---

PEDIATRIC PNEUMONIA - Complete Clinical Medicine Guide

---

1. DEFINITION

---

2. ETIOLOGY BY AGE GROUP

• Cystic fibrosis: S. aureus early in life, then Pseudomonas aeruginosa later
• Sickle cell disease: Encapsulated bacteria - S. pneumoniae, Salmonella, Klebsiella (acute chest syndrome risk)
• Immunocompromised: Pneumocystis jirovecii (PCP), CMV, fungi
• Post-influenza: S. aureus (notorious for rapid progression, high fever, pulmonary abscesses)
• Unvaccinated children: H. influenzae type b, all pneumococcal serotypes, measles, varicella

---

3. PATHOGEN-SPECIFIC CLINICAL PATTERNS ("TYPICAL" vs "ATYPICAL")

Typical Pneumonia

• Abrupt onset, high fever, chills, pleuritic chest pain, productive cough
• Classically caused by S. pneumoniae

Atypical Pneumonia

• Gradual onset over days to weeks
• Low-grade fever, nonproductive (dry, hacking) cough, malaise, headache
• Caused by Mycoplasma pneumoniae or Chlamydophila pneumoniae
• Mycoplasma: may also cause wheezing in school-age children, sore throat, dysphagia
• Extrapulmonary manifestations with Mycoplasma: arthralgias, rash, CNS symptoms (meningitis, encephalitis)

Pattern Recognition Table

---

4. CLINICAL FEATURES

Symptoms by Age

• Tachypnea (most sensitive sign)
• Nasal flaring
• Grunting
• Fever
• Intercostal/subcostal retractions
• Cyanosis (severe cases)

• Rales (crackles)
• Tactile fremitus
• Pleural rub
• Bronchial breath sounds
• Productive cough, pleuritic chest pain

Tachypnea Thresholds (WHO/IMCI):

---

5. DIAGNOSIS

Clinical Diagnosis

• Mild, uncomplicated CAP can be diagnosed clinically - no investigations required in outpatient setting.
• The combination of fever + respiratory signs remains the foundation of diagnosis.

Chest X-Ray

1. Infants/children with toxic appearance + respiratory findings
2. Age 0-3 months with fever + respiratory symptoms (full sepsis evaluation)
3. Child < 5 years with temperature > 39°C for ≥ 5 days + WBC ≥ 20,000/mm³ with no clear source
4. Suspicion of complication (pleural effusion, pneumothorax)
5. Prolonged or treatment-unresponsive pneumonia
6. Biphasic illness (URTI followed by acute worsening + high fever)
7. Suspected foreign body aspiration

• Not 100% sensitive or specific
• Cannot reliably distinguish bacterial from viral etiology
• Alveolar infiltrates suggest bacterial; interstitial infiltrates suggest viral - but overlap is common
• Viral bronchiolitis can mimic bacterial CAP radiographically (patchy atelectasis)
• A false "consolidation" appears with poor inspiration in infants (classic exam trap - same child looks normal with proper inspiration)

Laboratory

• Routine blood cultures: NOT recommended for healthy children with mild CAP (bacteremia rates are low)
• Blood cultures ARE indicated: toxic-appearing children, severe disease requiring hospitalization, complicated pneumonia (obtain before antibiotics)
• Sputum culture: For severe illness; adequate specimen needs > 25 WBCs and < 10 squamous cells per low-power field
• Nasopharyngeal swabs for RSV, influenza, hMPV: Quick, specific - if positive, may obviate need for antibiotics and imaging
• CBC: Not useful for distinguishing viral vs bacterial; useful for detecting complications (e.g., pneumococcal HUS)
• CRP / ESR / Procalcitonin: NOT routinely recommended to distinguish bacterial from viral, but may be used to trend resolution in severe pneumonia
• Tuberculosis workup: Induced sputum (older children) or gastric aspirates (infants) for AFB smear and culture; indicated in high-risk patients

---

6. MANAGEMENT

Antibiotic Selection

• First-line: High-dose Amoxicillin × 5 days (covers S. pneumoniae)
• If atypical suspected (school-age, subacute course): add Macrolide (azithromycin, clarithromycin)
• If penicillin allergy: second-generation cephalosporin or macrolide

