Drowning — Viva

Q1: Definition and terminology (2 min)

Examiner: Define drowning. And tell me — why do we no longer talk about "near-drowning" or "dry drowning"?

Expected answer:

• Drowning is the process of experiencing respiratory impairment from submersion or immersion in liquid — the 2002 World Congress on Drowning definition, published by van Beeck et al. in the Bulletin of the World Health Organization in 2005, now adopted by the WHO, ILCOR, AHA, and ERC.
• The word process is deliberate — drowning is a continuum, not a single event.
• Outcomes are recorded as fatal drowning (death), non-fatal drowning with morbidity, or non-fatal drowning without morbidity (a rescue).
• The old terms are obsolete because they were inconsistently defined, made studies un-comparable, and did not map onto physiology or management. 'Near-drowning' mixed survivors and deaths; 'dry' vs 'wet' drowning suggested management differed when it does not (both are treated by oxygenation); 'secondary drowning' is simply post-immersion ARDS, a well-recognised evolution of the same injury, not a separate entity; 'active drowning' is a lay term. The retained distinction is by clinical severity (the Szpilman grade), not by water volume or type.

Follow-up: What is the Utstein consensus and why does it matter? A standardised dataset for reporting drowning resuscitation (the 2015 Utstein-style ILCOR advisory, Idris et al.) so that studies and registries can be compared — a precondition for evidence-based practice and for the 2024 AHA/AAP update.

Q2: Pathophysiology and the asphyxial arrest (3 min)

Examiner: Walk me through the pathophysiology from submersion to cardiac arrest. Why is the rhythm almost always asystole or PEA — and why does that change what I do?

Expected answer:

• The cascade: submersion -> voluntary breath-hold -> struggle -> irresistible urge to breathe -> either laryngospasm (about 10 to 20 percent) or aspiration of water into the alveoli (about 80 to 90 percent) -> hypoxia -> unconsciousness within 1 to 2 minutes -> hypoxic cardiac arrest.
• Aspirated water damages the lung by: (1) surfactant washout and dysfunction -> alveolar collapse (atelectasis); (2) non-cardiogenic pulmonary oedema from capillary-alveolar injury (in saltwater, hypertonic fluid also osmotically pulls water from the circulation into the alveolus); (3) ventilation-perfusion mismatch and shunt (blood perfusing non-ventilated alveoli — poorly responsive to supplemental oxygen); (4) inflammation evolving into ARDS over hours (the basis of post-immersion respiratory failure).
• Why asystole/PEA, not VF? A primary cardiac arrest (ischaemic, channelopathic) begins as an electrical event in a well-oxygenated myocardium and tends to present as a shockable rhythm. A drowning arrest begins as asphyxia: the myocardium becomes progressively hypoxic and bradycardic before it stops, so the rhythm at arrest is asystole or PEA.
• Management consequence — drowning is an asphyxial arrest, so ventilation comes before circulation: give 5 initial rescue breaths, then 30:2 CPR (rather than starting with compressions). The defibrillator is rarely the first tool; shock only if a shockable rhythm appears. Circulating desaturated blood through the brain and coronaries before oxygenating it does harm.

Follow-up: What is the role of cold water? The mammalian diving reflex (apnoea, bradycardia, peripheral vasoconstriction shunting blood to brain and heart) plus hypothermia reduce cerebral metabolic rate — paradoxically neuroprotective, especially in children. This is the basis of 'not dead until warm and dead'. And autonomic conflict? Cold-water immersion triggers a simultaneous sympathetic cold-shock surge and parasympathetic dive-reflex bradycardia; in a susceptible heart (long-QT, Brugada, CPVT) this triggers fatal arrhythmia — so an unexplained drowning warrants an ECG and family screening.

Q3: Resuscitation — the BLS modification and what NOT to do (3 min)

Examiner: You are first on scene at a pool. A child is pulled out, no breathing, no pulse. What do you do — and what must you NOT do?

Expected answer — the BLS sequence:

1. Safe rescue: reach/throw before go; remove from water onto a hard surface. Do not do chest compressions in the water (ineffective).
2. Open airway; check for breathing for up to 10 seconds. Agonal gasps are NOT breathing.
3. Give 5 initial rescue breaths (each about 1 second, enough to make the chest rise) — oxygenate the flooded, hypoxic lungs FIRST.
4. Check for a pulse; if no pulse, start chest compressions at 30:2.
5. Continue CPR; attach an AED as soon as the chest is dry; defibrillate only if a shockable rhythm (VF/pVT).
6. Use bag-valve-mask + oxygen as soon as available; prepare for early intubation if arrest continues.

