Chapter 72 Near drowning
DEFINITIONS
The American Heart Association Guidelines for Resuscitation1 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
| At site of immersion: |
| In the emergency department |
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. kerosene23), 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.
MANAGEMENT
BASIC LIFE SUPPORT
Prompt retrieval from the water is essential as is immediate on-site resuscitation. Expired air resuscitation and external cardiac compression should be applied immediately after retrieval. If trauma is suspected, especially in diving and surfing accidents, head and spinal injuries are assumed and due caution in stabilising the cervical spine during airway manipulation and transport is required. The Heimlich manoeuvre is no longer recommended in the management of submersion injury as the volume of aspirated water removed at the time of attempt is small and the risk of gastric aspiration is great.1 Rewarming should be commenced immediately with the use of blankets and further heat loss should be avoided. When experienced personnel arrive, bag and mask ventilation and advanced cardiac life support is initiated.
ASSESSMENT
INVESTIGATIONS
These depend on the clinical circumstances and could include:
ADMISSION CRITERIA
Asymptomatic patients with no clinical findings on cardiorespiratory examination and a normal chest radiograph and blood gas are unlikely to develop ALI and pneumonia and thus do not require hospital admission.18,29 All other patients should be admitted to a high-dependency area or intensive care unit for continuous monitoring and rewarming.
RESPIRATORY SUPPORT
Severe agitation or coma mandates intubation and mechanical ventilation; otherwise oxygenation is initially maintained with high-flow oxygen or continuous positive airway pressure (CPAP) by tight fitting facemask. Superimposed ventilatory failure may be managed with non-invasive inspiratory pressure assistance in addition to CPAP (often termed bilevel positive airway pressure or non-invasive pressure support). The use of intravenous and inhaled bronchodilators may reduce airflow resistance and the work of breathing. Selective pulmonary vasodilators such as inhaled nitric oxide or inhaled prostacyclin may be useful in severe refractory hypoxaemia. In severe cases, extracorporeal membrane oxygenation has been used in some centres.30
CARDIOVASCULAR SUPPORT
Patients with ALI are often hypovolaemic regardless of the type of water ingestion. Cautious volume expansion and the use of catecholamine infusion may improve cardiac output and blood pressure. Fluid replacement with isotonic fluids is aimed at restoring adequate end-organ perfusion without compromising respiratory function. The use of a central venous or pulmonary artery catheter may be necessary to achieve these goals. In cases where severe circulatory insufficiency or cardiac arrest is associated with severe hypothermia, cardiopulmonary bypass has been used successfully.31
CEREBRAL PROTECTION
Recent data show a better neurological outcome with induced hypothermia (32–34°C) after cardiac arrest due to ventricular fibrillation.32 Although no specific data for the cerebral protective effects of hypothermia exist for patients suffering hypoxic brain injury associated with submersion, the data would suggest that comatose drowning victims should not be actively rewarmed above 34°C.
No other specific cerebral protective measures have proven efficacy in post anoxic encephalopathy associated with drowning.33 Maintenance of an adequate cerebral perfusion pressure (mean arterial pressure >90 mmHg in adults, 60–70 mmHg in children) is the most important goal of therapy. Prevention of cerebral venous and thus intracranial hypertension can be achieved by neutral neck positioning, avoiding occlusive endotracheal tube ties and head-up positioning. Avoiding hypocapnia (PaCO2 <30 mmHg), reducing cerebral metabolic rate with sedation, preventing hypoglycaemia and hyperthermia, and the use of anticonvulsants in those with documented seizures are simple measures to prevent secondary cerebral injury.
OTHER THERAPIES
There is no role for prophylactic corticosteroid therapy in the prevention of acute lung injury after submersion.12 Prophylactic antibiotic therapy is unproven and the decision to commence therapy is made on the degree of water contamination, need for mechanical ventilation and severity of respiratory failure in each case.18 Baseline microbiological studies should be sent prior to commencement of therapy.
PROGNOSIS
Mortality rate for those surviving more than 24 hours was 24% in a recent large series,18 with three quarters succumbing in the early stages after injury. Moderate to severe brain damage is reported in 33% of survivors.8 The outcome in children is similar, with 30% having selective deficits and 3% with persistent vegetative state.34 No difference in mortality between fresh and salt water submersion has been documented.11 Lower core temperatures appear to be associated with a better prognosis, except if this occurs after rescue. However, hypothermia in warm water immersion and severe hypothermia (<30°C) in cold water immersion is indicative of prolonged immersion and poor outcome.27Table 72.1 lists some factors associated with death or severe neurological impairment. None of these predictors is infallible and survival with normal cerebral function has been noted despite the presence of some or all of these factors.12
1 AHA Resuscitation Guidelines. Submersion or near-drowning. Circulation. 102(Suppl I), 2000.
2 World Health Organization. The World Health Report, 2002: Reducing risks, promoting healthy life. Geneva: WHO, 2002.
3 National Center for Injury Prevention and Control. WISQARS Leading Causes of Death Reports, 1999–2000. http://webappa.cdc.gov/cgi-bin/broker.exe.