• Ampicillin × 5 days (IV)
• If atypical coverage needed: add Azithromycin
• If S. aureus / MRSA suspected (severe, rapidly progressive, post-influenza): Ceftriaxone + MRSA coverage (vancomycin, clindamycin, or TMP-SMX); vancomycin not preferred as first-line

• Ceftriaxone + MRSA coverage empirically
• Consider additional antifungals or antivirals based on context

Antibiotic Notes

• Duration: 7-10 days total
• Macrolide controversy: Azithromycin is NOT routinely first-line in children < 5 years (atypical organisms less common; high macrolide resistance to S. pneumoniae up to 50% in some regions; azithromycin liquid NOT approved < 6 months due to risk of pyloric stenosis; azithromycin driving S. pyogenes resistance)
• If failing amoxicillin at 48-72 hours: Consider adding a macrolide (suggests atypical co-infection)
• Fluoroquinolones: Not established for children due to theoretical arthropathy risk
• Doxycycline: Active against atypicals and streptococci but restricted to adolescents/adults (causes permanent tooth staining in young children)

Viral Pneumonia

• Supportive management (hydration, oxygen, fever control)
• Ribavirin: NOT routinely used for RSV (evidence insufficient for routine use)
• Antivirals (oseltamivir) for influenza

Hospitalization Criteria

• Neonates (birth - 20 days): ALWAYS admit
• Febrile infants 3 weeks - 3 months: ADMIT (may not mount reliable signs)
• Toxic-appearing children: ADMIT
• Hypoxia (SpO2 < 90-92%)
• Moderate-to-severe respiratory distress
• Failed outpatient antibiotic therapy
• Inability to tolerate oral medication
• Unreliable caregiver/follow-up

---

7. COMPLICATIONS

Viral Pneumonia Complications

• Dehydration
• Apnea (especially RSV, C. trachomatis, B. pertussis in very young infants)
• Bronchiolitis obliterans (rare)

Bacterial Pneumonia Complications

• Pleural effusion (most common; seen with S. pneumoniae, Mycoplasma, H. influenzae type b)
• Empyema (S. aureus, S. pneumoniae)
• Pneumothorax
• Pneumatocele / lung abscess (S. aureus hallmark)
• Bacteremia / Sepsis
• Hemolytic-uremic syndrome (HUS) - complication of pneumococcal pneumonia
• Extrapulmonary Mycoplasma: arthritis, meningitis/encephalitis, hemolytic anemia (cold agglutinins), erythema multiforme (Stevens-Johnson)

---

8. FOLLOW-UP IMAGING

• Routine follow-up CXR: NOT indicated unless clinical condition does not improve.
• Repeat imaging warranted if: prolonged fever, clinical deterioration, or suspected complication.

---

9. PREVENTION (VACCINES)

---

10. HIGH-YIELD EXAM POINTS (MCQ TRAPS)

---

11. CLINICAL CASE VIGNETTE (Exam Style)

• Diagnosis: Community-acquired pneumonia (bacterial, right lower lobe)
• Most likely organism: Streptococcus pneumoniae
• Management: Admit (hypoxia + respiratory distress); IV Ampicillin
• If toxic/no improvement: Add MRSA coverage
• If no improvement at 72 hours: Consider atypical co-infection - add azithromycin; evaluate for empyema with repeat imaging/ultrasound

---

1. Definition & Epidemiology - incidence, global burden
2. Etiology by Age Group - from neonate to adolescent, with special populations
3. Typical vs Atypical Pneumonia - pathogen-specific clinical patterns
4. Clinical Features - WHO diagnostic criteria, tachypnea thresholds by age
5. Diagnosis - when to order CXR, limitations of imaging, lab investigations, role of biomarkers
6. Management - outpatient vs inpatient vs ICU antibiotic regimens, antibiotic controversies (macrolides, fluoroquinolones), hospitalization criteria
7. Complications - effusion, empyema, pneumatocele, HUS, extrapulmonary Mycoplasma
8. Prevention - vaccines
9. High-yield MCQ traps - 15 classic exam questions
10. Clinical vignette - worked case with diagnosis and management

• Tachypnea = most sensitive sign in young children
• High-dose amoxicillin = first-line outpatient treatment
• S. pneumoniae = most common bacterial cause
• Mycoplasma = walking pneumonia in school-age
• S. aureus = post-influenza + rapid deterioration + pneumatocele
• Routine CXR and blood cultures are NOT required for mild uncomplicated CAP

