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NEONATAL EMERGENCIES MANAGEMENT MASTER GUIDE FROM BASIC TO MASTER LEVEL WITH REASONING WITH MNEMONICS

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This is a very large topic, so I'll start with a map of it and go deep on one area at a time.

Neonatal emergencies: map of topics

  1. Resuscitation at birth (NRP, the ABC approach, drugs, when to stop)
  2. Respiratory emergencies (RDS, TTN, meconium aspiration, pneumothorax, CDH, PPHN, apnea)
  3. Neonatal sepsis and meningitis (early vs late onset, empiric antibiotics)
  4. Cardiac emergencies (duct-dependent lesions, cyanotic vs shock, PGE1, SVT)
  5. Metabolic emergencies (hypoglycemia, hypocalcemia, inborn errors of metabolism, hyperammonemia)
  6. Neonatal seizures (causes, EEG, phenobarbitone and second-line drugs, HIE and cooling)
  7. Jaundice and hemolytic disease (phototherapy and exchange transfusion thresholds, kernicterus)
  8. Surgical emergencies (NEC, esophageal atresia/TEF, intestinal atresia, malrotation/volvulus, gastroschisis/omphalocele, anorectal malformation)
  9. Hematologic emergencies (vitamin K deficiency bleeding, polycythemia, severe anemia, DIC)
  10. Thermoregulation, fluids, electrolytes and shock (hypothermia, hypernatremia, shock types)

Overview

The core logic. Neonates deteriorate fast and show the same few signs whatever the cause: poor feeding, lethargy, temperature instability, apnea, cyanosis, grunting, hypotonia, and a "just not right" look. Because of this, the framework is the same for every case:
  • Stabilize first. Airway, breathing, circulation, temperature and glucose.
  • Treat the common, treatable causes empirically. Sepsis and hypoglycemia come before you have a diagnosis.
  • Then find the cause.
Mnemonics you will meet.
  • TACTIC: the causes of respiratory distress.
  • TORCH: congenital infections.
  • I-ONE-GLUC (my own working aid, not a standard textbook mnemonic): Infection, Oxygen (hypoxia), Neurologic, Electrolytes, Glucose, Lungs, Unusual metabolic, Cardiac.
  • NRP "HAD" sequence: the order of steps in resuscitation.
  • SOAP-ME: equipment check before a resuscitation.
  • Neonatal seizure causes: a "HIE, ICH, infection, metabolic" stack.
Reasoning pillars.
  1. Is the baby blue, pale, floppy or bilious? Each points to a different system.
  2. Does it respond to oxygen? The hyperoxia test separates lung disease from cyanotic heart disease.
  3. Is the problem duct-dependent? If it is, give prostaglandin E1 (PGE1) early.
  4. Is it surgical? Bilious vomiting is a surgical emergency until proven otherwise.
I'll check the clinical details (doses, thresholds, algorithms) against the textbooks and current evidence once you choose a topic.
Asking for Preferences

Which topic should I cover in full depth first (basic to master level, with reasoning and mnemonics)?

This is a very large topic, so I'll start with a map of it and go deep on one area at a time.

Neonatal emergencies: map of topics

  1. Resuscitation at birth (NRP, the ABC approach, drugs, when to stop)
  2. Respiratory emergencies (RDS, TTN, meconium aspiration, pneumothorax, CDH, PPHN, apnea)
  3. Neonatal sepsis and meningitis (early vs late onset, empiric antibiotics)
  4. Cardiac emergencies (duct-dependent lesions, cyanotic vs shock, PGE1, SVT)
  5. Metabolic emergencies (hypoglycemia, hypocalcemia, inborn errors of metabolism, hyperammonemia)
  6. Neonatal seizures (causes, EEG, phenobarbitone and second-line drugs, HIE and cooling)
  7. Jaundice and hemolytic disease (phototherapy and exchange transfusion thresholds, kernicterus)
  8. Surgical emergencies (NEC, esophageal atresia/TEF, intestinal atresia, malrotation/volvulus, gastroschisis/omphalocele, anorectal malformation)
  9. Hematologic emergencies (vitamin K deficiency bleeding, polycythemia, severe anemia, DIC)
  10. Thermoregulation, fluids, electrolytes and shock (hypothermia, hypernatremia, shock types)

Overview

The core logic. Neonates deteriorate fast and show the same few signs whatever the cause: poor feeding, lethargy, temperature instability, apnea, cyanosis, grunting, hypotonia, and a "just not right" look. Because of this, the framework is the same for every case:
  • Stabilize first. Airway, breathing, circulation, temperature and glucose.
  • Treat the common, treatable causes empirically. Sepsis and hypoglycemia come before you have a diagnosis.
  • Then find the cause.
Mnemonics you will meet.
  • TACTIC: the causes of respiratory distress.
  • TORCH: congenital infections.
  • I-ONE-GLUC (my own working aid, not a standard textbook mnemonic): Infection, Oxygen (hypoxia), Neurologic, Electrolytes, Glucose, Lungs, Unusual metabolic, Cardiac.
  • NRP "HAD" sequence: the order of steps in resuscitation.
  • SOAP-ME: equipment check before a resuscitation.
  • Neonatal seizure causes: a "HIE, ICH, infection, metabolic" stack.
Reasoning pillars.
  1. Is the baby blue, pale, floppy or bilious? Each points to a different system.
  2. Does it respond to oxygen? The hyperoxia test separates lung disease from cyanotic heart disease.
  3. Is the problem duct-dependent? If it is, give prostaglandin E1 (PGE1) early.
  4. Is it surgical? Bilious vomiting is a surgical emergency until proven otherwise.
I'll check the clinical details (doses, thresholds, algorithms) against the textbooks and current evidence once you choose a topic.

All

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"Infant, Newborn"[MeSH Terms] AND "Resuscitation"[MeSH Terms]

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NRP 9th edition 2025 neonatal resuscitation algorithm changes AHA AAP guidelines

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https://journalfeed.org/article-a-day/2025/2025-new-aha-nrp-…

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Neonatal emergencies master guide

This guide is for learning and revision. I took the resuscitation updates from the 2025 AHA/AAP guidelines (summary at JournalFeed). Several items come from the textbooks, and I label them below. Doses marked "(verify)" are from my own knowledge and not from the retrieved sources. Check them against your local formulary or the Harriet Lane Handbook before using them.
Some mnemonics below are my own teaching aids, not standard textbook ones. I mark those "(my aid)". In my earlier overview I called TACTIC and I-ONE-GLUC mnemonics. Neither is a standard mnemonic, so ignore both. The ones below replace them.

PART 0. The core logic of the sick neonate

Neonates have a small repertoire of responses, so very different diseases look the same. Tintinalli's lists the causes of critical neonatal illness as sepsis, ductal-dependent heart disease, pneumonia, air leak, airway anomalies, neuromuscular disease, inborn errors of metabolism (IEM), congenital adrenal hyperplasia (CAH), intracranial hemorrhage and abdominal catastrophe (malrotation, volvulus, necrotizing enterocolitis, NEC) - Tintinalli's Emergency Medicine, Neonatal Emergencies chapter (Table 116-2).
Sepsis is the most common cause of neonatal cardiorespiratory distress. Fever (rectal ≥38.0°C) or hypothermia (<36.5°C) means serious infection until proven otherwise.
Universal first 10 minutes: "A-B-C-D-E-F-G-S" (my aid)
  • Airway, Breathing, Circulation
  • Dextrose (check glucose in every sick neonate)
  • Expose and keep Euthermic (36.5 to 37.5°C)
  • Fever or Fluid status
  • Gas (blood gas, lactate)
  • Sepsis cover (cultures, then antibiotics without delay)
Five-question reasoning filter
  1. What colour is the baby: blue, pale or grey, jaundiced, or mottled?
  2. What is the vomit: bilious means surgical until proven otherwise.
  3. Does it respond to oxygen? Lung disease responds. Cyanotic heart disease does not.
  4. Is it duct-dependent? Think of this in any baby who is shocked or cyanosed in the first 2 weeks.
  5. What is the timing? Hours point to birth events, days to infection, metabolic disease or heart disease, and weeks to cholestasis or pyloric stenosis.

