In the fourth century BC, India was invaded by Alexander the Greats army, which was accompanied by a number of Macedonian physicians and observers. They were impressed by the achievements of the local Ayurvedic practitioners, particularly in the treatment of snake bite (1). Unfortunately, the legacy of ancient skills, experience and wisdom may have held back rather than encouraged the application of modern scientific research methods to manage this continuing scourge of rural life in India (2).In India, snake envenomation is a huge public health problem, but unfortunately it hasn’t got its due attention. There is scant information on epidemiology and minimal research on anti venom. Most of the quoted figures on snake bite are hospital based though most bites occur in villages and among poor population, who rely largely on traditional treatment. Recent Global Snake Bite Initiative of the International Society on Toxicology and by the World Health Organisation, is expected to throw more light on epidemiology and treatment of snake bites (3). Of the 3,000 or so snake species that exist in the world, only about 15% are venomous. Venomous snakes exist on every continent except Antarctica. In India the ‘Big Four’ (Cobra, Krait, Saw scaled and Russel’s viper) are the key poisonous snakes(4).Though the hospital records show only 1,300 annual deaths but a recent Nationally Representative Mortality Survey puts this figure to approx. 45,900 deaths a year. Snakebite remains an underestimated cause of accidental death in modern India. Community education, appropriate training of medical staff and better distribution of antivenom, especially in the states with the high prevalence, could reduce snakebite deaths in India(5).
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Historical Background: Since time immemorial snake has been an object of worship in many countries. According to Hindu mythology this world is resting on a many-headed cobra. Lord Vishnu lies on Sheshnag. The Cobra coils around Lord Shiva. Old Egyptian nobility are pictured with cobra hood on their forehead. Some cultures held snakes in high esteem as powerful religious symbols. Quetzalcoati, the mythical “plumed serpent” was worshipped as the “master of life” by ancient Aztecs of Central America. Some African cultures worshipped rock pythons and considered the killing of one to be a serious crime. In Australia, the Aborigines associated a giant rainbow serpent with the creation of life. In Jewish texts, in the old Maya civilization, in Kundalini yoga, theosophy and in many medieval society emblems the world over, snakes form an essential symbol. This shows how intimate has been the historical, social and mythological association of snakes with the mankind and no wonder the cobra is worshipped in India on Naga Panchami day. Ayurvedic texts written by Vagbhata and Sushruta, have given in fair detail the classification of snakes according to their symptoms and their poisoning. There are many stories about constrictors, particularly anacondas in the Amazon and pythons in the east, which are said to have strangled adult humans, these need to be treated with great deal of skepticism (6,7,10).
In practice it is only the poisonous snakes that are of interest. Poisoning from snake bite is an important medical emergency in Africa, South America, India, Pakistan and greater part of south East Asia.
As snake bite is not a notifiable illness, there is little reliable information on incidence of snakebite in many parts of the world. Snake bite is an important occupational injury affecting farmers, plantation workers, herders, and fishermen. Open-style habitation and the practice of sleeping on the floor also expose people to bites from nocturnal snakes. Bites are more frequent in young men, and generally occur on lower limbs. The incidence of snake bites is higher during the rainy season and during periods of intense agricultural activity (6). Available data shows 30,000-40,000 deaths from snakebites every year but this figure probably is an underestimate (8), because of incomplete reporting. Recent global estimates suggest 2.5 million bites and 85000 annual deaths. In India recent published literature suggests yearly 45,900 deaths due to poisonous snakebites and 5.6-12.6 deaths per 100,000 population in some states appears to be realistic(4,5). Upto 80% of snake bite patients in developing countries, first contact traditional practitioners, before visiting a medical center (6,7,9). Owing to the delay in reaching hospital many patients die enroute. Going by the fact that around 85-90 % snakes are non-poisonous and even 50% of bites by poisonous snakes are dry runs, number of snakebites in India are enormous(4). Myanmar probably has highest mortality figure in Asia, where over 70% bites are by Russell’s viper. In India, Maharashtra records the highest number of snakebites, followed by West Bengal, Tamil Nadu, Uttar Pradesh and Kerala. In Maharashtra alone, 70 bites per 100,000 population occur yearly with 2.4 per 100,000 mortality. Rajasthan and Jammu region of J&K also report large number of viper bites (up to 95% of all bites (10). During rains and floods number of cases shows a steep rise. Most bites occur between 0400 hours to midnight and mere observation that majority of bites are on lower extremity suggest that snake is inadvertently trodden upon.
