GC204 The Newborn Baby Cannot Breathe Oesophageal Atresia, Diaphragmatic Hernia, And Other Surgery Of Lung
Neonatal respiratory distress caused by congenital surgical conditions such as oesophageal atresia, congenital diaphragmatic hernia, and other thoracic anomalies that obstruct or compromise the airway and lung function, requiring urgent surgical intervention.
The Newborn Baby Cannot Breathe: Oesophageal Atresia, Diaphragmatic Hernia, and Other Surgery of the Lung
Big Idea: A newborn presenting with respiratory distress may have a surgical cause that requires urgent recognition and intervention — this lecture focuses on distinguishing surgical from medical causes, and on the definitive management of two landmark neonatal surgical conditions: Congenital Diaphragmatic Hernia (CDH) and Oesophageal Atresia/Tracheo-Oesophageal Fistula (OA/TOF).
Learning Objectives (directly from the deck [1]):
- Surgical care of the newborn
- Principles of management of neonatal respiratory distress
- Causes of airway obstruction
- Specific management of two major anomalies: CDH and OA/TOF
Part 1: Principles of Neonatal Surgical Care
"Newborn infants are not small adults" — Children differ from adults in anatomy, physiology, psychology, pathology. [1]
This is a core exam concept. Key differences include:
- Thermoregulation: High surface-area-to-volume ratio → rapid heat loss → hypothermia risk during surgery
- Fluid balance: Proportionally higher total body water, kidneys immature → narrow margin for fluid errors
- Metabolism: Higher basal metabolic rate per kg, limited glycogen stores → hypoglycaemia risk
- Airway: Smaller, more anterior larynx; obligate nasal breathers; subglottic region is the narrowest part (not glottis as in adults)
- Immune function: Immature → higher infection risk
Paediatric Surgery Scope
Paediatric surgery is a broad specialty defined by age, treating the child as a whole rather than an organ/system. It is divided into: (a) Neonatal surgery, (b) Major/complex surgery of older infants and children, (c) Paediatric urology.* [1]
Key advances: Neonatal intensive care (pre- and post-operative), neonatal anaesthesia, TPN, and minimally invasive surgery (MIS). [1]
- TPN (Total Parenteral Nutrition): Critical because many neonatal surgical patients cannot feed enterally for days–weeks (e.g., post OA repair, CDH repair)
- MIS: Size is not a contraindication to MIS surgery [1]. Modern instruments — thoracoscope (5mm or 3mm diameter, 20cm or 40cm length, 30° HD camera) — allow even premature neonates to undergo thoracoscopic procedures.
Part 2: Neonatal Respiratory Distress — Presentation and Initial Management
Tachypnoea — ↑ breath rate Dyspnoea — laboured breathing, not CNS Stridor:
- Inspiratory → pharyngeal, glottic level
- Biphasic → subglottic, tracheal level
- Expiratory → bronchial level Cyanosis, tachycardia [1]
Why stridor localization matters: The phase of stridor tells you where the obstruction is. Inspiratory stridor = obstruction above the glottis (airway collapses inward during inspiration). Biphasic = fixed obstruction at the subglottis/trachea. Expiratory = intrathoracic airways collapsing during expiration.
| Stridor Phase | Level | Examples |
|---|---|---|
| Inspiratory | Supraglottic / Glottic | Laryngomalacia, epiglottitis, croup |
| Biphasic | Subglottic / Tracheal | Subglottic stenosis, tracheomalacia, vascular ring |
| Expiratory | Bronchial | Bronchomalacia, bronchial FB |
Resuscitate — ABC: airway, breathing, circulation; suctioning, tongue forward, oxygenation, intubation, ventilation, IV fluid Monitor — vital signs, oximetry Diagnosis + review antenatal (AN) history → specific treatment [1]
Why review AN history? Antenatal ultrasound may have already detected polyhydramnios (→ OA), absent stomach bubble (→ OA), intrathoracic bowel (→ CDH), or cystic lung lesions (→ CPAM). This gives you a head-start on diagnosis.
