Merigian K S, Park L J, Leeper K V, Browning R G, Giometi R
Department of Emergency Medicine, University of Tennessee, Memphis 38163.
J Emerg Med. 1994 Jul-Aug;12(4):485-90. doi: 10.1016/0736-4679(94)90345-x.
We report the historical, clinical, and laboratory findings in 5 patients after crack cocaine ingestion. All patients exhibited adrenergic crisis as a result of their ingestion. Analysis of their history revealed a latency period before signs and symptoms occurred as well as a wide variation in the number of crack cocaine nuggets ingested. Signs of intoxication were hypertension, tachycardia, hyperthermia, agitation, and generalized seizure activity. Treatment included therapeutic sedation with lorazepam and adrenolysis with esmolol infusion. The majority of patients showed electrocardiographic evidence of cardiac ischemia, but not elevations in serum creatinine phosphokinase enzymes--MB fraction. One patient died of complications associated with subclinical status epilepticus. The toxicities of crack cocaine ingestion are seldom appreciated. Prompt reversal of both cardiovascular and neurological signs and symptoms with appropriate pharmacologic agents is indicated.
我们报告了5例吸食快克可卡因后的历史、临床和实验室检查结果。所有患者因吸食快克可卡因均出现了肾上腺素能危象。对他们病史的分析显示,在体征和症状出现之前有一段潜伏期,且吸食的快克可卡因块数量差异很大。中毒体征包括高血压、心动过速、体温过高、躁动和全身性癫痫活动。治疗包括用劳拉西泮进行治疗性镇静以及用艾司洛尔静脉输注进行肾上腺能阻滞。大多数患者有心电图显示的心肌缺血证据,但血清肌酸磷酸激酶同工酶-MB部分未升高。1例患者死于与亚临床癫痫持续状态相关的并发症。吸食快克可卡因的毒性很少被认识到。建议使用适当的药物迅速逆转心血管和神经体征及症状。