In India 2/3rd of bites are due to saw scaled viper, about 1/4th due to Russell’s and a smaller proportion due to cobra and Krait. In neighboring Sri Lanka Daboiarussellii accounts for 40% and in Myanmar 70% of snake bites (11,12).
For correct epidemiological studies one requires enzyme-linked immunosorbent assay to identify antigen and antibody. This permits reliable identification and sensitive quantification of venom antigens and antibody. Natural antibody is detectable in serum by one week of bite, which rises to peak by one year and falls to low levels by 3 years, though may be detectable for up to 40 years after bite. Anti snake venom reduces but doesn’t abolish the generation of antibodies. In some countries e.g. Australia, ELISA is routinely used for identification of poison (13).
Anatomy and Habits
Snakes belong to order Ophidia of the Reptilia general class. Over 3000 species are encountered in the world of which less than 15% are poisonous. Most of these are found in tropical and subtropical regions, Australia and throughout USA except in Alaska, Maine and Hawaii. In India 216 species from 9 families are reported of which 52 species from 3 families are poisonous. Most snakes are non-venomous, have no fangs and belong to colubrid family; a few colubrids are technically poisonous having a venom gland connected to a solid fang at the back of mouth. Bites from back fanged colubrids are generally harmless to man but with some species like African boomslang, Dispholidustypus, serious and even fatal poisoning has been reported in the snake handlers(13). The three families of front fanged poisonous snakes are elapids, vipers and sea snakes. Elapids are land snakes with non-mobile 3-5 mm long fangs in adults. Vipers have 10-30 mm long fangs which are easy to see when erected, but difficult to see when folded against upper gum. Vipers are divided into crotalids or pit vipers who have heat sensing pit between eye and nose and viperidae which don’t have the pit. Sea snakes have very short immobile fangs and flat rudder like tails. There are mainly 4 poisonous snakes encountered in India i.e. Cobra, Krait, Saw scaled and Russell’s viper. New addition to ‘Big Four’ is Hump-nosed Pit viper (Hypnale hypnale), recently being reported from India though existent for more than 100 years(16). This has been mistaken for Saw Scaled Viper by most. It is identified by larger, triangular head ending in a snout with large scales on the head in contrast to the small scales of saw scaled viper. The envenomation is manifested by coagulopathy and renal failure. It is reported as one of the most poisonous snakes in India but specific anti venom against this is not available (12).
Common poisonous snakes found in India are as below;
Viperidae * Saw scaled viper (Echis carinatus)
* Russell’s viper (Vipera russelli)
Elapidae * Indian Cobra (Naja naja)
* Common Krait (Bungarus caeruleus)
Crotalidae * Pit Viper
Hydrophidae * Sea snakes
Cobra is 1.2-2.1 meters long while King Cobra may be as long as 5.5 meters. Cobra is usually slate gray to brown. The back of hood may or may not have a pattern. They raise their hood when aroused or threatened. They try to avoid mankind unless they are too close or are trodden upon. The distance a cobra can strike in forward direction is the height its hood rises above the ground. Some cobras however can spit venom upto a distance of 3 meters. This can cause redness, corneal abrasions/ulcers etc. King cobra is uniformly olive, brown or green with ringlike cross bands of black. Although it is the largest venomous snake in the world but it avoids attacking another venomous snake for fear of being bitten, therefore it feeds only on harmless species. Females build a nest and then deposit the eggs. Lying close by, she guards the nest and is highly aggressive towards anything which approaches the nest.The king cobra is found in the forests or their vicinity in the Himalayas, Bengal, Assam and South India. The common Indian cobra is found in jungles but also in open country with or without vegetation; in gardens, drains, cultivated fields, and populated areas in man’s proximity; in stacks of wood and under rubbish, in loose masonry, crevices of walls and building ruins; in old cemeteries, in temples or mosques.It is often seen in dark corners of bathrooms, stables and servant quarters of old bungalows. It may be found in old hole of a tree, in ant-hill or a rat burrow. It can climb trees and swim well. It feeds on rats, mice, frog; less frequently on birds or their eggs; and sometimes on chickens, squirrels, lizards and other snakes. It is usually diurnal in habit but in populated areas it is more nocturnal(14,15).
Krait is black or bluish black with white narrow crossbands and a narrow head. It’s average length is 90cm – 150 cm. It is found only in Asia. It is active during night and passive during the day. It is found in plains, cultivated fields and human habitations. It has tendency to seek shelter in sleeping bags, boots and tents.Kraits are mostly found in Eastern India, Assam, Bengal and parts of South India and patches all over the country. There are two varieties, banded and non-banded. Although it has most potent venom of all land snakes, it is rather shy and bites human beings least commonly (13,15).