Part 3: Causes of Respiratory Distress — Complete Classification
Congenital heart diseases CNS disorders causing apnoea — cerebral haemorrhage, oedema, drugs GI disorders — OA/TOF, gastro-oesophageal reflux Systemic — metabolic acidosis, sepsis [1]
Meconium aspiration Transient tachypnoea (TTN) Hyaline membrane disease (HMD / RDS) — LBW Persistent fetal circulation (PPHN), pneumonia, pulmonary haemorrhage, pneumothorax, phrenic nerve palsy [1]
| Condition | Key Feature | CXR Finding |
|---|---|---|
| TTN | Term/C-section, resolves 12-72h | Fluid in fissures, perihilar streaking |
| RDS (HMD) | Preterm/LBW, surfactant deficiency | Ground-glass with air bronchograms |
| MAS | Post-dates, meconium-stained liquor | Bilateral patchy/fluffy densities |
| PPHN | Persistent high PVR, R-to-L shunt | Can be normal; echo diagnostic |
| Pneumothorax | Sudden deterioration | Visible lung edge, absent lung markings |
Choanal atresia Pierre-Robin syndrome Laryngomalacia Subglottic stenosis Tracheal malacia, stenosis Lymphatic malformation Vascular ring [1]
Key Airway Disorders for Exams
- Choanal atresia: Bilateral = neonatal emergency (obligate nasal breathers). Unilateral may present later. Diagnosis: failure to pass catheter through nose; CT confirms.
- Pierre-Robin syndrome: Micrognathia + glossoptosis + cleft palate → airway obstruction. Prone positioning helps.
- Laryngomalacia: Most common cause of neonatal stridor. Inspiratory stridor worse when supine/feeding. Usually self-limiting by 12–18 months.
- Vascular ring: Aberrant vessels encircling trachea/oesophagus → biphasic stridor + feeding difficulties.
Cystic hygroma / Lymphangioma Neck (75%), axilla Treatment: Injection sclerotherapy (OK432, bleomycin) or Excision [1]
Why it causes respiratory distress: Large cervical lymphatic malformations can compress the airway externally. They are soft, transilluminant, and non-tender. Can enlarge acutely with infection or haemorrhage into cyst.
Cystic lesions Congenital Pulmonary Airway Malformation (CPAM) Congenital Lobar Emphysema (CLE) Congenital Diaphragmatic Hernia (CDH) Diaphragmatic splinting (distended abdomen) [1]
Congenital Pulmonary Airway Malformation (CPAM)
1 : 5,000 live births Antenatal diagnosis Potential recurrent pneumonia, malignancy Lobectomy as definitive treatment [1]
From first principles: CPAM (formerly CCAM — congenital cystic adenomatoid malformation) is a hamartomatous developmental abnormality of the lower respiratory tract. Abnormal bronchiolar proliferation creates cystic or solid masses that communicate with the tracheobronchial tree but have abnormal alveolar structure.
Why treat even if asymptomatic?
- Recurrent pneumonia — the abnormal tissue acts as a nidus for infection
- Malignancy risk — rare but documented transformation to pleuropulmonary blastoma or bronchoalveolar carcinoma
- Therefore, elective lobectomy (often thoracoscopic) is recommended
Imaging: Antenatal USS shows echogenic lung mass ± cysts. Postnatal CT chest delineates anatomy for surgical planning. [1]
CT findings (from lecture imaging) [1]:
- Axial CT (lung window): well-defined, air-filled cystic/lucent lesion in the affected lobe (e.g., left lower lobe) with smaller adjacent cystic areas
- Coronal reconstruction: confirms the cystic lesion near the hemidiaphragm with surrounding altered lung texture
- These images guide the extent of thoracoscopic lobectomy
Part 5: Congenital Diaphragmatic Hernia (CDH) — A Major Neonatal Surgical Emergency
1 : 4,000 live births (1 : 2,000 births including stillbirths) Survival 60% (range 40–95%) Left side (80–90%) Posterolateral defect (Bochdalek) [1]
Why left-sided? The left pleuroperitoneal canal closes later during embryonic development (approximately week 8–10) than the right. The liver on the right side also acts as a partial plug, protecting the right hemidiaphragm.
