Determination of the size and depth of a burn sets the guidelines for resuscitation, as well as the indications for surgical intervention (Table 52-7: New Proposed Rule to Estimate Body Surface Areas of Normal and Obese Patients). Thermal trauma caused by flames in a closed space is likely to be associated with airway damage. Burns caused by electrocution may show little external evidence but may be associated with severe fractures, hematomas, visceral injury, and skeletal and cardiac muscle injury. A severe burn is a systemic disease that stimulates the release of mediators producing wound edema and immune suppression, hypermetabolism, protein catabolism, insulin resistance, sepsis, and multisystem organ failure. Patients with burns >40% of total body surface are consistently develop catabolism and weight loss.

1. Airway Complications
   1. Respiratory distress in the initial phase of a burn is usually caused by airway injury involving the pharynx or the trachea.
   2. The development of parenchymal lung injury takes approximately 1 to 5 days and presents with the clinical picture of ARDS.
   3. Administration of the highest possible concentration of O₂ by facemask is the first priority in moderately to severely burned patients with patent airways.
   4. The chest radiograph, ABGs, and pulmonary function test results are usually normal in the immediate postburn period (should be performed at this time for later comparison).
2. Ventilation and Intensive Care
   1. Hypoxemia may persist despite tracheal intubation, ventilation with PEEP, bronchodilators, and suction of airway secretions. In the first 36 hours, this is caused by acute pulmonary edema. From the second to the fifth day, hypoxia may result from atelectasis, bronchopneumonia, and airway edema after mucosal necrosis and sloughing, viscous secretions, and distal airway obstruction. Later the patient may develop nosocomial pneumonia, hypermetabolism-induced respiratory failure, and ARDS.
   2. Treatment of these complications includes ventilatory maneuvers such as low tidal volume (5–6 mL) with titrated PEEP, bronchoscopic lavage, antibiotics, and chest physiotherapy.
3. Carbon Monoxide Toxicity (Table 52-8: Symptoms of Carbon Monoxide Toxicity as a Function of the Blood Carboxyhemoglobin Level)
   1. In burn victims, CO inhalation is almost always associated with smoke inhalation.
   2. A normal oxygen saturation on a pulse oximeter does not exclude the possibility of CO toxicity, although low arterial O₂ saturation measured by a cooximeter should raise the suspicion.
   3. The patient's inspired oxygen should be maintained at the highest possible concentration, even when there is no evidence of significant smoke-induced lung injury, until CO toxicity is ruled out by measurement of blood carboxyhemoglobin (COHb).
4. Cyanide Toxicity. Another cause of tissue hypoxia in burned patients is CN^– toxicity. Cyanide (hydrocyanic acid) is produced by incomplete combustion of synthetic materials and may be inhaled or absorbed through mucous membranes.
   1. As in CO toxicity, the usual clinical presentation is unexplained metabolic acidosis.
   2. Nonspecific neurologic symptoms such as agitation, confusion, or coma are also common findings.
   3. Elevated plasma lactate levels in severe burns may result from hypovolemia or CO or CN^– toxicity. (Lactic acidosis after smoke inhalation in a patient without a major burn suggests CN^– toxicity.)
   4. The definitive diagnosis can be made only by determination of the blood cyanide level, which is toxic above 0.2 mg/L and lethal at levels beyond 1 mg/L.
   5. The pulse oximetry reading will be accurate in the absence of CO toxicity and nitrate therapy–induced methemoglobinemia.
5. Fluid Replacement (Table 52-9: Guidelines for Initial Fluid Resuscitation after Thermal Injury)
   1. Crystalloid solutions are preferred for resuscitation during the first day following a burn injury; leakage of colloids during this phase may increase edema.
   2. An increase in Hct during the first day suggests inadequate fluid resuscitation.
   3. Blood replacement is usually not initiated until the Hct is below 20%.
   4. Standard clinical end points of resuscitation such as urine output and vital signs are used routinely to guide fluid therapy.

Trauma and Burns

1. Initial Evaluation and Resuscitation
2. Cervical Spine Injury
3. Direct Airway Injuries
4. Management of Breathing Abnormalities
5. Management of Shock
6. Early Management of Specific Injuries
7. Burns
8. Operative Management
9. Management of Intraoperative Complications
10. Electrolyte and Acid–Base Disturbances
11. Early Postoperative Considerations