Burn, chemical, and electrical injuries

Thermal (high temperature) burns

A thermal burn results when tissue temperature exceeds the level in which molecular kinetic energy exceeds the bond energies that stabilize biomolecular structure. This results from conduction, convection, and/or radiative heating and are usually not spontaneously reversible, although immediate cooling can modify some critical aspects. Thermal burn injury may also result from internal heat generation in diseases such as malignant hyperthermia. The extent of tissue heat damage depends on the tissue type, the immediate tissue temperature history, and the amount of preconditioning.

Cells have the capabilities to increase their tolerance to heat stress through an adaptive preconditioning process. This process involves upregulating synthesis of stress proteins that repair or remove heat-damaged molecules, seal membrane disruptions, and suppress oxidation stress. Only when the extent of thermal damage exceeds cellular repair capabilities does loss of cell and subsequent tissue viability result, which manifests as a burn injury. Basically induced thermal tolerance increases cellular injury repair rates, thus allowing tissues to subsequently survive more than normal heat exposure.

Characteristic molecular alterations that occur at supraphysiological temperatures include disruption of cell membranes, aggregation of unfolded proteins, onset of a cellular oxidative stress response to unfolded proteins in cellular organelles and in the cytoplasm, and extracellular damage to collagen, non-collagenous proteins, and activation of degradative proteases, vascular disruption with hemorrhage, blood coagulation, and dehydration. Of course, the skin temperature history (i.e., magnitude and duration) in nearly all cases of skin burn injury is anatomically non-uniform, which results in a non-uniform distribution of thermal burn injury and is clinically classified according to skin burn depth ( Fig. 18.1 ).

Flash and flame burns

Although the tissue damage mechanisms associated with “flash” and “flame” burns are similar, they are used in different ways. Both flame and flash phenomena pertain to hot, ionized combustion aerosols emanating from a fire or explosion. Flash and flame burn injuries are the most common cause of adult burn admissions. Flame burns result from exposure to heat produced by an ongoing fire. The exposure likely involves longer contact time because it involves a human response time. This results in deeper burn injuries such as partial- and full-thickness skin burns. In contrast, flash burns result from brief exposure to a propagating thermal energy pulse emanating from ignition of flammable gases, high-energy electrical arc ( Fig. 18.2 ), or ionizing radiation. Although the temperatures of arc or flash may reach 10–20 thousands of degrees, they are composed of gases with very low heat capacity which means the efficiency of heat energy transfer is fortunately low. Because of this and the brief exposure, flash burns usually do not penetrate clothing. Typically, flash burns are manifested only on exposed areas of skin and are superficial.

Scald burns

Scald burns result from skin contact with hot liquid or steam. In modern societies, scald burns are second in incidence to flame burns. Most often, the burns result from a cooking accident and often involve a mixture of water and grease. Tragically, children are the most common victims.

Scald burn depth is often more difficult to clinically judge because scalds are lower temperature thermal injuries than flame injury ( Fig. 18.3 ). This is particularly true for patients with darker skin. Thus, scald-injured skin’s structural changes are less noticeable compared to flame burns unless there are petechial hemorrhages visible indicating rupture of mid-dermal and subdermal microvasculature. In the absence of petechial hemorrhage, the depth of scald burn skin injuries is often not visually apparent for 48–72 hours when the manifestation of autolytic degradation is obvious. Duration of hot liquid contact is a major deterministic factor in the depth of burn in scald injuries. Thus, hot water immersion scalds are typically deeper than a hot water spill scald with liquid at the same temperature. Skin surface contact with 60°C (140°F) water creates a deep dermal burn in 3 seconds but will cause the same injury in 1 second at 69°C (156° F). Also, the burn tends to be a bit deeper in skin folds and clefts.

Scald burn damage kinetics depend on the barometric pressure, being slower in higher altitudes than at sea level. Unless superheated at pressures higher than 1 atmosphere or in a microwave, the maximum skin temperature reached in hot water can be 100°C at sea-level. Also, because wet skin cools by evaporation, the duration of tissue contact with scalding temperatures depends on factors that limit evaporation rate such as clothing, oil, or other water vapor barriers. If the water contains oils or lipids, as in soups, evaporative cooling is slowed, resulting in longer burn duration and a deeper skin injury.

