Pathophysiological and Clinical Features of Drowning

Human series of near drowning cases do not show the electrolyte, haematological and cardiac changes seen in animals whose lungs are flooded.

Aspiration causes lung changes and hypoxaemia, which in turn may result in acute respiratory distress syndrome, hypoxic brain damage or cardiac, multisystem or renal disease.

Many patients have survived without brain damage despite total immersion for durations of 15 to 45 minutes. Thus, resuscitation has to be implemented energetically.

Many patients deteriorate or die hours or days after rescue and resuscitation, and therefore observation in hospital is required over this time.

Most patients recover without sequelae, but those with hypoxic encephalopathy may have residual neurological and neuropsychiatric problems.

The pathophysiological process of drowning has been the focus of many attempts to classify and sub-classify, with terms such as ‘drowning’ versus ‘near drowning’, ‘wet drowning’ versus ‘dry drowning’ and ‘secondary drowning’ enjoying periods of popularity. However, a 2010 international consensus determined that these terms contribute little to understanding of the problem and discouraged their use1. A unifying definition of drowning published by the International Liaison Committee on Resuscitation (ILCOR) is as follows: ‘a process resulting in primary respiratory impairment from submersion/immersion in a liquid medium. Implicit in this definition is that a liquid/air interface is present at the entrance of the victim’s airway, preventing the victim from breathing air. The victim may live or die after this process, but whatever the outcome, he or she has been involved in a drowning incident’.

Drowning: Radiology and Pathology

Death may occur during immersion, soon after or from delayed complications.

In recreational scuba deaths, drowning is the most common cause – but it is usually a secondary effect, with the primary cause leading to loss of consciousness. Drowning reflects the fact that unconsciousness occurred in a watery environment.

Accidents (e.g. hypoxia, gas toxicities, immersion pulmonary oedema, dysbarism, medical illnesses, trauma) that occur while someone is immersed or submerged may result in the secondary complication of drowning, with all its pathological sequelae. Drowning then complicates the interpretation of the diving accident and contributes to a combined disorder.

Certain external characteristics of drowned victims are common, although these are more specific for immersion than for drowning (see Chapter 51). These include the following: pale, wrinkled, ‘washerwoman’s’ skin; post-mortem decomposition; lacerations and abrasions from impact with rocks, coral, shells, motor boats and their propellers; post-mortem injuries from aquatic animals, varying from the nibbling of protuberances (fingers, ears, nose and lips) by crustaceans and fish to the large tearing wounds of sharks and crocodiles.

Radiology, and especially computed tomography scans, may be of value in drowning cases. These studies are likely to detect pulmonary interstitial oedema, sub-glottic fluid in the trachea and main bronchi, frothy airway fluid, hyper-expanded lungs, high-attenuation particles (indicating sand or other sediment), pleural effusion, haemorrhage or effusion in the middle ear and para-nasal or mastoid sinuses, gas and fluid in the stomach and other contributory causes of death.

The theory and the procedures for autopsies of drowning victims are surprisingly contentious for such a common disorder. An autopsy can imply, but not reliably prove, that death is the result of drowning. There is no pathological feature that is pathognomonic for drowning.

Respiratory system

At autopsy, the main macromorphological changes associated with drowning are caused by the penetration of the liquid into the airways. These are external foam from the mouth and nose, frothy fluid in the airways and overexpansion of the lung. They are not specific to drowning and can be found, usually to a lesser degree, in other cardiorespiratory disorders.

The mushroom-like foam or ‘plume’ from the mouth and nostrils, often exacerbated by resuscitation efforts, is composed of the drowning aspirant (usually sea water), pulmonary oedema, mucus and pulmonary surfactant, together with fine air bubbles. It extends into the lower airways, is relatively resistant to collapse and may last some days. It is particularly common with salt water drowning. It is thought to develop only if there is some inspiratory action (i.e. it is not a passive, post-mortem event). Respiratory epithelial cells and CD68+ alveolar macrophages have been detected in the foam.

The lungs are water-logged, often heavier than normal, and overdistended (emphysema aquosum). The lung weights reduce over the subsequent few days, as fluid is redistributed, and sometimes fluid accumulates in the pleural cavity. This is another reason for performing early autopsies. The overdistension may cause the ribs to be imprinted on the pleural surfaces, and the lungs may extend over the mediastinal midline. The lung surfaces may be pale and mottled, and areas of distended alveoli or bullae may be evident, as may subpleural haemorrhages (Paltauf’s spots). The lungs retain their shape and size on sectioning.

