Clinical Features of Snakebite

Clinical Features of Snakebite  


some people who are bitten by snakes (or suspect or imagine that they have been bitten) may develop quite striking symptoms and signs, even when no venom has been injected. This results from an understandable fear of the consequences of a real venomous bite. Anxious people may hyperventilate so that they develop pins-and-needles sensation in the extremities, spasm of their hands and feet, and dizziness. Others may develop vasovagal shock after the bite or suspected bite, with faintness and collapse with profound slowing of the heart. Others may become highly agitated and irrational and may manifest a wide range of misleading symptoms.
The clinical presentation of a snakebite victim varies with the age and size of the patient, the species of snake, the number and location of the bites, and the quantity and toxicity of the venom.

Morbidity and mortality depends rather much on the age and size of victim (young people receive larger envenomation relative to body size) along with comorbid conditions (elderly patients succumb more easily to snake venom).  Other factors affecting severity and outcome are listed in. Factors not contributing to outcome are size of the snake and time of bite (day/evening).

Elapid bites
      Bites by krait, coral snake, and some cobras are associated with minimal local changes; however, bite by the Indian cobra (Naja naja) results in tender local swelling, blistering, and necrosis. Local necrosis causes a picture of "wet gangrene" with a characteristic putrid smell due to the direct cytolytic action of the venom. "Skip lesions" are typical findings. Systemic absorption occurs through venous channels and result in neurotoxic symptoms. Nausea, vomiting, malaise, prostration, and abdominal pain are the usual initial systemic symptoms. Paralysis is heralded by ptosis, followed by ophthalmoplegia. Paralysis of facial, palatal, tongue, and neck muscles follow. Respiratory failure, precipitated by upper airway obstruction and paralysis of intercostals and diaphragm, is the usual cause of death.

Viper bites
        Viper bite is primarily vasculotoxic. It causes rapidly developing bruising and growth of the bitten part. Local necrosis is mainly ischemic as thrombosis blocks the local blood vessels and causes a dry gangrene. Systemic absorption is slow; it occurs via the lymphatics and leads to lymphangitis. Hemostatic abnormalities are characteristic of viper bites and are the cause of the complications that lead to death. A persistent ooze from the bite mark and the site of the IV cannula is an indication of the altered clotting mechanism. Hemorrhage and increased capillary permeability leads to shock and pulmonary edema. Oliguria ensues, followed by loin pain due to renal ischemia. Renal failure is the common event before death.

Sea snake bite
     The effects of a sea snake bite are both myotoxic and neurotoxic and result in clinical and pathological changes typical of segmental myopathic lesions in the skeletal muscles. Muscle pains may last for several months unless treated. Myoglobin and potassium released from damaged skeletal muscle can cause renal failure, while the hyperkalemia thus produced may lead to cardiac arrest.
The average fatal dose, LD50, in mice and the average time to fatality of various snakes poison is given in.
 Management of Snakebite  
    WHO/SEARO has published guidelines, specific for the South East Asia region, for the clinical management of snakebites; these guidelines appeared in the supplementary issue of the South East Asian Journal of Tropical Medicine and Public Health.