Pediatrics

INTRODUCTION

Birth is the most dangerous journey of life. Approximately 10% of newborns require some assistance to begin breathing at birth, and about 1% need extensive resuscitation. The single most important and effective step of neonatal resuscitation is the establishment of adequate ventilation of the lungs. Resuscitation is carried out according to the NRP (Neonatal Resuscitation Program) 2020 algorithm.

OVERVIEW OF THE ALGORITHM

Rapid assessment (term? tone? breathing?) → Initial steps (warm, position, clear, dry, stimulate) → Evaluate breathing + heart rate → PPV if apnoeic or HR < 100 → Chest compressions if HR < 60 → Adrenaline if HR < 60 persists

PREPARATION & ANTICIPATION

• Every delivery must have at least one person skilled in initiating resuscitation whose sole responsibility is the baby.
• Prepare a pre-warmed radiant warmer, warm linen, functioning self-inflating bag & masks (sizes 0 and 1), suction, oxygen source with blender, laryngoscope, ET tubes and a functioning clock.
• Identify antenatal / intrapartum risk factors — prematurity, meconium-stained liquor, fetal distress, multiple gestation, maternal fever, antepartum haemorrhage.
• Perform a pre-resuscitation team briefing and equipment check.

INITIAL RAPID ASSESSMENT (at birth, within seconds)

Ask three questions: Term gestation? Good tone? Breathing or crying?

• If all three are YES → routine care with the mother (warmth, dry, skin-to-skin, delayed cord clamping ≥ 30–60 s).
• If any is NO → move the baby to a radiant warmer and begin the initial steps.

INITIAL STEPS — the 'Golden Minute'

The initial steps and, if needed, the start of ventilation must be completed within the first 60 seconds ('Golden Minute'):

• Provide warmth — place under a radiant warmer (preterm < 32 weeks: place in a polyethylene bag/wrap without drying, add a cap).
• Position the airway — slight extension ('sniffing' position); a shoulder roll may help.
• Clear the airway if needed — suction mouth before nose ('M before N') only if secretions obstruct or PPV is anticipated.
• Dry, stimulate, reposition — flick the soles / rub the back; remove wet linen.

EVALUATION — Two vital signs

After the initial steps, evaluate respirations and heart rate. Heart rate is the most important indicator of successful resuscitation; it is best assessed with ECG leads / auscultation (a pulse oximeter responds more slowly).

POSITIVE PRESSURE VENTILATION (PPV) — the key intervention

Indications for PPV: apnoea / gasping, OR a heart rate < 100/min despite the initial steps.

• Start PPV with a mask covering the nose & mouth (not the eyes/chin), at a rate of 40–60 breaths/min ('Breathe… two… three…').
• Start with 21% O2 (room air) for term and 21–30% for preterm, titrated to the target pre-ductal SpO2.
• The best sign of effective PPV is a rising heart rate (also chest rise and improving colour).

If the HR does not rise or the chest does not move, apply the MR SOPA corrective steps in sequence:

TARGET PRE-DUCTAL SpO2 (right hand)

CHEST COMPRESSIONS

• Indicated if HR < 60/min despite 30 seconds of effective PPV (ideally after an alternative airway is placed and O2 increased to 100%).
• Technique: two-thumb encircling technique (preferred) over the lower third of the sternum; depth ≈ one-third of the AP chest diameter.
• Coordinate with PPV in a 3:1 ratio → 90 compressions + 30 breaths = 120 events/min. Rhythm cue: 'One-and-Two-and-Three-and-Breathe-and'.
• Reassess HR every 60 seconds.

MEDICATIONS

Rarely needed if ventilation is effective. Indicated if the HR remains < 60/min despite effective PPV and 60 s of coordinated compressions:

• Adrenaline (epinephrine) 1:10,000 — IV/UVC preferred: 0.01–0.03 mg/kg (0.1–0.3 mL/kg); ET route (0.05–0.1 mg/kg) only while access is being secured. Repeat every 3–5 min.
• Volume expansion — Normal saline / Ringer lactate 10 mL/kg over 5–10 min, or O-negative blood, if hypovolaemia / blood loss is suspected and there is no response.
• Sodium bicarbonate and naloxone are NOT recommended during acute resuscitation.

