Snake Bite Instructions

SNAKES, VENOM & SNAKE BITE
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Dr Joseph.K.Joseph
Introduction Anatomy & Physiology Species
INTRODUCTION
Snake bite is a preventable public health hazard in tropical and subtropical countries which abound with dense vegetation and vast tracts of agricultural land. India has always been a land of exotic snakes.
India is estimated to have the highest snake bite mortality in the world with WHO estimates placing the number in between 15,000 to 30,000 per annum. The oft quoted figure till recently was around 50,000. Some experts think that it could be as low as 10,000 per annum. Why the discrepancy is because of our very poor system of entry, retrieval and reporting of morbidity and Venom & Bite mortality. These figures does not count various deaths due to snake bites in villages and other remote areas in our country including the tropical mountainous zones in various hill states. It is quite unfortunate that most of the deaths in our country are Occupational due to fright and wrong line of treatment
Risk and Other Ecological Factors Prevention
ANATOMY & PHYSIOLOGY

Reptiles are more primitive than mammals in their origin. Snakes belong to the generic class, reptilian, under the order Ophidia.
Anatomically speaking snakes have an elongated body divided into head, trunk or body and tail. A snake has no external appendages. The body is covered by scales, which have distinctive characteristics, in highly evolved and poisonous varieties. They have eyes with round or vertical pupil but no eyelids. They have a pair of primitive internal ears without external Investigation appendages. The tongue is bifid and quivers in and out through the opening in the jaw. In poisonous varieties there are modified teeth usually two in number and occasionally more than one pair called fangs which are present in the pre-maxilla and Snake Bite not in the mandibles. The fangs are channels for pouring venom, either in the form of a gutter as in Cobra or hollow with a tiny Treatment opening at the pointed end, like a hypodermic needle, as seen in Russells Viper (Daboia Russeli). At the base of the fangs Protocol opens the duct of the poison gland, one on either side of the upper fang below the orbit. Anteriorly the gland opens into a narrow venom duct which ends in an ampulla like dilatation at the base of the fangs. Snakes are provided with an elementary Complications digestive system, respiratory system, urogenital system, circulatory system and nervous system.
and Treatment Future
Snakes have no thermoregulatory mechanisms and therefore they are described as cold blooded animals. They have no sweat glands and a three chambered heart with a solitary lung makes them inefficient in physiological adjustment to high or very low external temperature and bright light. Except for certain species like saw Scaled Viper (Echis Carinatus Carpet Viper), snakes prefer a tolerable amount of humidity, darkness and quietness. Snakes are non vegetarians by feeding habit and live mainly on insects, smaller snakes, frogs, lizards and young mice or rats. It prefers food killed by it. The range of vision in the snake is limited and is mainly confined to a very close range and is more active on moving objects. The incidence of bite is therefore very much restricted to moving objects at closest proximity to its head. The eyes of snakes are without lids and hence they are fixed or unblinking vision. To substitute the loss of eye lids, a scale on the head is modified as a transparent covering to protect the eyes. This covering looks like goggles on the eyes of snakes and called epidermal membrane. The intricate apparatus of hearing is absent in them. They feel vibrations coming from solid objects through their skin and get sufficient warning of danger. The sense of taste is poor in snakes and it is compensated by a strong sense of smell. Most snakes rely heavily upon their keen sense of smell in the location of food, the avoidance of predators and for perceiving their environment. For their acute and efficient sense of smell therefore, they use their long forked and flickering tongues to taste the ground and air for detecting scent particles. The tongue is waved intermittently with flickering movement. During this act the scent particles from their surroundings are collected and absorbed on the surface and are brought into the mouth where they are introduced to the Jacobsons Organ which is a special organ of smell in reptiles. This organ of scent smell is located in the roof of mouth cavity. With their remarkable sense of scent smell the snakes can trace their prey with the help of the scent trail left behind by them. Some venomous snakes of tropical countries possess this amazing device known as pit organ to see in the darkness in a well developed form. It has now been discovered that they contain an organ of amazing complexity which is highly sensitive to even the slightest traces of infra red radiation that naturally emanates from the body of warm blooded animals such as rats, mice or birds, which constitute the normal food of these snakes. It is remarkable to note that the pit organs which are infrared receptors is the most efficient of all the thermal receptors found in the animal world. They are so sensitive that they can detect a temperature change of as minute as 1/3000th of a degree Celsius in the surrounding environment. In contrast to it, the most sensitive thermal receptors of the human eyelids can discriminate a temperature difference of only 1/20th of a degree Celsius.
