Chapter 20 Drowning
It is estimated that there were more than 400 000 victims of drowning worldwide in the year 2000.1 In several countries drowning is a major cause of accidental death, particularly amongst children. Drowning is more common in low- or middle-income countries than high-income countries,1 and is around three times more common in men than women. Alcohol is a major aetiological factor.2 For each victim of death by drowning, there are estimated to be between several cases of ‘near-drowning’ that are severe enough to require hospital admission, and probably hundreds of other less severe incidents.2 Death from pulmonary complications (‘secondary drowning’) may occur a considerable time after the accident, in patients who were initially normal.
The essential feature of drowning is asphyxia, but many of the physiological responses depend on whether aspiration of water occurs and upon the substances that are dissolved or suspended in the water. The temperature of the water is crucially important, and hypothermia following drowning in very cold water is a major factor influencing survival, though the mechanism underlying this observation remains controversial.
The hydrostatic pressure exerted on the body during immersion can be substantial. As a result there is a huge increase in venous return, causing increased pulmonary blood volume, cardiac output and, soon afterwards, a significant diuresis. Cephalad displacement of the diaphragm from raised abdominal pressure coupled with direct chest compression increases the work of breathing by about 65%. Three reflexes affect the respiratory system and come into play in drowning:
Airway irritant reflexes play a major part in drowning. Aspiration of water into the mouth initially stimulates swallowing followed by coughing, glottic closure and laryngospasm. If water penetrates deeper into the respiratory tract, below the vocal folds, bronchospasm results.
Cold shock describes a combination of several cardiovascular and respiratory reflexes that occur in response to sudden total-body immersion in cold water.4 Sudden immersion in water below 25°C is a potent stimulant to respiration and causes an initial large gasp followed by substantial hyperventilation. The stimulus is increased with colder temperatures, reaching a maximum at 10°C.2 Functional residual capacity is acutely increased, and individuals may find themselves breathing almost at total lung capacity, giving a sensation of dyspnoea. Breath-hold time is severely reduced, often to less than 10 seconds, which impairs the ability of victims to escape from a confined space underwater or to orientate themselves before seeking safety.
Diving reflex. In response to cold water stimulation of the face and eyes, the diving reflex produces bradycardia, peripheral vasoconstriction and apnoea in most mammals. It is particularly well developed in diving mammals, to reduce oxygen consumption and facilitate long duration dives. The reflex is present in humans,5 though of small magnitude compared with other species, and is believed to be more significant in infants than adults.2
Glottic closure from inhaled water, pulmonary aspiration, cold shock and the diving response all influence the course of events following submersion in water; the relative importance of each depends, amongst many other factors, on the age of the victim and the temperature of the water. Conflicting influences on the heart from activation of both the parasympathetic (diving reflex) and sympathetic (cold shock) systems are believed to contribute to death from cardiac dysrhythmia in some victims.2,4
This occurs in less than 10% of drowning victims.6 In thermoneutral water, when cold-stimulated reflexes will be minimal, the larynx is firmly closed during submersion and some victims will lose consciousness before water is aspirated. The rate of decrease of alveolar, and therefore arterial, Po2 depends on the lung volume and the oxygen consumption. Oxygen stored in the alveolar gas after a maximal inspiration is unlikely to exceed 1 litre, and an oxygen consumption of 3 l.min−1 would not be unusual in a subject either swimming or struggling. Loss of consciousness from decreased alveolar Po2 usually occurs very suddenly and without warning.
In cold water, hypoxia secondary to glottic closure may still occur. In addition, the cold shock and diving reflexes both leave the victim vulnerable to cardiovascular complications such as arrythmias and sudden circulatory failure leading to death before aspiration can occur. This is likely to be more common in elderly individuals.
Almost 90% of drowning victims have aspirated significant volumes of water. Following sudden immersion in cold water the cold shock response is believed to be more common than the diving reflex, and hyperventilation rapidly leads to aspiration. In thermoneutral water, glottic closure may either be overcome by the conscious victim or will eventually subside due to hypoxia, and in both circumstances aspiration is likely to continue. Once aspiration occurs, reflex bronchospasm quickly follows, further worsening respiratory function.
Fresh water. Aspiration of fresh water further down the bronchial tree causes rapid and profound changes to the alveolar surfactant, leading to loss of the normal elastic properties of the alveoli and a disturbed ventilation/perfusion ratio. In fresh water drowning, alveolar water is quickly absorbed, resulting in alveolar collapse and a pulmonary shunt, this being in addition to the changes resulting from dilution of surfactant. A significant shunt is therefore quickly established, with resulting hypoxia. Some studies indicate that neurogenic pulmonary oedema due to cerebral hypoxia might coexist with alveolar flooding from aspirated water.7 The pulmonary changes caused by immersion appear to be quickly reversible,7 with good prospects of return to normal pulmonary function in those who survive near-drowning.