APGAR SCORE — for documentation, NOT to guide resuscitation

Recorded at 1 and 5 minutes (and every 5 min up to 20 min if low). Resuscitation is guided by respirations and heart rate and is never delayed to assign an Apgar score.

POST-RESUSCITATION CARE

• Monitor temperature, glucose, oxygenation and perfusion; shift to the NICU.
• Consider therapeutic hypothermia for moderate–severe HIE in term/late-preterm babies (start within 6 hours of birth).
• Watch for post-asphyxial multi-organ complications (renal, cardiac, metabolic).
• Communicate with and support the parents; document events accurately.

WHEN TO STOP / WHEN NOT TO START

• If the heart rate remains undetectable after 20 minutes of adequate, effective resuscitation, discontinuation may be reasonable after team and family discussion.
• Non-initiation may be considered for confirmed extreme prematurity or lethal anomalies, per local ethical guidelines.

• Newborn resuscitation is A-B-C; effective ventilation is the single most important step.
• Complete initial steps within the 'Golden Minute'; PPV if apnoeic or HR < 100.
• Corrective steps = MR SOPA; chest compressions if HR < 60 despite effective PPV (3:1).
• Adrenaline 0.01–0.03 mg/kg IV/UVC if HR stays < 60; start air (21%) for term.
• Apgar is for documentation, never to delay resuscitation.

DEFINITION

Neonatal jaundice (icterus neonatorum) is the yellowish discolouration of the skin, sclera and mucous membranes due to accumulation of bilirubin. It is clinically visible when the serum bilirubin exceeds 5 mg/dL in a newborn, and is the most common condition requiring evaluation in the newborn period. About 60% of term and 80% of preterm babies develop visible jaundice.

KRAMER'S RULE (clinical estimation of severity)

Jaundice progresses cephalo-caudally (head to toe); the area involved roughly estimates the bilirubin level:

BILIRUBIN METABOLISM (why newborns are prone)

• Increased production — high RBC mass + a shorter RBC lifespan (70–90 days).
• Decreased uptake & conjugation — immature hepatic UDP-glucuronyl transferase.
• Increased enterohepatic circulation — high intestinal β-glucuronidase, a sterile gut, and delayed feeds.

CLASSIFICATION — Physiological vs Pathological

CAUSES BY TIME OF ONSET

< 24 hours (always pathological): Rh incompatibility, ABO incompatibility, G6PD deficiency, hereditary spherocytosis, concealed haemorrhage, congenital (TORCH) infections.

24–72 hours: physiological jaundice (commonest), sepsis, polycythaemia, cephalhaematoma / bruising, breastfeeding-failure jaundice.

> 72 hours – 2 weeks: sepsis, neonatal hepatitis, breast-milk jaundice, ongoing haemolysis, extravasated blood.

Prolonged (> 2 weeks):

• Unconjugated — breast-milk jaundice, hypothyroidism, ongoing haemolysis, Crigler-Najjar syndrome.
• Conjugated — biliary atresia (surgical emergency — needs Kasai portoenterostomy by 8 weeks), neonatal hepatitis, choledochal cyst, galactosaemia, TORCH, sepsis.

CLINICAL EVALUATION

• History — onset, gestation, feeding adequacy, maternal blood group, family history of haemolysis, sibling jaundice.
• Examine — degree (Kramer zone), pallor, plethora, hepatosplenomegaly, cephalhaematoma, signs of sepsis and of bilirubin encephalopathy.
• Assess hydration and weight loss.

INVESTIGATIONS

• Total & direct serum bilirubin (TcB for screening).
• Blood group & Rh (baby & mother); Direct Coombs test (DCT).
• CBC, reticulocyte count, peripheral smear.
• G6PD assay; sepsis screen if indicated; TSH; and LFT / urine reducing substances if conjugated.

MANAGEMENT

Decisions are plotted on the Bhutani nomogram / AAP or NICE charts against age in hours, gestation and risk factors.

1. Phototherapy — first-line for unconjugated hyperbilirubinaemia:

• Blue-green light (460–490 nm) converts bilirubin into water-soluble, excretable isomers by photoisomerisation & structural isomerisation (lumirubin).
• Expose maximum skin, cover the eyes with pads and cover the genitalia; maintain hydration and monitor temperature.
• Side-effects: loose stools, rash, hyperthermia, dehydration, and bronze baby syndrome (with conjugated hyperbilirubinaemia — a relative contraindication).