PART 1. Resuscitation at birth (NRP, 2025 update)

Pre-birth questions. Is the baby term? Is tone good? Is the baby breathing or crying? If all three are yes, the baby stays with the mother for skin-to-skin contact.
Flow of care
  1. Delayed cord clamping. The 2025 update recommends deferring clamping for at least 60 seconds in term and preterm babies who need no immediate resuscitation. Intact cord milking may be reasonable for babies of 28 to 36+6 weeks when delayed clamping is not possible. Do not do it below 28 weeks because of the risk of severe intraventricular hemorrhage (IVH).
  2. Initial steps. Warm, dry, stimulate, position the airway. Suction only if the airway is obstructed.
  3. HR <100, apnea or gasping. Start positive pressure ventilation (PPV) at 30 to 60 breaths/min. The primary feedback is a rising heart rate.
  4. Oxygen. Start at 21% for babies over 35 weeks. Use 21 to 30% for 32 to 34+6 weeks. Very preterm babies below 32 weeks may need 30 to 100%. Titrate to the pulse oximeter target.
  5. Ventilation not working: "MR. SOPA" (a standard NRP mnemonic)
    • Mask adjustment
    • Reposition the airway
    • Suction
    • Open the mouth
    • Pressure increase
    • Alternative airway. The laryngeal mask is now an earlier option for babies ≥34 weeks.
  6. HR <60 despite effective ventilation with an advanced airway. Start chest compressions at 3:1 with the two-thumb encircling technique (90 compressions plus 30 breaths per minute). Raise FiO2 to 100% during compressions.
  7. HR still <60. Give epinephrine, preferably IV or via an umbilical venous catheter. IO access is acceptable if the umbilical vein cannot be used. The endotracheal route is only a bridge while access is secured.
  8. Volume. Give normal saline or blood if hypovolemia is suspected and HR remains <60.
  9. Stopping. Consider redirecting care if there is no detectable heart rate after 20 minutes of high-quality resuscitation.
Textbook support: epinephrine is the primary resuscitation drug and is given if the HR stays below 60 after 45 to 60 seconds of PPV plus compressions - Miller's Anesthesia, Neonatal Resuscitation. Few neonates need drugs. Medications are for bradycardia or asystole unresponsive to ventilation and compressions, and for hemorrhage - Rosen's Emergency Medicine, Medications.
Doses (verify)
  • Epinephrine 1:10,000: IV/UVC 0.01 to 0.03 mg/kg (0.1 to 0.3 mL/kg), repeated every 3 to 5 min. Endotracheal 0.05 to 0.1 mg/kg (0.5 to 1 mL/kg).
  • Normal saline 10 mL/kg over 5 to 10 min.
Mnemonics
  • APGAR: Appearance (colour), Pulse, Grimace (reflex), Activity (tone), Respiration. The score is not used to decide whether to start resuscitation.
  • SOAP-ME (equipment check before delivery): Suction, Oxygen, Airway equipment, Pharmacy (drugs), Monitor, Equipment.
  • "Ventilation is king": nearly all newborn bradycardia is hypoxic. Fix the airway before reaching for compressions or drugs.
Post-resuscitation. Check glucose and keep the baby warm. Watch for pneumothorax, meconium aspiration syndrome (MAS), transient tachypnea of the newborn (TTN), electrolyte problems, hyperbilirubinemia and sepsis - Rosen's, Complications. Start therapeutic hypothermia for moderate to severe hypoxic-ischemic encephalopathy (HIE) at ≥36 weeks. Start within 6 hours, cool to 33 to 34°C and continue for 72 hours.
Recent evidence: a 2026 systematic review addresses initial vascular access (IO versus umbilical or peripheral) in neonatal resuscitation (PMID 42508602). I did not read its findings, so check it before changing practice.

PART 2. Respiratory emergencies

Grunting, flaring, retractions, tachypnea >60 and cyanosis all mean respiratory distress.
Causes (my aid, "4 S + lung")
  • Sepsis or pneumonia
  • Structural: choanal atresia, congenital diaphragmatic hernia (CDH), tracheoesophageal fistula (TEF), airway anomalies
  • Shunt (heart disease)
  • Sugar and metabolic (hypoglycemia, acidosis from IEM)
  • Lung: respiratory distress syndrome (RDS), TTN, MAS, pneumothorax, persistent pulmonary hypertension of the newborn (PPHN)
ConditionClueKey management
RDSPreterm, ground-glass lungs with air bronchogramsCPAP early, surfactant, caffeine, minimal ventilation
TTNTerm or C-section, fluid in fissures, resolves in 24 to 72 hOxygen, observe, rule out sepsis
MASPost-term, meconium-stained liquor, hyperinflationVentilate if apneic, no routine suction. Watch for PPHN and air leak
PneumothoraxSudden deterioration, one side hyperlucent, transilluminationNeedle decompression (2nd intercostal space mid-clavicular line, or 4th to 5th anterior axillary line), then chest tube
CDHScaphoid abdomen, bowel sounds in chestAvoid bag-mask ventilation. Intubate, place an orogastric tube, treat PPHN
PPHNPre/post-ductal SpO2 gap >10%, labile hypoxiaAvoid hypoxia and acidosis, inhaled nitric oxide, gentle ventilation
Choanal atresiaBlue at rest, pink when cryingOral airway
ApneaPreterm: prematurity. Term: always look for a causeCaffeine for prematurity. Work up sepsis, seizures, hypoglycemia, ICH
Hyperoxia test (reasoning). Give 100% oxygen for 10 minutes. A PaO2 that rises above about 150 mm Hg suggests lung disease. A PaO2 that stays low suggests cyanotic heart disease or PPHN. A simpler version is to compare pre-ductal (right hand) and post-ductal (foot) SpO2.
Bronchiolitis in neonates: this is a clinical diagnosis. Apnea can occur even with mild distress and is most common in the first 3 days of illness. Use supportive care only, with no antibiotics, steroids or beta-agonists. Send a urinalysis if the baby is febrile - Tintinalli's.

PART 3. Neonatal sepsis and meningitis

  • Early onset (<7 days): fulminant, linked to maternal risk factors (fever, group B streptococcus (GBS), prolonged rupture of membranes). It is more often septic shock and neutropenia.
  • Late onset (>7 days): gradual, with meningitis more common - Tintinalli's.
  • Organisms: "GEL" (my aid): GBS, E. coli and enterics, Listeria. Add HSV in a sick neonate with seizures, vesicles or a hepatitis picture.
  • Signs: "T-C-R-F-J-R" (my aid): Temperature instability, CNS signs, Respiratory distress, Feeding problems, Jaundice, Rash (Table 116-3).
  • Work-up: CBC, blood culture, catheter urine culture, lumbar puncture (LP) if stable, CRP or procalcitonin, and a chest X-ray if there are respiratory signs. Nuchal rigidity is absent in most neonates with meningitis.
  • Empiric treatment: ampicillin (about 50 mg/kg) plus gentamicin (2.5 mg/kg) - Tintinalli's. Add cefotaxime for meningitis. Avoid ceftriaxone in neonates because it displaces bilirubin and precipitates with calcium (my knowledge, the retrieved text was truncated).
  • Add acyclovir (20 mg/kg/dose per Harriet Lane) if HSV is plausible - Red Book Table 4.12 and Harriet Lane.
  • Reasoning: never delay antibiotics for an LP in an unstable baby. Give antibiotics within the hour.

