Frequently Asked Questions in Pediatric & Adolescent Practice A Parthasarathy, Dhanya Dharmapalan, Alok Gupta, Anupama S Borker
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NewbornCHAPTER 1

Contributors: Rhishikesh Thakre,
Naveen Jain
Reviewer: Alok Gupta
  • 1. Rapid Newborn Assessment
  • 2. Care of the Normal Newborn
  • 3. Antenatal Steroids
  • 4. Common Congenital Anomalies
  • 5. Basics of Inborn Error of Metabolism
  • 6. Breastfeeding
  • 7. Kangaroo Care
  • 8. Newborn Vaccination
  • 9. Approach to Respiratory Distress
  • 10. Neonatal Infections
  • 11. Neonatal Jaundice
  • 12. Chickenpox Infection
  • 13. Neonatal Hypoglycemia
  • 14. Oxygen Therapy
  • 15. Low Birth Weight Feeding and Supplements
  • 16. Shock2
Q1. How to categorize a newborn on first evaluation?
Quickly assess consciousness (alert, drowsy, nonresponsive), breathing (rate and work of breathing, audible sounds) and color (pink or pallor, plethora, icterus, cyanosis) to identify the newborn as stable or unstable. If stable, assess history and perform head to toe evaluation. If unstable, identify life threatening event (non-responsive, apnea, jerky breathing and cyanosis) to initiate life saving measures. If unstable, but with no life threatening event, initiate stabilization measures or consider referral with focused history and physical examination.
Q2. How do you know the newborn is “well”?
A newborn is considered to be well if it is asymptomatic, has no risk factors on history (medical, familial, pregnancy, peripartum), is term, weight >2.5 kg, with stable vital parameters with no localization on physical examination.
Q3. How do you know the newborn is “at risk”?
A newborn is considered to be “at risk” even if it is asymptomatic and has no physical signs if one of the following is present:
  1. There are risk factors on history (medical, familial, pregnancy, peripartum)
  2. Is preterm (< 37 weeks gestation)
  3. Weight <2 kg
  4. Has abnormal lab results
Such “at risk” newborns may develop problems in due course of time if not supervised.
Q4. How do you know the newborn is “sick”?
A newborn is sick if it has unstable vital parameters, loss of sleep, activity or feeding over 6 hours, or abnormal movements.
Q5. What should you do for a “well” newborn?
A well newborn parent needs response to their concerns, assurance, emphasis on breastfeeding, thermal and hygiene care, vaccination, information on when to report and periodic follow-up.
Q6. What should you do for a “at risk” newborn?
All “at risk” newborns need careful monitoring, anticipation of problems, investigation of suspicious findings and timely treatment. They should not be discharged but be under supervision, evaluated every 4–6 hours to detect early signs of problems if any.
Q7. What should you do for a “sick” newborn?
All sick newborns need urgent referral based on scope of practice, stabilization, continuous monitoring, aggressive supportive care 3(temperature, sugar, oxygen, perfusion assessment and support) and re-evaluation. Based on the likely cause specific investigations are done and specific therapy initiated.
Q8. How do you identify “why” the newborn is sick?
Initiation of supportive treatment is half the job done. To define the cause of the problem one needs to assess the history, perform focused examination and relevant investigations. For example, with significant jaundice starting phototherapy is not enough. The cause of jaundice needs to be identified based on history, examination and lab tests.
Q9. How should you prioritize your management?
Any life threatening event needs initiation of resuscitation. Priority should be to assess, support and maintain temperature, airway, breathing, circulation and dextrose (TABCD). Ensuring temperature, oxygenation, perfusion and sugar (TOPS) is a priority.
Q10. How do you interpret vital signs and what should you observe?
Temperature should be maintained between 36.5 and 37°C, RR should be 40–60 per minute, HR 120–160 per minute, BP 60/40 with spO2 > 89% in room air. Trend in vital parameters is more important. Any change of 10 per minute in baseline heart rate or respiration is abnormal. Fall in BP 10 mm Hg from baseline is abnormal. Urine output should be monitored in all sick newborns and should be > 1 cc/kg/hour.
  1. Singh M. Care of the Newborn, 5th edition. Sagar Publications;  New Delhi:  1999.
  1. Van den Bruel A, Haj-Hassan T, Thompson M, Buntinx F, Mant D, et al. Diagnostic value of clinical features at presentation to identify serious infection in children in developed countries: a systematic review. Lancet. 2010;375(9717):834-45.
Q11. Should suction be done routinely at the time of birth in newborn?
Oral suction is to be done only if there is an obstructed airway due to secretions or the newborn is requiring PPV. Routine suctioning is potentially damaging hence discouraged.
Q12. What is the role of pulse oximeter in the delivery room (DR)?
Pulse oximeter is recommended for assessment of minute specific oxygen saturation, babies requiring ventilation, titrating supplemental oxygen, and monitoring CPAP in the DR. Pulse 4oximeter working on a “signal extraction technique (SET)” that is designed to reduce movement artifact with a neonatal probe is ideal for delivery room resuscitation.
Q13. When should cord clamping be done in normal newborn?
Delayed cord clamping for more than 1 minute is a safe procedure in all newborns including preterm/LBW babies’ not requiring resuscitation at birth. There are apparently no negative effects. It offers major benefits with the reduction in blood transfusions and the incidence of IVH in preterm infants and improved iron status in infants up to six months after birth.
Q14. What should be routine cord care?
Keep the cord dry and clean. There is no role of local antibiotics or antiseptics to be applied routinely.
Q15. What minimum should be done routinely before the newborn leaves the delivery room?
Ensure normo-thermia and regular breathing. Assign sex. Weigh the baby. Look for external anomaly. Ensure anus is patent; there is no cleft of palate or frothing at mouth and no single umbilical artery. Administer vitamin K. Keep the baby skin to skin with mother and encourage breastfeeding.
Q16. Should vitamin K be given to all the newborns?
Newborn babies are at particular risk of vitamin K deficiency, as placental transfer is limited and human milk is a poor source. Vitamin K deficiency bleeding (VKDB) disorder is a preventable disorder with potential to cause neurologic sequelae if intracranial bleeding occurs. Vitamin K 1 mg IM should be given to all newborns.
Q17. What about baby wipes, diapers, soap, powder and shampoo?
Baby wipes contain preservatives, fragrances, or aloe that are potentially topically sensitizing. The use of wipes should be discontinued when the skin is broken open. The disposable diapers are also less likely to cause irritant diaper dermatitis relative to cloth diapers. When possible, the diaper should be changed immediately after urinating or defecating and can be as frequent as every hour in neonates. Tight-fitting diapers should be avoided. If possible, diaper-free time with exposure to air is needed to completely dry the affected areas. There is no added benefit of using soap, powder or shampoo except for increasing cost.
Q18. How to assess for thermal well-being?
The assessment for thermal well-being is made by observing the color of the sole and touching with dorsum of hand over abdomen and feet. A pink color is assuring while dusky hue warrants evaluation. In a baby with normal temperature both abdomen and feet are warm to touch. When feet are cold and abdomen is warm, it indicates that 5the baby is in cold stress. In hypothermia, both feet and abdomen are cold to touch.
Q19. What are simple measures to ensure temperature maintenance?
Postpone baby bath till cord falls. Keep the newborn close to the mother in a clean, dry and warm room. Dress the baby in adequate clothing (1–2 layers in summer and 3–4 layers in winter). Always cover the baby head with a cap/cloth. Provide skin-to-skin contact, as long as possible, day and night, by placing the baby on the mother's chest, between the breasts. Cover the baby and the mother with additional blanket or shawl in cold weather. Use gloves and socks as required. Warm the room with a room heater or use a 200 W bulb placed at a distance of 50 cm, as needed. Prevent air currents in the room.
Q20. How to know whether a warm baby has environment related elevation of temperature or due to underlying infection?
Table 1.1   Differentiating overheated and febrile infant
Overheated infant
Febrile infant
  1. Extended posture.
  2. Healthy appearance.
  3. Pink skin color.
  4. Warm hands and feet.
  5. High rectal temperature.
  6. Abdo – skin temperature difference < 2 °C.
  1. Flexed posture.
  2. Looks unwell.
  3. Pale skin.
  4. Cool hands and feet.
  5. High rectal temperature.
  6. Abdo – skin temperature Difference > 3 °C.
Q21. What should be done if the baby has fever?
If the baby appears warm, the baby is unclothe, efforts to lower the room temperature are taken (open the windows, turn on the fan), the baby kept away from sources of heat, direct sunlight and breastfeeding is ensured. Paracetamol is avoidable as it works only when there is reset of thermostatic mechanism. Both hypothermia and hyperthermia can be signs of sepsis and one should seek evaluation at earliest.
Q22. What should be done if baby appears cold?
If the baby appears cold, re-warming is done by skin-to-skin contact, covering and wrapping the baby, taking efforts to raise room temperature, providing warmth by a heater and offering additional breastfeed. Use of hot water bottle for re-warming the baby is avoided. One should evaluate for cause and rule out possibility of underlying infection.
Q23. What simple measure should be taken to keep baby infection free?
Clean hands, clean bed, clean room can prevent many infections in the baby and mother. Hand washing with soap is one of the most effective ways of preventing infection. Ensure clean clothes, blanket/6sheets for the baby and mother. Infant can be bathed once every few days. There should not be attempt to remove vernix from the body, as it can result in trauma to skin and increase chance of infections. Eyes of the infant must be cleaned with a clean swab soaked in normal saline or sterile water. The umbilical cord must be kept open and dry with no local applications. Keep nails clean and trimmed regularly of both—mother and baby.
Q24. How to identify a sick newborn?
The following danger signs must be explained to the mothers:
  • Difficulty in feeding
  • Convulsions
  • Lethargy (movement only when stimulated)
  • Fast breathing (respiratory rate of >60)
  • Severe chest in-drawing
  • Temperature of 37.5 degrees C or more or below 35.5 degrees.
    All such babies should be managed in hospital.
Q25. How to evaluate newborn with pustules?
All pustules need local cleaning. A baby with pustules (>10), needs local antiseptic and oral antibiotic (Fig. 1.1). Sick newborn with a pustule needs hospitalization.
zoom view
Fig. 1.1: Pustule
Q26. What nutritional supplements are given to newborn?
All preterm should receive drops of a multivitamin preparation, and iron (2 mg/kg/day) every day till at least for one year of age. In addition preterm should also receive calcium (100 mg/kg/day) and phosphorous (50 mg/kg/day) till 3 months. Term newborns need only vitamin D (400 IU till 1 year) and iron at 6 months age.
Q27. What minimum checkup is done for newborn evaluation in well OPD?
7Respond to parental queries. Plot the anthropometry on growth chart. Ensure adequacy for breastfeeding. Perform physical examination for “danger signs”. Confirm vaccination. Assurance to parents if the baby feeds well, sleeps well, is active and alert. Allot next date for follow-up.
Q28. Which growth charts should be followed?
For all term newborns, WHO (2005) growth charts for boys and girls for weight, height and head circumference should be followed. For preterms till they reach term equivalent age should be followed on Wright's chart or modified Fenton's chart.
Q29. Till what age is corrected age used for preterm?
Most centers continue to correct for prematurity till the age of 18 months to 24 months after that there is no correction for prematurity.
  1. Bhat BV. Neonatal care In: Parthasarthy A, Menon PS, Nair MK, Bhave SY (Eds). Partha's Fundamentals of Pediatrics, 1st edition. Jaypee Brothers Medical (P) Ltd;  New Delhi:  2007.pp.29-62.
  1. Lisa Stellwagen, Eyla Boies. Care of the well newborn. Pediatrics in Review 2006;27(3):89-98.
  1. Perlman JM, Wyllie J, Kattwinkel J, et al. Part 11:Neonatal resuscitation: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Circulation. 2010;122:S516-S38.
Q30. What is the status of maternal use of antenatal steroids?
Antenatal steroids is a simple, evidence based, low cost intervention to accelerate fetal lung maturation significantly reducing the incidence of respiratory distress syndrome in the neonate.
Q31. What is the benefit in giving antenatal steroids?
Given to mothers in threatened preterm labor, antenatal steroids decrease the risk of RDS and reduce the risk of neonatal death. Additionally antenatal steroids decrease the risk of IVH and NEC, respiratory support, intensive care admissions, and systemic infections in the infant in the first 48 hours of life. There are no adverse effects on the mother or fetus.
Q32. Who should receive antenatal steroid?
All mothers in threatened preterm labor between 24 and 34 weeks gestation considered to be at risk of delivery within 7 days should receive a course of antenatal steroids.
Q33. What is the optimal interval of steroid action?
8The greatest benefit against RDS is seen 24 hours after the lasts up to 7 days.
Q34. Should steroids be given even if the preterm delivery is likely to be eminent?
Therapy should be initiated even when delivery is anticipated within a few hours as it still helps maturation of fetal lung offering some protection.
Q35. Should a course of steroids be repeated if pregnancy continues beyond 7 days?
