Burns and Scalds

Introduction

A burn is an injury caused by heat or by a chemical or physical agent having an effect similar to heat. Most burns are produced by dry heat, and result from contact with a flame or a heated solid object, or alternatively from exposure to the radiant heat of an object. Burns caused by moist heat are described as scalds. Chemical burns are produced by acids and alkalis, or by vesicants especially developed as chemical warfare agents. Microwaves and electricity also produce burns.

Cause and Manner of Death

The severity of a burn caused by dry heat is assessed by two parameters, firstly the depth of the burn injury, and secondly the extent of injury, that is the size of the burn relative to the total body surface area. In assessing burn severity, it is helpful to keep in mind that a common error is to underestimate the depth and to overestimate the extent. In addition to burn depth and extent, other factors determining mortality are the location of the burn, the age of the victim and the presence of other injuries or natural disease. In general, burns involving more than 50% of the body surface carry a poor prognosis. However, age is a major factor for children under 2 years and adults over 60 years, so that in these victims more than 20% surface area involvement carries the same poor prognosis. In the first 48 h period after burning the major threats to life are hypovolemic shock and shock-induced organ failure, primarily renal failure.
The majority of burn deaths are related to accidental domestic fires, in which children and the elderly are particularly at risk, as a result of carelessness coupled with an inability to effectively combat or escape the fire. Alcoholics and drug addicts are a third at-risk group. Suicide by burning is rare, likely because of the pain involved. It is more common in eastern cultures than in the west, and the ritual suicide of a Hindu widow on the funeral pyre of her husband, Suttee, is now prohibited in India. During the period of the Vietnam war, the self-immolation of Buddhist monks during political protests was shown on television worldwide. Rarely a homicide victim may be doused in flammable liquid and then set alight.
Petrol bombs, or Molotov cocktails, are improvised incendiary devices which have become popular in urban disturbances, but do not usually result in death. Necklacing is a method of homicidal burning developed in South African black townships during the apartheid era as a form of punishment for political opponents. It involves placing a vehicle tire around the neck of the victim (hence ‘necklacing’) and setting it alight.
Burns resulting from flaming clothing have a pattern reflecting both the nature of the clothing and the position and movements of the victim. The type of fabric can influence the burn severity. The area and depth of burn tends to be greater with the faster-burning cotton fabrics than with polyester. Higher fabric weight reduces burn severity, and woven fabrics are associated with larger burns than knitted fabrics. Flash burns result from sudden deflagrations burning exposed skin surfaces which are not protected by clothing. These uniform, typically partial thickness, flash burns may be then partly masked by subsequent flame burns from ignited clothing. Burns produced as a result of contact with a hot solid object often leave a brand-mark in the shape of the object, for example the triangular base of an iron. Burns from cigarettes are of the expected size, round and punched out. To produce cigarette burns requires firm contact for some seconds, and cannot occur simply as the result of the accidental dropping of a cigarette, or brushing against one. A cigarette burn implies deliberate infliction, more obviously so when multiple burns are present. They may be seen in victims of child abuse, torture in custody, interprisoner violence and as the result of self-harm in individuals with low self-esteem and personality disorders. Whether fresh injuries or old scars, cigarette burns seen at autopsy always raise serious concerns which demand further investigation.