Vipers are so called because they are viviparous. There are 110 kinds of vipers and all are poisonous. Vipers have broad plates extending right across the belly and small scales on the head similar to those on the body. Body is light brown and their back is usually covered with black blotches of inverted V shaped markings. Some of the pit vipers have large shield on the head. Russell’s viper or Daboia is a big stumpy snake ½-2 meters long with short tail and characteristic marking as described above. It is irritable. When threatened it coils tightly, hisses and strikes with a lightning speed, that victim has no chance of escaping. Indian pit vipers are generally found in hilly areas of Western Ghats and Sunderbans in West Bengal.Russell’s viper prefers open country, cultivated fields and bushy or grassy fallow lands. It is nocturnal in habit. It is commonly found in plains of Punjab, Bombay, Madras area and Brahamputravalley(4,6,20).
Saw scaled viper (Echiscarinatus) is found all over India but particularly in Western India, Punjab, and around Tiruchirapalli. It prefers open dry rocky country or arid deserts.Saw Scaled Viper (Phoorsa) is responsible for maximum bites and deaths all over the world than any other snake. This small stumpy snake measures 25-60cmand camouflages well with the surroundings. Colour is light buff with shades of brown, dull red or gray. Its sides have a white or light coloured pattern. Its head usually has dark stripes that start behind the eye and extend to the rear. It gets its name from the fact it rubs its own body from sides and produces rasping sound. This ill- tempered snake attacks any intruder. It is common in rural settlements, cultivated fields and regions, barns, and rock walls(4,14).
Sea snakes resemble cobra and its allies in structure of their fangs and most other characters. Most of them are 3-4 ft. long, and a few may attain a length of 8 feet. Their tails are laterally flattened and are sculled in paddle -like fashion during swimming. Most sea snakes are covered with small round scales and lack the enlarged ventral scales found in terrestrial species. The nostrils are valvularand hey can be closed when snake submerges- and may be displaced towards the top of the head. Excess salt from the sea water and diet is excreted through special glands in the snake’s mouth. Venomous sea snakes mostly inhabit the waters of Australia, Indonesia, Southeast Asia and India. Of the more than 50 species some are many times more poisonous than land snakes, with venom 10-40 times more potent than that of cobra. Except for a single species found in creeks and river estuaries sea snakes are all poisonous. They however have a narrow gape and rarely bite effectively.Their bite is relatively painless and, amazingly very low percentage of patients suffer significant envenomation during the attack. In a census in Malay Peninsula less than 25% developed features of poisoning and a small percentage became critically ill (4,12,14).
Snakes have a good sensory perception with primitive ears. Their vision is limited to few meters only, with better acuity for moving objects. Lower jaw is a pair of bones joined together centrally by an elastic ligament which doesn’t articulate with maxilla thus enabling the snake to swallow its prey as a whole. Fangs are modified teeth on pre maxilla. Venom is secreted from parotid glands and is meant to immoblise the small creatures like rat. Man is an innocent coincident victim. Bite is a well coordinated act involving movement of head and body. It involves coordinated positioning of head, opening of mouth, attack by forward thrust of body and head, piercing the skin by fangs and injecting the venom while the wound is deepened by contraction of temporalis muscle. Vipers have holes at the tip of fangs while elapids have gutters in the fangs(14,15).
Identification of Poisonous Snakes
Most of the bites are by non-poisonous snakes, but the intense fear of snake bites may cause acute panic reaction or feeling of impending death. If the patient has brought snake to the attending doctor, proper identification can help institute early and appropriate treatment to the victim and also alleviate undue emotional disturbance. Some of the important differentiating features of poisonous from non-poisonous snake are appended below(13,18).
(a) Fangs: The most distinctive feature of poisonous snakes is the fangs. These are modified teeth in the upper jaw, generally two in number, one on either side. They communicate with salivary glands and are hollow or grooved. In elapidae and sea snakes they are located in front, are short and immobile while they are large, curved and have wide range of movement in vipers.
(b) Scales on Belly: In poisonous snakes the belly scales are large and extend all across the belly. In non-poisonous snakes belly scales are small and generally don’t extend across the belly.
