Drowning & Near-Drowning

Overview & definition

The drowning — the respiratory impairment from the submersion / the immersion in the liquid. The aspiration → the surfactant the dysfunction → the atelectasis, the V/Q the mismatch, the non-cardiogenic the pulmonary the oedema / the ARDS. The hypoxia → the brain the injury (the leading the cause of the death). The key principle: the correct the hypoxia the first (the oxygen, the ventilation, the PEEP).[1][3]

The pathophysiology

• The breath-holding → the panic → the aspiration (the water into the lungs). The laryngospasm (the initial — the 'dry drowning' in the 10 to 20 per cent; the no the water in the lungs but the hypoxia from the laryngospasm).[1][3]
• The aspiration → the surfactant the washout / the dysfunction → the atelectasis, the V/Q the mismatch, the shunt, the non-cardiogenic the pulmonary the oedema / the ARDS.[1][3]
• The hypoxia → the brain the injury (the anoxic-the-ischaemic the encephalopathy — the leading the cause of the death). The cardiac (the VF / the asystole from the hypoxia).[2][3]
• The salt vs the fresh: the clinically the same (the small the volume the aspirated; the lung the injury from the surfactant + the hypoxia the identical).[2][3]

The management — correct the hypoxia first

1. The scene — the rescue + the EARLY CPR.[1][3]

• The rescue the from the water (the safe).[1]
• The EARLY the CPR (the chest the compressions the FIRST if the pulseless — the drowning is a the asphyxial the arrest → the CPR the with the rescue the breaths).[1]
• The NOT the Heimlich / the abdominal the thrusts (the ineffective — the water the in the lungs the not the stomach; the delay the CPR).[1]

2. The respiratory the support — correct the hypoxia.[1][3]

• The 100 per cent the oxygen. The intubation if the coma / the respiratory the failure.[3]
• The lung-the-protective the ventilation if the ARDS (the low the TV, the plateau below 30).[3]
• The PEEP (the alveolar the recruitment — the surfactant the dysfunction → the atelectasis).[1][3]

3. The neuroprotection.[1][3]

• The TTM (the same as the post-the-cardiac-the-arrest — the 32 to 36 degrees C for the comatose post-the-arrest the patient). The normothermia (the avoid the fever).[3]

4. The NOT.[1][3]

• The NOT the prophylactic the antibiotics (the contamination → the colonisation; the culture-the-guided the only the if the infection).[1]
• The NOT the corticosteroids (the ineffective for the pulmonary / the neuro).[3]

5. The other.[1][3]

• The rewarm if the associated hypothermia (the cold the water the drowning → the hypothermia).[3]
• The check the cervical the spine (the diving → the injury).[3]

Prognosis

The submersion the time → the outcome (the longer → the worse). The cold the water → the protective (the better the neurological the outcome — the cold brain). The TTM. The mortality the high if the prolonged. The survivors → the full the recovery if the early the CPR.[1][2][3]

Red flags

The 2005 WHO redefinition — terminology that is OBSOLETE

The single highest-yield conceptual point in this topic 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.[7][5]

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).[5]

[1]

The drowning pathophysiological cascade — the six stages

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.[6]

• Stage 1 — Breath-holding and panic. The conscious victim holds their breath, often with panic and an instinctive struggle. Voluntary apnoea and small aspiration events raise arterial carbon dioxide and lower oxygen.
• Stage 2 — Laryngospasm. Contact of water with the larynx triggers reflex closure of the vocal cords, producing a period in which little water enters the lungs — the historical basis of the obsolete 'dry drowning'. Laryngospasm cannot be sustained; it breaks as hypoxia deepens, and the victim then gasps.
• Stage 3 — Aspiration of a small volume of fluid. Once laryngospasm relaxes, the victim gasps and aspirates water. Critically, the volume aspirated is small — typically 1 to 4 mL per kilogram — far below the volumes that would meaningfully alter serum sodium, serum potassium or haematocrit, which is why the salt-versus-fresh and dry-versus-wet debates are obsolete.[6]
• Stage 4 — Surfactant dysfunction, atelectasis and an ARDS-pattern injury. Aspirated water (fresh or salt) washes out and denatures surfactant, destabilises surface tension, and produces widespread alveolar collapse, ventilation-perfusion mismatch, intrapulmonary shunt and non-cardiogenic pulmonary oedema. Contaminants (particulate matter, bacteria, vomitus) add a chemical or infective pneumonitis. The result is an ARDS-pattern lung injury often apparent within hours and worsening over the first day.
• Stage 5 — Hypoxia, bradycardia and asystolic arrest. Progressive hypoxia produces bradycardia, pulseless electrical activity and finally asystole (occasionally ventricular fibrillation, more often with underlying cardiac disease, hypothermia, or a primary arrhythmia such as a long-QT swimming-triggered event). Drowning is therefore an asphyxial arrest, not a primary cardiac arrest.
• Stage 6 — Hypoxic-ischaemic brain injury. The brain is the organ that determines outcome. Duration of cerebral hypoxia and the quality of post-return-of-spontaneous-circulation care (oxygenation, perfusion, temperature, glucose, seizure control) govern the neurological result. This is why targeted temperature management applies.[8]

[1]

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.[8]

[1]

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.[8][9]

Rescue and resuscitation — the first minutes

[1]

Oxygenation and ventilation in ICU — 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.[6][1]

