Clinical Protocols of NICU

Hand book of clinical
management of
common scenarios in
NICU
Clinical Protocols
JSS Neonatal
Compiled by
Dr Srinivasa Murthy D
Dr Sushma K
Dr Deepti T
ADMISSION TO NICU - CRITERIA .................................................................................................................... 4
AIR LEAK ............................................................................................................................................................ 5
ANO-RECTAL ANOMALIES .............................................................................................................................. 6
APNOEA ............................................................................................................................................................. 8
ARTERIAL OCCLUSION / THROMBOSIS ........................................................................................................ 9
BLEEDING NEONATE...................................................................................................................................... 11
BRONCHIOLITIS .............................................................................................................................................. 12
CHRONIC LUNG DISEASE (CLD) - MANAGEMENT ..................................................................................... 13
CONGENITAL DIAPHRAGMATIC HERNIA (CDH) ......................................................................................... 16
CONGENITAL HYPOTHYROIDISM ................................................................................................................. 18
CONGENITAL INFECTION - GENERAL PROTOCOL .................................................................................... 21
CONVENTIONAL MECHANICAL VENTILATION ........................................................................................... 35
CRANIAL ULTRASOUND SCANNING ............................................................................................................ 39
DECLARING NEONATAL DEATH ................................................................................................................... 40
EXOMPHALOS (OMPHALOCOELE) ............................................................................................................... 41
GASTRO-ESOPHAGEAL REFLUX (GER) ...................................................................................................... 42
GASTROSCHISIS ............................................................................................................................................. 43
GRAVES’ DISEASE - INFANTS BORN TO MOTHERS .................................................................................. 44
HEART MURMURS DETECTED AT ROUTINE NEWBORN EXAMINATION ................................................ 47
HIE - ANTICONVULSANTS .............................................................................................................................. 48
HYPOGLYCEMIA IN THE NEWBORN............................................................................................................. 49
HYPOTENSION................................................................................................................................................. 54
HYPOTONIA ..................................................................................................................................................... 57
INBORN ERROR METABOLISM – SUSPECTED ........................................................................................... 58
INTRAVENTRICULAR HEMORRHAGE (IVH) ................................................................................................. 59
LOW BIRTH WEIGHT CARE GUIDELINES..................................................................................................... 63
LOW BIRTH WEIGHT FEEDING ...................................................................................................................... 71
MECONIUM ASPIRATION SYNDROME (MAS) .............................................................................................. 74
NECROTISING ENTEROCOLITIS ................................................................................................................... 75
NEONATAL ENCEPHALOPATHY ................................................................................................................... 77
NEONATAL SEIZURES .................................................................................................................................... 80
NEONATAL SEPSIS ......................................................................................................................................... 82
PATENT DUCTUS ARTERIOSUS (PDA) IN PRETERM INFANTS ................................................................ 86
PULMONARY HYPERTENSION – MANAGEMENT (SIPHON PROTOCOL) ................................................. 89
PULMONARY HAEMORRHAGE ..................................................................................................................... 91
RESPIRATORY DISTRESS - INITIAL MANAGEMENT .................................................................................. 93
1
Clinical Protocols, NICU, JSS Hospital
RESUSCITATION ............................................................................................................................................. 94
RETINOPATHY OF PREMATURITY SCREENING IN NICU ......................................................................... 102
SURFACTANT ................................................................................................................................................ 104
TRACHEO OESOPHAGEAL FISTULA (OESOPHAGEAL ATRESIA) ......................................................... 106
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Neonatal unit Clinical protocols
JSS Hospital, Mysuru.
This manual contains clinical guidelines we follow in our unit. We have used best available
evidence at the time of preparation of this manual. In the areas where evidence is unavailable or
lacking, we have relied upon the consensus opinion of the neonatal team experts and have taken
into consideration the ground realities of social and economic aspects of patient care.
This manual is not intended to replace the excellent text books in Neonatology. Doctors
under training are expected to follow the guideline without deviation. We recognize each and every
baby is different, and the management has to be tailored according to the need of individual baby.
Staff consultants responsible for the care of the baby can take management decisions which may
deviate from the guideline provided in this manual. Doctors under training are obliged to follow the
instructions of the responsible staff consultant in case it deviates from the guidelines in this
manual.
We have arranged the topics according to the alphabetical order for easy search.
We have deliberately not cited the references with an intention of keeping this manual
simple. This manual is intended to be used in Neonatal unit of JSS hospital, Mysooru and is not
suitable for being used as reference literature. This document is not copyrighted and hence can be
used by any health care provider if they find it useful. However, the onus of content and accuracy
lies on the user.
3
ADMISSION TO NICU - CRITERIA
i. Gestation and weight
a. Babies <34weeks
b. Birth weight < 2.0 Kg
ii. Clinical conditions
a. Birth asphyxia and not rapidly responding to resuscitation (APGAR 7 or less at 5
minute)
b. Suspected sepsis (See sepsis protocol)
c. Respiratory issues
i. RR>60/min for more than 30 mins
ii. Grunting
iii. Chest recessions
iv. Low respiratory rate < 30/min or apnea
v. Cyanosis
iii. Feeding problem severe enough to cause clinical concern/ bilious vomiting/ abdominal
distension/ Other signs suggestive of bowel obstruction
iv. Jaundice requiring phototherapy or exchange transfusion (feeding term babies with no
other risk factors can be treated at mother side with phototherapy)
v. Cardiovascular- severe anemia, congestive cardiac failure, Hematocrit >65%
vi. CNS- lethargy, convulsions, bulging AF
vii. Bleeding from any site
viii. Life threatening congenital malformations
ix. Hypoglycemia despite adequate feeding (See Hypoglycemia protocol)

Consider Admission:
1. Babies born through meconium, not needing resuscitation but are tachypneoic
2. Hypothermia (Axillary temp < 35)/Fever (Axillary temp > 37)
3. Babies requiring resuscitation with bag and mask for more than 1 min
4. Infant of Diabetic mother
Babies >1 month - weighing < 5 Kg (non - transmissible infection)

* Any baby > 1 month requiring admission to NICU has to be decided by the Consultant
4
AIR LEAK
Pneumothorax:
Signs: Respiratory distress, increasing oxygen and ventilation requirements, reduced air entry on
the affected
side, hypotension, increased PCO2, metabolic acidosis.
Tension pneumothorax: occurs when intrapleural pressure is greater than atmospheric pressure.
Investigations:
1. Transillumination (unreliable in term babies or on high frequency oscillation)
2. Chest x-ray
Treatment:
1. Small, asymptomatic pneumothorax – close observation even if ventilated. Try 100% oxygen
for 1-2 hours in term babies to ‘wash out’ nitrogen.
2. Needle drainage: if urgent decompression is required i.e. in case of tension pneumothorax
with poor
Oxygenation and hypotension.
3. Chest drain: see protocol for details of needle drainage and chest drain insertion and
maintenance
Pneumomediastinum
Air is near the heart with elevation of thymus and lucency between the heart and sternum. It rarely
needs
evacuation. Close observation for associated pneumothorax.
Pneumopericardium
Air completely surrounding the heart with associated shock (tamponade)
Pulmonary interstitial emphysema (PIE)
Air leak from alveoli but contained within interstitial space. CXR appearance typical with tiny
‘bubbles’ of air
throughout affected area.
Try reducing PIP if on conventional ventilation or use a ‘low volume’ strategy on HFO. Otherwise
ventilate as
clinical condition and blood gases determine.
5
ANO-RECTAL ANOMALIES
Incidence: 1:2500-5000 live births
Associations: V ACTERL
Trisomy 22 (cat-eye syndrome)
Short-rib
Polydactyly Syndrome
Caudal Regression
Antenatal detection unusual as only rarely associated with polyhydramnios or dilated bowel on u/s
scan
Types: Anal/Rectal stenosis
Imperforate anus (membranous)
Imperforate anus + blind-ending rectum
Normal anus/lower rectum with blind rectum above
All +/- fistulae (rectourethral, rectovesicular, rectoperitoneal, rectovaginal)
Presentation (usually from 24hrs)
• Usually noted at routine 1st examination

• Vomiting +/- dehydration
• Abdominal distension, visible bowel loops
• Failure to pass meconium
Clinical Examination
• Abdo. distension with visible loops,
• Imperforate anus, signs of fistulae
• Genitalia + placement of urethral opening (cloaca)
• Any other associated anomalies including spine
Management
• Admit to NNU
• NBM and place wide bore NGT to decompress abdomen
• IV access
• Bloods (FBC, G+S, neonatal profile, blood culture, blood glucose, blood gas, karyotype)
• IV fluids
6
• Replacement of NG losses 4 hourly (0.9% saline + 10mmol KCl/ 500mL)
• CXR/AXR + lateral x-ray pelvis
DELAYED PASSAGE OF MECONIUM
Most healthy babies pass meconium within 24 hrs. of birth. Delay after 24 hrs. is unusual and
underlying pathology should be considered.
Review full history with mother & midwives.
• Look in maternal notes for any evidence of polyhydramnios or other abnormalities on antenatal
scans e.g. dilated loops of bowel.
• Fully examine baby and check anus is patent.
• If < 24 hrs. old, baby is well with no vomiting and normal examination then observe closely
• If > 24 hrs. old, or < 24 hrs. but with concerning features in the history or on examination,
consider bowel obstruction, Hirschprung's Disease, enterocolitis and sepsis:
• admit to the neonatal unit
• inform SpR / Consultant
• request AXR and discuss with consultant +/- Paediatric Surgeon
• In cases of early discharge, it must be stressed to the mother and midwives that if there is delay
in passage of meconium greater than 24 hrs. then the baby should be reviewed as soon as
possible.
• If a baby has been given a suppository to aid passage of meconium, then this baby should still be
discussed with a Paediatric Surgeon in view of the possibility of Hirschprung's Disease.
If a meconium plug is passed, IRT (spot of blood on Guthrie card) and CF genetic studies
should be checked. Hirschsprung’s disease should also be considered.
7
APNOEA
Apneic episodes lasting up to 20 seconds are common and most often will resolve spontaneously
without any intervention. It can be physiological (e.g. associated with passing stool!), but is most
often associated with prematurity.
Always consider Sepsis, Abdominal Pathology, IVH, Seizures, gastro esophageal reflux and
hypoglycemia before considering physiological causes.
Note!!
If the baby remains apneic with a fall in heart rate and/or saturations, intervention is required.
1. Gentle stimulation by flicking the sole of the foot will usually cause the baby to cry thereby re-
establishing regular breathing.
2. Monitor Saturation – It is essential to check the level of desaturation during an apneic episode
3. Consider Mechanical factors – Reposition the head, oral suction if necessary. Administer Oxygen
by face mask if baby shows signs of recovery with the above action and saturations are not back to
normal.
4. Failure to respond to gentle or even more vigorous stimulation should prompt the nurse to
commence bag and mask ventilation.
5. Apnea and the interventions carried out should be documented in the case notes and nursing
monitoring sheet. Documentation of episodes should include nadir of heart rate and saturation.
6.Recurrent, severe apnea, 2 or more episodes in an hour if baby is > 30 weeks and 3 or more
episodes if the baby is < 30 weeks, needs stepping up of respiratory support and investigations.
Investigations - Blood gas, CBC & PS, Biochemistry, Sepsis screen (including CXR, LP and urine
culture), Blood glucose, AXR if NEC suspected and cranial ultrasound
7. Treatment
i. Treat underlying cause. IV antibiotic cover should be given until culture results are known.
ii. Provide suitable ventilatory and hemodynamic support.
iii. Babies with symptomatic anemia should be transfused.
iv. Ensure correct NG tube positioning,
v. Positioning the baby with a head up tilt – prone or lateral, decreasing feed volume by increasing
frequency
vi. Caffeine for apnea of prematurity. (10mg/kg loading dose followed by a once daily dose of
5mg/kg IV or NG/PO).
vii. Commence Caffeine for all preterm infants <32 weeks corrected gestational age.
8
ARTERIAL OCCLUSION / THROMBOSIS
1. Loss of the peripheral pulses after arterial cannulation (including after cardiac
catheterization) with large catheters may be due to:
i. Vessel spasm - usually combined with some thrombus formation.
ii. Occlusive thrombus at the puncture site - less commonly.
iii. Vessel dissection - very rarely.
2. Heparin is used to prevent propagation of thrombus while natural thrombolysis and
relaxation of the spasm takes place.
3. Pulses that can only be found on Doppler may be due to collateral flow when the major
limb artery is occluded.
4. Doppler ultrasound assessment of vascular occlusion may be helpful in the diagnosis and
assessment after treatment. However, treatment should not be delayed by waiting for an
ultrasound scan if circulation is compromised
Management:
1. If the limb is warm, normal colour and pulses are easily felt: observe puncture site and
peripheral pulses at least hourly.
2. If the limb is warm, normal colour but pulses are weak:

- GTN patch – place half a 5mg patch over proximal part of affected limb
- Heparin bolus of 75 U/kg. If pulses have not recovered after 1 hour, repeat bolus and start
heparin infusion of 25-40U/kg/hr.
- If there is no improvement after 6-12 hours of heparin infusion, consider rT-PA. Both of
these drugs may be contraindicated in preterm infants due to the risk of Intraventricular
and pulmonary hemorrhage. Therefore, always discuss with the consultant (and Pediatric
Cardiology team if post cardiac catheter) before starting.
3. If the limb is cool, or colour pale or pulses absent:

- Give heparin bolus & infusion (as above) immediately.
- start rT-PA if above status after 2-4 hours of heparin. Again, always discuss with the
Consultant (and Pediatric Cardiology team if post-cardiac catheter) before starting.
Notes on use of rT-PA (Alteplase)
9
1. Start IV 500μg/kg/hr. Continue for 3-4 hours and reassess.
2. If pulses and perfusion have returned to normal, stop rT-PA. If pulses and / or perfusion are not
normal,
Continue rT-PA and reassess every 3-4 hours.
4. Check serum fibrinogen level 2 hours after starting rTPA and then 4 hourly thereafter.
5. If fibrinogen level is <1.0 g/dl stop infusion for 1 hour and restart at 750U/kg/hr. Recheck
fibrinogen at 2
hours and then 4 hourly.
6. If after 6 hours, pulses are still absent increase infusion by 500U/kg/hr every 4 hours if fibrinogen
level is
still >1.4g/dl.
7. Continue until the pulses return, then stop streptokinase and recommence the heparin. If after
stopping the
rTPA infusion, the pulse disappears again, then stop heparin and restart the infusion (at the same
dose) then reassess 6 hourly.
8. Puncture site hemorrhage commonly occurs in recanalization and should be managed by local
pressure
and stopping the infusion. FFP may be considered.
Contraindications to rT-PA
i. recent major surgery
ii. Recent traumatic intracardiac catheter manipulation or recent major vessel
angioplasty. E.g. coarctation or pulmonary artery stenosis where ‘tissue tearing’ is
therapeutic.
iii. abnormal clotting / low platelet count (<50x109/l)
iv. recent intracranial hemorrhage (no documented evidence but theoretical risk of
exacerbating this)
v. hypersensitivity
vi. prematurity is a relative contraindication
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BLEEDING NEONATE
Hemorrhagic disease of newborn is seen in otherwise normal neonates

Bleeding in the newborn is often a serious problem because of
 Hemodynamic effects associated with a loss of intravascular volume

 Pressure effect (SOL) on the tissue
Babies in the neonatal intensive care unit (NICU) more commonly have abnormal bleeding or
conditions that increase the risk of bleeding
 Bleeding in the newborn may be manifested by signs of shock, anemia, signs related to pressure from
‘hidden’ bleeding (eg, intraventricular hemorrhage), or bleeding from the gastrointestinal tract,
respiratory system or skin.
 It is important to distinguish between the maternal blood and the bleeding from baby
 Once abnormal bleeding in the newborn is identified, the first management approach is to ensure
cardio-respiratory stability.
Once stabilized, a detailed Family history of bleeding disorder should be obtained.

Maternal illness (eg, infection, HELLP syndrome)
Maternal drugs (eg, acetylsalicylic acid, Coumadin, anticonvulsants)
The following Differential Diagnosis should be considered:
Management should initially be directed replacement of intravascular volume. in addition to

