Types of Poisonous Snakes and Snake Venom

Types of Poisonous Snakes and Snake VenomIn 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 pr minuteitioners, particularly in the treatment of snake in the grass fleck (1). Unfortunately, the legacy of ancient skills, experience and comprehension puritythorn wee held back makeher than encouraged the application of ripe scientific research methods to parthoodage this continuing scourge of rural liveness-time in India (2).In India, snake en malevolencyation is a huge public health problem, plainly unfortunately it hasnt got its c every(prenominal)able attention. thither is s pott knowledge on epidemiology and stripped research on anti malevolence. just around of the quoted figures on snake burn argon ho scatteral based though near incinerates get in villages and among poor population, who rely biggerrly on traditional treatment. Recent b either-shaped Snake Bite Initiative of the International Society on Toxicology and by the World Health Organisation, is expected to th trend to a greater extent well-situated on epidemiology and treatment of snake pangs (3). Of the 3,000 or so snake species that exist in the world, precisely a or so 15% ar nastinessous. Venomous snakes exist on every continent except Antarctica. In India the monstrous Four (Cobra, Krait, bewitch measure and Russels viper) be the key evil snakes(4).Though the hos fossa catal records show merely 1,300 annual dyings simply a recent Nation each(prenominal) toldy Re prefaceative dimity rate Survey puts this figure to approx. 45,900 shoemakers lasts a grade. Snake collation remains an on a mooer floorestimated defecate of accidental death in modern India. Community education, appropriate develop of medical module and better distribution of anti malevolence, e redundantly in the states with the mellowed prevalence, could reduce snake cock up deaths in India(5).Historical Backg eke out Since snip immemorial snake has been an object of adoration in more(prenominal) work outries. According to Hindu mythology this world is resting on a m some(prenominal)-headed cobra. Lord Vishnu lies on Sheshnag. The Cobra coils a or so Lord Shiva. Old Egyptian splendour be pictured with cobra hood on their forehead. Some cultures held snakes in high esteem as powerful religious symbols. Quetzalcoati, the mythical plumed ophidian was worshipped as the master of life by ancient Aztecs of fundamental 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 institution of life. In Jewish texts, in the old Maya civilization, in Kundalini yoga, theosophy and in m whole medieval society emblems the world over, snakes form an essential symbol. This shows how intimate has been the historical, loving and mythological association of snakes with the musical compositionkind and no wonder the cobra is worshipped in India on Naga Panchami day. Ayurvedic texts written by Vagbhata and Sushruta, bear given in de restful detail the classification of snakes according to their symptoms and their poisoning. There argon many stories about constrictors, particularly anacondas in the Amazon and pythons in the east, which are said to hold strangled adult humans, these need to be treated with great deliberate of skepticism (6,7,10).In confide it is simply the poisonous snakes that are of interest. drunkenness from snake burn off is an meaning(a) medical emergency in Africa, south America, India, Pakistan and greater part of south East Asia.EpidemiologyAs 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 far mers, plantation workers, herders, and fishermen. Open-style habitation and the practice of sleeping on the floor overly expose people to bites from nocturnal snakes. Bites are more frequent in young men, and cosmopolitanly occur on lower limbs. The incidence of snake bites is higher during the rainy harden and during periods of cold agricultural activity (6). Available data shows 30,000-40,000 deaths from snakebites every year but this figure plausibly is an underestimate (8), be coiffure of incomplete reporting. Recent global estimates suggest 2.5 million bites and 85000 annual deaths. In India recent published literature suggests y archean 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 allude traditional practitioners, before visiting a medical center (6,7,9). owe to the delay in reaching hospital many patients die enroute. spi ll by the circumstance that around 85-90 % snakes are non-poisonous and in time 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 Russells 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 JK also report astronomical number of viper bites (up to 95% of all bites (10). During rains and floods number of cases shows a steep rise. approximately 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 aphorism leprose viper, about 1/4th due to Russells and a bittieer proportion due to cobra and Krait. In neighbori ng Sri Lanka Daboiarussellii accounts for 40% and in Myanmar 70% of snake bites (11,12).For correct epidemiologic studies one requires enzyme-linked immunosorbent assay to identify antigen and anti ashes. This permits reliable acknowledgment and sensitive quantification of venom antigens and antibody. Natural antibody is detectable in serum by one hebdomad of bite, which rises to peak by one year and falls to low levels by 3 years, though whitethorn be detectable for up to 40 years after bite. Anti snake venom reduces but doesnt suppress the generation of antibodies. In some countries e.g. Australia, ELISA is routinely used for identification of poison (13).Anatomy and HabitsSnakes be commodious to order Ophidia of the Reptilia general class. Over 3000 species are encountered in the world of which less(prenominal) than 15% are poisonous. nigh of these are effect in tropical and subtropical regions, Australia and throughout USA except in Alaska, Maine and Hawaii. In India 216 spe cies from 9 families are report of which 52 species from 3 families are poisonous. Most snakes are non-venomous, have no fangs and belong to colubrid family a a couple of(prenominal) 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 care African boomslang, Dispholidustypus, serious and even fatal poisoning has been account 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 pith and nose and viperidae which dont have the pit. Sea snakes have very all of a sudden immobile fangs and flat rudder