Types of CDH:
| Type | Location | Frequency | Notes |
|---|---|---|---|
| Bochdalek | Posterolateral | ~80% | Most common, usually left |
| Morgagni | Anterior/retrosternal | ~2-3% | Usually right, often presents later |
| Central/hiatal | Oesophageal hiatus | Rare |
Contents: intestines, stomach, spleen, liver (left); liver, intestines (right) Non-rotation of intestines Associated anomalies 20–40%, mostly cardiac [1]
Pulmonary hypoplasia — compression (ipsilateral, contralateral) Pulmonary hypertension — persistent fetal circulation, immaturity, hypoxia [1]
Why pulmonary hypoplasia? The herniated abdominal organs occupy the thoracic cavity during fetal lung development (canalicular and saccular stages). This compresses the ipsilateral lung severely and pushes the mediastinum, compressing the contralateral lung too. The result is bilateral pulmonary hypoplasia (ipsilateral > contralateral) with fewer bronchial generations and reduced alveolar surface area.
Why pulmonary hypertension? Hypoplastic lungs have fewer and abnormally muscularized pulmonary arteries. At birth, the normal drop in pulmonary vascular resistance (PVR) fails to occur → persistent fetal circulation (right-to-left shunting via PDA and foramen ovale) → systemic hypoxia → further pulmonary vasoconstriction → vicious cycle.
CDH: The Two Killers
The mortality in CDH is NOT primarily from the hernia itself but from:
- Pulmonary hypoplasia (not enough lung tissue)
- Pulmonary hypertension (can't perfuse what lung is there)
This is why rushing to surgery does NOT improve outcomes — stabilization first is critical.
Antenatal USS — heart displaced, intrathoracic intestines Respiratory distress (early onset → pulmonary insufficiency) Apparent dextrocardia (heart pushed to the right by left-sided hernia) Scaphoid abdomen (empty because contents are in the chest) Reduced air entry, abnormal bowel sounds in affected chest [1]
Why scaphoid abdomen? The abdominal viscera have herniated into the thorax, so the abdomen is empty/flat — the opposite of the distended abdomen you'd expect in intestinal obstruction.
Why apparent dextrocardia? The mediastinum is pushed contralaterally by the herniated viscera. On examination and CXR, the heart appears to be on the right side (in left CDH). This is NOT true dextrocardia — it's a mediastinal shift.
CDH Physical Signs Summary (from lecture diagram) [1]:
- Cyanosis
- Heart sounds shifted to the right (in left-sided CDH)
- Bowel herniated into the left hemithorax — with dullness to percussion and absent breath sounds over the affected side
- Scaphoid abdomen
- Contralateral lung compressed; liver may be displaced into the thorax
Management
Chest X-ray Resuscitation: oxygen, NO BAGGING WITH MASK, endotracheal intubation Oxygen saturation: blood gases, oximetry Orogastric tube Systemic support: fluid, inotropes [1]
NEVER Bag-Mask Ventilate a Suspected CDH
No bagging with mask — this is the single most critical initial management point for exams. Bag-mask ventilation forces air into the stomach and bowel that are in the chest, further inflating them and further compressing the already-hypoplastic lungs. This will worsen the respiratory distress and can be fatal. Intubate directly. [1]
Why orogastric (OG) tube? To decompress the stomach and intestines sitting in the chest. Decompression reduces the volume of herniated contents, potentially improving lung expansion.
Vasodilators: nitric oxide to reduce pulmonary hypertension Gentle ventilation (to avoid barotrauma): high-frequency oscillation (HFO), permissive hypercapnia (pCO₂ up to 65 mmHg) Extracorporeal membrane oxygenation (ECMO) Surgical repair after stabilization: laparotomy / thoracoscopy, primary closure / patch repair Fetal surgery [1]
Why "gentle ventilation" and permissive hypercapnia? The hypoplastic lungs are extremely vulnerable to barotrauma. Aggressive ventilation with high pressures causes pneumothorax of the contralateral (only functioning) lung — which is catastrophic. High-frequency oscillatory ventilation (HFOV) delivers tiny tidal volumes at very high rates, achieving gas exchange with lower peak pressures. Accepting a higher-than-normal pCO₂ (up to 65 mmHg) avoids the need for dangerously high ventilatory pressures.