ensuring adequate vitamin K, many coagulation factor abnormalities may be corrected with
intravenous administration of 10 to 15 mL/kg fresh frozen plasma.
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BRONCHIOLITIS
1. Bronchiolitis (viral lower respiratory tract infection of the terminal bronchioles) can cause
severe illness in newborn infants. Ex preterm infants with chronic lung disease are
particularly at risk.
2. Infection is transmitted via droplets from the respiratory tract of an infected person caused
by RSV (most common), adenovirus, influenza A and B, parainfluenza 1, 2 and 3, and human
metapneumovirus.
3. Likelihood of hospitalization due to bronchiolitis and pneumonia due to RSV is 25% for
premature infants (<33 weeks) without CLD and higher for those with CLD
Clinical presentation
1. coryzal symptoms associated with worsening respiratory status (↑ FiO2, increased
ventilatory requirements)
2. inspiratory crackles, expiratory wheeze, cough.
Diagnosis
1. nasopharyngeal aspirate (NPA) or ET secretions; (Yet to have this service)
Management
2. Isolate or cohort affected patients (involve Infection Control for advice)
3. No antiviral therapy; supportive treatment only - ventilation may be necessary.
Prevention
1. Handwashing most important – staff, visitors, family
2. Avoidance of individuals with coryzal symptoms (staff and family members).
Prophylaxis
1. Palivizumab (Synagis®) – Humanized monoclonal antibody against RSV. (Reduces admission
rate by 55%). Indications: CLD, CHD on respiratory support
2. Paluvizumab may also be considered for all ventilator or chronically oxygen dependent
babies on NICU if there is an outbreak (i.e. 2 or more cases at the same time despite
isolation of cases.)
• Schedule: - Give monthly from October for 6 months up to and including March. May be given
anytime in
Relation to routine immunizations.
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CHRONIC LUNG DISEASE (CLD) - MANAGEMENT
Respiratory
Mechanically ventilated
1. Wean by first reducing peak pressures and inspired oxygen concentration (as in ventilation
protocol)
according to blood gas results.
2. Blood gas samples should be arterial if an arterial line is sited. Capillary samples are
satisfactory if
peripheral perfusion is good and oxygen saturation (SaO2) is constantly monitored.
3. Blood gas samples should be taken approximately 30 minutes after any ventilator change.
All ventilated babies should have at least one arterial blood gas sample taken per day, if
possible.
4. PCO2 levels as high as 55 – 65 mmHg are common (acceptable even higher if pH >7.25).
5. Arterial PO2 levels should ideally be 50 -75 mmHg (in preterm infants <34 weeks corrected
gestational age) 75 – 95 mHg (in infants >34 weeks corrected gestational age), - SaO2 should be 90 -
94% for babies <34 weeks corrected gestational age and >94% for babies >34 weeks.
6. Additional oxygen should be provided before handling and other nursing and medical
procedures.
1. Consider nebulized bronchodilators for infants with clinical evidence of lower airway
obstruction.
Salbutamol 2.5mg 4-6 hrly; Ipratropium bromide 62.5mg 4-6 hrly.
2. Consider inhaled steroids in infants not being weaned from the ventilator by 2 weeks of
age. Nebulized budesonide 0.5mg BD.
3. Ipratropium bromide via the ET tube can be used for ventilated babies when there are
problems with ET tube blockage due to excess secretions. Dose - 10mg in 0.5mL 0.9% saline
for babies <1000g; 20mg in 0.5mL 0.9% saline for babies >1000g.
4. Physiotherapy and regular repositioning should be considered if secretions are difficult to
clear
5. If FiO2 persistently high, Pediatric Cardiology opinion to assess for pulmonary
hypertension.
6. Systemic steroids
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i. These are used increasingly uncommonly for CLD, due mainly to concerns about their
effects on
neurodevelopment
ii. Consider steroid therapy in a baby with severe developing CLD whose ventilatory
requirements remain high or very high after:
- Exclusion of significant infection
- Exclusion or treatment of a significant PDA
- Consideration of treatment with diuretics
- Obtaining oral consent from the parents after discussion about the risks (including possible
increase
neurodevelopmental problems) and benefits of steroid therapy
iii. This is rarely before 4 weeks’ postnatal age
iv. Dose (this is a guide only) - dexamethasone 0.3mg/kg/day for 3 days, then 0.2mg/kg/day for
3 days, then 0.1mg/kg for 3 days, then stop. Give as 2-3 divided doses.
v. Blood sugar and blood pressure should be checked at least twice daily whilst babies are
receiving systemic steroids
vi. Consider excluding CMV infection before starting a course of steroids (send urine CMV DEAFF
test)
7. Self-ventilated, but oxygen dependent in hospital
Use low flow oxygen (rather than via head box) unless contraindicated. SaO2 should be
continuously monitored and blood gas samples taken when clinically indicated. Additional inspired
oxygen should be provided before certain nursing and medical procedures. Low-flow oxygen should
be humidified for flow rates >0.5L/min. Oxygen saturations, PO2 and PCO2 levels should be as for
ventilated babies (above).
8. CVS & fluids
i. Early diagnosis and treatment of PDA is important.
ii. If heart failure is suspected clinically, do CXR, ECG and discuss need for echocardiogram
with Pediatric Cardiology team. Start fluid restriction and diuretics (frusemide (1mg/kg
BD or TDS) and spironolactone (1mg/kg BD)). Chlorthiazide (10-20mg/kg BD should be
used if diuretics are needed for more than 2 weeks.
iii. Request Pediatric Cardiology review for all oxygen dependent babies at term to assess
pulmonary hypertension
14
9. Nutrition
i. If parenterally fed, prescribe TPN according to the TPN protocol.
ii. Enteral feeds according to protocol
iii. Daily weight should be measured and charted in any unstable baby, less frequently in a
stable growing baby. A satisfactory weight gain is ≥10-15g/kg/day. It is important that
this is maintained, and calorie supplements should be started if weight gain is
inadequate. Babies with chronic lung disease often require up to 150kcal/kg/24 hours.
iv. Serum calcium, phosphate and alkaline phosphatase should be monitored weekly and
osteopenia treated appropriately.
10. Infection
i. Deteriorations in respiratory status and other signs of infection should be treated with
antibiotics after carrying out a septic screen. This should include a CXR and tracheal
aspirate sample for M, C&S. If bacteria are identified in the tracheal aspirate, appropriate
antibiotics should only be given if the baby has deteriorated clinically.
ii. Consider sending a nasopharyngeal aspirate for virology to exclude RSV and a per - nasal
swab for pertussis.
iii. Routine vaccinations (DPT, HIB) should commence 6 weeks after birth. Oral polio vaccine
should be delayed until the day of discharge or alternatively give inactivated polio vaccine.
11. Hematology
i. Ventilator dependent infants should have CBC at least 1-2 times per week. Self-
ventilated babies with chronic lung disease should have FBC at least once per week
whilst in hospital.
ii. Hemoglobin levels should be maintained above 11 g/dl in all ventilator dependent
babies.
iii. Iron supplements should be started at 3 weeks of age.
Vitamins and folate supplements should be started at 2 weeks of age.
15
CONGENITAL DIAPHRAGMATIC HERNIA (CDH)
Anatomy and pathophysiology
1. 85-90% occur as a defect of the posterolateral segment (Bochdalek hernia).
2. 80% are left-sided and the hemi thorax contains herniated bowel, spleen, stomach and
often part of the left lobe of the liver. The bowel is usually malrotated.
3. Right-sided hernias usually contain the right lobe of the liver.
4. In virtually all cases, there is a degree of lung hypoplasia – there may be just a small
amount of lung tissue on the side of the hernia and the contralateral side is also hypo-
plastic.
5. PPHN is common and the pulmonary vasculature is hyper-responsive to hypoxia, acidosis
and hypercarbia.
6. Up to 50% of affected fetuses will have other associated anomalies e.g. chromosomal.
7. Anterior or Morgagni diaphragmatic hernia is much less common and usually right sided.
Clinical features
1. Antenatal diagnosis is frequently possible.
2. Postnatal presentation is of increasing respiratory distress and cyanosis soon after birth.
3. The abdomen is typically scaphoid.
4. CXR: air-filled loops of bowel in the hemi thorax with mediastinal displacement.
5. Differential diagnosis: Congenital cystic adenomatoid malformation of the lung (in this the
loops of bowel. are below the diaphragm – if the diagnosis is still uncertain, contrast can be
passed into NG tube).
Resuscitation
Staff to attend the delivery
Set up ready for draining pneumothorax, umbilical lines and intubation
Minimal bag and mask ventilation
Intubation at the earliest
Gut decompression by nasogastric tube with 8F tube
Obtain vascular access (Umbilical line can be used in case of emergency only)
NICU
Pulmonary management
Ventilation – SIMV pressure support mode (or pressure control mode)
PIP not to exceed 25 Cm H2O. Keep PEEP at 5 Cm H2O, MAP <16 Cm H2O
16
Target saturation in first 2 hours >70%, after 2 hours >85%
Pain relief, Sedation and muscle relaxation should be used as necessary
Surfactant may be used if necessary
Cardiac management
ECHO as soon as possible
Assess RV function, PA pressure, Duct shunting
Manage Pulmonary hypertension as per SIPHON protocol.
Note: use of inotrope in this condition is not aimed at increasing the systemic pressure to reverse
the shunt across fetal channels. It is used to maintain the optimal contractility of the ventricles!!
Use of inotrope: Dobutamine, Dopamine and Adrenaline in that order
Consider fluid bolus if ventricles are under filled
Inotrope use should be judicious to avoid hyperinotrophy
Additional drugs to be considered for management of pulmonary hypertension
a. Inhaled nitric oxide (currently not used in our unit)
b. Milrinone – if the systemic pressure is adequate and need to improve RV function
c. Alprostin – if duct shows signs of closing
d. Alkali – last resort
e. Hydrocortisone for inotrope resistant shock
Weaning: FiO2 followed by pressure followed by pulmonary vasodilator in that order
Consider weaning FiO2 when PaO2 is > 80mmhg
Weaning FiO2 should be slow with each decrement done at 60 minutes’ interval as tolerated.
ECMO
Consider ECMO if
Vent settings
PIP >25 cm H2O
MAP > 16 cm H2O
FiO2 – 100% and Preductal SpO2 < 85%
Oxygenation Index > 30 in two ABGs 3 hour apart after intensive treatment
ECMO is not offered in our institution
Consider Surgery after Stabilization for 24 to 48 hours
FiO2 needed <40%, PIP needed < 24 cm H2O, MAP needed < 12 cm H2O
No pneumothorax (if present, surgical can decide if it needed to be drained prior to surgery)
17
CONGENITAL HYPOTHYROIDISM
Every baby should be tested for TSH (as part of newborn screening) before discharge from hospital,
optimally by 48 hrs. to 4 days of life.
If the first sample TSH is high, then a second sample is sent along with a venous sample for TSH and
free T4 levels for confirmation.
The following babies should have a repeat testing done irrespective of TSH levels
1. Preterm babies (<31 wks. of gestation)
2. If sample sent <48 hrs. of life
3. Sick neonates
4. Sample sent immediately after transfusion
Specimen (sample):
3 drops of blood should be collected by heel prick on an approved filter paper, dried at room
temperature, not subjected to excessive heat.
The blood should completely saturate the filter paper and be applied to 1 side only. Filter-paper
spots should not be handled, placed on wet surfaces.
Test results:
The abnormal test results should be intimated to the responsible consultant.
The same is communicated to the parents, counseling to be done and repeat sampling to be
organized.
Low T4 and Elevated TSH Values: (TSH values should be checked with our Biochem lab)
If TSH is 20-40, then repeat NBS to be sent along with serum sample and age related normative
values should be used.
If TSH values > 40, same to be confirmed by serum TSH and Free T4 levels
High TSH >40 with low Free T4 levels, primary hypothyroidism is to be considered and therapy to be
initiated.
Parents to be counseled and educated regarding the
• Benefit of early diagnosis in preventing mental retardation
• Need for therapy
• Appropriate manner in which TH is administered and the substances
(ex: iron, calcium, and fiber) that can interfere with TH absorption
• Importance of adherence to the treatment plan
• Importance of periodic follow-up care.
18
Normal T4 and Elevated TSH Values:
Elevated serum TSH levels along with normal T4 levels can be transient or permanent thyroid
abnormality.
Persistent elevation of TSH >10 after the first 2 weeks of life is considered abnormal and treatment
should be initiated.
If such infants are not treated, measurement of FT4 and TSH should be repeated in 2 and 4 weeks,
and treatment should be initiated promptly if the FT4 and TSH concentrations have not normalized.
Before 2 weeks of life, age-related normative values are to be considered.
Treatment:
The goal of therapy is to normalize T4 within 2 weeks and TSH within 1 month.
An initial dosage of 10 to 15 μg/kg of L-thyroxine is recommended.
The pill should be crushed and suspended in a few milliliters of breast milk, or water.
Care should be taken to avoid concomitant administration of fiber, or iron. Breastfeeding can
continue.
FT4 is expected to increase to more than 2 ng/dL by 2 weeks after initiating therapy, and TSH
should normalize by 1 month.
The L-thyroxine dose should be adjusted according to the infant’s clinical response and serum FT4
and TSH concentrations.
Follow-up:
Because poor compliance and non-compliance have major sequelae, initial and ongoing counseling
of parents is of great importance.
Clinical examination, including assessment of growth and development, should be performed every
few months during the first 3 years of life.
Infants need to undergo frequent laboratory and clinical evaluations of thyroid function, growth,
and development to ensure optimal T4 dosage and adherence to their therapy regimen.
Serum T4 and TSH measurements should be performed:
1. 2, 4 and 8 weeks after the initiation of L-T4 treatment
2. every 2 months till 6 months of life (ie @ 4 and 6 mths of life)
3. every 3 months once till 18 mths of life.
4. Every 6 months from 18 mths of life till 3 years
5. At more frequent intervals when compliance is questioned, abnormal values are
obtained, FT4 and TSH measurements should be repeated 4 weeks after any change in
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dosage.
The aim of therapy is to ensure normal growth and  development by maintaining the serum total
T4 or FT4 concentration in the upper half of the reference range in the first year of life, with a
serum TSH in the reference range (optimally 0.5–2.0 mU/L).
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CONGENITAL INFECTION - GENERAL PROTOCOL
• The subheading of congenital infection has traditionally described as the “TORCH” infections:
toxoplasmosis, rubella, cytomegalovirus (CMV), herpes simplex (HSV). However, not all are truly
congenital, but more often perinatal (e.g. HSV) and the whole group of pathogens associated with
neonatology should be extended to encompass syphilis, group B streptococcus (GBS), human
immunodeficiency virus (HIV), varicella-zoster virus (VZV), human T-cell leukaemia virus (HTLV),
hepatitis B and C, parvovirus B19 and enteroviruses.
• Take care in requesting congenital infection investigations in babies, as there are a number of
reasons why
they may be inappropriate:
- some of these infections can usually be ruled out on clinical evidence alone e.g. perinatal
hepatitis B and C are almost always asymptomatic and thus are unlikely causes of neonatal jaundice
- serological diagnosis may be better made on mother’s blood, and some viral infections can be
ruled out by testing mother (e.g. hepatitis B, C, HIV, HTLV)
- baby’s serology may simply reflect mother’s long-term past infections
- babies make their own IgM, but this is not always reliable as a marker of true congenital
infections (e.g. CMV)
• Much of the positive diagnosis of true viral congenital infection is best done by direct detection,
either through molecular techniques such as PCR to detect viral genomes, rapid culture and/or
immunofluorescence for viral proteins (e.g. CMV in urine).
• In the absence of positive evidence for a congenital infection, for some diseases the baby will
need follow- up for up to 18 months before maternal antibody has decayed, allowing more
confidence to the prediction that a particular infection has not occurred e.g. toxoplasmosis,
syphilis, hepatitis C, HIV.
• Discuss with Microbiology staff if unsure of appropriate tests.
Clinical features of the TORCH infections
Consider congenital infection in infants with the following features:
• Unexplained IUGR/low birth weight – particularly if IUGR symmetrical (CMV, rubella,
toxoplasma)
• Cardiac structural defects – mainly rubella, also CMV, toxoplasma
• Cardiac inflammation – parvovirus B19, enterovirus and, rarely, CMV
21
• Ocular defects: cataract, retinitis, conjunctivitis
• Jaundice and hepatitis (toxoplasmosis, rubella, CMV, HSV, bacterial sepsis)
• Purpura or petechiae (usually first day) especially in CMV infection but also toxoplasmosis,
rubella, syphilis
and HSV
• Hepatosplenomegaly – CMV, rubella, toxoplasma
• Pneumonitis – consider in preterm infants with unexpectedly severe chronic lung disease
• Central nervous system involvement
- Microcephaly in toxoplasmosis, rubella, CMV
- Cerebral calcification: wide spread in toxoplasmosis, periventricular in
- Hydrocephalus especially parvovirus B19, toxoplasmosis
Investigations
• Use the above features to make a presumptive diagnosis and send appropriate laboratory
investigation requests. Please see specific guidelines for GBS, syphilis, hepatitis B & C, CMV, rubella,
toxoplasmosis, and HSV
• Maternal demographic details for assisting in the laboratory diagnosis are essential.
BABIES BORN TO HEPATITIS B POSITIVE MOTHERS.

• There is routine antenatal screening of mothers for hepatitis B
• At birth, the midwife informs the Neonatology PG that the baby requires Hepatitis B
immunisation. If required, HBIG should be given ASAP but certainly within 24 hours of birth
High risk mother
May be any of the following:
• Hepatitis BsAg positive and Hepatitis BeAg positive or e Ab negative
• Hepatitis BsAg positive and no "e" markers. Infectivity in this group is variable. HBV DNA level
should have been done in pregnancy. Discuss the interpretation of viral load with Microbiologist.
• Mother with acute hepatitis B in pregnancy
Baby requires:
1. Hepatitis B Vaccine and HBIG - (see below)
2.There is no contraindication to breast feeding
Low risk mother

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• Hepatitis BsAg positive and anti-HBe Ab positive
• Hepatitis BsAg positive with no “e” markers and a low HBV DNA level (discuss with virologist)
Baby requires:
1. Hepatitis B Vaccine only
2. There is no contraindication to breast feeding
Hepatitis B vaccine:
• Dose is 0.5mL of vaccine
• 1st dose: ASAP after birth and certainly within 24 hrs.
• 2nd dose: at 1 month of age
• 3rd dose: at 6months of age
HBIG
• Give ASAP after birth
• 200 IU/2mL IM for babies >1500g
• 100 IU/1mL IM for babies <1500g
• Give in contra-lateral thigh to vaccine
BABIES BORN TO HIV POSITIVE MOTHERS

• When a baby is born to a HIV positive mother,
• Blood should be taken from the baby (N.B. cord blood not suitable) for:
(i) Virology HIV antibody
HIV DNA PCR
HIV RNA viral load
Send minimum 2-3mL blood in EDTA bottle – in separate specimen bag from CBC sample
(ii) CBC
(iii) Hepatitis B & C screen (these need only be done if maternal serology not known)
• Breast feeding should be considered after discussion
• BCG should not be given
1. Most HIV positive mothers will have a low viral load due to treatment with combination
therapy or Zidovudine (AZT) alone to reduce vertical transmission.
- zidovudine 4 mg/kg/12 hourly for 4 weeks
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2. If maternal viral load is very high or unknown due to late presentation, a plan for neonatal
treatment should have been made antenatally and this should be followed
However, in the event of such a baby being delivered out of hours without a treatment plan,
consider
triple antiretroviral therapy:
- zidovudine 4mg/kg/12 hourly for 4 weeks
- lamivudine 2mg/kg/12 hourly for 4 weeks
- nevirapine 5mg/kg once daily for 2 weeks, then 5mg/kg 12 hourly for 2 weeks
3. AZT for preterm babies (<36 weeks): 1.5mg/kg/12 hourly for 2 weeks, then 2mg/kg/8 hourly for
2 weeks
4. AZT for sick infant unable to tolerate oral medication: term 1.5mg/kg/6 hourly IV; preterm
1.5mg/kg/8 hourly IV
BABIES BORN TO HEPATITIS C POSITIVE MOTHERS.
Mothers found to be HepC Ab positive antenatally should have been tested for HepC RNA. Babies
of mothers who are HepC RNA positive have a 6-8% risk of acquiring Hep C vertically. Hepatitis C is
unlikely to present in the neonatal period and usually causes a low grade chronic hepatitis in
childhood. At the present time, the natural history of the progression of vertically transmitted
hepatitis C is not known.
• Check mothers HepB and HIV status from antenatal testing.
• Baby should receive Hepatitis B Vaccine course regardless of mother’s HepB status (see
Protocol for management of babies born to Hepatitis B positive mothers
• Breast feeding should not be discouraged (unless the mother is also HIV positive) as the risks
are likely to be negligible.
• Take infants blood for PCR for HepC RNA.
• Arrange out-patient follow-up for 3 months in order to investigate further as follows:
- 3 months Hep C RNA
- 6 months Hep C RNA
- 12 months Hep C RNA, Hep C Abs
- 18 months If Hep C Abs +ve at 12 months repeat Hep C RNA, Hep C Abs
24
BABIES BORN TO MOTHERS WITH POSITIVE TESTS FOR SYPHILIS
Syphilis is caused by the spirochaete, Treponema pallidum, which has a cardiolipin-containing
membrane.
Serological tests for syphilis
Serological markers may not appear for a few weeks after infection
IgM first followed by IgG. IgG may ↓ with Rx but in 75% persists for life.
• Specific treponemal antibodies eg TPHA, TPPA, EIA

- may also cross react with other treponemal infections eg Yaws
• Non-specific treponemal antibodies (cardiolipin ab) eg VDRL, RPR
- cross-react with other treponemal infections (eg yaws)
- false-positives in other infections, autoimmune diseases and occasionally in pregnancy
Use one specific and one non-specific IgG test
May need to confirm with FTA-ABS or PCR for treponemal DNA (high sensitivity and specificity)
IgM helpful to diagnose recent or recurrent infection.
(FTA-ABS, PCR, IgM not done on site but in reference laboratory)
Maternal syphilis
• Transmission to fetus at any stage of pregnancy
• For one year after infection fetal transmission in 80-90%
- 25% SB
- 25-30% neonatal death
- 40% congenital syphilis but survive (40% late congenital syphilis)
• Transmission rare > 4 years after infection (even if mother untreated)
• If mother treated with adequate regime of penicillin 98% fetuses also treated
- failures↑ - 2° syphilis, short Rx – delivery interval, high VDRL titres, severe fetal disease
Congenital syphilis
There is no primary stage.
• 60% asymptomatic
• 40% symptomatic (mild → fatal) often with multiorgan involvement :–
- Early (2°) - IUGR; hydrops; rhinitis, rashes (including soles and palms, perioral and perianal);
osteochondritis and periostitis; hepatosplenomegaly; thrombocytopenia and anaemia; meningitis;
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renal.
- Late (3°) - developmental delay, 8 th nerve deafness, interstitial keratitis, bones and joints,
teeth
Diagnosis – clinical; dark field microscopy of lesions or eg amniotic fluid; X-rays; serology
• Serology
- Maternal IgG crosses the placenta but –ve in most uninfected babies by 6/12 and all by 1 year
- Neonatal titres often x1-2 dilutions ↓ than maternal in uninfected babies
- If IgM +ve baby has congenital syphilis (but may not become +ve for 3/12)
(Not done locally but +ve results phoned through)
Management
• Do not treat
- baby asymptomatic and mother adequately Rxed (titres ↓x4 in 6/12)
- but check serology at birth, 3/12, 6/12 and 18/12 (to check IgG antibody absent or titres falling).
(see “laboratory testing”)
• Treat (based on CDC recommendations)
- inadequate or no maternal Rx (even if baby asymptomatic)
- maternal Rx with erythromycin (does not reliably cross the placenta)
- <30 days between maternal Rx and delivery
- symptomatic +/- abnormalities on XR, FBC,CSF or microscopy
- IgM +ve or IgG non-treponemal titres x4 maternal at birth
- IgG titres static or rising at 3/12 and 6/12
- poor follow-up predicted
Treatment
• x-ray chest and long bones, FBC, LFTs, LP
• Symptomatic (or +ve X-ray and lab findings)
- benzylpenicillin 30mg/Kg IV 12hrly for 7 days then 8hrly for 3 days
• Asymptomatic (with –ve X-ray and lab findings)
- procaine penicillin 30mg/Kg IM daily for 10 days
- or benzathine penicillin 30mg /Kg (or 50,000u/Kg) IM x1
Follow-up
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• Serology at 3/12 and 6/12 (should be ↓x4 or –ve), treat or retreat if static or rising
• If treated, check treponemal antibodies at 15/12

• If CSF abnormal at birth repeat LP 6 monthly until normal
• Outlook for congenital syphilis treated at birth is good, but treponemes may remain in eye →
interstitial keratitis (and ? also in CNS). Refer to Paediatric Ophthalmologist.