A substantial volume of water may be absorbed from the lungs, and profound hyponatraemia, leading to fits, has been described in infants drowned in fresh water.8 However, most human victims absorb only small quantities of water and redistribution rapidly corrects the blood volume. Hypovolaemia is the more common problem following near-drowning.8
Sea water. Sea water is hypertonic, having more than three times the osmolarity of blood. Consequently, sea water in the lungs is not initially absorbed and, on the contrary, draws fluid from the circulation into the alveoli. Thus, in laboratory animals that have aspirated sea water, it is possible to recover from the lungs 50% more than the original volume that was inhaled.9 This clearly maintains the proportion of flooded alveoli and results in a persistent shunt with reduction in arterial Po2.
There appears to be no conclusive test for aspiration of either fresh or sea water. Tests based on differences in specific gravity and chloride content of plasma from the right and left chambers of the heart are unreliable. The demonstration of diatoms in bone marrow tissue is also controversial. For example, to improve the accuracy of the diatom test the species, morphology and number of diatoms found at post-mortem need to be compared with those in a sample of the water in which the victim allegedly drowned.10
Some degree of hypothermia is usual in near-drowned victims and body temperature is usually in the range 33–36°C. Hypothermia induced reduction in cerebral metabolism is protective during hypoxia and is believed to contribute to the numerous reports of survival after prolonged immersion in cold water, particularly in children. There have been reports of survival of near-drowned children and adults trapped for periods as long as 80 minutes beneath ice.8 However, for the reasons outlined above, arterial hypoxia is believed to develop very quickly, and there is controversy surrounding how body temperature can decrease quickly enough to provide any degree of cerebral protection. Surface cooling is not believed to allow a rapid enough fall in temperature as normal physiological responses to cold such as peripheral vasoconstriction and shivering limit the decline in temperature. Even so, the greater body surface area of children relative to their body size will theoretically result in more rapid cooling by heat conduction from the body surface.3
Absorption of cold water either from the lungs or stomach will contribute to hypothermia during prolonged immersion, but quantitatively the volumes required are unlikely to be absorbed, particularly in sea water. Heat loss from the flushing of cold water in and out of the respiratory tract, without absorption occurring, is another possible explanation. Animal studies have shown that airway flushing with cold water reduces carotid artery blood temperature by several degrees within a few minutes,11 which is sufficient to produce a useful reduction in cerebral oxygen requirement. Finally, repeated aspiration of cold water may directly cool deep areas of the brain through conductive heat loss to the nasopharynx.3
In spite of these potential benefits, hypothermia in most drowning victims probably does more harm than good. Consciousness is lost at around 32°C, making further aspiration almost inevitable, and ventricular fibrillation or asystole commonly occur at temperatures below 28°C. Once rescued, near-drowned patients often cool further before arrival at hospital.
There is a high measure of agreement on general principles of treatment.2,6,8
Circulatory failure and loss of consciousness may occur when a patient is lifted from the water in a vertical position, as for example by a helicopter winch. This is probably due to the loss of water pressure resulting in relative redistribution of blood volume into the legs. It is now recommended that victims are removed from the water in the prone position wherever possible.
At the scene of the drowning, it can be very difficult to determine whether there has been cardiac or even respiratory arrest. However, there are many records of apparently dead victims who have recovered without evidence of brain damage after long periods of total immersion. It is therefore essential that cardiopulmonary resuscitation be undertaken in all victims until fully assessed in hospital, no matter how hopeless the outlook may appear at the scene.
Early treatment of near-drowning is crucial and this requires efficient instruction in resuscitation for those who may be available in locations where drowning is likely to occur. The normal priorities of airway clearance, artificial ventilation and cardiac massage should be observed. Out of hospital, mouth-to-mouth ventilation is the method of choice, but high inflation pressures are usually required when there has been flooding of the lungs. Attempts to drain water from the lungs by postural drainage or an abdominal thrust (the Heimlich manoeuvre) are generally unsuccessful. These manoeuvres are likely to cause regurgitation of stomach contents with possible aspiration, and will delay the institution of artificial ventilation. Tracheal intubation should be performed as soon as possible to protect the airway from aspiration. Most survivors will breathe spontaneously within 1–5 minutes after removal from the water. The decision to discontinue resuscitation should not be taken until assessment in hospital, particularly if the state of consciousness is confused by hypothermia.
On arrival at hospital, patients should be triaged into the following categories:
There should be better than 90% survival in the first two categories, but patients should still be admitted for observation and followed up after discharge. Late deterioration of pulmonary function may occur and is known as ‘secondary drowning’, which is a form of acute lung injury (see Chapter 31). This can develop in any patient who has aspirated water, and the onset is usually within 4 hours of the aspiration.3 Patients who are comatose or hypoxic will require admission to a critical care unit. Treatment follows the general principles for hypoxic cerebral damage and aspiration lung injury. If spontaneous breathing does not result in satisfactory levels of arterial Po2 and Pco2, continuous positive airway pressure (CPAP) may be tried and is frequently useful. If this is unsuccessful, or in a patient with neurological impairment, artificial ventilation is required (Chapter 32).
References
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*8. Harries M. Near drowning. BMJ. 2003;327:1336-1338.
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