Case 6-2004: Severe Burns from a Nightclub Fire
http://www.100md.com
《新英格兰医药杂志》
To the Editor: Sheridan et al. (Feb. 19 issue)1 fail to consider that carbonaceous sputum, confusion, agitation, dyspnea, and lactic acidosis in their burned patient are all signs of potential cyanide poisoning from smoke inhalation. This oversight is troubling and, unfortunately, common. Since one of us and our colleagues described the role of cyanide in death due to smoke inhalation and its strong association with increased plasma lactate concentrations,2 numerous investigators have confirmed the importance of cyanide in this setting. The patient under discussion had multiple potential sources of lactate, including possible crush injury, extensive burns, carbon monoxide intoxication, and hypovolemia. The source of lactic acid in patients with burns is of more than academic interest. Jeng et al.3 confirmed that lactate values are inversely related to survival in patients with burn injuries. They suggested many potential sources of hyperlactatemia but never considered cyanide. We have recently shown that lactate is a valuable early marker in pure cyanide poisoning4 but not in pure carbon monoxide poisoning.5 Cyanide poisoning is a deadly but treatable complication of smoke inhalation that should be considered in every patient who presents with altered mental status, hypotension, a low respiratory rate, or lactic acidemia.
Stephen W. Borron, M.D.
George Washington University
Washington, DC 20037
Bruno Mégarbane, M.D.
Frédéric J. Baud, M.D.
INSERM Unité 26
75010 Paris, France
sborron@intoxicon.com
References
Case Records of the Massachusetts General Hospital (Case 6-2004). N Engl J Med 2004;350:810-821.
Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med 1991;325:1761-1766.
Jeng JC, Jablonski K, Bridgman A, Jordan MH. Serum lactate, not base deficit, rapidly predicts survival after major burns. Burns 2002;28:161-166.
Baud FJ, Borron SW, Megarbane B, et al. Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med 2002;30:2044-2050.
Benaissa ML, Megarbane B, Borron SW, Baud FJ. Is elevated plasma lactate a useful marker in the evaluation of pure carbon monoxide poisoning? Intensive Care Med 2003;29:1372-1375.
The discussants reply: Dr. Borron and colleagues bring up the issue of cyanide toxicity in inhalation injury. This consideration did not apply to this patient, since she presented to our institution approximately 11 hours after the injury and her measured cyanide concentration (0.4 mg per deciliter) was well within the normal range. Her lactic acidosis was due to hypovolemia. Specific treatment for cyanide exposure in patients with inhalation injury is an area of ongoing controversy. In what is perhaps the most comprehensive study of cyanide toxicity in inhalation injury, 364 cases of death due to fire were evaluated.1 Cyanide poisoning was found infrequently and was not itself an important cause of death. The authors concluded that specific treatment of cyanide poisoning is rarely necessary and that even if cyanide poisoning is present, it can be well managed with standard supportive care.
Robert Sheridan, M.D.
John Schultz, M.D.
Colleen Ryan, M.D.
Massachusetts General Hospital
Boston, MA 02114
References
Barrillo DJ, Goode R, Esch V. Cyanide poisoning in victims of fire: analysis of 364 cases and review of the literature. J Burn Care Rehabil 1994;15:46-57.
Stephen W. Borron, M.D.
George Washington University
Washington, DC 20037
Bruno Mégarbane, M.D.
Frédéric J. Baud, M.D.
INSERM Unité 26
75010 Paris, France
sborron@intoxicon.com
References
Case Records of the Massachusetts General Hospital (Case 6-2004). N Engl J Med 2004;350:810-821.
Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med 1991;325:1761-1766.
Jeng JC, Jablonski K, Bridgman A, Jordan MH. Serum lactate, not base deficit, rapidly predicts survival after major burns. Burns 2002;28:161-166.
Baud FJ, Borron SW, Megarbane B, et al. Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med 2002;30:2044-2050.
Benaissa ML, Megarbane B, Borron SW, Baud FJ. Is elevated plasma lactate a useful marker in the evaluation of pure carbon monoxide poisoning? Intensive Care Med 2003;29:1372-1375.
The discussants reply: Dr. Borron and colleagues bring up the issue of cyanide toxicity in inhalation injury. This consideration did not apply to this patient, since she presented to our institution approximately 11 hours after the injury and her measured cyanide concentration (0.4 mg per deciliter) was well within the normal range. Her lactic acidosis was due to hypovolemia. Specific treatment for cyanide exposure in patients with inhalation injury is an area of ongoing controversy. In what is perhaps the most comprehensive study of cyanide toxicity in inhalation injury, 364 cases of death due to fire were evaluated.1 Cyanide poisoning was found infrequently and was not itself an important cause of death. The authors concluded that specific treatment of cyanide poisoning is rarely necessary and that even if cyanide poisoning is present, it can be well managed with standard supportive care.
Robert Sheridan, M.D.
John Schultz, M.D.
Colleen Ryan, M.D.
Massachusetts General Hospital
Boston, MA 02114
References
Barrillo DJ, Goode R, Esch V. Cyanide poisoning in victims of fire: analysis of 364 cases and review of the literature. J Burn Care Rehabil 1994;15:46-57.