kg/hr,
 Broad spectrum ABx
Class I Class II Class III Class IVPage 206 of 217
Blood loss (ml) 750 750–1500 1500–2000 2000
Blood loss (%) 15 15–30 30–40 40
HR (per min) <100 >100 >120 140
Blood pressure Normal Normal  
Pulse pressure Normal or    
RR 14–20 20–30 30–40 <35
Urine ml/hr 30 20–30 5–15 Negligible
Mental status Slightly Mildly Anxious and Confused,
anxious anxious confused lethargic
Fluid (3:1 rule)‡ Crystalloid Crystalloid Crystalloid + Crystalloid +
blood blood
Shoulder Sx: Page 207 of 217
 Arthroplasy, and arthroscopy, and rotator cuff repair
 Use of a beach chair position  VAE risk
 Limited access to the airway tighten the connection, reinforce with tap
 Possible eye and ears injury
 Avoid excessive head rotation brachial plexus injury
 Options GA, interscalene or combined
 Assess the arm before doing the block for any neurological deficit
 Risk of post-op neurological deficit  the level of the injury is at the level
of the trunk (same as interscalene) difficult to determine the cause (surgical
Vs block) Neurapraxia  90% resolve within 3-4 months
Inappropriate Secretion of Antidiuretic Hormone (SIADH) Page 208 of 217
 Causes: head injuries,intracranial tumors, pulmonary infections, small cell
carcinoma of the lung and hypothyroidism.
Clinical manifestations
occur as a result of a dilutional hyponatremia,  serum osmolality, and a reduced
urine output with a high osmolality. Weight gain, skeletal muscle weakness, and
mental confusion or convulsions are presenting symptoms. Peripheral edema
and hypertension are rare. The diagnosis of the (SIADH) is one of exclusion,
and other causes of hyponatremia must first be ruled out. The prognosis is
related to the underlying cause of the syndrome.
 Pt with mild/mod H2O intoxication is restriction of fluid intake to 800 ml·day–
 Pt with severe water intoxication associated with hyponatremia and mental
confusion may require more aggressive therapy, with the iv administration of a
hypertonic saline solution. This may be administered in conjunction with lasix
 Caution must be observed in patients with poor LV function. Isotonic saline is
substituted for hypertonic solutions once the serum Na is in a safe range.
Sickle cell anemia Page 209 of 217
 The defect in -chain, position 6  glutamic acid substituted by valine
 3 types of crisis
o hemolytic further anemia
o sickling  pain & vaso-occlusive
o Aplastic  may cause death.
 Ethnic background: Mediterranean and African-American.
 In infancy Hb F is protective.
 % of Hb S
o trait (mild)
o < 50% is Hb S
o sickling do not occur under normal physiological conditions
o may happen under extreme conditions e.g severe hypoxemia.
o Disease (severe)
o Hb S > 75% may up to 95%
o Could be associated with other abnormal Hb e.g Hb C
o Pt with Hb SC have a normal Hb level, but at a greater risk of sickling.
 Pre-op you need to knew what is the result of the Hb electrophoresis.
  mortality with  in the number of the painful crisis in adult per-year.
Status asthmaticus Page 210 of 217
 Emergency and life threatening
 Result in respiratory failure with hypoxia, hypercarbia, and
respiratory/metabolic acidosis
 Management:
o ABC, 100% O2
o Intubate deep/ also may consider BiPAP
o Ventoline, ipratrupium bromide, steroids, thiophylline, leukotrine
inhibitor, ABx if suspect infection
o Other consider Ventoline IV, Isoprel/pei gtt, Ketamine, BNZ
o Last volatile agent, and paralyze
o Ventilation: volume control Vt 6-10ml/kg, PEEP 5-10, target
normal PO2, pH, and PCO2, keep the platue pressure < 30cmH2O
o If need switch to pressure control
o Also may consider Heliox
o Be aware of AutoPEEP disconnect the bag, if on vent  reverse
ratio ventilation
Stroke & TIA: Page 211 of 217
 Hemorrhagic or ischemic
 Etiology: Atherosclerosis, embolic  MI, A.fib, VHD, post-op  CEA,
trauma, severe HTN
A  LOC, loss of A/W reflux (RSI)
B hypoventilation
C HTN, CAD, VHD, A.fib, arrhythmias  ECG, Echo
D anti-PLT, ASA, coumadin, Avoid Sux, N. stimulator  resistance
N   LOC, neuro deficit

 Avoid swinging in BP, and hyperglycemia
 With chronic HTN the cerebral autoregulation curve shifted to the Rt
Supratentorial Intracranial Tumors Page 212 of 217
 Review Pt overall medical condition
 Focus on Neuro-evaluation:  LOC, S/S of  ICP: headache, N&V, papilledema,
