The majority of burnt bodies recovered from fires will not have died from the direct effect of burns, but from exposure to the products of combustion (smoke, carbon monoxide, cyanide and a cocktail of toxic combustion by-products) and/or the inhalation of hot air/gases (Box 17.3).
Deaths occurring after a fire may occur because of the large variety of potential complications of thermal injury such as hypovolaemic shock follow- ing fluid loss, overwhelming infection, the inhalation of combustion products (causing acute lung injury), renal failure or blood-clotting abnormalities.
While the determination of ‘manner of death’
usually rests with the appropriate medico-legal authority, an opinion from the forensic pathologist is frequently sought. The interpretation of injury in bodies recovered from fire is complicated by arte- facts related to exposure to fire:
■ the so-called ‘pugilist attitude’ of the body reflects differential heat-related contraction of
Figure 17.11 Thermal injury to the back of the throat provides evidence of the inhalation of hot gases during a fi re, and provides a useful sign of vitality at the time of a fi re.
Figure 17.10 Soot staining can be seen in the oesophagus in this body recovered from a house fi re. Such staining indicates that the deceased was alive – and able to swallow – at the time of the fi re.
Box 17.3 Examples of mechanisms of death in fi res
● Interference with respiration (owing to a reduction in environmental oxygen and/or the production of carbon monoxide and other toxic substances)
● Inhalation heat injury leading to laryngospasm, bronchospasm and so-called ‘vagal inhibition’ and cardiac arrest
● Exposure to extreme heat and shock
● Trauma
● Exacerbation of pre-existing natural disease or burns
Box 17.2 Examples of reasons for failure to escape from a fi re
● Deceased was already dead before the start of the fi re
● Deceased was intoxicated (alcohol and/or drugs)
● Deceased was elderly and/or disabled
● Deceased was immobile
● Deceased was rapidly overcome by fumes/smoke because of ‘poor physiological reserve’ (e.g. ischaemic heart disease or chronic obstructive airways disease)
● Deceased had insuffi cient time to escape the fi re owing to the nature of the fi re itself (an explosion or ‘fl ash fi re’)
● There was panic/confusion
● Escape routes were obstructed (deliberately or accidentally)
● Deceased was in an unfamiliar environment (and did not know where the escape route was)
Cold injur y (hypothermia)
muscle, leading to flexion of the forearms, hands and thighs (Figure 17.12);
■ post-mortem splitting of fragile burnt skin (Figure 17.13);
■ fire- and heat-related fractures; and
■ heat-related ‘extradural haemorrhage’, caused when severe heat has been applied to the scalp, resulting in expansion of the blood in the skull diplöe and the intracranial venous sinuses, which rupture, resulting in the formation of a collection of brown and spongy blood outside the meninges (Figure 17.14).
Such artefacts often cause concern to police and/or fire officers attending the scene, and may be misin- terpreted as representing the effects of ante mortem violence.
Careful consideration of all apparently traumatic lesions must be made in order to determine the true nature of such post mortem lesions; the lack of na- ked eye or microscopic evidence of vitality (such as erythema, blistering, tissue swelling, bruising or an acute inflammatory reaction) will frequently distin- guish artefact from trauma inflicted before death, unless they were inflicted at, or around, the time of death. In cases where there is doubt, an evalu- ation of the overall pattern and distribution of such lesions may assist in the interpretation of artefact versus ante-mortem trauma.
The manner of death may be homicide (following arson or where death was caused by violence be- fore the fire being set), accident (e.g. an intoxicated individual attempting to cook, or from a discarded cigarette) or, rarely, suicide (self immolation).
■ Cold injury (hypothermia)
Cold injury (hypothermia) has both clinical and forensic aspects, as many people suffer from and die of hypothermia even in temperate climates in winter. In marine disasters, hypothermia may be as common a cause of death as drowning. In the very cold waters of seas, and lakes in high lati- tudes, death from immersion may occur within a
Figure 17.13 Post-mortem artefactual skin splitting in charred skin. No haemorrhage can be seen in the depths of the splits and they should not be confused with ante-mortem injuries.
Figure 17.14 Post-mortem fi re-related skull fractures in a severely charred body. There is a reddish-brown heat haematoma/extradural haemorrhage on the inner surface of the carbonized cranial vault.
Figure 17.12 Appearance of ‘pugilistic attitude’ as a respose to heat effect more on fl exor than extensor muscle grasp.
17 Heat, cold and ele ctrical tr auma
few minutes from sheer heat loss and before true drowning can occur.