Why inhaled nitric oxide (iNO)? iNO is a selective pulmonary vasodilator. It relaxes pulmonary vascular smooth muscle → reduces PVR → reduces right-to-left shunting → improves oxygenation. It has no systemic vasodilatory effect because it is rapidly inactivated by haemoglobin.
Why ECMO? In severe cases where the lungs cannot provide adequate gas exchange despite maximal medical therapy, ECMO provides extracorporeal oxygenation and CO₂ removal, acting as a temporary lung bypass. This allows time for pulmonary hypertension to stabilize.
Why surgery AFTER stabilization? Historical approach was emergency surgery. Evidence now shows that stabilizing pulmonary hypertension and optimizing ventilation BEFORE surgery improves survival. Surgery on an unstable baby worsens pulmonary hypertension and can be fatal.
1. Reduce the abdominal contents back into the abdominal cavity 2. Repair the diaphragm by direct closure or mesh repair [1]
Approach: Via laparotomy (abdominal) or thoracoscopy (thoracic). If the defect is small, primary closure with sutures. If the defect is large and there is insufficient native diaphragm, a prosthetic patch (e.g., Gore-Tex) or muscle flap is used.
Why fetal surgery? Fetal surgery includes FETO (Fetoscopic Endoluminal Tracheal Occlusion): A balloon is placed in the fetal trachea in utero. By obstructing tracheal fluid outflow, the lungs are kept distended, which promotes lung growth and counters hypoplasia. The balloon is removed before or at delivery. This is reserved for severe cases with poor predicted survival. [1] [5]
Part 6: Oesophageal Atresia (OA) and Tracheo-Oesophageal Fistula (TOF)
1 : 4,000 births Anatomical variations (n = 5) Associated anomalies (50%) VATER, CHARGE [1]
Vertebral, Anorectal, Cardiac, Tracheo-oesophageal fistula, Esophageal atresia, Renal, Limb [1]
VACTERL Association — High Yield
50% of OA/TOF patients have associated anomalies. When you diagnose OA/TOF, you MUST screen for:
- Vertebral anomalies (hemivertebra — visible on the CXR!)
- Anorectal malformations (imperforate anus — check at birth exam)
- Cardiac defects (echocardiography)
- TE — already diagnosed
- Renal anomalies (renal USS)
- Limb anomalies (radial ray defects — examine hands)
CHARGE = Coloboma, Heart defects, choanal Atresia, Retardation of growth/development, Genital anomalies, Ear anomalies.
The five types of OA/TOF are classified by the relationship between the oesophageal pouch and any tracheal fistula [1] [2] [5]:
| Type | Description | Frequency | Key CXR Feature |
|---|---|---|---|
| A | Pure OA (no fistula) | ~8% | Gasless abdomen |
| B | OA + proximal TOF | ~1% | May be gasless |
| C | OA + distal TOF | ~86% | Gas in stomach/bowel |
| D | OA + double TOF (proximal + distal) | ~1% | Gas in bowel |
| E | H-type fistula (no atresia) | ~4% | Normal, may present late |
Type C (OA with distal TOF) is by far the most common (~86%).
What the Gross schematics show: five drawings (a–e) of trachea + oesophagus — pure blind ends (A), proximal fistula only (B), blind proximal pouch + distal TOF (C, ~86%), double fistula (D), and continuous oesophagus with an H-type tract (E). Match the drawing to the gas pattern on AXR. [1]
Why does type matter?
- Gas in the stomach on X-ray = a fistula exists between the trachea and the distal oesophageal segment (allowing air to enter the GI tract). This means it is NOT pure OA.