Hot object “contact burns”

Contact burns involve mechanical contact with a hot, thermally conducting object (e.g., cooking pan or radiator). Domestic contact burns are caused by direct mechanical contact with lit cigarettes, space heaters, stoves, ovens, irons, exhaust pipes, etc. Resultant burn depth depends on the capability to transfer heat energy to the skin. Thus, skin contact with a hot metal rod can be expected to produce a deeper burn than a hot plastic rod at the same temperature.

Contact burns are often associated with workplace-related hands, patients prone to seizures, and use of intoxicating substances. They are also seen in elderly people after a loss of consciousness; such a presentation requires a workup of the cause of syncope. In the industrial setting, contact burns commonly result from contact with hot metals, thermoplastic composites, glass, or coals. Because the heat energy transfer is large, contact burns often involve full-thickness skin and subcutaneous tissue.

Tar and asphalt burns

Hot tar and asphalt burns occur in workers engaged in surfacing pavement and roads, roofing, and other industrial applications. Tar is an oil composite that solidifies when cooled to body surface temperatures. When hot tar makes contact with skin, it adheres and solidifies in the wound making it difficult to remove without causing further injury. The tar usually retains sufficient heat to produce prolonged damaging temperatures resulting in deep skin burns. Tar itself is also chemically toxic to tissues.

Often, the tar is cool by the time the patient arrives at the medical facility. Injuries typically occur on the exposed skin of the face and extremities, and the burn is of variable depth ranging from deep partial to full thickness.

Electrical injury

Electrical injuries represent 3%–5% of burn trauma admissions. However, injuries are often among the most devastating and therefore challenging to manage. Electrical injuries are more difficult to clinically assess because tissues can be injured by either or both thermal and non-thermal injury processes. Furthermore, various modes of electrical injuries can result from electrical current exposure at any frequency in the electromagnetic spectrum ( Table 18.1 ). The abbreviation “DC” (i.e., direct current) indicates the current frequency to be zero, the current flows constantly in one direction, and “AC” (i.e., alternating current) indicates that the current is changing direction of flow (i.e., alternating polarity) with time. The injury mode(s) depend on the voltage, power capacity, and frequency of the power source. The vast major of electrical shock patients seeking medical attention have had contact with commercial electrical power sources which operate between 50 and 60 Hz (i.e., 1 Hz = 1 wave cycle per second). However, electrical power in the form of radiowaves, microwaves, infrared, visible, and ionizing irradiations are also capable of inflicting injury, and they each have unique pathophysiology and clinical manifestations.

At frequencies greater than approximately 50,000 Hz (i.e., low frequency radio waves), electrical power can radiate across air gaps from the power source into the body. However, the body does not absorb ambient radio waves very efficiently, so very high power is needed to cause injury. However, a thermal burn injury can result when direct mechanical contact is made with an energy low radiofrequency power source. Electrocautery devices used for surgical procedures operate in the low radiofrequency range. At much higher frequencies, mechanical contract with the conductor is not required for tissue injury. Common domestic microwave ovens operate in the gigahertz frequency range (10 ⁹ Hz), and infrared food warmers operate in the terahertz (10 ¹⁸ Hz) range. Although they induce electrical current flow in tissues, these devices cause injury by heating rather than cellular disruption by electrical forces (i.e., electroporation). Accidental brief microwave and infrared radiation burns are usually superficial. To summarize the effects of electrical shock over a range of electrical field frequencies, Table 18.1 presents a classification of electrical injury according to frequency regime.

Electrical shocks from commercial electrical power are the second most common cause of workplace injury. The clinical manifestations depend on the amount of electrical current, the duration of contact, and the anatomic path of the current through the body. When relating the amount of current to the contact voltage, the length of the current path between electrical contact points, the resistance of skin coverings such as gloves, shoes, and clothing are essential to consider. With moist skin, the VLF electrical resistance of a current path from one hand to the other is about 1000 ohms and from hand to both feet is about 750 ohms. The highly resistive epidermal layer is instantly penetrated by voltages greater than 60–100 volts.