Deaths from exposure occur through heat loss from radiation, convection, conduction, respiration and evaporation. Environmental temperatures be- low 10°C are probably sufficient to cause harmful hypothermia in vulnerable individuals.
Hypothermia occurs when a person’s normal body temperature of around 37°C (98.6°F) drops be- low 35°C (95°F). It is usually caused by being in a cold environment. It can be triggered by a combina- tion of factors, including prolonged exposure to cold (such as staying outdoors in cold conditions or in a poorly heated room for a long time), rain, wind, sweat, inactivity or being in cold water.
It is usually healthy individuals who succumb to death from hypothermia caused by a cold envi- ronment. If a body gets cold, the normal response is to warm up by becoming more active, putting on more clothing layers or moving indoors. If exposure to the cold continues, other physiological processes will attempt to prevent any further heat loss. These processes include shivering (which keeps the major organs at normal temperature), restricting blood flow to the skin and releasing hormones to generate heat.
After prolonged exposure to the cold, these respons- es are not enough to maintain body temperature. At this point, shivering stops and heart rate decreases.
This can happen quickly. Alcohol consumption wors- ens hypothermia as it causes vascular dilatation and increased heat radiation. Wind and rainfall exacer- bate the drop in body temperature. The body may rapidly lose temperature when immersed in cold water, as water has a cooling effect that is 20–30 times that of dry air. Hypothermia may confer a protective effect on survival following cold water immersion, but survival may be accompanied by severe hypoxic brain injury.
In many patients there may be an underlying medical cause (such as thyroid or pituitary dys- function), or it may be associated with immobile or demented patients or conditions such as pneumonia.
It is characterized by depression (poor functioning) of the cardiovascular and nervous systems.
Generally, the elderly, children and trauma patients are susceptible to hypothermia. Hypother- mia can be classified into mild (core temperature 32–35°C compared with a normal of 37.5°C), moder- ate (30–32°C), or severe (< 30°C). Below a core temperature of 32°C, shivering ceases and thus this extra muscle activity will no longer generate heat,
worsening the situation. Unconsciousness may occur between core temperatures of 27°C and 30°C, while ventricular fibrillation and apnoea occur at core temperatures below 27°C. Those who may be prone to developing hypothermia are those in extreme weather conditions (e.g. climbers, walkers, skiers, sailors), homeless people who are unable to find shelter, heavy drug and/or alcohol users (collapsing in the open) and those who have been immersed in cold water.
Hypothermia is usually diagnosed on the basis of typical symptoms and environment, and can be divided into mild, moderate and severe cases (Box 17.4). When unconscious, a person will not appear to have a pulse or be breathing. Treatment of severe hypothermia may not be successful. The key to treatment is a controlled rewarming that must be under medical supervision, and may require inter- vention such as dialysis.
It is important to remember that the weather does not have to be unusually cold for hypothermia to develop and, even in moderately cold winter weather, many elderly individuals will become hypothermic.
Box 17.4 Features of mild, moderate and severe hypothermia
● Mild cases – shivering – feeling cold – lethargy – cold, pale skin
● Moderate cases
– violent, uncontrollable shivering – cognitive impairment – confusion
– loss of judgment and reasoning
– loss of coordination, including diffi culty moving around or stumbling – memory loss
– drowsiness – slurred speech – apathy
– slow, shallow breathing – weak pulse
● Severe cases
– loss of control of hands, feet and limbs – uncontrollable shivering that suddenly stops – unconsciousness
– shallow or no breathing, weak – irregular or no pulse – stiff muscles – dilated pupils
Cold injur y (hypothermia)
Children have a high body surface-to-weight ratio and lose heat rapidly. In some cases of deliber- ate neglect or careless family circumstances, infants may be left in unheated rooms in winter and suffer hypothermia.
In an unrefrigerated body, the finding of indistinct red or purple skin discoloration over large joints, such as the elbows, hips or knees (and in areas of skin in which such discoloration cannot be hypostasis) raises the possibility of hypothermia and is found in approximately 50 per cent of presumed hypothermia deaths (Figure 17.15). The nature of such discolora- tion (‘frost erythema’) is not completely understood, but may reflect capillary damage and plasma leak- age; microscopy reveals no red blood cell extravasa- tion, distinguishing it from bruising.
Classically, haemorrhagic gastric lesions (Wischnewsky spots) may be seen in hypothermia
deaths; these lesions represent mucosal necrosis with haematin formation (Figure 17.16). However, their presence is not specific to hypothermia as they are identical to those lesions seen in some deaths following sepsis and shock, as well as in cases of alcohol misuse. They are thought to be caused by a disturbance of gastric microcirculation and exposure of haemoglobin to gastric acid.