Repeat course of steroids is not recommended. After 7 days the treatment should only be repeated after careful consideration because the risks and benefits of repeated courses of antenatal steroids are still unknown. Possibility of decreased birth weight and head circumference at birth has been reported. There are concerns of increased risk of cerebral palsy.
Q36. What are contraindications to antenatal steroid therapy?
Contraindications to antenatal corticosteroids are maternal thyrotoxicosis, cardiomyopathy, active maternal infection or chorioamnionitis.
Q37. What is the role of steroids in maternal diabetes, pre-eclampsia, preterm prelabor rupture of the membranes or treated suspected chorioamnionitis?
It is safe to give steroids to mothers with these conditions.
Q38. Which steroids are to be used? Which is preferred steroid?
Both betamethasone and dexamethasone have been studied and found to be more effective than placebo, but these steroids have not been examined head-to-head. Betamethasone is the preferred steroid as it may cause a larger reduction in RDS than dexamethasone. Further, antenatal exposure to betamethasone, but not dexamethasone, is associated with a decreased risk of periventricular leukomalacia (PVL) in preterm infants.
Q39. What is the ideal dose of steroids?
Betamethasone, 12 mg, IM, once a day, 2 doses or dexamethasone, 6 mg, IM, 12 hours, 4 doses is the optimal dose regime for use of steroids.
Q40. Is there role for steroids in the era of surfactant?
Infants who received both antenatal steroids and surfactant had significant reductions in mortality, severity of respiratory distress, and frequency of air leaks compared with infants who received neither treatment, or only antenatal steroids, or only surfactant. The effects of antenatal steroids and surfactant are thus synergistic and additive improving mortality and clinical outcomes. 9The non- respiratory benefits of steroids and very low cost with immense benefits still make steroids an essential intervention for all mothers with threatened preterm labor irrespective of availability of surfactant.
  1. Alan H Jobe. Prenatal Corticosteroids: A Neonatologist's Perspective. Neo Reviews 2006;7:e259-e67.
Q41. How should preauricular tags/pits be managed?
Isolated ear pits and tags can have an autosomal dominant inheritance pattern within families hence family history should be sought. It is of utmost importance to assess hearing in both ears. Examination of face should exclude microtia and facial asymmetry, which can be suggestive of oculo-auriculo-vertebral spectrum. Examine the neck for evidence of branchial cleft fistulae. Evidence is mounting that it is unnecessary to obtain routine renal ultrasonography in patients who have isolated pre-auricular ear pits or tags. Renal USG should be done in patients who have three or more minor anomalies that include ear pits or tags or for patients in whom a genetic syndrome is suspected.
Q42. How should sacral dimple be evaluated?
A midline dimple measuring less than 5 mm that is located within 2.5 cm of the anus and not associated with other cutaneous findings is benign and routine spinal ultrasonography is not warranted in these patients. High-risk dorsal cutaneous stigmata for occult spinal dysraphism include hemangioma, cutis aplasia, raised lesions (masses, tail-like appendages, and hairy patches), the presence of multiple cutaneous lesions in a given patient, and atypical dimples, defined as dimples that are large (>5 mm) or high on the back (>2.5 cm from the anus). All such lesions should have an USG of spine (<3 months) or MRI spine (> 3 months age).
Q43. What should be done for newborns with asymmetric crying facies?
Congenital absence or hypoplasia of the depressor anguli oris muscle (DAOM) is a common cause of asymmetric crying facies in neonates. These patients can be distinguished from patients who have the less common finding of facial nerve palsy by the ability of the former patients to wrinkle the forehead and close the eye equally well on both sides of the face. In addition, the naso-labial fold depth remains intact and equal on both sides in patients in whom the 10DAOM is absent. Patients who have asymmetric crying facies have an increased risk for concomitant congenital heart defects, systemic anomalies and have been described in patients with velo-cardio-facial syndrome (VCFS).
Q44. How to evaluate a single transverse palmar crease?
Approximately 45% of patients who have Down syndrome have single transverse palmar creases. It is reasonable to search for other congenital anomalies. It could be a normal phenotypic variation in otherwise well newborn and no workup is required.
Q45. How to evaluate café au lait spots?
These are sharply defined, round to oval, homogeneous macules, usually varying in size from 2 mm to 20 cm. They are more prevalent on unexposed skin and are found more frequently on the buttocks, trunk, and lower limbs. Although it is common to see one spot, the finding of three or more is uncommon and neurofibromatosis needs to be ruled out.
Q46. How to evaluate a case of congenital hydronephrosis?
Confirm the anomaly postnatally on 3–7 days of life. If normal, repeat at 4–6 weeks. Do not start prophylactic antibiotics. No role for MCU if both USG normal.
  1. Unilateral hydronephrosis (HDN): Is ureter present?
    Yes: Do MCU
    No: Tc99 DTPA renal scan with diuretic renography should be done to detect PUJ obstruction
  2. Bilateral hydronephrosis: As above + BUN/S creatinine
Q47. Asymptomatic HDN or HDN which is mild to moderate and stable after USG within 3–7 days, with no obstruction should be followed as follows:
  1. Antibiotic prophylaxis is no longer recommended for all infants with antenatal hydronephrosis (APD >5 mm). Families should be counseled on signs and symptoms of urinary tract infections (UTIs)
  2. Urine cultures may be necessary if fever occurs.
  3. Diuretic renography, MCU are recommended if there is UTI episode
  4. USG after a year.
Q48. If VUR is detected,
  1. DMSA renal scan to detect renal scars
  2. Surgery may be needed if scars are present or there is presence of Grade IV-V VUR.
  3. Repeat MCU/diuretic venography at 2 years to decide about resolution of VUR.
  4. DMSA renal scan should be done every 2–3 yearly if scars are persistent or to detect presence of new scars.
  5. 11BP; growth monitoring; S. creatine/BUN, USG should be done yearly till 15–20 years.
Following are candidates for surgical consideration (Table 1.2):
Table 1.2   Indications for surgery in VUR
Initial at diagnosis
On follow-up
  1. PUJ obstruction
  2. At initial diagnosis:
    1. Symptomatic HDN (UTI, renal mass, growth failure),
    2. Solitary kidney with impaired function,
    3. Bilateral severe HDN
  3. Relative renal function of obstructive kidney <30%.
  1. 10% decline in relative renal function on DTPA renal scan when repeated after 6–12 weeks
  2. Increasing HDN
  3. Posturethral valves, ureterocele
  4. VUR Grade IV-V persisting beyond infancy
  5. New renal scars or recurrent UTI despite antibiotic prophylaxis.
Q49. Which newborns should be screened for developmental dysplasia of hip (DDH)?
Ideally all newborns during first well newborn examination, on follow-up every 3 months till infancy or when clinically suspected should be examined for DDH. There is a higher preponderance in the left hip of the firstborn female baby. Factors like a positive family history, breech presentation and oligo-hydramnios increase the predisposition by a factor of 10. Such newborns should be subjected to USG hips at 6 weeks irrespective of initial clinical finding. Pavlik harness should be used in first 3 months of age. Delayed diagnosis, beyond 3 months, is almost synonymous with surgical intervention.
Q50. What should be done for a newborn with solitary kidney?
Infants with a normal-appearing solitary kidney on postnatal ultrasound, does not require further imaging studies. If any abnormality is detected on postnatal ultrasound, investigate with a VCUG and diuretic renography. Close monitoring for the development of hypertension and/or proteinuria is required lifelong.
Q51. How to evaluate newborn detected to have a multicystic dysplastic kidney (MCDK)?
Non-communicating cysts of various sizes, lack of identifiable renal parenchyma, and atretic proximal ureter are classic ultrasound findings of MCDK. Verification of a nonfunctioning kidney with a DMSA scan was necessary to confirm the diagnosis of MCDK. Recent studies have shown that the DMSA scan is not necessary in the setting of well done ultrasound with features diagnostic of MCDK. MCDK are associated with a high rate of contralateral renal abnormalities. Infants with unilateral MCDK and a normal contralateral kidney on postnatal ultrasounds can be conservatively managed without routine VCUG screening. Abnormalities of the 12contralateral kidney (hydronephrosis, small size, lack of cortico-medullary differentiation, dilated ureter) should be investigated with a VCUG.
Q52. Antenatal US shows f/s/o posterior urethral valve. What should be the plan?
Ultrasound findings of PUV include bilateral hydronephrosis, hydroureter, posterior urethral dilatation, and a distended, thick-walled bladder. Postnatal renal ultrasound and voiding cysto-urethrogram should be done within 48 hours of birth in prenatally suspected bladder outlet obstruction. A thorough evaluation including renal ultrasound, VCUG, urinalysis, urine culture, and serum electrolytes, creatinine, and blood urea nitrogen should be completed on all infants suspected of having PUV followed by urologist evaluation.
Q53. How should a case of suspected trachea-esophageal fistula (TOF) be stabilized?
Presence of frothing at mouth or unexplained respiratory distress should raise suspicion of TOF. Nurse the baby prone to prevent aspiration. Keep the baby nil by mouth. Minimize handling and crying (which fills the stomach with excessive air). Suction the upper esophageal pouch frequently. Search for VACTERL anomalies. If a fistula exists between the esophagus and the trachea, abdominal distention will develop as air builds up in the stomach. Use 10 G (term), 8G (preterm) rubber catheter via mouth to detect the proximal pouch on X-ray. Presence of gas shadows in stomach suggest fistula. Do dye study selectively in high-risk cases only.
Q54. When should congenital diaphragmatic hernia (CDH) be suspected?
A newborn that worsens on positive pressure ventilation should be suspected of CDH. Presences of decreased air-entry, shift of heart sounds to the right, scaphoid abdomen are subtle clues.
Q55. How to interpret fetal echogenic bowel?
Echogenic bowel may be present with meconium ileus and isolated bowel atresia; therefore, genetic counseling and consideration of carrier screening of the parents for the common DNA mutations seen in cystic fibrosis is indicated. Echogenic bowel also has been associated with chromosomal abnormalities and cytomegalovirus infections, and should also be excluded.
Q56. How to manage encephalocele?
Encephalocele is confirmed on MRI. There may be associated intracranial malformations including agenesis of the corpus callosum and dysmorphic cerebral cortex. Microcephaly and hydrocephalus accompany malformations in which there is extensive herniation of cerebral tissue and are associated with a higher incidence of seizures, developmental delays, and mental retardation. Emergency 13closure is warranted when there is CSF leak; otherwise most repairs are completed in the first few days of life.
Q57. What should be done for tooth at birth?
Well implanted teeth should be left in the arch and their removal should be indicated only when they interfere with feeding or when they are highly mobile, with the risk of aspiration. Other oral manifestations that may be confused with natal tooth are cysts of the dental lamina and Bohn nodules, both differentiated from natal and neonatal teeth by radiographic examination (Fig. 1.2). Extraction is usually scheduled in second week of life ensuring vitamin K prophylaxis.
zoom view
Fig. 1.2: Natal tooth
Q58. How should isolated cleft palate managed?
Systemic examination is indicated because every sixth newborn that has the disorder may have additional malformations, such as congenital heart disease or urinary tract anomalies. Parental anxiety should be addressed as it may negatively affect the mother infant bond and lead to further feeding difficulties. No significant difference in terms of weight increase, developmental progress, and parental satisfaction was seen between infants fitted with a maxillary plate and those who had no plate hence are no longer recommended. Breastfeeding with the head supported, upright and attaching from above to seal the defect is a practical and most effective way to maintain nutrition. Use of squeezable bottles and teats with wide apertures to provide sufficient flow rates, syringe feeding or spoon feeding are inferior alternatives. To maximize chances of achieving normal speech and hearing, correction of the cleft palate (Fig. 1.3) is usually scheduled at approximately 8 months post-term. Operative 14repair of palatal fistula and placement of tympanostomy tubes is frequently needed in the first 4 years after birth. Speech hypernasality can be treated by a pharyngeal flap procedure.
zoom view
Fig. 1.3: Isolated cleft palate
Q59. How should hemangioma be managed?
During the first 2 months of life, nearly all hemangioma double in size (Fig. 1.4). Maximum size is generally fulfilled at 9 months and almost always by 12 months of age. Plateau in growth then occurs and is followed by involution, which occurs over several years, with the most rapid phase of involution occurring between ages 1 and 4 years. The growth cycle is dynamic, and within the same lesion, central graying and regression may begin to occur as the periphery is still proliferating. Most IH follow a benign course without the need for intervention aside from anticipatory guidance. Size and location on the face are the other most important predictors of complications and need for treatment. The first 4 months of life are the period of highest risk for the development of ulceration, and the occurrence of a gray-white discoloration akin to that typically seen and described as graying in the involuting hemangioma can herald impending ulceration and should be a cause for worry, because it seems to represent necrosis of the overlying epidermis. Indications for systemic therapy (steroids, propranolol or both) include threat to a vital function (vision, feeding, and cardiac function), risk of disfigurement, ulceration, and bleeding.15
zoom view
Fig. 1.4: Hemangioma
  1. Behrman RE, Kliegman RM, Jenson HB (Eds). Nelson Textbook of Pediatrics, 18th edition. Elsevier Saunders;  Philadelphia:  2007.
