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Venomous snakebites are still a public health problem in tropical countries. Even in metropolitan areas, such as Bangkok, green pit viper (Cryptelytrops albolabris and C. macrops) bites are still prevalent. As we are invading their territory, they adapt to live among humans in our backyards. With some exceptions, clinical syndromes of snakebites can be divided simply into two classes: elapid envenomation attacks neuromuscular junctions, causing muscular paralysis; viper envenomation targets the haemostatic system, resulting in bleeding disorders. Therefore, viper venoms are of great interest to haematologists.
Vipers (Viperinae) are members of the snake family that develops the most advanced venom-injecting organs, the long sheathed fangs that can be folded like switchblades. Some vipers possess pit organs, infrared detectors for locating warm-blooded prey in the dark. This specialised subfamily is termed crotalidae (Pit viper), separating them from viperidae (True viper). Vipers found in the Americas are pit vipers, while African vipers are true vipers. Asia and Europe are homes to both subfamilies.
Clinically, viper bites cause both local tissue damage and systemic effects: local tissue swelling, blisters from dermo-epidermal separation, ecchymoses and gangrene. Snake venom metalloprotease (SVMPs) have been implicated in these tissue injuries, both directly and indirectly via vascular damage1 and inflammatory responses.2 The most prominent systemic effects of pit viper venoms are towards fibrinogen and platelets. Although the venoms clot fibrinogen (thrombin-like effect) and activate platelets in vitro, these friable clots and platelet aggregates are rapidly cleared from circulation in vivo, resulting in hypofibrinogenaemia, termed defibrination syndrome, and thrombocytopenia.3 On the other hand, true vipers, such as Russell’s viper and Daboia russelii, activate common pathways of coagulation via factor X and V, causing bleeding from disseminated intravascular coagulation. Kinetics studies in humans showed that the viper venom is rapidly absorbed. However, the effects on blood may be delayed and prolonged as the half-life of viper venoms is over 24 hours.4 Antivenoms, the specific treatment of venomous snakebites, are polyclonal antibodies derived from horses or sheep. Older versions of antivenoms may cause potentially fatal early reactions mediated by complement activation from the immunoglobulin (Ig)-G (fragment, crystallisable) Fc portion.5,6 Current F (ab)’2 antivenoms in Thailand, the products of Queen Saovabha Memorial Institute, are pure and devoid of the Fc portion. A study revealed that the incidence of reactions is low (3.5%) and unpredictable by the intradermal test.7 Therefore, a hypersensitivity skin test for immunoglobulin (Ig)-E-mediated reactions is unnecessary, but close observation is essential during administration in all patients. Although antivenoms are efficacious in reversing coagulopathy and thrombocytopenia from viper venoms, this efficacy in treating local tissue injuries is limited.8,9 This is consistent with animal studies showing that venom-induced local damages was rapid, and unable to be treated even by immediate antivenom.10 Therefore, local tissue injury is the current management problem after snakebites, and further research is needed.