Laboratory testing
General points:
• Problems will occur with understandably small blood samples from neonates
• Maternal serostatus should be obtained prior to testing neonatal sample
• Priority of testing
If mother known seropositive:
1. IgM first at birth
2. If IgM negative, then repeat at 3 months of age, with TPPA + RPR
3. If still negative, repeat IgM at 6 months and this time with EIA (instead of TPPA as less likely to
be positive)
4. If still negative just repeat EIA at 18 months of age
If mother serostatus unknown:
1. EIA (manual) first on neonate to establish maternal IgG
2. If mother positive, do IgM on baby and follow rationale from (2) above
3. If mother negative, no further action
• Serum volumes required for all tests:
- EIA (automated) 100μL
- EIA (manual) 30μL
- TPPA 25μL
- RPR 50μL
- RPR titre 50μL
- IgM ref. Lab 100μL
Total (all tests) ~350μL
Since neonatal blood has a higher PCV, approx 750μL (0.75mL) whole blood needed to yield enough
serum
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CYTOMEGALOVIRUS (CMV)
Perinatal acquisition of CMV usually has no implications for the baby.
For the diagnosis of congenital CMV, it is extremely important to collect urine within the first 2
weeks of life, otherwise perinatal infection (as opposed to congenital infection) cannot be ruled
out.
Investigations
• Cranial ultrasound scan (and consider need for MRI scan)
• Ophthalmology assessment (contact Mr Calver)
• Hearing screening – see separate protocol
• Virology tests
- send urine for CMV DEAFF (this test is definitive in the first 2 weeks of life)
- saliva and bronchial washings if available
- EDTA blood for CMV PCR
- clotted blood for CMV IgM
- also check maternal CMV serology (IgG and IgM)
• LFT’s, clotting and FBC
Treatment
Ganciclovir has been used for life threatening infection in individual cases and evidence has
emerged recently
that long-term hearing loss in babies born with congenital CMV central nervous system disease can
be prevented
with a regimen of IV ganciclovir. Such cases should be discussed with Virology consultant
The dose and length of treatment is debatable. Suggested dose is 5mg/kg BD IV for 3 weeks.
Neutropenia and thrombocytopenia are possible side effects.
Infection control
Most babies congenitally infected with CMV shed virus in urine and body secretions. Barrier nursing
is indicated.
RUBELLA
Congenital rubella may be expected to increase with reduced uptake of MMR.
Classical congenital rubella exhibits a triad of cataract, congenital heart disease and nerve deafness.
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Confirmation of maternal rubella immune status and immunisation history and whether there has
been a rubella-
like illness in pregnancy is important.
Investigations
• Cardiology opinion and echocardiogram
• Ophthalmology assessment (contact Mr Calver)
• Hearing screening (see separate protocol)
• Blood tests
- LFT’s, clotting and FBC
- viral serology on baby for rubella IgM (EPR order ‘congenital/perinatal infection serology’)
- check maternal booking viral serology and order current maternal IgG and IgM
- further specialist tests such as rubella PCR or culture may be advised by Virology
Treatment
There is no safe, proven, effective treatment for congenital rubella.
Infection control
Most babies congenitally infected with rubella shed virus in urine and body secretions. Barrier
nursing is indicated.
CONGENITAL TOXOPLASMOSIS
Consider a diagnosis of congenital toxoplasmosis in infants with:
• Unexplained IUGR (particularly if asymmetrical)
• Hydrocephalus
• Microcephaly
• Hepatosplenomegaly
• Hepatitis
• Petechiae
• Thrombocytopenia
• Chorioretinitis
Evaluation of suspected case should proceed following discussion with a Virology consultant. It will
usually
involve the following: -
Mother
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• Maternal history during pregnancy including possible exposure (travel, handling or ingestion of
previously
uncooked meat, kittens/cat litter) and illness (lymphadenopathy, fatigue, infectious mononucleosis-
like
illness). Note that such illness prior to conception is unlikely to be relevant to a diagnosis of
congenital
toxoplasmosis.
• Maternal serology results if available – liase with Obstetricians
• Send maternal serology as indicated by Virology
• Results of antenatal ultrasound scans
Baby
• Physical examination looking for above signs
• Discuss with consultant virologist and send samples to Virology as advised.
• FBC and film
• Liver function tests
• Urinalysis and serum creatinine
• Eye examination by a Paediatric Ophthalmologist (contact Mr Calver)
• Hearing screening (see separate protocol)
Treatment
Even in moderately affected babies, considerable improvement can occur with aggressive
treatment.
Symptomatic babies
• Pyrimethamine 1mg/kg daily
• Sulphadiazine 25-50mg/kg BD
• Folinic acid 1mg/kg, 2 times per week
Continue all 3 for one year. Monitor LFT’s and FBC every 4-6 weeks (risk of myelosuppression and
hepatitis).
Asymptomatic infants with positive serology
• Treatment of these babies is not straightforward. Discuss individual cases with Virologists.
Follow up
30
Infants born to women with a definite toxoplasma infection in pregnancy will need to be followed
up for up to
18 months. Frequency of testing will be determined by rate of maternal antibody decay or
appearance of infant’s
intrinsic immune response to toxoplasma. Liaise with Virology for frequency.
• Toxoplasma antibodies and/or PCR
• Monitor liver and marrow function as above
• Ophthalmology review as suggested by Paediatric Ophthalmologists
• Audiology assessment according to hearing screening result or clinical indication
• Neurosurgical referral if hydrocephalus occurs
N.B.
• Breastfeeding by an infected mother provides no risk to her infant
• Infected babies are not contagious
HERPES SIMPLEX VIRUS INFECTION
Most often, the infant acquires HSV at the time of delivery, through direct contact with infectious
secretions or lesions. Congenital HSV infection in the neonate is rare, but all cases of neonatal HSV
are associated with high rates of mortality and morbidity unless treated.
Primary maternal genital HSV infection is far more dangerous than is secondary, since there is no
maternal
antibody to afford protection.
Prevention
Babies born to mothers with active lesions should be delivered by elective caesarean section
Breast-feeding is not contraindicated as long as there are no breast lesions.
Investigation
1. Send swabs for viral HSV detection from:
• vesicular lesions
• the conjunctiva (separately)
• nasopharynx
• ears, mouth, anal, vulval
2. Send EDTA blood and CSF for HSV PCR
3. Send urine and blood for HSV culture
4. Blood Tests
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FBC, LFT’s, CRP, electrolytes, clotting (looking for evidence of viral hepatitis)
Management
1. Observation
Monitor for:
• skin or scalp rashes (especially vesicular lesions)
• respiratory distress (neonatal HSV infection may cause pneumonitis),
• seizures
• signs of sepsis
Babies born to mothers without genital lesions or those born by Caesarian section may be
discharged early,
but parents should be instructed to look out for any rashes or signs of viraemia.
Babies born vaginally to mothers with active lesions should be observed for at least 4 days.
2. Babies with suspected Herpes simplex infection
• If signs of viraemia are present or the diagnosis is strongly suspected start aciclovir (20mg/kg
daily IV
8 hourly for 14-21 days)
• Barrier nurse, preferably in an isolation room
PERINATAL CHICKENPOX
Maternal chickenpox
• Herpes Zoster (shingles) infection in mother is not an indication for concern in the newborn.
• If mother develops chickenpox ≥ 7 days before birth, the baby is likely to have received
maternal antibodies
transplacentally, therefore Varicella Zoster Immunoglobulin (VZIG) or other treatment is not
indicated.
• If mother develops chickenpox from < 7 days before birth until 4 days after birth, VZIG should
be given.
• There is no contra-indication to breastfeeding.
• The mother and baby should be isolated from other mothers and babies.
• The appearance of any vesicular leasions in an infant should be treated with IV aciclovir
whether VZIG has
32
been given or not.
• Early shingles may occur following perinatal chickenpox
• Maternal chickenpox during early pregnancy is associated with embryopathy (microcephaly,
microphthalmia, limb atrophy etc.) – risk <13 weeks ~0.4%, 13-20 weeks ~2%
Chickenpox contact (baby within 1 month of birth)
• Contact is defined as being in the same room for 15 minutes or more or face-to-face contact for
5 minutes or
more. Chickenpox is infectious from 48 hours before the rash and until ~5-7 days after (traditionally
taken as when all lesions have become scabs).
• If baby is ≤28 weeks gestation and/or ≤1000g at birth, regardless of mother’s previous
chickenpox exposure, he/she is unlikely to have received adequate antibody transplacentally and
should be given VZIG.
• If baby is >28 weeks gestation, the mother needs to have her chickenpox serology performed,
regardless of
history of chickenpox (this may be done on booking blood samples).
- If mother is seropositive for VZV, the baby is likely to be immune and will not need prophylaxis or
treatment.
- If maternal serology is negative, the baby requires VZIG.
• Anyone with chickenpox infection must not visit NNU until no longer infectious (see above).
• Any chickenpox contacts must not visit the NNU from days 7 to 21 after the contact.
• Babies who are contacts should be isolated (and cohorted if there are more than one) from
days 7 to 21 after
contact (or from days 7 to 28 after contact if they received VZIG).
• Babies who are contacts should be nursed by staff immune to chickenpox.
• When indicated, VZIG should be given as soon as possible, certainly within 72 hours of contact,
but is
recommended up to 10 days following contact.
Treatment of chickenpox in newborn
• Request that virologist performs lesion scrape for electron microscopy and viral culture.
• Treat with IV Aciclovir if within first 1 month of life, regardless of previous provision of VZIG or
maternal
33
chickenpox status.
TUBERCULOSIS
TB is due to infection with Mycobacterium tuberculosis
Neonatal tuberculosis
• Neonates are very susceptible to Mycobacterium tuberculosis.
• Virtually all infections are acquired from maternal TB and only rarely from staff with open TB.
• TB is most commonly acquired postnatally but can be acquired antenatally (congenital TB)
Congenital tuberculosis
In congenital TB, 50% of the mothers have previously undiagnosed TB, usually a 1° infection.
Pleural effusion, meningitis and disseminated infection are the commonest manifestations.
Mode of transmission
• Infection from genital tract rare and usually → abortion or SB
• Transplacental
- haematogenous with 1° in liver
- via amniotic fluid by ingestion or aspiration
Presentation
• Asymptomatic at birth but most have an abnormal CXR and are symptomatic by 2-3 weeks.
• Symptomatic at birth, very sick and may be infectious
- hepatosplenomagaly, lymphadenopathy, fever
- respiratory distress
- meningitis (present in 1/3 of cases)
- papules and petechiae, discharging ear
Diagnosis
• Microscopy for AFB - only 10% +ve
• PCR – 25-83% +ve
• Culture (takes weeks)
• Tuberculin skin test may be –ve for 3/12
• Diagnosis often has to rely on making the diagnosis in the mother
Treatment
Isoniazid, rifampicin and pyrazinamide + ethambutol or streptomycin - until sensitivities known.
Continue appropriate antituberculosis medication for 9-12 months
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CONVENTIONAL MECHANICAL VENTILATION
Indications
Respiratory illness – Respiratory failure
Central Nervous system disorders Failure of respiratory drive (e.g. convulsions, Coma, iatrogenic,
metabolic).
Cardiovascular diseases – Pulmonary congestion, poor cardiac output and metabolic acidosis etc.
1. Arterial PaO2 < 60 Torr whilst FiO2 > 0.6
2. PaCO2 > 65 Torr with no compensation
3. Arterial pH < 7.20 if mainly respiratory
4. Loss of central respiratory drive for any reason
5. Severe respiratory distress with impending respiratory exhaustion irrespective of diagnosis or lab
parameters. (this is quite subjective. However, most responsible senior doctor/staff should be
taking the decision)
Principle
The aim is to maintain oxygenation and allow adequate clearance of carbon dioxide. Care must be
taken to maintain humidification of inspired gas, control of airway temperature and provision of
adequate end expiratory pressure.
1. Oxygenation is dependent on mean airway pressure (MAP) which can be derived from:
MAP = PEEP + ({PIP - PEEP} × {Ti / (Ti + Te)}). Thus oxygenation can be improved by increasing
a) Peak Inspiratory Pressure (PIP), b) Positive End Expiratory Pressure (PEEP), c) inspiratory time (Ti)
2. Carbon dioxide clearance is dependent on alveolar minute ventilation and thus is proportional to
tidal volume and ventilator rate. Tidal volume can be increased by increasing PIP or decreasing
PEEP, which will in turn lead to more CO2 clearance (and vice versa).
3. Infants should initially be treated with morphine if there is no contraindication. Morphine is
predominantly used for pain relief and the babies may be initially sedated with morphine. Prescribe
this in a way that allows the dose to be adjusted. The initial bolus is 100μg/kg followed by an
infusion of 10-20μg/kg/hr. Midazolam is sedative and can be considered if the baby is still not
calmed down with morphine. See sedation protocol.
4. Suggested initial ventilator settings
For Pressure control mode (IMV/SIMV)
i. PIP should be just great enough to produce adequate chest inflation. Starting PIP can be
gauged by the pressure needed to inflate the lung during bagging. Otherwise starting
35
PIP should be kept at 18 and titrated against chest wall raise and improve in the
saturation.
ii. PEEP 5-6cmH2O – Start PEEP at 5 and can go up to 6 if needed. Do not escalate PEEP
beyond this without a CXR and Staff consultant opinion.
iii. Ti 0.35-0.4 sec. - Start I Time at 0.35 sec. For most of the restrictive lung disease we deal
in our unit, this is sufficient. May need to go up to improve oxygenation. Do not
increase without the consent of the responsible staff consultant.
iv. Rate – initially 40/min. in preterm infant with surfactant deficiency and high PCO2 may
start at 60/min (N.B. usually need to decrease rate after administration of surfactant)
v. FiO2 – adjust to maintain O2 sats. 90-94 % in preterm infants <35 weeks; >95% in more
mature infants with MAS and PPHN
5. Changing ventilator settings
i. In order to improve oxygenation:
• Increase FiO2 by steps of 0.05 (at high concentrations O2 is likely to be toxic and may increase
atelectasis)
• Increase PEEP to 6-7cmH2O (may also increase PaCO2)
• Increase PIP by steps of 2 (may increase risk of barotrauma). Stop increments if the chest raise is
adequate.
• Increase Ti – by 0.05 sec (need to be decided by staff consultant)
• Obtain synchrony (see later for trigger ventilation)
• Increase Sedation if "fighting" ventilator
• Paralyze with Rocuronium/Vacuronium bolus then infusion (N.B. may need to increase PIP once
paralyzed)
ii. In order to increase carbon dioxide clearance
• Suction or change ETT if possibly blocked/coated with secretions
• Increase ventilator rate
• Decrease PEEP
• Increase PIP
• Decrease system dead space (shorten ETT)
iii. Consider blood gas approximately 30 minutes after each ventilator change.
6. PRVC mode
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PRVC mode is a hybrid mode of ventilation. It is important to remember that it is still pressure
control mode of ventilation. Tidal volume is set on this mode and ventilator varies the pressure
control to achieve this Tidal volume. If the tidal volume cannot be achieved even at the highest PIP
set, the set tidal volume is not delivered and the pressure is capped at the maximum set PIP
i. Set Tidal volume to 4 – 5 ml/Kg
ii. Set the Maximum PIP – check the PIP needed to achieve the required tidal volume. Set
PIP 2 above that value
iii. Set the backup rate, PEEP and I Time similar to pressure control mode.
iv. Minute ventilation alarms to be set between 150 ml/Kg and 300 ml/Kg
7. Changing ventilator settings – See Above. No need to change the PIP
PRVC mode is the preferred mode in our unit as it is believed to reduce barotrauma.
In case of Apnea, PRVC mode functions as IMV with set PIP and rate.
Weaning and extubation from Conventional mechanical ventilation

Weaning the baby from ventilator is more of an art than science!
Once the baby is stable and lung disease is resolved to a reasonable extent consider weaning
It is good practice to have all the vitals and numbers in normal range before embarking on weaning
and extubation. FiO2 should be less than 0.3
Pressure control mode
1. Start weaning Morphine – 2 mcg/ hr every 2 hours
2. Wean PIP by 2 every 4 to 6 hours (or as decided by the responsible staff consultant) Wean
the peak inspiratory pressure initially down to < 15 cmH2O, then start weaning the rate.
3. Wean the rate by 5/min every 4 – 6 hours
4. Do not do two changes at a time. (Some consultants may prefer alternating the weaning
parameters. Check with them for the weaning plan)
5. If there is increase in the need of oxygen, go a step backward.
6. Decrease and discontinue sedation and start caffeine if appropriate
7. Once the ventilator rate is <20/min. PIP is < 15 and fiO2 is < 0.3 change to pressure support
mode. Delta PIP on pressure support mode needs to be 10 to 12.
8. In no setback on PS mode for more than 4 hours, extubated to NCPAP or low flow nasal
prongs with 1 lit/min of flow.
PRVC mode
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1. Follow same principle as above.
2. There is no need to wean PIP
3. If the PIP needed to achieve the tidal volume is less 15 cm H2O, switch to pressure support
mode. Rest follow as above.
Worsening oxygenation or blood gases in ventilated infants
Action required:
1. Assess initially by prompt clinical examination
2. Resuscitate as necessary
3. Reassess
4. Arrange appropriate investigations – usually blood gas and CXR
Possible causes :
1. Blocked or malposition of ETT
2. Pneumothorax - auscultate and Trans illuminate
3. Ventilator malfunction
4. Pulmonary hemorrhage - increase ventilation especially PEEP. See separate protocol.
5. Massive IVH
6. Infection
7. Pulmonary hypertension
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CRANIAL ULTRASOUND SCANNING
The following babies should have a cranial ultrasound scan within the 1st 12 hours if possible:
• < 32 weeks gestation or birth weight < 1500g
• Any baby with seizures or other neurological signs or symptoms (e.g. neonatal encephalopathy)
• Antenatally detected intra-cranial anomalies
• Babies with craniofacial anomalies or other syndromic features associated with intracranial
anomalies
• Babies born to mothers known to use cocaine
• Suspected congenital infection (e.g.CMV , toxoplasmosis)
• Monochorionic twins
Schedule for routine cranial ultrasound scans in babies < 32 weeks gestation or birth
weight < 1500g
• Within 6 hours of birth
• At 2-3 days or sooner if unstable
• At 7 days
• Then 2-4 weekly depending on the baby’s condition
• At term (i.e. 40 weeks corrected gestational age) or prior to discharge whichever
comes first
N.B. further scans should be done:
After any adverse event – e.g. major cardiovascular collapse, NEC etc.
Depending on results of previous scans – schedule needs to be individualized if significant
abnormalities are detected. Any scan with major abnormalities should also be reviewed by a
consultant radiologist.
Images to save
• Coronal view through frontal horns
• Coronal view through 3rd ventricle