• High-flow oxygen initially, then titrate FiO2 down to the lowest value that keeps arterial oxygen saturation at 92 to 96 per cent, avoiding both hypoxia and hyperoxia.
• Positive end-expiratory pressure (PEEP) is the cornerstone — it recruits collapsed alveoli, restores functional residual capacity, improves ventilation-perfusion matching and reduces shunt. Start at 5 to 10 cmH2O and titrate upward, balancing oxygenation against haemodynamic compromise and the risk of pneumothorax (particularly after aspiration of particulate matter).
• Lung-protective ventilation — tidal volume 6 mL per kilogram predicted body weight, plateau pressure under 30 cmH2O, permissive hypercapnia if needed. This is the same strategy as for ARDS and is appropriate given the ARDS-pattern pathology of the drowning lung.
• Adjuncts for refractory hypoxaemia — recruitment manoeuvres, prone ventilation (which improves oxygenation and mortality in moderate-to-severe ARDS), inhaled pulmonary vasodilators (nitric oxide) as a bridge, and extracorporeal membrane oxygenation for refractory hypoxaemia or hypercapnia.
• Airway froth — pulmonary oedema often produces copious pink or white froth. Do NOT repeatedly suction to dryness; the froth clears as oxygenation and PEEP improve. Continuous suction can injure the airway and interrupt ventilation. [1]

[1]

Targeted temperature management — drowning IS a cardiac arrest

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. The 2010 American Heart Association special-situations guidance is explicit on this point.[8]

• Targeted temperature management (TTM) at 32 to 36 degrees C for at least 24 hours in any adult or child who remains comatose (no purposeful response to verbal commands) after return of spontaneous circulation. Choose a single target within that range and maintain it tightly; the TTM trial (Nielsen and colleagues) showed that 33 degrees C and 36 degrees C give equivalent outcomes, so either is acceptable.[10]
• Avoid fever for 72 hours after arrest — pyrexia worsens neurological injury; treat with antipyretics and cooling devices.
• Normoglycaemia — avoid both hypoglycaemia and hyperglycaemia; moderate glucose control (6 to 10 mmol per litre) is reasonable.
• Normocapnia — ventilate to PaCO2 35 to 45 mmHg; avoid prophylactic hyperventilation (which causes cerebral vasoconstriction) except as a temporising measure for impending herniation.
• Seizure detection and control — treat clinical and electrographic seizures aggressively; consider continuous electroencephalography in the comatose patient.
• Concurrent immersion hypothermia — distinguish THERAPEUTIC hypothermia (intended, controlled TTM) from ACCIDENTAL hypothermia (the cold-water exposure that brought the patient in). Rewarm accidental hypothermia to at least 30 to 32 degrees C before declaring futility, and then transition to controlled TTM at the chosen target.[3]

[1]

Co-existing injuries — cervical spine, hypothermia and trauma

The intensivist must not be so focused on the lung and the brain that the co-existing injuries of drowning are missed. Three are particularly important: cervical spine injury, accidental hypothermia, and traumatic injury from the mechanism.[8][6]

• 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 per cent) but much higher in diving accidents.
• Accidental hypothermia — cold water cools the body rapidly. Measure core temperature (oesophageal, bladder or rectal). Severe hypothermia (under 30 degrees C) risks ventricular fibrillation and warrants careful handling, rewarming and, if arrest occurs, extracorporeal rewarming. Remember that hypothermia is also PROTECTIVE — the cold brain tolerates hypoxia far longer than the warm brain.
• Traumatic injury — boating and watercraft accidents, falls from height into water, and surf injuries can produce head injury, chest and abdominal trauma, and long-bone fractures. Assess and manage per standard trauma principles once the airway, breathing and circulation are secure.
• Immersion-related syndromes — prolonged immersion can produce immersion pulmonary oedema in divers and swimmers (even without aspiration), and cold-water immersion can trigger the mammalian diving reflex, particularly in children, contributing to the occasionally remarkable preservation of neurological function after prolonged cold submersion.
• Decompression sickness and gas embolism — consider in breath-hold or compressed-gas diving presentations with neurological symptoms; manage with 100 per cent oxygen and hyperbaric referral where appropriate. [1]

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.[8][6][5]

[1]

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'.[7][6]

[1]

Exam practice — SAQs

[1] [1]

Clinical pearls — high-yield points for the CICM, FFICM and EDIC exam

Landmark trials and guidelines

[1] [1] [1] [1] [1]

References

1. [1]Schmidt AC, et al. Management for the Drowning Patient Chest, 2021.PMID 33065105
2. [2]Modell JH. Near drowning Crit Care Clin, 1999.PMID 10331129
3. [3]Szpilman D, Bierens JJ, Handley AJ, Orlowski JP Drowning N Engl J Med, 2012.PMID 22646632
4. [4]Szpilman D, Morgan PJ Management for the Drowning Patient Chest, 2021.PMID 33065105
5. [5]van Beeck EF, Branche CM, Szpilman D, Modell JH, Bierens JJLM. A new definition of drowning: towards documentation and prevention of a global public health problem Bull World Health Organ, 2005.PMID 16302042
6. [6]Szpilman D, Bierens JJLM, Handley AJ, Orlowski JP. Drowning N Engl J Med, 2012.PMID 22646632
7. [7]Idris AH, Berg RA, Bierens J, Bossaert L, Branche CM, Gabrielli A, et al. Recommended guidelines for uniform reporting of data from drowning: the Utstein style Resuscitation, 2003.PMID 14580734
8. [8]Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, et al. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Circulation, 2010.PMID 20956228
9. [9]Szpilman D, Webber J, Quan L, Bierens J, Morizot-Leite L, Langendorfer SJ, Beerman S, Lofgren B. Creating a drowning chain of survival Resuscitation, 2014.PMID 24911403
10. [10]Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest N Engl J Med, 2013.PMID 24237006