---

NEONATOLOGY - Comprehensive Exam Notes

---

QUICK REFERENCE: CAUSES OF CRITICAL ILLNESS IN NEONATES

---

1. RESPIRATORY DISTRESS SYNDROME (RDS) / HYALINE MEMBRANE DISEASE

Definition & Epidemiology

• Disease of prematurity - most common cause of respiratory insufficiency in the newborn
• Incidence (without antenatal steroids):
  • < 28 weeks gestation: ~60%
  • 28-34 weeks: ~30%

  • 34 weeks: < 5%

• More common in: male sex, infant of diabetic mother (IDM), cesarean delivery (especially before labor onset)

Pathophysiology

• Fundamental defect: insufficient surfactant (dipalmitoyl phosphatidylcholine - lecithin) production by immature Type II pneumocytes
• Without surfactant → alveolar collapse (atelectasis) → hypoxia → epithelial and endothelial injury → hyaline membrane formation (fibrin + necrotic type II pneumocytes)
• Hormonal regulation of surfactant:
  • Corticosteroids STIMULATE surfactant synthesis → stress/IUGR DECREASES RDS risk
  • High insulin levels in IDM SUPPRESS surfactant → IDM at INCREASED risk despite large size
  • Labor stimulates surfactant → C-section before labor increases risk

Clinical Features

• Onset: within minutes to hours of birth
• Grunting, nasal flaring, subcostal/intercostal retractions
• Tachypnea (RR > 60)
• Cyanosis
• Progressive respiratory failure - infant "tires out" because each breath requires massive effort

Morphology / CXR

• Lungs: heavy, airless, mottled purple (like liver)
• Microscopy: eosinophilic hyaline membranes lining respiratory bronchioles, alveolar ducts, alveoli
• CXR: ground-glass (reticulogranular) opacification with air bronchograms, low lung volumes, "white-out" in severe cases

Management

1. Antenatal corticosteroids (betamethasone/dexamethasone) to mother at 24-34 weeks → most effective prevention
2. Exogenous surfactant therapy - given via endotracheal tube; transforms outcomes
3. Respiratory support: CPAP, mechanical ventilation
4. Supplemental oxygen (with careful monitoring to avoid hyperoxia)

Complications of RDS Therapy

• Retinopathy of Prematurity (ROP) - from high O2 exposure
• Bronchopulmonary Dysplasia (BPD) - chronic lung disease from mechanical ventilation/O2 injury
• Both complications decreased with modern surfactant protocols

---

2. TRANSIENT TACHYPNEA OF THE NEWBORN (TTN)

• Caused by delayed clearance of fetal lung fluid
• Classic history: term or near-term, born by C-section (without labor), or rapid vaginal delivery
• Presents: tachypnea within first few hours, usually resolves within 24-72 hours
• CXR: perihilar streaking, fluid in fissures, mild hyperinflation, "wet" appearance
• Management: supportive (supplemental O2, often CPAP); self-limited
• Distinguish from RDS (earlier onset, more severe, premature infant)

---

3. MECONIUM ASPIRATION SYNDROME (MAS)

• Occurs when meconium-stained amniotic fluid is aspirated before, during, or after delivery
• Seen in term or post-term infants (meconium passage rare before 37 weeks)
• Risk factors: fetal distress, post-maturity, low APGAR scores

Pathophysiology

• Mechanical obstruction → air trapping ("ball-valve") → gas trapping, hyperinflation
• Chemical pneumonitis from bile salts
• Surfactant inactivation
• Often complicated by PPHN

Clinical Features

• Respiratory distress at birth
• Barrel-shaped chest (hyperinflation)
• CXR: coarse, patchy infiltrates with hyperinflation; pneumothorax common (up to 30%)
• Yellow-green staining of skin, nails, umbilical cord

Key Management Point

• Current evidence: tracheal suctioning of depressed meconium-stained neonates does NOT reduce morbidity or mortality (guideline change from 2015/2019)
• Management: CPAP/ventilation, surfactant, inhaled NO for PPHN

---

4. PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN (PPHN)

Risk Factors

• Term or post-term infants
• Meconium aspiration syndrome, pneumonia
• Asphyxia / hypoxia / acidosis
• Polycythemia (hyperviscosity)
• Congenital diaphragmatic hernia, pulmonary hypoplasia, renal agenesis