2. Exchange transfusion — for very high or rapidly rising levels / signs of encephalopathy / failed phototherapy:

• Removes bilirubin, antibody-coated red cells and circulating antibody; a double-volume exchange (≈ 2 × 80 mL/kg ≈ 160 mL/kg) replaces ~85% of the blood volume.
• Use fresh, irradiated, cross-matched blood; monitor for hypocalcaemia, hypoglycaemia, thrombocytopenia, sepsis, apnoea and arrhythmia.

3. IVIG — in isoimmune haemolytic disease (Rh/ABO) to reduce the need for exchange transfusion. 4. Treat the cause — sepsis, hypothyroidism, and surgery for biliary atresia.

COMPLICATION — KERNICTERUS (Bilirubin Encephalopathy)

Unconjugated (lipid-soluble) bilirubin crosses the blood-brain barrier and deposits in the basal ganglia, hippocampus and brainstem nuclei.

• Acute (ABE): lethargy, poor feeding, hypotonia → hypertonia, retrocollis-opisthotonus, high-pitched cry, seizures.
• Chronic (kernicterus): choreoathetoid cerebral palsy, sensorineural hearing loss, upward-gaze palsy, dental enamel dysplasia.

• Jaundice in the first 24 h is pathological until proven otherwise (usually haemolysis).
• Physiological: after 24 h, peaks day 3–5, rise < 5 mg/dL/day, resolves by 1–2 weeks.
• Conjugated (direct > 2 mg/dL) is always pathological — think biliary atresia (Kasai by 8 wk).
• Phototherapy first-line; exchange transfusion for very high/rapidly rising levels.
• Kernicterus (basal ganglia) is preventable but irreversible.

DEFINITION

Neonatal sepsis is a clinical syndrome of systemic illness with bacteraemia occurring in the first 28 days of life, characterised by signs and symptoms of infection with or without a positive blood culture. It is a leading cause of neonatal mortality in India, contributing to a large share of preventable newborn deaths.

WHY THE NEWBORN IS SUSCEPTIBLE (Pathogenesis)

The neonate — especially the preterm — has an immature immune system and vulnerable barriers:

• Immature innate immunity — reduced neutrophil reserve, impaired chemotaxis and phagocytosis, low complement levels.
• Immature adaptive immunity — low IgG (transplacental IgG mainly transferred in the 3rd trimester → preterm deficient), and IgM & IgA do not cross the placenta, so the newborn cannot fight Gram-negative organisms well.
• Vulnerable barriers — thin skin, the umbilical stump as a portal of entry, and an immature gut mucosa.
• Once organisms invade, a cytokine cascade (TNF-α, IL-1, IL-6) drives the systemic inflammatory response, shock and DIC.

ROUTES OF INFECTION

• Transplacental (haematogenous) — e.g. Listeria, TORCH agents.
• Ascending / intrapartum — from the birth canal after rupture of membranes (early-onset).
• Postnatal / nosocomial — from the environment, hands, equipment and invasive lines (late-onset).

CLASSIFICATION

RISK FACTORS

For early-onset (maternal):

• PROM > 18–24 hours; maternal fever / chorioamnionitis.
• Foul-smelling / meconium-stained liquor; maternal UTI or GBS colonisation.
• Prematurity and low birth weight; unclean or prolonged / instrumental delivery.
• More than 3 vaginal examinations in labour.

For late-onset (baby / environment):

• Prematurity / LBW; prolonged hospital stay; invasive lines & ventilation.
• Poor hand hygiene, overcrowding, prolonged antibiotics, lack of breastfeeding.

CLINICAL FEATURES

Signs are non-specific and subtle — 'the baby is not doing well'. A high index of suspicion is vital.

• General: lethargy, refusal to feed, poor cry, temperature instability (fever OR hypothermia).
• Respiratory: tachypnoea, grunting, retractions, apnoea, cyanosis.
• CVS: tachycardia, poor perfusion, prolonged CRT, shock, sclerema.
• GIT: vomiting, abdominal distension, diarrhoea, poor feeding, hepatosplenomegaly.
• CNS: lethargy, irritability, seizures, bulging fontanelle, high-pitched cry (meningitis).
• Others: jaundice, bleeding / DIC, petechiae, hypo/hyperglycaemia.