• Coronal view through posterior horns
• Mid line sagittal
• Left and right parasagittal through lateral ventricles
Left and right parasagittal view of parenchyma lateral to the lateral ventricles
39
DECLARING NEONATAL DEATH
Neonate: baby aged 28 days or less
1. Prerequisites
a. Baby should not be on any of the following medications
i. muscle relaxant
ii. CNS Depressants/sedation
iii. Mydriatics
b. Cardiopulmonary resuscitation for at least 20 mins (Ref NRP – 2017)
2. Clinical examination:
• No spontaneous movement
• No spontaneous breathing
• No heart rate on auscultation (do not depend on pulse oximeter). If in doubt, perform
bedside ECHO to note the cardiac activity
• Pupils dilated and fixed on shining focus light
Perform 12 lead ECG - Iso-electrical activity on ECG (Rhythm strip)
Baby is declared dead
Note the time
Most responsible physician (Duty Staff) should convey the message to the parents
Breaking the bad news under video recording in the AV room
Relevant documents should be immediately prepared.
Rest of the handing over procedure according to hospital policy
40
EXOMPHALOS (OMPHALOCOELE)
- Anterior abdominal wall defect involving the umbilicus with abdominal contents outside
the abdominal wall but covered by a membrane
- Diagnosis is usually made on antenatal ultrasound scan.
- Associations – approximately 50% have another major anomaly and of these 37% have GI
problems (midgut volvulus, Meckel’s diverticulum, and atresia). ~20% have cardiac
anomalies and 30% have karyotype abnormalities.
Initial management
- Birth – SHO/NNP & Registrar/Consultant to attend. There is no contraindication to vaginal
birth.
- Avoid giving bag & mask ventilation and have a low threshold for intubation during initial
resuscitation.
- Insert a large bore NG tube as early as possible, aspirate and then leave on free drainage.
- Wrap omphalos in sterile cling film for protection and in order to prevent fluid and heat loss if
sac
ruptured.
- The omphalos should be handled minimally as the membrane can be very fragile and easily
damaged.
- Examine carefully for other congenital anomalies.
- Establish IV access and start IV fluids as early as possible.
- Replace NG losses 4 hourly with 0.9% saline + KCl (10mmol/500mL)
- Monitor urine output and assess fluid requirements carefully on a daily basis.
- Start IV antibiotics - penicillin, gentamicin and metronidazole.
- Arrange echocardiogram, renal and cranial u/s scan and karyotype (if not done antenatal).
Surgical management
• It is usual to aim for early initial surgery i.e. within 24 hours.
• Operation depends on size of lesion and its contents. It is usual to aim for primary closure but
may need silo
Post-operative establishment of enteral feeds - see under gastroschisis.
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GASTRO-ESOPHAGEAL REFLUX (GER)
Definition - flow of gastric contents back up into the esophagus.
This increases in incidence with increasing prematurity (up to 18% in preterm infants overall). It
usually resolves by one year of age.
GER occurs because of:
small gastric capacity with delayed emptying times
increased gastric pressures due to abdominal breathing,
lower esophageal sphincter relaxation and upper sphincter disco-ordination, positioning and
drugs (eg caffeine).
It can be just physiological or there may be pathological symptoms:
- frequent vomiting
- irritability with feeds
- apneas, bradycardias & desaturations recurrent cough/ wheeze/ stridor aspiration pneumonia
These may lead to poor weight gain, mucosal ulceration, strictures, chronic respiratory symptoms,
and increased incidence of SIDS.
Diagnosis: Usually clinical
pH study is the gold standard for the diagnosis of acid reflux and should be considered if there is no
improvement with basic medical management. However, this facility is not available in our unit as
of now. Upper GI contrast study may be helpful if there is thought to be an underlying anatomical
problem (malrotation, hiatus hernia etc.).
Treatment
- Positioning (prop up at 30o angle 24 hours per day or place prone with monitor)
- Feeds – often reducing the volume slightly will help – therefore increase frequency or try
continuous feeds or even naso-jejunal feeds
Drugs:
- Domperidone – 200-400mcgm/kg/dose 3-4x day (doses up to 1000mg/kg qid are rarely used)
- Ranitidine – 1mg/kg dose po/iv tds (remember theoretical risk of worsening pulm hypertension)
– use if oesophagitis suspected
- Omeprazole – 0.7-1.4mg/kg po od or 0.5-2.0mg/kg od IV
Surgery – Consider surgical referral for Nissan’s fundoplication for severe cases refractory to above
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GASTROSCHISIS
• This is a defect of the anterior abdominal wall with abdominal contents outside the abdominal
cavity with no covering membrane and separate from the umbilicus.
• Diagnosis is usually made on antenatal ultrasound scan.
• Associations - ~15% have associated anomalies of these ~20% are GI i.e. malrotation and atresia
and ~2% are cardiac
Initial management
• Birth - There is no contraindication to vaginal birth.
Wrap visible intestine in sterile plastic bag or cling film to prevent fluid and heat loss. It may be
necessary to put whole baby in bag from waist down if defect is large.
• The visible intestine should be minimally handled.
Avoid giving bag & mask ventilation and have a low threshold for intubation during initial
resuscitation.
Insert a large bore NG tube as early as possible, aspirate and then leave on free drainage.
• Establish IV access and start IV fluids as early as possible.
• Replace NG aspirates 4 hourly with 0.9% saline + KCl (10mmol/ 500mL)
• Monitor urine output and carefully evaluate fluid requirements daily.
• Start IV antibiotics - penicillin, gentamicin and metronidazole.
• Arrange an echocardiogram and renal and cranial u/s scans.
Surgical management
• Urgent surgery is recommended to prevent further bowel ischemia
• Primary repair may be possible depending on the size of the defect
If staged repair is carried out, the baby will return from theatre with silo and pediatric surgeons will
guide further management.
Ventilation may initially be more difficult post-operatively as the abdominal cavity is now tense and
can impede chest movement. Initially paralysis may ease silo reduction.
Usually keep nil by mouth on TPN until secondary repair, but if secondary repair likely to be delayed
enteral feeds may be considered especially if gastric aspirates are minimal and the baby is opening
his/her bowels. Decisions to start enteral feeds should be discussed with the Paediatric Surgeons.
Dysmotility is common and it may take a long time to establish enteral feeds.
43
GRAVES’ DISEASE - INFANTS BORN TO MOTHERS
Infants at risk of, or diagnosed with hyperthyroidism, because of:
1. Being born to mothers with, or having a history of Graves’ disease, an autoimmune
disorder:
• Most common cause where maternal antibodies are transferred to the fetus in utero
• Thyrotropin receptor antibodies then attach to and activate the fetal thyrotropin
receptors on the thyroid gland
• This leads to increased production of thyroid hormones Free T4, Free T3 (FT4, FT3) and
the clinical findings of hyperthyroidism.
2. Other causes, although rare:
• Activating mutations of the TSH receptor
• McCune-Albright syndrome.
Note: Prevalence
1. Graves’ disease in pregnant women is 0.1 – 0.4%. Hyperthyroidism or Neonatal Graves’
disease in offspring of women with Graves’ disease is 1 – 5%.
2. Male and female infants affected equally.
At risk infants
Includes infants born to mothers: With a previously affected infant
• Who have received ablative treatment with radioiodine(RAI)
• With elevated maternal thyrotropin receptor antibodies (TRAb) at the time of delivery.
Diagnosis of Infants with Hyperthyroidism
In utero
• Diagnosis with high TRAb titres during pregnancy.
Post-natal
• Cord Blood - Diagnosis with high TRAb titres. Infants may be asymptomatic at the time of
delivery. Samples of cord blood may be sent in non-confirmed “high-risk” pregnancies.
• Infant blood may be sent for:
o Thyroid Stimulating Hormone (TSH)
o FT4
o FT3
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at 48 hours of age or sooner, if symptomatic or discharged. These levels may be repeated at 5-7
days post delivery, as an outpatient.
o Elevated FT4, FT3 and a suppressed TSH level indicate hyperthyroidism (see chart below).
Normal Thyroid levels in neonates
Test Age Normal Values
FT4 level 1-4 days 27-54 pmol/l
FT4 level 4 days-1year 13.9-26.1 pmol/l
TSH level by 7 days of age Less than 12 mU/l
Free T3 levels 3.0 – 9.1 pmol/L
Note: If infant is less than 1 month of age, the lab will call to identify a FT4 greater than 100 pmol/l
as a critical value.
Presentation of Other Clinical Features
May present at birth or several days after birth for infants born to mothers taking antithyroid drugs
(ATD).
Clinical signs that are commonly seen in neonates with hyperthyroidism
Tachycardia Hepatomegaly
Goiter Bilateral gynecomastia
Hyper excitability Stare, eyelid retraction
Poor weight gain Cardiac insufficiency
Additional Clinical Features
Intra Uterine Growth Retardation IUGR Tachypnea Microcephaly
Premature birth Jaundice Fever
Thrombocytopenia Vomiting Diarrhea
Advanced skeletal maturation Craniosynostosis
Treatment of the Infant:
High Risk Infants
1. Consider the diagnosis of Neonatal Graves’ disease in infants born to mothers with high
TRAb titres during pregnancy or in the cord blood.
2. Consult Pediatric Endocrine service for “high-risk” symptomatic or asymptomatic infants.
3. If asymptomatic, infant may be cared for in the post-natal ward. Monitor:
• Vital signs every 6 hours
• Serum TSH, FT4, FT3 levels at 48 hours and again at 5-7 days
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• Physical exam pre-discharge.
4. If symptomatic, infant is admitted to the NICU.
• Check TSH, FT4, FT3 levels after birth and as per endocrinologist’s advice.
Post discharge, follow in “Belaku” clinic
Low Risk Infants
1. Full term infant who is asymptomatic and considered to be at “low-risk” and can be
nursed in the post natal ward. Monitor:
• Vital signs every 6 hours
• Serum TSH, FT4, FT3 levels at 48 hours and again at 5-7 days
• Physical exam pre-discharge.
Potential Medication Choices
Medication Dosage Comments
Propylthiouracil (PTU) 5-10 mg/kg/day given orally TID (safe for breast-feeding)
Propranolol 2 mg/kg/day given orally TID
Lugol’s solution (iodine) 1 drop (8 mg) given orally TID Started only after PTU
Notes:
1. Minimum 48 hr stay for infant even if asymptomatic.
2. TSH, FT4, FT3 at 48 hrs for asymptomatic baby and repeated at 5-7 days.
3. Any infant who becomes symptomatic is admitted to the NICU.
* Contact pediatrics if heart rate, at rest, is > 200 bpm taken on 2 occasions one hour apart.
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HEART MURMURS DETECTED AT ROUTINE NEWBORN EXAMINATION
1. If a heart murmur is detected during routine newborn examination, complete a thorough
clinical examination including looking for signs of Dysmorphism and other congenital
malformations. Check transcutaneous oxygen saturation using a pulse oximeter and 4 limb
BP.
2. If the baby is unwell, has cyanosis, signs of cardiac failure, or decreased or absent femoral
pulses admit to NICU for urgent assessment and referral to the Paediatric Cardiology team.
3. If there is a family history of congenital heart disease, other congenital malformations,
Dysmorphism or an abnormal antenatal echocardiogram discuss with responsible staff
consultant.
4. Ask Responsible staff consultant to review if baby is well but murmur significant i.e. ≥3/6,
harsh, diastolic, pansystolic, continuous or associated with an ejection click or precordial
hyperactivity. If consultant confirms signs, ensure that Consultant referral to Paediatric
Cardiology has been made before discharge. Paediatric Cardiology assessment (+/-
echocardiogram) is likely to be necessary prior to discharge. Arrange follow-up as decided
by Paediatric Cardiology team.
5. If the baby is well with grade 1-2/6 murmur loudest at the left sternal edge, has normal
pulses, no ejection clicks and no signs of respiratory distress then review before discharge.
If still present then arrange for Neonatology OPD follow-up in 4 - 6 weeks (Discuss with
consultant on for postnatal wards).
6. Warn the parents about significant signs to observe for (poor feeding, lethargy, pallor,
sweatiness, cyanosis, apnoea and breathlessness) and to seek medical advice early should
there be any concerns. Ask consultant to review if there is any uncertainty. ECG and CXR are
unnecessary. If the murmur is still present when baby is seen in the Neonatology OPD
referral to Paediatric Cardiology will be arranged by the Consultant Neonatologist for that
clinic.
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HIE - ANTICONVULSANTS
48
HYPOGLYCEMIA IN THE NEWBORN
Definition: The operational threshold for Hypoglycemia is defined as that concentration of plasma
or whole blood glucose at which clinicians should consider intervention, based on the evidence
currently available in literature.
Operational threshold has been defined as CAP BLD SUG of less than 40 mg/dl (plasma glucose level
less than 45 mg/dl). In our unit, we measure capillary whole blood glucose using “Hemacue”. This
has a better agreement with lab glucose compared to regular glucometers. Hence our cut off for
action is 40 mg/dl by Cap bld sug.
WHO defines Hypoglycemia as blood glucose level of less than 45 mg/dl.
Healthy full-term infant (No symptoms)

a) <24 hrs. of age: 30-35mg/dl may be accepted at one time but should be > 45mg/dl
b) After 24 hrs., threshold should be increased to 45 mg/dl.
As there are no different values for preterm and SGA babies, the Cap bld sug cut off is taken as
45mg/dl
Indication for routine blood glucose screening
At risk of Hypoglycemia (who needs to be under Hypoglycemia protocol)
1. Low birth weight infants (<2000 grams)

2. Preterm infants (36 weeks)
3. Small for gestational age infants (SGA) : birth weight <10th centile
4. Infant of diabetic mothers (IDM)
5. Large for gestational age (LGA) infants: birth weight >90th percentile
6. Infants with Rh-hemolytic disease
7. Infants born to mothers receiving therapy with terbutaline/propranolol/labetalol/oral
hypoglycemic agents
8. Infants with morphological IUGR. This group includes neonates with birth weight between
10th to 25th and possibly up to 50th percentile, with features of fetal under-nutrition such
as three or more loose skin folds in gluteal region, overall decreased subcutaneous fat, and
head circumference to chest circumference difference greater than 3 cm
9. Any sick neonate such as those with perinatal asphyxia, polycythemia, sepsis, shock etc.,
when they are in active phase of illness. The screening may be discontinued once their
condition gets stabilized.
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10. Infants on total parenteral nutrition
Screening for hypoglycaemia is not recommended in term healthy breast-fed appropriate-for-

gestational age (AGA) infants. However, term infants with poor feeding, presence of inadequate
lactation or presence of cold stress may be considered for screening on an individual basis.
Time schedule for screening
At risk neonates 1, 3,6, 12, 24 and 48 hrs
Later 6th hourly till 72 hours of age
After 72 hours 8th hourly till one week of age
After one week of age – twice a day (Cap bld sug threshold is >50 mg/dl)
Growing preterm on full feeds after two weeks – once a day
This schedule is followed only if the Cap bld sug is normal. If abnormal, proceed with management
plan
Clinical signs associated with hypoglycaemia
 Asymptomatic: It is well known that low CAP BLD SUG may not manifest clinically and be
totally asymptomatic.
 Symptomatic: A smaller proportion of infants with hypoglycaemia can be symptomatic.
Clinical signs of hypoglycaemia are variable and may include stupor, jitteriness, tremors, apathy,
episodes of cyanosis, convulsions, intermittent apneic spells or tachypnea, weak and high-
pitched cry, limpness and lethargy, difficulty in feeding, and eye rolling. Episodes of sweating,
sudden pallor, hypothermia and cardiac arrest have also been reported.
Diagnosis
 Asymptomatic hypoglycaemia is said to be present when CAP BLD SUG is less than 45 mg/dL
(to be confirmed by laboratory estimation) and the infant does not manifest with any clinical
features
 Symptomatic hypoglycaemia should be diagnosed if hypoglycaemia (CAP BLD SUG is less than
45 mg/dL) coexists with clinical symptoms.
Management plan of infants with asymptomatic hypoglycaemia
1. Blood sugar 30 - 45 mg/dL - Trial of oral feeds (expressed breast milk or formula) and
repeat blood test after 1 hour.
If repeat Cap bld sug is >45 mg/dL,
50
 two hourly feeds
 6 hourly CAP BLD SUG for 48 hrs (the target blood glucose value is 50 to 120 mg/dL)
If repeat blood sugar is <45 mg/dl
 IV dextrose start at GIR of 6mg/kg/min

 Cap bld sug 1 hrly X 2, 2 hrly X 2, 4 hourly X 2 (if in normal range)
 If any of the Cap bld sug suggest Hypoglycemia – Increase GIR
All symptomatic infants should be treated with IV fluids.

2. Blood sugar < 30 mg/dl
 IV dextrose start at GIR of 6mg/kg/min

 Cap bld sug 1 hrly X 2, 2 hrly X 2, 4 hourly X 2 (if in normal range)
 If any of the Cap bld sug suggest Hypoglycemia – Increase GIR
For symptomatic hypoglycaemia including seizures, a bolus of 2 mL/kg of 10% dextrose (200 mg/kg)
should be given. The bolus should be followed by continuous glucose infusion at an initial rate of 6-
8 mg/kg/min. CAP BLD SUG should checked after 30 min, and then every 1 hour until blood sugar is
>50 mg/dL.
If CAP BLD SUG stays below 45 mg/dL despite bolus and glucose infusion, glucose infusion rate (GIR)
should be increased in steps of 2 mg/kg/min every 30 min until a maximum of 12 mg/kg/min.
Central line should be considered once the GIR is 10mg/kg/min
How to increase GIR?
Initial increment can be done by increasing the volume of infusion and keeping the dextrose
concentration unchanged
If the volume of fluids is 20 ml/kg/day more than recommended for the age, the increments should
be in the concentration of dextrose infused.
If the urine output is good (3 – 4 ml/kg/hr), and the fluid balance is either neutral or negative, one
can go up further on the volume before increasing the concentration of dextrose.
However, if the total increment in the fluid volume is 40ml/kg/day in excess of the fluid
recommended for the age, do not increase the volume further and GIR should be increased by
increasing the concentration of dextrose infused.
After 24 hours of IV glucose therapy, once two or more consecutive CAP BLD SUGs are >50 mg/dL,
the GIR can be tapered off at the rate of 2 mg/kg/min every 6 hours with CAP BLD SUG monitoring.
51
Initially, the concentration of dextrose is decreased to a minimum of 10% and later the volume to
match the need of the baby.
Tapering has to be accompanied by concomitant increase in oral feeds. Once a GIR of 4 mg/kg/min
of is achieved and oral intake is adequate and the CAP BLD SUGs are consistently >50 mg/dL, the
infusion can be stopped.
Do not stop glucose infusion abruptly as severe rebound hypoglycaemia may occur. Avoid using
more than 12.5% dextrose infusion through a peripheral vein due to the risk of thrombophlebitis.
Recurrent / resistant hypoglycaemia: This condition should be considered when infant fails to
maintain normal CAP BLD SUG despite a GIR of 12 mg/kg/min or when stabilization is not achieved
by 7 days of therapy.
Important causes of resistant hypoglycaemia:
 Congenital hypopituitarism
 Adrenal insufficiency
 Hyperinsulinemic states
 Galactosemia
 Glycogen storage disorders
 Maple syrup urine disease
 Mitochondrial disorders
 Fatty acid oxidation defect
Investigations to be done in resistant hypoglycemia

blood glucose < 45mg/dl with GIR of 12mg/kg/min (Critical labs)
 Serum insulin levels

 Serum cortisol levels
 Growth hormone levels
 Thyroid function test
 Urine ketones and reducing substances
If suspecting inborn error of metabolism (discuss with consultant before sending)
 Serum ammonia
 Serum lactate levels
 Free fatty acid levels
52
Besides increasing GIR for resistant hypoglycaemia, certain drugs may be used. Ensure that central
line access is available, and the necessary investigations as mentioned above.
 Hydrocortisone 5 mg/kg/day IV or PO in two divided doses for 24 to 48 hrs

 Diazoxide can be given orally 5-8 mg/kg/day in three divided doses.
 Glucagon 100 g/kg (0.025 to 0.2 mg/kg intramuscular, subcutaneous or intravenous
maximum 1.0mg) subcutaneous or intramuscular (max 300 g) – maximum of three doses.
Side effects of glucagon include vomiting, diarrhoea and hypokalaemia and at high doses it
may stimulate insulin release. For IDM 0.3mg/kg (maximum 1.0 mg)
 Octreotide (synthetic somatostatin in dose of 5-20 µg/kg/day subcutaneously two to three
times a day.
Useful formulae
(a) GIR(mg/kg/min) = % of dextrose being infused x rate (mL/hr)