Diagnosis

• Presents within 12-24 hours of birth
• Severe hypoxemia disproportionate to CXR findings - key distinguishing feature
• Pre/post-ductal SpO2 gradient ≥7-15 mmHg (right hand vs. foot/left hand)
• Echo: right-to-left shunt at foramen ovale and/or ductus arteriosus; structurally normal heart
• Hyperoxia test: PaO2 < 100 mmHg in 100% O2 in room air → suggests PPHN or cyanotic CHD

Treatment

1. Supplemental O2 - goal: vasodilation of pulmonary vasculature
2. Treat underlying cause
3. Avoid noxious stimuli, minimize handling; sedation if intubated
4. Avoid hypocarbia (PCO2 < 30 mmHg) → myocardial ischemia + decreased cerebral flow
5. Inhaled Nitric Oxide (iNO): First-line pulmonary vasodilator; starting dose 20 ppm; reduces PVR
   • Watch for: methemoglobinemia (reduce if > 4%), NO2 toxicity
6. Sildenafil (PDE5 inhibitor): oral pulmonary vasodilator - second-line
7. ECMO for refractory cases

---

5. NEONATAL JAUNDICE (HYPERBILIRUBINEMIA)

Types - Unconjugated vs Conjugated

Physiologic Jaundice (Normal)

• Appears on day 2-3 (never on day 1 - pathologic if day 1!)
• Peaks by day 4-5
• Rarely rises > 5 mg/dL/day
• Usually < 20 mg/dL
• Resolves by day 7-10 in term, day 14 in preterm
• Mechanism: high RBC turnover + immature hepatic conjugation capacity

Breast Milk Jaundice

• Appears in week 2, can persist 3-12 weeks
• Caused by beta-glucuronidase in breast milk → increases enterohepatic circulation
• Do NOT stop breastfeeding routinely

Pathologic Jaundice - Red Flags

• Jaundice on day 1 of life = always pathologic → usually hemolysis (HDFN, G6PD)
• Bilirubin rising > 5 mg/dL/day
• Total bilirubin > 20 mg/dL in term
• Jaundice persisting > 2 weeks (term) or > 3 weeks (preterm) → evaluate for conjugated hyperbilirubinemia

Most Common Causes of Severe Hyperbilirubinemia

1. Hemolytic Disease of Fetus and Newborn (HDFN)
2. Sepsis

Kernicterus (Bilirubin Encephalopathy)

• Unconjugated bilirubin crosses BBB → deposits in basal ganglia, hippocampus, brain stem nuclei
• Acute: lethargy, hypotonia, poor feeding → opisthotonos, high-pitched cry, seizures
• Chronic: athetoid cerebral palsy, hearing loss, dental enamel hypoplasia, upward gaze palsy
• Premature infants more susceptible (lower albumin binding, immature BBB)

Treatment

• Phototherapy: Blue light (450-490 nm) converts unconjugated bilirubin to water-soluble isomers (lumirubin) via photo-isomerization → excreted in bile/urine without conjugation
• Exchange transfusion: For severe/rapidly rising bilirubin unresponsive to phototherapy; replaces ~85% of neonatal blood
• IVIG: For HDFN to reduce hemolysis and need for exchange transfusion

---

6. NEONATAL SEPSIS

Definition

• Fever in neonate = rectal temp ≥ 38°C (100.4°F)
• Hypothermia = rectal temp < 36.5°C (97.7°F)
• Both are serious signs in neonates

Early-Onset vs Late-Onset Sepsis

Organisms

Clinical Signs (Non-specific!)

• Temperature instability (fever OR hypothermia)
• CNS: lethargy, irritability, seizures
• Respiratory: apnea, tachypnea, grunting
• Feeding: poor feeding, vomiting, abdominal distention, diarrhea
• Jaundice (especially conjugated)
• Rash, petechiae, purpura

Workup

• Full sepsis evaluation is the standard for febrile/hypothermic neonates (lower threshold than older infants)
• CBC with differential, CRP, blood cultures (before antibiotics!)
• Lumbar puncture (LP) for CSF analysis + culture
• Urinalysis + urine culture
• CXR if respiratory symptoms
• Important: Height of temperature does NOT distinguish viral from bacterial etiology in neonates