Pleural effusions are common and increase with the duration between death and autopsy.

When non-breathing bodies are immersed, significant quantities of fluid usually do not enter the lower respiratory system, but some may enter with the descent of the body as a result of replacement of the contracting gas space (Boyles’ Law). This is unlike the foam referred to earlier.

Histological evidence of focal alveolar damage and emphysema is frequent. Microscopic changes may demonstrate toxic effects both of chemicals and of the specific aspirant. The surfactant changes, including denaturation, can progress even after apparent clinical improvement. Epithelial and endothelial changes, with detachment of the basilar membrane and cellular disruption, have been described. Sand, marine organisms, algae and diatoms may be observed in the lungs.

The finding of water, effusion or blood in the middle ears, mastoid or para-nasal sinuses is not evidence of drowning per se, but it may indicate descent of the body while still alive (see Chapter 51). Other explanations include the inflow of water after death and the effects of venous congestion during the agonal struggle.

Usually the death results from hypoxia from the acute pulmonary damage and the shunting of blood through non-aerated tissue. Sometimes there is progressive or irreversible lung damage, for various reasons. They include progressive surfactant damage, pneumonitis from the aspirant, vomitus and foreign bodies. Even victims who appear normal on arrival at hospital can deteriorate over the next 6 to 12 hours. Respiratory infections and abscesses are not infrequent if death is delayed. Pulmonary oxygen toxicity, associated with prolonged resuscitation attempts, may also be present (see Chapter 17).

Other organs

The stomach often contains free fluid, water inhaled during the incident, together with debris and organisms. Wydler’s sign is a three-layer separation of foam, fluid and solids in the stomach.

Local haemorrhages in the upper torso musculature are sometimes claimed to be drowning induced, but this finding is controversial and non-specific.

The major effects on the neurological system are those of hypoxic brain damage with petechial haemorrhages and subsequent cerebral oedema and raised intracranial pressure.

Autopsies on drowning victims who submerged while still alive, although unconscious, may also show other cranial haemorrhages, which are sometimes misinterpreted as a cause of the accident. Meningeal haemorrhages, both dural and arachnoid, may be observed. These are usually not extensive and are quite different from the brain haemorrhages of arterial gas embolism or decompression sickness or from the petechial haemorrhages of asphyxia. They are probably derived from the bleeding of descent sinus barotrauma, which ruptures into the cranial cavity when the enclosed gas spaces expand during ascent.

There is often considerable venous congestion of the viscera, especially the brain, kidneys and other abdominal organs. Hypoxic cerebral necrosis and acute renal tubular necrosis with blood pigment casts are both described.
Because of the relatively small amount of fluid usually aspirated in drowning, it is considered unlikely that victims die acutely of electrolyte imbalance and/or associated ventricular fibrillation.

Cardiac arrhythmias may be initiated by hypoxia, but this is not demonstrable at autopsy. Cases of prolonged QT interval causing death from immersion have been postulated, but support for this as a common cause of death is lacking in drowning surveys.

The possibility of vagally induced death immediately following immersion has also been proposed when dealing with water colder than 15°C.

In the event of delayed drowning deaths, the lungs, brain or kidneys may all be involved.

Laboratory findings

A series of biochemical tests has been designed to verify drowning as the cause of death. The rationale is that the inhaled fluid, because it has different osmotic pressures, electrolytes and particulates compared with the pulmonary blood flowing past it, will change the latter and alter the character of the blood in the pulmonary veins, the left side of the heart and the systemic arterial system.

Thus, one can compare the left-sided heart blood with the right-sided heart blood and deduce the nature of the aspirate. In fresh water drowning, the left-sided heart blood should have a lower osmotic pressure and a dilution of most electrolytes. The hypo-osmolarity could result in haemolysis with a raised serum haemoglobin and potassium levels. Sea water aspirate should draw fluid from the circulating blood, thereby causing a rise in specific gravity and most blood constituents in the arterial blood. Such changes can be verified in animal experiments when the lungs are flooded with large volumes of fluid and the parameters are measured immediately post mortem.