PART 4. Cardiac emergencies

Presentation by timing
  • Cyanotic lesions present in the first days.
  • Left-sided obstructive (duct-dependent) lesions present at about days 5 to 14 with feeding difficulty and shock, after a day or two of poor feeding or lethargy - Tintinalli's.
Cyanotic lesions: "5 Ts" (a standard mnemonic): Truncus arteriosus, Transposition of the great arteries, Tricuspid atresia, Tetralogy of Fallot, Total anomalous pulmonary venous return (TAPVR).
Left obstructive lesions (shock): hypoplastic left heart syndrome (HLHS), critical aortic stenosis, coarctation, interrupted aortic arch. Closure of the duct cuts off either pulmonary flow (cyanosis, for example tricuspid atresia) or systemic flow (shock, for example HLHS) - Rosen's.
Management
  • Suspect any shocked neonate with hepatomegaly, weak or unequal femoral pulses, or no response to fluids of having a duct-dependent lesion.
  • Start prostaglandin E1 (PGE1) early. The usual start is 0.05 to 0.1 mcg/kg/min, then titrate down to the lowest effective dose (verify). Be ready for apnea and intubate if needed.
  • Exception: obstructed TAPVR, where PGE1 can worsen the obstruction - Creasy & Resnik.
  • Use small fluid boluses of 10 mL/kg with reassessment. Avoid excess oxygen in left-sided lesions.
  • Supraventricular tachycardia (SVT, HR >220): ice-water to the face, then adenosine 0.1 mg/kg rapid IV push. Use synchronized cardioversion at 0.5 to 1 J/kg if unstable (verify).
  • Screening: pulse-oximetry screening at 24 hours or more.

PART 5. Metabolic emergencies

Hypoglycemia
  • Treat when the glucose is <40 mg/dL with symptoms (jitteriness, apnea, seizures, lethargy, poor feeding). Give 2 to 4 mL/kg of 10% dextrose, then start an infusion - Rosen's, Medications. Tintinalli's Table 146-1 lists a larger neonatal D10 bolus of about 5 mL/kg, so local protocols differ.
  • Persistent hypoglycemia means hyperinsulinism, adrenal insufficiency or an IEM. Take a critical sample before treating if it does not delay treatment.
Hypocalcemia: seizures or jitteriness. Give calcium gluconate 10% at 1 to 2 mL/kg by slow IV infusion on a cardiac monitor (verify). Check magnesium too.
Inborn errors of metabolism (IEM)
  • Clue: a baby who was well for 1 to 3 days after birth and then deteriorates after feeds start, looking like sepsis (poor feeding, vomiting, lethargy, tachypnea, seizures).
  • Tests: glucose, gas, anion gap, lactate, ammonia, ketones, urine reducing substances, plasma amino acids, urine organic acids.
  • Management:
    • Stop protein feeds and give high-rate glucose (D10 infusion).
    • Give fluid boluses carefully, and reassess after each one because heart disease can look similar - Tintinalli's.
    • Treat hyperammonemia with ammonia scavengers and early dialysis in a metabolic center.
  • Reasoning pattern: hyperammonemia with respiratory alkalosis suggests a urea cycle defect. Metabolic acidosis with a high anion gap suggests an organic acidemia.
Congenital adrenal hyperplasia (salt-wasting): presents at days 7 to 14 with vomiting, dehydration, hyponatremia, hyperkalemia and hypoglycemia. Girls may have ambiguous genitalia. Give saline and stress-dose hydrocortisone (about 50 to 100 mg/m2, verify).

PART 6. Neonatal seizures

Causes: "HISS-MEND" (my aid)
  • Hypoxic-ischemic encephalopathy (day 0 to 2, most common)
  • Intracranial hemorrhage or infarct
  • Sepsis or meningitis (including HSV)
  • Sugar (hypoglycemia)
  • Minerals: calcium, magnesium, sodium
  • Errors of metabolism (including pyridoxine dependency)
  • Narcotic or drug withdrawal
  • Developmental or genetic (channelopathies, benign familial seizures)
Management
  1. ABC, check glucose and give dextrose if low.
  2. Check calcium, magnesium, sodium and a gas. Do a sepsis work-up.
  3. Phenobarbital 20 mg/kg IV is the usual first line (verify).
  4. Second line: levetiracetam, phenytoin or midazolam.
  5. Pyridoxine trial (100 mg IV, verify) if the seizures are refractory.
  6. Seizures can be subtle (eye deviation, lip smacking, cycling movements, apnea). EEG is the gold standard, and EEG-clinical dissociation after phenobarbital is common.
  7. Cool for HIE if criteria are met.

PART 7. Neonatal jaundice

Timing logic
  • <24 hours: always pathologic. Think hemolysis (Rh, ABO, G6PD), congenital infection or sepsis.
  • Day 2 to 3: physiologic peak, but also ABO disease and sepsis.
  • Week 1: breastfeeding jaundice and breast milk jaundice, sepsis, hypothyroidism.
  • >2 weeks, or direct (conjugated) bilirubin >1 mg/dL: cholestasis. Look for biliary atresia (pale stools, dark urine) and refer urgently. A Kasai procedure before about 60 days gives the best outcome.
Mnemonic for hemolytic causes (my aid, "RAGS"): Rh disease, ABO incompatibility, G6PD deficiency, Spherocytosis.
Management
  • Treat using the 2022 AAP phototherapy and exchange thresholds, which depend on gestational age, hours of life and neurotoxicity risk factors (gestation <38 weeks, low albumin, isoimmune hemolysis or G6PD deficiency, sepsis, clinical instability). Use a tool such as BiliTool.
  • Escalate care when the bilirubin is within 2 mg/dL of the exchange threshold. Escalation means intensive phototherapy, IV fluids, a repeat bilirubin every 2 hours and NICU transfer.
  • IVIG (0.5 to 1 g/kg) for isoimmune hemolysis. Exchange transfusion for failure of intensive phototherapy or signs of bilirubin encephalopathy.
  • Warning signs of encephalopathy: lethargy, hypotonia changing to hypertonia, arching (opisthotonos), high-pitched cry, and fever. Treat as an emergency.

PART 8. Surgical emergencies

Rule: bilious vomiting in a newborn is mechanical obstruction until proven otherwise - Mulholland and Greenfield's Surgery. A lethargic baby with bilious emesis needs urgent investigation for malrotation with midgut volvulus, a true surgical emergency because of progressive ischemia - Sabiston.
ConditionCluesInitial management
Malrotation with volvulusBilious vomiting, abdominal tenderness, shockResuscitate, urgent upper GI contrast study, then Ladd procedure. Do not wait if the baby is unstable
NECPreterm, feed intolerance, bloody stool, distension. Pneumatosis, portal venous gas, pneumoperitoneumNPO, nasogastric decompression, broad-spectrum antibiotics, fluids, serial X-rays, surgical review
Esophageal atresia with TEFDrooling, choking with feeds, orogastric tube coils, gasless abdomen in pure atresiaHead-up, continuous upper pouch suction (Replogle), avoid PPV if possible, look for VACTERL
Duodenal atresia"Double bubble", Down syndromeOrogastric tube decompression, fluids, surgery
GastroschisisDefect to the right of the cord, no sacCover bowel with warm saline-soaked gauze or a plastic bowel bag, lay the baby on the side, give extra fluids, orogastric tube
OmphaloceleSac present, associated anomalies and syndromesProtect the sac, keep warm, look for cardiac and chromosomal anomalies
Hirschsprung diseaseNo meconium by 48 hoursRectal washouts, antibiotics if enterocolitis
Anorectal malformationNo anus on inspectionLook for VACTERL, check urine for meconium
VACTERL: Vertebral, Anorectal, Cardiac, Tracheo-Esophageal, Renal, Limb anomalies.
Also remember testicular torsion and posterior urethral valves (weak urine stream, distended bladder) among neonatal urologic emergencies.