  1. Cloherty JP, Echenwald EC, Stark AR (Eds). Manual of Neonatal Care, 6th edition. Lippincott Williams and Wilkins;  Philadelphia:  2008.
Q60. What are inborn error of metabolism?
Inborn error of metabolisms (IEMs) are a group of heritable genetic disorders interfering with the body metabolic pathways in different ways, leading to inadequate functioning of a particular pathway. This interference in the normal enzymatic or metabolic pathway has varying consequences, including deficiency of a particular end product or excessive accumulation of a substrate that may be toxic.
Q61. How is IEM inherited?
The most common mode of inheritance for metabolic disorders is autosomal recessive (AR) followed by X linked recessive and least common being autosomal dominant (AD). Mitochondrial DNA inherited from mother is also one of the modes of inheritance. Consanguinity has an increased chance of expression of an AR 16disorder. De novo mutations are observed in any of the above inheritance leading to expression of the disorder. It is important to detail a three- to four-generation pedigree to evaluate the mode of inheritance accurately.
Q62. When should one suspect IEM?
  1. Unexplained–lethargy, refusal to feed, vomiting, altered sensorium, convulsions, and coma.
  2. Unexplained neonatal death.
  3. Unexplained jaundice/hepatomegaly.
  4. Severe hypotonia and respiratory difficulty.
  5. Refractory convulsions.
  6. History of early unexplained neonatal deaths.
  7. Family history of mental retardation, especially when there is consanguineous marriage.
Q63. What are clinical clues to IEM?
Table 1.3   Clinical clues to IEM
IEM Disorders
Peroxisomal disorders, Zellweger syndrome, lysosomal storage disorders, mucopolysaccharidosis, mucolipidosis, gangliosidosis, homocystinuria, Smith-Lemli-Opitz syndrome.
Pyridoxine dependent, folinic acid dependent, secondary to hypoglycemia, molybdenum co-factor deficiency, mitochondrial disorders, lysosomal storage disorders.
Fatty acid oxidation disorders, peroxisomal disorders, urea cycle disorders, mitochondrial disorders, Pompe's disease, glycogen storage disorders.
Glycogen storage diseases, fatty acid oxidation disorders, mitochondrial disorders.
Peroxisomal disorders, mitochondrial disorders, lysosomal storage disorders.
Lethargy or coma
Aminoaciduria, organic acidemias, urea cycle disorders, fatty acid oxidation defects, mitochondrial disorders.
Hepatomegaly or splenomegaly
Lysosomal storage disorders, glycogen storage diseases.
Jaundice or liver dysfunction
Galactosemia, hereditary fructose intolerance, tyrosinemia, citrullinemia, GSD type IV, α1-Antitrypsin deficiency, hemochromatosis, Niemann-Pick disease, fatty acid oxidation defects.
Cardiac manifestations
Fatty acid oxidation disorders, carnitine deficiency, Mitochondrial disorders, glycogen storage disease: type 2, Pompe's disease, mucopolysaccharidosis
Cherry red spot (e.g. Tay-Sachs disease), lenticular cataracts (e.g. Galactosemia, Fabry disease), dislocated lens (e.g. Homocystinuria), retinitis pigmentosa (e.g. Mitochondrial disorders).
Q64. What are initial tests to be done for suspected IEM?
Table 1.4   Baseline lab tests for suspected IEM
General laboratory tests
Metabolic screening tests
  • CBC
  • BUN, creatinine
  • Ca, Po4, Mg
  • Liver enzymes
  • Uric acid
  • Creatine kinase
  • CSF study
  • Cultures of blood, urine, CSF
  • B Sugar
  • S Electrolytes
  • Urine for glucose-non glucose reducing Substances
  • Blood gas
  • Ammonia
  • Lactate, pyruvate
  • Quantitative plasma/urine amino acids
  • Urine organic acids
  • Acylcarnitine profile
Q65. What are characteristic lab findings in IEM?
Table 1.5   Interpretating labs in IEM
Lab Finding
Metabolic acidosis with increased anion gap
Organic acidemias
Metabolic acidosis with normal anion gap
Galactosemia, hereditary fructose intolerance, glycogen storage disease, types I and III, phosphoenolpyruvate carboxykinase deficiency, tyrosinemia, type I, cystinosis, carnitine palmitoyltransferase 1 deficiency, mitochondrial respiratory chain disorders. Lowe syndrome, carbonic anhydrase II deficiency
Respiratory alkalosis
Urea cycle disorders
Urea cycle disorders, Organic acidemias
Lactic acidosis
Mitochondrial disorders, glycogen storage disorders, organic acidemias, fatty acid oxidation disorders, aminoacidurias, disorders of glyconeogenesis, pyruvate metabolism
High lactate/pyruvate ration
Mitochondrial disorders, pyruvate carboxylase deficiency
Acylcarnitine profile abnormalities
Fatty acid oxidation disorders, organic acidemias
Hypoglycemia with ketosis
Glycogen storage disease, organic academia
Hypoglycemia without ketosis
MSUD, fatty acid oxidation disorders, disorders of ketogenesis
Quantitative amino acid profile
Specific defects in amino acid metabolism
Urine organic acids
Specific defects in amino acid metabolism
Q66. What precautions should be taken while collecting samples for IEM?
  • Ammonia values can be significantly elevated if the sample is not immediately rushed on ice to the laboratory and analyzed.
  • 18Lactate and pyruvate concentrations must be obtained simultaneously for comparison.
  • The samples for plasma ammonia, lactate, and pyruvate should be obtained without the use of a tourniquet and need to be transported on ice for immediate analysis in the laboratory; pyruvate samples should be collected in perchlorate to prevent degradation.
  • The venous ammonia sample must be collected, stored, and transported on ice to the laboratory. Once in the laboratory, this specimen must be rapidly analyzed and not run as a routine and must be reported with an adjustment for the newborn age.
  • When ordering measurements of plasma amino acids, it is important to ask for a quantitative analysis. Analysis of amino acids generally is more informative in plasma rather than urine.
  • Free and total carnitine measurements often are ordered erroneously instead of the plasma acylcarnitine profile.
  • Lactate concentrations between 4 and 6 mmol/L can result from improper sample collection technique, such as prolonged tourniquet use, infant struggling, or seizure activity.
  • Whole blood glucose concentrations are 15% lower than those measured in plasma or serum.
  • Samples collected while the infant is hypoglycemic are more likely to show diagnostic metabolites, but, unlike hormone studies which must be collected during hypoglycemia, many metabolic tests are abnormal in IEMs, even if the infant is normoglycemic.
  • Concentrations of ketones in arterial blood are approximately 20% higher than venous concentrations.
  • Urine tests for ketones detect only acetoacetate, a positive urine dipstick test for ketones in an infant less than 1 month of age is indicative of severely altered metabolism, usually an organic acidemia or disorder of ketone body utilization.
  • For infants receiving parenteral nutrition, holding the amino acid-containing solution for 30 to 60 minutes is sufficient to avoid artifactual elevation of amino acids due to the parenteral nutrition.
Q67. What are clues to IEM on MRI?
  • Abnormal hyperintense signal in the globus pallidus and periatrial white matter of the centrum semi-ovale is often present in mitochondrial disease.
  • The globus pallidus is particularly vulnerable in metabolic disorders.
  • Nonketotic hyperglycinemia and MSUD primarily affect the white matter.
  • Different patterns of abnormality may suggest other underlying inborn errors of metabolism. For example, basal ganglia 19“metabolic strokes” may occur in organic acidemias, and involvement of the caudate nucleus, in addition to the putamen, is seen in glutaric aciduria type I and juvenile Huntington disease.
Q68. Which IEM have significant encephalopathy with normal lab tests?
Maple syrup urine disease, phenylketonuria, galactosemia, peroxisomal disorder, nonketotic hyperglycinemia (plasma amino acids may show an elevated glycine, CSF glycine diagnostic), disorders of neurotransmitters, Zellweger syndrome, cobalamin C defects and pyridoxine dependency.
Q69. What samples should be collected in suspected IEM on verge of dying?
Table 1.6   Sampling for IEM in terminally ill
Amino acids
1 mL EDTA/heparin tube
1 mL lithium heparin tube on ice
Blood gas
0.3 mL in heparin coated syringe
Carnitine (Free and total)
1 mL lithium heparin tube on ice
Comprehensive metabolic panel
0.5 mL lithium heparin tube on ice
Fatty acid profile
0.3 mL fluoride heparin tube on ice
0.5 mL EDTA
Lactic acid
0.6 mL in 0.6 mL sodium fluoride tube on ice
pH, reducing substances, ketones, organic acids, amino acid
5 mL, freeze at –20 °C
Amino acids, cells, proteins, glucose, lactic acid
0.5 mL in plastic tube
Q70. What is practical approach for IEM?
What is the predominant clinical picture?
Encephalopathy, seizures, disorder of breathing, dysmorphism, organomegaly–liver, spleen, heart, eye abnormalities, cardiac disorder, skin changes, cholestasis, abnormal odor.
What is the primary problem of IEM?
  • Is it hypoglycemia?
  • Is it metabolic acidosis?
  • Is it hyperammonemia?
  • Is it multisystem involvement?
20 How do you narrow down the above disorders?
For metabolic acidosis
  • Anion gap: Is it increased or normal
  • S lactate levels: If increased what is lactate pyruvate ratio
    : If normal what is b glucose
For hyperammonemia:
  • Is the sample collection, transportation, analysis appropriate?
  • What is the timing of presentation < 24 hr vs > 24 hr?
  • Is there acidosis, ketosis or hypoglycemia?
For hypoglycemia:
  • Is it ketotic or nonketotic?
Q71. What are management strategies in suspected IEM?
Table 1.7   Management options in IEM
For all
Organic acidemia
Lactic acidosis
Start GIR
Start lipids
Add amino acids
Control seizures, sepsis, shock, acidosis,
Sod. Bicarb
Vit B12
Sod. benzoate
PO, (IV)
Sodium phenylbutyrate
L Arginine
PO, (IV)
L Carnitine
Sod. Bicarb
Coenzyme Q
Folinic acid
Pyridoxol phosphate
Dextrose feeds
Repeat screen
Breast feeds
Monitor 6 hr
  1. Manmohan Kamboj. Clinical approach to the diagnoses of inborn errors of Metabolism. Pediatr Clin N Am. 2008;55:1113-27.
  1. MP Champion. An approach to the diagnosis of inherited metabolic disease. Arch Dis Child Educ Pract Ed. 2010;95:40-6.
Q72. Why should a mother start breastfeeding within the first hour after birth?
Most newborns have a strong suck reflex and are alert and ready to suck in the hour after birth. The newborn's immediate sucking at the breast stimulates milk production to begin. The newborn will begin immediately to get the benefits of colostrum: a) It is high in vitamin A and antibodies to prevent infection. b) It helps expel meconium and prevent jaundice. c) It is very concentrated and helps prevent low blood sugar in the first hours of life.
Q73. Its summer time. Explain why babies do not need extra water?
21Breast milk (even colostrum) is almost all water and contains plenty of fluid for the baby's needs. Breastfeeding on demand supplies all the fluid a baby needs. Mother should have adequate fluids to keep herself well hydrated.
Q74. What is the harm of using in addition to breastfeeding, one bottle-feed a day when I am boiling the bottles carefully?
Sucking at the breast is reduced, which causes decreased milk production and may lead to lactation failure. The baby may lose the ability to suck effectively on the breast, which can cause sore nipples, poor and/or refusal of the breast. The chance of baby getting sick are more often, and more severe, with higher mortality. Babies who receive other foods or liquids stop breastfeeding earlier.
Q75. Mother says I am sick from cold, can I still breastfeed my baby?
Yes. Minor illnesses do not come in the way of breastfeeding. Commonly used medications also do not affect lactation or affect the baby.
Q76. Should washing the breast before and after each feed be done?
Not routinely. In fact more the cleaning more would be the risk of sore nipple.
Q77. I have pain while feeding the baby. What should I do?
A good breastfeeding infant-dyad should not feel any pain. Pain suggests problem with positioning or attachment. Evaluate the breastfeeding process in details.
Q78. My milk leaks from breast after feeding the baby. What should I do?
It is normal for breast to leak. It suggests lactation sufficiency. Ensure baby is getting enough milk and is not partly sucking and leaving the breast. Express milk if you feel breast engorgement.
Q79. Which is the best position to breastfeed the baby?
Any position which is comfortable to the mother is acceptable.
Q80. My milk looks thin and watery. Is it alright?
No two mothers’ milk is the same in appearance and composition. In fact in the same mother the milk composition varies from time to time and in fact within the day. Hence the appearance, consistency of milk has no bearing.
Q81. Should I breastfeed from both the breasts each time I feed my baby?
First offer one breast to the baby. Once it is emptied offer the second. Many a times baby may feed only on one breast and stop feeding. Next time when you feed offer the other breast.
Ensure alternate emptying of breasts.
Q82. How does the breast size influence the breastfeeding?
22Breast size does not influence the breastfeeding. Milk is produced by the lactiferous ducts and sinuses and not by the breast.
