ICU · Resuscitation
Near-drowning and drowning in the ICU
Also known as Drowning · Near-drowning · Submersion injury · Secondary drowning · Non-fatal drowning · Surfactant dysfunction drowning
Drowning is defined as 'the process of experiencing respiratory impairment from submersion/immersion in liquid.' 'Near-drowning' (old term) — now ALL submersion injuries are 'drowning' (fatal or non-fatal). Primary injury: HYPOXIA (from aspiration/laryngospasm causing hypoxaemia → brain injury + multi-organ failure). NOT salt-water vs fresh-water distinction (clinically irrelevant — both cause hypoxia). Management: ABCDE + HIGH-FLOW OXYGEN + early intubation if respiratory distress or decreased GCS. LUNG INJURY: non-cardiogenic pulmonary oedema (ARDS-like) from aspiration + surfactant washout. BRAIN INJURY: hypoxic ischaemic encephalopathy — PRIMARY cause of death and disability. Management: neuroprotection (avoid hypoxia, hyperoxia, hypotension, hyperthermia). Rescue breaths FIRST (5 breaths) — drowning is an asphyxial arrest. Lung-protective ventilation + PEEP for ARDS-pattern lung. TTM 32–36°C for comatose post-arrest patients. Surfactant may be considered for severe refractory ARDS.
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Target exams
Red flags
Drowning definitions — the WHO 2005 consensus
The single highest-yield conceptual point is the uniform World Health Organization definition. The 2003 Utstein-style consensus (Idris and colleagues) standardised data reporting, and van Beeck and colleagues consolidated the definition in the 2005 WHO Bulletin. The committee deliberately abolished a list of imprecise modifiers because they implied distinct pathophysiology that does not exist and because they fragmented surveillance data.[3]
Drowning is the process of experiencing respiratory impairment from submersion or immersion in liquid. Every submersion or immersion event is a DROWNING, classified only by outcome as fatal drowning (death) or non-fatal drowning (with morbidity, or without morbidity).[3]
Obsolete drowning terminology — what to say instead
| Obsolete term | What it used to mean | Why it is abolished | Correct modern term |
|---|---|---|---|
| Near-drowning | Survival for at least 24 h after submersion | The 24-hour outcome cut-off is arbitrary and implies a separate disease | Non-fatal drowning (with or without morbidity) |
| Dry drowning | No water aspirated (laryngospasm only) | Autopsy and animal data show most victims aspirate fluid; distinction is not actionable | Drowning |
| Wet drowning | Water aspirated into the lungs | Aspiration is the norm, not a subtype; aspirated volume is small | Drowning |
| Salt-water / fresh-water drowning | Different osmotic effects on blood | Real aspirated volume is too small to change serum electrolytes or haematocrit | Drowning |
| Secondary drowning | Delayed pulmonary oedema hours later | Delayed oedema is part of the same surfactant or inflammatory injury, not a new event | Drowning (observe all symptomatic patients) |
| Active / passive / silent drowning | Distinction by observed behaviour | No pathophysiological or management implication | Drowning |
Pathophysiology — the six-stage cascade
Drowning is fundamentally a hypoxic event driven by respiratory failure. Every downstream consequence — cardiac arrest, brain injury, multi-organ failure — is secondary to hypoxia and ischaemia. Understanding the cascade explains why ventilation is the first intervention and why fluid or electrolyte manipulation is irrelevant.[4]
The drowning pathophysiological cascade — six stages from breath-holding to brain injury
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BREATH-HOLDING AND PANIC — the conscious victim holds their breath, often with panic and an instinctive struggle. Voluntary apnoea and small aspiration events raise PaCO₂ and lower PaO₂. The urge to breathe eventually overcomes breath-holding. (Treatment implication: remove from water, give oxygen.)[4]
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LARYNGOSPASM — reflex vocal-cord closure triggered by water contacting the larynx and hypopharynx. This is the obsolete basis of 'dry drowning.' Laryngospasm provides transient protection (no aspiration into alveoli) but itself causes hypoxia because gas exchange ceases. Breakthrough aspiration follows as the larynx fatigues or the victim gasps. (Treatment implication: restore ventilation urgently.)[4]
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ASPIRATION OF SMALL VOLUME OF WATER — only 1–4 mL/kg of water is typically aspirated. This is far too small to cause clinically important haemodilution (fresh water), hypernatraemia (salt water), haemolysis or electrolyte shifts. The old teaching about osmotic differences between fresh and salt water was based on massive-volume animal experiments that do not reflect real drowning. However, even this small volume is sufficient to wash out and dysfunction pulmonary surfactant and to trigger inflammatory injury. (Treatment implication: PEEP and lung-protective ventilation; NOT fluid restriction or diuresis.)[4]