PART 9. Hematologic emergencies

  • Vitamin K deficiency bleeding: give vitamin K 1 mg IM at birth (0.5 mg if <1.5 kg, verify). For active bleeding, give IV vitamin K plus FFP or PCC. Intracranial hemorrhage can be the first sign - Tintinalli's.
  • Polycythemia: venous hematocrit >65%. Partial exchange transfusion if symptomatic.
  • Severe anemia: think fetomaternal hemorrhage, twin-twin transfusion, hemolysis. Transfuse.
  • Thrombocytopenia: immune (NAIT or maternal ITP) or sepsis, DIC. Treat the cause. Give matched platelets for severe bleeding.

PART 10. Shock, fluids, temperature and electrolytes

  • Shock types: hypovolemic (dehydration, hemorrhage), septic, cardiogenic (duct-dependent lesions, SVT, myocarditis), obstructive (tension pneumothorax) and adrenal crisis.
  • Fluids: crystalloid boluses of 10 to 20 mL/kg in neonates, with reassessment after each - Tintinalli's. Use smaller boluses (10 mL/kg) if cardiac disease is possible.
  • Vasoactives: dopamine or epinephrine early if fluid-refractory. Give hydrocortisone for catecholamine-resistant shock.
  • Hypernatremic dehydration: exclusively breastfed babies with poor intake and weight loss. Correct slowly.
  • Weight loss: normal loss is up to 10 to 12% in the first 3 to 7 days, and babies gain 20 to 30 g/day in the first 3 months - Tintinalli's.
  • Temperature: cold stress raises oxygen and glucose consumption. Prevent it with skin-to-skin contact, hats, plastic wrap for preterm babies and warmed rooms.

PART 11. Master-level quick map

PresentationFirst thoughtFast action
Blue, no response to O2Cyanotic heart disease, PPHNPGE1, echo
Pale or grey with shock, day 5 to 14Duct-dependent left heart lesion, sepsisPGE1 and antibiotics both
Bilious vomitingMalrotation with volvulusSurgical review, contrast study
SeizureHIE, glucose, calcium, sepsisDextrose, phenobarbital, work-up
Jaundice <24 hHemolysisPhototherapy, bilirubin and Coombs
Poor feeding after a well intervalIEM, sepsisGlucose, ammonia, antibiotics
Scaphoid abdomen with respiratory distressCDHIntubate, no bag-mask
Drooling, choking with feedEsophageal atresiaReplogle tube, no oral feeds
Ambiguous genitalia with vomitingCAHSaline, hydrocortisone
Master-level principles
  1. Treat as one: sepsis and duct-dependent heart disease can look identical. Cover both until separated.
  2. Always check glucose in any sick neonate.
  3. Bilious vomiting and weak femoral pulses are red flags.
  4. Preterm babies behave differently: NEC, IVH, apnea of prematurity and RDS apply.
  5. Neonates tolerate fluids and drugs poorly. Dose by weight, reassess often and avoid nephrotoxins and ceftriaxone.
I can turn any part into a one-page quick card, a quiz or a case-based exam set. I can also go deeper on any one topic with textbook figures and images. Tell me which you want.

With textbook figures and images

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neonatal resuscitation algorithm

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respiratory distress syndrome newborn chest radiograph ground glass air bronchograms

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congenital diaphragmatic hernia chest radiograph neonate bowel in thorax

A postoperative portable anteroposterior (AP) radiograph of a neonate in the supine position, capturing the chest, abdomen, and pelvis. The image shows the lungs are well-expanded with the mediastinum and cardiac shadow in a midline position. A pigtail chest tube is visible in the left hemithorax, placed to manage a small subpulmonic pneumothorax. Additional medical support devices include an endotracheal tube, a nasogastric tube extending into the stomach, and multiple external monitoring leads and cables across the thorax. The abdomen demonstrates a typical neonatal bowel gas pattern with air-filled loops visible in the lower quadrants. Skeletal structures, including the ribs, spine, and pelvis, appear unremarkable for the age group. The image illustrates postoperative management and device placement following surgical correction of a congenital diaphragmatic hernia, serving as a pedagogical tool for neonatal radiology and critical care monitoring.

A postoperative portable anteroposterior (AP) radiograph of a neonate in the supine position, capturing the chest, abdomen, and pelvis. The image shows the lungs are well-expanded with the mediastinum and cardiac shadow in a midline position. A pigtail chest tube is visible in the left hemithorax, placed to manage a small subpulmonic pneumothorax. Additional medical support devices include an endotracheal tube, a nasogastric tube extending into the stomach, and multiple external monitoring leads and cables across the thorax. The abdomen demonstrates a typical neonatal bowel gas pattern with air-filled loops visible in the lower quadrants. Skeletal structures, including the ribs, spine, and pelvis, appear unremarkable for the age group. The image illustrates postoperative management and device placement following surgical correction of a congenital diaphragmatic hernia, serving as a pedagogical tool for neonatal radiology and critical care monitoring.

A portable anteroposterior (AP) supine chest and abdominal radiograph of a neonate demonstrating a classic presentation of a left-sided congenital diaphragmatic hernia (CDH). The left hemithorax is occupied by multiple radiolucent, air-filled loops of bowel, which have herniated from the abdomen into the thoracic cavity. This mass effect has resulted in the total collapse of the left lung and a significant mediastinal shift toward the right, as evidenced by the displacement of the cardiac silhouette and trachea. The right lung appears partially collapsed due to the contralateral pressure. Iatrogenic structures are visible, including an endotracheal tube and a nasogastric tube (the latter seen following an abnormal course toward the herniated stomach/bowel). An ECG lead is noted on the right abdominal wall. This diagnostic image is a critical educational example of neonatal respiratory distress caused by anatomical defects, illustrating the hallmark radiological features of CDH, including a 'scaphoid' appearance of the lower abdominal gas pattern due to the displacement of abdominal contents into the thorax.

A portable anteroposterior (AP) supine chest and abdominal radiograph of a neonate demonstrating a classic presentation of a left-sided congenital diaphragmatic hernia (CDH). The left hemithorax is occupied by multiple radiolucent, air-filled loops of bowel, which have herniated from the abdomen into the thoracic cavity. This mass effect has resulted in the total collapse of the left lung and a significant mediastinal shift toward the right, as evidenced by the displacement of the cardiac silhouette and trachea. The right lung appears partially collapsed due to the contralateral pressure. Iatrogenic structures are visible, including an endotracheal tube and a nasogastric tube (the latter seen following an abnormal course toward the herniated stomach/bowel). An ECG lead is noted on the right abdominal wall. This diagnostic image is a critical educational example of neonatal respiratory distress caused by anatomical defects, illustrating the hallmark radiological features of CDH, including a 'scaphoid' appearance of the lower abdominal gas pattern due to the displacement of abdominal contents into the thorax.