INVESTIGATIONS

Definitive:

• Blood culture — the gold standard (before starting antibiotics; ≥ 1 mL blood).
• Lumbar puncture / CSF study — mandatory in late-onset / positive culture / neurological signs.
• Urine culture (suprapubic / catheter) in late-onset sepsis.

Sepsis screen (supportive; ≥ 2 positive = probable sepsis):

• Total leukocyte count (< 5000 or high); Absolute Neutrophil Count (neutropenia is ominous).
• Immature-to-Total neutrophil (I:T) ratio ≥ 0.2.
• C-reactive protein (CRP) elevated; micro-ESR > 15 mm in the 1st hour.
• Others: procalcitonin, thrombocytopenia, toxic granules, chest X-ray if respiratory.

MANAGEMENT — Supportive care (equally important)

• Maintain temperature (warmth), oxygenation, and perfusion (fluid boluses / inotropes for septic shock).
• Maintain euglycaemia; correct electrolyte, acid-base and coagulation abnormalities (FFP/platelets for DIC).
• Continue breast / expressed milk feeds if tolerated; IV fluids if not; nurse in a thermoneutral environment.

MANAGEMENT — Antibiotics (start empirically after cultures; do not wait)

• First-line (community EOS): Ampicillin + Gentamicin (add Cefotaxime if meningitis).
• Nosocomial LOS: as per the unit antibiogram — e.g. Piperacillin-tazobactam / Vancomycin + Amikacin, or Meropenem for resistant Gram-negatives; antifungal (fluconazole/amphotericin) if Candida.
• Duration: 7–10 days for sepsis, 14–21 days for meningitis; de-escalate as per culture & sensitivity.
• Adjuncts: IVIG in selected cases; exchange transfusion for sclerema / DIC (not routine).

COMPLICATIONS

• Septic shock and multi-organ dysfunction; DIC and bleeding.
• Meningitis and its sequelae — hydrocephalus, seizures, deafness, developmental delay.
• Pneumonia, necrotising enterocolitis, osteomyelitis / septic arthritis, endocarditis.

PROGNOSIS

Mortality is high, especially in preterm babies, Gram-negative sepsis and meningitis. Early recognition and prompt antibiotics dramatically improve survival. Meningitis survivors need long-term neurodevelopmental and hearing follow-up.

PREVENTION

• Clean delivery practices (WHO '5 cleans'); asepsis and strict hand hygiene in the nursery.
• Early exclusive breastfeeding; KMC; minimise invasive procedures and rationalise antibiotics.
• Intrapartum antibiotic prophylaxis for GBS-colonised mothers; good antenatal care; antenatal steroids to reduce prematurity morbidity.

• Ampicillin 50 mg/kg/dose IV (meningitis 100 mg/kg/dose).
• Gentamicin 5 mg/kg/day IV (term) — once daily.
• Cefotaxime 50 mg/kg/dose (for meningitis / Gram-negative cover).
• Duration: 7–10 days (14 days culture-positive sepsis; 21 days meningitis).

• 'Not doing well' = sepsis until proven otherwise; start antibiotics after cultures, don't wait.
• EOS ≤ 72 h (maternal); LOS > 72 h (nosocomial); Indian NICUs — Gram-negatives predominate.
• Sepsis screen: TLC, ANC, I:T ratio ≥ 0.2, CRP, micro-ESR (≥ 2 positive = probable).
• Empirical: ampicillin + gentamicin (+ cefotaxime for meningitis).
• Supportive care (warmth, glucose, perfusion) is as important as antibiotics.

DEFINITION

Respiratory distress in a newborn is the presence of at least two of the following three signs: respiratory rate > 60/min (tachypnoea), chest retractions, and grunting. Its severity is graded by the Silverman-Andersen score.

SILVERMAN-ANDERSEN SCORING

Five parameters, each scored 0–2 (total 0–10). Higher score = worse distress (the opposite of Apgar).

CAUSES OF RESPIRATORY DISTRESS

Pulmonary: hyaline membrane disease (RDS), transient tachypnoea of the newborn (TTN), meconium aspiration syndrome (MAS), pneumonia, pneumothorax, pulmonary haemorrhage, congenital malformations (CDH, TEF).

Non-pulmonary: congenital heart disease, sepsis, metabolic acidosis, hypoglycaemia, anaemia / polycythaemia, hypothermia, and CNS causes.