For triage purposes, electrical shock injuries are often categorized as “low-voltage” or “high-voltage” depending on whether the contact voltage is below or above 1000 volts, respectively. The scientific basis for this stratification is not clearly defined, but it does correlate with the probability that arc-mediated electrical contact will precede direct body mechanical contact with the energized conductor. For low-voltage shocks, direct mechanical contact with the power source is usually required to initiate current flow, whereas for high-voltage shocks, the current begins to flow through an electrical arc before mechanical contact is made. Some have proposed a mid-voltage (i.e., 400–1000 volts) shock category which makes medical sense in terms of predicting therapy and prognosis. In addition, other important injury-determining factor parameters are duration of electrical contact and the anatomic path of the current through the body. For example, although static electrical shocks typically involve more than 1000 volts, they do not cause injury because the current is small and it only passes on the outer surface of the body.

If mechanical contact with the power source occurs, it can be difficult to impossible to voluntarily disconnect from the contact because the skeletal muscle stimulation is dominated by the electrical shock current rather than the central nervous system. Thus, shock times are typically longer in low-voltage shocks. Electrical shock by commercial electrical power can produce a range of neuromuscular effects ( Table 18.2 ). Of course, the most life-threatening is the immediate risk for cardiopulmonary arrest when the current passes through the heart, especially during the myocardial repolarization phase.

In the case of contact with an energized high-voltage conductor, electrical arcing will mediate electrical current flow to the victim before mechanical contact. This introduces a third mechanism of injury: mechanical trauma from the thermoacoustic blast. This is a particularly important mechanism of injury and mortality in short circuits involving very high capacity electrical power in a closed space. The gases released from the arc will further short circuit paths that generate thunderous pressures and temperatures. High-voltage contact arcs can reach very high temperatures leading to corneal burns and clothing ignition.

A common misconception is to identify skin contact wounds as “entrance” and “exit” wounds. The skin contact wounds resulting from passage of commercial AC current are all “entrance” and “exit” wounds because the current travels in and out of each body contact ( Fig. 18.4 ). If the skin is wet, especially from salt water, the skin’s electrical resistance drops allowing subcutaneous tissue damage to occur without skin burns. For electrical shock injury, the skin surface area damage is not reflective of the injury extent. The damage is more volumetric and scattered along the current path, often requiring diagnostic imaging to locate and quantify ( Fig. 18.5 ).

Peripheral nerve and skeletal muscle tissues are most vulnerable to the damaging effects of the electrical field during electrical shock. Just 14–16 milliamperes of current passing through the forearm induces tetanic contractions of muscles controlling handgrip, which may prevent a person from voluntarily releasing the electrical conductor (see Table 18.2 ). Joint dislocations and fractures may result from the muscle spasm as well. A current of 50 milliamperes or more passed through the chest can result in cardiopulmonary arrest within 1 second. Non-thermal electric injury to nerves and muscles can occur in milliseconds while taking seconds for burns to occur. Thus brief shocks commonly result in neuromuscular function disturbances in the absence of thermal burns.

Disruption of skeletal muscle membranes leads to release of myoglobin and hemoglobin that enter the circulation and muscle edema, which results in muscle compartment syndromes. Release of myoglobin into the urine is a characteristic feature of severe electrical shock injury. Renal failure may result from intrarenal aggregation of myoglobin. Direct electrical shocks to the head may cause increased intracranial pressure as well. Case reports of electrical injury also have been reported secondary to cardioversion.

Lightning is another common form of electrical shock. Approximately 200 deaths occur per year in the United States due to lightning injury. Most of the lightning current passes along the skin surface and around the body to ground through the lightning arc. There are often superficial epidermal burn marks that have a characteristic fern-leaf pattern, but the burn does not extend into the dermis for various reasons. Cardiac and central neurological arrest often occurs due to the magnetic pulse-induced electrical currents. Transient central and peripheral neurological arrest is called keraunoparalysis that causes delay in recovery of brain function as well as autonomic nervous system malfunction. CNS viability signs are not useful to guide CPR efforts. Thus, CPR should be continued longer than for other causes of cardiac arrest. Peripheral autonomic neurological malfunction can persist for longer time periods in lightning injury survivors.