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necrotizing enterocolitis pneumatosis intestinalis abdominal radiograph

This diagnostic image is a plain anteroposterior abdominal radiograph of a pediatric patient, demonstrating significant pathology of the upper gastrointestinal tract. The primary finding is a grossly distended, gas-filled stomach and proximal duodenum, occupying much of the upper and middle abdomen. Key diagnostic features include gastroduodenal pneumatosis (pneumatosis intestinalis), characterized by linear and curvilinear radiolucent gas streaks within the walls of the distended stomach and duodenum, highlighted by red arrows. This intramural air gives the gastric and duodenal walls a bubbly or mottled appearance. The distal bowel appears relatively gas-less, suggesting a proximal high-grade obstruction. These findings are clinically significant for identifying conditions such as duodenal web, stenosis, or necrotizing enterocolitis involving the proximal gut. This radiograph serves as a critical educational example of pneumatosis intestinalis and gastric emphysema, highlighting the visual cues for identifying gas within organ walls as distinct from intraluminal gas.

This diagnostic image is a plain anteroposterior abdominal radiograph of a pediatric patient, demonstrating significant pathology of the upper gastrointestinal tract. The primary finding is a grossly distended, gas-filled stomach and proximal duodenum, occupying much of the upper and middle abdomen. Key diagnostic features include gastroduodenal pneumatosis (pneumatosis intestinalis), characterized by linear and curvilinear radiolucent gas streaks within the walls of the distended stomach and duodenum, highlighted by red arrows. This intramural air gives the gastric and duodenal walls a bubbly or mottled appearance. The distal bowel appears relatively gas-less, suggesting a proximal high-grade obstruction. These findings are clinically significant for identifying conditions such as duodenal web, stenosis, or necrotizing enterocolitis involving the proximal gut. This radiograph serves as a critical educational example of pneumatosis intestinalis and gastric emphysema, highlighting the visual cues for identifying gas within organ walls as distinct from intraluminal gas.

**Imaging Modality:** Anteroposterior (AP) abdominal radiograph (X-ray).

**Imaging Modality:** Anteroposterior (AP) abdominal radiograph (X-ray).

**Imaging Modality:** Anteroposterior (AP) abdominal radiograph (plain film/X-ray).

**Imaging Modality:** Anteroposterior (AP) abdominal radiograph (plain film/X-ray).

**Imaging Modality:** Abdominal Radiograph (X-ray), AP view/scout film.

**Imaging Modality:** Abdominal Radiograph (X-ray), AP view/scout film.

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malrotation midgut volvulus upper GI corkscrew

Two-panel diagnostic image featuring an upper gastrointestinal (GI) contrast study (fluoroscopy/radiography) demonstrating classic signs of midgut volvulus secondary to intestinal malrotation. Panel (a) illustrates the 'corkscrew sign,' characterized by the spiral or helical twisting of the distal duodenum and proximal jejunum around the superior mesenteric artery axis. Panel (b) reveals an incomplete duodenal obstruction with marked dilation of the first and second portions of the duodenum. A tapered, 'beak-like' appearance is visible at the point of obstruction where the bowel twists. The contrast study identifies the abnormal right-sided position of the duodenojejunal flexure, rather than the normal position to the left of the spinal column. These radiographic findings are critical for diagnosing pediatric surgical emergencies such as midgut volvulus, where torsion of the narrow mesenteric base leads to intestinal ischemia and high-grade obstruction.

Two-panel diagnostic image featuring an upper gastrointestinal (GI) contrast study (fluoroscopy/radiography) demonstrating classic signs of midgut volvulus secondary to intestinal malrotation. Panel (a) illustrates the 'corkscrew sign,' characterized by the spiral or helical twisting of the distal duodenum and proximal jejunum around the superior mesenteric artery axis. Panel (b) reveals an incomplete duodenal obstruction with marked dilation of the first and second portions of the duodenum. A tapered, 'beak-like' appearance is visible at the point of obstruction where the bowel twists. The contrast study identifies the abnormal right-sided position of the duodenojejunal flexure, rather than the normal position to the left of the spinal column. These radiographic findings are critical for diagnosing pediatric surgical emergencies such as midgut volvulus, where torsion of the narrow mesenteric base leads to intestinal ischemia and high-grade obstruction.

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esophageal atresia tracheoesophageal fistula radiograph coiled tube

Anteroposterior (AP) neonatal chest and abdominal radiograph demonstrating diagnostic findings for esophageal atresia (EA) with an associated tracheoesophageal fistula (TEF). The primary finding is a radiopaque orogastric feeding tube that terminates abruptly in the proximal esophagus, visualized as a blind pouch in the upper mediastinum, indicating atresia. Despite the esophageal obstruction, there is significant bowel gas distributed throughout the stomach and small intestine in the abdomen. This presence of distal air confirms the existence of a distal tracheoesophageal fistula, allowing air to pass from the trachea into the lower gastrointestinal tract. The skeletal structures show normal neonatal development, and the abdominal gas pattern suggests patency distal to the stomach. This combination of a coiled or superiorly terminating feeding tube and subdiaphragmatic air is a classic radiological sign used in pediatric surgery to classify Type C esophageal atresia. The image is a critical educational example for neonatal intensive care and pediatric radiology training.

Anteroposterior (AP) neonatal chest and abdominal radiograph demonstrating diagnostic findings for esophageal atresia (EA) with an associated tracheoesophageal fistula (TEF). The primary finding is a radiopaque orogastric feeding tube that terminates abruptly in the proximal esophagus, visualized as a blind pouch in the upper mediastinum, indicating atresia. Despite the esophageal obstruction, there is significant bowel gas distributed throughout the stomach and small intestine in the abdomen. This presence of distal air confirms the existence of a distal tracheoesophageal fistula, allowing air to pass from the trachea into the lower gastrointestinal tract. The skeletal structures show normal neonatal development, and the abdominal gas pattern suggests patency distal to the stomach. This combination of a coiled or superiorly terminating feeding tube and subdiaphragmatic air is a classic radiological sign used in pediatric surgery to classify Type C esophageal atresia. The image is a critical educational example for neonatal intensive care and pediatric radiology training.

This composite figure illustrates the prenatal and postnatal imaging findings of a 21-week fetus with esophageal atresia. Image (a) is a sagittal fetal MRI using the FIESTA sequence, demonstrating a well-defined, hyperintense mediastinal cyst (thick arrow) posterior to the trachea (thin arrows). The fetal bladder is marked with 'B'. Image (b) provides a coronal HASTE fetal MRI view, showing a detailed perspective of the same hyperintense mediastinal duplication cyst (thick arrow). Image (c) is a postnatal anteroposterior thoraco-abdominal radiograph. It reveals a gastric tube coiled in the upper esophageal pouch (black arrow), characteristic of esophageal atresia. Notably, there is a total absence of gas in the bowel and abdomen, indicating a type I or II esophageal atresia without a distal tracheoesophageal fistula. A radiopaque venous umbilical catheter is also visible (white arrow). The constellation of findings—polyhydramnios, absent gastric bubble on ultrasound, and the identification of a mediastinal cyst—serves as critical diagnostic indicators for enteric duplication cysts and associated esophageal anomalies.

This composite figure illustrates the prenatal and postnatal imaging findings of a 21-week fetus with esophageal atresia. Image (a) is a sagittal fetal MRI using the FIESTA sequence, demonstrating a well-defined, hyperintense mediastinal cyst (thick arrow) posterior to the trachea (thin arrows). The fetal bladder is marked with 'B'. Image (b) provides a coronal HASTE fetal MRI view, showing a detailed perspective of the same hyperintense mediastinal duplication cyst (thick arrow). Image (c) is a postnatal anteroposterior thoraco-abdominal radiograph. It reveals a gastric tube coiled in the upper esophageal pouch (black arrow), characteristic of esophageal atresia. Notably, there is a total absence of gas in the bowel and abdomen, indicating a type I or II esophageal atresia without a distal tracheoesophageal fistula. A radiopaque venous umbilical catheter is also visible (white arrow). The constellation of findings—polyhydramnios, absent gastric bubble on ultrasound, and the identification of a mediastinal cyst—serves as critical diagnostic indicators for enteric duplication cysts and associated esophageal anomalies.