- Gasless abdomen = pure OA (no connection between trachea and distal oesophagus → no air enters the GI tract) [1]
- H-type (Type E): No atresia, so the baby can feed, but has recurrent aspiration pneumonia. Often presents later in infancy, not at birth.
| Group | Birth Weight | CHD | Survival |
|---|---|---|---|
| I | > 1500 g | − | > 95% |
| II | > 1500 g | + | 60% |
| II | < 1500 g | − | 60% |
| III | < 1500 g | + | 20% |
Why these prognostic factors? Low birth weight reflects prematurity (→ immature lungs, higher surgical risk), and congenital heart disease adds haemodynamic instability. Together, they dramatically worsen outcomes.
Polyhydramnios, preterm labour A/N USS (18–20 weeks) — absent stomach bubble Frothy salivation Cyanosis, choking, respiratory distress (aspiration, reflux, gastric distension) [1]
Why polyhydramnios? Normally, the fetus swallows amniotic fluid → absorbed by GI tract. In OA, the fetus cannot swallow effectively → amniotic fluid accumulates → polyhydramnios. (Note: polyhydramnios has many causes, but OA is a classic surgical one.)
Why absent stomach bubble on USS? If there is pure OA, no fluid reaches the stomach. Even in Type C (distal TOF), the amount reaching the stomach may be reduced.
Why frothy salivation? Saliva produced by the baby cannot pass through the atretic oesophagus → it pools in the blind upper pouch and overflows through the mouth and nose → characteristic persistent "frothiness."
Why respiratory distress? Three mechanisms:
- Aspiration of pooled saliva from the blind pouch into the trachea
- Reflux of gastric contents through the distal TOF into the trachea
- Gastric distension from air entering through the fistula → diaphragmatic splinting
Arrest of orogastric tube X-ray — tube in blind pouch — stomach gas (TOF) / gasless (pure OA) Contrast study, CT, bronchoscopy [1]
Clinical test: Pass an orogastric tube — it will arrest at approximately 10–15 cm from the upper gum [2] [3]. It cannot be advanced further because it hits the blind-ending upper oesophageal pouch.
CXR findings (high-yield for exams):
- Coiling of tube in blind pouch [1]
- Presence of bowel gas = presence of tracheo-oesophageal fistula [1]
- Hemivertebra (known association — VACTERL) [1]
CT scan with sagittal reconstruction: Shows the blind-ending oesophageal pouch with the Replogle tube, the TOF connecting trachea to distal oesophagus, and allows measurement of gap length (critical for surgical planning — determines whether primary anastomosis is feasible) [1]
Oropharyngeal suction (Replogle tube) Electrolytes, crossmatch, IV fluid, antibiotics Transfer to specialist centre [1]
The Replogle Tube — Know This
A Replogle tube is a dual-flow gastric aspiration tube. One lumen provides continuous low-pressure suction to aspirate saliva from the upper oesophageal pouch. The other lumen allows air (and saline irrigation) inflow to prevent the suction from damaging the pouch mucosa by adherence. This prevents aspiration of pooled secretions into the lungs. [1]
Division and ligation of TOF (thoracotomy / thoracoscopy) Short gap → primary anastomosis Long gap → delayed primary repair or substitution (stomach, colon) Postoperative ICU [1]
Surgical steps (from slides):
- Step 1: Clip and divide the tracheo-oesophageal fistula [1] — The fistula is the immediate danger (allows gastric acid reflux into the lungs). It is identified, clipped, and transected.
- Step 2: Oesophageal anastomosis [1] — The two oesophageal ends (proximal blind pouch and distal segment) are mobilized and sutured together.
Short gap vs. Long gap:
- Short gap: The two ends are close enough that they can be brought together for primary end-to-end anastomosis. This is the case in most Type C OA/TOF.
- Long gap: The gap is too large for primary repair. Options include:
- Delayed primary: Allow the baby to grow with a gastrostomy for feeding, then attempt repair later when the pouch has elongated
- Oesophageal substitution using stomach (gastric pull-up), colon interposition, or jejunal interposition [1]
Approach: Traditionally via right posterolateral thoracotomy. Increasingly done thoracoscopically — the lecture emphasizes that size is not a contraindication to MIS surgery [1].
Supporting case: A 1.5 kg baby girl born at 35 weeks (antenatal polyhydramnios detected at 27 weeks) underwent successful thoracoscopic repair of OA at Queen Mary Hospital in July 2021, demonstrating feasibility of MIS even in very low-birth-weight neonates [1].
