Snake Bite Epidemiology and Proper Treatment

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Snake bite

A correct recording and analysis of the global problem of snake bite envenoming happens to be an illusion in spite of many efforts to estimate it and study it. Snake bite envenoming evokes a lot of fear across the board irrespective of nationalities and, other than a few countries, proper documentation on incidence, morbidity, and mortality are hard to come by (Alirol et al., 2010) .The real number of snake bite victims who succumb are not yet known as most of the data and its analysis are based on records and inputs as received from hospitals of country side areas. Latest study has shown that actual scale of this disease is much more threatening than what was previously thought because most of the snakebite victims might never get to reach hospitals on time as they are likely to pass away on their way to a nearby hospital or health care center (Gutie´ rrez et al., 2013).

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Hardly any reliable information on snake bites can be gathered from rural areas due to lack of sound technological and other essential means. On the other hand, developed countries are more vulnerable for mortality and morbidity from snake bite. Hence, the characteristics and other parameters of snake bite envenoming largely remain an uncharted territory for all of us. However, data on number of bites, their consequent death cases as well as frequency of long term impact of snake bites is important for evaluating the intensity of the problem, planning about it, learning how to combat its onset and also in training medical staff to confront it effectively. Kasturiratne et al., 2008 have estimated from the available literatures, which is rather lower than the true estimate, that, globally, at least 421,000 envenomings and 20,000 deaths occur each year due to snake bite. They have concluded that these figures can be as high as 1,841,000 envenomings and 94,000 deaths, which was later found by WHO to be on the higher side. Since about one in every four snake bites results in envenoming it can be deduced that between 1.2 million and 5.5 million snake bites occur annually.

Snake bites cause considerable morbidity and mortality worldwide. The highest burden exists in South Asia, Southeast Asia, and sub-Saharan Africa. Regarding number of snake bites and the related mortality in India, World Health Organization WHO (2010) guidelines state that estimates as low as 61,507 bites and 1124 death in 2006 and 76,948 bites and 1359 deaths in 2007 and as high as 50,000 deaths each year have been published (Warrell DA , 2010). In hospital-based studies, mortality rates ranged from 3% in northern India (Sharma et al., 2005) to 20% in Nepal (Sharma et al., 2003).

In Maharashtra, a state in India, an estimated 10,000 annual venomous snake bites account for 2000 deaths (Warrell DA, 2010). Maharashtra has the highest incidence of snake bite among all states in India. Other states with a large number of snake bite cases include West Bengal, Tamil Nadu, Uttar Pradesh, and Kerala (Philip E, 1994). Based upon an epidemiological survey of 26 villages with a total population of nearly 19,000 individuals in Burdwan district of West Bengal state in India, Hati et al., 1992 worked out an annual incidence of snake bite of 0.16% and mortality rate of 0.016% per year. However this information may not be exhaustive in nature as many snake bite incidents go unnoticed or unreported due to dearth of proper health care facilities.

Venom and venomous snakes

Among the 3000 species of snakes existing worldwide 410 are considered venomous (Cruz et al., 2009). The four major venomous biting species of India, known as big four, are cobra or Naja naja ,krait or Bungarus caeruleus , Russell’s viper or Vipera russelli , and saw-scaled viper or Echis carinatus . While cobra and krait belong to the Elapidae, Russell’s viper and saw-scaled viper belong to the Viperidae family. Echis carinatus, the saw-scaled viper is responsible for the majority of deaths in India (Kumar et al., 2006)

Snake venoms are the most complex of all natural venoms and poisons, and the components may act independently, synergistically or antagonistically (Kohli et al., 2003). The characteristic venom effect may be considered as quite regular to a given family for simplification but the actual mix of toxins in the venom vary in individual species, and also by age and season. Equally, the quantity of venom injected in a bite is highly variable, though ineffective or ‘dry bites’ account for more than 50% of all bites.

Symptoms and treatment of snake envenomation

Symptoms and signs of snake envenomation vary according to the species of snake responsible for the bite and the amount of venom injected. The identification of the snake is important for proper treatment and done by examining the dead snake, patient’s description, circumstances of the bite, or from the clinical effects of the venom (Warrell DA, 1999) and from bed side ELISA in developed countries only.