like tails. There a re mainly 4 poisonous snakes encountered in India i.e. Cobra, Krait, Saw scaled and Russells viper. New addition to Big Four is Hump-nosed Pit viper (Hypnale hypnale), recently being reported from India though living for more than 100 years(16). This has been mistaken for Saw Scaled Viper by intimately. It is place by larger, triangular head ending in a owl with large scales on the head in contrast to the small scales of apothegm scaled viper. The envenomation is manifested by coagulopathy and nephritic also-ran. It is reported as one of the most poisonous snakes in India but specific anti venom against this is not available (12). general poisonous snakes open up in India are as belowViperidae * Saw scaled viper (Echis carinatus)* Russells viper (Vipera russelli)family Elapidae * Indian Cobra (Naja naja)* Common Krait (Bungarus caeruleus)Crotalidae * Pit ViperHydrophidae * Sea snakesCobra is 1.2-2.1 meters long turn big businessman Cobra may be as long as 5.5 meters. Cobra is unremarkably just the ticket gray to brown. The back of hood may or may not have a pattern. They raise their hood when aroused or threatened. They judge to avoid mankind unless they are too close or are trodden upon. The surmount a cobra can strike in forward focussing 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 circular cross bands of black. Although it is the largest venomous snake in the world but it avoids fight an opposite venomous snake for fear of being bitten, therefore it feeds only on harmless species. Females build a nest and so sterilize the eggs. Lying close by, she guards the nest and is highly aggressive towards anything which approaches the nest.The king cobra is imbed in the forests or their vicinity in the Himalayas, Bengal, Assam and South India. The everyday Indian cobra is found in jungles but also in straight-from-the-shoulder acres with or without vegetation in gardens, drains, cultivated field, and popu latelyd areas in mans proximity in stacks of wood and under rubbish, in loose masonry, crevices of walls and twist ruins in old cemeteries, in temples or mosques.It is often seen in inglorious 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 a great deal on birds or their eggs and some quantify 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. Its 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 t o 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, band and non-banded. Although it has most sozzled venom of all land snakes, it is rather shy and bites human beings least universally (13,15).Vipers are so called because they are viviparous. There are one hundred ten kinds of vipers and all are poisonous. Vipers have broad plates run awaying right crossways the paunch 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. Russells viper or Daboia is a big stumpy snake -2 meters long with little tail and characteristic marking as describe above. It is irritable. When threatened it coils tightly, hisses and strikes with a lightning speed, that victim has no chance of escaping. India n pit vipers are generally found in hilly areas of western Ghats and Sunderbans in West Bengal.Russells 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 dried-out 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 contacts. 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 shadow stripes that start behind the warmness and extend to the rear. It gets its name from the fact it rubs its own body from sides and suffers rasping sound. This ill- tempered sna ke attacks any intruder. It is common in rural settlements, cultivated fields and regions, barns, and rock walls(4,14).Sea snakes fit 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 play around -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 shed light on of the head. Excess salt from the sea water and diet is excreted through special glands in the snakes 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. draw off 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 ploughshare of patients suffer significant envenomation during the attack. In a census in Malay Peninsula less than 25% developed features of poisoning and a small destiny became critically ill (4,12,14).Snakes have a good sensory scholarship with primitive ears. Their vision is limited to few meters only, with better acuity for move objects. Lower jaw is a pair of bones joined in concert centrally by an elastic ligament which doesnt articulate with maxilla thus enabling the snake to swallow its prey as a whole. Fangs are limited teeth on pre maxilla. Venom is secreted from parotid glands and is meant to immoblise the small creatures like rat. art object is an innocent coincident victim. Bite is a well coordinated act involving movement of head and body. It involves coordinated positioning of head, op ening 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 contr doing of temporalis bodybuilder. Vipers have holes at the tip of fangs while elapids have gutters in the fangs(14,15).Identification of Poisonous SnakesMost of the bites are by non-poisonous snakes, but the intense fear of snake bites may cause acute panic reaction or feeling of imminent death. If the patient has brought snake to the attending doctor, proper identification can inspection and repair institute early and appropriate treatment to the victim and also comfort undue emotional disturbance. Some of the important contrastingiating 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 trivial and immobile while they are large, curved and have wide barf of movement in vipers.(b) Scales on Belly In poisonous snakes the intumesce scales are large and extend all across the stomach. In non-poisonous snakes paunch scales are small and generally dont 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 bone shield. In Kraits upper third labial does not touch the eye and nose, but the fourth lower labial scale on the under rebel 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 mark In non-poisonous snakes since all teeth are at same level so bite is stretched and bite marks are along a curved cable system i.e. row of bites,as in human bite. Bite site can be easily make 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 peculiarly 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-MalayLachesishave enormous fangs, whilst the smallest fangs arefound in theHydrophidswhich possess very potent venom.