Radiation Injuries

Radiation injury results from tissue absorption of either ionizing or non-ionizing radiating electromagnetic waves or both at doses above tissue tolerance. Sub-atomic particle beam irradiation is classified as ionizing irradiation because it can ionize molecules that absorb the particle. Radiation effects on tissue are dependent on both fraction of the radiation energy absorbed and the relative biological effectiveness of the absorbed radiation on the tissue. Both of these factors depend on the tissue type, water content, oxygenation, and other variables.

Regarding non-ionizing radiation, such as infrared or microwave radiation, the radiating energy is absorbed by tissue molecules resulting in tissue heating. Light is absorbed at the sub-molecular level, resulting in heating and shifts in electron orbitals, but does not have enough energy to ionize the molecule. Intense laser light may cause thermal burns or explosive water boiling to disrupt tissues. Non-ionizing radiation from a hot fire or an electrical arc is a frequent cause of industrial thermal burns.

Ionizing radiation transmits higher energy and shorter wavelength than non-ionizing radiation. Ionizing radiation disrupts atomic structure and causes chemical reactions in the tissue. In tissue, water is the primary absorber. Ionizing irradiation causes water and molecular oxygen to react and produce hydroxyl radicals with an unpaired electron in the valence shell. Unpaired radicalized electrons on the outer shell are very reactive with other biomolecules causing damage to DNA, proteins, lipids, etc. Most commonly, the cell and extracellular matrix damage is caused by generation of hydroxyl (OH*) free radicals in oxygenated water. The higher the tissue water and oxygen content, the greater the radiation-induced cell injury.

The intensity of ambient ionizing irradiation energy to which a person can be exposed is measured in Roentgens (R); the amount absorbed into the tissue is measured in Gray (Gy). For a typical person, absorbing X-ray or gamma-ray doses greater than 5 Gray (Joules/kilogram) to a body part like the hand or scalp causes molecular alterations in proteins and nucleic acids that results in radiation fibrosis or burns. With preconditioning that upregulates DNA repair and intracellular protein removal mechanisms, higher doses of radiation could be better tolerated by tissue. Total body absorption of more than 2–3 Gy is associated with a high mortality rate.

The most common cause of radiation burn is heavy sun exposure. Sunlight produces a wide spectrum of radiating energy from infrared to cosmic energies. In typical sunburn, it is the heavy dose of the infrared heating and ionizing ultraviolet (UV) that does the most damage. Cosmic irradiation also contributes. UV radiation produces aqueous phase oxidative free radicals in the epidermis and dermis. When free radical scavenging mechanisms are exceeded, biomolecular damage occurs. It is rare that the burn depth is greater than epidermal or superficial dermal. Also, nucleic acids are able to directly adsorb some wavelengths of UV radiation known as the UVB wavelength spectrum. UVB radiation causes direct damage to DNA in the form of cross-links and double-stranded breaks. If this damage is not reparable by the cell the result is an increased risk of cell death or malignant transformation. Clinical manifestations are painful partial-thickness burns and blistering. Sunscreen lotions absorb the UV and increase the amount of sun exposure required to cause a burn. However, until recently they did not totally shield the entire UV range. There is some evidence that use of narrow-band (i.e., UVB) sunblock is associated with other long-term consequences related to prolonged exposure to DNA reactive irradiation outside of the blocked UVB band.

Radiation injuries also occur from therapeutic, accidental, space travel, or military use of ionizing irradiation. The molecular target of the radiation depends on the type of radiation. Severe immune compromise due to neutropenia and bleeding secondary to thrombocytopenia are seen over a period of 3–5 weeks. At higher levels of exposure (30–100 Gy), the membranes of cells, even non-proliferating nerves and muscle, are damaged leading to loss of tissue viability within 6–24 hours. Radiation injury during space travel is a major unsolved problem. Outside of planetary magnetic fields, the electrons emitted from the sun at relativistic speeds would certainly cause burns and must be shielded. Also, subatomic particles, especially fragments of heavy metal nuclei (High Z), traveling through space are almost impossible to shield. Of course, such High Z radiation would damage tissue.

