Physiologic Implications of Burn Injury

Physiologic Implications of Burn Injury

1. Deep thermal injury destroys skin, the body's barrier to the external environment. Skin plays a vital role in thermal regulation, fluid and electrolyte homeostasis, and protection against bacterial infection. Significant heat and protein loss, massive fluid shifts, and infections all commonly occur in patients with severe thermal injuries. In major burns, circulating mediators trigger systemic inflammation, hypermetabolism, and immune suppression. There is also diffuse alteration in the permeability of cell membranes to sodium, resulting in generalized cellular swelling. Microvascular injury results from local damage by heat and from the release of vasoactive substances from the burned tissue. Therefore, edema occurs in both burned and unburned tissues.
   1. Cardiovascular effects
      1. Alterations in microvascular permeability result in a transcapillary fluid flux and significant tissue edema 12 to 24 hours after a thermal injury. Large amounts of water, electrolytes, and proteins are lost into the extravascular space leading to intravascular fluid depletion and hypovolemic shock (burn shock).
      2. Immediately after a burn injury, the cardiac output is frequently reduced due to decreased preload and myocardial depression, possibly due to circulating humoral factors. Blood pressure may be normal due to increased systemic vascular resistance (SVR). The magnitude of these pathophysiologic changes depends on the size and the depth of the burn injury.
      3. The cardiovascular response 24 to 48 hours after successful resuscitation of a major burn is characterized by an increase in cardiac output and reduced SVR, consistent with the pathophysiology of the systemic inflammatory response syndrome.
   2. A hypermetabolic state develops 3 to 5 days after the burn injury. For major burn injuries, the estimated caloric need is 1.5 to 1.7 times the calculated basal metabolic rate, and the protein need is near 2.5 g/kg/d. Early initiation of enteral feeding may decrease muscle catabolism and reduce bacterial translocation through the intestinal mucosa. Ambient temperature should be kept within the thermoneutral range to avoid cooling and a further increase in the metabolic rate.
   3. Capillary leakage results in hemoconcentration immediately after injury. Despite apparent adequate fluid resuscitation, the hematocrit level often remains increased during the first 48 hours after injury. Bleeding from wounds and a shortened erythrocyte half-life, however, can result in anemia.
   4. Microaggregation of the platelets in the skin and smoke-damaged lung and aggressive volume resuscitation result in early thrombocytopenia after major burns. Thrombotic and fibrinolytic mechanisms are activated, and disseminated intravascular coagulation may complicate the course of a massive burn injury. A decrease in antithrombin III, protein C, and protein S levels can increase the thrombogenicity of these patients later in their clinical course and theoretically can cause venous thrombosis and pulmonary embolism.
   5. Acute renal failure is not uncommon in patients with major burn injury and is associated with high mortality. Decreased renal blood flow secondary to hypovolemia and decreased cardiac output, as well as increased levels of catecholamines, aldosterone, and vasopressin, can contribute to renal failure. Other mechanisms include nephrotoxic effects of drugs, rhabdomyolysis, hemolysis, and sepsis (see Chapter 4).
   6. Gastrointestinal function is diminished immediately after burn injury, secondary to the development of gastric and intestinal ileus. The stomach should be adequately vented with a nasogastric tube.
      1. Curling ulcers (mucosal erosion) will occur at variable times after major burns and may lead to gastric hemorrhage or perforation. These ulcers seem to be more common in children than in adults. Therapy consists of antacids, histamine (H₂) receptor antagonists, and proton pump inhibitors.
      2. Other gastrointestinal complications of burns include esophagitis, tracheoesophageal fistula (from prolonged intubation and the presence of a nasogastric tube), hepatic dysfunction, pancreatitis, acalculous cholecystitis, and mesenteric artery thrombosis.
   7. Infection of burned areas delays healing and prevents successful skin grafting. Bacterial invasion of underlying tissue may result in septicemia. Common organisms involved are staphylococci, β-hemolytic streptococci, and gram-negative rods such as Pseudomonas and Klebsiella species. Local treatment with topical antimicrobials and early skin grafting are important measures to reduce risk of infection.
2. In electrical burns, current creates thermal energy that destroys tissue, particularly tissues with high resistance such as skin and bone. Exposure to high voltage can result in compartment syndromes, fractures of long bones and the axial spine, myocardial injury, and rhabdomyolysis with subsequent renal injury.
3. In chemical burns, the degree of injury depends on the chemical, its concentration, duration of contact, and the penetrability and resistance of the tissues involved. Some substances producing chemical burns, such as phosphorus, are absorbed systemically, producing significant and often life-threatening injury. Hydrofluoric acid exposure will cause severe hypocalcemia and requires close monitoring of serum calcium levels. Subeschar injection of calcium gluconate and emergent wound excision may be indicated.