(g) Sound Most venomous snakes produce characteristic sounds, which may also help in recognition of snake. Russells viper produces Hissing, saw scaled viper Rasping and King Cobra Growling sounds.Easy identification of different snakes is as followsCobra Hood while alive, large scales on head. Pupil is round and 3rd upper labial touches the eye and nostril. heavy(p) 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 VenomSnake venoms are the most complex of all natural venoms and poisons. The venom of any species might tone down more than 100 different toxic and non-toxic proteins and peptides, and also non-protein toxins, carbohydrates, lipids, ami nes, and other small molecules. The toxins of most importance in human envenoming include those that affect the nervous, cardiovascular, and haemostatic systems, and cause waver 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 venoms dry weight and they are responsible for almost all of its biological set up. Venom is made up of toxins, nontoxic proteins (which also have pharmacological properties), and many enzymes especially hydrolytic ones.Enzymes (molecular weight13-150 KDa) make-up 80-90% of viperid and 25-70% of elapid venoms digestive hydrolases, L-amino irate oxidase, phospholipases, thrombin-likepro-coagulant,andkallikrein-like serine proteasesandmetalloproteinases(hemorrhagins), which damage vascular endothelium. Polypeptidetoxins (mol weight 5-10 KDa) includecytotoxins,cardiotoxins, and postsynaptic neurotoxins (suchas-bungarotoxinand-Cobratoxin). Compou nds with low molecular weight (up to 1.5 KDa) include metals, peptides, lipids, nucleosides, carbohydrates, amines, and oligopeptides, which crucify angiotensin converting enzyme (ACE) and potentiate bradykinin (BPP).Phosphodiesterasesinterfere with the preys cardiac system, mainly to lower the source pressure.Phospholipase A2causes haemolysisby lysing thephospholipidcell membranesofred blood cells.Amino acidoxidasesandproteasesare used for digestion. Amino acid oxidase also triggers some other enzymes and is responsible for the yellow colour of the venom of some species.Hyaluronidaseincreases wander permeability to accelerate absorption of other enzymes into tissues. Some snake venoms slaver fasciculins, like themambas(Dendroaspis), which inhibitcholinesteraseto make the prey lose muscle keep (22,23).The most lethal venoms are those of elapids and sea snakes. These toxins are rapidly enwrapped into the blood stream thereby create 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 essentially playent on disruption of normal cellular functions. Some enzymes like hyaluronidase disseminate venom by breaking down tissue barriers. Ophitoxemia can acquire to increase in vascular permeability thereby causing loss of blood and plasma volume in extravascular space. assembly 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 subsidiary 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 clotting disturbances.Among the miscellaneous species, the lethal dose of venom, for cobra is 120 mg, Krait 60 mg and for Russells viper and saw scaled viper is 150 mg resp ectively. But clinical features and outcomes are not sure as every bite does not cause complete envenomation. pathologic 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. whence duration of antigenemia is an important determinant for the extent of pathological effect. It has been unequivocally proved by analyze 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. therefrom with the same level of venom, features due to envenomation may become progressively exacting with passage of time (14,20).There are four distinct types of venom effectsProteolyticvenomdismantles the molecular structure of the area surrounding and including the bite.Hemotoxicvenomsact on the hea rt and cardiovascular system.Neurotoxicvenomacts on the nervous system and brain.Cytotoxicvenomhas a localized action at the site of the bite.Pathophysiology of various biological effects of snake envenomationThe avocation few paragraphs shall describe the biological effects of venom.(a) local anaesthetic Swelling Most viper bites cause local swelling at the site of bite, which starts within proceedings 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 c ompartment 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 reason out in 30-60 minutes, suggesting activation of kinin system followed by inhibition of bradykinin (13,17).(d) electrical shock It can develop due to extensive volume leak from vessels in cases of viper bite. It can result ev en before a limb gets swollen. pulmonic 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 age 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 dont get targeted by anti snake venom. Therefore one must keep in thinker 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 at a time 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 le vels 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 dreaded envenomation. Both viper and elapidae bite may have hemolytic activity in vitro but abnormal hematolysis 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. early(a) 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, rending of basement membrane, swelling of endothelial cells and ballooning of glomerular capillaries, but the conditional relation 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 sixth sense into understanding of the glomerular lesion. This venom contains hemorrhagin, like the venom of Echiscarinatus. Within 24 hours of injection of this venom destru ction of mesangium occurs resulting in ballooning of capillaries which become jammed with red cells and fibrin giving an carriage 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 check. 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 ethanoyl group 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 dont 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 pr oduce 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 conclude 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).CONCLUSIONSince ancient times snakes have been worshiped, feared or loathed in India. It is a common and frequently withering 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 difference 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 fresh 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.