(c) Head: Vipers have heavier triangular head with small scales all over. In case of pit vipers a pit is located between the nostril and the eye. Cobra and Krait have large head scales. In cobra upper third labial is largest and touches the eye and nasal shield. In Kraits upper third labial does not touch the eye and nose, but the fourth lower labial scale on the under surface of mouth is the largest. All the poisonous sea snakes have large scales on the head and valved nostrils.
(d) Pupil: Poisonous snake have generally elliptical or vertical slit. However pupils are round in elapidae (cobra) and most non-poisonous snakes.
(e) Body design: Krait has central row of large scales on dorsal side, which are almost hexagonal. It has paired white or black stripes across the body in the banded Krait. Some cobras have spectacle-like mark on their hood.
(f) Fang marks: In non-poisonous snakes since all teeth are at same level so bite is stretched and bite marks are along a curved line i.e. row of bites,as in human bite. Bite site can be easily made out. In poisonous snakes since poisonous teeth are generally two (fang marks) and other teeth areat lower level, so only two,1-2 cm spaced puncture marks are seen. A distance of less than 10 mm signifies a small snake while a distance of over 15 mm is suggestive of a large snake. Sometimes one requires hand lens to identify these marks especially in cases of cobra or Krait bite. It is noteworthy that the size of the venom fangs has no relation to the virulence of the venom. The comparatively innocent Indo-MalayLachesis have enormous fangs, whilst the smallest fangs arefound in the Hydrophids which possess very potent venom.
(g) Sound: Most venomous snakes produce characteristic sounds, which may also help in recognition of snake. Russell’s viper produces “Hissing”, saw scaled viper “Rasping” and King Cobra “Growling” sounds.
Easy identification of different snakes is as follows:
- Cobra: Hood while alive, large scales on head. Pupil is round and 3rd upper labial touches the eye and nostril. Large belly scales extend acrossthe width.
- Krait : The fourth lower labial scale on the under surface of the mouth isthe largest. Hexagonal large scales in the central row on dorsal side. Body may be banded. Belly scales extend across the width.
- Viper : Triangular heavy head with small scales all over. Large belly scales extend across the width.
Snake venoms are the most complex of all natural venoms and poisons. The venom of any species might contain more than 100 different toxic and non-toxic proteins and peptides, and also non-protein toxins, carbohydrates, lipids, amines, and other small molecules. The toxins of most importance in human envenoming include those that affect the nervous, cardiovascular, and haemostatic systems, and cause tissue necrosis (21).
Snake venom is primarily meant to paralyse the prey, man is only accidental victim to whom snake strikes if threatened. Proteins constitute 90-95% of venom’s dry weight and they are responsible for almost all of its biological effects. Venom is made up of toxins, nontoxic proteins (which also have pharmacological properties), and many enzymes especially hydrolytic ones. Enzymes (molecular weight 13-150 KDa) make-up 80-90% of viperid and 25-70% of elapid venoms: digestive hydrolases, L-amino acid oxidase, phospholipases, thrombin-likepro-coagulant,andkallikrein-like serine proteasesand metalloproteinases (hemorrhagins), which damage vascular endothelium. Polypeptide toxins (mol weight 5-10 KDa) include cytotoxins, cardiotoxins, and postsynaptic neurotoxins (suchas Î±-bungarotoxin and Î±-Cobratoxin). Compounds with low molecular weight (up to 1.5 KDa) include metals, peptides, lipids, nucleosides, carbohydrates, amines, and oligopeptides, which inhibit angiotensin converting enzyme (ACE) and potentiate bradykinin (BPP). Phosphodiesterases interfere with the prey’s cardiac system, mainly to lower the blood pressure. Phospholipase A2 causes hemolysis by lysing the phospholipid cell membranes of red blood cells. Amino acid oxidasesand proteases are used for digestion. Amino acid oxidase also triggers some other enzymes and is responsible for the yellow colour of the venom of some species. Hyaluronidase increases tissue permeability to accelerate absorption of other enzymes into tissues. Some snake venoms carry fasciculins, like the mambas (Dendroaspis), which inhibit cholinesterase to make the prey lose muscle control (22,23).