Q83. How long does it take to breastfeed?
It is variable and depends on baby to baby.
Q84. How long is expressed breast milk stable in room temperature?
At least 6 hours.
Q85. What are good practices to ensure enough milk?
  • Kangaroo care
  • Rooming in
  • Early and exclusive breastfeeding.
  • Feeding on demand—day and night.
  • Ensuring complete diet to mother with no restrictions.
  • Ensure adequate rest for mother.
  • Ensure positive frame of mind of mother. Make her relaxed and stress free.
  • Convey danger signs.
Q86. What are best practices to maintain lactation in NICU mothers?
  • Provide information, educational materials, equipment, supplies, during mother's hospital stay.
    • Actively encourage and support breastfeeding
    • Start milk expression in first 24 hours after birth
    • Aim for the first oral feedings to be at the breast
    • Encourage milk expression 8 to 10 times per day
    • Communicate about the progress of the baby and involve mother in day to day NICU baby care
    • Responding to maternal concerns, stress, anxiety, or insomnia related to infant's changing condition or other personal issues
    • Discuss identified maternal risk factors for lactation
    • Avoid hormonal birth control during early postnatal period
    • Make provision of hospital-grade breast pump and collection kit and storage containers with guidelines for their use.
    • Provide written educational information addressing common concerns, such as insufficient breast milk, maternal diet and medications, expressing breast milk, colostrum, benefits, etc.
    • Recommend specific medications to the mother that are compatible with lactation
    • Educate new staff to support breastfeeding
  • Provide non-pharmacologic interventions in the NICU that optimize maternal milk volume during the infant's hospitalization.
    • 24-hour visitation and access to infant
    • Consistent message about the importance of human milk from all NICU clinicians
    • 23Use of expression of breast milk at infant's bedside
    • Daily skin-to-skin holding in the NICU
    • Comfortable, supportive chairs should be available for mothers
    • Daily “tasting” of milk (suckling at emptied breast) regardless of infant weight and gestation
    • Peer support for expressing milk and other NICU-specific activities.
    • Review of maternal milk volume records to identify expressing patterns and detect potential problems.
    • Observations of mother using manual expression or electric pump in the NICU to detect problems that may compromise milk volume and incomplete breast emptying.
    • No free formula samples or other promotion of artificial feeding.
    • Ensure the entire system supports breastfeeding.
Q87. How to overcome common problems in breastfeeding?
  • Breast discomfort and pain: Frequent unrestricted breastfeeding, analgesia compatible with breastfeeding, breast massage; hand expression if necessary; cabbage leaves or cold compresses may help, but observed effects could be a placebo effect
  • Sore nipples: Correct positioning and attachment may prevent pain, consider treating thrush infection, topical nipple treatments, nipple shells, or nipple shields have not been shown to be effective; evidence for the safety of nipple cream is weak
  • Mastitis: Continue breastfeeding or expressing milk, analgesia compatible with breastfeeding; increase fluid intake; gently massage, if symptoms continue for more than a few hours of self management, seek professional advice to decide whether a β lactamase resistant antibiotic is indicated
  • Inverted or flat nipples: Require skilled help with positioning and attachment, not a contraindication to breastfeeding.
  • Difficulty getting the baby to suck: Assessment of effective breast feeding, encourage kangaroo care, allay anxiety, stress or pain, express milk
  • Not gaining weight: Assessment of effective breastfeeding, check urine output, activity, stool frequency and character
  • Neonatal jaundice: Breastfeed frequently, do not give trial off breastfeeding and investigate jaundice persisting beyond 14 days
  • Multiple births: Intense maternal support, advice and counseling, frequent feeding, feed consecutively or simultaneously, alternate breasts when breastfeeding twins, use cradle or football or combination position method, even partial breastfeeding may be beneficial.
  • Preterm baby: Expressing milk, Mother-infant skin-to-skin contact as early as feasible, fortified human milk for < 1500 g 24who do not gain weight on adequate breast milk feed, maternal support and counseling
  • Cleft lip/palate: Assistance in position and attachment, breastfeeding offers several benefits over bottle-feeding
  • HIV: Individualized counseling, screening for acceptable, feasible, affordable, sustainable and safe (AFASS) criteria, promote and actively counsel on exclusive breastfeeding (EBF) for 6 months if ALL AFASS criteria not met, avoid mixed feeding, early weaning, abrupt weaning, prepare for stopping BF at 6 months if AFASS criteria met.
  1. Amanda Black. Breastfeeding the premature infant and nursing implications. Advances in Neonatal Care. 2012;12(1):10-4.
  1. Lucas A, Fewtrell M. Feeding low birth weight infants In: Rennie JM (Ed). Roberton's Textbook of Neonatology, 4th edition. Churchill Livingstone;  Edinburgh:  2005.pp.314-24.
Q88. What are the three key basics of kangaroo care (KC)?
Warmth, breast milk and love.
Q89. How do you get the parents into KC?
Counseling before and after birth about technique, benefits to mother/baby, intermixing with KC practicing mothers, ensure staff education and acceptance to practice and preach, provide practical assistance at every stage.
Q90. Apart from making most of KC in NICU/Step down nursery and at home where else can KC be beneficial?
During transport (within and between hospitals); during painful minor procedures.
Q91. When do you consider initiating KC?
Initiation should be based on physiological assessment. As soon as the LBW baby is stable.
Q92. Which babies are not eligible for KC?
Sick babies; unstable babies.
Q93. How do you prepare baby for KC?
Unclothe the baby. Cover only the head and genitals. Use socks and gloves as required. Ensure proper positioning and support to the baby.
Q94. How do you prepare mother for KC?
25Counsel mother about KC, benefits and respond to all her concerns. Use loose top with front open. A semi reclining chair or back support is provided. Ensure proper positioning and support to the baby.
Q95. Kangaroo position is the hallmark of KC. What is kangaroo position?
Baby is kept in upright position. Baby's abdomen is at level of mother's xiphisternum. Head turned to one side slightly extended. Hands and legs in flexed posture. Support the baby hips.
Q96. What is the ideal position for mother for providing KC?
No ideal position like for breastfeeding. Mother can provide KC during sleep, rest-provided she is comfortable.
Q97. Do you always need special clothes for KC?
No. You just need a garment to form a sling to support the baby.
Q98. What additional staff is required to implement KC?
Q99. What do you monitor for a baby on KC?
Neck is not too flexed or extended. Breathing is regular. Color is pink. Baby maintaining temperature.
Q100. How is baby fed in KC?
Depending upon baby physiologic condition–tube feeds, wati spoon feeds, syringe feeds or paladin feeds.
Q101. How long KC should be given?
Individualize but take into consideration—infant's GA at birth, current postmenstrual age and medical condition, and the family's situation. As long as possible ensuring mother comfort level. Begin in small sessions up to 1 hour and extend as mother becomes confident.
Q102. When to discontinue KC?
When the baby or mother get uncomfortable. By and large continue up to term and weight of 2500 g.
Q103. Do you need to take consent for KC?
Some units take consent. We don't. It is part of essential routine care for all stable LBW babies. We do write and document in daily orders and notes.
Q104. What are the nonthermal benefits of KC?
Increased breastfeeding rates, increased duration of breastfeeding, earlier discharge from nursery, better weight gain, lesser risk of apnea, nosocomial infections, stronger bonding with the baby and lesser stress and more confidence amongst mothers (Fig. 1.5).26
zoom view
Fig. 1.5: Kangaroo care
  1. Conde-Agudelo A, Díaz-Rossello JL. Kangaroo mother care to reduce morbidity and mortality in low birth weight infants. Cochrane Database Syst Rev. 2014;4:CD002771. doi: 10.1002/14651858.CD002771.pub3.
  1. Engmann C, Wall S, Darmstadt G, Valsangkar B, Claeson M. Participants of the Istanbul KMC Acceleration Meeting. Consensus on kangaroo mother care acceleration. Lancet. 2013;382(9907):e26-7.
Q105. Is there any difference in preterm and term vaccination?
Postnatal age rather than GA appears to be more important in response to immunization. The schedule, dose, site and mode of vaccination remain the same for all newborns irrespective of gestation. Vaccine dose should not be reduced or divided for preterm infants. Local and systemic reactions are similar in both. Studies demonstrate that vaccines are safe and immunogenic in preterm infants.
Q106. Should vaccines be delayed for LBW/preterm infants?
Birth weight and size are not factors in deciding whether to postpone routine vaccination of a clinically stable premature infant, except for 27hepatitis B vaccine. The severity of vaccine-preventable diseases in LBW/preterm infants precludes any delay in initiating the administration of these vaccines.
Q107. What should be the vaccination strategy for preterm/LBW infant?
Medically stable LBW/preterm infants should receive all routinely recommended childhood vaccines at the same chronologic age as recommended for full term infants. Under most circumstances, gestational age at birth and birth weight should not be limiting factors when deciding whether a LBW/preterm infant is to be immunized on schedule. Infants with birth weight less than 2000 g, however, may require modification of the timing of hepatitis B immuneprophylaxis depending on maternal HBsAg status.
Q108. Any special precautions for preterm vaccination?
Apnea has not been reported after administration of acellular. Pertussis-containing vaccines to extremely low birth weight infants. Cardio-respiratory events (apnea and bradycardia) that generally are mild, transient and self-resolving have been noted in multiple reports following immunization. Monitoring of infants at the highest risk of cardio-respiratory events for 48 hours post-immunization should be considered strongly.
Q109. Should paracetamol be given routinely/prophylactically for vaccination?
Administration of paracetamol at the time of vaccination or shortly afterward may interfere with the uptake of the vaccines hence routine or prophylactic administration is not recommended.
Q110. Should ice be applied at vaccination site?
Ice provides only 1 to 2 seconds of analgesia at the injection site and, therefore, is not recommended.
Q111. Do blood-products given during NICU stay interfere with vaccination?
Blood products do not interfere with inactivated antigen vaccines and can be administered simultaneously or at any time between doses. Blood products and live antigen should not be administered simultaneously. Blood products should preferably not be given till 2 weeks following live antigen administration.
Table 1.8   Blood product and vaccine administration
Blood + inactivated antigen
Can be given simultaneously
Blood + live antigen
Cannot be given simultaneously
Q112. Do antibody containing products (intravenous immune globulin, specific hyperimmune globulin (e.g. hepatitis B immune globulin, tetanus immune globulin, Varicella zoster immune globulin) interfere with vaccination schedule?
Table 1.9   Blood products and vaccination
Interval between doses
Inactivated antigen
Live antigen
Inactivated antigen
Live antigen
Dose related
2 weeks
Q113. Which vaccine administrations should be considered invalid?
Doses administered ≥5 days earlier than the minimum interval or age should not be counted as valid doses and should be repeated as age-appropriate. Any vaccination using less than the standard dose should not be counted, and the person should be revaccinated according to age, unless serologic testing indicates that an adequate response has been achieved.
Q114. Once reconstituted how long is BCG vaccine stable?
6 hours
Q115. Any special concerns about use of DPT vaccine?
Under normal circumstances, vaccinations should be deferred when a precaution is present.
Table 1.10   Precautions but not contraindications for DPT
  • Fever of >40.5°C ≤48 hours after vaccination with a previous dose of DTP or DTaP
  • Collapse or shock-like state (i.e. hypotonic hypo-responsive episode) ≤48 hours after receiving a previous dose of DTP/DTaP
  • Seizure ≤3 days of receiving a previous dose of DTP/DTaP
  • Persistent, inconsolable crying lasting >3 hours <48 hours after receiving a previous dose of DTP/DTaP
  • Moderate or severe acute illness with or without fever.
Q116. Can OPV or pulse polio be given in NICU?
No. The virus is shed in stools which may be cause infection to other newborns that are already immune-compromised.
Q117. What should be the strategy for hepatitis B vaccination in LBW?
Table 1.11   Hepatitis B immuno-prophylaxis scheme for PT and LBW infants
Maternal status
Infant ≥2000 g
Infant <2000 g
HBsAg positive
Hepatitis B vaccine + HBIG (within 12 h of birth)
Hepatitis B vaccine + HBIG (within 12 h of birth)
Immunize with 3 vaccine doses at 0, 1, and 6 months of chronologic age
Immunize with 4 vaccine doses at 0, 1, 2–3, and 6–7 months of chronologic age
Check anti-HBs and HBsAg at 9–15 months of age
Check anti-HBs and HBsAg at 9–15 months of age
If infant is HBsAg and anti-HBs negative, re-immunize with 3 doses at 2-months intervals and retest
If infant is HBsAg and anti-HBs negative, re-immunize with 3 doses at 2-months intervals and retest
HBsAg status unknown
Hepatitis B vaccine (by 12 h) + HBIG (within 7 days) if mother tests HBsAg positive
Hepatitis B vaccine + HBIG (by 12 h)
Test mother for HBsAg immediately
Test mother for HBsAg immediately and if results are unavailable within 12 h, give infant HBIG
HBsAg negative
Hepatitis B vaccine at birth preferred
Hepatitis B vaccine dose 1 at 30 days of chronologic age if medically stable, or at hospital discharge if before 30 days of chronologic age
Immunize with 3 doses at 0–2, 1–4, and 6–18 months of chronologic age
Immunize with 3 doses at 1–2, 2–4, and 6–18 months of chronologic age
May give hepatitis B-containing combination vaccine beginning at 6–8 weeks of chronologic age
May give hepatitis B-containing combination vaccine beginning at 6–8 weeks of chronologic age
Follow-up anti-HBs and HBsAg testing not needed
Follow-up anti-HBs and HBsAg testing not needed
Q118. What happens if accidentally vaccine is administered after the expiry date?