unilateral pupil dilation, and the presence and extent of focal neurological deficit
 May have fluid and lytes abnormality
 Review CT/MRI head
 Lab: CBC, lytes, BUN, creat, ECG
 The main effect of Supratentorial masses is intracranial HTN
 The main anesthetic goal is to maximize the therapeutic modality to  ICP, and to
avoid any factor that may  ICP
 ICP control SEE ICP card
 Monitoring: Standard + Art line, CVP, Foley cath, for the art-line have the
transducer at the level of external auditory meatus ( level of circle of Willis)
 Induction: may need RSI, if CN involvement or  LOC, give Lidocaine IV, with
other standard induction drugs, Avoid Sux
 Maintenance: Isoflurane, No N2O
 Emergence: give Lidocaine IV 90 sec before extubation, and consider using
antihypertensive Meds(labetolol), assess for any neurological deficit
Systemic Lupus Erythematosus Page 213 of 217
A cricoarytenoid arthritis  hoarseness, stridor, or airway obstruction (awake
intubation), post-extubation edema
B effusion, pneumonitis, pul HTN, and alveolar hemorrhage. high correlation
of pul HTN with Raynaud's phenomenon in patients with SLE.(CXR, PFT)
C pericardial effusion, tamponade, Cardiomyopathy, cardiac conduction
abnormalities,  ventricular function, and coronary arteritis, noninfectious
endocarditis (Libman-Sacks endocarditis)  mitral insufficiency (ECG, ECHO)
D immunosuppressants (corticosteroids) or cytotoxic drugs
(cyclophosphamide, azathioprine, cyclosporine),avoid Drug-induced lupus
quinidine, hydralazine, methyldopa, captopril, enalapril, clonidine, isoniazid,
Hanti-phospholipid antibodies  thromboembolic complications, anemia
R common cause of M&M in patients with SLE, CRF
CNS seizures, stroke, dementia, psychosis, and peripheral neuropathy
GI peritonitis, pancreatitis, bowel ischemia, protein-losing enteropathy, and
lupoid hepatitis
Tamponade: Page 214 of 217
 Emergency and life threatening
 In acute as little as 200 ml cause S/S
 In chronic up to 1000 ml cause S/S
 Causes:
o Infection: bacterial, viral, fungal, TB
o Inflammatory disease with vasculitis: R.Arthritis, SLE, scleroderma
o Metabolic: RF, myxedema
o Radiation, malignancy, trauma, post-heart
 Pathophysiology:  VEDV,  SV,  CO,  SBP,  CVP, Rt=Lt pressure
 Dx by keeping in mind a high index of suspicion with clinical S/S and lab
 Beck’s triad: hypotension, distended neck veins, muffled heart sound
 S/S: tachypnea, BP, narrow pulse pressure, HR, pulses paradoxus
 Signs of systemic hypoprefusion: oliguria, lactic acidosis, cool extr
 DDx: tension Pneumo, RV infarction, Pul HTN, cardiac herniation
 ECG: diffuse ST-changes, low voltage
 Lab: ECG, Echo, CXR, CT
TCA overdose: Page 215 of 217
 Gives anticholinergic syndrome, So no Atropine
 Cardiac toxicity is the major cause of death
 No correlation between serum level and symptom
A  LOC  RSI
B depression, ARDS
C toxicity,  QT, wide QRS, sinus tach, heart block, hypotension due 
contractility, and vasodilation by -blockade, arrest
CNS hallucination, coma, seizure
M metabolic acidosis
 Management:
o Gastric lavage
o Activated charcoal 1g/kg with 60 ml sorbitol
o Bicarb is the Key in the management 2 mEq/kg bolus then infusion
150mEq in 850 D5W to maintain pH 7.45-7.50
o For Vent arrhythmia give Lidocaine, Class 1A,1C are C/I
o Hypotension  Norepi gtt
o Bradycardia Isoprel or pacing No Atropine
TEF Page 216 of 217
 30% premature, associated CHD, and VATER, VACTREL syndromes
 Depend on the infant stability if stable complete repair, if not stage repair, with
insertion of G-tube under LA, the ligation of the fistula, and reanastomosis of the
A subglottic stenosis
B resp distress, RDS, pneumonia
C CHD, decompensation and CHF
M dehydration, metabolic acidosis
 Worm up the room, big IV, standard CAS monitors, Art-line
 Lab CBC-D, lytes, ABG, Cap gas or VBG, CXR, Echo, X-match with 2U peds
in the room
 Give atropine, not muscle relaxant until chest open,
 Inhalation induction  bronch, then intubate after further mask ventilation to
deepen the Pt, have different size ETT, after intubation with the bevel directed
posteriorly, listen to the chest and initially intubate the Rt main bronchus, with
listening to the chest withdraw the tube slowly till you here bilateral breath sound.
 Consider caudal epidural for post-op pain
 Run maintenance fluids with glucose maintenance as well
Page 217 of 217