Other gastrointestinal lesions sometimes found in deaths caused by hypothermia include haemorrhagic erosions and infarction in the small bowel (because of red blood cell ‘sludging’ and submucosal thrombo- sis), and haemorrhagic pancreatitis with fat necrosis.
Cold injury to the extremities may be severe enough to cause frost bite, which reflects tissue injury that varies in severity from erythema to infarc- tion and necrosis following microvascular injury and thrombosis (Figure 17.17).
Hypothermia may cause behavioural abnormali- ties that can lead to death-scene findings that appear suspicious. Paradoxical undressing is a phenomenon that describes the finding of partially clothed – or naked – individuals in a setting of lethal hypother- mia. The pathophysiology of this is uncertain but it may reflect confusion and abnormal processing of peripheral cutaneous stimuli in a cold environment, leading the individual to perceive warmth and thus to shed clothing.
The phenomenon of ‘hide and die syndrome’
describes the finding of a body that appears to be hidden, for example under furniture or in the cor- ner of a room, etc., often surrounded by disturbed furniture, clothes or other artefacts. It is thought that this phenomenon reflects a terminal primitive ‘self- protective’ behaviour and may be more commonly
Figure 17.16 Numerous superfi cial haemorrhagic gastric erosions of the lining of the stomach in hypothermia. These are
often called ‘Wischnewsky’ spots. Figure 17.17 Frostbite of the knuckles.
Figure 17.15 Pinkish discoloration over the large joints in fatal hypothermia.
17 Heat, cold and ele ctrical tr auma
observed where there is a slow decrease in core body temperature.
■ Electrical injury
Injury and death from the passage of an electric cur- rent through the body is common in both industrial and domestic circumstances. The essential factor in causing harm is the current (i.e. an electron flow) which is measured in milliamperes (mA). This in turn is determined by the resistance of the tissues in ohms () and the voltage of the power supply in volts (V). According to Ohm’s Law, to increase the current (and hence the damage), either the resist- ance must fall or the voltage must increase, or both.
Almost all cases of electrocution, fatal or other- wise, originate from the public power supply, which is delivered throughout the world at either 110 V or 240 V. It is rare for death to occur at less than 100 V. The current needed to produce death varies according to the time during which it passes and the part of the body across which it flows. Usually, the entry point is a hand that touches an electrical appliance or live conductor, and the exit is to earth (or ‘ground’), often via the other hand or the feet. In either case, the current will cross the thorax, which is the most dangerous area for a shock because of the risks of cardiac arrest or respiratory paralysis.
When a live metal conductor is gripped by the hand, pain and muscle twitching will occur if the current reaches about 10 mA. If the current in the arm exceeds about 30 mA, the muscles will go into spasm, which cannot be voluntarily released because the flexor muscles are stronger than the extensors:
the result is for the hand to grip or to hold on. This
‘hold-on’ effect is very dangerous as it may allow the circuit to be maintained for long enough to cause car- diac arrhythmia, whereas the normal response would have been to let go so as to stop the pain.
If the current across the chest is 50 mA or more, even for only a few seconds, fatal ventricular fibril- lation is likely to occur, and alternating current (AC, common in domestic supplies) is much more danger- ous than direct current (DC) at precipitating cardiac arrhythmias.
The tissue resistance is important. Thick dry skin, such as the palm of the hand or sole of the foot, may have a resistance of 1 million ohms, but when wet, this may fall to a few hundred ohms and the cur- rent, given a fixed supply voltage, will be markedly
increased. This is relevant in wet conditions such as bathrooms, exterior building sites or when sweating.
The mode of death in most cases of electrocution is ventricular fibrillation caused by the direct effects of the current on the myocardium and cardiac con- ducting system. These changes can be reversed when the current ceases, which may explain some of the remarkable recoveries following prolonged cardiac massage after receipt of an electric shock.
The victims of such an arrhythmia will be pale, whereas those who die as a result of peripheral res- piratory paralysis are usually cyanosed. Even rarer are the instances in which the current has entered the head and caused primary brain-stemparalysis, which has resulted in failure of respiration. This may occur when workers on overhead power sup- ply lines or electric railway wires touch their heads against high-tension conductors, usually 660 V.
The scene of a suspected electrical death should be reviewed to try and identify causative agents and ensure that no risk persists. Health and safety legislation may require that an electrical death (e.g.
in the work setting) should be fully reviewed to pre- vent further electrical exposure.