Doses of expired vaccines that are administered inadvertently generally should not be counted as valid and should be repeated. Inactivated vaccines should be repeated as soon as possible. Live vaccines should be repeated after a 28-day interval from the invalid dose to reduce the risk for interference from interferon on the subsequent doses.
Q119. How to ascertain that the vaccine has been given intradermal?
During an intradermal injection, considerable resistance is felt and a raised, blanched bleb showing the tips of the hair follicles is a sign that the injection has been correctly administered. A bleb of 7 mm in diameter is approximately equivalent to 0.1 mL and is a useful indication of the volume that has been injected. If no resistance is felt, the needle should be removed and reinserted before more vaccine is given.
Q120. How should one optimize the use of hepatitis B vaccine in preterm/LBW?
Hepatitis B vaccines, which should be delayed until at least age 6 weeks and weight greater than 2 kg. For infants who weigh less 30than 2,000 g, the first HBV dose is not counted as part of the vaccine series; they receive a total of four doses.
When HBsAg testing of pregnant women is not feasible (i.e. in remote areas without access to a laboratory), all infants should receive hepatitis B vaccine ≤12 hours of birth and should complete the hepatitis B vaccine series according to a recommended schedule for infants born to HBsAg-positive mothers.”
Hepatitis B administered by any route other than intramuscular should not be counted as valid and should be repeated.
Q121. When should hepatitis B immunoglobulin be given?
All newborns born to HBsAg +ve mothers should be given hepatitis B vaccine and immunoglobulin preferably < 12 hours and not beyond 72 hours age regardless of the e-antigen status of the mother. Infants should be tested at 9 to 18 months of age after completion of the series to document that a protective anti-HBs concentration of at least 10 mIU/mL has been achieved. Responders with anti-HBs levels of 10 to 100 mIU/mL should receive one additional dose of vaccine at that time. If protection has not been achieved, the infant should be re-immunized with three doses at 2-month intervals and retested.
Table 1.12   Hepatitis B vaccination in newly born
Hepatitis B status of mother
Newborn should receive
HB vaccine
HBsAg +ve, HBeAg+ve
HBsAg +ve, HBeAg –ve, Anti-HBe -ve
HBsAg, e markers not determined
Acute hepatitis B infection during pregnancy
HBsAg +ve, Anti-HBe +ve
Q122. Which vaccines can be given safely during pregnancy?
Whether live or inactivated vaccines are used, vaccination of pregnant women should be considered on the basis of risks versus benefits—i.e. the risk of the vaccination versus the benefits of protection in a particular circumstance. Risk for a developing fetus from vaccination of the mother during pregnancy primarily is theoretical and largely unknown. Initiation of the vaccine series should be delayed until after completion of the pregnancy. Live vaccines (MMR, varicella and HPV) are contraindicated during pregnancy.
Hepatitis B, Td, Tdap, inactivated influenza, rabies vaccines can be safely given during pregnancy. When Td or Tdap is administered during pregnancy, the second or third trimester is preferred.
Q123. If mother has inadvertently received a live vaccine should pregnancy be terminated?
31If a live-virus vaccine is inadvertently given to a pregnant woman, or if a woman becomes pregnant within 4 weeks after vaccination, she should be counseled about the potential effects on the fetus. But vaccination is not ordinarily an indication to terminate the pregnancy.
Q124. What should be the vaccine strategy for immunodeficiency disorders in newborn?
Decisions to vaccinate immunocompromised children must be made individually.
Table 1.13   Vaccination in special circumstances
Vaccine safety
Defects in phagocyte function
(e.g. chronic granulomatous disease or
myeloperoxidase deficiency)
Can receive live, attenuated viral vaccines in addition to inactivated vaccines but should not receive live, attenuated bacterial vaccines (e.g. BCG or Ty21a oral typhoid vaccines)
Complement deficiency
Can receive live, attenuated viral and live, attenuated bacterial vaccines
Severe cell-mediated immunodeficiency
Should not receive live, attenuated viral or bacterial vaccines
Chemotherapy has been discontinued for at least 3 months
Can receive live-virus vaccines
Prednisolone, 2 mg/kg/day for at least one week, or 1 mg/kg/day for one month
Until at least three months after treatment has stopped
Immunosuppressive drugs (e.g. azathioprine, cyclosporin, methotrexate, cyclophosphamide, leflunomide and the newer cytokine inhibitors)
Until at least six months after terminating such treatment
Currently being treated for malignant disease with immunosuppressive chemotherapy or radiotherapy, or who have terminated such treatment within at least the last six months
No live vaccines
Have received a solid organ transplant and are currently on immunosuppressive treatment
No live vaccines
Received a bone marrow transplant, on- immunosuppressive treatment
No live vaccines at least 12 months after finishing all immunosuppressive treatment
Aerosols or topical or intra-articular non- systemic steroid preparations
No C/I
Live vaccines can be given
Replacement schedules of corticosteroids for people with adrenal insufficiency
No C/I
Q125. Which is an absolute contraindication for immunization?
32The only absolute contraindication for immunization is the known severe allergic reaction to a previous dose of a given vaccine or vaccine constituent.
Q126. Should influenza vaccine be given to NICU graduates?
Influenza vaccine should be given to all NICU graduates starting from 6 months age. The susceptibility and morbidity of influenza is very high in NICU graduates. For preterm infants younger than 6 months of age who are not direct candidates for vaccination, immunization of contacts (parents, siblings) becomes their only immunologic means of influenza prevention. This is called “cocooning”.
Q127. How should one vaccinate an infant with congenital bleeding disorder?
When [any] intramuscular vaccine is indicated for a patient with a bleeding disorder or a person receiving anticoagulant therapy, the vaccine should be administered intramuscularly if, in the opinion of a physician familiar with the patient's bleeding risk, the vaccine can be administered with reasonable safety by this route. If the patient receives anti-hemophilia or similar therapy, intramuscular vaccinations can be scheduled shortly after such therapy is administered. A fine needle (≤23 gauge) should be used for the vaccination and firm pressure applied to the site, without rubbing, for ≥2 minutes.
Q128. How should infants born to HIV infected mothers be vaccinated?
For severe immunosuppression (age specific CD4 T lymphocyte count) and in symptomatic live vaccines are contraindicated. Measles and varicella vaccinations are recommended for children with asymptomatic or mildly symptomatic human immunodeficiency virus (HIV) infection but are contraindicated for persons with severe immunosuppression from HIV or any other immunosuppressive disorder.
  1. Ashraf Gad, Shetal Shah. Special Immunization Considerations of the Preterm Infant. J Pediatr Health Care. 2007;21:385-91.
  1. C Mary Healy. Immunization Strategies to Protect Preterm Infants. Neo Reviews. 2010;11:e409-e418.
  1. IAP Guidebook on Immunization. 2000-2010.33
Q129. What are clues on history to identify etiology of respiratory distress?
Table 1.14   Clues on history
Previous sibling with CHD
Maternal fever, leaking PV > 12 hours, pPROM, chorio-amnionitis
Congenital pneumonia
CS without labor
Course of AN steroids
Resuscitation, fetal distress
Asphyxial lung disease, air leak, PPHN, metabolic acidosis, myocardial dysfunction
TTNB, CHD, air leak, RDS, birth trauma, polycythemia, hypoglycemia
Neonatal deaths
Tracheo-esophageal fistula
Lung hypoplasia
Placenta previa or abruption
Post feed worsening
Aspiration, GERD, isolated cleft palate, TEF, IEM
Chronic course, oxygen dependency
BPD, CHD (TAPVC), atypical infection (CMV, fungus, pneumocystis carinii, chlamydia), Wilson-Mikity syndrome, recurrent aspiration (GER, pharyngeal in-coordination, H shaped TOF), osteopenia of prematurity
Q130. What are clinical signs diagnostic of cause for respiratory distress?
Table 1.15   Diagnostic signs on examination
Look for
Potter facies
Hypo-plastic lungs
Single umbilical artery
Tracheoesophageal fistula
Frothing at mouth
Tracheoesophageal fistula
Crying aggravating cyanosis
Congenital heart defect
Crying relieving cyanosis
Choanal atresia
Inability to pass feeding tube
Tachycardia, delayed CRT, cold extremities, weak pulses,
mottling, oliguria, altered sensorium, hypotension
Temperature instability, core periphery temperature difference > 3C
Multiple pustules, foul smell, umbilical discharge
Scaphoid abdomen
Congenital diaphragmatic hernia
Absent femorals
Coarctation of aorta
Barrel chest
Meconium aspiration syndrome
CHD, cardiomyopathy
Q131. How to grade severity of respiratory distress clinically?
Table 1.16   Grading severity
Type of respiratory distress
Sub-costal, intercostal, sub-sternal in-drawing
Mild to moderate
Supraclavicular, suprasterna, sternal in-drawing
Head bobbing
Q132. How do breathing pattern helps define the underlying cause?
Table 1.17   Breathing pattern interpretation
Breathing pattern
Isolated tachypnea
CHD, metabolic acidosis, anemia, hypoglycemia, temperature instability, renal failure
RDS, pneumonia, TTNB
CHD, severe lung disease, polycythemia, abnormal hemoglobin, CNS dysfunction
UAO, laryngo-tracheomalacia
Apneic spells
Severe lung disease, anemia, termal instability, GER, IVH, PDA, fungal infection, CNS dysfunction
Q133. How to differential respiratory from cardiac distress?
Table 1.18   Differentiating respiratoy and cardiac cause for distress
Gallop, weak pulses, hepatomegaly,
Absent femorals
Parenchymal lesion
Shape, size of heart abnormal,
abnormal pulmonary vasculature
Pulse oximeter
Improvement with oxygen
Not much improvement with oxygen,
differential cyanosis
Hyperoxia test
PaO2 up to 150 mm Hg
PaO2 > 150 mm Hg
Q134. How does X-ray helps to define the underlying cause of RD?
Table 1.19   Interpreting X-ray chest
Radiological signs
Low lung volume
RDS, pulmonary hypoplasia
High lung volume
MAS, TTNB, cystic lung disease, hyperventilation
Air bronchograms
RDS, pneumonia
Diffuse parenchymal infiltrates
TTN, MAS, pneumonia
Lobar consolidation
Pneumonia, CLE, CCAM
Pleural effusion
Pneumonia, pulmonary lymphangiectasia
Reticular granular pattern
RDS, pneumonia
TTN, MAS, pulmonary lymphangiectasia
Fluid accumulations in inter-lobar spaces
TTN, pulmonary lymphangiectasia
“Cystic” mass
CCAM, CDH, pulmonary sequestration
Spontaneous, MAS, RDS, pneumonia
Q135. How do you objectively assess respiratory distress in newborns bedside?
Trend in Silverman Anderson Score (preterm), Downes Score (term), Pulse oximetry and FiO2.
Silverman Anderson Score
Table 1.20   Silverman Anderson score
Upper chest retraction
Lower chest retraction
Xiphoid retraction
Nares dilatation
Expiratory grunt
Grade 0
Grade 1
Lags on inspiration
Just visible
Just visible
On steth.
Grade 2
See saw
Downe's Score
Table 1.21   Downe's score
Air entry
Score 0
< 60
Mild to moderate
Room air
On steth
Score 2
On FiO2 > 40%
Interpret the score looking at the trend, FiO2 and sensorium of the patient.
Q136. What is the 30–60–90 rule for pulse ox?
The “30–60–90” rule is a useful bedside indicator when using the pulse oximeter. This means that at a saturation of 90% the paO2 is around 60 mm Hg and at 60% it is around 30 mm Hg in a newborn. This is due to high HbF in neonatal blood which causes the left shift 36of oxygen dissociation curve. At saturation of 90–95%, the paO2 may be between 60 and 98 mm Hg and above 95% saturation, paO2 is well above 100 mm Hg.
Q137. What are nonrespiratory, noncardiac causes of breathing difficulty?
Asphyxia, renal failure, anemia, polycythemia, raised ICT, metabolic acidosis, sepsis, intracranial hemorrhage, medications.
Q138. What is the diagnostic test for TTNB?
TTNB is a diagnosis of exclusion.
Q139. How do you clinically suspect air-leak?
Sudden deterioration/collapse, shift of heart sounds.
Q140. Which is the single most important risk factor for developing respiratory distress syndrome in preterm babies?
Maternal history of steroids.
Q141. What are good practices for stabilization for baby with RD?
Minimal handling, ensure normo-thermia, keep airway patent, suction as required, monitor objectively-score, pulse ox, maintain normoxia, normo-tension and normo-glycemia.