HYALINE MEMBRANE DISEASE (RDS) — Definition

HMD is respiratory distress in a preterm neonate due to deficiency of pulmonary surfactant, causing widespread alveolar collapse (atelectasis). It is the commonest cause of respiratory distress in preterm babies.

PATHOPHYSIOLOGY

Surfactant deficiency → ↑ Alveolar surface tension → Progressive atelectasis → ↓ Lung compliance + V/Q mismatch → Hypoxia + hypercapnia + acidosis → Pulmonary vasoconstriction → ↓ pulmonary blood flow → Ischaemic injury → protein-rich exudate → hyaline membranes

RISK FACTORS

• Prematurity (the major factor — risk ↑ with decreasing gestation).
• Infant of a diabetic mother (insulin antagonises surfactant maturation).
• Male sex, second twin, elective caesarean without labour, perinatal asphyxia, hypothermia.
• Protective: antenatal steroids, chronic intrauterine stress, PROM, IUGR.

CLINICAL FEATURES

• Onset within minutes to hours of birth, worsening over the first 48–72 hours (then improving as endogenous surfactant appears).
• Tachypnoea, grunting, retractions, nasal flaring, cyanosis.
• Reduced air entry; may progress to respiratory failure and apnoea.

INVESTIGATIONS

• Chest X-ray (classic): low lung volumes, a fine reticulogranular 'ground-glass' pattern with air bronchograms; severe disease → 'white-out' lungs.
• ABG — hypoxaemia, hypercapnia, respiratory + metabolic acidosis.
• Sepsis screen (to exclude pneumonia), blood glucose, and echocardiography if PDA/PPHN suspected.

DIFFERENTIAL DIAGNOSIS (high-yield comparison)

MANAGEMENT — Supportive

• Neutral thermal environment; IV fluids; maintain glucose & perfusion; minimal handling.
• Monitor continuously — SpO2 (target 90–95%), heart rate, ABG, blood pressure.

MANAGEMENT — Respiratory support

• Early CPAP (nasal CPAP 5–6 cmH2O) — first-line; maintains functional residual capacity and prevents collapse.
• Mechanical ventilation if CPAP fails / severe apnoea / respiratory failure.
• Surfactant replacement via ET tube — INSURE (Intubate-Surfactant-Extubate to CPAP) or LISA (less-invasive surfactant administration); give early ('rescue') for established RDS.

Others: antibiotics until sepsis is excluded; caffeine for apnoea of prematurity; treat a haemodynamically significant PDA.

COMPLICATIONS OF RDS / ITS THERAPY

• Air leaks — pneumothorax, pneumomediastinum, pulmonary interstitial emphysema.
• Bronchopulmonary dysplasia (BPD) — chronic lung disease (O2 dependence at 36 weeks corrected age).
• Patent ductus arteriosus; intraventricular haemorrhage; retinopathy of prematurity.
• Complications of mechanical ventilation and oxygen toxicity.

PREVENTION

• Antenatal corticosteroids — betamethasone / dexamethasone to the mother at 24–34 weeks when preterm delivery is anticipated (most effective if given > 24 h and < 7 days before delivery).
• Prevent prematurity; prevent birth asphyxia and hypothermia; optimise diabetic control in pregnancy.

• Respiratory distress = ≥ 2 of tachypnoea, retractions, grunting; grade by Silverman score.
• HMD = surfactant deficiency in preterm; CXR shows ground-glass + air bronchograms.
• Early CPAP + surfactant (INSURE/LISA) is the key treatment.
• Antenatal steroids (24–34 wk) prevent RDS.
• Always cover with antibiotics — GBS pneumonia mimics RDS.

DEFINITION

Perinatal asphyxia is an insult to the fetus / newborn due to lack of oxygen (hypoxia) and/or lack of perfusion (ischaemia) to various organs. The WHO defines birth asphyxia as failure to initiate and sustain breathing at birth.

The National Neonatology Forum (NNF) defines it as an Apgar score ≤ 6 at 1 minute (or slow / absent gasping requiring resuscitation). HIE is the neurological syndrome resulting from asphyxia.

ETIOLOGY

Antepartum (~20%): maternal hypotension / hypertension, pre-eclampsia, diabetes, APH, IUGR, post-maturity.

