小黄鼠咬伤后的深度昏迷和原因不明的低钾血症:两个病例的病理生理机制探讨。

Journal of Venom Research Pub Date : 2010-12-14
Indika Bandara Gawarammana, Senanayake Abeysinghe Mudiyanselage Kularatne, Keerthi Kularatne, Roshita Waduge, Vajira Senaka Weerasinghe, Sunil Bowatta, Nimal Senanayake
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引用次数: 0

摘要

存在于小黄鳝(BC)中的黄鳝毒素可导致危及生命的呼吸肌肉麻痹。深度昏迷和低钾血症在很大比例的患者中被观察到,但原因尚不清楚。我们假定这两种现象背后的可能机制。我们研究了两例入院的深度昏迷患者的临床细节,并进行了脑电图(EEG)和脑干听觉和视觉诱发电位(BAEP和VEP)。测定每日血清钾和尿钾排泄量,作为细胞外体钾总量的标志。两例患者入院时均无脑干反射,脑电图显示α和δ活动缺失,θ活动占优势。1例患者在第3天恢复了α节律,另1例患者没有恢复,后者因弥漫性血管内凝血于第13天死亡。死亡患者BAEP延迟,VEP缺失。两例患者均有低血钾和低尿钾排泄。补钾(高达1.5mmol/kg/天)没有改善血清钾和尿钾排泄。脑电图α和δ活动的缺失,BAEP的延迟和VEP的缺失提示了毒液对皮质和脑干神经元的中枢作用。持续低血钾和尿钾排泄减少提示细胞内移位是低钾血症的致病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Deep coma and hypokalaemia of unknown aetiology following Bungarus caeruleus bites: Exploration of pathophysiological mechanisms with two case studies.

Deep coma and hypokalaemia of unknown aetiology following Bungarus caeruleus bites: Exploration of pathophysiological mechanisms with two case studies.

Deep coma and hypokalaemia of unknown aetiology following Bungarus caeruleus bites: Exploration of pathophysiological mechanisms with two case studies.

Deep coma and hypokalaemia of unknown aetiology following Bungarus caeruleus bites: Exploration of pathophysiological mechanisms with two case studies.

Bungarotoxin present in Bungarus caeruleus (BC) causes life threatening respiratory muscle paralysis. Deep coma and hypokalaemia have been observed in a significant proportion of patients, but the cause is unknown. We postulate the likely mechanism behind these two phenomena. We studied clinical details of two patients admitted with deep coma and performed electroencephalograms (EEG) and brain stem auditory and visual evoked potentials (BAEP and VEP). Daily serum potassium was measured along with urinary potassium excretion as a marker of total extracellular body potassium. Both patients had no brain stem reflexes on admission and the EEG revealed absent alpha and delta activity and presence of dominant theta activity. Alpha rhythm returned on the 3(rd) day in one patient, while in the other it did not, and the latter patient died on the 13(th) day due to disseminated intravascular coagulation. BAEP were delayed and VEP were absent in the deceased patient. Both had low serum potassium and low urinary potassium excretion. Replacement of potassium (up to 1.5mmol/kg/day) did not improve serum potassium and urinary potassium excretion. Absent alpha and delta activity in EEG and delayed BAEP and absent VEP are suggestive of a central action of the venom on both the cortical and brain stem neurones. Persistently low serum potassium and reduced urinary potassium excretion are suggestive of intracellular shift as the causative mechanism of hypokalaemia.

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