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gastroschisis omphalocele newborn

This clinical photograph displays a neonate with gastroschisis, a congenital ventral abdominal wall defect. The image shows a full-term newborn lying on a medical surface shortly after delivery. A significant periumbilical defect is visible, through which multiple loops of small intestine have herniated. The eviscerated bowel appears erythematous and edematous, lacking a protective peritoneal sac (distinguishing it from omphalocele). A healthcare provider, wearing blue sterile surgical gloves, is positioned to stabilize the exposed viscera. Visible neonate details include a blue identification band on the right ankle and standard newborn limbs. The image serves as a clinical example of a major abdominal wall defect requiring immediate neonatal intensive care and surgical intervention. It illustrates the typical presentation of gastroschisis where the bowel is exposed directly to amniotic fluid in utero, leading to its characteristic thickened and inflamed appearance at birth.

This clinical photograph displays a neonate with gastroschisis, a congenital ventral abdominal wall defect. The image shows a full-term newborn lying on a medical surface shortly after delivery. A significant periumbilical defect is visible, through which multiple loops of small intestine have herniated. The eviscerated bowel appears erythematous and edematous, lacking a protective peritoneal sac (distinguishing it from omphalocele). A healthcare provider, wearing blue sterile surgical gloves, is positioned to stabilize the exposed viscera. Visible neonate details include a blue identification band on the right ankle and standard newborn limbs. The image serves as a clinical example of a major abdominal wall defect requiring immediate neonatal intensive care and surgical intervention. It illustrates the typical presentation of gastroschisis where the bowel is exposed directly to amniotic fluid in utero, leading to its characteristic thickened and inflamed appearance at birth.

This clinical photograph shows a large omphalocele in a newborn infant, representing a midline abdominal wall defect. The protrusion is encased in a smooth, translucent amnioperitoneal sac. The sac exhibits a yellowish-brown hue with a focal area of dark purple discoloration, suggestive of bruising or underlying visceral congestion. Small, white, bubble-like surface irregularities are noted on the membrane. The umbilical cord is visible at the inferior aspect of the sac, appearing as a pale, whitish, fibrous structure with irregular texture against the reddish-brown skin of the abdominal wall. This image demonstrates the initial presentation of a congenital omphalocele before conservative treatment with eschar-inducing agents (e.g., aqueous eosin). Key educational features include the distinction between omphalocele (covered by a sac) and gastroschisis, and the assessment of sac integrity for pediatric surgical or neonatal management.

This clinical photograph shows a large omphalocele in a newborn infant, representing a midline abdominal wall defect. The protrusion is encased in a smooth, translucent amnioperitoneal sac. The sac exhibits a yellowish-brown hue with a focal area of dark purple discoloration, suggestive of bruising or underlying visceral congestion. Small, white, bubble-like surface irregularities are noted on the membrane. The umbilical cord is visible at the inferior aspect of the sac, appearing as a pale, whitish, fibrous structure with irregular texture against the reddish-brown skin of the abdominal wall. This image demonstrates the initial presentation of a congenital omphalocele before conservative treatment with eschar-inducing agents (e.g., aqueous eosin). Key educational features include the distinction between omphalocele (covered by a sac) and gastroschisis, and the assessment of sac integrity for pediatric surgical or neonatal management.

A clinical photograph of a newborn in an operating room setting illustrating gastroschisis, a congenital abdominal wall defect. The image shows a large evisceration of abdominal contents, including loops of the small and large intestines and a portion of the stomach, protruding through a right-sided paraumbilical defect. The herniated bowel loops exhibit significant edema, characteristic of prolonged exposure to amniotic fluid (matted, thickened appearance), and appear erythematous with a moist, glistening surface. The umbilical cord is visible and intact to the left of the defect. Gloved surgical hands are shown assessing the abdominal wall fissure and the visceral mass. This clinical finding is a hallmark of gastroschisis, where the bowel is not covered by a peritoneal sac, distinguishing it from an omphalocele. The case demonstrates the immediate postnatal presentation prior to the implementation of silo bag placement or primary surgical closure.

A clinical photograph of a newborn in an operating room setting illustrating gastroschisis, a congenital abdominal wall defect. The image shows a large evisceration of abdominal contents, including loops of the small and large intestines and a portion of the stomach, protruding through a right-sided paraumbilical defect. The herniated bowel loops exhibit significant edema, characteristic of prolonged exposure to amniotic fluid (matted, thickened appearance), and appear erythematous with a moist, glistening surface. The umbilical cord is visible and intact to the left of the defect. Gloved surgical hands are shown assessing the abdominal wall fissure and the visceral mass. This clinical finding is a hallmark of gastroschisis, where the bowel is not covered by a peritoneal sac, distinguishing it from an omphalocele. The case demonstrates the immediate postnatal presentation prior to the implementation of silo bag placement or primary surgical closure.

This clinical photograph displays a newborn infant in a neonatal care setting with a large, midline abdominal wall defect characteristic of a giant omphalocele. The defect presents as a substantial, hemispherical sac originating from the umbilical region, estimated at approximately 8 cm in diameter. The sac is covered by a thin, translucent peritoneal-amniotic membrane, through which the underlying visceral contents—primarily a significant portion of the liver and intestinal loops—are visible. Parts of the liver show a dark, purplish hue through the membrane. Concurrent medical management is visible, including a nasogastric tube for decompression, several adhesive dressings on the chest and upper abdomen, and white gauze packing at the base of the omphalocele sac. The image illustrates a major congenital anomaly requiring staged surgical closure and neonatal intensive care. Key educational concepts include midline abdominal wall defects, differentiation from gastroschisis by the presence of a covering sac, and initial neonatal stabilization.

This clinical photograph displays a newborn infant in a neonatal care setting with a large, midline abdominal wall defect characteristic of a giant omphalocele. The defect presents as a substantial, hemispherical sac originating from the umbilical region, estimated at approximately 8 cm in diameter. The sac is covered by a thin, translucent peritoneal-amniotic membrane, through which the underlying visceral contents—primarily a significant portion of the liver and intestinal loops—are visible. Parts of the liver show a dark, purplish hue through the membrane. Concurrent medical management is visible, including a nasogastric tube for decompression, several adhesive dressings on the chest and upper abdomen, and white gauze packing at the base of the omphalocele sac. The image illustrates a major congenital anomaly requiring staged surgical closure and neonatal intensive care. Key educational concepts include midline abdominal wall defects, differentiation from gastroschisis by the presence of a covering sac, and initial neonatal stabilization.

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duodenal atresia double bubble sign

A plain anteroposterior (AP) X-ray of a neonate's chest and abdomen demonstrating situs inversus totalis and duodenal atresia. The cardiac silhouette is predominantly located in the right hemithorax (dextrocardia). In the abdomen, the liver shadow is positioned on the left side, while the stomach gas bubble is located on the right. A classic 'double bubble' sign is visible in the upper right quadrant, representing a dilated, gas-filled stomach and proximal duodenum, characteristic of duodenal atresia. A radiopaque nasogastric tube (NGT) is seen traversing the midline and terminating in the right-sided gastric bubble. A circular metallic temperature probe is visible on the right lateral abdominal wall. The image illustrates the complete reversal of thoracic and abdominal organs in a neonatal patient presenting with signs of intestinal obstruction.

