Cardiovascular, gastrointestinal and renal system manifestations

During the hypovolemic shock phase, only vital areas of circulation are maintained. As a result of decreased circulating volumes post-burn, the average cardiac output for a moderate to large burn is reduced by 30 – 50 %. Patients with burns over 40 % body surface area experience this drop as early as 15 – 30 minutes post-injury. Cardiac monitoring is essential and concerns are increased if the patient has a pre-burn history of cardiac problems. Electrical burn patients, who arrest at the scene or who experience cardiac arrhythmias post-injury, warrant particular vigilance. Hypovolemic shock and hypoxemia also produce the initial gastrointestinal complications seen post-burn. Lack of circulating blood volume to the splanchnic area results in decreased peristalsis and the development of abdominal paralytic ileus. The stress response post-burn releases catecholamines and may produce stress (Curling’s) ulcers in burns > 50 % body surface area. Sepsis is primarily responsible for ulcers in patients with burns > 50 %. Renal complications are predominantly caused by hypovolemia and the lack of blood volume necessary to adequately perfuse the kidneys. If perfusion remains poor, high circulating levels of hemoglobin from damaged red blood cells and myoglobin from damaged muscle collect in the renal tubules and may clog them, causing acute tubular necrosis.

Table 4. Causes of thermal burns

Chemical

The types of chemical injuries seen are usually related to the geography, industry and culture of the local population. There are more than 25,000 chemicals in the world and most can be divided into 2 major groups: acids and alkalis. Necrotizing substances in the chemicals cause tissue injury and destruction (Fig. 8). Acids, in general, cause coagulation necrosis with protein precipitation. Alkalis produce liquefaction necrosis with loosening of the tissue, which allows the alkali to diffuse more deeply into the tissues.

Fig. 7. Scald burn

Therefore, on a volume-to-volume basis, alkaline material can produce far more tissue damage than acids. The extent and depth of a chemical injury is directly proportional to the amount, type and strength of the agent, its concentration, extent of penetration, mechanism of action and length of contact time with the skin. Chemicals will continue to destroy tissue until they are inactivated by reaction with tissues, are neutralized or are diluted with water. The burning process may continue for variable and, often prolonged, periods of time (i. e. up to 72 hours) after the initial contact with the chemical agent. It is important to remove the person from the burning agent as soon as possible and to begin copiously flushing the area with water. Neutralizing agents should not be used as they may produce additional tissue damage through heat production. Dry chem-

Fig. 8. Chemical burn

icals should be gently brushed off the skin before flushing begins. Most industries have detailed information on the chemicals their workers are exposed to and are required, by Occupational Health and Safety law, to have portable eyewash and shower stations for first aid use. Chemical burns to the eye require an ophthalmology consult, on admission, as late complications, such as corneal ulceration, secondary glaucoma and cataracts, are fairly common. Ingestion of caustic materials may cause chemical burns to the oropharynx, tongue, esophagus, stomach and duodenum. The patient should be given nothing by mouth, closely monitored and fluid resuscitated. Laryngeal edema may occur, producing upper airway obstruction. Endotracheal intubation or tracheostomy may be required to maintain airway patency.

Electrical

Electrical injuries comprise a small portion of the burn population, but the outcomes can be devastating, including deep tissue damage and potential loss of one or more limbs (Fig. 9). Injuries occur mainly in males and are usually occupation-related. When electrical current passes through the body, intense heat is generated and coagulation necrosis results. Tissue anoxia and death are also the result of direct damage to nerves and vessels. The severity of the electrical injury is determined by the type and voltage of the circuit (whether alternating current –AC or direct current – DC), amperage of the current, resistance of the body, pathway of the current and duration of contact. Electrical current takes the path of least resistance through the body. Least resistance is offered by nerves and blood vessels, whereas bone and fat offer the most resistance. If major body organs, such as the heart, brain or kidneys are involved, the damage is more profound than if the current only passed through tissue. In some situations, electrical sparks may ignite the person’s clothing, causing a flame burn, in addition to the electrical injury. If there is an explosion at an electrical panel and the clothing catches fire but no electricity passes through the body, it is termed an electrical flash burn, not an electrical burn. It is an important distinction to make in the early hours post-injury. The severity of an electrical injury can be difficult to

Fig. 9. Electrical burn

Smoke and inhalation injury

determine as most of the damage may be below the skin at the level of muscle, fat and bone. This phenomenon is referred to as the “iceberg” effect. Entry and exit points, produced at the time of the injury, may help determine the probable path of the current and potential areas of injury. The history of the event can provide valuable clues as to what actually transpired at the accident scene. Many electrical injuries occur when a worker is suspended from an aerial basket or ladder and makes contact with a live wire. If the person has fallen post-injury, precautions to protect the head and cervical spine must be taken during transport. Spinal x-rays and neurological assessment are necessary following admission to hospital. Contact with electrical current can cause tetanic muscle contractions that may produce long bone and vertebral fractures.

The person, who has sustained an electrical burn injury, may have also experienced cardiac arrhythmias or arrest post-injury. Immediate CPR is essential following cardiac arrest. He/she then continues to be at risk for cardiac arrhythmias for 24 hours post-burn, and must be monitored and have an electrocardiogram performed on admission to hospital.

Severe metabolic acidosis develops shortly after the injury occurs, because of extensive tissue destruction and cell rupture. Assessment includes arterial blood gas analysis and, if necessary to maintain normal serum pH levels, infusions of sodium bicarbonate. The kidneys also need to be closely

Exposure to smoke and inhalation of hot air, steam or noxious products of combustion can seriously impair ventilatory function. Irritation of the mucosa can cause laryngeal edema and airway obstruction or pulmonary edema and severe respiratory insufficiency. In combination with a major burn, the presence of an inhalation injury can double or triple one’s mortality rate.

Signs and symptoms of smoke inhalation include burns to the head and neck, singed nasal hairs, darkened oral and nasal membranes, carbonaceous sputum, stridor, hoarseness, difficulty swallowing, history of being burned in an enclosed space, and exposure to flame, including having clothing catch fire near the face out of doors (Fig. 10). The most critical period for patients with inhalation injuries is 24 to 48 hours post-burn. The airway becomes edematous and there is increased airway resistance. The respiratory mucosa sloughs, along with loss of ciliary function and poor diffusion of gases.

Smoke and inhalation injuries can be divided into 3 types:

1. Inhalation injury above the glottis. Most smoke/inhalation injury damage (60%) is limited to the upper airway (pharynx, larynx, vocal cords), since the vocal cords and glottis close quickly as a protective mechanism following exposure to smoke or thermal agents, such as hot air or steam. There is redness and blistering. Edema and the onset of rapid airway obstruction, resulting in a respiratory emergency, are the primary concerns with this type of inhalation injury.