What you must NOT do:

• No Heimlich manoeuvre / abdominal thrusts — useless (water is in the alveoli, not the upper airway) and harmful (delays CPR, causes regurgitation/aspiration/injury).
• No routine cervical spine immobilisation — hampers CPR and rescue breathing; immobilise ONLY if the mechanism suggests trauma (diving, water-slide, fall, seizure with head strike, alcohol, unexplained adult submersion). Most pool submersions in swimmers are non-traumatic.
• Do not attempt to drain water from the lungs — a small volume is in the alveoli; it will absorb; do not delay CPR.
• Do not terminate resuscitation prematurely, especially if hypothermic.

Follow-up: Why 5 breaths specifically? The first few breaths recruit and oxygenate the collapsed, flooded alveoli before there is any point in circulating blood through them; the AHA/AAP and ERC both specify 5 initial rescue breaths before compressions in drowning.

Q4: Definitive management, ventilation, and the post-ROSC patient (2 min)

Examiner: The child has ROSC but is comatose and hypoxaemic with pulmonary oedema. Walk me through definitive management.

Expected answer — stepwise:

1. Oxygenation and lung-protective ventilation — intubate; tidal volume 6 mL/kg ideal body weight; plateau pressure under 30 cmH2O; titrate PEEP (high PEEP often needed to recruit collapsed alveoli); permissive hypercapnia (allow PaCO2 to rise provided pH acceptable); SpO2 94 to 98 percent. Consider prone positioning and inhaled nitric oxide for refractory hypoxaemia.
2. Haemodynamic support — balanced crystalloid (Hartmann's / Plasma-Lyte) 10 to 20 mL/kg boluses titrated to perfusion (lactate, capillary refill, urine output over 0.5 mL/kg/h, MAP over 65 mmHg); noradrenaline first-line vasopressor; adrenaline if myocardial stunning dominates.
3. Targeted temperature management (TTM) — comatose post-arrest: target 32 to 36 degrees C for 24 hours, then controlled normothermia (avoid fever). Reduces hypoxic-ischaemic brain injury.
4. Neuroprotection — maintain cerebral perfusion (avoid hypotension), normoglycaemia, normocapnia (both hypo- and hypercapnia raise intracranial pressure), treat seizures. Do not prognosticate before 72 hours of normothermia; use a multimodal assessment (clinical, SSEP, EEG, imaging, biomarkers).
5. Antibiotics — selective, never routine. Most aspiration is sterile chemical pneumonitis. Give antibiotics only for clinical infection, gross aspiration of contaminated water (sewage, hot-tub), or positive culture; cover oral flora plus Gram-negatives; add Aeromonas/Vibrio/Pseudomonas cover for brackish/sea water.
6. Not recommended routinely: corticosteroids (no benefit), exogenous surfactant (inconclusive), barbiturate coma, aggressive hyperventilation.
7. ECMO/ECPR for refractory arrest, refractory hypoxaemia, or hypothermic arrest under 28 degrees C — extracorporeal rewarming is the method of choice for hypothermic circulatory arrest.

Q5: Observation, prognosis, and prevention (2 min)

Examiner: A 6-year-old is brought in well-looking after a brief submersion. Can you send her home? And how do you prognosticate the one who arrested?

Expected answer:

• Observation period. Every rescued victim needs observation because post-immersion ARDS can develop over minutes to 24 hours. An asymptomatic victim with normal observations and normal exam can be observed for 6 hours (some guidelines 4 to 6 hours) and discharged if well, with a safety-net to return immediately if cough, breathlessness, chest pain, or drowsiness develops. Any symptom (cough, dyspnoea, vomiting) or any abnormal observation (SpO2 under 95 percent, tachypnoea) means admission and observation for up to 24 hours. A normal initial chest X-ray does NOT exclude later deterioration.

• Prognosis. Outcome is driven by the severity and duration of hypoxia. Favourable: submersion under 5 to 10 minutes, prompt bystander CPR (especially rescue breaths), good neurological status at scene, cold water (neuroprotective), sinus or shockable rhythm, young age. Poor: submersion over 10 to 25 minutes, no bystander CPR, asystole at scene, warm water, high lactate, persistent coma, GCS under 5. No single factor is reliable — survival with good neurological outcome after prolonged cold-water submersion (especially in children) means early prognostication is unreliable and dangerous.

• When to stop. In a normothermic victim, no ROSC after 20 to 30 minutes of good-quality ALS with reversible causes addressed. In hypothermia, the rule does not apply — continue until core temperature at least 32 degrees C.

• Prevention (the public-health message): four-sided isolation pool fencing (the most evidence-based single intervention), constant adult supervision within arm's reach, lifejackets, alcohol avoidance in and around water, swimming and water-safety instruction, trained lifeguard presence. The WHO Global Report frames drowning as a neglected public-health problem, with over 90 percent of deaths in low- and middle-income countries.