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.
- 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.
- Laryngospasm does not typically persist until death. It is a possible but temporary response.
- 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.
- 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:
- 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.
- Hypothermia and/or cardiac arrhythmias, leading to loss of function and drowning, have been well described by Keatinge and others.
- 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.
- 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.
- 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.
- 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).