SPECIES
There are some 2700 described species of snakes in the world coming under 402 genera and 18 families, of these some 500 species are venomous. 275 species of snakes have been described from India belonging to 71 genera and 11 families. Out of these 275 species 62 species can be categorized as Venomous 42 as mildly venomous and 171 as non venomous. Of the 62 venomous species, 42 are seen on land and 20 in the sea.
http://www.physicianbyte.com/SnakesVenomAndSnakeBite.aspx
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Substantial number of snake bites in India is due to non poisonous snakes. Even, many a bites by the poisonous snakes are dry bites implying that the snakes fail to inject the venom. However, the non poisonous bites and the dry bites may cause panic reaction and local injury. In a generalized form one can say that about 70% of bites are due to non poisonous snakes; of the rest 30%, 15% are dry bites and only 15% bites are the one which causes envenomation. In India the poisonous snakes belong to three broad families; Family Elapidae (Cobras, Kraits & Coral Snakes) Family Viperidae The family of Viperidae has two subfamilies Viperidae (Russells Viper, Saw Scaled Viper) Crotalinae (Pit Viper) Family Hydrophidae Sea Snakes So Four among the poisonous snakes in India are highly venomous namely 1. Cobra Naja naja (Spectacled Cobra) 2. Russells Viper (Vipera russelli or Daboia Russelli) 3. Saw Scaled Viper (Echis Carinatus) 4. Krait (Bungarus Caerules) However this concept has led to some serious problems 1. ASV manufactures only produce antivenom against these species 2. The assumption that only The Big 4 can cause serious symptoms and death has led to misidentification of species. Other deadly snakes may be going unnoticed and causing death and disability. The recent discovery of the Hump nosed Pit Viper (Hypnale Hypnale) as a species capable of causing life threatening symptoms has demonstrated this. In order to determine the actual list of medically significant species in India, the old concept of The Big 4 is to be abandoned for a newer more flexible model that enables better classification of species. About 80% of venomous snake bite in India by the saw-scaled Viper. However it may show geographic variation. Most of the bites in the Western states Rajasthan & Maharashtra are from saw scaled viper. In Kerala at the southern tip of the peninsular India most of the bites are due to the Russells Viper and Cobra. In Tamil Nadu, the bites are mainly from Cobra, Krait and some by saw-scaled Viper. In Bengal it is mostly due to Russells Viper, Krait and Cobra except the saw-scaled Viper. In hill terrain of the northern Himalayas Krait bites are common. Bites from the hump nosed pit viper (Hypnale Hypnate) are being reported from the states of Kerala, Tamil Nadu and Maharashtra. Rajasthan reports bites from Sochurekis saw scaled viper (Echis Carinatus Sochureki). The polyvalent snake anti venom used in India is found less effective for bites from Hump nose Viper and Sochureks saw scaled Viper. The only rear-fanged snake definitely known to be venomous is the Himalayan keelback (Rhabdophis Himalayans). The W.H.O classification developed in 1981, has been adopted in India as the preferred method for categorizing snakes of medical importance. Class I : Commonly cause death or serious disability Russells Viper/Cobra/Saw-scaled Viper Class II : Uncommonly cause bites but are recorded to cause serious effects (death or local necrosis) Krait/Hump nosed Pit Viper/King Cobra/Mountain Pit Viper Class III : Commonly cause bites but serious effects are very uncommon Snake Venom: The snake Venom is a complex fluid with powerful ingredients and is secreted by the parotid glands, mainly for immobilizing, killing & digesting small animals like rats. Hence snake bite in humans is a mere accident not designed by nature. Elapidae inject venom through gutters in fangs, while the viperidae do so through tiny holes at the tip of the fangs. A snake can bite and continue to secrete the venom a number of times in succession. The lethal dose of the venoms for a man has been reported to be (Deoras 1965). Cobra - 0.12 g Krait 0.06 g Russells Viper 0.15 g Echis Carinatus- 0.08 g The Venom output in all the species appear to vary in season to season. During the summer months the output is more than in the winter, when the venom is viscous and comes out in small quantities. This may explain the higher mortality rate by Snake bites in the summer months including the monsoon. It is estimated that most snakes inject about 10% percent of the available venom in a single strike.
