Chapter 72 Near drowning

DEFINITIONS

The American Heart Association Guidelines for Resuscitation ¹ suggest that the term ‘submersion victim’ be used to describe a person who experiences some swimming-related stress that is sufficient to require support in the field plus transportation to an emergency facility for further observation and treatment. ‘Drowning’ refers to death within 24 hours following a submersion event and the term ‘near drowning’ should no longer be used.

Table 72.1 Predictors of death or severe neurological impairment after submersion

EPIDEMIOLOGY

Drowning causes over 400 000 deaths worldwide.² Of these, 4000 are reported from the USA (approximately 1.5 deaths per 100 000 population),³ 500 from Australia⁴ and 700 from the UK.⁵ The incidence of non-fatal submersion events has been estimated to be 2–20 times more common than drowning.⁶ More than half of all submersion events occur in children less than 5 years old, the majority being 1–2 years old.^7,⁸ Males predominate, with peaks at 5 and 20 years of age. Private swimming pools and natural water bodies close to home present the greatest risk to young children.⁸ Other sites include bathtubs, fish tanks, buckets, toilets and washing machines. Adolescent drowning tends to occur in rivers, lakes, canals and beaches.⁹ Lack of adult supervision is almost always to blame for toddler accidents; however, child abuse must also be considered. Alcohol and drug intoxication is associated with up to 40% of adolescent drowning.¹⁰ Other risk factors include epilepsy (18%), trauma (16%) and cardiopulmonary disease (14%).¹¹ Hyperventilation prior to underwater swimming suppresses the physiological response to rising carbon dioxide tension, allowing hypoxia to ensue with consequent loss of consciousness and water breathing.¹²

PATHOPHYSIOLOGY

Voluntary apnoea and reflex responses occur upon submersion. The diving response is characterised by apnoea, marked generalised vasoconstriction and bradycardia in response to cold-water stimulus of the ophthalmic division of the trigeminal nerve. Blood is thus shunted preferentially to the brain and heart. In infants the response may be marked,¹³ but only 15% of fully clothed adults show a significant response. Although the diving reflex appears to play a powerful role in oxygen conservation in animals, its role in humans is unknown but may be protective.¹⁴

At some point after submersion involuntary inspiration occurs which leads to aspiration of water and often vomitus. Laryngeal spasm may occur which may explain the approximate 15% incidence of dry drowning, where little or no fluid is found in the lungs.^15,¹⁶ Gasping then occurs and water aspiration continues. Up to 22 ml/kg of water has been estimated to be the maximal survivable inhaled water volume.¹⁷ This is followed by a phase of secondary apnoea and loss of consciousness. Hypoxaemic death ensues if the person is not retrieved and resuscitated. Acute lung injury (ALI) – often termed secondary drowning, the pathophysiology of which is discussed elsewhere in the book – occurs in up to 72% of symptomatic survivors.¹⁸ Multiple organ dysfunction and cerebral damage may become evident in those that survive to hospital.

SALT VS FRESH WATER ASPIRATION

The differences between salt and fresh water drowning should be downplayed.¹ On the basis of animal studies it was thought that hypertonic seawater aspiration would draw plasma volume into the pulmonary interstitial space, leading to hypovolaemia, hypernatraemia and haemoconcentration. Similarly, aspiration of hypotonic fresh water was thought to lead to the passage of large volumes into the blood stream, leading to hypervolaemia, dilutional hyponatraemia, haemolysis and haemoglobinuria.

Modell et al.¹⁹ showed that volumes of water normally aspirated rarely translate into clinically meaningful syndromes. Orlowski and colleagues²⁰ showed little difference in observed cardiovascular effects in a canine model using six solutions of differing tonicity. They concluded that the cardiovascular effects seen with drowning and aspiration of water are not dependent on the tonicity of the aspirated fluid, but are the direct result of anoxia. Of 91 patients seen with severe submersion, no patient had serious electrolyte abnormalities or haemolysis. In another series, only 15% of retrieved but unresuscitatable patients had any of the expected electrolyte changes.¹⁷ Generally, most patients with ALI/pulmonary oedema will be hypovolaemic by the time they reach hospital.¹² No clinically detectable difference in the patterns of lung injury is seen between salt and fresh water drowning; both types reduce pulmonary surfactant quantity and function.²¹

WATER CONTAMINANTS

The incidence of pneumonia complicating submersion injury may be greater than 15% in those who survive long enough.¹⁸ Rivers, lakes and coastal waters are greater reservoirs for microbes than well-kept swimming pools. In fresh water, Gram-negative bacteria predominate along with anaerobes and Staphylococcus spp., fungi, algal and protozoan species. Aeromonas spp. are ubiquitous water-borne bacteria and can be responsible for severe pneumonia.²²

Chemicals in polluted water (e.g. kerosene ²³), chlorine²⁴ and particulate matter (e.g. sand²⁵) can cause severe pulmonary dysfunction.

TEMPERATURE

Victims of submersion may develop primary or secondary hypothermia. If submersion occurs in icy water (<5°C) hypothermia may develop rapidly and provide some protection against hypoxia. Surface cooling is unlikely to produce adequate protective hypothermia before hypoxia ensues.¹⁴ Most survivors of prolonged submersion almost always involve small children in icy water and it has been postulated that protective core cooling occurs rapidly due to cold-water aspiration, ingestion and absorption, though the mechanisms remain controversial.²⁶

Of more importance in cold-water submersion are the detrimental ‘cold-shock’ responses.²⁷ These responses include a ‘gasp’ followed by uncontrollable hyperventilation and reduction in maximal breath-hold times, vasoconstriction, tachycardia, hypertension and increased myocardial oxygen consumption. These responses may lead to motor dyscoordination and swimming failure as well as cardiac arrhythmias, hence even strong swimmers may drown quickly in icy waters.

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