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SURFACTANT DYSFUNCTION, ATELECTASIS, V/Q MISMATCH, OEDEMA — aspirated water disrupts the surfactant monolayer, producing alveolar collapse (atelectasis), massive ventilation-perfusion mismatch and intrapulmonary shunt. The resulting non-cardiogenic pulmonary oedema is clinically and radiologically indistinguishable from ARDS. Copious pink or white froth fills the airways. Refractory hypoxaemia follows. (Treatment implication: PEEP to recruit alveoli; high FiO₂; consider prone ventilation.)[4][6]
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HYPOXIA → BRADYCARDIA → ASYSTOLIC ARREST — progressive hypoxaemia and hypercapnia produce initial tachycardia then reflex bradycardia (diving reflex) progressing to pulseless electrical activity (PEA) or asystole. Ventricular fibrillation is uncommon because the arrest is asphyxial, not primary cardiac. This is the critical difference from a witnessed primary cardiac arrest. (Treatment implication: rescue breaths FIRST, then compressions; prolonged CPR if hypothermic.)[2][4]
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HYPOXIC-ISCHAEMIC BRAIN INJURY — the organ that determines outcome. Cerebral hypoxia produces neuronal injury through excitotoxicity (glutamate release), calcium influx, mitochondrial dysfunction, reactive oxygen species, and delayed apoptotic and necrotic cell death. The pattern is identical to post-cardiac-arrest brain injury from any cause. (Treatment implication: TTM 32–36°C for comatose post-arrest patients; normoglycaemia, normocapnia, seizure control; avoid hypoxia, hyperoxia, hypotension, hyperthermia.)[2][6]
Pathophysiological cascade and its treatment implication — stage-by-stage
| Stage | Event | Consequence | First-line treatment implication |
|---|---|---|---|
| 1 | Breath-holding, panic | Rising CO₂, falling O₂ | Remove from water, give oxygen |
| 2 | Laryngospasm | Transient protection, then breakthrough aspiration | Restore ventilation urgently |
| 3 | Aspiration of small volume of water | Surfactant washout, contamination | PEEP, lung-protective ventilation; NOT fluid restriction or diuresis |
| 4 | Surfactant dysfunction, atelectasis, V/Q mismatch, oedema | Severe shunt, hypoxaemia | PEEP to recruit alveoli; high FiO₂; consider prone ventilation |
| 5 | Hypoxia, bradycardia, asystolic/PEA arrest | Cardiac arrest (asphyxial) | Rescue breaths FIRST, then compressions; prolonged CPR in cold water |
| 6 | Hypoxic-ischaemic brain injury | Determines neurological outcome | TTM 32–36°C for 24 h; normoglycaemia, normocapnia, seizure control |
Ventilation comes FIRST — the asphyxial arrest principle
Because drowning produces a respiratory arrest that progresses to cardiac arrest, the primary defect is failure of oxygen delivery to the blood. Chest compressions without oxygenation merely circulate deoxygenated blood and cannot reverse the process. This is the central reason that resuscitation of drowning differs from a primary witnessed cardiac arrest, in which compression-only CPR may be acceptable.[2]
Primary cardiac arrest versus drowning (asphyxial) arrest
| Feature | Primary cardiac arrest (e.g. VF) | Drowning (asphyxial) arrest |
|---|---|---|
| Initial problem | Electrical or pump failure | Respiratory failure, hypoxia |
| Initial rhythm | VF or VT common | Asystole or PEA (bradycardic) |
| Blood oxygen at arrest | Often still adequate initially | Already severely depleted |
| Compression-only CPR | Acceptable for witnessed adult arrest | NOT acceptable — rescue breaths essential |
| Sequence | Compressions first (C-A-B) | Ventilation prioritised — give 5 rescue breaths, then 30:2 |
| Defibrillation | Early, central to survival | Only if shockable rhythm; secondary to oxygenation |
| Prognostic modifier | Bystander CPR, time to defibrillation | Submersion time, water temperature, bystander CPR |
The practical rule for the drowning arrest: as soon as the victim is on a firm surface give 5 initial rescue breaths, then continue cardiopulmonary resuscitation at a 30:2 ratio of compressions to ventilations. If an automated external defibrillator is available, attach it, but do not interrupt ventilation — the rhythm is usually non-shockable until oxygenation improves. In-water rescue breathing by trained lifeguards may be initiated before reaching shore if feasible.[2][13]
SAQ — Drowning: prehospital and ED resuscitation
10 minutes · 10 marks
A previously well 18-year-old man is pulled from a cold lake after a witnessed submersion of approximately 8 minutes. He is unconscious, apnoeic, with a carotid pulse. Bystanders have started chest compressions. On paramedic arrival his SpO2 is 60% on high-flow oxygen.