  • Local symptoms and signs in the bitten part: fang marks, local pain, local bleeding, bruising, Lymphangitis, lymph node enlargement, inflammation (swelling, redness, heat), blistering, local infection, abscess formation, necrosis
  • General symptoms and signs: Nausea, vomiting, malaise, abdominal pain, weakness, drowsiness, prostration
  • Cardiovascular (Viperidae): Visual disturbances, dizziness, faintness, collapse, shock, hypotension, cardiac arrhythmias, pulmonary oedema, conjunctival oedema
  • Bleeding and clotting disorders (Viperidae): bleeding from recent wounds (including fang marks,venepunctures etc) and from old partly-healed wounds, spontaneous systemic bleeding – from gums , epistaxis, bleeding into the tears, haemoptysis, haematemesis, rectal bleeding or melaena, haematuria, vaginal bleeding, bleeding into the skin (petechiae, purpura, ecchymoses) and mucosae (eg conjunctivae), intracranial haemorrhage (meningism from subarachnoid haemorrhage, lateralising signs and/or coma from cerebral haemorrhage)
  • Neurological (Elapidae, Russell’s viper): Drowsiness, paraesthesiae, abnormalities of taste and smell, “heavy” eyelids, ptosis, external ophthalmoplegia, paralysis of facial muscles and other muscles innervated by the cranial nerves, aphonia, difficulty in swallowing secretions, respiratory and generalised flaccid paralysis
  • Skeletal muscle breakdown (sea snakes, Russell’s viper): Generalised pain, stiffness and tenderness of muscles, trismus, myoglobinuria, hyperkalaemia, cardiac arrest, acute renal failure
  • Renal (Viperidae, sea snakes): Loin (lower back) pain, haematuria, haemoglobinuria, myoglobinuria, oliguria/anuria, symptoms and signs of uraemia (acidotic breathing, hiccups, nausea, pleuritic chest, pain)
  • Endocrine (acute pituitary/adrenal insufficiency) (Russell’s viper): Acute phase: shock, hypoglycaemia Chronic phase (months to years after the bite): weakness, loss of secondary sexual hair, amenorrhoea, testicular atrophy, hypothyroidism etc (Warrell DA, 2010)

Treatment for snake bite according to WHO/SEARO guidelines (Warrell DA, 1999) is as following:

First aid

Reassurance, immobilization of the affected limb (but not by tight arterial compression) and prompt transfer of victim to hospital

Hospital treatment

The only available treatment against snake envenomation is anti snake venom serum (ASVS) which is given intravenously after hospitalization. Monovalent antivenom is recommended by WHO when it is available and when the snake is identified but polyvalent antivenom is mostly given. However it has several shortcomings as – adverse reaction to antivenom, cost, cost chain dependence and dependence on animals (horse) for production, which is often a issue for animal rights. In special cases symptomatic treatment is given as – ventilation in respiratory problems, dialysis in renal problems etc.

Nephrotoxic snake envenomation

Hemotoxic and myotoxic snakes are the major causes of SAKI (Sitprija V, 2006) among which three genera of snakes viz Russell’s viper, Bothrops and Crotalus together are responsible for most of the cases of snakebite-induced AKI reported. All of these snakes belong to the viperidae family (Pinho et al., 2008). Hemotoxic bites cause hemorrhagic diathesis, intravascular hemolysis and rhabdomyolysis, leading to renal complications. Intravascular coagulation, another effect of hemotoxic venom, affects renal function through disseminated intravascular coagulation. Hemodynamic changes contribute by causing renal ischaemia and consequent AKI. Though Sitprija, (2006) has concluded that immunologic mechanisms are minor, it is responsible for hemodynamic changes brought about by cytokines and vasoactive mediators. Hemodynamic changes are also brought about by myotoxic venoms and venoms acting through neuromuscular changes (Sitprija V, 2008).

Effects on kidney resulting from Russell’s Viper bites: The major share of SAKI in India is due to Russell’s Viper bites. It is reversible in mild conditions, but the venom usually causes cortical necrosis, making the condition irreversible (Kumar, 2012). The Viperinae, or viperines, is a subfamily of venomous vipers endemic to Europe, Asia and Africa. They are distinguished by their lack of the heat-sensing pit organs. Russell’s Viper (Daboia Russelii), a supernasal sac with sensory function. The supernasal sac is an invagination of the skin between the supernasal and nasal scales and is connected to the ophthalmic branch of the trigeminal nerve. The component of the snake venom can be grouped into four braod categories : enzymes(phospholipase A2, hyaluronidase, protease), polypeptides, glycoproteins and small molecular weight compounds. The toxic effects results from both the protein as well as nonprotein components of snake venom. Metalloproteases and phosphilipase A2 are the venom components responsible for direct nephrotoxicity (Sitprija V, 2006).

Proteases and phospholipase A2 can also cause systemic and renal hemodynamic by initiating inflammatory responses (Sitprija V, 2008). Direct nephrotoxicity has also been demonstrated in case of Russell’s Viper venom (Ratcliffe et. al., 1989). Some of the major toxic components and the way the bring about their toxic effects are as follows : Phospholipase A2, the enzyme most widely studied, is present in the venom of all families of venomous snakes. It inhibits electron transfer at cytochrome C level and renders mitochondrial-bound enzymes soluble.

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