Neonatology & Newborn Care
The first minutes, the yellow baby, and the breathless newborn
The delivery room: APGAR and resuscitation
APGAR. Five signs (Appearance, Pulse, Grimace, Activity, Respiration) are each scored 0–2 at 1 and 5 minutes. A 5-minute score under 7 prompts continued scoring every 5 minutes. The score describes the baby's condition but does not direct resuscitation: interventions are triggered in real time by breathing and heart rate.
| Sign | 0 | 1 | 2 |
|---|---|---|---|
| Appearance (color) | Blue or pale all over | Pink body, blue extremities | Pink all over |
| Pulse | Absent | <100/min | ≥100/min |
| Grimace (reflex irritability) | No response | Grimace | Cry, cough, or active withdrawal |
| Activity (tone) | Limp | Some flexion | Active motion |
| Respiration | Absent | Slow, irregular, weak cry | Strong cry |
Ventilation first. Unlike adult arrest, neonatal arrest is almost always respiratory, so ventilation comes before compressions, and heart rate is the most important indicator of response throughout.
- Warm, dry, stimulatePosition the airway; suction only if secretions obstruct it.
- Apneic, gasping, or HR <100Positive-pressure ventilation (PPV), the single most important step.
- HR <60 after 30 s of effective PPVChest compressions coordinated with ventilation at a 3:1 ratio, with an advanced airway in place and oxygen raised to 100%.
- HR still <60Epinephrine, preferably intravenous via the umbilical vein.
If the heart rate is not rising, the ventilation is usually ineffective: check that the chest moves, then adjust the mask seal, reposition the airway, suction, raise the pressure, or place an advanced airway before escalating to compressions.
Neonatal jaundice
Physiologic jaundice. It appears after 24 hours, peaks on days 3–5, and is unconjugated, reflecting immature UDP-glucuronosyltransferase (UGT) and high RBC turnover.
Red flags. Jaundice in the first 24 hours is always pathologic and usually hemolytic: ABO incompatibility (type O mother, type A or B infant), Rh incompatibility, or G6PD deficiency. Check total and direct bilirubin, infant blood type and direct Coombs test, CBC with smear, and reticulocyte count. A rapid rise also needs evaluation, and jaundice persisting beyond 2 weeks (formula fed) or 3 to 4 weeks (breastfed) needs a direct bilirubin to exclude cholestasis.
| Type | Timing | Mechanism | Management |
|---|---|---|---|
| Hemolytic | Within 24 h | ABO or Rh isoimmunization, G6PD deficiency | Phototherapy; exchange transfusion if extreme |
| Physiologic | After 24 h, peaks days 3–5 | Immature UGT, high RBC turnover | Observe; phototherapy per AAP hour-specific thresholds |
| Breastfeeding jaundice | First week | Inadequate intake and dehydration increase enterohepatic circulation ("not enough milk") | More frequent, effective feeding |
| Breast milk jaundice | After day 7, peaks around 2 weeks | Factors in the milk impair conjugation ("the milk itself") | Benign; continue breastfeeding |
| Conjugated (direct) | Any time | Biliary atresia, sepsis | Always pathologic: urgent workup |
Kernicterus. Very high unconjugated bilirubin, which is fat-soluble, crosses the blood-brain barrier and deposits in the basal ganglia. Acute bilirubin encephalopathy (lethargy, hypotonia, poor suck, then arching and a high-pitched cry) progresses to kernicterus: choreoathetoid cerebral palsy, sensorineural hearing loss, and upgaze palsy. Prematurity, hemolysis, sepsis, and drugs that displace bilirubin from albumin (ceftriaxone, sulfonamides) raise the risk.
Treatment. Phototherapy converts bilirubin into water-soluble isomers excreted without conjugation; thresholds come from the AAP hour-specific phototherapy curves, which shift with gestational age and neurotoxicity risk factors. Exchange transfusion is reserved for dangerously high levels or signs of acute bilirubin encephalopathy.
