The pharmacologic modulation of the hypermetabolic response to burns.
Patients with burns less than 40% TBSA do not have catabolism unless sepsis develops. Those with burns more than 40% TBSA always experience catabolism, which causes metabolic derangements that persist for at least 1 year after the injury in most body tissues. The accomplishments of the past decade have placed us in the midst of an exciting paradigm shift from what used to be a primary concern (ie, mortality) to areas that are more likely to enhance the quality of life of burn survivors. Modulating postburn hypermetabolism for the burned patient is of overwhelming importance in both the immediate care stage and the rehabilitative stage. Postburn hypermetabolism cannot be completely reversed but may be manipulated by nonpharmacologic and pharmacologic means. Early burn wound excision and complete wound closure, prevention of sepsis, the maintenance of thermal neutrality for the patient by elevation of the ambient temperature, and graded resistance exercises during convalescence are simple, highly effective primary treatment goals. Although the initial burn injury and sepsis-related complications principally determine the extent of the metabolic response in burn victims, obligatory activity, background- and procedural-related pain, and anxiety also greatly increase metabolic rates. Judicious maximal narcotic support, appropriate sedation, and supportive psychotherapy are mandatory if their effects are to be minimized. Several anabolic and anticatabolic agents are available for use during immediate care and rehabilitation. Exogenous, continuous low-dose insulin infusion, beta-blockade with propranolol, and the use of the synthetic testosterone analogue oxandrolone are the most cost-effective and least toxic therapies to date. These greatly assist therapeutic minimization of the loss of lean body mass and linear growth delay and are effective in burned patients with and without sepsis. Adverse effects, cost benefits, and the ease of administration and monitoring must be examined when considering the possibility of their use.
Pereira
Clifford T
CT
Department of Surgery, University of Texas Medical Branch, Shriners Hospitals for Children, Galveston, Texas, USA.
Herndon
David N
DN
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D045930:Anabolic Agents / Q000627:therapeutic use; D002056:Burns / Q000378:metabolism*; D002395:Catecholamines / Q000037:antagonists & inhibitors; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D007334:Insulin-Like Growth Factor I / Q000627:therapeutic use; D008066:Lipolysis; D010074:Oxandrolone / Q000627:therapeutic use; D011433:Propranolol / Q000494:pharmacology / Q000627:therapeutic use
D000319:Adrenergic beta-Antagonists; D045930:Anabolic Agents; D002395:Catecholamines; D007004:Hypoglycemic Agents; D007328:Insulin; D007334:Insulin-Like Growth Factor I; D010074:Oxandrolone; D011433:Propranolol