Q142. How to interpret pulse ox reading?
Table 1.22   Interpreting pulse oximeter
Check probe placement
Cold stress, abnormal hemoglobin
Pulmonary hypertension
Normal in upper limb, low in lower limb
Shunt or pulmonary hypertension
No improvement despite oxygen
Congenital cyanotic heart, fixed pulmonary hypertension
Q143. What are the general principles of respiratory support?
Table 1.23   Management strategy for respiratory support
SA Score <3
SA Score 4–6
SA Score >7
IV fluids, ensure normo-thermia, normo-glycemia, normo-tension, RD scoring, vitals, urine output and SpO2 monitoring, X-ray, lab tests
Early CPAP
Exit from CPAP
If FiO2 > 0.4, consider surfactant
If apnea, FiO2 >0.7, CPAP pressure >7, respiratory failure = consider intubation and ventilation
  1. Hermansen CL, Lorah KN. Respiratory distress in the newborn. Am Fam Physician. 2007;76:987-94.
  1. Edwards MO, Kotecha SJ, Kotecha Sailesh. Respiratory distress of the term newborn infant. Paediatr Respir Rev, doi:10.1016/j.prrv.2012.02.002
  1. Hany Aly. Respiratory Disorders in the Newborn: Identification and Diagnosis. Pediatrics in Review. 2004;25:201-8.
Q144. What is clinical, probable and proven sepsis?
Clinical sepsis is a subjective diagnosis based on clinical assessment without any lab evidence. Probable sepsis is a diagnosis made when sepsis screen is positive but blood culture is not done or is sterile. Proven sepsis is isolation of the organism on culture.
Q145. How does evolution of sepsis takes place?
A newborn with sepsis may be at one of the following stage of the evolving sepsis cascade.
  • Systemic inflammatory response syndrome: Tachypnea, tachycardia, increase or decrease in WBC count, hypo or hyperthermia.
  • Sepsis: SIRS + hypotension in response to infection.
  • Severe sepsis: Sepsis with organ dysfunction, hypoperfusion or hypotension, may include changes in mental state, oliguria, hypoxemia or lactic acidosis.
  • Septic shock: Severe sepsis with persistent hypotension despite adequate fluid resuscitation.
  • Multiorgan dysfunction syndrome: Presence of altered organ function which cannot be maintained without intervention.
Q146. What risk factors on history should be taken into consideration while evaluating newborn?
Table 1.24   Risk factors for sepsis
Early onset sepsis
Late onset sepsis
Intrapartum factors
Community factors
Unexplained preterm labor
Febrile mother
PROM > 24 hours
Preterm PROM
Prolonged labor/difficult labor
Foul liquor
Meconium stained liquor in preterm
Apgar< 6 at 5 minutes
Prelacteal feeds
Poor hygiene
Poor cord care
Cultural practices
Top feeds
Prolonged NICU stay
Prolonged antibiotics
Invasive procedures
Congested NICU
Prolonged ventilation
No enteral feeds
No breast feeds
Indwelling catheters
Gut surgery
Q147. What are subtle clinical markers to suggest neonatal infection?
38Core axillary temperature mismatch, fluctuating temperature, unexplained tachycardia, changing body color, upcoming direct jaundice, unexplained metabolic acidosis.
Q148. What are signs of advanced sepsis?
Sclerema, bleeding tendency, direct hyperbilirubinemia, cyanosis, grunt, abdominal fullness and or redness, persistent gastric residue, neck retractions, bulging fontanel, thrombocytopenia.
Q149. When should I do a sepsis screen?
If there is clinical ambiguity, i.e. you are not sure whether to give antibiotics or not to give, e.g. fullness of abdomen, tachypnea and otherwise baby looks well–in this situation, if screen is negative, withhold antibiotics; if positive, start antibiotics.
In a situation where you feel antibiotics need not be started, sepsis screen will not serve any purpose. If the sepsis screen is going to change your decision about antibiotics, do it; if not, do not do it—you will save time and money.
On the other hand, if in your clinical judgment, you feel antibiotics have to be started, e.g. sick baby, shock-screen serves no purpose, draw a blood culture and start antibiotics. Do not use sepsis screen as a substitute for blood culture.
Do not use sepsis screen to decide duration of antibiotics. Bottom line remains, treat the baby/bacteria and not the screen.
Q150. How reliable is CRP in sepsis?
An elevated CRP level (greater than 10 mg/liter) is abnormal. It is always associated with pathological changes. The positive predictive value for a raised CRP is poor so a positive test is poorly predictive of sepsis. False positives arise from noninfectious condition such as intraventricular hemorrhage, meconium aspiration, respiratory distress syndrome, fetal hypoxia, intraventricular hemorrhage, NEC, pneumothorax, surgery and immunization.
Sensitivity of the test at presentation is only 40%, i.e. 60% of subsequently proven sepsis episodes will have a normal initial CRP. With this in mind CRP level should not be checked at birth or at initial presentation with symptoms suggestive of sepsis.
The C-reactive protein level is not recommended as a sole indicator of neonatal sepsis, but it may be used as part of a sepsis work-up.
Q151. How to make the most of CRP?
The test is most likely to be useful when the case history and the condition of the patient leave the clinician in serious doubt about the presence of infection, in which case the diagnostic test may be used as a decision rule: start treatment if the test is positive; delay treatment if the test result is negative.
CRP should be considered in cases in which diagnosis of sepsis is unclear, and where negative cultures may not give sufficient 39reassurance to discontinue antibiotics. Common examples may include when maternal intrapartum IV antibiotics were given, and in late onset sepsis where lumbar puncture specimens were unobtainable or blood-stained.
CRP helps to differentiate bacterial (significant elevation) from viral infection (minimal elevation).
In the absence of clinical or bacteriological factors, an isolated slight rise in CRP is not a sufficient reason for starting antibiotics, as the rise may be a false positive result unrelated to infection.
A decrease in CRP by 25% or more from previous day's level is a good indicator of resolution of sepsis, with a sensitivity of 97%, specificity of 95% and predictive value of 97%. At least 2 CRP levels, obtained 24 hours apart, with levels < or = 10 mg/L, are needed to identify infants unlikely to be infected. Negative predictive value of serial serum CRP is 100% in deciding duration of antibiotics therapy in neonatal septicemia up to 7 days.
Q152. Is it worthwhile doing a blood culture? The yields are so poor?
Isolation on blood culture of 20–30% is a very good rate. Trust your lab and stop antibiotics if culture is sterile and baby is well. In general, we would suspect sepsis at least 10 times more than it is actually there. This is OK because symptoms and signs of so many illnesses overlap in the newborn. If there is culture positivity of 70%, either they are under-suspecting or there is contamination (at collection or in lab).
Q153. What is the status of CSF study in sepsis?
  • Suspicion of meningitis (lethargy, hypo- or hypertonia, seizures, apnea, excessive irritability, bulging fontanel, or septic shock)
  • Positive blood culture
  • Refractory seizures.
Q154. What is the utility of procalcitonin in diagnosis of sepsis?
Procalcitonin is an excellent marker for severe, invasive bacterial infection in children. However, the use of procalcitonin in the diagnosis of neonatal bacterial infection is complicated, but if correctly used procalcitonin results in a higher specificity than C-reactive protein. In addition, procalcitonin has been shown to correlate with severity of disease and can therefore be used as a prognostic marker.
Q155. Which newborns should be started on antibiotics?
All symptomatic term and preterm babies need septic evaluation and treatment for infection regardless of the presence or absence of risk factors.
Q156. How should one interpret positive sepsis screen in an asymptomatic newborn?
Asymptomatic preterm babies with either: Strong maternal risk factors for sepsis like chorio-amnionitis, PPROM, PROM, maternal 40UTI, intrapartum maternal fever >38°C and positive sepsis screen should be initiated on antibiotics.
Asymptomatic term babies:
  1. If there are no risk factors, apart from the PROM, the infant is usually observed closely and treated only if sepsis screen is positive or symptoms develop
  2. If there is a risk factor present in addition to PROM, such as maternal intrapartum fever or suspected chorio-amnionitis that infant should be treated as potentially septic, even if completely asymptomatic.
Q157. When should I suspect fungal infection?
There are no specific symptoms or signs. Fungal infections should be considered in infants who have been receiving broad spectrum antibiotics, TPN and/or ventilation, if they develop deterioration or new symptoms/signs. Appearances of new thrombocytopenia, hyperglycemia and/or abdominal symptoms/signs which suggest NEC but AXR does not confirm are suggestive. Routine blood culture bottles are able to grow Candida and usually growth occurs within 96 hours but can be delayed till 7 days. CSF must be done in all proven cases.
Q158. Is there role for fluconazole prophylaxis?
Fluconazole prophylaxis may be useful in units dealing with ELBW infants and documented high incidence of fungemia (> 10% at least). For others, it will lead to more problems. Not having a culture facility and hence not knowing how much is the incidence is no justification. Candida grows very well in routine blood culture bottles.
Q159. What is the status of IVIG, G-CSF, FFP and exchange transfusion in sepsis management?
There is insufficient evidence to support the routine administration of IVIG preparations investigated to date to prevent mortality in infants with suspected or subsequently proved neonatal infection. Use of IVIG should be restricted to severe infection. There is currently insufficient evidence to support the introduction of either G-CSF or GM-CSF into neonatal practice, either as treatment of established systemic infection to reduce resulting mortality, or as prophylaxis to prevent systemic infection in high-risk neonates. FFP is used in cases of DIC. There are anecdotal reports of exchange transfusion cases of sclerema but it is not standard of care.
Q160. If the culture reports are available after starting therapy and they do not correlate with the present management do we need to change the drugs?
When the therapeutic response to initial therapy is excellent it can be continued because of lack of correlation between in vivo and in vitro antibacterial sensitivity pattern.
Q161. What conditions mimic “refractory sepsis”?
41Metabolic disorders (IEM, hypoglycemia), polycythemia, TORCH complex, congenital anomaly and immunological disorder.
  1. Lam HS, Pak C Ng. Diagnostic markers in neonatal sepsis. Fetal and Maternal Medicine Review. 2007;18:153-65.
  1. Thaver Durrane, Ali Syed Asad, Zaidi Anita KM. Antimicrobial resistance among neonatal pathogens in developing countries. The Pediatric Infectious Disease Journal. 2009;28(1).
  1. Yu Z, Liu J, Sun Q, et al. The accuracy of the procalcitonin test for the diagnosis of neonatal sepsis: a meta-analysis. Scand J Infect Dis. 2010;42(10):723-33.
Q162. How to clinically look for jaundice?
Jaundice is assessed by looking at the baby's skin, sclera, or mucous membranes for yellowish discoloration. The extent of jaundice is estimated in a well lit room or preferably in natural light in a naked infant. The skin is blanched by digital pressure over bony parts to reveal underlying yellowing (Fig. 1.6). This is done at several sites on the baby's body, ranging from the face where the jaundice appears first, to the mid sternum, knee, palms and soles. The extent of cephalo-caudal progression of jaundice is judged by the Kramer's criterion. The clinical assessment for severity does not strongly correlate with measured bilirubin values, is not of help in preterms and in infants under phototherapy.
zoom view
Fig. 1.6: Jaundice assessment is by inspection and applying digital pressure to see for yellowish underlying skin
Q163. Is clinical evaluation for jaundice estimate reliable?
42Review of the evidence shows that, in most term babies, healthcare professionals and parents are capable of recognizing jaundice but not very good at assessing its severity clinically. However if they consider that a baby is not visibly jaundiced, this assessment is generally reliable in ruling out hyper-bilirubinemia. It must be realized that visual examination of the infant is not a reliable measure of jaundice alone to estimate the bilirubin level and is prone to errors especially in dark pigmented babies, preterms and in babies receiving phototherapy.
Q164. How should discharge planning be done for every newborn so that we do not miss significant jaundice appearing later?
All newborns at the time of discharge should undergo assessment for presence of risk factors predicting for severe hyper-bilirubinemia. Based on the risk factors (Table 1.25) the follow-up schedule should be planned.
Table 1.25   Pre-discharge assess for risk factors for significant jaundice (NNF CPG, 2010)
Risk factors
  • Primi-para mother
  • Visible jaundice at discharge
  • Gestation < 38 weeks
  • History of jaundice requiring treatment in previous sibling
  • ABO/Rh. incompatibility
  • Geographic prevalence for G6PD deficiency
  • Weight loss at discharge >3% per day or >7% cumulative weight loss
Newborns with risk factors should be seen within 24–48 hours of discharge. More the risk factors present more is the chance of developing severe jaundice.
Q165. Why should breastfeeding be assessed for every jaundice newborn?
Insufficient breast milk aggravates hyper-bilirubinemia. Hence all mothers should be assessed during hospital stay and at discharge for lactation sufficiency. Every effort must be made to support, promote and practice exclusive and frequent breastfeeding (8–10 times every 24 hours). Use of top feeds, pre-lacteals should be discouraged.
Q166. What physical findings should always be looked for on clinical examination in newborn with jaundice?
Table 1.26   Focused clinical assessment
Look for
Preterms are more at risk for significant jaundice.