SAQ — Post-ROSC care in the drowned patient
10 minutes · 10 marks
A 30-year-old man who drowned in a swimming pool has achieved ROSC after 25 minutes of CPR. He is intubated, GCS 4 (post-intubation), with pulmonary oedema and a PaO2/FiO2 of 180. Outline your ICU management.
Clinical pearls
Management — prehospital and ICU
Rescue and the first minutes
Acute drowning — rescue and the first minutes in the emergency department or ICU
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RECOGNISE THE DROWNING and ensure rescuer safety — the rescuer must not become a second victim. Note the mechanism (diving, surf, boating, seizure, immersion hypothermia), the estimated submersion time and the water temperature. Cold-water submersion is a strong reason to prolong resuscitation.[1][13]
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REMOVE FROM WATER WITH CERVICAL SPINE PRECAUTIONS IF INDICATED — immobilise the cervical spine for diving accidents, boating trauma, surf injuries, water-slide accidents or unwitnessed trauma. Routine spinal immobilisation is NOT required for simple unwitnessed shallow-water immersion.[1]
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ASSESS RESPONSIVENESS AND BREATHING — if not breathing normally, begin resuscitation. If breathing normally, place in recovery position, give oxygen, monitor, transport to hospital for observation.[2]
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GIVE 5 INITIAL RESCUE BREATHS — in-water or onshore, trained rescuers should give 5 rescue breaths first (mouth-to-mouth or bag-mask). Drowning is an asphyxial arrest — ventilation must precede compressions. Each breath: 1 second, visible chest rise.[2]
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START CHEST COMPRESSIONS IF NO PULSE — after 5 rescue breaths, check for pulse (max 10 seconds). If no pulse, begin chest compressions at 30:2 ratio (compressions:ventilations). Compression depth 5–6 cm, rate 100–120/min. Minimise interruptions.[2]
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ATTACH AED WHEN AVAILABLE — analyse rhythm. Defibrillate if shockable (VF/VT). Continue CPR. Do NOT interrupt ventilation for defibrillation preparation.[2]
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DO NOT PERFORM HEIMLICH OR ABDOMINAL THRUSTS — contraindicated. Delays CPR, risks aspiration of gastric contents, may cause visceral injury. Suction only visible solid airway obstruction.[1]
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TRANSPORT ALL DROWNING PATIENTS TO HOSPITAL — even asymptomatic patients require observation for delayed pulmonary oedema (minimum 6–8h). Monitor SpO₂, ECG, and mental status. Notify receiving hospital.[1][6]
ICU respiratory management — oxygenation, PEEP, and lung-protective ventilation
The post-arrest or symptomatic drowning patient typically has a stiff, oedematous, poorly compliant lung from surfactant dysfunction, aspiration and inflammation — functionally an ARDS-pattern injury. The respiratory strategy mirrors ARDS: recruit collapsed alveoli with positive end-expiratory pressure, oxygenate, and ventilate protectively to avoid further volutrauma and barotrauma.[4][6]
ICU respiratory management of the drowning patient — stepwise escalation
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INITIAL OXYGENATION — high-flow oxygen 100% via non-rebreather mask or nasal high-flow. Titrate FiO₂ to lowest value maintaining SpO₂ 92–96%. Avoid hypoxia (SpO₂ <90%) and unnecessary hyperoxia (FiO₂ >0.6 if avoidable — oxidative stress).[6]
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NON-INVASIVE VENTILATION (CONSCIOUS PATIENT) — CPAP or BiPAP for Szpilman Grade 3 patients with pulmonary oedema who are alert and cooperative. CPAP 5–10 cmH₂O recruits alveoli and counters pulmonary oedema. Close monitoring — be ready to intubate if worsening.[6]
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INTUBATION AND MECHANICAL VENTILATION — for Szpilman Grade 4–6, decreased GCS (<8), severe respiratory distress, refractory hypoxaemia, or cardiac arrest. RSI with maximal pre-oxygenation (expect rapid desaturation). Use cuffed ETT (large-bore suction catheter for froth).[6]