body weight (in kg) x 6
(b) Infusion rate (mg/kg/min) = IV rate (mL/kg/day) x % of dextrose) / 144
Infusion rate(mg/kg/min) = Fluid rate (mL/kg/day) x 0.007 x % of dextrose infused
53
HYPOTENSION
Hypotension is usually a feature of uncompensated shock in neonates. Signs of compensated shock
may precede hypotension and include mottling, mild tachycardia and reduced spontaneous
movement. Signs of
uncompensated shock includes hypo - perfusion with prolonged capillary refill time, widening of
peripheral - core
temperature difference, tachycardia, metabolic acidosis and reduced urine output.
Causes of shock
1. Hypovolemia
- Acute blood loss
- Fluid losses (diuresis, insensible etc.)
- Third spacing (hydrops, NEC, sepsis, postoperative)
2. Distributive (aberrant local regulation or generalized vasodilation)
- Common in extreme preterm infants
- Sepsis
3. Cardiogenic
- Impaired venous return
- Hyper inflated lungs
- Pneumothorax
- abdominal distension
- myocardial dysfunction
- perinatal asphyxia
- more common in SGA babies if placental function poor
- congenital heart disease (e.g. hypo plastic left heart syndrome)
- post cardiac surgery
- cardiomyopathy
- arrhythmias
-
Definition of hypotension:
54
1. This is difficult to define accurately. If the lower 95% confidence interval is used for mean
blood pressure, this approximates the baby’s gestational age in weeks - i.e. if a 25-week
gestation baby is 1 week old, the minimal accepted mean BP should be 26mmHg
2. Markers of tissue hypo perfusion should also be considered when deciding on the
threshold for intervention of circulatory support
3. Babies with a PDA are likely to have a decreased mean BP due to the increased pulse
pressure. It may be reasonable to consider a minimal accepted mean BP of up to 3mmHg
below the baby’s corrected gestational age in these cases, in the absence of markers of
tissue hypo perfusion
Action:
1. Confirm the BP reading is accurate and the transducer has been calibrated and positioned
correctly.
Continuous intra-arterial BP monitoring is preferable in any unstable baby (Currently not practiced
in our unit)
2. Look for signs of tissue hypo perfusion – e.g. prolonged capillary refill time, metabolic acidosis
(likely to be with increased anion gap (>16mmol/L) and raised lactate (>2mmol/l) – reduced urine
output (< 1ml/Kg/hr.)
3. Echocardiogram – exclude congenital heart disease, assess PDA, and assess markers of
hypovolemia
Treatment -
1. Volume expansion
• This should be used cautiously unless there is good evidence of hypovolemia (i.e. recent
blood/fluid Loss, echocardiographic findings +/- low CVP)
• 10 mL/kg 0.9% saline IVI over 20-30 minutes
• Packed red blood cells may be used if there is evidence of recent acute blood loss or if
PCV is <0.35
• Repeat boluses of fluid should only be given if there is good evidence of hypovolemia
2. Dopamine
• Start if no evidence of hypovolemia on echocardiogram or following lack of response to
volume expansion
• Give via central venous line if available
55
• Start at dose of 10 μg/kg/min.
• Increase by 2μg/kg/min. every 15 minutes according to hemodynamic response to a
maximum of 20μg/kg/min.
3. Dobutamine
• Consider if there is evidence of myocardial dysfunction on ECHO. This may be useful to
add if there is inadequate response to dopamine and/or volume expansion. It may be also
be a good first choice inotrope if there is marked peripheral vasoconstriction
• Give via central venous line if available
• Start at dose of 10 μg/kg/min.
• Increase by 2 μg/kg/min. every 15 minutes according to hemodynamic response to a
maximum of 20μg/kg/min.
4. Epinephrine (Adrenaline)
• Discuss with consultant prior to use.
• may need to be used with a peripheral vasodilator such as dobutamine
• Dose – 0.1 - 1.5μg/kg/min. according to response.
5. Hydrocortisone
• Relative adrenocortical insufficiency is a recognized cause of hypotension in preterm
infants. Therefore, consider hydrocortisone in hypotensive preterm infants failing to respond to the
above. Send sample for cortisol levels before commencing steroids.
• Dose - 2.5mg/kg IV every 4 hours for 2 doses then 6 hourly.
6. Phosphodiesterase inhibitors - Milrinone
• Discuss with consultant (+/- Pediatric Cardiology team) prior to use
• Phosphodiesterase inhibitors inhibit NO release and have inotropic and vasodilator activity
• Do not mix with dobutamine, dopamine or epinephrine (adrenaline) because of pH
incompatibility.
Weaning inotropes:
• Decisions about weaning of inotropes should usually be made on ward rounds
• Usually wean in reverse order that inotropes were started
• Wean one inotrope at a time
• Avoid hypertension
56
HYPOTONIA
Maternal history – fetal movements, polyhydramnios, maternal myotonia (direct questions re.
grip, screwing up eyes etc.), maternal myasthenia
Perinatal history –? HIE, birth trauma – particularly cervical spine injury, history of respiratory
problems, feeding problems etc.
Examination:
• Any dysmorphism
• Deep tendon reflexes
• Fasciculations (including tongue)
• Contractures
Investigations: Electrolytes, Bone profile and Thyroid function test should be sent ASAP
If neuro-muscular problem is suspected, liaise with Paediatric Neurology team before arranging
detailed investigations. These may include
- Cervical spine x-rays
- Cranial U/S scan
- MRI brain / spinal cord
- CK (N.B. may be high for a few days after vaginal delivery)
- EMG , Nerve conduction study, Muscle biopsy, Myasthenia antibodies (baby and
maternal), Edrophonium test
If Genetic or metabolic disorder is suspected, liaise with Genetic team
- Blood gas
- Blood sugar
- Serum lactate
- Serum ammonia
- Serum amino acids
- Urine organic acids
- Serum carnitine and acyl carnitines
- CSF – lactate, glycine
DNA analysis for SMA, Congenital Myotonia (2 mls in EDTA bottle) DNA analysis for Prader-
Willi Syndrome Karyotype
57
INBORN ERROR METABOLISM – SUSPECTED
Suspect IEM in following conditions
a. As D/D for Sepsis
b. Encephalopathy
c. Failure to thrive
d. Hurried breathing (if pulmonary cause is less likely)
e. Previous neonatal death/Bad obstetric history
f. Previously well baby becoming suddenly ill
g. Recurrent neurological manifestation – Seizure, hypotonia, lathergy etc
h. Unexplained vomiting
Approach and management
Keep the baby nil by mouth
Start TPN with reduced protein (1gm/kg/day)
Treat for possible sepsis
Investigations – First line should be done at suspicion
 CBC with PS
 Urea Creatinine and electrolytes
 Bone profile (Ca, Phosphorus and alkaline phosphatase)
 Liver function test
 Thyroid function test (if not done earlier)
 Coagulation studies (if there is evidence of bleeding)
 Arterial blood gas: very important investigation. Take at most precaution to avoid pre-
analytical errors.
 Serum Ammonia
 Serum lactate
Site urinary catheter or bag to collect 24-hour urine sample
Other investigations as per clinical need. (e.g. X-ray, LP etc.)
Inform duty consultant for further management orders
Inform Dr Deepa Bhat for consultation
Inform parents about the possible need for extended metabolic screen
58
INTRAVENTRICULAR HEMORRHAGE (IVH)
Peri/intraventricular haemorrhage (PIVH), Post-haemorrhagic ventricular dilatation (PHVD) and
Hydrocephalus (PHH)
Definitions
• PIVH is bleeding limited to the sub ependymal area, into the cerebral ventricles, or involving the
adjacent cerebral parenchyma. It commonly occurs silently and is diagnosed
ultrasonographically. There are several grading schemes, but description of the morphology of
the IVH is recommended using the table below.
• Ventricular dilatation (ventricular index) is measured by comparison of the width of the lateral
ventricle (measured on the coronal view in the plane of the 3rd ventricle – midline to most
lateral part of lateral ventricle on either side) to the normal width for corrected gestational age.
Conventional wisdom is to define PHVD as growth of the lateral ventricles to above 4 mm wider
th
than the 97 centile for corrected gestational age following PIVH
PIVH with dilatation and HPI are termed “complicated PIVH” and lesser degrees of PIVH as
“uncomplicated”.
Pathogenesis
It is thought that PIVH is usually a consequence of bleeding from the vascular but immature
germinal layer, which overlies the head of the caudate nucleus in the fetus until about 30-32 weeks
gestation. The bleeding comes about mainly because of unstable perfusion, a consequence of
cardiovascular immaturity in the preterm infant, aggravated if they are sick/unstable.
HPI probably occurs due to venous infarction due to compromised venous drainage, rather than
direct extension of bleeding from the germinal matrix.
Aetiology
The major factor is prematurity
Others correlate to the degree of sickness and instability of the infant:
• Hypoxia
• Hypercapnia (or rapid changes in PCO2)
• Acidosis; need for bicarbonate
• Hypothermia
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• Unstable blood pressure; hypotension
• Maternal smoking
• Asphyxia
• Coagulopathy (this is also an important predisposing factor in the rare term baby with IVH)
Prophylaxis
• Stop prematurity!
• Antenatal steroids
• Scrupulous maintenance of physiological stability (blood gases, BP, clotting etc.)
• Minimal handling, gentle handling
Clinical presentation
• Majority of PIVH is clinically silent

• Acute hypovolaemia (rare)
• Neurological symptoms – apnea, seizures, hypotonia, reduced level of
consciousness, signs of raised ICP) There is a very high mortality rate in babies
presenting with shock or neurological signs due to PIVH.
Acute management of PIVH
• Maintain normal physiological parameters (blood gases, BP, clotting etc.)

• Treat hypovolaemia and neurological manifestations symptomatically
• Repeat cranial ultrasound scan within 24-48 hours and then weekly in any baby witH
• complicated PIVH
• Measure OFC twice weekly in babies with PIVH complicated by ventricular dilatation
More frequent ultrasound scans and OFC measurement may be necessary in babies with rapidly
progressing abnormalities.
Complications:
• Intracranial hypertension – this occasionally occurs in babies with developing PHH and
may be symptomatic with hypotonia, drowsiness, poor feeding and tense fontanelle
• Outcome of PHVD
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- ~ 1/3 normalise spontaneously
- ~ 1/3 retain ventriculomegaly – likely to represent cerebral atrophy
- ~ 1/3 require CSF diversion (shunt)
• Infants with IVH + dilatation and HPI are at risk of cerebral palsy. This is usually evident by1 year,
occasionally later, and may be of variable severity because of brain plasticity. There is
also an increased risk of learning difficulties, which may vary in severity from almost
indiscernible to very severe. The longer the delay before presentation, the less severe the
neurodevelopmental impairment. Other less common complications include epilepsy,
hearing impairment and impaired visuomotor coordination.
Management of PHVD and hydrocephalus
• Early (or elective) drainage of accumulating CSF does not improve neurodevelopmental outcome
• Indications for CSF removal are:
- Ventricular index >4mm over 97th centile for corrected gestational age
- OFC with abnormal growth acceleration (i.e. increasing relative to centiles)
- symptoms suggesting raised intracranial pressure (apnoea, vomiting, lethargy,
seizures etc.)
• Always attempt lumbar puncture (LP) as initial choice for CSF removal, regardless of ultrasound
evidence of CSF communication, as this is less invasive and may reduce the risk of
iatrogenic brain injury. See separate protocol for LP. If LP unsuccessful, do ventricular tap.
See separate protocol for ventricular tap.
• Always measure pressure prior to removing CSF by LP or ventricular tap (see protocol for
ventricular tap).
- if pressure 􏰏6mmHg (8cmH20), remove CSF for microbiological investigation only
- if pressure >6mmHg, remove 10-15ml/kg CSF, send samples for microbiological
investigation and
protein concentration
• Repeat CSF removal as in indications above. Any baby requiring CSF removal more than once
should be discussed with the neurosurgery team at KCH. Temporary measures to drain
CSF via a reservoir may be considered in babies requiring very frequent CSF removal by LP
or ventricular tap prior to permanent CSF drainage via a shunt. The timing of shunt
insertion may be determined by the baby’s general condition, weight and CSF protein
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concentration and cell count. CSF drainage from a reservoir should be carried out
according to the baby’s symptoms or as directed by the neurosurgical team (see separate
protocol)
It is likely that permanent CSF diversion via a shunt is appropriate more for cosmetic and practical
reasons than for improvement in neurodevelopmental outcome
Hydrocephalus Grade Location of blood Immediate symptoms Outcome
Subependymal haemorrhage I Adjacent and just below the lateral Silent No long term effects
(SHE), germinal matrix ventricle, over the head of the
haemorrhage (GMH) caudate nucleus, outside the
ependyma
Uncomplicated II Within the lateral ventricle but Silent No long term effects
intraventricular without change in its size or shape
haemorrhage (IVH)
IVH with ventricular III Within and distending the lateral Occasionally shock from Risk of CP and cognitive
dilatation ventricle blood volume depletion delay. Sometimes
hydrocephalus
Haemorrhagic parenchymal III (Levene), IVH plus echogenic wedge-shaped Occasionally shock. Very Very high risk of CP
infarction (HPI) echolucency adjacent to the lateral rarely neurological signs (spastic hemiplegia), and
IV (Papile)
ventricle (usually superolateral) (fits, hypotonia, reduced maybe cognitive delay.
level of consciousness, Sometimes hydrocephalus
raised ICP)
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LOW BIRTH WEIGHT CARE GUIDELINES
Objective
To reduce preventable mortality and short & long-term morbidities by providing health care
providers with a clinical practice guideline that promotes a consistent, individualized care approach
for low birth weight infants, based on physiologic principles and the best available evidence
Acknowledgement: This document is prepared by adopting small baby protocol practiced in sick
kids, Toronto, Canada. Reproduction of the document verbatim at places indicates our appreciation
of the presentation by the original authors. The authors of this document should be credited only
for compilation and modification according to local need, and do not deserve the credit of full
authorship.
Developmental care
Developmental care is both a philosophy of care and a practice model aimed at minimizing
the adverse effects of the NICU environment on high-risk infants. Developmental care has been
shown to reduce days of parenteral feedings, shorten the transition to full enteral feeds, improve
weight gain, reduce days in NICU and lower total medical costs. No adverse events have been
reported.
Light
The ambient lighting levels must be 20 foot-candles (fctcs) or less, unless task lights are required
(one per bed space)
Light sources need to have flexibility so that the disparate needs of the infants at various stages of
development and at various times of day can be accommodated, as well as the needs of the
caregivers
Control of illumination should be accessible to bedside staff with the ability to adjust lighting levels
Incubators are to be covered with opaque material
Eyes are to be covered following ROP exams
Eyes are to be covered when task lights are used (as they exceed 300 fctcs)
Noise
Infant bed areas and the spaces opening onto them should be designed to produce minimal
background noise (<45 dB) and absorb transient noise
Room design to include careful placement of travel paths, size and location of bed spaces, careful
selection of equipment and communication systems, and sound absorbent characteristics of
surfaces.
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Equipment will have noise criterion (NC) rating of 40 dB or less
Minimize intercoms and mobile usage
Avoid loud discussions at bedside
Avoid placing objects on incubators
Temperature and Humidity
Decrease Evaporative Heat Losses
Dry infants immediately after birth and bathe using warm towels/blankets. Minimize rubbing due
to risk of abrasive skin injury
Admit preterm infants to pre-warmed and pre-humidified isolettes/Incubator
Provide humidity to prevent trans-epidermal water loss
Decrease Radiant Heat Losses
Use pre-warmed, humidified, double-walled isolette/Incubator
Place an insulating cover over isolette/Incubator
Place polyethylene plastic wrap over infants to reduce water losses, oxygen consumption, heat
convection and heat demands if the baby is less than 30 weeks
Decrease Convective Heat Losses
Maintain constant air temperatures (use isolette temperature range chart)
Limit air currents
Minimize removal of infant from isolette (i.e. for weighing), especially during the first week of life
Decrease Conduction Heat Losses
Place infant on pre-warmed blankets and mattresses
Pre-warm surfaces such as scales, x-ray plates
Avoid Hyperthermia
Overheating on radiant warmers or within isolettes can occur quickly if not closely monitored.
Phototherapy and sunlight further increases the risk of hyperthermia developing
Humidity guideline
<1000 grams
Day 0-7 - humidity level ~75-80%
Day 8 - Gradually reduce isolette humidity level to 50% over 12-24 hours by reducing humidity
level by ~5% every 4 hours. To ensure tolerance to changing humidity levels, measure temperature
q3h. No supplemental humidity required after the first month of life
1000-1250 grams
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Day 0-7 - humidity level ~ 70%
q3h. No supplemental humidity required after the first month of life.
1250-1500 grams
q3h. No supplemental humidity required after the first month of life
1500-1800 grams
> 7 days - No humidity required after the first week of life
>1800g - No supplemental humidity required
Newborn Skin
At birth, the infant ‘s environment abruptly changes from an intrauterine fluid filled environment to
an extra uterine gaseous low humidity environment.
The skin has several primary functions:
 controls trans epidermal water losses o prevents dehydration from excessive water loss
 maintains fluid and electrolyte balance o thermoregulation and minimization of caloric
losses
 antimicrobial defense
 protection from environmental toxins, trauma, ultraviolet radiation o tactile sensation
Immature infants have a poorly developed stratum corneum that may only be two-three layers
thick with poor keratin development
Keratinization does not occur until the sixth to seventh month of fetal life
The skin of very immature infants is poorly developed with structural and functional immaturity
that is inversely related to gestational age.
Fortunately, the skin maturation process is accelerated following birth, hypothesized to be a result
of air exposure.
By 2-3 weeks of age, regardless of gestational age at birth, the epidermis has matured significantly
with a skin integrity that is similar to a term infant’s skin.
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Skin care
General care
Minimize adhesive use as much as possible
Double back tape or dab the portion of tape that will be exposed to the skin with cotton to reduce
adhesive exposure
Use hydrogel-based cardiorespiratory leads. Remove only when not functioning
Use a semi-permeable barrier between skin and the adhesive (e.g., Tegaderm) to secure umbilical
catheters, temperature probes, nasogastric tubes
Avoid adhesive removal but if adhesive removal is necessary use cotton balls soaked with warm
sterile water to facilitate removal
Avoid the use of adhesive removers (Dermasol) and plasticized polymers (e.g. skin prep)
Toxic epidermal necrolysis has been reported with the use of distillate-containing adhesive remover
Avoid bonding agents (e.g., tincture of benzoin)
The bond is usually stronger between the adhesive and epidermis than the bond between the
epidermis and dermis, risking epidermal stripping with adhesive removal
To reduce skin pressure and the development of pressure sores use sheepskin or gel mattress or
water bags underneath the mattress
Ensure infant is not lying on foreign objects that may result in pressure injuries (i.e. needle caps, IV
luer locks)
Transcutaneous monitor probes should use the lowest effective temperature
When a heating pad is used, regular monitoring for skin irritation or skin compromise is required
Emollient Use
Emollients can provide a mechanical barrier to water loss and promote skin integrity and function.
Studies evaluating the use of emollients have conflicting findings. Some studies have found a
reduction in infection rates while other have found higher rates of bloodstream infection among
infants <750 grams; therefore, prophylactic emollient use is not currently recommended
Emollient (e.g. Aquaphor*) use is to be reserved for infants with dry, flaking or fissured skin. In
our unit, we use coconut oil lightly applied once the baby is stable and no longer need humidity.
The risk of infection must be weighed against the benefit of emollient use If required
Bathing
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Bathing may result in hypothermia, increased oxygen consumption & respiratory distress. The first
bath is to be delayed until vital signs are stable and there is clinical stability present for several
hours. Bathing should be gentle with minimal infant stress incurred
Universal precautions (e.g., gloves) must always be employed but is of particular importance
before and during the first bath to prevent exposure to pathogens in body fluids
Gloves should continue to be used if vernix or other body fluids remain on the infant after the first
bath
Premature Infants <1500
 Use sterile, warm water for removal of maternal bodily fluids

 Clean skin surfaces with warm sterile water for the first week of life
 When soap is needed due to soiling, a neutral pH synthetic soap should be used to minimize
interruption of the acid mantle
 Infants <1500 grams should have non-immersion bathing only
 Immersion bathing, except the head and neck, is only commenced when infants are
clinically stable, at least 3 weeks of age, >1500 grams and the infant is able to maintain their
temperature
 Rubbing or scrubbing can easily injure and must be avoided
 Completely rinse skin with warm water after cleansing agents or antiseptics are used
Monitoring
Weight
Weight loss in the first week of life results primarily from contraction of the extracellular fluid space
Onset of the postnatal diuresis is primarily determined by a fall in pulmonary vascular pressure
Expected postnatal weight loss: Preterm-10%-20%; Full term-5% to 10%
Weigh the baby every day till steady weight gain is achieved
Once baby on substantial feeds and gaining weight, weight measurement can be made twice a
week. Babies on ventilator may not be stable enough to be weighed every day (we do not have
inbuilt weighing scale). They should be weighed at least every 48 hours
Weigh more frequently if consultant requests
Urine
Urine output should be measured every day
Sick babies are generally catheterized, and the volume of urine can be accurately measured
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In babies who are not catheterized, the diaper weight is measured every 4th hourly and the urine
volume is calculated (conversion 1 gm = 1 ml)
Glucose
Measure glucose on admission then q12h x 3 days unless clinical circumstances or abnormal values
mandate more frequent testing
Day 4-5: daily glucose measurement, then with other labs
For glucose levels > 100 mg/dl, dip urine to assess for glycosuria
Refer to NICU Glucose Monitoring Guidelines for recommended management of hypoglycemia
Electrolytes, Urea and creatinine
All babies less than 1500 grams – 24, 48 and 72 hours. Later as per the clinical indication
Babies > 1500 grams – 24, 72 hours and later as per clinical indication
All preterm infants should have twice weekly electrolyte levels while on PN and then weekly once
off PN Urine electrolyte levels should be assessed as clinically indicated (i.e., suspect increased
urinary sodium losses). Include urine creatinine levels with urine electrolyte evaluations
CBC and coagulation
Complete CBC on day 1 and day 3; thereafter measurements are as clinically indicated.
Minimum once weekly for the first 3 weeks then every two weeks until discharge
Request for modified hematological septic score if infection is suspected
Routine coagulation evaluation is not required; measurements are based on clinical indication
Arterial blood gas
Babies < 1500 grams and respiratory status stable (SOPI of <1.6, or OI of <8)
ABG at admission, 24 and between 48 to 72 hours
If fluid requirement is more than 20 ml/kg/day than stipulated for gestation and post-natal age
After one week of age, once a week
More frequently if clinically indicated
Nutritional labs
All preterm/low birth weight babies who are stable and on > 50% feeds should have nutritional labs
done once a week. The day of the week nutritional labs should be sent will be decided by the
consultants
Nutritional labs include CBC, Electrolytes, Urea, Creatinine, Bilirubin, Albumin, Calcium, Phosphorus
and alkaline phosphatase.
Neuro imaging
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Which infants should have cranial ultrasound completed?
 All infants with BW <1500g and/or <32 weeks’ gestation.

 High risk infants >32 weeks.
 Infants with severe hemodynamic compromise (i.e., shock, hypoxia, bleeding, NEC).
 Infants with apnea of unexpected frequency, severity or if occurring after 40 weeks’
gestation.
When should cranial ultrasound be completed?