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The most lethal venoms are those of elapids and sea snakes. These toxins are rapidly absorbed into the blood stream thereby causing rapid systemic effects. Large molecular weight viper toxins are absorbed slowly through lymphatics thereby staying longer at local site, hence more local effects. Pathophysiology of ophitoxemia is basically dependent on disruption of normal cellular functions. Some enzymes like hyaluronidase disseminate venom by breaking down tissue barriers. Ophitoxemia can lead to increase in vascular permeability thereby causing loss of blood and plasma volume in extravascular space. Collection of this fluid is responsible for edema and fluid loss, if significant it can lead to shock. Venom also has cytolytic effect leading to necrosis and secondary infection. Neurotoxic effect may lead to paralysis, cardiotoxic effect can cause cardiac arrest and likewise myotoxic or nephrotoxic effect can lead to rhabdomyolysis and renal failure. Ophitoxaemia also can lead to coagulation disturbances.
Among the various species, the lethal dose of venom, for cobra is 120 mg, Krait 60 mg and for Russell’s viper and saw scaled viper is 150 mg respectively. But clinical features and outcomes are not predictable as every bite does not cause complete envenomation.
Pathological effects of venom may not be noticed until about six hours (varying between 1.5-72 hours), and it may remain functionally active causing persistent coagulopathy even after three weeks of bite. Hence duration of antigenemia is an important determinant for the extent of pathological effect. It has been unequivocally proved by studying the venom levels by enzyme linked immunosorbent assay (ELISA), that effects due to envenomation depend on venom hours (i.e. Blood venom level x time elapsed between bite and institution of treatment) rather than blood levels alone. Hence with the same level of venom, features due to envenomation may become progressively severe with passage of time (14,20).
There are four distinct types of venom effects:
- Proteolytic venom dismantles the molecular structure of the area surrounding and including the bite.
- Hemotoxic venoms act on the heart and cardiovascular system.
- Neurotoxic venom acts on the nervous system and brain.
- Cytotoxic venom has a localized action at the site of the bite.
Pathophysiology of various biological effects of snake envenomation
The following few paragraphs shall describe the biological effects of venom.
(a) Local Swelling: Most viper bites cause local swelling at the site of bite, which starts within minutes of bite and massive swelling of the limb may develop within 48-72 hours. This is usually the result of hemorragins in the venom. This opens the endothelial pores resulting in leakage of plasma or whole blood. At times leakage may be so much that patient develops hypovolemic shock. This swelling is not due to any venous occlusion or infection. If the exudation is of whole blood, then later discoloration of the limb may develop. In contrast to Echis, in European adder V berus bites, spontaneous bleeding is rare but discolouration is common. Sometimes local swelling is delayed and compartment syndrome may result(10,13,17).
(b) Local Necrosis: In viper bites local necrosis appears late if at all and if it occurs, it is due to ischemia, mimicking dry gangrene. On the other hand in Cobra bite local necrosis appears early. Local swelling may develop after 2-3 hours but necrosis develops rapidly after that. It is due to cytolytic factors present in the venom and is a wet gangrene. As this dead tissue provides ideal setting for anaerobes, hence the putrid smell. An early excision is warranted (13).
(c) Non-specific early symptoms: With bites of some vipers e.g. V berus, V xanthina, Australian elapids, some rattle snakes etca few symptoms are common. Vomiting, headache, abdominal pain, explosive diarrhea and collapse can occur. These features resolve in 30-60 minutes, suggesting activation of kinin system followed by inhibition of bradykinin (13,17).
(d) Shock: It can develop due to extensive volume leak from vessels in cases of viper bite. It can result even before a limb gets swollen. Pulmonary intra vascular clotting, pulmonary edema and cardiac effects can be contributory factors for shock.
(e) Spontaneous haemorrhage: Haemorrhages can develop in patients with viper bites even days after the bite. These at times may be life threatening especially if they occur in brain. Local blisters at bite site appear to be depot of venom, which don’t get targeted by anti snake venom. Therefore one must keep in mind the delayed absorption from bite site in patients who present with late bleeding manifestations despite having been given anti-snake venom a few days back.
(f) Effect on Circulation: Some viper venoms contain procoagulant activity which activates prothrombin to thrombin; which in turn converts fibrinogen to fibrin while in others procoagulant venom may directly affect fibrinogen. This fibrin formed is susceptible to lysis unlike natural fibrin thus resulting in poorly clottable or non-clottable blood because of absent or very low levels of fibrinogen. It should be remembered that bleeding manifestations during envenomation are not generally due to coagulation disturbances but rather due to haemorrhagin. Platelet count may also be low though usually it is normal. Low platelet count is due to consumption of platelets in the repair of endothelial damage. Polymorphonuclearleucocytosis is common in all forms of envenomation especially severe envenomation. Both viper and elapidae bite may have hemolytic activity in vitro but abnormal hemolysis is rarely of clinical importance except probably in renal failure (13,17).