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LUNG-PROTECTIVE VENTILATION — tidal volume 6 mL/kg predicted body weight. Plateau pressure <30 cmH₂O. Driving pressure <15 cmH₂O. Permissive hypercapnia (pH ≥7.20) if necessary. This is the same strategy as ARDS.[4][6]
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PEEP OPTIMISATION — start at 5 cmH₂O, titrate upward (10–15 cmH₂O typical; may need 15–20 cmH₂O for severe oedema). PEEP is the KEY intervention — it recruits collapsed alveoli and counters surfactant dysfunction. Titrate to best oxygenation without compromising haemodynamics.[4][6]
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PRONE POSITIONING — for severe ARDS (PaO₂/FiO₂ <150 despite FiO₂ ≥0.6 and PEEP ≥5). Proning improves V/Q matching and oxygenation. 16+ hours per day. May be life-saving in refractory hypoxaemia after drowning.[4]
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RESCUE THERAPIES FOR REFRACTORY HYPOXAEMIA — if PaO₂/FiO₂ <80 despite optimised ventilation and proning: (a) consider exogenous surfactant (calfactant/poractant) — case-report evidence of dramatic improvement. (b) Consider veno-venous ECMO. (c) Inhaled pulmonary vasodilators (nitric oxide, epoprostenol) — may improve oxygenation as temporising measure.[7][9]
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SUCTION AIRWAY FROTH AS NEEDED — copious pink/white froth is pulmonary oedema fluid. Suction only enough to maintain ETT patency — do not suction to dryness (damages airway, interrupts ventilation). Let PEEP resolve the oedema.[1][4]
Respiratory support in drowning — escalating by Szpilman severity grade
| Szpilman grade | Clinical features | Respiratory support |
|---|---|---|
| Grade 1 — asymptomatic | Normal examination, normal SpO₂ | Observe 6–8h; oxygen only if SpO₂ falls |
| Grade 2 — mild | Cough, basal crackles, SpO₂ normal on room air | Supplemental oxygen, observe |
| Grade 3 — moderate | Pulmonary oedema on auscultation, SpO₂ low on room air | High-flow oxygen; consider NIV (CPAP/BiPAP) or intubation |
| Grade 4 — severe | Acute pulmonary oedema, hypoxaemia, may be conscious | Intubate; mechanical ventilation with PEEP and lung-protective ventilation |
| Grade 5 — respiratory arrest, pulse present | Apnoeic, pulse present | Immediate bag-mask then intubation; mechanical ventilation |
| Grade 6 — cardiopulmonary arrest | No pulse, no breathing | Full CPR; 5 rescue breaths first then compressions; prolonged CPR if cold |
Neuroprotection — targeted temperature management and post-arrest care
Because the mechanism of death in drowning is hypoxic cardiac arrest, the comatose post-arrest drowning patient should receive exactly the same post-resuscitation neuroprotective care as any other cardiac-arrest survivor.[2]
Post-arrest neuroprotective bundle for the comatose drowning patient
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TTM 32–36°C for at least 24 hours — choose a single target within range and maintain tightly. The TTM trial (Nielsen et al 2013) showed 33°C and 36°C are equivalent. If patient is already hypothermic from water exposure, do NOT actively rewarm above target. Use surface or endovascular cooling. Avoid shivering (sedation, analgesia, counter-warming).[14][2]
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MAINTAIN NORMOGLYCAEMIA — target blood glucose 6–10 mmol/L. Avoid hypoglycaemia (<4 mmol/L — worsens brain injury) and hyperglycaemia (>10 mmol/L — associated with worse outcome). Insulin infusion if needed.[2]
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MAINTAIN NORMOCAPNIA — PaCO₂ 35–45 mmHg (4.7–6.0 kPa). Avoid hypocapnia (cerebral vasoconstriction → ischaemia) and hypercapnia (cerebral vasodilation → raised ICP). Monitor with arterial blood gas.[2]
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AVOID HYPOTENSION — target MAP ≥65 mmHg (≥70 if hypertensive baseline). Use noradrenaline if needed. Hypotension after ROSC is strongly associated with worse neurological outcome. Avoid fluid overload (may worsen pulmonary oedema).[2]