Neither situation is likely in human drowning, in which the volume of aspirate is relatively small. There are usually many hours between death and autopsy, thus allowing blood constituents and electrolytes to equilibrate. Effective resuscitation is also likely to diminish any variations in venous and arterial blood.

For the foregoing reasons, the Gettler test (chloride variation) and sodium, magnesium, calcium, strontium, haematocrit, haemoglobin, pulmonary surfactant protein and specific gravity levels are unlikely to contribute to the autopsy diagnosis of drowning, although all have had their proponents. Some pathologists use the measurement of vitreous electrolytes to support the diagnosis. Atrial natriuretic peptide levels may increase in drowning, but also in immersion per se, in cardiac disease and in any hypervolaemic state. They also only persist for short periods.

Identification and comparison of environmental and systemic diatoms and algae in the lungs, blood, kidneys and vertebrae have been recommended. The single-celled diatoms, usually 10 to 80 micrometres long, are ubiquitous with about 15 000 different species – some inhabiting most waterways. They do not enter the tissues from the lungs unless there is an active circulation. Their presence in both the water environment and the body tissues does not prove drowning, merely the aspiration of that water while the body’s circulation is still functional. The silica shell makes diatoms stable and thus detectable by complex autopsy procedures. Despite its potential, the detection of diatoms is not often employed in pathological laboratories because of its complexity and the possibility of contamination. In addition, pollution of waterways reduces the presence of diatoms.

Further discussion relevant to drowning is found in Chapters 22 to 25.

‘Dry’ Drowning

This misnomer continues to be reported, despite the absence of experimental and clinical support for drowning without aspiration. The proponents originally quoted the observations of Charles Cot7, a Belgian doctor who reported in the French literature in 1931. He observed the ‘dry’ lungs of dogs fished from the Seine. Because there was no reason to believe that the dogs had drowned, as opposed to being disposed of in the water after death, this support was dubious.

The colourful terminology ensured the popularity of ‘dry drowning’, and many clinicians observed that persons who drowned may not have had obvious water in the lungs at autopsy. This was attributed to laryngospasm caused by asphyxia, continuing until death. Virtually every review of drowning over the rest of that century acknowledged this concept, without question, although the incidence was often increased to 20 to 40 per cent. It did conflict with the findings of earlier animal experiments.

Clinicians who dealt with sea water drownings, such as in scuba divers, never witnessed this paradox – indeed, they marveled at the degree of foam in the lungs and airways, whereas clinicians who dealt with fresh water drownings were much more enthusiastic about the ‘dry drowning’ pathological observation. Now the incidence of presumed ‘dry’ drownings has sunk to less than 2 per cent, even among the earlier proponents of this concept. It is a pathological entity, not a clinical one.

As it has been stated, fresh water is absorbed very rapidly from the lungs after death, and therefore autopsy findings cannot be used to imply (let alone prove) the absence of a previous aspirant. This is especially so when these investigations are performed sometime after the event or after cardiopulmonary resuscitation. ‘Dry drowning’ is probably an artefact of fluid absorption from the lungs, or it may indicate death from other causes. The deleterious effects of the aspiration can proceed even after the absorption of the fluid.

In the absence of more information, it would be prudent to presume that all victims of near drowning or drowning have aspirated and base one’s first aid and management on this presumption. This is supported by the knowledge that laryngospasm does not usually continue until death, and thus even if it does occur during the drowning process, it will not prevent aspiration as hypoxic death is approached.

Drowning: Animal Experiments

Biochemical and circulatory changes after flooding animals’ lungs with fresh water and sea water. Cl, chloride; K, potassium; Mg, magnesium; Na, sodium.

In the early 1900s many animal experiments conducted both in Europe and North America demonstrated that if an animal was immersed and drowned in water containing chemical traces or dyes, these would spread through the tracheo-bronchial tree to the alveolar surfaces. In the case of fresh water, this was also absorbed into the bloodstream.

A consistent fall in arterial oxygen content was observed, followed by a rise in arterial carbon dioxide and sometimes cardiac arrhythmias.