Anastomotic leak, stricture Recurrent TOF Tracheomalacia Gastro-oesophageal reflux Disordered peristalsis Failure to thrive [1]
| Complication | Mechanism | Management |
|---|---|---|
| Anastomotic leak | Tension on suture line, poor blood supply | Conservative (small leak) vs. re-operation |
| Anastomotic stricture | Scarring at anastomosis site | Serial balloon dilatation |
| Recurrent TOF | Incomplete closure or breakdown | Re-operation |
| Tracheomalacia | Intrinsic weakness of tracheal cartilage (associated developmental defect) | Usually self-limiting; aortopexy if severe |
| GOR | Disordered oesophageal motility, shortened oesophagus | Anti-reflux medication; fundoplication if severe |
| Disordered peristalsis | Abnormal intrinsic innervation of oesophagus | Dietary modification, prokinetics |
| Failure to thrive | Feeding difficulties from all of the above | MDT approach, nutritional support |
Long-Term Follow-Up
OA/TOF patients need lifelong surveillance. They are at risk of Barrett's oesophagus due to chronic GOR, and chronic respiratory issues from tracheomalacia and recurrent aspiration. [3]
Part 7: Other Airway and Lung Conditions (Completing the Lecture Scope)
- Hyperinflation of one or more lobes due to air trapping (cartilage deficiency in lobar bronchus)
- Presents with respiratory distress and mediastinal shift
- CXR: hyperlucent lobe with compression of adjacent lung
- Treatment: lobectomy if symptomatic
- A distended abdomen (from any cause — e.g., intestinal obstruction, ascites) pushes the diaphragm up, restricting lung expansion
- This is a secondary cause of respiratory distress — treat the underlying cause
- Aberrant vessels (e.g., double aortic arch, right aortic arch with aberrant left subclavian + ligamentum arteriosum) encircle the trachea and oesophagus
- Presents with biphasic stridor ± feeding difficulties
- Diagnosis: CT angiography, barium swallow (posterior oesophageal indentation)
- Treatment: surgical division of the ring
Exam Intelligence
| Trap | Correct Answer | Why Students Get It Wrong |
|---|---|---|
| Bag-mask ventilation in CDH | NEVER bag-mask → intubate directly | Students default to standard NLS algorithm |
| Gasless abdomen on CXR in OA | This means pure OA (no fistula) | Students forget that bowel gas = TOF present |
| CDH presented as "dextrocardia" | It's apparent dextrocardia (mediastinal shift), not structural | May confuse with congenital dextrocardia |
| Scaphoid abdomen in CDH | Pathognomonic — empty abdomen because viscera are in chest | May be confused with dehydration |
| Polyhydramnios DDx | OA is ONE cause; also duodenal atresia, CNS anomalies, etc. | Students anchor on OA only |
| Type C OA/TOF is most common | ~86% — OA with DISTAL TOF | Students confuse proximal vs distal |
| Replogle tube vs NG tube | Replogle = dual-lumen, continuous suction for OA | Students call it a "NG tube" — loses marks |
| CDH: surgery timing | After stabilization, NOT emergency | Older teaching said emergency surgery |
| CPAM: why operate if asymptomatic? | Risk of recurrent pneumonia + malignancy | Students say "observe" |
| VACTERL: what to screen | Cardiac echo, renal USS, spinal X-ray, limb exam, anorectal exam | Students forget to screen other systems |
Both can present with:
- Mediastinal shift
- Absent breath sounds on one side
- Respiratory distress
| Feature | CDH | Tension Pneumothorax |
|---|---|---|
| Bowel loops in chest | Yes | No |
| Scaphoid abdomen | Yes | No |
| Bowel sounds in chest | Possible | No |
| NG tube in chest | May be seen | No |
| Onset | From birth | Usually sudden deterioration |
- GC 205 (Neonatal Intestinal Obstruction): Lists CDH as a "neonatal emergency" alongside NEC and abdominal wall defects [10]. CDH causes non-rotation of intestines — this is why malrotation is nearly universal in CDH.