Well being
Sick babies (unstable vital parameters, change in activity, sleep or feeding) are more at risk for severe jaundice and bilirubin encephalopathy.
Weight loss at discharge >3% per day or >7% cumulative weight loss is suggestive of inadequate feeds which is a contributory factor for significant jaundice.
Age in hours
Hour specific bilirubin nomogram can predict babies likely to develop significant jaundice. The decision making is based on interpretation of total serum bilirubin (TSB) in relation to age in hours. Visible jaundice in first 24 hours is always pathological. A jaundice beyond 21 days merits investigations.
Extent of jaundice
Not reliable in preterms, under phototherapy and in dark pigmented babies.
Urine/stool pattern
High colored urine and clay stools suggest direct hyper-bilirubinemia. Frequent passage of urine which is colorless assures adequacy of feeding.
Pallor, hepatomegaly or splenomegaly
Suggests hemolytic jaundice and high-risk for developing severe hyper-bilirubinemia.
Signs of sepsis
Assess for activity, pustules, umbilical discharge, temperature fluctuation, foul smell, rash, signs of poor perfusion.
Aggravates jaundice.
Activity, feeding
Decreased activity, sleepy and not feeding well on the breast needs evaluation of underlying cause and bilirubin encephalopathy.
Q167. What are signs of bilirubin encephalopathy?
Table 1.27 and Figure 1.7 show signs of bilirubing encephalopathy.
Table 1.27   Signs of bilirubin encephalopathy
Nonspecific, subtle
(First 1–2 days)
Progressive toxicity
(Up to 7 days)
Advanced toxicity
(After 1st week)
Mental status
Sleepy, poor feed,
weak suck,
decreased alertness,
Lethargy + irritability
minimal feeding
Stupor, coma or seizures
No feeding
Muscle tone
Slight decrease
Hyper or hypotonia
depending on arousal
state or mild nuchal/
truncal arching
Marked retrocollis or
opisthotonus or
decreased tone, or
bicycling movements
High pitched
zoom view
Fig. 1.7: Bilirubin encephalopathy
Q168. How to objectively assess jaundice bedside?
Transcutaneous bilirubinometry (TcB) is more accurate than visual inspection when used to assess the degree of jaundice in term and near-term babies (Fig. 1.8). When placed against forehead or sternum it displays a bilirubin value by measuring reflected light via a micro-spectrometer or by calculating changes in optical density between reflected light sources. The measurements are within 2–3 mg/dL of the TSB and can replace a measurement of serum bilirubin in many circumstances, particularly for TSB levels less than 15 mg/dL. Proper staff training is must. It is not recommend using TcB measurements in high-risk population (< 35 weeks) and in infants receiving phototherapy.
TcB values are interpreted using nomograms.
zoom view
Fig. 1.8: Transcutaneous bilirubinometer
Q169. What is the role of cord blood in jaundice management?
45Current evidence does not support measuring umbilical cord blood bilirubin levels for the prediction of subsequent hyper-bilirubinemia in healthy babies with the exception of Rh iso-immunized pregnancy. If the mothers blood group is not known cord blood should be collected for baby blood group. Umbilical cord blood direct Coombs test is useful particularly in a baby of a woman who did not receive anti-D during pregnancy.
Q170. Which jaundice newborns should be subjected to investigations?
  • Visible jaundice in the first 24 hours
  • Any baby, if there is clinical doubt about the degree of jaundice
  • Any unwell baby with jaundice
  • Any baby with clinical signs of obstructive jaundice
  • Prolonged jaundice, greater than 3 weeks
  • Babies at or above the relevant treatment threshold for their postnatal age, and for all subsequent measurements.
Q171. Which investigations should be done in a newborn with jaundice?
Table 1.28   Investigations for significant hyper-bilirubinemia (Adapted from Pediatrics. 2004;114(1):297-316)
For all jaundice babies
  • Total serum bilirubin or TcB
  • Mother and baby blood group
  • Hemoglobin or PCV
Unexplained rapidly rising TSB
  • Total and direct bilirubin
  • Peripheral blood smear
  • Reticulocyte count
  • Direct Coombs test (if mother is ‘O’ or Rh negative)
  • G6PD assay
  • S albumin (optional)
Elevated direct hyper-bilirubinemia
  • Total and direct bilirubin
  • Urine examination and urine culture
  • Evaluation for infection, as indicated
  • Thyroid profile (T3, T4, TSH)
  • Expert referral
Prolonged jaundice
OR Sick infant with jaundice
  • CBC
  • Total and direct bilirubin
  • Evaluate for cholestasis, if indicated
  • Urine examination and culture
  • Evaluate for infection, as indicated
  • Urine for reducing substances
  • Thyroid profile (T3, T4, TSH)
  • Evaluation for infection, as indicated
Q172. How to interpret bilirubin value?
Total serum bilirubin (TSB) levels should be used to guide management. Previous practice of subtracting direct bilirubin from the total serum bilirubin when deciding on management in babies with hyper-bilirubinemia is not advocated. All bilirubin levels are interpreted according to the baby's postnatal age in hours and 46hyper-bilirubinemia managed according to threshold values. Direct reacting or conjugated bilirubin level should not be subtracted from the total bilirubin unless it is greater than 50% of the total. Direct bilirubin > 2 mg% or direct fraction > 20% of total bilirubin suggests direct hyper-bilirubinemia.
zoom view
Fig. 1.9: Hour specific bilirubin nomogram for predicting jaundice (Pediatrics. 2004;114(4):297–314)
  1. American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. 2004;114(1):297-316.
  1. Guruprasad G, Chawla D, Aggarwal S. Management of neonatal hyperbilirubinemia In: NNF Clinical Practice Guidelines. 2010 [online] Available from pdf [Accessed July, 2014].
Q173. How to manage a newborn with maternal chickenpox during delivery?
If maternal infection occurs one to four weeks before delivery, up to 50% of babies are infected and approximately 23% of these develop clinical varicella despite high titers of passively acquired maternal antibody. Severe chickenpox is most likely to occur if the infant is born within seven days of onset of the mother's rash. Risk to the neonate includes severe disseminated chickenpox, pneumonia, and fulminant hepatitis.
47If there is contact with chickenpox, no intervention is required if the mother had past history of chickenpox.
While in hospital, a mother and/or infant with lesions should be isolated from other patients. An infected mother does not need to be isolated from her own baby. Newborns with the congenital varicella syndrome are not infectious and need not be isolated. Continue to encourage breastfeeding unless lesions are on or near the nipple. Ensure routine newborn care. Infants should be closely monitored for signs of infection for 14–16 days. Admit infant into hospital isolation room if rash develops or is unwell.
Give the infant ZIG (2 mL IMI) as soon as possible after delivery or onset of maternal illness within 72 hours if:
  • Mother is sero-negative
  • Her sero-status cannot be determined and history is negative.
  • Infant born at less than 28 weeks gestation or <1000 g birth weight
  • If mother develops chickenpox 1 week on either side of delivery ZIG should be given to infants to avoid overwhelming disease regardless of other contacts.
    The dose—regardless of weight—is 2 mL (=2000 IU) IM for newborns.
    Acyclovir is given to infants who develop chickenpox and/or:
  • Did not receive ZIG prophylaxis within 24 hours
  • Are immunocompromised
  • Are premature (less than 28 weeks gestation at birth)
  • In infants whose mothers develop chickenpox 4 days before to 2 days after delivery, because these babies are at highest risk of a fatal outcome despite VZIG prophylaxis.
Routine acyclovir prophylaxis in conjunction with ZIG is not currently recommended in the neonatal population, due to lack of evidence. Acyclovir cream/ointment are not recommended in chickenpox (Fig. 1.10).
zoom view
Fig. 1.10: Chickenpox rash
Q174. How to evaluate a newborn with chickenpox exposure during postnatal ward or at home from siblings?
48The risk of the newborn developing severe disease from postnatal exposure is considerably less than from transplacentally acquired varicella, but some babies with postnatal exposure will develop severe disease. The risk to the newborn baby is determined primarily by the presence or absence of transplacentally acquired maternal IgG antibody. If the mother has had chickenpox, the risk from siblings is negligible. If not, the baby should be given ZIG, which will minimize the risk. Newborn baby does not need to be isolated from its siblings with chickenpox, whether or not the baby was given ZIG.
Q175. What should be done for chickenpox exposure within the neonatal unit?
Spread of VZV is primarily by the respiratory route, so isolation in a separate room is desirable for babies with pneumonitis, and essential if they require artificial ventilation. Staff hand-washing is important in reducing spread of the virus. Infants born after 28 weeks’ gestation should only be given ZIG if they have had significant exposure (defined above) and serological tests show the mother to be sero-negative. All infants born at or before 28 weeks’ gestation or born weighing under 1000 g with significant exposure should be given ZIG regardless of the results of serological testing of the mother.
All staff who have had significant exposure to an index case and who do not have a history of previous chickenpox infection or of VZV vaccination should have serological tests. If they are VZV antibody negative, they should be removed from clinical duties from days 7–21 after exposure (days 7–28 if they receive ZIG). Quarantine of cases should continue until all lesions have crusted. Quarantine of contacts should be from days 7–21 after exposure and from days 7–28 after exposure if they received ZIG. Infants with pneumonitis requiring ventilation must be isolated. Where isolation facilities are unavailable, cases should be transferred to a unit with isolation facilities.
  1. Michael Paul Tan, Gideon Koren. Chickenpox in pregnancy: Revisited. Reproductive Toxicology. 2006;21:410-20.
  1. Smith CK, Arvin AM. Varicella in the fetus and newborn. Seminars in Fetal and Neonatal Medicine. 2009, doi:10.1016/j.siny.2008.11.008.
Prevention of hypoglycemic brain injury requires attention to babies at risk of poor metabolic adaptation at birth and with clinical symptoms of low glucose to brain and not just blood sugar levels. All babies have a physiological drop 49in blood glucose in the first few hours after birth; this will not be associated with any symptoms of hypoglycemia and will show “normal blood sugars” within 3–4 hours after birth.
Babies with disturbed adaptation do not recover from the physiological drop in blood sugar levels and continue to remain hypoglycemic, may show early and definite symptoms of low glucose on brain. They need close monitoring and early therapy. Hence, perinatal history and observing for symptoms are equally important as is monitoring of blood glucose on bed side with an accurate point-of-care method of glucose assay.
  1. Babies at-risk of poor adaptation—which babies need monitoring for hypoglycemia—in a recent trial by Harris et al, on hypoglycemia employing an accurate method of glucose monitoring (glucose oxidase method), 50% of infant of diabetic mothers, late preterms (35–37 weeks), small infants (<10th centile/<2500 g birth weight) and large infants (>90th centile/2500 g birth weight) had hypoglycemia.
    1. Hyperinsulinemia—babies requiring high glucose infusion rates–often up to 10 mg/kg/minute and have severe hypoglycemia even after starting intravenous glucose infusion must be considered as having hyperinsulinemia, e.g. infant of mother with gestational diabetes, some babies with perinatal asphyxia, and sepsis, primary hyperinsulinemia.
    2. Low body stores–in preterm and IUGR deposition of glycogen and fat have been very less in last trimester. These babies have hypoglycemia in the fasting phase (before the next feed), but often improve with feeding or minimal glucose infusion rates 5 mg kg/min (3 mL/kg/hour of 10% dextrose)
    3. Endocrine and metabolic causes—less common—must consider when severe hypoglycemia not responding to high infusion rates refractory and taking longer to stabilize—persistent (7–10 days)—adrenal insufficiency, pituitary insufficiency, disorders not allowing fat or amino acids to be concerted to glucose in hypoglycemic states—assay of cortisol levels, pH, ammonia, urine reducing substances as a screen and tandem mass spectrometry, gas chromatography studies of blood and urine in reference labs for IEM.
    4. Any sick baby mostly on parenteral nutrition (no/minimal enteral feeds)
  2. Clinical signs of low glucose on brain—there is a significant difference in the incidence of brain injury among babies with symptomatic hypoglycemia vs. babies with low sugar levels and asymptomatic. It is critical to record whether any of symptoms were noted when blood sugar levels are recorded as low.
    1. Early nonspecific—irritability, lethargy, poor feeding, jitteriness
    2. Severe and definite signs—seizures and coma—even at this stage prompt correction of glucose may prevent permanent brain injury
  3. 50Point of care tests (glucometers) are not designed for monitoring low blood sugar levels, and are likely to sometimes miss hypoglycemia. Many of them have low sensitivity in picking up hypoglycemia. Hence, babies with symptom of hypoglycemia and those at risk of poor adaptation may require confirmation of borderline sugar values 50–60 mg/dL with lab sugar, and may be treated with feeds/intravenous glucose till lab values are available.
  4. Feeding a baby with hypoglycemia–breast milk has alternate fuels, especially for brain, i.e. fat (ketones) and lactate. Babies on some or full enteral feed are less likely to have permanent brain injury even with low blood glucose levels. Formula milk does not have the same protective abilities. Baby not on any feeds is at very high-risk of brain injury if blood glucose levels fall.