Swann and his colleagues from Texas3,4, in a series of accurate but misleading experiments, flooded animals’ lungs with fresh or salt water and demonstrated the significant differences between the two, attributable to osmotic pressures. In both cases, flooding of the lungs produced a reduction in PaO2 and pH, with a rise in the arterial partial pressure of carbon dioxide (PaCO2).

Because fresh water was osmotically much weaker than blood, it moved into the bloodstream and produced haemodilution – reducing blood concentrations of proteins, sodium, chloride and so forth. The subsequent reduction in the osmotic pressure of the blood caused haemolysis and a liberation of both haemoglobin and potassium, with resultant metabolic and renal complications, aggravated by hypoxia. Deaths were often cardiac and resulted from ventricular fibrillation.

When, however, the animals’ lungs were flooded with sea water – which has a higher osmotic concentration than blood – water was drawn from the bloodstream into the lungs, thereby producing pulmonary oedema and haemoconcentration. This caused an increase in the haematocrit, blood proteins and electrolytes.

For many years physicians attempted to correct these presumed electrolyte, metabolic and cardiac abnormalities in human drownings, but their cases did not replicate the animal model (Figure 21.1).

Biochemical and circulatory changes after flooding animals’ lungs with fresh water and sea water. Cl, chloride; K, potassium; Mg, magnesium; Na, sodium.
Figure 21.1 Biochemical and circulatory changes after flooding animals’ lungs with fresh water and sea water. Cl, chloride; K, potassium; Mg, magnesium; Na, sodium.

Earlier workers had shown that in dogs that drowned, there were still large volumes of air in the lungs, as there are in humans.

Colebatch and Halmagyi5, working in Australia in 1961, produced an animal model more relevant to the clinical management of patients, by aspiration of only 1 to 3 ml/kg body weight. By using these smaller volumes, these researchers demonstrated the sudden arterial hypoxia, not directly proportional to the amount of fluid inhaled. Pulmonary hypertension, vagal inhibition and reduced compliance were also observed. These investigators demonstrated that the weight of the lungs increased threefold the weight of the instilled sea water. Sea water aspiration usually caused significant pulmonary oedema, but aspirated fresh water was often absorbed from the lungs within 2 to 3 minutes.

Subsequent animal experiments by Modell6 and others, using intermediate volumes of aspirant, demonstrated that shunting of blood was the predominant cause of persistent arterial hypoxaemia, as a result of perfusion of blood through non-ventilated areas of lung. Destruction of lung surfactant in fresh water installation also resulted in alveolar wall damage and pulmonary oedema.

Behaviour During Drowning

Over the range of animals tested and observed, consciousness is usually lost within 3 minutes of submersion and death between 4 and 8 minutes, as a result of cerebral hypoxia.

Observations of human drowning parallel those of the animal experiments, involving a panic reaction with violent struggling followed by automatic swimming movements. There may be a period of voluntary breath-holding or involuntary laryngospasm as fluid strikes the nasopharynx or larynx. During this period of apnoea, hypoxia, hypercapnoea and acidosis develop, and respiratory attempts may result in much swallowing of water and even vomiting. With increasing hypoxia, unconsciousness supervenes, and any laryngospasm abates. Inhalation of water into the lungs may then have many respiratory, cerebral, haematological and biochemical consequences. These are documented later.

Some misunderstandings need to be addressed.

  1. The lungs do not usually ‘flood’ with water. Once death has occurred, and respirations have stopped, aspiration ceases. Hypoxaemia becomes evident from minimal aspirations (1 to 3 ml/kg body weight). Volumes greater than 11 ml/kg are needed before blood volumes are altered, volumes greater than 22 ml/kg are needed to produce obvious biochemical alterations and volumes greater than 44 ml/kg are needed to induce ventricular fibrillation. In humans, volumes exceeding 22 ml/kg are uncommon and they are usually much less, as inferred from the lung weights at autopsy.
  2. Laryngospasm does not typically persist until death. It is a possible but temporary response.
  3. There is no such clinical entity as ‘dry drowning’. This is a pathological finding in some cases of drowning and in which the aspirated fluid has subsequently been absorbed.
  4. For many years, drowning was characteristically associated with a ‘fight for survival’, but this is not inevitable, and it is uncommon in divers underwater. It is more common in swimmers on the surface.

From observations in children exposed to drown-proofing, as it is euphemistically called, there is usually a failure of the infant to struggle. Breath-holding and automatic but ineffectual paddling-type movements are evident as the infant sinks to the bottom.