Basic differences between modes of cellular burn injury can be appreciated in Fig. 18.6 .

Frostbite

Tissue tolerance to hypothermic temperatures is tissue type specific. Neurological and neuromuscular tissues stop functioning at temperatures less than 21°C for more than 20–30 minutes because electrical and chemical signaling stops working. Skin tolerates hypothermia for longer time frames (i.e., 19–24 hours). At temperatures below freezing the mechanism of injury changes. Freezing with ice formation in any tissue causes damage by disrupting cell membranes and denaturing cellular proteins.

Frostbite is a clinical diagnosis applied to tissues injured by freezing. Freezing temperatures result in disruptive intracellular ice formation and denaturation of proteins. Ice formation in tissues concentrates electrolytes around proteins that leads to protein unfolding and aggregation. Tissue freezing also dehydrates cells in addition to promoting ice crystal propagation through cell membranes. The thaw cycle also causes injury by osmotic rupture of tissue cells that survived the freezing process.

Loss of circulation in the frozen tissue, as well as the reperfusion consequences on rewarming, also contribute substantially to the molecular denaturation of frostbite injury. Demographically, the majority of frostbite cases arise in the homeless or disabled populations in climates with cold winters. Ethanol consumption accelerates cool-down by increasing vasodilatation and rapid heat loss. Most commonly, distal extremities, ears, and other ambient air-exposed areas of the face are involved.

Burn injury in children

Burn injuries in children typically involve home cooking accidents. Another 10% of pediatric burns are due to non-accidental injury, and these burn victims will occasionally have other non-burn-related trauma. Diagnosing pediatric burns also involves an investigative component to understand the risk factors that precipitated the burn. A social history is extremely important. Abuse is more common in poor households with single or young parents. Detecting these injuries is important, as many children who are repeatedly abused eventually suffer a fatal injury. Usually children less than 3 years old are affected. As with other non-accidental injuries, the history and the pattern of injury may arouse suspicion ( Fig. 18.7 ).

Burn center care with experienced pediatric burn resuscitation and pain management is more important than for young adults.

Chemical injuries and burns

Chemical injury occurrences are roughly equally distributed between industrial and domestic situations. They most commonly result from inadvertent contact with toxic polishers, paints, cleaners or solvents. Cement burns make up approximately one-quarter of all chemical burns.

Current classification of chemical burns began with the efforts of Carl Jelenko III, who proposed stratification of chemical injuries into six broad categories based upon mechanism of action: reducing agents, oxidizing agents, corrosive agents, protoplasmic poisons, desiccants/vesicants, and acids/bases. The toxic chemicals involved are often strong acids or alkalis, especially in domestic disputes. Extent of tissue resulting from toxic chemicals are almost always dependent the concentration of the chemical, the duration of contact, mechanism of action of the chemical, and phase of the chemical agent (liquid, solid, or gas). The various mode of tissue damage range from redox reactions, corrosion, denaturation of proteins, disruption of cell membrane lipid bilayers, chelation of important ions, vesicants, and desiccants. Some chemicals actually cause thermal burns through exothermic reactions.

Chemicals diffuse into tissues causing damage until they are inactivated by reaction with tissue and/or removed by therapeutic intervention or by blood perfusion of the tissue. Different taxic chemicals behave the differently when in contact with tissue. Tissue injury caused by strong acid spills are characteristically less deep than those caused by strong bases. Acids denature proteins and dehydrate tissues, which makes the tissue less permeable to the acid (i.e., tanning). Tissue injury resulting from contact with strong bases results in hydrolysis, peroxidation and liquefication of tissue lipids. This facilitates tissue penetration to cause deeper penetration and damage to tissues. Some toxic chemical injuries to the skin may appear superficial because of minimal discoloration, but are actually deep dermal or full thickness. An example of this type of chemical injury is caused by skin contact with wet cement (i.e., calcium oxide [CaO]).

Acid burns