Burn Severity

The traditional classification of burn depth is into three degrees. A first degree burn destroys only the epidermis. It is characterized by erythema, edema and pain. Sunburn, produced by the radiant heat of the sun, is the most common first degree burn. In general, first degree burns are produced by prolonged exposure to low intensity heat or very brief exposure to high intensity heat. Healing, associated with skin peeling, is usually uneventful and completed in 5-10 days with no residual scarring.
A second degree burn involves both the epidermis and a variable depth of the underlying dermis. The most superficial second degree burns implicate only the upper third of the dermis and are characterized by blister formation. They are extremely painful but heal in 7-14 days with no or minimal scarring. A deep second degree burn extends beyond the upper third of the dermis but not beyond the dermis itself. Paradoxically these deeper burns are less painful as a result of destruction of nerve endings in the dermis. Healing is extremely slow, sometimes requiring months and usually leading to dense scarring, if not treated by skin grafting.
A third degree burn destroys the full thickness of the epidermis and dermis. Heat coagulation of dermal blood vessels leaves the tissue avascular with a characteristic waxy white appearance. If there is prolonged contact between subcutaneous fat and flame then the burn has a leathery brown or black, charred appearance. There is characteristic lack of pain, due to heat destruction of all nerve endings. Spontaneous regeneration of skin (primary re-epithelialization) will not occur and such burns require skin grafting. Burns can also be classified, according to the modern classification, as partial thickness or full thickness, depending on the depth of skin involved. Beneath any burned tissue there is usually a zone of marginally viable tissue which is readily converted into nonviable tissue by physiological stressors. In this way a second degree burn frequently converts into a third degree burn.
The second parameter of burn severity is the extent of injury. This is expressed as the percentage of the total body surface area which is burnt. It can be estimated using the ‘rule of nines’ which divides the body into areas representing 9% or multiples of 9% of the total body surface. Thus the head and neck are 9%, each arm 9%, each leg 18%, the anterior trunk 18%, the posterior trunk 18%, and the genitalia and perineum 1%. In making the assessment a very rough guide is that the victim’s palm is approximately 1% of the total body surface area. In children under 15 years body proportions differ and the estimates must be age-adjusted.

Bodies from Fires

When a body is recovered from a fire, a common problem is to distinguish burns produced during life from postmortem burning of the corpse. Most fire deaths result from carbon monoxide poisoning and smoke inhalation, and the burns to the body are postmortem, but this generality does not assist in resolving the issue in an individual case. It is commonly impossible to exclude burning during life, firstly because postmortem burns may be superimposed on and mask antemortem burns, and secondly because antemortem burns may be indistinguishable from postmortem burns. When the interval between burning and death is short there may be insufficient time for the development of the typical red margin of vital reaction around the burnt area. If time is sufficient then the margin is pronounced and distinctive, measuring 1-2 cm in width. Postmortem burns may be associated with marginal congestion, thought to be the result of tissue contraction, but this is typically a narrow band only a few millimeters wide. In the face of these diagnostic difficulties, and the social pressure to minimize the perceived suffering of the deceased in the eyes of the next of kin, most of these burns are dismissed, rightly or wrongly, as postmortem.
The burning of a corpse produces other artifacts which may create confusion. Characteristically, heat contraction of the muscles causes the limbs to flex and the body to assume a pugilistic (boxer’s) posture, an appearance which does not reflect in any way a struggle at the time of death. Desiccation and loss of the distal limbs may give a false impression of small body size. Heat contraction of the skin produces splits, which are distinguished from wounds produced in life by the fact that they involve charred areas of skin, are uniformly shallow and show no evidence of hemorrhage, as a consequence of heat coagulation of the blood vessels. Contraction of the skin of the torso may induce a prolapse of the rectum and vagina, and contraction of the neck and face forces protrusion of the tongue. Bones may be fractured by the intensity of the heat, but the fractures are unlike those produced by trauma during life. Complex right-angled fractures of long bones (‘street and avenue fractures’) and repeated arcs of fractures are characteristic. Burning of the scalp produces not only an eggshell fracturing of the skull vault but also a postmortem extradural hematoma. This is thought to result from blood boiling in the diploe of the skull and then being forced into the extradural space.

Scalds

Scalds are produced by moist heat which may be steam or any hot liquid, such as water, oil or even molten metal. They are typically less severe than burns produced by dry heat. The scalded area appears erythematous with desquamation and blistering of the usually sharply demarcated area of injury. Unless the liquid is superheated, such as oil, there is no singeing of hairs or charring and carbonization of tissues. Scalds generally occur on exposed skin. In clothed areas the influence of the clothing on the severity of the injury is variable. Fabrics which are poorly permeable protect the skin, whereas absorbent fabrics may hold the hot liquid against the skin, reduce natural cooling, and make the scald more severe.
The pattern of the scald can give an indication as to how it occurred. Major areas of scalding are sharply demarcated with trickle marks reflecting the flow of hot liquid under the influence of gravity. There may be splash marks. Dipping injuries of the limbs appear as well-demarcated glove and stocking scalds. Distinguishing accidental from deliberately inflicted scalds, by evaluating the pattern of injury against the alleged circumstances, is of particular importance in childhood injuries, both fatal and nonfatal. Industrial accidents involving superheated steam produce severe scalds in a pattern similar to flash burns.