Generally, early cranial ultrasound is used for the detection of hemorrhagic lesions while later
ultrasounds are primarily used for the detection of cystic lesions, PVL or ventriculomegaly and
predicting long term outcome
Timing of Head Ultrasounds
Complete head ultrasound day 4 with follow-up 7-14 days of age irrespective of initial findings. If
first two head ultrasounds are normal, repeat every 2-3 weeks for evolution of ischemic changes
(PVL).
If grade II IVH or greater, follow with serial head ultrasounds every two weeks until ventricular size
stable. More frequent evaluation may be necessary depending on the degree and rate of increase
of ventricular dilatation.
If early signs of increased echogenicity are identified on cranial ultrasound, repeat cranial
ultrasounds every 2-3 weeks is recommended to follow for the development and evolution of PVL.
Of note, infants born to mothers with chorioamnionitis are at higher risk of developing PVL
ROP screening – See ROP protocol/SOP
Growth monitoring
Anthropometric measurement should be done as soon as possible and plotted on the growth chart
There are two types of growth charts provided in our case notes
a. weight chart for daily charting: this has to be used for daily weight charting and is very essential
for assessing our fluid and nutrition management plan
b. Fenton’s growth chart: this has to be plotted every week to assess the growth. Preferably done
on the day of nutritional labs for stable babies
Parenteral nutrition
Very low birth weight (VLBW) and extremely low birth weight (ELBW) infants have unique
nutritional requirements in order to maintain tissue integrity, metabolism and growth. Duplication
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of normal in-utero fetal growth rates is the principle nutrition management goal in preterm infants.
However, achieving this goal is frequently very difficult and growth failure is very common.
Growth in the early weeks of life has been associated with improved neurodevelopmental scores.
As well, poor early nutrition may predispose these infants to health issues later in life. Therefore, it
is imperative that attention is paid to nutrient quality and quantity; that nutritional practices are
timely, cost-effective and based on the best available evidence
The provision of nutrition for preterm infants may consist of either parenteral nutrition (PN) or
enteral nutrition (EN) or a combination of both. PN is provided to compensate for the inability of
the preterm infant to meet their metabolic needs in the first few weeks of life with EN alone
Efforts should be made to provide IV amino acids as soon as possible after birth to prevent a state
of catabolism.
A minimum of 1.5 g/kg/d is necessary to provide neutral/positive nitrogen balance and as much as
3 g/kg/d as soon after delivery as possible will further enhance protein deposition leading to earlier
growth. As much as 4 g/kg/d of IV protein may be necessary to maintain stores and facilitate
optimal growth especially in very preterm infants
The initial parenteral fluid in our unit is modified pediatric electrolyte solution (EP-10% with
additions)
Please follow the PN calculator for maintenance fluid to prepare the above solution
Tailor made parenteral nutrition (TPN) is used for all sick babies or stable babies with need for
electrolyte and fluid management
Below table gives the general guideline of adding protein and fat to the TPN
Use the TPN calculator provided for achieving required recipe for the given baby
Parenteral Nutrition (PN)

Timing
Protein Fat
Day 1 1.5 g/kg/day 1 g/kg/day
Day 2 2.5 g/kg/day advance by 0.5 g/kg/day
g/kg/day-do not exceed 2.5 g/kg/day

Day 3 3-3.5 g/kg/day
Maximize protein to 3-3.8

Day 4
g/kg/day
Enteral nutrition – See LBW feeding guideline
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LOW BIRTH WEIGHT FEEDING
Adequate nutrition is essential for optimal growth and recovery from illness in low birth weight
infants. Enteral nutrition should be commenced as soon as the clinical condition permits with an aim
of sustained graduation and achieving full feeds in about 2 weeks.
In our unit, full feeds constitute 160 ml/kg/day after 5 days of life. However, many LBW babies may
require more (up to 220 ml/kg/day) than this. The increment in the volume of feeds beyond regular
full feeds has to be on case to case basis as decided by the primary consultant.
Commencement of feeds:
Trophic feeds – this is the minimal volume of feeds that stimulate gut function and does not have
significant nutritional value. In our unit we start trophic feeds at a rate of 15 ml/kg/day divided into
eight or twelve feeds. Trophic feeds should be considered for all babies less than 34 completed
weeks of gestation before graduating to higher volume of feeds. Commence the feed as soon as baby
is clinically stable. For small for gestational age babies with documented “Absent/reversed end
diastolic umbilical flow (AREDF), we commence the feed after 24 hours of physiological
stabilization.
For babies with gestation of less than 30 weeks, trophic feeds are continued for about 48 hours
before graduating up. For babies greater than 30 weeks of gestation, trophic feed of 24 hours is
sufficient to consider graduating up the feed volume
Contraindication: proved or suspected intestinal obstruction is contraindication for commencing
enteral feeds. Babies who are very sick due to asphyxia, severe resistant hypotension, increasing
need for ventilation should be considered precarious and hence caution in introducing trophic feeds.
Trial feeds – late preterm or term babies who are nil by mouth for their clinical needs who are now
fit to be fed can be offered trail feeds. Trial feeds constitutes 15 ml/kg/day divided into 8 feeds. Once
they tolerate trial feeds well, the frequency of increment of feeds depends on the nursing and clinical
assessment of the condition.
Graduation/Increments of feeds: for babies less than 34 weeks of gestation, the feeds graduated to
avoid feed intolerance. The feeds are increased at a rate of 15 ml/kg/ day for first 24 to 48 hours and
later it can go up to 30ml/kg/day. Once the feed reaches 30ml/kg/day, it is considered as nutritionally
significant and no more a trophic feed. Full feeds are expected to be achieved by one week after
commencement of nutritional feeds.
For SGA babies with AREDF, the advancement of feeds should be slow. We increase feeds by
15ml/Kg/day for first week to 10 days of life.
Frequency of feeds: in babies less than 1500 grams, initial trophic feeds are given every 3 to 4 hourly
as the EBM becomes available. Once nutritional feeds are achieved and EBM is sufficient, the
choice of frequency is 3 hourly feeds. However, as the volume of feeds increases, some babies may
be unable to cope up with the volume. Nursing feedback is essential in this regard. If the baby is
unable to tolerate the volume, the frequency of feeding can be changed to 2 hourly feeds. In some
cases, very tiny babies may tolerate the feeds but not the volume in spite of 2 hourly frequencies.
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Pump feeds: all the babies are initially fed via gavage under gravity. The feed rate variation is too
huge and hence may result in some babies not tolerating the planned volume of feeds. If the baby is
well and appear to initially tolerate certain volume but becomes distressed and starts vomiting after
feed is near complete, he/she might be a good candidate for pump feeds. The planned volume of milk
feed is slowly fed via gavage and syringe pump over a period of 30 to 45 mins. If the pump feed
duration is less than 20 mins, consider going back to slow bolus feeds. Very rarely, continuous
gastric infusion of the milk feed is ordered by the in charge consultant in order to overcome
feed/volume intolerance.
Note: calculation of aliquots – each baby will have the aliquots per feed calculated based on his/her
weight and feed of 15ml/kg/day. E.g. the aliquot for one Kg baby would be 15ml per day which is
divided into 8 feeds = 15/8 = 1.9 ml per feed. But for the sake of ease, it is rounded up as 2ml per
feed. Due to rounding up practice, the exact amount of feed baby would receive will not be exactly
what has been calculated. However, we use the calculated volume for our clinical discussions.
Type of milk: First and default choice is expressed mother’s milk. Second choice is frozen and
thawed mother’s own milk (MOM). This facility is yet to be commissioned in our unit. Once
commissioned, this will be the second natural choice. Third choice is donor’s milk. As we do not
have milk bank in our unit, this service is not offered. Commercially available donor’s milk is
available at request (call Neolacta/Amara). If the parents agree and are affordable, this can be
considered as second choice till MOM facility is made available.
The least preferred choice is appropriate formula milk. Parents have to be explained about the need
and possible disadvantages of formula milk and a written consent should be taken before
commencing formula milk. Please check with the treating consultant about the appropriate formula
to be prescribed.
Withholding the feeds: in case of abdominal distension, or significant pre-feed aspirate (> 50% of the
previous feed), blood or bile in the aspirate is the indication for withholding the feeds. Call
consultant for further management plan.
Checking pre-feed aspirate: the evidence to support routine checking of pre-feed aspirate is thin.
However, we have noticed several cases of tube migration back to esophagus causing bradycardia
and respiratory distress during feeds, which has been picked up by our practice of pre feed gastric
aspirate check. Hence, it is the practice which is continued in our unit. Nurses check the pre-feed
aspirates. If the aspirate is minimal or less than 25% of previous feed, it is returned back to stomach
and the feeding is continued as planned. If the aspirate is greater than 25% and less than 50%, the
aspirate is returned back and the same volume is subtracted from the current feeds. If the aspirate is
greater than 50% of the previous feed, the current feed is withheld and the consultant informed for
further evaluation. If the pre-feed check does not yield anything, please check for NG/OG tube
position with PH paper and if needed a check X – ray. Do not continue feeds till the issue of tube
position is resolved.
Human Milk Fortifiers: we add HMF to the breast milk after achieving a volume of 180 ml/kg of
EBM and still unable to achieve expected growth (15 gm/Kg/day). One sachet of HMF has to be
dissolved in 50 ml of EBM.
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Glycerin enema: we strongly discourage using Glycerin enema on a routine basis or even with soft
indications such as not passing stools for 24 to 48 hours. Babies with significant abdominal
distension due to non-passage of stool will be reviewed with pediatric surgeon. After necessary
investigations are done and if the surgical team is convinced then glycerin enemas are considered. If
the babies are on glycerin tips, they must be reviewed every day by surgical team and stopped at the
earliest.
Supplements: all low birth weight babies receive nutrition supplements. We use three group of
nutrition supplements.
a. supplements to counter metabolic bone disease – calcium, phosphorus and Vit D3
b. multivitamins
c. supplements to counter anemia associated with prematurity and infancy. – Iron and folic acid
supplements a and b should be started once the baby is tolerating 50% of the required fluid as enteral
feeds. Commencement of supplement c should be postponed till 4 weeks of postnatal life. In case of
significant anemia, iron and folic acid supplementation can be commenced after 2 weeks of postnatal
age.
Calcium and multivitamins should be continued till it gains birth weight of 2.5 Kg. Iron – folic acid
and Vitamin D3 should be continued till one year of age.
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MECONIUM ASPIRATION SYNDROME (MAS)
Pathophysiology
1. Atelectasis with ball-valve obstruction of airways leads to hyper-expansion and predisposes
to air-leaks.
2. A chemical pneumonitis contributes to respiratory distress and inactivates endogenous
surfactant.
3. Hypoxemia also occurs because of a right to left shunting due to pulmonary hypertension.
4. Secondary infection may also occur.
Strategy
This should follow the basic guidelines on respiratory distress (see respiratory distress protocol)
specific points:
1. Antibiotic therapy and intravenous fluids (see appropriate protocols)
2. Aim for SaO2 >98% to decrease pulmonary vascular resistance
3. Obtain arterial blood gas. Consider UAC or PAL if ventilated or if FiO2 >0.3 and rising
4. CO2 retention indicates significant distress in hyperventilating baby
5. CXR - atelectasis, hyper expansion, and meconium plugs. May progress to a more diffuse
pneumonitis
6. If on CPAP and SOPI is > 1.6, intubate and ventilate
7. If baby’s work of breathing is more and blood gases shows hypoxia, hypercarbia or acidosis
intubate and ventilate. If in doubt, ask responsible staff consultant to decide.
8. Surfactant has been shown to reduce need for ECMO and improve lung mechanics and
should be considered. Discuss with responsible staff consultant
9. Avoid high end expiratory pressures Start with a PEEP of 5. Rarely needs increasing- may
exacerbate air trapping
10. Adopt ventilatory strategy with long expiratory times to avoid gas trapping (I:E should be
>2)
11. Adequate analgesia and sedation with Morphine and midazolam. Consider rocuronium
infusion in case of severe PPHN
Complications:
1. Pneumothorax (drain)
2. Pneumomediastinum (usually requires no treatment)
3. Pulmonary hypertension
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NECROTISING ENTEROCOLITIS
Clinical staging (“Mod Bell staging”) Stage 1 – suspected NEC
- GI symptoms/signs (mild Abdominal distension, poor feeding, vomiting, increased gastric

aspirates, fecal occult blood)
- Systemic signs (temperature instability, lethargy, apnea)

- Abdo. XR (dilated loops, thickened bowel wall but no pneumatosis)
Stage 2 – confirmed NEC
Any features of stage 1 disease, plus:
- persistent occult or frank GI bleeding, marked Abdominal distension

- AXR – gross intestinal distension, bowel wall thickening, unchanging bowel loops, intramural gas,
portal vein gas
- features of NEC at laparotomy
- Stage 3 – advanced NEC
Any features of stage 1 or 2 disease, plus:
- shock, severe sepsis or gross GI bleeding

- abdomen XR shows evidence of perforation (or confirmed at laparotomy)
Investigations : (Urinary IFABP may be considered. Check with consultant)
AXR - ask for AP (+/- lateral decubitus or shoot through)
- serial x-rays can be helpful ( 6-12 hourly in first incidence)
- look for thickened bowel wall, intramural gas (pneumatosis intestinalis), free air “football
sign” or (rarely in neonates) air under diaphragm in AP films or uppermost in lateral, air in
portal system (sign of severe illness), large distended loops of bowel which do not change
from film to film (may suggest gangrenous bowel). is useful to detect pneumatosis, free
peritoneal fluid, air in portal vein or biliary tree and for
Abdo USG: assessment of focal signs (e.g. mass)
- FBC & film - May show leukocytosis or neutropenia - left shift & toxic granulations,
thrombocytopenia, hemolysis, clotting screen, biochemistry profile including CRP
- blood cultures
- stool for M, C+S (including C. difficile)
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Stool for occult blood - this method is oversensitive and is usually positive if the baby has received
oral iron and in some babies with NG tube
Blood gas – check on presentation and then subsequently as needed
Initial medical management
- nil by mouth
- large bore nasogastric tube with free drainage
- IV fluids - clear fluids initially then TPN once stable biochemically
- IV antibiotics - usually clindamycin and metronidazole
- frequent reassessment by clinical examination +/- abdo. XR
- contact Pediatric Surgeons early
- adequate analgesia with morphine IVI
- low threshold for intubation and ventilation. Avoid nasal CPAP.
Subsequent medical management
- 7-14 days NBM & IV fluids from time of resolution of symptoms/signs. This may vary
depending on the
certainty of diagnosis
- trophic feeds (i.e. 1mL/kg/hr.) for 24-48 hours initially and then increase by no more than
1mL/kg/hr. 24 hourly until fully enteral feed use EBM if available.
- consider upper or lower GI contrast studies if stricture(s) are suspected in babies who
have had confirmed or suspected NEC. Always do lower GI contrast study before upper if
both indicated.
Surgical
- in acute phase, may be considered if medical management is failing, or if there is
perforation, abdominal mass, portal venous gas, fixed loop of bowel on serial
Abdominal XR suggestive of gangrenous bowel
- late surgery may be considered due to stricture formation or abscess /
inflammatory mass
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NEONATAL ENCEPHALOPATHY
Definition
Neurological manifestations of acute disturbance of brain function
Incidence: 2-6/1000 live births (1-2/1000 severe)
Aetiology
Some cases have a hypoxic-ischaemic aetiology (therefore sometimes called hypoxic ischaemic
encephalopathy – HIE). However, only 5-10% of the cases have identifiable evidence of intrapartum
events that may have caused this. Therefore, terms such as birth asphyxia should be avoided. Other
causes are antenatal hypoxia- ischaemia, infection (particularly with chorioamnioitis) and inborn
errors of metabolism.
Clinical features and staging
This was previously described by Sarnat and Sarnat, as 3 states of HIE with baby assigned to the
maximum level reached. Levene’s staging scheme may be more practical as the categories are more
mutually exclusive.
Stage 1 – mild Stage 2 – moderate Stage 3 – severe
Conscious level hyper alert lethargic comatose
Muscle tone minor disturbances more disturbed reduced
Feeding slight difficulties poor absent suck
seizures no yes yes
Able to maintain vital yes yes no

functions
Other systems are also commonly involved as a further consequence of inadequate organ
perfusion. This may be manifested as:
• Acute tubular necrosis leading to acute renal failure (see separate protocol
• Hypoglycaemia secondary to glucose and glycogen consumption during compensatory anaerobic
metabolism, which is energy inefficient. This may cause hypoglycaemic convulsions
• Necrotising enterocolitis or dysmotility with ileus and dilated loops
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• (Transient) myocardial ischaemia, which may result in systemic hypotension, possibly
exacerbated by poor
• peripheral vasomotor tone
• Disseminated intravascular coagulation (DIC)
• Shock lung/acute RDS
• Pulmonary hypertension
• Hepatic failure
• Acute cold injury to skin
Management
• Resuscitate as necessary including ventilatory support as required. Hyperventilation may be
harmful, therefore maintain PCO2 >3.5kPa
• Treat another organ failure as appropriate

• Consider the diagnosis and etiology and investigate as appropriate. Always check blood culture
and early arterial (not capillary) blood gas.
• Carefully monitor fluid balance. Fluid restriction may be appropriate if there is concurrent acute
renal failure (see separate protocol) but there is no evidence that fluid
restriction/diuretics are beneficial for encephalopathy per se, unless there is fluid
overload or cerebral edema. Cerebral edema is very difficult to diagnose: full or tense
fontanelle with invisible ventricles on cranial ultrasound can (but ventricles are normally
very small in term infants). In established cerebral edema, fluid restrict as tolerated (start
at 40ml/kg/24 hours and increase according got urine output, daily weight etc.) It is
important to maintain systemic blood pressure if possibly, so that cerebral perfusion
pressure (difference between mean arterial pressure and intracranial pressure) and hence
cerebral blood flow is kept up.
• Treat seizures according to HIE anticonvulsant protocol. Request EEG early. Prior to the EEG,
consider anticonvulsants even if baby is very irritable but not obviously seizing.
MRI including Diffusion Weighting Imaging (DWI) should be performed within 5 days if possible; this
is likely to give useful prognostic information too. Keep parents well informed
Prognosis and follow-up
• The baby’s staging is done as per modified Sarnat staging, according to their worst clinical
condition is probably the best guide to prognosis.
- Stage 1 – 100% full recovery with normal neurological follow-up
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- Stage 2 – 75% full recovery with normal neurological follow-up
- Stage 3 – 90% mortality or have significant neurodevelopmental abnormalities
• The rate of improvement in the baby’s neurological condition may also have prognostic value but
note that anticonvulsants may interfere with neurological assessment for weeks
after discontinuation.
• Results of cranial imaging (particularly if MRI scan done in 1st 5 days) and EEG may also provide
valuable prognostic information. These should be considered along with the baby’s
neurological examination findings and discussed with the relevant subspecialist on
a case by case basis.
Those from other areas should be followed up by their local pediatrician as well.
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NEONATAL SEIZURES
Incidence
Term infants 2.6 / 1000 live births
Preterm infants 11.1/ 1000 live births
Etiology:
HIE
CNS infection
Intracranial hemorrhage
Cerebral artery infarction
Acute metabolic disorder
Inborn error of metabolism
CNS malformations
Maternal drug intoxication
Benign Neonatal Seizures
Idiopathic
Neonatal seizures are often subtle and difficult to recognize, often including repetitive movements,
staring and apnea.
Clinical features
• Onset
- 36% in 1st 24 hours
- 64% in 1st 48 hours
- 83% in 1st week

• Type - may be:
- multifocal or generalized
- clonic, myoclonic or tonic
- electrographic with no clinical signs
Investigations:
• Initial investigations / monitoring
- oxygen saturation, heart rate and apnea monitoring
- blood glucose
- neonatal biochemistry profile including Ca, Mg
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- FBC
- blood gas
- septic screen including lumbar puncture
- cranial ultrasound scan
- EEG
• If seizures persist or if otherwise indicated from results of initial investigations

- brain MRI
- urine for toxicology
- investigations for congenital infection
- plasma ammonia
- plasma amino acids
- urine organic and amino acids
- plasma and CSF lactate and pyruvate
- CSF glycine
• Treat the underlying cause

• Treat if more than 2 seizures/hour or one seizure of more than 3 minutes’ duration
- Phenobarbitone 20mg/kg over 30 min. loading dose. If seizures uncontrolled, give up to 2 further
doses of 10 mg/kg over 30 minutes (i.e. max. total dose of 40 mg/kg), then maintenance dose
5mg/kg/day
nd
• If seizures uncontrolled with phenobarbitone, use 2 line treatment of phenytoin or
lignocaine (Lignocaine is currently not used in our unit)
- Phenytoin – 20mg/kg (slow IVI over ~20 mins.). If seizures not controlled, give 2nd dose of
10mg/kg (slow IVI over ~20 mins.), then maintenance dose 2-4mg/kg BD (IV or oral)
- Lignocaine – loading dose 2mg/kg followed by 6mg/kg/hour (ECG monitoring necessary)
Aim to stop anticonvulsant treatment early if seizures well controlled, within 1st week of life if
possible
81
NEONATAL SEPSIS
Clinical Categories
1. Risk of sepsis
2. Suspected sepsis (Admission diagnosis only, should be changed to appropriate category at
the time of discharge)
3. Probable (Clinical) sepsis
4. Culture proven sepsis
Early and late onset sepsis (< 3 days/> 3 days) to guide antibiotic therapy and need for LP
Risk of Sepsis:
The following factors seem to be associated with an increased risk of sepsis:
1. Low birth weight (<2500 grams)
2. Prematurity (< 37 weeks)
3. Febrile illness in the mother with evidence of bacterial infection within 2 weeks prior to delivery
4. Foul smelling and/or meconium stained liquor
5. Rupture of membranes >24 hours
6. Babies requiring resuscitation for > 1 min
7. Respiratory Distress
In our unit we consider Infants with two risk factors will be at higher risk of sepsis and should be
investigated and then treated accordingly.
Table 1: Septic Screen: * (always send blood and urine culture when sepsis is suspected)
Modified Septic score (incidence of Sepsis in our unit 35% of L3 admissions)
A score of 3
Positive Likelihood ratio 2.66 4.60
Negative Likelihood ratio 0.28 0.19
If certain parameters have not been reported on HIS – Please call hematology for information.
If the screen is negative but clinical suspicion persists, it should be repeated between 12 and 24
hours.
If the screen is still negative, sepsis can be excluded with reasonable certainty.
Consider LP in stable baby with clinical suspicion of sepsis.
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Modified Hematological septic score
Parameter Value Mod HSS