Conjugated hyperbilirubinemia with acholic stools and dark urine suggests biliary atresia, which needs a Kasai portoenterostomy early (ideally before about 2 months) to prevent cirrhosis.
Respiratory distress in the newborn
| Feature | Respiratory distress syndrome | Transient tachypnea (TTN) | Meconium aspiration |
|---|---|---|---|
| Who | Premature infants; also infants of diabetic mothers | Term or late-preterm, often after cesarean delivery | Post-term, meconium-stained fluid |
| Cause | Surfactant deficiency | Retained fetal lung fluid | Aspirated meconium: obstruction, inflammation |
| Chest x-ray | Reticulogranular ground glass, air bronchograms, low volumes | Fluid in the fissures | Patchy infiltrates, hyperinflation |
| Course | Surfactant and CPAP | Resolves in 24–72 h with support | Risk of persistent pulmonary hypertension |
RDS prevention. Antenatal betamethasone given to the mother accelerates fetal surfactant production and prevents RDS. A lecithin-to-sphingomyelin (L/S) ratio below 2 in amniotic fluid indicates immature lungs. Maternal diabetes delays surfactant maturation because fetal insulin inhibits it. Oxygen and ventilation in preterm infants carry risks of bronchopulmonary dysplasia and retinopathy of prematurity.
Persistent pulmonary hypertension complicates meconium aspiration: right-to-left shunting through the ductus and foramen ovale causes hypoxemia, often with a higher preductal than postductal saturation. Treat with oxygen, ventilation, and inhaled nitric oxide, with ECMO for refractory cases.
Neonatal sepsis and GBS prevention
Early-onset sepsis (under 72 hours) is most often group B Streptococcus, followed by E. coli and Listeria. Risk factors are maternal GBS colonization, rupture of membranes over 18 hours, maternal fever, and prematurity. Signs are nonspecific: temperature instability, poor feeding, lethargy, apnea, respiratory distress.
Empiric therapy is ampicillin plus gentamicin, which covers GBS, Listeria, and E. coli. Ceftriaxone is avoided in neonates because it displaces bilirubin from albumin. Add acyclovir when herpes simplex is suspected (vesicles, seizures, elevated transaminases).
Febrile neonate. Per the AAP 2021 guideline, a febrile (38 °C, 100.4 °F) well-appearing infant aged 8 to 21 days needs blood, urine, and CSF cultures and empiric antibiotics. At 22 to 28 days, blood and urine studies and inflammatory markers are obtained; LP and antibiotics are required if markers are abnormal and may be withheld, with hospital observation, if markers and urinalysis are normal.
GBS prevention. Screen mothers by rectovaginal culture at 36–37 weeks. Colonized mothers receive intrapartum penicillin (or ampicillin), ideally at least 4 hours before delivery. GBS bacteriuria during pregnancy or a previous infant with invasive GBS disease warrants prophylaxis without screening.
Hypoglycemia and routine newborn care
Infant of a diabetic mother. Maternal hyperglycemia crosses the placenta and drives fetal hyperinsulinemia. After cord clamping, the glucose supply stops but insulin stays high, causing hypoglycemia (jitteriness, poor feeding, lethargy, seizures). The same hyperinsulinism explains macrosomia, and these infants also develop hypocalcemia, polycythemia (with hyperbilirubinemia), RDS, and hypertrophic cardiomyopathy.
Treatment. Feed the infant; give IV dextrose (a D10 bolus, then infusion) if the infant is symptomatic or the glucose is severely low.
Routine prophylaxis. Every newborn receives intramuscular vitamin K, because gut flora and placental transfer are minimal and breast milk is low in vitamin K; refusing it risks vitamin K-deficient bleeding, including intracranial hemorrhage. Erythromycin eye ointment prevents gonococcal ophthalmia. The first hepatitis B vaccine dose is given at birth, and newborn screening covers metabolic disorders, hearing, and pulse oximetry for critical congenital heart disease.