Chemical Burns

Chemical burns are produced by corrosive acids and alkalis. The pattern on the skin surface resembles that of scalds caused by liquids, but the injuries differ in physical appearance, reflecting different mechanisms of tissue damage. The amount of tissue damage caused in a chemical burn will depend on the strength of the chemical, its concentration, the quantity applied to the skin surface, the duration of contact, and the extent to which the chemical penetrates the tissues. Chemical burns continue to develop for as long as the causative agent is not neutralized by another chemical, or inactivated as a result of reaction with the body tissues.
Acids with a pH less than 2 precipitate proteins causing coagulation necrosis. The resultant burns are clearly demarcated, dry and with a leathery scab, the color of which depends on the acid. Nitric acid gives a yellow-brown scab, sulfuric acid (vitriol) a black-brown scab, hydrochloric acid (spirit of salt) a white to gray scab, and carbolic acid (phenol) a light-gray to light-brown scab. Prolonged contact with cement may produce a chemical burn since the pH of cement is less than 2. Alkalis with a pH above 11.5 also produced chemical burns. They generally produce more tissue damage than acids because they cause liquefactive necrosis, which facilitates ever deeper penetration of the alkali. The caustic alkalis and ammonium hydroxide leave a gray-white mucoid burn.
Chemical burns from acids and alkalis are almost invariably accidental, and homicide by this method is rare. Throwing liquid corrosives, such as acid, over a victim is more often intended to produce facial disfigurement than death, and to be the act of a spurned suitor. Suicide by the ingestion of strong acid or alkali has now become rare in the developed world because of the ready availability of drugs, which are painless. However, suicide by this method is still seen in poorer countries. Typically there is staining of the lips, and often the cheeks, chin and neck, as well as chemical burns of the mucosa from lips to stomach, sometimes extending into the small bowel. Esophageal and gastric perforations are most common with sulfuric and hydrochloric acids.

Chemical Warfare Agents

One group of chemical warfare agents produce skin burns. The best known of these vesicants is ‘mustard gas’, or more correctly sulfur mustard. It was given its name because of the smell, which has been likened to garlic, mustard, horseradish or leeks. Mustard gas was first used by Germany during World War I, at Ypres. Since then it has been used by the Italians in Ethiopia in 1936, the Japanese against Chinese troops during World War II, and Iraq against Iranian troops in the 1980s. During World War I total mustard gas casualties may have been as high as 400 000, but with a low mortality rate of around 2-3%. Death within 24 h of exposure is very rare, whereas later deaths are the result of respiratory effects or bone marrow depression with associated infections. It was the incapacitating, rather than the lethal, effects of mustard gas that caused it to be named the ‘King of the Battle Gases’ during World War I.
The vapour given off by liquid sulfur mustard rapidly penetrates clothing to damage the underlying skin. The production of blisters is a characteristic of mustard gas, by contrast with acids and alkalis which do not produce blistering when they burn the skin. The mechanism of blister formation is unknown, but it is a specific response of human skin which is not seen in animal studies. Following exposure to sulfur mustard there is a latent, symptom- and sign-free period of some hours. If the exposure is severe, the first sign is erythema, reminiscent of scarlet fever. There is mild skin edema, and itching is common. As the erythema fades, areas of hyperpigmentation are left behind, as occurs with sunburn. By 18 hours typical vesicles appear. These blisters are uncomfortable but not painful in themselves, although they are delicate and easily rubbed off, leaving the now painful blister base. Crops of new blisters may appear as late as the second week after exposure. Analysis of the aspirated blister fluid for thiodiglycol may assist in distinguishing mustard gas blisters from those produced by other chemical warfare vesicants, such as lewisite. Deep burning, leading to full thickness skin loss, is followed by eschar formation. The effects of liquid sulfur mustard on the eye mirror those in the skin. Late onset blindness is a distressing effect of exposure.
Lewisite is another chemical warfare agent which, like mustard, is a vesicant when applied to human skin but not to animals. Unlike mustard gas it is nonpersistent, making it possible for attacks to be launched on previously contaminated ground. However, lewisite is rapidly hydrolyzed when mixed with water, making it ineffective as a weapon under wet conditions. Although the chemical warfare effectiveness of both lewisite and mustard depend on their vesicant properies, lewisite is also lethal. Less than 3 g applied to the skin of an average man, and not washed off or otherwise decontaminated, would be expected to be fatal. Death is typically the result of damage to the respiratory tract, with necrosis of the mucosa and formation of a false diphtheria-type membrane, together with pulmonary edema and congestion, with secondary bronchopneumonia. It has not been used in warfare and deaths have resulted from accidental exposure. A related arsenical vesicant, phenyldichlor-arsine, was used on a large scale during World War I because it was capable of penetrating the respirators then available. Other vesicants similar to lewisite are ethyl-phenyldichlorarsine (known as dick) and methyl-phenyldichlorarsine (known as methyl-dick).