< 5000 2
>25000 (at birth) 1
Total Leucocyte Count
> 30000 (12 - 24 hrs) 1
> 21000 (day 2 onwards) 1
Normal 0
No neutrophils 2
Total Neutrophil Count Increased / Decreased 1/2
Normal (1800 - 0
5400/cumm)
Increased NA
Immature Neutrophils
Not increased NA
> 0.2 1
Immature: Total Neutrophil ratio (IT Ratio)
< 0.2 0
Immature: Mature > 0.3 NA
Neutrophil ratio (IM ratio) < 0.3 NA
Present 1
Degenerative changes
Absent 0
<150000 1
Platelet count
>150000 0
> 5% 1
Nucleated RBC
< 5% 0
Normal CSF Findings in Neonates:
CSF Components Normal Range
Cells/mm3 5 - 20 cells
PMN 60%
PROTEIN (mg/dl) 90 (20-170)
GLUCOSE (mg/dl) 53(32-119)
CSF/Blood glucose 50%
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Suspected sepsis
Babies with soft indications of infection such as decreased activity, feed intolerance, with border
line septic screen and improves within 24 to 48 hours. Antibiotics may be stopped after 72 hours if
culture is negative and baby clinically well. Please note – this is very subjective diagnosis and
responsible staff consultant may decide a longer course of antibiotics.
Probable (Clinical) sepsis (culture negative sepsis) - Babies who fit into clinical diagnosis of sepsis
Systemic inflammatory response syndrome
Organ dysfunction
Positive septic screen
Cultures negative
This could be fungal or viral sepsis. As the blood culture yield is quite low, treat all clinical sepsis
with at least 7-day course of appropriate antibiotics.
Duration of antibiotic therapy in neonatal sepsis
Diagnosis Duration
Meningitis (with or without positive blood/CSF 21 days

culture)
Blood culture positive but no meningitis 14 days
Culture negative sepsis (screen positive and 7 - 10 days

clinical course consistent with sepsis)
Septic Arthritis 4 wks. - minimum of 2 weeks IV

Antibiotics
UTI (Culture positive) 10 days
Pneumonia 10 days
Choice of antibiotics: In our unit, commonest organism causing neonatal sepsis (Nosocomial) is
Klebsiella sp. Our empirical antibiotic policy reflects the need to cover Klebsiella with the antibiotics
for which is sensitive to as noted in our hospital.
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1st line: Inj Piperacillin – Tazobactum and Inj Gentamicin
2nd line: Inj Cefipime with gentamicin/Amikacin
3rd line: Inj Colistin
Community acquired pneumonia: Inj Amoxicillin Clavulonic acid
Severe Staphylococcal sepsis: Inj.Cloxacillin. if it is not available consider Vancomycin or Linezolid
Septic Arthritis: Cloxacillin and gentamicin or Linezolid and Gentamicin
Urinary Tract infection: Inj. Gentamicin
Currently we are not doing Gentamicin levels
Hold Gentamicin if serum creatinine is > 1.4 or urine output is < 1ml/Kg/hr
UTI Prophylaxis: Cephalexin 10 mg/Kg HS
Note: Antibiotic policy is frequently revised by the infection control committee and that needs to
be adopted for treatment of neonatal sepsis.
Fungal Sepsis:
Suspect in:
1. Preterm < 28 wks
2. VLBW
3. Prolonged use of broad spectrum antibiotics for > 7 days
4. Any foreign body (ET tubes, central lines)
6. Surgical procedures(abdominal)
7. Failure to thrive
Send for fungal blood culture, Supra pubic urine sample for fungal hyphae, CSF and abdominal
ultrasound, ECHO, Opthalmology review
Inj Fluconazole 12 mg/kg loading dose followed by 6mg/kg once daily - 10 days (uncomplicated)
14 days – funguria or mycetoma
85
PATENT DUCTUS ARTERIOSUS (PDA) IN PRETERM INFANTS
Clinically significant PDA occurs in 30-40% VLBW infants. It is associated with increased mortality,
pulmonary hemorrhage, chronic lung disease, peri/Intraventricular hemorrhage and NEC.
Diagnosis:
1. Clinical signs
- Low-pitched, continuous murmur
- bounding pulses
- Wide pulse pressure (i.e. >20-25mmHg)
- Active precordium
- Poor lower body perfusion (poor capillary refill, mottled skin)
- Increased ventilator requirements/Swinging saturation
- Metabolic acidosis
- Pulmonary hemorrhage
N.B. absence of a murmur does not exclude PDA. ∴ if PDA suspected due to presence of other signs,
investigate further and consider treatment
2. CXR : May show cardiomegaly and pulmonary edema
3. Echocardiogram
Confirm the presence of PDA prior to medical treatment to assess the degree of volume loading of
the left atrium and ventricle and R/O other congenital heart disease particularly coarctation of
aorta. Medical treatment should not be delayed if an echocardiogram is unavailable and there are
clinical signs suggesting a hemodynamically significant PDA. Following features suggest significant
PDA
- Ductal diameter > 1.5 mm in the first 30 hrs. after delivery (<1500g)
- Left atrial/aortic root ratio > 1.6
- Pulsatile transductal flow (Vmax) < 1.8m/sec
- Reverse end diastolic flow in the descending aorta/mesenteric artery
- LPA diastolic flow velocity of more than 20cm/sec
- Low velocity L-R flow (<1.5m/s) through the ductus in the 1st 4 days in ventilated babies
<1500 g s/o high risk for PDA
Any 2 clinical criteria and any 2 ECHO criteria constitutes the definition of HS-PDA, and hence needs
to be treated.
Medical treatment:
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Do not close PDA if the shunt across the duct is right to left
1. Optimize oxygenation by appropriate ventilatory management. Use of higher PEEP (i.e >6cmH2O)
may be beneficial to minimize the effects of pulmonary oedema and risk of pulmonary
haemorrhage.
2. Treat anaemia. Maintain Hgb >12g/dL (Hct 35 – 40)
3. Fluid restrict – fluid requirements need to be evaluated on an individual daily basis but fluid
restriction may be necessary. If baby is not fluid depleted, decrease fluids by 20 ml/Kg/day
4. Frusemide should be considered if there is evidence of pulmonary oedema or fluid overload
5. Medications
i. Ibuprofen – is the drug of choice (IV preparation is not available in our unit)
Unless there are contraindications, ibuprofen should be started as early as possible in all
VLBW infants with a clinically significant PDA in the first 2-3 weeks of life – i.e. those at
greatest risk of increased mortality, pulmonary hemorrhage, chronic lung disease, peri/
intraventricular haemorrhage and NEC.
Contraindications to ibuprofen:
• Renal failure – urine output <0.5-1.0ml/kg/hr. or creatinine >1.5 mg/dl and rising
• Severe thrombocytopenia (platelet count <40000/cumm) – transfuse platelets prior to
starting Ibuprofen or before next dose
Severe hyperbilirubinaemia (i.e. serum bilirubin at exchange transfusion level)
Evolving IVH
Dose: 3 IV doses 24 hours apart
1st dose 10mg/kg
2nd dose 5mg/kg
3rd dose 5mg/kg
Monitor urine output and document average 6 hourly. Check electrolytes, urea and creatinine and
CBC once daily (or more frequently if indicated) during ibuprofen treatment.
If signs of PDA persist after 1st course of ibuprofen, repeat echocardiogram and consider a second
course of ibuprofen.
If signs of PDA persist after 2nd course of ibuprofen or if there are contraindications to treatment
with ibuprofen, consider surgical ligation.
Alternatively Paracetamol can be used as iv prep. See “Neonatal drugs” for dosages.
2. Paracetamol (IV preparation is available)
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Evidences regarding efficacy of paracetamol is emerging. Consider if there is GI bleed precluding
use of oral ibuprofen
Surgical ligation:
• Ensure echocardiogram has been done and discuss clinical details and echocardiogram findings
with Paediatrics Cardiology team
Prior to surgery:
- Maintain Hgb >12g/dL
- Check platelet count and clotting times are within normal limits
- Cross match 1 Pediatric unit of packed red blood cells 24 hours before
- Check written parental consent has been obtained (to be done by Cardiothoracic Surgery team)
- If possible, insert peripheral arterial line and check blood gas immediately prior to transfer to
operating theatre
• Post-operatively
- Check ventilation and (arterial) blood gas, CBC, serum electrolytes, urea and creatinine and CXR
immediately after return from operating theatre
- Respiratory function frequently worsens immediately post-operatively and it is likely that
increased
ventilatory pressures will be required (Post PDA ligation syndrome)
- Ensure adequate analgesia – regime needs to be individualized but IVI morphine at 10mg/kg/hour
is suggested for the 1st 12-24 hours post-operatively
- Monitor urine output 6 hourly and fluid restrict as appropriate total fluids usually 80-100mL/kg/24
hours for 24-48 hours post-op)
- A post-operative echocardiogram should be done by the Pediatric cardiology team routinely,
usually
within 24 hours of the operation
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PULMONARY HYPERTENSION – MANAGEMENT (SIPHON protocol)
Diagnosis
a. Oxygen requirement (any amount) - essential
b. Arterial blood gas – Calculate Oxygenation index – OI >15 - Desirable
c. ECHO – (any two)
RVSP>40mmHg,
RVSP/Syst.pressure - >0.5
Bidirectional flow /Rt-lt shunt (clinically pre and post ductal saturation difference of >10%)
Ventricular septal flattening
Management
Start inotropes,
Sedation
Soda Bicarbonate infusion if PH<7.2
Inotropes *Target MBP to be maintained RVSP +5
Dopamine – 10 mics to be started for all babies
If BP low
Dopamine to be increased by 2 every 20 mins to max 20 mics
If BP low
Adrenaline infusion 0.1mics/kg
If BP low
Adrenaline to be increased by 0.1 every 20 mins to max 1 mic
**Dobutamine to be added to the inotrope if Fractional excretion<25%
***Inotrope is weaned off in reverse order if BP maintained
Sedation:
Morphine infusion 100mics stat followed by 10 mics/kg
If not sedated
To increase by 2 mics to maximum of 15 mics/kg
If not sedated
Midazolam infusion 0.1 mics/kg
If not sedated
Increase by 0.1 mics every 20 mins to max – 0.5 mics
Muscle relaxant
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Ventilation Strategies:
Mode: SIMV-PS+PC Target Spo2 – 94 – 98%
Weaning: To be done in the same order – Every 30 mins
Once baby stable
To reduce Fio2 by 0.5
To reduce Fio2 by 0.5
To reduce mean pressure by 2
To reduce RR by 5
Sildenafil infusion should be considered if the consultant orders at any stage of management
Dose: 0.7mg/kg loading followed by 0.04mg/kg/min infusion
ECHO should preferably do q 12 hourly
90
PULMONARY HAEMORRHAGE
This usually occurs due to increased pulmonary blood flow or pulmonary venous congestion.
Diagnosis
• Clinical signs
- Massive pulmonary haemorrhage (MPH), which is usually a result of haemorrhagic pulmonary
oedema, should be distinguished from minor bleeding due to local trauma. MPH is usually
associated
with an acute deterioration in the baby’s condition, often requires extensive resuscitation and is
associated with high mortality
- Clinical signs of PDA are often present
• CXR
- Usually shows bilateral uniform opacification (often ‘white out’)
Management
1. Following rapid initial assessment start ABC of resuscitation as required. Vigorous airway
/ET tube suction with a wide-bore suction catheter is likely to be necessary
2. Intubate and commence positive pressure ventilation if baby not already ventilated
3. Use relatively high PEEP (i.e. 6-8cmH2O)
4. Adjust PIP so that chest wall has adequate movement and according to subsequent CXR and
(arterial)
blood gases
5. Consider HFO if oxygenation problematic
6. Insert an arterial line if not already in place. Adjust ventilation according to frequent (1-2
hourly initially) arterial blood gases
7. Check CBC and coagulation profile. Correct any abnormalities. Maintain Hgb >12g/dL
8. Send blood for culture and start broad spectrum IV antibiotics according to antibiotic
protocol
9. Once the acute haemorrhage has stopped, give surfactant if FiO2 has increased
significantly (i.e. >0.1)
following the pulmonary haemorrhage or if new changes suggesting surfactant deficiency are seen
on the
CXR
10. Likely to need initial fluid resuscitation with blood or FFP
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11. Later may need restriction of fluids if there are signs of fluid overload, congestive cardiac
failure or PDA.
12. Consider IV furosemide 1-2mg/kg BD if there are signs of fluid overload, congestive cardiac
failure
13. Perform ECHO for diagnosis of PDA
14. Start IV Paracetamol as soon as possible if there are signs of PDA and there are no
contraindications to treatment
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RESPIRATORY DISTRESS - INITIAL MANAGEMENT
1. ABC resuscitation (follow NRP guidelines)
2. Review history - Gestation, PROM, type of delivery, meconium stained liquor, maternal diabetes
3. Examine baby - Well/unwell, pink/pale/cyanosed, perfusion.
4. Start Pulse oximeter saturation monitoring – Maintain sats. 90 -94% if <34 weeks’ gestation.
Maintain sats > 95% if MAS or PPHN
5. BP – Non - invasive blood pressure (Invasive monitoring may be needed in very sick neonates –
check with staff consultant before embarking on invasive blood pressure monitoring)
6. Temperature – Axillary temperature is generally preferred. In case of suspected sepsis or shocked
baby consider rectal temperature
4. Establish IV access – one peripheral IV for all babies. In case of sick babies consider two IV access.
If baby is < 30 weeks’ gestation, consider UVC at this stage if clinically appropriate.
5. Blood tests – CBC, CRP, Blood culture and Blood sugar. Additionally, consider urea, creatinine,
electrolytes, Bilirubin and Calcium as needed.
6. Blood gas- needs to be done for babies needing respiratory support needing oxygen of >30%.
Preferably arterial blood gas. If peripheral perfusion is good Capillary gas can be done.
7. Start IV fluids (See Fluid guidelines)
8. Start IV antibiotics – First line of antibiotics is Ciprofloxacin and Gentamicin.
9. CXR – Get CXR if Chest retractions is significant, oxygen requirement is > 30%, if no improvement
in respiratory condition after 4 hours of CPAP.
10. Respiratory support
Guided by clinical state, oxygen requirement and blood gases.
A) Nasal cannula O2 - if baby is > 30 weeks or > 1 Kg
(i) looks comfortable, (ii) FiO2 < 0.3, (iii) Blood gas normal (pH>7.25, PCO2<55 Torr).
B) CPAP – consider for any of the following:
(i) > 28 weeks, > 750 g, (ii) Baby looks well, (iii) FiO2 < 0.4, (iv) PH>7.20, PCO2< 65 Torr
C) Positive pressure ventilation – consider for any of the following :
(i) No improvement on CPAP, (ii) < 28 weeks, < 750 g, (iii) Baby unwell, marked recession
(iv) FiO2 > 0.4 in preterm or > 0.5 in term infants
(v) pH<7.20, PCO2> 65 Torr
11. Surfactant - see Surfactant guidelines.
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RESUSCITATION
Equipment needed for resuscitation:
1. Radiant warmer
2. Warm towel and blankets
3. Resuscitation bag and mask:
❍ Self-inflating bags with reservoir
❍ The resuscitation mask should comfortably cover the mouth and nose whilst sitting on
top of the chin. Circular silicone masks result in less air-leak and are easier to clean
4. Endotracheal tube Size 2.5, 3.0, 3.5 and 4.0
5. Laryngoscope with blades 00,0,1
6. Stethoscope
7. Oxygen source and tubing
8. Suction source, tubing and size 6/8/10 FG Y-suction catheters and ‘meconium aspirators’.
When to do:
1. Any Neonate > 26 wks. have to be
resuscitated, complications involved to be counselled to parents in detail.
2. Babies born between 25 to 26 weeks’ gestation should be resuscitated unless parents’ object for
resuscitation.
3. Babies born between 23 to 25 weeks’ gestation should be resuscitated only after discussion with
the parents about the prognosis and financial implications involved in the care.
4. Any neonate having trouble to initiate or sustain breathing
5. Any neonate with the heart rate of less than 100/min
6. Any neonate who is either very pale or grossly cyanosed (barring acral cyanosis)
Cessation of cardiopulmonary resuscitation:
Call responsible staff consultant
The decision to cease cardiopulmonary resuscitation should be based on cause of arrest response
to resuscitation, and remediable factors.
Death or severe neurological abnormality is predicted by a failure to obtain a heart rate by 10
minutes (Apgar score 0 at 10’) despite adequate resuscitation and failure to respond to adrenaline.
Newborn infants who do not require resuscitation can generally be identified by a rapid assessment
of the following 3 characteristics: (See NRP flow chart)
94
• Term gestation?
• Crying or breathing?
• Good muscle tone?
If the answer to all 3 of these questions is yes, the baby does not need resuscitation and should not
be separated from the mother. The baby should be dried, placed skin-to-skin with the mother, and
covered with dry linen to maintain temperature. Observation of breathing, activity, and colour
should be ongoing.
Dry and stimulate the infant after delivery. The Apgar score is used to document postnatal
adaptation at 1and 5 minutes (and at 10, 15 and 20 minutes if < 8 at 5 minutes). It includes: Heart
rate, respiratory efforts, tone, reflex irritability and colour, which guide resuscitation.
Assessment of heart rate should be done by intermittently auscultating the precordial pulse. When
a pulse is detectable, palpation of the umbilical pulse can also provide a rapid estimate of the pulse
and is more accurate than palpation at other sites.
Infants with low Apgar scores, or persisting cyanosis and/or bradycardia and/or irregular
respiratory effort should receive assistance.
b. Minimize heat loss:
Prevention of cooling reduces the mortality of low birth weight infants. Infants gain and lose heat
by 4 modalities: evaporation, radiation, convection and conduction. Steps taken in the delivery
room to prevent heat loss that have been shown to be
effective include
1. If resuscitation is not required - early skin to skin contact with mother under warm blankets in
term infants.
2. Dry the infant (and wrap in warm blankets when resuscitation completed)
3. Radiant heater
4. Polyethylene wrap for infants <1500g. Plastic covering when moving the resuscitaire.
Avoid overheating, particularly with infants wrapped in polyethylene under radiant heaters. Infant
temperature should be monitored carefully as soon as the infants is stabilized with initial
resuscitation. Hyperthermia has been associated with exacerbation of cerebral injury following
ischemic injury in animal studies; infants born to febrile mothers have been found to have an
increased risk of death, respiratory depression, seizures and cerebral palsy.
c. Suctioning of the airway:
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Suctioning of the upper airways should be restricted to who have obvious obstruction to
spontaneous breathing. Meconium stained liquor: Suctioning as the head delivers when meconium
is present is no longer routinely recommended. However, if thick meconium appears to be in the
mouth causing obstruction, it should be suctioned out.
Suctioning below the cords when thick meconium is in the liquor:
In the absence of randomized, controlled trials, there is insufficient evidence to recommend a
change in the current practice of performing endotracheal suctioning of non-vigorous babies with
meconium-stained amniotic fluid. However, if attempted intubation is prolonged and unsuccessful,
bag-mask ventilation should be considered, particularly if there is persistent bradycardia.
If the baby is vigorous and breathing established, do not attempt to suction below the cords as
there is evidence that this does not reduce the incidence or severity of meconium aspiration and
may do harm.
d. Assisted ventilation:
Effective ventilation is the most important part of neonatal resuscitation in an infant that has not
established regular breathing and good heart rate following initial drying and stimulation.
Start with t-piece or Bag and mask intermittent positive pressure ventilation (IPPV):
The mask should cover the mouth and nose, but not be as high as the eyes and it should sit below
the mouth on the chin. There should be a good seal. The head position should be neutral or sniffing
(not overly extending the neck), with jaw thrust if needed to help open the airway.
Ventilate at 30 - 60 breaths per minute PIP 20 cmH2O PEEP 5cmH2O. (during BMV, PIP and PEEP
cannot be set) – look for the chest raise
If heart rate and colour do not improve with mask IPPV, check that the airway is adequate
(appropriate head position) and the seal of the mask is good, and that the chest is moving higher
inflation pressures may be needed. If mask IPPV is not producing a response, intubation could be
attempted. Call for assistance.
Oxygen use with ventilation (IPPV and mask or via endotracheal tube):
Oximetry should be used when resuscitation can be anticipated, when positive pressure is
administered for more than a few breaths, when cyanosis is persistent, or when supplementary
oxygen is administered. Place a pulse oximeter on the right arm/hand (preductal SpO2). Applying
the sensor to the infant before connecting it to the cable yields the fastest acquisition of accurate
HR data.
96
Preductal targeting of SpO2 should approximate physiological levels see targeted preductal SpO2
after birth
For term and late term infants (34-36 weeks): Start in air and adjust clinically as needed increasing
after 30 seconds if there is a poor response, and decreasing as able as colour/oxygen saturations
improve.
For very preterm infants (<32 weeks): Start in 30 - 40% FiO2 and adjust clinically as needed
increasing after 30 seconds if there is a poor response, and decreasing as able as colour/oxygen
saturations improve.
Titrating from an initial oxygen concentration of 100% was more effective than giving a static
concentration of 100% oxygen in maintaining preterm infants in a target oxygen saturation range.
e. Tracheal intubation:
Indications for endotracheal tube intubation include:
i. Tracheal suctioning for meconium if infant born through thick meconium and non-vigorous (no
respiratory effort)
ii.Failure to provide adequate ventilation using a bag and mask despite adequate attempts at
obtaining an airway
iii. Respiratory distress likely to require continued ventilatory support
iv. Congenital abnormalities as indicated (e.g. diaphragmatic hernias)
Tube placement should always be checked clinically (Air entry and chest raise)
Once stabilized a chest x-ray should be done to check placement as well as for condition of the
lungs, air leaks etc.
Checking position of the ETT:
i. Ensure you see the ETT going through the cords; insert to 2cm (slightly less in infants <750g)
which is the end black mark (2cm).
ii. Listen for air entry in each side of the chest; if the tube is too far down (usually it would be down
the right main bronchus) there will be decreased breath sounds on the unventilated side (usually
the left) withdraw the ETT until breath sounds are equal. No single technique is without limitations
and clinicians should utilize a combination.
iii. Adequate chest raise
iv. Misting of the ET tube (Not very reliable)
iv. If there is doubt as to whether it is in the trachea despite the measures above, look again with a
laryngoscope to see if the tube is through the cords.
97
f. Combined external cardiac compression and assisted ventilation:
Check for pulse: either by auscultation, palpating umbilical arteries or apex beat.
Perform cardiac massage: If initial heart rate after initiation of ventilation is < 60-bpm4 or remains
60-80 bpm after initiation of adequate ventilation.
Chest compression:
Compressing the lower half of sternum either by:
Encircle the chest with both hands and use 2 thumbs preferred method; or by:
Using 2 fingers over the lower sternum. The 2-finger technique may be preferable when access to
the umbilicus is required during insertion of an umbilical catheter.
Avoid the chest margins and xiphisternum and do not restrict chest re-expansion.
Compress the chest 1/3rd of its depth4
Provide chest compression in combination with ventilation. There should be at least 90
compressions and 30 breaths per minute, with a ratio of 3 compressions with 1 breath (i.e. 3:1
ratio: c-c-c-v-c-c-c-v-c-c-c-v).
g. Assess the response:
Reassess the response to ventilation every 30-60 seconds
Continue to ventilate until there is an adequate response crying or adequate sustained
spontaneous breathing and heart rate > 100 bpm
With infants receiving coordinated chest compressions and ventilations, Respirations, heart rate,
and oxygenation should be reassessed periodically, and coordinated chest compressions and
ventilations should continue until the spontaneous heart rate is 60 per minute.
Frequent interruptions of compressions should be avoided, as they will compromise artificial
maintenance of systemic perfusion and maintenance of coronary blood flow.
h. Failure to respond to resuscitation:
If there is an initial heart beat this is usually due to inadequate ventilation
If bag and mask ventilation: ensure an adequate airway (chin lift and slight head tilt)
Failure to respond to bag and mask ventilation is an indication for intubation.
If endotracheal tube: usually a misplaced endotracheal tube (i.e. esophageal). See Checking
position of the ETT.
If the above have been checked and optimized and there is inadequate response, then there may
be blocked endotracheal tube, blocked airway or severe lung disease. Change tube under suction.
Preterm infants with surfactant deficiency may respond to surfactant treatment.
98
Deterioration after initial response to resuscitation may indicate a misplaced endotracheal tube or
air leak. Consider the possibility of anatomical anomalies or pleural effusions (suggested by
antenatal findings).
If none of the above, then increase ventilatory effort and follow Newborn Resuscitation Algorithm
Call for assistance
i. Vascular access:
Use umbilical vein where possible,
Alternative routes include: peripheral vein (eg scalp vein), femoral vein, or endotracheal (ETT)
routes for adrenaline.
The umbilical artery and subclavian veins should be avoided where possible due to the potential
complications of these routes.
j. Drugs in resuscitation:
1. Adrenaline:
The recommended IV dose is 0.01 to 0.03 mg/kg per dose. If the endotracheal route is used, doses
of 0.01 or 0.03 mg/kg will likely be ineffective. Therefore, IV administration of 0.01 to 0.03 mg/kg
per dose is the preferred route. While access is being obtained, administration of a higher dose
(0.05 to 0.1 mg/kg) through the endotracheal tube may be considered, but the safety and efficacy
of this practice have not been evaluated.
Dosage regimen used at JSS:
1. Adrenaline 0.03 mg/kg intravenously via UVC = 0.3 ml/kg of 1:10000 Adrenaline, or
2. If unable to obtain rapid venous access give: adrenaline 0.1 mg/kg via ETT = 1 ml/kg of 1:10000
Adrenaline.
Repeat dose once if no response after 60 seconds.
2. Naloxone:
This should only be considered in infants who are depressed by opiates once an infant has first
been stabilized with ventilatory support, and has good heart rate and colour.
DO NOT give Naloxone to infants of narcotic dependent mothers. It can precipitate acute
withdrawal.
Opiates given to the mother in Labor (within 4 hours of delivery), can affect the infants drive to
breathe at the time of delivery, and possibly in the first few hours of life. If a mother has received
Pethidine, the infant needs close observation for at least the first 4 hours of life Dose: Naloxone 100
99
μg/kg via intravenous or intramuscular injection (preferred)49. For term or near-term infants, if
weight is not known, then give 0.5ml of Naloxone 400μg/ml (ie 200μg).
Naloxone is quick acting and should work within a couple of minutes of giving it. Effect after giving
this IM is only slightly delayed compared with IV.
3. Bicarbonate:
Bicarbonate should be restricted to post-resuscitation correction of acidosis. Obtain an early blood
gas after resuscitation.
If there is a significant metabolic acidosis the dose is: 4.2% NaHCO3 ml = 0.3 x weight kg x BE given
over 30-60 minutes.
4. Volume replacement in resuscitation:
Hypovolemia is difficult to diagnose in the neonate. Volume expansion should be considered when
blood loss is known or suspected (pale skin, poor perfusion and weak pulse) and the baby’s heart
rate has not responded adequately to other resuscitative measures. An isotonic crystalloid solution
or blood is recommended for volume expansion in the delivery room.
k. Cord Blood Sampling:
A cord gas should be taken for every baby who requires resuscitation. Take blood from an umbilical
artery. There are two umbilical arteries that are smaller, muscular and blue (compared with one
larger purple coloured umbilical vein). Sample from the placental surface if necessary (arteries go
over the veins). An umbilical venous-arterial pH difference of 0.15 is an effective cutoff value in
differentiating cord prolapse from abruptio placentae (accuracy 92%).
Normal values for cord gases:
Umbilical artery:
pH: 7.24 ± 0.07 [range 7.37 7.10]
BE: -5.0 ± 3.0 mmHg [range +0.3 to -11.5]
Umbilical Vein:
pH: 7.32 ± 0.06 [range 7.43 7.20]
BE: -4.5 ± 2.4 mmHg [range +0.2 to -9.2]
Measures of hypoxia
- pH <7.0 (important for diagnosis of HIE)
- pH <7.10 (2SD below mean)
Sample before 60 minutes (Preferably before 30 mins or soon) from a clamped cord
100
A blood gas is stable in syringe for 30 minutes. With delayed sampling placental pH values fall at
twice the rate as umbilical pH values.
l. Management after resuscitation (see asphyxia):
Seek the cause of the arrest and treat specifically.
Complications of the resuscitation procedure should be sought, including air leaks (pneumothorax,
Pneumomediastinum or Pneumopericardium), esophageal injury and blood loss from organ
damage (e.g. liver).
Obtain cord arterial and venous blood gas analysis (may be obtained from placental vessels -
arteries cross veins). Perform Apgar at 1 and 5 mins and every 5 mins until Apgar > 7.
Document time to sustained spontaneous respiration.
Obtain early arterial blood gas and CBG. Correct persisting acidosis and hypoglycemia.
Respiratory support: continue ventilation till adequate sustained spontaneous respiration and
without severe respiratory distress. Ventilate to ensure adequate oxygenation and normocarbia.
Monitor vital organ function: cardiac dysfunction as determined by hypotension or poor cardiac
output (ECHO); renal dysfunction (oliguria < 0.5 ml/kg/hour or creatinine 1.2 mg/dl); hepatic
dysfunction (abnormal LFTs); and cerebral dysfunction (hypoxic ischemic encephalopathy).
Avoid running high fluid rates in asphyxiated infants, as fluid retention may occur resulting in
hyponatraemia.
101
RETINOPATHY OF PREMATURITY SCREENING IN NICU
Who should be screened?
All premature babies born before 34 weeks of gestation
All low birth weight babies who weigh less than 2 kgs at birth
• Congenital infection (TORCH).
• Congenital abnormalities of the eye or face.
• Disease associated with eye problems, e.g. Sturge-Weber, candida septicemia.
Concern about vision.
When to screen?
For premature babies:
Babies born earlier to 30 weeks will have their screening at 32 wks. PMA
Babies born between 30 and 34 weeks’ gestation will have their screening at 2 weeks of postnatal
age
Subsequent screening is done as per the ophthalmologist’s advice.
For LBW babies:
For babies with birth weight less than 2 Kgs and gestation > 34 weeks screening is done as soon as
the clinical condition is stable and is baby is more than one week of age.
Subsequent screening is done as per the ophthalmologist’s advice.
When to stop screening?
If there is no ROP, stop screening after 40 weeks post menstrual age
If ROP is detected, screening is to be continued till ROP is resolved or completely treated.
Who will screen for ROP?
Designated ophthalmologist will screen for ROP
When will be the screening done in the unit?
------ Day of every week, screening is done at bedside in NICU.
How does the ophthalmologist know which baby is to be screened?
During the rounds, the concerned Neonatal staff will notify the babies who need ROP screening. A
marker will be displayed at the bedside for the ophthalmologist to recognize the baby needing ROP
screening.
How to prepare the baby for ROP screening?
Concerned nurses have to administer the prescribed drops at prescribed time for preparation.
Where is the screening report documented?
102
There is a specific ROP form which needs to be filled in by ophthalmologist after screening. (The
format of the form needs to be decided after talking to the opthalmology team.)
Who will communicate to the patient about the ROP status?
Ophthalmologists after screening procedure will talk to the parents about ROP status.
What about the treatment of ROP?
Ophthalmologist will decide about the nature of the treatment dependent on their finding. They
will institute the treatment at the earliest convenient time in the neonatal unit
103
SURFACTANT
Composition of surfactant
Lipid (mostly phospholipids – 90%)
Protein (surfactant proteins A, B and C – 10%)
Préparations avalable
Natural surfactants – Neosurf and Survanta
Prophylactic - Elective intubation at birth with the administration of surfactant in the first 30
minutes of life
Before clinical or radiological confirmation of RDS. – Consider only in extreme premature births
such as gestation of < 28 weeks. This needs to be decided by the responsible staff consultant.
Surfactant.
Early Rescue - Surfactant administered to ventilated infants with clinical and radiological signs of
RDS. Consider this option if the parents can easily afford surfactant
Late Recuse – Surfactant administered for babies who fail to stabilize on CPAP with a SOPI of > 1.6
for more than an hour and does not show the trend to drop.
Administration of surfactant
Note!!
Please confirm the position of endotracheal tube before embarking on surfactant administration
1. Discuss need for surfactant with Consultant before use. Senior postgraduate needs to be present
during administration of surfactant and for at least 30 mins after administering surfactant.
2. Dose of surfactant is 100 – 200 mg/Kg. if using Neosurf give 5 ml/Kg and Survanta give 4 ml/Kg
3. Remove the vial of Surfactant from the fridge and check the Expiry date
4. Warm the vial to ambient temperature by holding in the hand for a few minutes, and gently turn
upside Down, without shaking in order to obtain a uniform suspension
5. Arrange following items - Nasogastric tube (size 6F), sterile 18F needle and appropriate size
syringe, Scissors or stitch cutter, Alcohol swabs, Tape measure and Sterile gloves
6. Prepare the vial by inverting gently a few times, without shaking, to obtain a uniform suspension.
Remove outer cap and sterilize inner cap by wiping with an alcohol swab
7. Cut the nasogastric tube to the correct length – i.e. 1cm shorter than the length of the ET tube
(including ET tube connecter etc.)
104
8. Attach the syringe to the nasogastric tube. To avoid contamination, remember to handle the
tube with a sterile glove. Push the surfactant to the end of the nasogastric tube ready for
administration
9. Monitor oxygenation during and after surfactant administration using saturation monitor
10. Oxygenate well before commencing surfactant administration (consider appropriate pressures
and fiO2 to keep the saturation > 95%)
11. Disconnect from ventilator and insert NGT into ET tube and inject surfactant down ET tube.
Injection should be done in 3 to 4 aliquots. Do not rapidly push surfactant! Bagging is needed in
between injection of aliquots. Changing the position of the baby during surfactant administration is
not practiced in our unit.
Once all surfactant has been administered, remove syringe and NG tube from ET tube.
12. Reconnect to ventilator, adjust PIP and FiO2 to ensure adequate chest inflation and
oxygenation.
13. Avoid suction for 4 hours
Note!!
Lung mechanics may change very rapidly (within minutes) and necessitate rapid adjustments of
ventilator Settings, therefore observe baby carefully for 10-20 minutes after administration
14. Repeat blood gas after 30 minutes.
2nd and subsequent surfactant doses may be needed in some babies. This should always be
discussed with a consultant. In general, a second dose should be considered ~12 hours after the 1st
in babies <30 weeks’ gestation, with FiO2 >0.3, despite adequate ventilator pressures. If a baby has
high or increasing ventilator requirements <12 hours after the 1st dose, consider giving the 2nd
dose earlier, but exclude other important causes of worsening respiratory function prior to this (e.g.
blocked or dislodged ET tube or Pneumothorax etc.)
Other indications for Surfactant
Surfactant is destroyed by FFA in meconium and also by certain proteins.Therefore, in the following
conditions, if high ventilatory requirements persist, surfactant may be helpful:
• Meconium aspiration syndrome
• Congenital pneumonia
• Pulmonary hemorrhage (when active hemorrhage subsided)
• ARDS
• Congenital diaphragmatic hernia
105
TRACHEO OESOPHAGEAL FISTULA (OESOPHAGEAL ATRESIA)
Presentation
1. Antenatal - polyhydramnios +/- absent stomach bubble
2. Postnatal
- difficulty placing NG tube during initial resuscitation / assessment (x-ray if in
doubt)
- Excessive oral / upper airway secretions ("frothy")
- Choking or cyanosis following feeds
- Recurrent pneumonia/ aspiration
Associated anomalies
3. VACTERL association(vertebral / anorectal /cardiac / tracheo-esophageal / renal / limb) -
~30-50% of babies
with esophageal atresia & TOF have this
4. CHARGE association (coloboma / heart / atresia choanae / restricted growth / genital
hypoplasia / ear)
duodenal atresia (“double bubble” only seen if TOF present with esophageal atresia)
5. diaphragmatic hernia
6. more common in karyotype abnormalities (trisomy 21 & 18, 22q deletion)
Diagnosis
1. Oesophageal atresia
- chest & AXR with NG or Replogle tube in situ
- ~85% have a blind ending proximal oesophageal
pouch with a distal TOF
~10% have no TOF
~5% have a TOF connected to the proximal
esophageal pouch +/- a distal TOF
2. TOF
isolated TOF (H-type) much rarer than with oesophageal atresia
Waterstone’s test - pass NG tube into the stomach and place free end under water slowly pull tube
back and if fistula is present you may see bubbles appearing
Tube oesophogram – NG tube is inserted and
withdrawn under x-ray screening whilst
106
simultaneously injecting water-soluble contrast
medium. If fistula is present contrast will be seen
to leak over into airways and lungs. (This
procedure is not always well tolerated and a doctor
should accompany the baby to the department with
resuscitation equipment).
Management
- after a thorough initial clinical examination, request karyotype (even if no other dysmorphic
features), echocardiogram, renal and cranial u/s scan and AP X-ray of whole spine in all babies with
esophageal atresia +/- TOF. Request an ophthalmological opinion if CHARGE suspected.
Oesophageal atresia
attempt to place a NG tube on first suspicion, then when diagnosis confirmed place a Replogle tube
(10F – smaller in VLBW baby) with suction sufficient to constantly drain pouch. Tube must be
placed as far as possible and kept in that position. Flush with 0.9% saline
Head end elevation and NBM / IV fluids or TPN
surgical management (not an emergency can wait for working hours) contrast study in theatre to
determine length of atretic segment attempt to rejoin esophagus
if primary closure not possible then gastrostomy feeding tube inserted with plan to wait for 6-8
weeks to allow growth
if segment very long then occasionally an esophagostomy is formed to allow drainage of saliva and
sham feeding
For closure of long gaps various procedures are used including prosthetic grafts and tubes
fashioned either from stomach or bowel
TOF: surgical closure required via thoracotomy approach
NBM until fistula closed to prevent aspiration
Gastro-esophageal reflux is very common
Esophageal dysmotility may lead to swallowing and feeding problems
Feeding problems due to oral aversion secondary to long term Replogle tube use. Refer to Speech
Therapist.
Strictures of anastomosis site may occur and later
esophageal dilatation may be necessary
- Tracheomalacia causing the characteristic chronic "TOF cough"
107