Intrapartum (~70% — commonest): cord prolapse / compression, abruptio placentae, prolonged / obstructed labour, uterine rupture, difficult instrumental delivery, tight nuchal cord.

Postpartum (~10%): severe RDS, cyanotic heart disease, recurrent apnoea, severe anaemia, shock.

PATHOPHYSIOLOGY — the two phases of injury

• Primary energy failure: hypoxia-ischaemia → anaerobic metabolism → ↓ ATP → failure of the Na/K pump → cytotoxic oedema and immediate necrosis.
• Reperfusion / secondary energy failure (6–48 h later): excitotoxicity (glutamate release), calcium influx, free-radical injury, and apoptosis. This delayed phase is the therapeutic window targeted by cooling.

SARNAT & SARNAT STAGING OF HIE

MULTI-ORGAN INVOLVEMENT ('asphyxia is a multi-organ disease')

• CNS: HIE, seizures, cerebral oedema.
• Renal: acute tubular necrosis, oliguria (the commonest organ affected).
• CVS: myocardial dysfunction, hypotension, tricuspid regurgitation.
• Lungs: PPHN, pulmonary haemorrhage, RDS / MAS.
• GIT: necrotising enterocolitis, feed intolerance.
• Metabolic / Haem: hypoglycaemia, hypocalcaemia, metabolic acidosis, DIC, SIADH.

INVESTIGATIONS

• Cord / arterial blood gas (pH, base deficit); blood glucose, calcium, electrolytes.
• Renal & liver function; coagulation profile.
• Cranial ultrasound / MRI (MRI best for prognosis — basal ganglia / thalamic and watershed injury).
• EEG / amplitude-integrated EEG (aEEG) — for subclinical seizures and prognostication.

MANAGEMENT — 1. Resuscitation

Prompt, effective resuscitation at birth (per NRP) to restore ventilation and perfusion and prevent ongoing hypoxic injury.

MANAGEMENT — 2. Supportive care (the 'golden Ns')

• Normal ventilation / oxygenation — avoid both hypoxia and hyperoxia; avoid hyperventilation (hypocapnia reduces cerebral flow).
• Normal perfusion / BP — treat hypotension with fluids / inotropes; avoid fluid overload.
• Normoglycaemia; normal electrolytes / calcium.
• Control seizures — first-line Phenobarbitone 20 mg/kg IV loading (repeat 10 mg/kg up to 40 mg/kg); second-line phenytoin / levetiracetam / midazolam.
• Restrict fluids (~2/3 maintenance) if renal failure / SIADH; monitor urine output and daily weight.

MANAGEMENT — 3. Therapeutic hypothermia (key neuroprotection)

• For moderate-to-severe HIE in babies ≥ 36 weeks, started within 6 hours of birth.
• Cool to a core temperature of 33–34 °C for 72 hours, then rewarm slowly (0.5 °C/hour).
• Proven to reduce death and major neurodevelopmental disability; requires monitoring facilities.

PROGNOSTIC INDICATORS (poor outcome)

• Sarnat stage 3 (severe HIE); prolonged, refractory seizures.
• Persistently abnormal aEEG/EEG; abnormal MRI (basal ganglia / thalamic injury).
• Apgar 0–3 beyond 10 minutes; failure to establish spontaneous respiration by 20–30 minutes.
• Multi-organ failure and persistent metabolic acidosis.

COMPLICATIONS / SEQUELAE

• Cerebral palsy (spastic quadriplegia / dyskinetic), epilepsy, intellectual disability.
• Microcephaly, sensorineural hearing loss, visual impairment, learning / behavioural problems.

PREVENTION & FOLLOW-UP

• Good antenatal & intrapartum care, partograph use, and fetal monitoring; timely caesarean for fetal distress.
• Skilled birth attendance and readiness for resuscitation at every delivery.
• Structured neurodevelopmental follow-up of survivors (development, hearing, vision) for early intervention.

• Asphyxia is a multi-organ disease (renal ATN is commonest organ affected).
• Sarnat staging (1 mild → 3 severe) grades HIE and predicts outcome.
• Therapeutic hypothermia (33–34 °C × 72 h) for moderate–severe HIE, within 6 h, ≥ 36 wk.
• Control seizures with phenobarbitone 20 mg/kg; maintain the 'golden Ns'.
• Prevention = good intrapartum care and readiness to resuscitate.