Electrical Burns

The principal bodily barrier to an electrical current is the skin, and once beyond the dermis the current passes easily through the electrolyte-rich fluids. Having entered the body at the entry point, usually the hand, the electricity then exits to earth (ground) via a pathway depending mainly on the relative resistance of the various potential exit points. The current tends to take the shortest route between entry and best exit irrespective of the varying conductivity of the different internal tissues. Alternating current (AC) is more dangerous than direct current (DC), and AC in the range 39-150 cycles per second has the highest lethality. The effects of AC depend on the magnitude, frequency and duration of the current, whereas the voltage is of importance only because it is a factor in determining the current. DC injuries are uncommon but examples include encounters with lightning, car batteries, electroplating, some public transportation systems and some industrial systems. The mechanism of death in electrocutions is most commonly a cardiac dysrhythmia, usually ventricular fibrillation, less commonly paralysis of the respiratory muscles, and rarely a direct effect on the brainstem as a result of passage of the current through the head and neck. Hand-to-hand passage of a high-voltage current has a reported immediate mortality of 60% as a result of cardiac arrhythmia.
Skin burns are a common form of electrical injury and are a pathognomonic marker for death by electrocution. When present, the typical skin lesion is a thermal burn resulting from the heating of the tissues by the passage of the electric current. Tissue damage from this heating effect may be insufficient to produce a visible injury if the surface contact area is broad and the conductivity of the skin is high because of a high water content, two conditions which are usual in electrocutions in the bath. Torture by electricity may be performed using broad wet contact electrodes in order to avoid leaving evidential marks. When they occur, electrical burns on the skin may be of firm contact or spark (arc) type. Both types can occur in the same victim as a result of the irregular shape or movement of the conductor, or movement of the victim during electrocution.
A firm contact electrical burn of entry typically leaves a central collapsed blister, which may reproduce the shape of the conductor, with a surrounding areola of pallor. The blister is created by the steam produced in the heating of the tissues by the electric current. When the current ceases, the blister cools and collapses to leave a crater with a raised rim. Should the blister burst during its formation, as a result of its large size or the continued passage of current, then the epidermis may peel off leaving a red base. Contact electrical burns at exit points are often not seen but should be searched for. When present, in low voltage deaths, they are similar to, but less severe than, the corresponding entry mark. In high-voltage (more than 1000 volts) electrical burns the contact injury of exit often appears as a ‘blow-out’ type of wound. Skin and subcutaneous tissue may be destroyed, exposing thrombosed vessels, nerves, fascia, bones or joints.
With the passage of an electric current, metallic ions from the metal conductor combine with tissue anions to form metallic salts which are deposited in tissues, and may be demonstrated by chemical, histochemical and spectrographic techniques. The histological appearance of electrical skin marks is closely similar to thermal injuries with cellular eosinophilia and nuclear streaming. Some researchers have claimed to be able to distinguish, at the histological level, electrical from thermal injury, but this is disputed. Certainly the combination of the gross appearance and histology will usually permit a firm diagnosis.
A spark (arc) burn occurs when there is an air gap between the conductor and the skin so that the current arcs across the gap as a spark. The distance which the spark can jump is proportional to the voltage, so that 1000 volts can jump a few millimeters, 5000 volts can jump 1 cm, and 100 000 volts can jump 35 cm. The extremely high temperature of sparks, which may be up to 4000°C, causes the epidermal keratin to melt over a small area. After cooling, this leaves a raised brown or yellow nodule of fused keratin surrounded by an areola of pale skin. A brief arc transmits only enough energy to cause a superficial skin burn. These are most commonly seen on the hands. Ocular burns, mostly caused by low voltage arcs, are a particular clinical problem in survivors. High voltage spark burns may cause large areas of skin damage resulting in an appearance of ‘crocodile skin’. Spark burns involving the clothing can cause the clothing to ignite, so that the victim suffers superimposed flame burns.
