Ischemic stroke following hump-nosed pit viper bite has previously been reported in a Sri Lankan patient who developed left-sided hemiparesis associated with acute kidney injury . In vitro studies confirmed that Hypnale venom has potent cytotoxic, mild procoagulant, weak neurotoxic, and myotoxic activity . However, procoagulant toxins of Hypnale venom have thus far not been isolated and characterized, and it is hypothesized that the procoagulant activity is due to thrombin-like enzymes (TLEs) of the venom , which may have caused the cerebral infarction in our patient. Thrombin-like enzymes activate clotting pathways, leading to the formation of thrombi, and hence deposit them as fibrin, causing vascular occlusion, which results in reduction of blood supply to the organ. This commonly occurs in vessels of kidneys, brain, heart, or pituitary gland. When red blood cells flow through these blocked vessels, they get distorted, which can be seen on peripheral blood microscopy as schistocytes (fragmented red blood cells). This condition is called microangiopathic hemolysis and can be observed in Hypnale bites . When this organ ischemia occurs together with thrombocytopenia and microangiopathic hemolysis, the process is called TMA, which can also be observed in hump-nosed pit viper bites . It was evidenced that, in our patient, cerebral infarction was due to the venom because he also had other venom effects, including bradycardia, mild reduction of hemoglobin (Hb), and mild elevation of creatinine. While thrombi are formed, circulating platelets can get trapped in fibrin mesh, resulting in thrombocytopenia as our patient’s platelet count on day 2 was near to the lower marginal limit (Table 1). As a drug therapy, these patients can be administered aspirin after the clotting abnormality is resolved, and physiotherapy plays a vital part in the management. To determine whether the type of snake venom is hemotoxic, neurotoxic, nephrotoxic, or myotoxic, there are various investigations that can be done according to the severity of the patient’s condition. Coagulopathy is detected from the clotting profile, including prothrombin time (PT)/international normalized ratio (INR), activated partial thromboplastin time (aPTT), WBCT20, fibrinogen, and D-dimers. Nephrotoxicity is detected from serum creatinine, blood urea, and renal ultrasound scan. Myotoxicity is assessed using laboratory findings related to rhabdomyolysis such as myoglobinuria, serum K+, and creatine phosphokinase.
Interestingly, the clotting profile of our patient was normal throughout (Table 1), and it could be hypothesized that he has depletion of the downstream clotting factors due to consumption and maintained factor levels marginally sufficient for normal clotting. At this stage, fibrinogen levels could be reduced. However, we were unable to measure fibrinogen levels owing to lack of that facility at the hospital. In Sri Lanka, both hemorrhagic and ischemic cerebral infarction is common with Russell’s viper (Daboia russelii) envenoming, and sometimes these may be fatal . Cardiac effects such as MI, atrial fibrillation, acute ischemic changes, bradycardia, and cardiac arrest have previously been reported following hump-nosed pit viper bites [4, 12]. Our patient had bradycardia throughout. However, we expect heart rate to be high because of the local pain. Therefore, reduction of heart rate may be the effect of venom on heart, as previously suggested . Initially, it was thought that bradycardia might also be due to the patient’s old age. However, his pulse rate improved to around 70 beats per minute 4 days after the snakebite. Our patient had pure motor involvement of arms, face, and legs, which was suggestive of ischemia mainly to the posterior limb of internal capsule and involvement of middle cerebral artery. Even though strokes are very rare in Hypnale bites, physicians should be aware of them, because as there is no antivenom, these patients should be managed with available supportive care. Otherwise, they may be administered available antivenom unnecessarily.