Management

• Empiric antibiotics: Ampicillin + Gentamicin (covers GBS, E. coli, Listeria)
• If MRSA suspected: add Vancomycin
• If meningitis: Ampicillin + Cefotaxime (aminoglycosides have poor CSF penetration)
• Duration: 7-10 days for bacteremia, 14-21 days for meningitis

---

7. HYPOXIC-ISCHEMIC ENCEPHALOPATHY (HIE)

Epidemiology

• 1-6 per 1000 live births
• Mortality: 20% in newborn period
• 25% of survivors have neurodevelopmental disability

Pathophysiology

• Perinatal asphyxia → hypoxia + ischemia → brain injury
• Primary energy failure → secondary reperfusion injury (free radicals, excitotoxicity) 6-24 hours later
• Important: Most cerebral palsy is NOT caused by intrapartum asphyxia alone - prenatal and postnatal factors matter

Sarnat Classification - HIE Severity

Diagnosis

• Sarnat exam - grading of encephalopathy
• Cord gas or first-hour blood gas: pH < 7.0 or base deficit > 16
• EEG: epileptiform activity + voltage suppression = unfavorable prognosis
• MRI: best for characterizing pattern of injury (basal ganglia/watershed)

Treatment - Therapeutic Hypothermia (TH)

• Indicated for infants ≥ 35 weeks with evidence of moderate-severe HIE
• Must be initiated within 6 hours of delivery
• Protocol: core body temperature cooled to 33-34°C for 72 hours, then slowly rewarmed
• Criteria for eligibility (one or more):
  • pH < 7.0 OR base deficit > 16 on cord/first-hour gas
  • pH 7.01-7.15 or BD 10-15.9 PLUS additional criteria (10-min APGAR ≤ 5, need for assisted ventilation ≥ 10 min, or evidence of moderate-severe encephalopathy)
• Reduces death/major neurodisability by ~15-20% NNT

Long-Term Sequelae

• Spastic quadriplegia / cerebral palsy
• Epilepsy
• Cognitive delay, intellectual disability
• Sensorineural hearing loss, visual impairment

---

8. INTRAVENTRICULAR HEMORRHAGE (IVH)

Epidemiology

• 30-40% of infants < 1500 g; 50-60% of infants < 1000 g
• 50% occur within 24 hours; 90% within first 96 hours of life
• Originates in the germinal matrix (highly vascular, fragile subependymal region)

Grading (by cranial ultrasound)

Diagnosis

• Cranial ultrasound (bedside, no radiation, can be done in incubator)
• Timing: screening at 7-14 days; repeat at 36-40 weeks corrected age

Complications

• Post-hemorrhagic hydrocephalus (from impaired CSF resorption)
• Periventricular leukomalacia (PVL) - white matter injury
• Cerebral palsy, cognitive delay

Prevention

• Antenatal corticosteroids
• Indomethacin prophylaxis (controversial)
• Vitamin K at birth
• Minimize unnecessary procedures, gentle handling

---

9. NECROTIZING ENTEROCOLITIS (NEC)

Epidemiology

• Most common GI emergency in neonates
• Incidence inversely proportional to gestational age
• Affects ~1 in 10 very-low-birth-weight infants (VLBW < 1500 g)

Pathogenesis (Multifactorial)

1. Immature intestinal mucosal barrier + immature immune system
2. Altered gut microbiome → pathogenic bacterial overgrowth
3. Exaggerated inflammatory response (platelet-activating factor, cytokines)
4. Associated with: prematurity + milk feeding (especially formula)

Location

• Terminal ileum, cecum, right colon most commonly (any segment can be involved)

Clinical Features (Bell's Staging)

Pathognomonic X-ray Finding

• Pneumatosis intestinalis - gas within the intestinal wall (submucosal gas bubbles)
• Portal venous gas - gas in portal veins (serious sign)
• Pneumoperitoneum - indicates perforation → surgical emergency

Management

• Conservative (medical): NPO, IV fluids, nasogastric decompression, broad-spectrum IV antibiotics (ampicillin + gentamicin + metronidazole)
• Surgical (20-60% of cases): Resection of necrotic bowel segments
• Key: In NEC patients, indomethacin for PDA is AVOIDED - use surgical ligation instead

Complications

• High perinatal mortality
• Short bowel syndrome (after extensive resection)
• Post-NEC strictures (from fibrosis during healing)

---

10. NEONATAL HYPOGLYCEMIA

Definition

• Serum glucose < 40 mg/dL in term and late preterm infants
• Hyperglycemia: > 125 mg/dL (term) or > 150 mg/dL (preterm)

