Coagulopathy and Haemorrhagin Effects

The severity and clinical presentation of coagulopathy will be determined, in part, by the species of snake. In general, first clinical evidence of coagulopathy is often persistent ooze of blood from the bite site, any other areas of recent trauma, venepuncture sites and often from the gums. The latter are particularly likely to bleed if there are haemorrhagins in the blood. The area around the bite site may show mild to gross and extensive ecchymosis. There may be haematuria; if myoglobinuria is also suspected, microscopic evidence of red cells or casts may assist in differentiating. Coagulopathy may be severe, yet the victim may be virtually symptom free and thus the severity of envenoming masked. It is particularly because of this danger that at least baseline clotting tests should be routine for most types of snakebite, the exception being regions where none of the culprit species cause coagulopathy. While full laboratory tests of coagulation might be ideal, in most parts of the world they are either unavailable or will take a long time. If detailed coagulation studies are unavailable the whole blood clotting time (discussed later) is an invaluable bedside test in snakebite victims. In the presence of major coagulopathy, any trauma has the potential to result in major or lethal haemorrhage. This is particularly true for head injuries.

Fibrin degradation products are cleared through the kidney and secondary renal failure is a potential complication of coagulopathy. A few species can cause quite specific haemorrhages, most notably Russell’s viper in Myanmar (Burma) can cause anterior pituitary haemorrhage, or Sheehan’s syndrome, with long term consequences.

While the net effect of most haemostatically active venoms is functional anticoagulation, often through consumption of fibrinogen, sometimes thrombosis is the most prominent effect. Bites by vipers in Martinique, in particular, are associated with DVT formation and a significant risk of pulmonary embolism.