  5. Blood glucose levels should best be tested pre-feed (before feeding) as the lowest values are expected at this time. A baby with two pre-feed blood sugar values in safe range is at low-risk of hypoglycemia.
  1. Hawdon JM. Neonatal hypoglycemia: are evidence based guidelines achievable? Neo Reviews. 2014;15:e 91.
  1. Ho HT, Yeung WKY, Young BWY. Evaluation of “point of care” devices in the measurement of LO glucose in neonatal practice. Arch Dis Child Fetal and Neonatal Edn. 2004;89:F356-9.
Oxygen is one of the most common therapies used in sick neonates. In the recent years, attention has been drawn to potential risks/toxicity of oxygen and questions are being asked as to how low oxygen targets can be set without increasing mortality/neurodevelopment.
Q176. What is the best way to deliver oxygen to a newborn?
Oxi-hood is preferred for babies requiring low FiO2 and nasal catheter for babies requiring high and consistent FiO2 (severely ill).
Oxi-hood generally delivers only up to 30–40% FiO2. The advantages of oxi-hood are that there is no need for humidification/warming the oxygen; it does not touch the baby and hence, does not irritate the baby. But, high flow rates are necessary up to 2–3 L/kg/min to prevent re-breathing of carbon dioxide. This adds cost, as oxygen is expensive. Also, baby cannot be held by mother and cannot be fed by breast/paladai.
Nasal catheter (6–8F) is passed to a distance of approximate 2.5 cm, (measured from side of nostril to inner margin of eye brow). At flow rates of 0.5–1 L/minute (lower flow rates for newborn) higher 51FiO2 can be delivered by nasal catheter. Humidification/warming are not necessary. Removing the catheter from nose and cleaning 12 hourly is recommended. Nasal catheter can generate a modest PEEP. This may be beneficial, but, caution must be exercised at higher flow.
Nasopharyngeal catheter (nose to ear tragus, about 7.5 cm) has risk of gastric distension, higher PEEP and high-risk of nose block; humidification and warming may be necessary.
Face mask delivers low FiO2, irritates the baby by contact.
Holding oxygen flow near to nose can be unreliable in oxygen delivery.
Q177. Is ABG necessary, can I manage monitoring oxygen therapy with pulse oximetry?
Pulse oximetry is probably the best method to monitor oxygen therapy. The pulse oximeter probe should preferably be fixed to right upper limb (preductal). Target saturations for preterm are 90–95%, alarm limits may be set at 88–96. Term babies target saturation is >95% (PaO2 60–90) and for PPHN >97% (PaO2 80–100).
Pulse-oximetry has many benefits—it is easy to use, continuous monitor and also a physiologically appropriate measure compared to PaO2 (ABG). The problem with pulse oximetry is that it cannot diagnose hyperoxia. Strict attention to upper saturation limits, and decreasing FiO2 (using blenders, decreasing flow rates in nasal catheter, opening side-holes/ports in oxi-hood) can overcome this risk; but, most often alarms are either inappropriately set at 100 or overlooked.
A good pulsating wave form is necessary to get a reliable record. Patient movement, shock, too tight pulse oximeter probe can result in false values. Excess light from phototherapy or examination lamp can interfere with pulse oximeter. Covering the probe site with a cloth will be necessary.
Disposable probes are better than reusable ones; they decrease risk of cross-infection, snugly fit to all size babies. They should be selected according to the type of pulse-oximeter in the unit; they cost about 1000 Indian rupees. Reusable probes are mostly difficult to fix well; they have the advantage of one-time nonrecurring cost; cleaning with spirit can decrease risk of cross-infection. They are expensive about 15–25,000 rupees can be repeatedly used if not damaged by rough use.
It is advisable to change pulse oximeter site once in 6–8 hours.
Transcutaneous PaO2 monitors should be used in preterm only after 2 weeks age.
Pulse oximeter with new signal extraction technology (SET) is faster to respond to oxygen changes in body and more sensitive in shock situations.
Oxygen in Labor Room
Term baby's resuscitation must be started with room –air, (21% FiO2, no “oxygen”) and preterm babies may be started with 30–40% FIO2. This makes it necessary to have blenders in labor rooms. Both 100% oxygen and room air may be associated with risk in preterms at birth.
Q178. What are the risks with oxygen therapy?
Hyperoxia due to unmonitored use is associated with ROP and lung injury. There is risk of toxicity even with brief exposures; hence, the importance of monitoring even from labor room.
Recently studies attempting restricted use of oxygen have reported higher mortality in preterm babies with saturations less than 90%.
Q179. How do I know the baby needs more than oxygen for his respiratory illness—CPAP/ventilation?
Severe retractions, grunting and tachypnea suggest low functional residual capacity and lung compliance and must be supported with distending pressure (CPAP/ventilation) and not just oxygen. High FiO2 needs also most often is due to poor ventilation.
  1. Frey B, Shann F. Oxygen administration in infants. Arch Dis Child Neonatal Edn. 2003;88:F 84-88.
Q180. If a mother is able to provide breast milk for a preterm baby, do we need to add any supplements/added nutrients?
Potential nutrient needs—calories, protein, iron, calcium, phosphorus, vitamin D.
Protein needs may be as high as 3–4 g/kg/day and mother milk may provide maximum up to 2 g/kg/days.
Iron may be supplemented at 2–3 mg/kg/day for 12–15 months, starting at least by one month of age. Recent trial from India found better ferritin, MCV and Hb after starting iron earlier at 2 weeks compared to 6 weeks in VLBW babies.
Vitamin D has been recommended at 400–800 IU/day till one year. Recent trial from India supported use of 800 IU in babies born between 28 and 34 weeks. Calcium (150–220 mg/kg/day) and phosphorus (75–140 mg/kg/day) supplementation is necessary for VLBW infants. Phosphorus and alkaline phosphatase levels should be monitored from 4 to 6 weeks after birth and then every 2 weekly. Phosphorus levels less than 4 and ALP more than 800–1000 are considered risk factors for rickets.
53Use of multi-nutrient human milk fortifiers added to expressed mothers milk seems to get benefits of mothers own milk and is targeted at closing the nutrition gap. In a recent RCT, comparing babies on fortified human milk vs. babies on un–fortified human milk, growth at one year was better in weight, length and OFC. On analyzing nutrient differences, protein and calories were similar in both arms; only calcium and phosphorus were far more in the intervention (fortifier) group, possibly pointing to role of mineral on bone growth. Problem with use of HMF is that mother has to express milk and direct breastfeeding is interrupted. Direct feeding is necessary to sustain breast milk for long durations. Studies evaluating short-term outcomes (till discharge/term) on preterm babies (<31 weeks) gestation found growth benefits HMF and suggest than 1.4 g/100 mL or more may be necessary. HMF with high protein is not yet available in India.
Controversies regarding selective use (in case of poor growth) or universal use are unresolved. In a survey on use of nutrient supplements from level II and III neonatal units from UK about 98% use HMF, iron and multi-vitamins and fewer units use folic acid. Seventy-eight percent units use HMF only in babies not gaining weight.
Q181. If a mother is unable to provide breast milk for a preterm baby, do we need a special formula?
If breast milk is not available in spite of best efforts, formula milk designed for preterm babies should be used. Fortified formula milk designed for preterm babies have not demonstrated consistent growth benefits over formula for term babies although biochemical mineral deficiency states are proven in babies fed term formula.
Q182. What should be the strategy for SGA or late preterm baby?
There are no definite guidelines for SGA neonates.
Q183. Do we wean at chronological age/corrected age?
If breast milk is available, weaning may be at the age of 6 months of chronological age like in term babies. Babies must develop sitting and swallowing maturity. Weaning may be required before 6 months of chronological age if growth falters. There is insufficient evidence to guide practice.

  1. 54 Abrams SA; committee on nutrition. Calcium and vitamin D requirements of generally fed preterm infants. Pediatrics. 2013;131(5):e1676-83.
  1. Ahmed M, Brent J, Ginn E. Use of enteral nutrition supplementation: a survey of level II and level III units in England. J Coll Sug Physicians Pak. 2013;23(9):683-5.
  1. Joy R, Krishnamurthi S, Bethou A, Rajappa M, Ananathanarayan PH, Bhat PV. Early vs. Late Enteral prophylactic iron supplementation in preterm VLBW infants: a RCT. Arch Dis Child fetal Neonatal Edn. 2014;99(2):F105-9.
  1. Morgan JA, Young L, McCormick FM, McGuire W. Promoting growth for preterm infants following discharge. Arch Dis Child fetal Neonatal Edn. 2012;97:F295-8.
  1. O Connor DL, Unger S. Post discharge nutrition of the breast fed preterm infant. Seminar in Fetal and Neonatal medicine. 2013;18:124-8.
Q184. How do we diagnose shock in a sick newborn?
Neonates differ from children/adults in their physiological responses to shock, hence, the same definitions are not applicable. Useful end points for diagnosing circulatory dysfunction are any one of the three after a 40 mL/kg bolus of saline in term born and 10 mL/kg in babies <32 weeks
  • MAP <5th centile in term babies, MAP <30 or <5th centile in preterm with capillary refill more than 4 seconds
  • Need for inotropes to maintain blood pressure
  • Capillary refill less than 4–5 seconds, urine output < 0.5 mL/kg / hour, lactate > 2 time's normal, base excess > 4, core peripheral temperature difference > 3 C in term babies (less specific in preterm).
Other pointers to critical circulatory dysfunction due to septic shock are altered mental status, need for high FiO2 (>50%) to maintain a saturation of 92%, drop in platelet count to <80,000, rise in ALT and S. creatinine two times normal.
Functional ECHO and NIRS may help identify poor cerebral perfusion with greater accuracy in ELBW babies in first 3 days where many parameters like blood pressure, capillary refill and urine output have innate fallacies in recognizing shock.
Q185. Is invasive BP monitoring better?
All published reference values of blood pressures in neonates are from indwelling arterial catheters. Noninvasive BP monitoring is easy to use and with low risk of vascular complications, if the sick neonate has an arterial line in place, invasive BP is the gold standard. Values obtained by NIBP are about 3–5 mm Hg higher. Correlation with IBP is reasonable, but, depends on use of appropriate cuff size.
Q186. What is the approach to resuscitation of a baby with shock?
55In term neonates with shock initial shock management is aggressive volume resuscitation with 40–60 mL/kg. In preterm babies, after a bolus of 10–20 mL/kg over 30–60 minutes, fluid boluses may be associates with risk of IVH and cardiac overload. Maintain blood sugar, ionized calcium, temperature, Hb > 10, airway and supportive ventilation, oxygen as necessary.
Q187. Which is the inotropes of choice in a baby with shock?
Dopamine at 5–10 microgram/kg/min may be the inotrope of choice in term born babies not responding to volume. In VLBW baby's dobutamine in low doses may improve cerebral perfusion better than dopamine; if tachycardia is significant, the dose must be decreases, at higher doses and cardiac oxygen demand may increase with use of dobutamine. Epinephrine, nor-epinephrine and Milrinone are not studied enough in neonatal shock. In one study adding NE was helpful when volume + dopamine/dobutamine was not effective in term babies, in another study low dose epinephrine was found to be equally effective as low dose dopamine in VLBW babies.
Q188. Steroids in shock?
In babies not responding to volume and vasopressors, hydrocortisone in the dose of 1 mg/kg/dose 8th hourly has shown to improve blood pressure, decrease heart rate especially in very preterm babies. Drawing a sample of serum cortisol prior to start of steroids may help characterize the cause of shock.
Q189. What is low systemic blood flow?
In very preterm babies, in the first 24 hours of life, blood pressure and clinical signs of hypo-perfusion fail to identify poor systemic blood flow (SBF), ECHO diagnosis. Babies <29 weeks, ventilated with MAP > 8 and FiO2 > 30% are at risk of poor SBF. Asphyxiated, infected babies also are at risk of low SBF. ECHO within one hour of life and use of indomethacin in babies with large PDA (>1.6 mm) are associated with improved SBF. In this setting, on day 1, with normal BP and ECHO proven low SBF, dobutamine is the inotrope of choice after a saline bolus of 10 mL/kg. Milrinone has been tired. Dopamine may be used if the baby has hypotension; dopamine is the inotrope of choice after the first day of life (Figs 1.11A and B).56
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Figs 1.11A and B: ACCCM consensus guidelines for treatment of shock in term infants (A) and suggested modifications for preterm infants (B)Abbreviations: RDS, respiratory distress syndrome; NRP, Neonatal Resuscitation Program; CVP, central venous pressure; MAP, mean arterial pressure; ScvO2-central venous oxygen saturation; SVC, superior vena cava; CI, cardiac index; VLBW, very low birth veight; PDa, patent ductus arteriosus; PPHN, persistent pulmonary hypertension of the newborn
  1. Osborn D, Evans N, Kluckow M. Diagnosis and treatment of low systemic blood flow in preterm infants. Neo Reviews. 2004: e109.

  1. 58 Wynn JL, Wong HR. Pathophysiology and treatment of septic shock in neonates. Clin Perinatol. 2010;37(2):439-79.