The severity of the electrical injury to the deep tissues depends on the amperage, i.e. the actual amount of current passing through the tissues. Although it is impossible to know the amperage, it can be inferred from the voltage of the source as either high or low. A low-voltage household source is capable of causing death if a sufficient current passes through the body and 60 mA will produce cardiac fibrillation. However, no deep tissue damage is evident at autopsy because the current pathway is too diffuse to cause thermal damage. Consequently, there are no characteristic internal findings in fatal electrocutions. Skeletal fractures and joint dislocations may occur as a result of tetanic contractions. Skeletal muscle damage leads to release of myoglobin, and muscle-specific intracellular enzymes, with resultant myoglo-binemia and myoglobinuria. A high-tension source producing a current of 5000 mA or more is usually required to produce severe widespread tissue necrosis. Experimental studies have shown that this tissue necrosis is a result of not just heat but also short-term nonthermal effects of electric fields. Although the severity of injury is directly proportional to the duration of the current flow, even very brief exposures to high amperage will produce massive deep tissue damage. These types of electrical injuries are more akin to crush injuries than to thermal burns in as much as the damage below the skin is usually far greater than the outward appearance would indicate. If, after death, the electric current continues to flow then there may be severe damage to the body with peeling and blistering of the skin, charring, and cooking of the underlying tissues. Rarely, thermal burns of this type may be found in a survivor, usually following prolonged contact with over 1000 volts. In these cases, necrosis of deep tissues, both immediate and delayed, often requires limb amputation. Generally, for those who survive an electric shock, the prognosis is good and the majority make a complete recovery, so that delayed deaths from electrocution are uncommon.
Most electrocutions are accidental and the bathroom is a place of particular danger in the home. An unusual and characteristic finding in electrocution in the bath is that the subsequent development of hypostasis is limited by the water-line, resulting in a stark and unusual demarcation. Currents of less than 0.2 mA will not cause a skin injury or death by electrocution but are sufficient to evoke a startle reaction and may precipitate a lethal accident, such as a fall from a height. Suicidal electrocution is uncommon but increasing, and may be difficult to distinguish from an accident. Homicidal electrocutions are also rare, except in a judicial setting, the first execution by electricity having been carried out in Auburn Prison, New York in 1890.

Lightning

Each year, lightning causes hundreds of deaths worldwide. A lightning bolt is produced when the charged undersurface of a thunder-cloud discharges its electricity to the ground. Very large electrical forces are involved with currents up to 270 kA. The lightning may directly strike the victim, strike a nearby object and then jump from the object to the victim (a side flash), or strike an object which conducts the lightning to a victim in contact with the object, e.g. a worker in contact with a metal crane. The lightning current may spread over the body surface, pass through the body or follow both routes. The resulting injuries may be electrical, burns, or blast from the wave of heated air created by the lightning strike. The pathological findings range from a completely unmarked body to bizarre and extreme trauma. An unmarked dead body found in the open should raise the possibility of a lightning strike. When injuries are present, the clothing may be torn and the shoes burst, with the body partly stripped and the clothing scattered. The hair may be seared, patterned skin burns reflect the heating of metal objects such as zippers, severe burns with blisters and charring may be present, and rupture of the tympanic membranes, fractures and lacerations may be found. Fern-like or arborescent patterns on the skin are pathognomonic of a lightning strike but are rarely seen. They appear as irregular red marks, several inches long, which tend to follow skin creases and the long axis of the body.

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