- GC 147 (Cyanotic CHD): CDH causes cyanosis that must be differentiated from cyanotic heart disease. Hyperoxia test: PaO₂ > 15 kPa = respiratory cause; remains low = cardiac cause. However, CDH with severe pulmonary hypertension may also have persistent low PaO₂ — echocardio is definitive [2].
- CFB Perinatal Medicine: Antenatal diagnosis of CDH and OA on morphology scan (18–20 weeks). These are indications for delivery at a tertiary centre with neonatal surgery capability.
- GC 220 (Upper Airway Obstruction): Overlaps with the airway disorder section of this lecture — choanal atresia, Pierre-Robin, laryngomalacia, subglottic stenosis.
- Adrian Lui Paediatrics Notes: Provides the OA classification (Types A–E with percentages), Spitz prognostic classification, and CDH management summary [2].
- Maksim Paediatric Notes: Emphasizes CDH CXR findings (absent hemidiaphragm, bowel loops in chest, mediastinal shift, contralateral lung collapse) and the importance of intubation over bag-mask [5].
High Yield Summary
-
CDH
- Left-sided (80-90%), Bochdalek (posterolateral).
- Scaphoid abdomen, apparent dextrocardia, bowel sounds in chest.
- NEVER bag-mask ventilate → intubate directly.
- OG tube to decompress.
- Gentle ventilation (HFO, permissive hypercapnia). iNO for pulmonary hypertension.
- ECMO if refractory.
- Surgery AFTER stabilization (reduce contents, close/patch diaphragm).
- Mortality from pulmonary hypoplasia + pulmonary hypertension.
-
OA/TOF
- 1:4,000. Type C (distal TOF) = 86%. Polyhydramnios, frothy salivation, OG tube arrest at ~10cm. CXR: tube coiled in blind pouch; gas in stomach = TOF present; gasless = pure OA. Replogle tube for continuous pouch suction. Screen for VACTERL. Surgery: divide/ligate fistula → primary oesophageal anastomosis (short gap) or delayed repair/substitution (long gap). Complications: leak, stricture, recurrent TOF, tracheomalacia, GOR, disordered peristalsis, FTT. Prognosis by Spitz classification (BW + CHD).
-
CPAM
- 1:5,000. Risk of recurrent pneumonia and malignancy → lobectomy even if asymptomatic.
-
Airway disorders
- Choanal atresia (bilateral = emergency), Pierre-Robin, laryngomalacia (most common neonatal stridor), subglottic stenosis, tracheomalacia, lymphatic malformation (neck 75%; sclerotherapy/excision), vascular ring.
-
Stridor localization
- Inspiratory = supraglottic/glottic. Biphasic = subglottic/tracheal. Expiratory = bronchial.
Active Recall - Lecture Notes
[1] Lecture slides: GC 204. The newborn baby cannot breathe Oesophageal atresia, diaphragmatic hernia, and other surgery of lung.pdf (all pages) [2] Senior notes: Adrian Lui Pediatrics Notes.pdf (pp. 52, 56–57, 195) [3] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p. 1039) [4] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (pp. 353, 357, 376) [5] Paediatric notes: Maksim Paediatric Notes.pdf (pp. 69–70, 83) [9] AOS material: AOS - Paeds.pdf (Q6) [10] Lecture slides: GC 205. The newborn baby is vomiting repeatedly Neonatal intestinal obstruction and other GI emergencies.pdf (p. 6)
GC203 The Child Needs An Operation Common Emergencies And Surgery In Childhood
An overview of common pediatric surgical emergencies and elective procedures, covering the recognition, initial management, and referral of conditions such as appendicitis, intussusception, pyloric stenosis, hernias, and undescended testes in childhood.
GC205 The Newborn Baby Is Vomiting Repeatedly Neonatal Intestinal Obstruction And Other GI Emergencies
Neonatal intestinal obstruction and other gastrointestinal emergencies are conditions such as atresias, malrotation with volvulus, meconium ileus, and necrotizing enterocolitis that present with repeated vomiting in the newborn and require urgent diagnosis and intervention.