4 Pearn J. Drowning in Australia: a national appraisal with particular reference to children. Med J Aust. 1977;ii:770-771.
5 Golden F St C, Rivers JF. The immersion accident. Anaesthesia. 1975;30:364-373.
6 Weinstein M, Kreiger BP. Near drowning: epidemiology, pathophysiology and initial treatment. J Emerg Med. 1996;14:461-467.
7 Centers for Disease Control. Fatal injuries to children – United States, 1986. MMWR. 1990;39:442-451.
8 Orlowski JP. Drowning, near drowning, and ice-water submersions. Pediatr Clin North Am. 1987;34:75-92.
9 Wintemute GJ. Childhood drowning and near drowning in the United States. Am J Dis Child. 1990;144:663-669.
10 Wintemute GJ, Kraus JF, Teret SP, et al. Drowning in childhood and adolescence: a population based study. Am J Public Health. 1987;77:830-832.
11 Spilzman D. Near drowning and drowning classification. A proposal to stratify mortality based on the analysis of 1831 cases. Chest. 1997;112:660-665.
12 Modell JH. Drowning. N Engl J Med. 1993;328:253-256.
13 Daly M deB, Angell-James JE, Elsner R. Role of carotid-body chemoreceptors and their reflex interactions in bradycardia and cardiac arrest. Lancet. 1979;1:764-767.
14 Gooden BA. Why some people do not drown; hypothermia versus the diving response. Med J Aust. 1992;152:629-632.
15 Karch SB. Pathology of the lung in near drowning. Am J Emerg Med. 1986;4:1.
16 Kringsholm B, Filskov A, Kock K. Autopsied cases of drowning in Denmark 1987–1989. Forensic Sci Int. 1991;52:85-92.
17 Modell JH, Davis JH. Electrolyte changes in human drowning victims. Anesthesiology. 1969;30:414-420.
18 van Berkel M, Bierens JJL, Lie RLK, et al. Pulmonary oedema, pneumonia and mortality in submersion victims: a retrospective study in 125 patients. Int Care Med. 1996;22:101-107.
19 Modell JH, Graves SA, Ketover A. Clinical course of 91 consecutive drowning victims. Chest. 1976;70:231-238.
20 Orlowski JP, Abulleil MM, Phillips JM. The hemodynamic and cardiovascular effects of near-drowning in hypotonic, isotonic, or hypertonic solutions. Ann Emerg Med. 1989;18:1044-1049.
21 Sachdev R. Near drowning. Crit Care Clin. 1999;15:281-296.
22 Ender PT, Dolan MJ, Farmer JC, et al. Near-drowning associated Aeromonas pneumonia. J Emerg Med. 1996;14:737-741.
23 Segev D, Szold O, Fireman E, et al. Kerosene-induced severe acute respiratory failure in near-drowning. Reports on four cases and review of the literature. Crit Care Med. 1999;27:1437-1440.
24 DeNicola LK, Falk JL, Swanson ME, et al. Submersion injuries in children and adults. Crit Care Clin. 1997;13:477-502.
25 Dunagan D, Cox J, Chang MC, et al. Sand aspiration with near drowning. Radiographic and bronchoscopic findings. Am J Respir Crit Care Med. 1997;156:292-295.
26 Conn AW, Miyassaka K, Katayama M, et al. A canine study of cold water drowning in fresh versus saltwater. Crit Care Med. 1995;23:2023-2036.
27 Golden F St C, Tipton MJ, Scott RJ. Immersion and near drowning. Br J Anaes. 1997;79:214-225.
28 Agar JW. Rhabdomyolysis and acute renal failure after near drowning in cold salt water. Med J Aust. 1994;161:686-687.
29 Causey AL, Tilelli JA, Swanson ME. Predicting discharge in uncomplicated drowning. Am J Emerg Med. 2000;18:9-11.
30 Thalmann M, Trampitsch E, Haberfellner N, et al. Resuscitation in near-drowning with extracorporeal membrane oxygenation. Ann Thorac Surg. 2001;72:607-608.
31 Letsou GV, Kopf GS, Elefteriades JA, et al. Is cardiopulmonary by-pass effective for treatment of hypothermic arrest due to drowning or exposure? Arch Surg. 1992;127:525-528.
32 Oddo M, Schaller MD, Feihl F, et al. From evidence to clinical practice: effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest. Crit Care Med. 2006;34:1865-1873.
33 Bohn DJ, Biggard WJ, Smith CR, et al. Influence of hypothermia, barbiturate therapy and intracranial pressure monitoring on morbidity and mortality after near drowning. Crit Care Med. 1986;14:529-534.
34 Pearn J. Medical aspects of drowning in children. Ann Acad Med Singapore. 1992;21:433-455.