A plain anteroposterior (AP) X-ray of a neonate's chest and abdomen demonstrating situs inversus totalis and duodenal atresia. The cardiac silhouette is predominantly located in the right hemithorax (dextrocardia). In the abdomen, the liver shadow is positioned on the left side, while the stomach gas bubble is located on the right. A classic 'double bubble' sign is visible in the upper right quadrant, representing a dilated, gas-filled stomach and proximal duodenum, characteristic of duodenal atresia. A radiopaque nasogastric tube (NGT) is seen traversing the midline and terminating in the right-sided gastric bubble. A circular metallic temperature probe is visible on the right lateral abdominal wall. The image illustrates the complete reversal of thoracic and abdominal organs in a neonatal patient presenting with signs of intestinal obstruction.

This abdominal X-ray of a neonate demonstrates the classic 'double bubble' sign, highly indicative of duodenal atresia. Two large, air-filled radiolucencies are visible in the upper abdomen: a larger gastric bubble on the patient's left and a smaller duodenal bubble on the right of the midline. A notable feature in this specific image is the 'caterpillar sign,' where the dilated gastric wall shows multiple waves of peristalsis (undulating borders), suggesting an attempt by the stomach to overcome the distal obstruction. There is a complete absence of bowel gas distal to the duodenum throughout the rest of the abdomen, signifying high intestinal obstruction. This diagnostic image is a key educational resource for pediatric radiology and neonatal surgery, illustrating the pathophysiology of congenital intestinal malformations and the radiographic markers used to differentiate them from other causes of neonatal emesis.

This abdominal X-ray of a neonate demonstrates the classic 'double bubble' sign, highly indicative of duodenal atresia. Two large, air-filled radiolucencies are visible in the upper abdomen: a larger gastric bubble on the patient's left and a smaller duodenal bubble on the right of the midline. A notable feature in this specific image is the 'caterpillar sign,' where the dilated gastric wall shows multiple waves of peristalsis (undulating borders), suggesting an attempt by the stomach to overcome the distal obstruction. There is a complete absence of bowel gas distal to the duodenum throughout the rest of the abdomen, signifying high intestinal obstruction. This diagnostic image is a key educational resource for pediatric radiology and neonatal surgery, illustrating the pathophysiology of congenital intestinal malformations and the radiographic markers used to differentiate them from other causes of neonatal emesis.

This diagnostic image is an anteroposterior plain radiograph of an infant's abdomen and thorax. The primary finding is the pathognomonic 'double-bubble' sign, characterized by two large, air-filled lucencies in the upper abdomen representing a dilated stomach (left) and a dilated proximal duodenum (right). There is a complete absence of gas throughout the distal intestinal tract, which indicates a high-grade proximal bowel obstruction. These radiographic features are classically associated with congenital duodenal atresia. The skeletal structures, including the rib cage, vertebral column, pelvis, and proximal femurs, appear appropriate for gestational age without obvious deformities or secondary complications. The image serves as a critical educational example of neonatal intestinal obstruction and the classic presentation of duodenal atresia in pediatric radiology.

This diagnostic image is an anteroposterior plain radiograph of an infant's abdomen and thorax. The primary finding is the pathognomonic 'double-bubble' sign, characterized by two large, air-filled lucencies in the upper abdomen representing a dilated stomach (left) and a dilated proximal duodenum (right). There is a complete absence of gas throughout the distal intestinal tract, which indicates a high-grade proximal bowel obstruction. These radiographic features are classically associated with congenital duodenal atresia. The skeletal structures, including the rib cage, vertebral column, pelvis, and proximal femurs, appear appropriate for gestational age without obvious deformities or secondary complications. The image serves as a critical educational example of neonatal intestinal obstruction and the classic presentation of duodenal atresia in pediatric radiology.

This diagnostic image is an anteroposterior babygram (plain film X-ray of the chest and abdomen) of a neonate. The thoracic cavity demonstrates dextrocardia, where the cardiac silhouette is predominantly positioned in the right hemithorax. In the upper abdomen, there is a prominent 'reverse double bubble' sign, characterized by two distinct gaseous shadows with air-fluid levels. The larger bubble (stomach) is located on the right side, and the smaller bubble (proximal duodenum) is located on the left, indicating situs inversus associated with duodenal obstruction. There is a complete absence of gas in the distal intestinal segments, suggesting a high-grade intestinal obstruction such as duodenal atresia or a perforated duodenal diaphragm. The clinical relevance of this visual includes the recognition of heterotaxy syndromes or situs inversus totalis in the context of neonatal bowel obstruction. This material is suitable for medical students and pediatric residents focusing on neonatal radiology and congenital gastrointestinal anomalies.

This diagnostic image is an anteroposterior babygram (plain film X-ray of the chest and abdomen) of a neonate. The thoracic cavity demonstrates dextrocardia, where the cardiac silhouette is predominantly positioned in the right hemithorax. In the upper abdomen, there is a prominent 'reverse double bubble' sign, characterized by two distinct gaseous shadows with air-fluid levels. The larger bubble (stomach) is located on the right side, and the smaller bubble (proximal duodenum) is located on the left, indicating situs inversus associated with duodenal obstruction. There is a complete absence of gas in the distal intestinal segments, suggesting a high-grade intestinal obstruction such as duodenal atresia or a perforated duodenal diaphragm. The clinical relevance of this visual includes the recognition of heterotaxy syndromes or situs inversus totalis in the context of neonatal bowel obstruction. This material is suitable for medical students and pediatric residents focusing on neonatal radiology and congenital gastrointestinal anomalies.

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transposition of the great arteries egg on a string chest radiograph newborn cyanotic heart disease

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neonatal jaundice kernicterus phototherapy bilirubin

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Neonatal emergencies: illustrated companion to the master guide

The images below are real case figures from the medical image library, matched to each part of the earlier guide. They come from published case reports and teaching sets, so they are not all from the textbooks I cited earlier. For each one I say what to look for and why it matters.
I found no usable images for the resuscitation algorithm flowchart or for classic kernicterus, so those are covered in text only. The NRP algorithm is available from the AAP/AHA 2025 guidelines.

Part 1. Resuscitation and access

Training for the first minute. In Helping Babies Breathe, the "golden minute" rule is that ventilation comes first. This photo shows an HBB training session in Sierra Leone.
Helping Babies Breathe training session in Sierra Leone
Chest compression position. This simulation uses a feedback device placed on the sternum, with a crosshair aligned to the sternum and the inter-nipple line. Compress over the lower third of the sternum, with the two-thumb encircling technique at 3:1.
Neonatal compression simulation with feedback sheet
Umbilical vein catheterization. This shows preparation for the preferred route for epinephrine and volume when compressions are needed.
Preparation for umbilical vein catheterization
Thermoregulation. A heat-reflecting patch on a newborn's sternum is one example of preventing cold stress.
Heat-reflecting patch on a newborn's sternum

Part 2. Respiratory emergencies: reading the neonatal chest X-ray

Reasoning approach: look at lung volume, the pattern (granular, patchy or hazy), and any air leak. Then match the pattern to gestation and history.

