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An injury commonly associated with burns is smoke inhalation (see 9) Suspicion of inhalation injury is aroused when the nasal hairs are singed, the mechanism of burn involves closed spaces, the sputum is carbonaceous, or the carboxyhemoglobin level exceeds 5% in nonsmokers This suspicion should lead the clinician to institute early intubation before airway edema supervenes The products of combustion, not heat, are responsible for lower airway injury Electrical injury that causes burns may also produce cardiac arrhythmias that require immediate attention Pancreatitis occurs in severe burns Prior alcohol exposure may exacerbate the pulmonary components of burn injury Toxic epidermal necrolysis (TEN) occasionally occurs following sulfonamide or phenytoin administration (see 6) If TEN is severe, patients are best transferred to a burn unit and treated as having severe burn injury Corticosteroid therapy should be avoided

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and subclavian vein laceration when such a line is placed in a volume-depleted patient Femoral lines provide good temporary access during resuscitation Venous access catheters placed in the emergency department should be changed within 24 hours because of the high risk of nonsterile placement Distal saphenous cutdown is occasionally necessary An arterial line is useful for monitoring mean arterial pressure and drawing blood

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The actual burn injury is only the incipient event in a cascade of deleterious local tissue and systemic inflammatory reactions leading to multiorgan system failure in the severely burned patient Locally, substance P, serotonin, prostaglandins E2 and F2 , histamine, platelet-activating factor, nitric oxide, bradykinin, and leukotrienes B4 and D4 play a role in the increased local capillary permeability and initiation of the systemic inflammatory cascade Systemically, levels of interleukin-2, -4, -6, and interferon-gamma (IFN- ) are elevated in proportion to the severity of the burn injury, perhaps as part of a generalized systemic release of inflammatory mediators and generalized macrophage dysfunction There is often an altered CD4/CD8 (T helper/T suppressor) cell ratio In addition, in the first 24 hours following a significant burn, there is production of tumor necrosis factor and IFN- , which in turn stimulate production of the enzyme nitric oxide synthetase in hepatocytes After 24 hours, lipopolysaccharide plays a dominant role in its production Nitric oxide has been proposed as a mediator of the acute inflammation Transforming growth factor beta and IL-10 and a markedly elevated level of IL-6 serve as harbingers of a declining clinical course in severely burned patients

Generalized capillary leak results from burn injury over more than 25% of total body surface area This often necessitates replacement of a large volume of fluid There are many guidelines for fluid resuscitation The Parkland formula relies on the use of lactated Ringer s injection The fluid requirement in the first 24 hours is estimated as 4 mL/kg body weight per percent of body surface area burned Half the calculated fluid is given in the first 8-hour period The remaining fluid, divided into two equal parts, is delivered over the next 16 hours An extremely large volume of fluid may be required For example, an injury over 40% of the total body surface area in a 70-kg victim may require 112 L in the first 24 hours [4 mL 40(%) 70 (kg) = 11,200 mL] The first 8-hour period is measured from the hour of injury These guidelines may be inadequate, since crystalloid solutions alone may be insufficient to restore cardiac preload during the period of burn shock Deep electrical burns and inhalation injury increase the fluid requirement Adequacy of resuscitation is determined by clinical parameters, including urinary output and specific gravity, blood pressure, and central venous catheter or, if necessary, Swan-Ganz catheter readings

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