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SEIZURE SURVEILLANCE AND TREATMENT — post-hypoxic seizures are common (20–30%). Continuous EEG monitoring if available. Treat clinical and electrographic seizures with levetiracetam or valproate. Avoid phenytoin (worse outcomes in post-arrest).[2]
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DEFER PROGNOSTICATION — wait ≥72h after return to normothermia AND off sedation/paralysis. Use multimodal: clinical examination (brainstem reflexes, motor response), EEG, somatosensory evoked potentials, neuroimaging, biomarkers (NSE). Premature prognostication is a well-described cause of inappropriately withdrawn care.[2][10]
Accidental hypothermia versus therapeutic hypothermia in drowning
| Feature | Accidental hypothermia (the immersion) | Therapeutic hypothermia (TTM) |
|---|---|---|
| Cause | Cold-water exposure lowering core temperature | Intentional cooling after arrest |
| Direction | Rewarm toward 32–34°C, then decide | Hold at chosen target (32–36°C) for 24h |
| Prognostic role | PROTECTIVE — lower cerebral metabolic rate; reason to prolong CPR | Neuroprotective — part of the post-arrest bundle |
| Risk | Arrhythmia below 30°C (ventricular fibrillation) | Shivering, infection, electrolyte shift, bradycardia |
| Key principle | 'Not dead until warm and dead' | Standard post-cardiac-arrest TTM applies |
| Rewarming rate | 0.25–0.5°C/hour (avoid rapid rewarming → arrhythmia, vasodilation) | Controlled rewarm 0.25–0.5°C/hour after 24h |
ECMO and extracorporeal life support
Extracorporeal membrane oxygenation has an emerging role in two scenarios after drowning: (1) refractory hypothermic cardiac arrest requiring ECPR (veno-arterial ECMO) and (2) severe ARDS with refractory hypoxaemia (veno-venous ECMO).[8][9]
Indications and evidence for ECMO in drowning
| Scenario | ECMO type | Indication | Evidence |
|---|---|---|---|
| Hypothermic cardiac arrest (core temp <30°C) | Veno-arterial (VA-ECMO) | Cardiac arrest unresponsive to conventional CPR; core temp <30°C | Bjertnæs et al 2021 systematic review: ECLS rewarming achieves best survival in hypothermic cardiac arrest (PMID 34055829) |
| Refractory hypoxaemia (severe ARDS) | Veno-venous (VV-ECMO) | PaO₂/FiO₂ <80 despite optimised ventilation and proning | Case reports of successful use after drowning; consistent with EOLIA trial criteria for ARDS |
| Prolonged submersion in cold water | VA-ECMO (ECPR) | Remarkable case: 14-year-old resuscitated with VA-ECMO after 43 min submersion | Scandroglio et al 2018: full neurological recovery (PMID 28882324) |
| Children with drowning-associated hypothermia | VA-ECMO preferred | Systematic review: ECMO rewarming has best survival in paediatric drowning-associated OOHCA | Andre et al 2023: PCCM systematic review (PMID 37133324) |
What NOT to do — the obsolete and harmful interventions
Several traditional interventions are now known to be useless or actively harmful and should be explicitly avoided. Examiners test these repeatedly.[2][4][3]
Interventions to AVOID in drowning
| Intervention | Why it is wrong | What to do instead |
|---|---|---|
| Heimlich manoeuvre / abdominal thrusts | Water is in the lungs, not the stomach; delays CPR, risks aspiration of gastric contents, may cause visceral injury | Suction only solid upper-airway obstruction; start rescue breaths |
| Compression-only CPR | Drowning is asphyxial — blood is already desaturated | Give 5 rescue breaths then 30:2 CPR |
| Prophylactic antibiotics | Initial lung injury is a chemical pneumonitis, not infection; cultures guide therapy | Send cultures; treat only if infection develops after 24h |
| Prophylactic corticosteroids | No benefit for the pulmonary or the neurological injury | Standard supportive care; no steroids |
| Fluid restriction or aggressive diuresis | Aspirated volume is small; oedema is hydrostatic or inflammatory | Treat hypoxia with PEEP; match fluid balance to perfusion |
| Salt-water versus fresh-water fluid logic | Electrolyte shifts are negligible at real aspirated volumes | Treat the patient, not the water type |
