Isbister G K, Little M, Cull G, McCoubrie D, Lawton P, Szabo F, Kennedy J, Trethewy C, Luxton G, Brown S G A, Currie B J
Tropical Toxinology Unit, Menzies School of Health Research, Charles Darwin University, Darwin, Northern Territory, Australia.
Intern Med J. 2007 Aug;37(8):523-8. doi: 10.1111/j.1445-5994.2007.01407.x.
Australian brown snake (genus Pseudonaja) envenoming causes a venom-induced consumptive coagulopathy (VICC). A proportion of cases go on to develop thrombotic microangiopathy characterized by thrombocytopenia, microangiopathic haemolytic anaemia (MAHA) and acute renal failure (ARF).
The aim of the study was to define better the natural history and empirical treatments for thrombotic microangiopathy in brown snake envenoming.
A review of brown snake bites recruited to the Australian Snakebite Project (ASP), a national multicentre study of snake envenoming was undertaken. Serial data are recorded on clinical effects and laboratory results, including measurement of venom concentrations. We describe cases of thrombotic microangiopathy and compare these to cases without thrombotic microangiopathy.
From 32 cases of brown snake envenoming with severe VICC, four (13%) developed thrombotic microangiopathy, we also included two cases of thrombotic microangiopathy from prior to ASP. All six developed severe thrombocytopenia (<20 x 10(-9)/L), worst 3 days after the bite and resolving over a week, MAHA with fragmented red blood cells on the blood film and five developed anuric ARF requiring dialysis and lasting 2-8 weeks. All six received antivenom, which was delayed compared with other brown snake-envenoming cases. Four were treated with plasmapheresis. The severity and recovery of the thrombocytopenia, anaemia and renal function were similar with and without plasmapheresis. The median length of stay for MAHA cases was 14 days (interquartile range (IQR) 12-14) compared to 1.8 days (IQR 1.3-2) for all other cases.
Thrombotic microangiopathy resulting from brown snake bite appears to have a good prognosis and management should focus on early antivenom therapy and supportive care including dialysis. The role of plasmapheresis is yet to be defined.
澳大利亚棕蛇（伪眼镜蛇属）咬伤可导致毒液诱导的消耗性凝血病（VICC）。一部分病例会发展为血栓性微血管病，其特征为血小板减少、微血管病性溶血性贫血（MAHA）和急性肾衰竭（ARF）。
本研究的目的是更好地明确棕蛇咬伤所致血栓性微血管病的自然病程及经验性治疗方法。
对纳入澳大利亚蛇咬伤项目（ASP）的棕蛇咬伤病例进行回顾，ASP是一项关于蛇咬伤的全国多中心研究。连续记录临床效应和实验室结果的数据，包括毒液浓度的测定。我们描述了血栓性微血管病病例，并将其与无血栓性微血管病的病例进行比较。
在32例发生严重VICC的棕蛇咬伤病例中，4例（13%）发展为血栓性微血管病，我们还纳入了2例ASP之前的血栓性微血管病病例。所有6例均出现严重血小板减少（<20×10⁻⁹/L），咬伤后3天情况最严重，一周内缓解，血涂片显示MAHA伴破碎红细胞，5例出现无尿性ARF需要透析，持续2 - 8周。所有6例均接受了抗蛇毒血清治疗，与其他棕蛇咬伤病例相比，治疗延迟。4例接受了血浆置换。有或无血浆置换时，血小板减少、贫血和肾功能的严重程度及恢复情况相似。MAHA病例的中位住院时间为14天（四分位间距（IQR）12 - 14），而所有其他病例为1.8天（IQR 1.3 - 2）。
棕蛇咬伤所致血栓性微血管病似乎预后良好，治疗应侧重于早期抗蛇毒血清治疗及包括透析在内的支持性护理。血浆置换的作用尚待确定。