In many diving-related circumstances drowning may proceed in a quiet and apparently unemotional manner. Examples of these quiet or silent drownings include the following:

  1. Hyperventilation before breath-hold diving (see Chapters 3, 16 and 61) is a common cause of drowning in otherwise fit individuals who are good swimmers, often in a swimming pool in which they could have stood up. Hyperventilation followed by breath-hold diving can result in loss of consciousness secondary to hypoxia. This occurs before the blood carbon dioxide levels rise sufficiently to force the diver to surface and/or breathe. In these cases, loss of consciousness can occur without any obvious warning, and the underwater swimmer then aspirates and drowns quietly.
  2. Hypothermia and/or cardiac arrhythmias, leading to loss of function and drowning, have been well described by Keatinge and others.
  3. Drugs and alcohol increase the likelihood of drowning by impairing judgement, reducing the struggle to survive and possibly reducing laryngospasm. It is likely that nitrogen narcosis may have a similar effect in divers.
  4. Diving problems may produce hypoxia. These include the dilution hypoxic effects with mixed gas breathing and ascent hypoxia (see Chapter 16) and carbon monoxide toxicity resulting from the interference with oxygen metabolism. These effects are likely to cause loss of consciousness without excess carbon dioxide accumulation, dyspnoea or distress.
  5. Water aspiration causing hypoxia (see Chapter 24). In animals, 2.2 ml of fresh water inhaled per kg body weight drops the arterial partial pressure of oxygen (PaO2) to approximately 60 mm Hg within 3 minutes, or to 40 mm Hg with sea water. A similar situation was observed clinically in the salt water aspiration syndrome of divers.
  6. Other causes of unconsciousness leading to drowning have been described, e.g. diving-induced cardiac arrhythmias, cerebral arterial gas embolism, some marine animal envenomations and coincidental medical illnesses such as epilepsy or cerebral haemorrhage. Sudden death induced by vagal inhibition can follow a sudden immersion (this is not drowning, although it can be confused with it, and the drowning syndromes may be precipitated by sudden cold water impact with the pharynx or larynx).

Drowning: Demography

Drowning causes half a million deaths per year, worldwide. In many countries, drowning is one of the most common causes of all deaths for children less than 12 years old. In the United States and Australia, it is the second leading cause of death, after motor vehicle accidents, in children less than 12 years old.

The worldwide death rate from drowning is 6.8 per 100 000 person years. The rate of drowning in different populations varies widely according to their access to water, the climate and the national swimming culture. The incidence in most developed countries has now dropped to less than 2 per 100 000. In Africa and in Central America, the incidence is 10 to 20 times higher than this. Island nations with dense populations, such as Japan and Indonesia, are more vulnerable than are large continental nations.

Key risk factors for drowning are male sex, age less than 14 years, alcohol use, low income, poor education, rural residency, aquatic exposure, risky behavior and lack of supervision. Epilepsy increases the risk of drowning by 15 times. The exposure-adjusted, person-time risk of drowning is 200 times higher than that from traffic accidents. For every person who dies of drowning, at least another 4 persons receive care in the emergency department for ‘non-fatal drowning’.

There is a predictable age distribution for specific types of drowning. Most swimming pool deaths occur in children, surf deaths occur mostly in teenagers and young adults, ocean deaths occur in sailors and fishers throughout the whole adult range and bathtub drowning occurs in either young babies or older infirm persons. Homicides occur in all ages.

Alcohol consumption is involved in more than half the adult male drowning cases. This may result from the following:

  • Increased risk-taking activities.
  • Reduced capacity to respond to a threatening situation.
  • Loss of heat secondary to peripheral vasodilatation.
  • Interference with the laryngeal reflex.
  • Increased vagal response.
  • Increased tendency to vomit.
  • Suicidal intentions.

‘Bacchus hath drowned more men than Neptune’. Old English Adage.

The demographic features of general drowning accidents are not reflected in the drowning of divers (see Chapter 25). Although it should be the simplest and most informed topic in diving medicine, drowning is plagued with paradoxes. It is responsible for most diving fatalities, but unless other explanations are added, it is a totally inadequate explanation. Divers, unlike other aquatic adventurers, carry their own breathable gas supply (their life support system) with them, and unless this is interrupted in some way, drowning per se is inexplicable. It is a grossly oversimplified diagnosis without determining what has compromised this respirable gas supply or what complications have ensued.