| Early termination of CPR in cold-water drowning | Hypothermia protects the brain; prolonged CPR can succeed | Continue until warm and dead, or validated futility criteria met |
| Suctioning froth to dryness | Damages the airway, interrupts ventilation | Suction to keep the tube patent; let PEEP resolve the oedema |
| Routine bronchoscopy/lavage | Water is rapidly absorbed; injury is inflammatory, not retained water | Only for suspected foreign body (seaweed, sand, debris) |
| Using the term 'near-drowning' | Abolished by WHO 2005; implies separate disease | Say 'non-fatal drowning' |
Prognostication — good and poor predictors
Prognostication in drowning rests on a small number of robust clinical variables available at or soon after presentation. The Szpilman stratification and the Utstein-style drowning dataset codify these. Two aphorisms dominate: 'not dead until warm and dead' (cold-water hypothermia is protective) and 'time submerged is the single most important predictor.'[1][11]
Prognostic factors in drowning — good versus poor indicators
| Predictor | Favourable direction | Poor direction | Detail |
|---|---|---|---|
| Submersion time | <5 min | >25 min | The single most powerful predictor. Submersion >25 min is associated with very poor outcome; <5 min is favourable |
| ROSC at scene | ROSC before hospital | No ROSC at scene | Sustained ROSC before hospital arrival is strongly favourable; asystole unresponsive to prolonged CPR is poor (unless hypothermic) |
| Initial rhythm | Sinus rhythm, VF/VT | Asystole, PEA | VF/VT implies shorter downtime; asystole/PEA (asphyxial pattern) is poor — but VF can occur if arrest was primary cardiac (e.g., MI while swimming) |
| GCS at presentation | >5 | 3 (persistently) | GCS <6 or absent motor response at 24h (off sedation) is poor; purposeful response is favourable |
| Serum potassium | <8 mmol/L | >8 mmol/L | K⁺ >8 in arrested drowning is strongly associated with death — UNLESS hypothermic, in whom the threshold does not apply |
| Water temperature | Cold (<10°C) — paradoxically protective | Warm (>20°C) | Cold water lowers cerebral metabolic rate; remarkable recoveries after prolonged cold submersion, especially in children |
| Age | Young children (diving reflex) | Adults with comorbidity | Paradoxical good outcomes in young children after cold submersion |
| Bystander CPR | Present | Absent | Early bystander ventilation and CPR improve survival and neurological outcome |
| Szpilman grade | Grade 1–3 | Grade 5–6 | Higher grade at presentation = worse outcome; Grade 6 mortality exceeds 90% |
Favourable versus unfavourable presentation profile — quick reference
| Favourable profile (expect good outcome) | Unfavourable profile (poor prognosis, but do NOT withdraw prematurely) |
|---|---|
| Submersion <5 min | Submersion >25 min |
| Cold water (<10°C) | Warm water (>20°C) |
| ROSC at scene | No ROSC at scene |
| GCS >5 on arrival | GCS 3 (persistently, off sedation at ≥72h) |
| Initial rhythm: VF/VT or sinus | Initial rhythm: asystole or PEA |
| K⁺ <8 mmol/L | K⁺ >8 mmol/L (unless hypothermic) |
| Szpilman Grade 1–3 | Szpilman Grade 5–6 |
| Bystander CPR with rescue breaths | No bystander CPR |
| Child with diving reflex | Adult with comorbidity or co-ingestant |
| No aspiration of contaminated water | Aspiration of sewage/contaminated water |
Co-existing injuries and conditions
The intensivist must not be so focused on the lung and the brain that the co-existing injuries of drowning are missed.[1][4]
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Cervical spine injury — a dive into shallow water, surf-board and watercraft impact, and boating trauma can produce cervical fracture and dislocation. Immobilise the cervical spine during rescue, extraction and intubation in any diving, boating or unwitnessed-trauma mechanism. Routine immobilisation is NOT needed for simple shallow-water immersion without a diving or trauma history. The proportion of drowning victims with spinal injury is low overall (under 0.5%) but much higher in diving accidents.[1]