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Hand book of clinical

ix. Hypoglycemia despite adequate feeding (See Hypoglycemia protocol)

Babies >1 month - weighing < 5 Kg (non - transmissible infection)

Presentation (usually from 24hrs)

• Usually noted at routine 1st examination

2. If the limb is warm, normal colour but pulses are weak:

3. If the limb is cool, or colour pale or pulses absent:

Hemorrhagic disease of newborn is seen in otherwise normal neonates

 Hemodynamic effects associated with a loss of intravascular volume

Once stabilized, a detailed Family history of bleeding disorder should be obtained.

Management should initially be directed replacement of intravascular volume. in addition to

BABIES BORN TO HEPATITIS B POSITIVE MOTHERS.

Low risk mother

BABIES BORN TO HIV POSITIVE MOTHERS

• Specific treponemal antibodies eg TPHA, TPPA, EIA

• 40% symptomatic (mild → fatal) often with multiorgan involvement :–

- Neonatal titres often x1-2 dilutions ↓ than maternal in uninfected babies

- baby asymptomatic and mother adequately Rxed (titres ↓x4 in 6/12)

• If treated, check treponemal antibodies at 15/12

interstitial keratitis (and ? also in CNS). Refer to Paediatric Ophthalmologist.

• Infection from genital tract rare and usually → abortion or SB

Weaning and extubation from Conventional mechanical ventilation

• Coronal view through 3rd ventricle

Rest of the handing over procedure according to hospital policy

Post-operative establishment of enteral feeds - see under gastroschisis.

Healthy full-term infant (No symptoms)

1. Low birth weight infants (<2000 grams)

Screening for hypoglycaemia is not recommended in term healthy breast-fed appropriate-for-

If repeat Cap bld sug is >45 mg/dL,

If repeat blood sugar is <45 mg/dl

 IV dextrose start at GIR of 6mg/kg/min

All symptomatic infants should be treated with IV fluids.

 IV dextrose start at GIR of 6mg/kg/min

Investigations to be done in resistant hypoglycemia

 Serum insulin levels

If suspecting inborn error of metabolism (discuss with consultant before sending)

 Hydrocortisone 5 mg/kg/day IV or PO in two divided doses for 24 to 48 hrs

(a) GIR(mg/kg/min) = % of dextrose being infused x rate (mL/hr)

(b) Infusion rate (mg/kg/min) = IV rate (mL/kg/day) x % of dextrose) / 144

Infusion rate(mg/kg/min) = Fluid rate (mL/kg/day) x 0.007 x % of dextrose infused

• Majority of PIVH is clinically silent

Acute management of PIVH

• Maintain normal physiological parameters (blood gases, BP, clotting etc.)

Hydrocephalus Grade Location of blood Immediate symptoms Outcome

 Use sterile, warm water for removal of maternal bodily fluids

 All infants with BW <1500g and/or <32 weeks’ gestation.

When should cranial ultrasound be completed?

Parenteral Nutrition (PN)

Day 1 1.5 g/kg/day 1 g/kg/day

Day 2 2.5 g/kg/day advance by 0.5 g/kg/day

g/kg/day-do not exceed 2.5 g/kg/day

Maximize protein to 3-3.8

Enteral nutrition – See LBW feeding guideline

- GI symptoms/signs (mild Abdominal distension, poor feeding, vomiting, increased gastric

- Systemic signs (temperature instability, lethargy, apnea)

- persistent occult or frank GI bleeding, marked Abdominal distension

- shock, severe sepsis or gross GI bleeding

Stage 1 – mild Stage 2 – moderate Stage 3 – severe

Conscious level hyper alert lethargic comatose

Muscle tone minor disturbances more disturbed reduced

Feeding slight difficulties poor absent suck

seizures no yes yes

Able to maintain vital yes yes no

• Treat another organ failure as appropriate