Drowning: Terminology

Drowning is defined as the death of an air-breathing animal as a result of submersion in fluid. When patients lose consciousness because of aspiration causing hypoxia, but subsequently recover, the term ‘near drowning’ is used. When symptoms are not severe enough to classify as near drowning, another term, the ‘aspiration syndrome’, is employed.

In divers, and others who submerge after losing consciousness, the pathology of drowning is complicated by the effects of barotrauma in air spaces (e.g. middle ear, sinus, face mask) and decompression artefact.

When I use a word it means just what I choose it to mean – neither more nor less.

Humpty Dumpty, from Lewis Carroll

General reviews indicating the importance of this topic to diving medicine have been presented by diving clinicians such as Sir Stanley Miles, Kenneth Donald, Carl Edmonds, Barbara Tabeling, Christopher Dueker, Tom Neuman and others (see the Further Reading list at the end of this chapter and also Chapters 24 and 25).

Other specialists such as forensic pathologists, epidemiologists, animal researchers and respiratory and emergency clinicians have an equal involvement, but they approach the topic from different aspects. This diversity of interests has had implications not only on terminology, but also on conventional beliefs and prejudices.


The drowning syndromes have been researched extensively for centuries, yet we cannot even agree on the definition.

Drowning, until the nomenclature was changed by the World Congress on Drowning in 2002, meant the death of an air-breathing animal as a result of submersion in a liquid. There were a number of related clinical diagnoses:

Near-drowning referred to a serious clinical syndrome with the loss of consciousness from the submersion, but not resulting in death. It was therefore a lesser condition, but one that could lead to drowning.

Delayed drowning or secondary drowning occurred when the victim appeared to recover from the near drowning incident, but then proceeded to die. This had important management implications.

The aspiration syndrome referred to the lesser effects of aspiration of fluid into the lungs, without death or loss of consciousness.

There was an escalating range in the severity of symptoms and signs among aspiration, near drowning and drowning. They were incorporated together as the drowning syndromes because they needed to be seen as a continuum, for a comprehensive understanding of this disorder.

Post-immersion syndromes referred to the complications that develop after immersion and subsequent rescue. These included pulmonary (infections and inflammations), brain, haematological, renal and multi-system disorders. They also had clinical and management implications.

Other nomenclatures have been proposed over the centuries, based on the type (sea water and fresh water drowning) and amount of fluid inhaled (wet and dry drowning). Modell’s classification of 19711, which was based on survival and on whether aspiration occurred, failed because although death was a clear differentiator, aspiration was not.

These classifications were less clinically valuable and may even be artefactual or misleading. They probably did add to the confusion and deserved the approbation of the World Congress on Drowning.

Thus, by 2002, when the World Congress on Drowning convened, it confronted the problem of a complicated nomenclature, some of which was not very informative. To promote an international statistical conformity for surveillance and comparison of research and epidemiological data, it was decided to use just one all-embracing term – drowning – to cover all such clinical eventualities and not imply an outcome. The World Congress thus succeeded in demographic standardization, but in doing so managed to oversimplify a genuinely complex subject. The Congress then relented with one demarcation qualification – based on outcome, whether the drowning was fatal or non-fatal. In doing so, the Congress managed to re-define a previously well-defined term (‘drowning’) and add an oxymoron (‘non-fatal drowning’). Other subsequent classifications included warm water or cold water drowning. The International Liaison Committee on Resuscitation’s (ILCOR) complex definition in 2010 similarly combined all forms of aspiration, from the most innocuous to the drowning deaths, into the one category (see Chapter 22). This all-embracing approach was not a problem for statisticians, but it resulted in a loss of information and direction for clinicians, most of whom revert to the more useful older definitions.

For clinicians, who need to make management decisions based on the client’s presentation, it is still preferable to distinguish among the following:

  • Those who died (drowning).
  • Those who lost consciousness and were at risk of dying (near drowning).
  • Those who had minor inhalation and transitory symptoms (aspiration).
  • Those who had later complications of the aspiration. These include the various forms of organ damage, such as lung, brain and kidney disease.