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Accidental hypothermia — cold-water immersion rapidly lowers core temperature. Severe hypothermia (<28°C) causes arrhythmia (VF below 28–30°C) and cardiac arrest. Rewarm at 0.25–0.5°C/hour. Consider ECMO for hypothermic cardiac arrest. The hypothermia is simultaneously protective (lowering cerebral metabolic rate) and dangerous (arrhythmia).[8][12]
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Rhabdomyolysis — vigorous struggling against water, prolonged immobilisation, or crush injury can produce rhabdomyolysis. Check creatine kinase on admission and monitor. Treat with IV fluids to maintain urine output 1–2 mL/kg/h. May require renal replacement therapy if severe AKI develops.[1]
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Co-ingestants — alcohol is detected in 30–50% of adult drowning victims. Other drugs (opioids, benzodiazepines) may coexist. Check glucose, paracetamol and salicylate levels, consider naloxone if opioid suspected. Co-ingestants complicate prognosis and may mask neurological signs.[1][5]
Red flags
Landmark trials and guidelines
van Beeck, Branche, Szpilman, Modell, Bierens 2005 — A new definition of drowning (WHO Bulletin) (PMID 16302042)
Source
Bulletin of the World Health Organization — international consensus statement
Purpose
To establish a uniform, internationally accepted definition and outcome taxonomy for drowning to enable surveillance, research and prevention
Definition
Drowning is the process of experiencing respiratory impairment from submersion or immersion in liquid
Outcome taxonomy
Fatal drowning, or non-fatal drowning subdivided into morbidity or no morbidity
Terminology abolished
Near-drowning, dry and wet drowning, salt-water and fresh-water drowning, secondary drowning, active, passive and silent drowning
Key finding
A single definition and outcome taxonomy adopted by WHO, ILCOR and the International Life Saving Federation, transforming surveillance and reporting
Clinical bottom line
Every submersion or immersion event is DROWNING; classify by outcome only. The bedrock of modern exam answers on this topic.
Szpilman, Bierens, Handley, Orlowski 2012 — Drowning (NEJM Current Concepts) (PMID 22646632)
Source
New England Journal of Medicine — Current Concepts review
Authors
Szpilman D, Bierens JJLM, Handley AJ, Orlowski JP
Scope
Comprehensive review of epidemiology, pathophysiology, rescue, resuscitation and in-hospital management of drowning
Key concepts
Unified WHO definition; asphyxial arrest with ventilation-first CPR; small aspirated volumes render salt/fresh and dry/wet distinctions obsolete; ARDS-pattern lung injury managed with PEEP and lung-protective ventilation; TTM for comatose post-arrest patients
Clinical tool
Szpilman 6-grade drowning severity classification (1 asymptomatic to 6 cardiopulmonary arrest) guiding the level of respiratory support
Key finding
Submersion time, age and water temperature are the dominant determinants of outcome; cold water is protective
Clinical bottom line
The definitive modern reference — treat the hypoxia with PEEP and protective ventilation, not the water type or the theoretical electrolyte problem.
Dezfulian, McCallin, Bierens, Idris, Topjian et al 2024 — AHA/AAP Focused Update on Resuscitation Following Drowning (PMID 39530204)
Source
Circulation — 2024 American Heart Association and American Academy of Pediatrics Focused Update
Scope
Updated evidence-based recommendations for drowning resuscitation, replacing earlier AHA special-circumstances guidance
Key recommendations
Begin ventilation first (5 rescue breaths then 30:2); do NOT use compression-only CPR; do NOT perform Heimlich; continue prolonged CPR in cold-water drowning ('not dead until warm and dead'); apply standard post-cardiac-arrest care including TTM 32–36°C; consider ECMO/ECPR for refractory hypothermic arrest
Key finding
Drowning resuscitation differs from primary cardiac arrest because the arrest is asphyxial — oxygenation must come first. Bystander CPR quality and time to ROSC are the strongest modifiable predictors.