RDS (preterm, surfactant deficiency)

Look for bilateral, symmetrical ground-glass opacification with a fine granular texture and low lung volumes, with air bronchograms in more severe disease.
RDS: diffuse ground-glass opacification with fine granular appearance
Severe disease obscures the cardiophrenic and costophrenic angles:
Severe RDS with homogeneous bilateral opacity
Mild (grade 1) disease shows a mild ground-glass appearance with increased central density:
RDS grade 1: mild ground-glass appearance

TTN (term or late preterm, often after C-section)

Look for diffuse hazy lungs with increased interstitial markings (retained fetal lung fluid). The picture usually clears in 24 to 72 hours. If it does not, reconsider sepsis, pneumonia or a cardiac cause.
TTN: bilateral hazy lungs with increased interstitial markings

Meningeal aspiration with air leak (MAS + pneumothorax)

Look for coarse patchy opacities with hyperinflation, and a pleural line with absent lung markings beyond it. This is why MAS babies on positive pressure can suddenly deteriorate.
MAS with right-sided pneumothorax

Pneumothorax

Bilateral pneumothoraces with visible visceral pleural lines:
Bilateral neonatal pneumothoraces
A small pneumothorax can hide on a supine film. A lateral decubitus view, as below, shows a thin radiolucent band between the lung and the chest wall.
Small right pneumothorax on lateral decubitus film

Congenital diaphragmatic hernia (CDH)

Look for air-filled bowel loops in the left hemithorax, mediastinal shift to the right and a scaphoid lower abdomen. Note the tubes: an endotracheal tube (intubation, not mask ventilation) and a nasogastric tube that follows an abnormal course toward the herniated stomach.
Left CDH with bowel in the chest and mediastinal shift
Post-repair, a pigtail chest tube manages a small residual pneumothorax and the lungs are well expanded:
Post-operative CDH with pigtail chest tube

Part 4. Cardiac emergencies

Transposition of the great arteries (egg-on-a-string). A globular heart with a narrow superior mediastinum. This is a cyanotic lesion that presents in the first days.
Egg-on-a-string cardiac silhouette in a neonate
Obstructed TAPVC (day 4 of life). Mild cardiomegaly with diffuse ground-glass lungs from pulmonary venous congestion. It can be mistaken for RDS or sepsis, and PGE1 can worsen it, which is why the guide flagged it as an exception.
Supracardiac TAPVC with pulmonary venous obstruction
Rashkind balloon septostomy. Used in a cyanotic neonate (for example TGA or HLHS) to improve atrial mixing while awaiting definitive surgery.
Rashkind balloon septostomy fluoroscopy series
Pulse-oximetry screening for critical CHD. This table lists the conditions detected by the screen:
Table of conditions detected by pulse oximetry screening for CCHD

Part 6. Neonatal seizures: monitoring

Amplitude-integrated EEG (aEEG) is used in the NICU for continuous bedside monitoring. Look for a continuous versus discontinuous background and for the sudden raised baseline that marks a seizure. This shows aEEG with raw EEG in a term infant:
aEEG and raw EEG in a term infant in the NICU
A preterm tracing shows a discontinuous background, which is normal for that gestation:
aEEG and raw EEG in a preterm newborn

Part 7. Jaundice

Bili-ruler screening. A colour-matched strip held against the infant's face gives a rough estimate of bilirubin. It is a screening aid only, and a serum or transcutaneous bilirubin is needed to decide on treatment.
Bili-ruler screening for neonatal jaundice
Jaundice resolution over time. The left panel shows yellow discolouration of the face at diagnosis, with the same infant over 3 months.
Resolution of neonatal jaundice over three months
Opisthotonos. This one-month-old infant shows severe arching with retrocollis. In a jaundiced neonate, arching is a late warning sign of bilirubin encephalopathy. This photo is not specifically a kernicterus case, so use it only to recognise the posture.
Infant with opisthotonos

Part 8. Surgical emergencies

Malrotation with midgut volvulus

Upper GI contrast study. Panel (a) shows the corkscrew sign, a spiral twist of the distal duodenum and proximal jejunum. Panel (b) shows a beak-like tapering at the obstruction, and the duodenojejunal flexure sits to the right of the spine instead of the left. Bilious vomiting plus this picture means the operating room, not more imaging.
Corkscrew sign and duodenal obstruction in midgut volvulus

Intramural gas (NEC family)

This film shows linear and curvilinear gas streaks in the walls of a distended stomach and duodenum, with a relatively gasless distal bowel. The caption raises duodenal web or stenosis as well as NEC. In classic NEC, look for pneumatosis in the small or large bowel, portal venous gas and free air.
Gastroduodenal pneumatosis intestinalis

Esophageal atresia with TEF

Type C (most common). The tube stops in the upper pouch, but gas fills the stomach and bowel because a distal fistula lets air pass from trachea to gut.
Esophageal atresia with distal TEF: tube in upper pouch, gas-filled abdomen
Without a distal fistula. The tube coils in the upper pouch and the abdomen is gasless (a type I or II pattern). Prenatal clues in this case were polyhydramnios and an absent gastric bubble.
Esophageal atresia without distal fistula: coiled tube and gasless abdomen
Reasoning pearl: gas in the abdomen means a distal fistula. A gasless abdomen means pure atresia.

Duodenal atresia (double bubble)

Two large air-filled bubbles (stomach and proximal duodenum) with no gas beyond. This film also shows a "caterpillar" pattern of gastric peristalsis:
Double bubble sign with caterpillar sign
A classic double bubble with a gasless distal tract:
Classic double bubble sign
A reverse double bubble with dextrocardia and situs inversus. Check heart position and liver side on the film before reading the bubbles.
Double bubble with situs inversus and dextrocardia

Gastroschisis versus omphalocele

Gastroschisis: a right paraumbilical defect, no sac, and edematous, matted, inflamed bowel from amniotic fluid exposure. The cord is intact to the left of the defect.
Gastroschisis: eviscerated bowel with no sac
Gastroschisis with right paraumbilical defect and edematous bowel
Omphalocele: a midline defect covered by a translucent sac, with the cord inserting into the sac. Look for associated anomalies.
Omphalocele with intact amnioperitoneal sac
A giant omphalocele with liver in the sac, a nasogastric tube and a protective dressing:
Giant omphalocele with liver in the sac
Memory aid (my aid): "Gastro = Gut out, no covering, right side. Omphalo = Covered, midline, other anomalies."

Anorectal malformations

Always inspect the perineum in the first newborn examination. A high malformation in a male has a visible perineal raphe:
High anorectal malformation in a male newborn
A rectovestibular fistula in a girl (red arrow):
Rectovestibular fistula in an infant with imperforate anus
A low imperforate anus with perineal ultrasound:
Low imperforate anus with clinical photo and ultrasound
Once found, look for VACTERL associations (cardiac, renal, spine, limb, tracheoesophageal).

One-page visual pattern recognition

What you seeThinkFirst action
Ground-glass, low volumes, pretermRDSCPAP, surfactant
Hazy lungs, term or C-sectionTTNOxygen, observe, exclude sepsis
Coarse patchy, hyperinflated, post-termMAS, watch for air leakVentilate gently, check for pneumothorax
Bowel in chest, shift, scaphoid abdomenCDHIntubate, orogastric tube, no mask ventilation
Egg-on-a-string heart, cyanosisTGAPGE1, urgent cardiology
Ground-glass with cardiomegaly in first daysObstructed TAPVCAvoid PGE1, urgent surgery
Corkscrew duodenum on contrastMidgut volvulusOperating room
Double bubble, gasless distal bowelDuodenal atresiaDecompress, check for Down syndrome and cardiac anomalies
Tube coils in upper chest, gas in abdomenEA with distal TEFReplogle suction, head-up
Defect right of cord, no sacGastroschisisCover the bowel, side-lying, extra fluids
Defect with a sacOmphaloceleProtect the sac, search for associated anomalies
Arching in a jaundiced babyBilirubin encephalopathyEmergency exchange transfusion assessment
I can turn this into a printable PDF or slide deck, or build an image-based quiz where you identify the diagnosis from the film. Tell me which you prefer.

Neonatal emergencies master guide With textbook figures and images

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