Causes

Clinical Features

• Many asymptomatic (incidental on screening)
• Symptomatic: jitteriness, tremors, apnea, cyanosis, poor feeding, seizures, lethargy, hypotonia

Management

• If glucose < 40 and asymptomatic: feed enterally (breast milk/formula) and recheck in 30-60 min
• If glucose < 40 and symptomatic: IV glucose bolus = 200 mg/kg (= D10W at 2 mL/kg), then continuous dextrose infusion
• Monitor glucose q30-60 min until stable

---

11. PATENT DUCTUS ARTERIOSUS (PDA) IN PREMATURITY

Physiology

• Ductus arteriosus connects pulmonary artery to aorta in fetal circulation; normally closes in first 24-72 hours with rising O2 and falling prostaglandins
• In premature infants, closure is delayed or absent

Clinical Presentation

• "Machinery murmur" (continuous), loudest at left infraclavicular area
• Bounding pulses, wide pulse pressure
• Hyperdynamic precordium (active praecordium)
• Worsening respiratory failure / increasing ventilator requirements in a premature infant
• Heart failure signs

Diagnosis

• Echocardiogram - gold standard

Management

• Medical closure: Indomethacin (COX inhibitor - blocks prostaglandin synthesis) OR Ibuprofen OR Acetaminophen (IV paracetamol increasingly used)
• Surgical ligation: When medical therapy fails or is contraindicated (NEC, renal impairment, thrombocytopenia, bleeding)
• Key: Indomethacin contraindicated in NEC - use surgical ligation

---

12. APNEA OF PREMATURITY (AOP)

Definition

• Cessation of breathing > 20 seconds, OR shorter pause with bradycardia (HR < 100), cyanosis, or pallor
• Central (most common) - no respiratory effort; Obstructive - effort present; Mixed

Pathophysiology

• Immature central respiratory drive (medullary immaturity)
• Exaggerated inhibitory reflexes to hypoxia
• Caffeine stimulates respiratory center (adenosine receptor antagonism)

Management

• Caffeine citrate - first-line; loading dose 20 mg/kg, maintenance 5-10 mg/kg/day
• CPAP / nasal ventilation for refractory cases
• Treat underlying causes (sepsis, anemia, hypoglycemia, hypothermia, reflux)
• Monitor until resolved: AOP typically resolves by 36-44 weeks corrected gestational age

---

13. SUDDEN INFANT DEATH SYNDROME (SIDS)

Definition

• Sudden death of infant < 1 year, unexplained after thorough investigation including autopsy
• Most likely basis: delayed development of arousal reflexes and cardiorespiratory control
• Leading cause of death between 1 month and 1 year of age

Peak Age

• 2-4 months (90% of cases < 6 months)

Risk Factors

Prevention

• "Back to Sleep" campaign (supine position) → reduced SIDS incidence dramatically
• Firm mattress, no loose bedding
• Room-sharing without bed-sharing
• Avoid smoking exposure
• Pacifier use is protective

---

14. HEMOLYTIC DISEASE OF FETUS AND NEWBORN (HDFN) / ERYTHROBLASTOSIS FETALIS

Mechanism

• Maternal IgG antibodies cross placenta → attack fetal/neonatal RBCs → hemolysis
• Rh incompatibility (anti-D) - most severe; mother Rh(-), fetus Rh(+)
• ABO incompatibility (anti-A or anti-B) - more common but milder; mother O, fetus A or B
• First pregnancy rarely affected (Rh) - sensitization occurs at delivery; second pregnancy at risk

Clinical Features

• Neonatal anemia, jaundice (day 1 - always pathologic)
• Hepatosplenomegaly (extramedullary hematopoiesis)
• Erythroblastosis fetalis - circulating nucleated RBCs
• Hydrops fetalis (severe - ascites, pleural effusion, anasarca)
• Kernicterus if untreated

Management

• Antenatal: Anti-D immunoglobulin (Rh prophylaxis) at 28 weeks and within 72 hours of delivery → prevents sensitization
• Postnatal: Phototherapy, IVIG, exchange transfusion for severe cases
• Intrauterine transfusion (IUT) for severe fetal anemia detected in utero

---

HIGH-YIELD EXAM MCQ TRAPS - NEONATOLOGY

---

---