Clinical bottom line
The current guideline of record for drowning resuscitation — ventilation-first CPR, prolonged resuscitation in hypothermia, and standard post-arrest TTM.
Nielsen, Wetterslev, Cronberg et al 2013 — TTM trial (PMID 24237006)
Source
New England Journal of Medicine — multicentre randomised controlled trial
Population
Comatose adult survivors of out-of-hospital cardiac arrest of presumed cardiac cause
Intervention
Targeted temperature management at 33°C versus 36°C for 36 hours
Primary outcome
All-cause mortality through end of trial; composite of death or poor neurological outcome at 180 days
Key finding
No difference in mortality or neurological outcome between 33°C and 36°C — both targets are acceptable
Clinical bottom line
For the comatose post-arrest drowning patient, choose any single target between 32 and 36°C and maintain it tightly; 33 and 36 are equivalent.
Szpilman, Webber, Quan, Bierens et al 2014 — Creating a drowning chain of survival (PMID 24911403)
Source
Resuscitation — consensus advisory statement (International Life Saving Federation and ILCOR-aligned)
Purpose
To define a simple, universal chain of survival for drowning spanning prevention through post-resuscitation care
Chain links
(1) Prevent drowning, (2) Recognise distress, (3) Provide flotation, (4) Remove from water, (5) Provide care as needed — culminating in on-scene resuscitation and definitive hospital care
Key emphasis
Rescue and rescue-breath-first CPR must start at the scene; earlier links (prevention, supervision, barriers) determine how much hypoxic injury reaches hospital
Key finding
A standardised chain that integrates public-health prevention with pre-hospital and in-hospital resuscitation, applicable in high- and low-to-middle-income settings
Clinical bottom line
The intensivist is the final link; outcomes depend on the strength of the whole chain, especially early bystander ventilation and CPR.
Varisco, Palmatier, Alten 2010 — Exogenous surfactant for refractory hypoxaemia in paediatric drowning (PMID 20693854)
Source
Pediatric Emergency Care — case report
Clinical scenario
A paediatric drowning victim with intractable hypoxaemia despite conventional mechanical ventilation and PEEP
Intervention
Exogenous surfactant (calfactant) administered via endotracheal tube
Outcome
Rapid reversal of hypoxaemia; complete neurological recovery
Key finding
Surfactant replacement can reverse refractory hypoxaemia by restoring surfactant function and reopening collapsed alveoli in drowning-induced ARDS
Clinical bottom line
Consider exogenous surfactant as rescue therapy when conventional ventilation and PEEP fail to oxygenate the drowning patient with severe ARDS.
Bjertnæs, Hindberg, Næsheim, Suborov 2021 — Rewarming from hypothermic cardiac arrest with ECLS: systematic review (PMID 34055829)
Source
Frontiers in Medicine — systematic review
Scope
Extracorporeal life support (ECLS/ECMO) for rewarming patients in hypothermic cardiac arrest
Key finding
ECLS rewarming achieves the best survival rates in hypothermic cardiac arrest compared to other rewarming methods
Clinical bottom line
VA-ECMO is the rewarming method of choice for hypothermic drowning-associated cardiac arrest when available.
Slomine, Nadkarni, Christensen, Silverstein et al 2017 — Neurobehavioural outcomes after paediatric drowning cardiac arrest (PMID 28274812)
Source
Resuscitation — multicentre observational cohort (THAPCA-associated dataset)
Population
Children who survived cardiac arrest due to drowning and other respiratory etiologies
Key finding
Children who survive drowning-associated cardiac arrest can have meaningful neurobehavioural recovery, but outcomes are generally poorer than after primary cardiac arrest
Clinical bottom line
Aggressive early resuscitation and post-arrest TTM are justified — quality of bystander CPR and time to ROSC are the strongest modifiable predictors.
Key summary
[1]References
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