2 g/dl, total

leukocyte count of 13,500, with 80% neutrophils, platelet count of 178,000/mm3. Coagulation profile showed prothrombin time (PT) 18 seconds (control 12 s) with INR of 1.44 thromboplastin time with kaolin (PTTK) was 38 seconds (control-35 s) and fibrinogen degradation products was 2.72 mg/l (Normal-<0.20 mg/l). The biochemical investigations including blood urea, serum creatinine, plasma glucose, serum bilirubin and transaminases were with in normal limit. An urgent Digital Subtraction Angiography (DSA) of the intracranial vessel was performed and which was normal excluding the possibility of Inhibitors,research,lifescience,medical ruptured aneurysm or an arterio-venous malformation. Since his clinical parameters were improving, he was managed conservatively without any neurosurgical intervention. He was discharged home a week later Inhibitors,research,lifescience,medical in good health without any neurological deficit. Discussion and conclusion Saw- scaled viper venom is a highly complex mixture of a variety of biological substances including protein and non protein toxins [7,8]. Multiple mechanisms have been suggested for coagulopathy following SSV envenoming. The most common coagulopathy associated with snake bite envenoming is venom induced consumptive coagulopathy(VICC) [9]. A VICC result from the activation of the coagualation pathway in varied Inhibitors,research,lifescience,medical points by procoagulant toxins. SSV venom contains

two metalloproteinases that are prothrombin activators namely ecarin and carinactivase [7,8]. Activation of prothrombin by these factors

result in consumptive coagulopathy with variable deficiency in fibrinogen, factor V and factor VII [9]. Simultaneous injury Inhibitors,research,lifescience,medical to the blood vessel integrity increases the risk of bleeding. The venom also contains factor X activator and many other compounds Inhibitors,research,lifescience,medical which increases its capacity to cause coagulopathy such as platelet KPT-330 manufacturer aggregation inhibitors [7-9]. VICC and direct endothelial injury due to haemorrhagin in the venom might be responsible for the near fatal intracerebral haemorrhage in our patient. VICC is characterized by prolonged 20WBCT, PT and PTTK and a marked increase in fibrinogen degradation products. Personal communication with many practicing physicians in the Island revealed that there is a wide variation in the treatment methods used in SSV envenoming. Because of the belief, that the Sri Lankan subspecies of SSV is never fatal to man, AVS is not used by all. Although subspecies of SSV in Sri Lanka is regarded as a ‘non lethal and venomous snake’, the occurrence of rare potentially fatal complications such as intracerebral haemorrhage should be considered in their management. AVS should be administered promptly if features of systemic envenoming are present. In our patient neurological deficit was progressive despite the prompt use of AVS. It indicates either AVS was less effective in preventing progression of intracerebral haemorrhage or inadequate dose of AVS was used.