(g) Renal Failure: Renal failure is a common manifestation of viperine envenomation especially where treatment has been delayed. On renal biopsy acute tubular necrosis is the commonest underlying lesion in 50-70% of cases and acute cortical necrosis (patchy / diffuse) has been found in 20-25% of cases. Hypovolemia and shock are the usual underlying mechanism. Other contributory factors are hemo/ myoglobinuria, hemolysis, associated sepsis and disseminated intravascular coagulation (24). Glomerular lesions have also been described in snake bite cases. Merchant et al(25) have reported mesangial proliferation, splitting of basement membrane, swelling of endothelial cells and ballooning of glomerular capillaries, but the significance of these lesions in causing renal failure is not clear and is debatable. Seedat et al(26) reported two cases due to puff adder who developed oliguric renal failure and biopsy showed crescenticglomerulunephritis. Authors suspected hypersensitivity of venom as the cause. Occasional casesof severe glomerulonephritis related renal failure have been reported in the literature. Experimental studies carried out on the effect of Habu snake venom (found in Japan) has given some insight into understanding of the glomerular lesion. This venom contains hemorrhagin, like the venom of Echiscarinatus. Within 24 hours of injection of this venom destruction of mesangium occurs resulting in ballooning of capillaries which become packed with red cells and fibrin giving an appearance of blood cysts. This is followed by proliferation of mesangial cells giving appearance of segmental proliferative glomerulonephritis. Rarely crescents are observed. These studies provide evidence that these glomerular changes are due to vasculotoxic effects of hemorrhagin. However about tubular necrosis or cortical necrosis, the commonest lesion encountered in snake envenomation, there is no consensus that venom has any direct toxic effect in producing these lesions (27,28).
(h) Neurotoxic effects: Elapidae venom and sea snake venom cause neurotoxic effects due to neuromuscular blockade. Commonly affected muscles in elapidae bite are those of eye, tongue, throat and chest (leading to respiratory paralysis in severe envenomation). Neurotoxins are small molecular weight positively charged molecules with less antigenecity. Neuro- muscular blockade is produced by one of the following mechanisms. (a) Post synaptic block (Cobra) cobratoxin and alpha-bungarotoxins act similar to d-tubocurarine on the post synaptic membrane. There is no decrease in acetyl choline. Response to neostigmine is satisfactory. (b) Pre-synaptic blockade (Krait)beta- bungarotoxin acts like botulism toxin pre synaptically to block the neuro-muscular junction. Post junctional membrane remains sensitive to acetyl choline. The time required for neuromuscular block varies with impulse traffic, therefore intense physical activity shortens the interval between envenomation and neuromuscular block. Response to neostigmine is less satisfactory. It is important to note that these neurotoxins don’t cross the blood brain barrier and therefore do not cause alteration in consciousness. Hence in case of altered sensorium an alternative cause should be found (23,29).
(i) Cardiotoxic Effects: Cardiotoxin (Cobra) acts on cell membrane of skeletal, smooth and cardiac muscle to produce paralysis and cardiac asystole. Cobramine B and cytoxin cause irreversible depolarization of cell membrane and systolic cardiac arrest. Hyperkalemia following massive hemolysis or rhabdomyolysis also depresses cardiac function.
(j) Myotoxic Effects: Although sea snake venom appears to be neurotoxic in animal experiments, the effects in man are primarily myotoxic. There is diffuse effect on all muscles though local effects at the site of bite are minimal. In humans bitten by sea snakes the findings are typical of generalized myopathic lesions in skeletal muscle. Damage to muscles- rhabdomyolysis and hyperkalemia resulting from it may be life threatening. Snake envenomation has so diverse effects that every system of the body is affected directly or indirectly (20,29).
Since ancient times snakes have been worshiped, feared or loathed in India. It is a common and frequently devastating environmental and occupational disease, especially in rural areas of our country. India has the highest number of death to snake bite in the world. One of the major gaps in the battle against snakebite in India is the lack of qualitative work. Most Herpetology text books give snake identification data that is overtly complex and of little use to doctors. Snakes are misidentified by doctors in most cases where snake is brought to the hospital. Without the snake, identification based on symptomatology is clearly fraught with problems. The doctors should be aware of discovery of a new poisonous snake, the Hump-nosed Pitviper (Hypnale Hypnale) which has no available antivenom at present. Community education, appropriate training of medical staff and better distribution of anti venom, especially in the states with the high prevalence, could reduce snakebite deaths in India.
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