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.
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).
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.
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.