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The snakes have the most complex of all venoms. More than 90% dry weight is protein comprising a rich variety of Enzymes, non-enzymatic polypeptide toxins and nontoxic proteins such as nerve growth factor. Non protein ingredients of venom include carbohydrate and metals (often part of glycoproteins & metalloprotein enzymes) lipids, free amino acids, nucleosides and biogenic amines such as serotonin and Acetyl Choline. About 80 90% of Viperidae & 25% to 70% of Elapidae Venom consists of enzymes. The role of enzymes in envenoming is most clearly seen in the case of Venom pro coagulants. For example, Vipera Russelli Venom contains : a) Glycoprotein which activates Factor X b) Arginine esterhydrolase which activates Factor V Echis Carinatus Venom (Saw-scaled Viper) contains a zinc metalloprotein Ecarin which activates prothrombin. Many crotalinae venoms (Pit Viper) contain proteases which cleaves fibrinogen molecule, for example Arvin or ancrod (c rhodostoma) and botorxin or Reptilase (B. atrain). Phospholipase A2 is the most wide spread and extensively studied of all venom enzymes. Up to 30% of protein content is Phospholipase A2, presenting in the form of seven isoenzsymes. Under experimental condition it damages mitochondria, red blood cells, leucocytes, platelets, peripheral nerve endings skeletal muscle, vascular endothelium and other membrane and produces presynaptic neurotoxic activity, opiate like sedative effects and autopharmacological release of histamine. Hence Phospoholipase A2 activity contributes to many of the clinical manifestation of envenoming. They include, hemolysis, Rhabdomyolysis, pre-synaptic neurotoxicity, hepatic necrosis, platelet damage, oedema formation, vasodilatation causing shock, release of endogenous autacoids such as histamine serotonin and slow releasing substances, may contribute to the local pain and permeability changes at the site of snake bite. Polypetide Toxins (Neurotoxins): The Polypeptide toxins often called neurotoxins are low molecular weight, non enzymatic proteins found almost in elapidae and hydrophidae venoms. Post synaptic (alpha-Neurotoxins) such as Alpha Bungarotoxins and Cobrotoxin, contain about 60-62 Short chains or 66-74 long chains aminoacid residues and bind to acetyl choline receptors on the motor end plate.Toxic phospholipase-A2 can block neuromuscular transmission by acting pre or post synaptically, can damage skeletal muscles and may be cardio toxic. Pre-synaptic (beta) neurotoxins such as Beta-bungarotoxins, Crotoxin and Taipoxin contain about 120-140 aminoacid residues and a phospholipase A subunit. These release acetyl choline at the nerve endings at Neuromuscular junction and then damage the endings, preventing further release of Acetyl choline. It is now well established that the neurotoxins of Elapid venoms induce neuromuscular block of non-depolarizing type similar to that of curare. However the action differs from that of Curare in the slowness of development and blockade of long duration, acting only on nicotinic acetyl choline receptors by competitive antagonism. Neurotoxins in elapid venom fall into one of two groups according to the mechanism by which they block neuromuscular transmission. The first comprising of alpha bungarotoxin, Cobrotoxin. They produce anti-depolarising neuromuscular block by acting on the post junctional membrane. Short Chain neurotoxins Cobrotoxin, Erabutoxin Long Chain neurotoxins alpha bungarotoxin Blockade by Short Chain neurotoxin is more readily reversible than that with long chain toxins. Both Cobrotoxin and alphabungaratoxins do not inhibit Acetylcholine output from nerve endings; both neurotoxin produce competitive inhibition of the motor end plate similar to d - tubocurarine. On the other hand, the second group beta-bungarotoxin produces the block by acting pre-synaptically on the motor nerve endings, having the sensitivity of the end plate to Acetyl Choline unaffected. Alpha Bungarotoxin and Cobrotoxin has no direct action on the muscle. Experimental studies have shown that the neuromuscular blockade caused by Alpha Bungarotoxin &Cobratoxin can be reversed by neostigmine. Electrophysiologically Alpha bungarotoxin and Cobratoxin depress the End plate Potential (EPP) without affecting Terminal nerve spike, resting membrane potential and action potential by the muscle. An exclusively pre-synaptic action is characteristic of second group of neuro-toxins Beta bungarotoxin. This neurotoxin produces a neuromuscular block and severe reduction in Acetyl Choline output only after a latent period of more than one hour. In clinical practice this would mean an early precipitation of neuromuscular paralysis by physical activity after envenomation, while a restful muscle relaxation would retard the onset of neuromuscular block. Haemorrhagins (HR 1 & HR 2): Haemorrhagins, two immunologically distinct non enzymatic haemorrhagic principles (HR 1 & HR 2) are typical components of Crotalid (Pit viper) and Viperid (true Viper) venoms. They cause acute, rapid haemorrhage. In many instances of serve envenomation, the haemorrhagins play a major lethal role by causing haemorrhage in the vital organs. eg. the Brain, Lungs, kidneys, heart and gastro-intestinal tract. Pharmacologically, the haemorrhagins have been demonstrated to be seperate entities from proteolytic enzymes in the venom. It has been observed that they cause severe vasoconstriction followed by vasodilatation of micro-vessels and arterioles with haemorrhage in the capillary bed. The haemorrhagins act by directly disrupting the endothelial lining and by inhibiting platelet aggregation. Pharmacological studies have further shown that the haemorrhagic principles induce the release of certain autopharmacological mediators such as histamine and 5-HT from various tissues which open up endothelial cell junction and disrupt the isolated basement membrane, presumably in an enzymatic mode of action thus causing vascular damage and haemorrhage. Similarily vasculotoxic changes have also been observed in the renal and cerebral vessels with crotalid venom. The observed vasculotoxic changes resulting in severe cutaneous and systemic haemorrhage particularly in kidneys, lungs and brain, bear a close resemblance to that of experimental schwartzman phenomenon with bacterial toxins.
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name="Introduction" id="A4" class="articlesubtitle_txt">TABLE Enzymatic components in Snake Venom ENZYME EFFECTS
Arginin ester hydrolase Bradykinin release, interference with clotting Collagenase Hyaluronidase A Phospholipase A Phospholipase B Phosphodiesterase Digestion of Collagen Reduction of Collagen Viscosity. Promotes the spread of venon through tissues Uncoupling of oxidative phasphorilation Hydrolysis of lysophosphatids Inhibition of DNA, RNA, arabinose derivatives
Acetyl cholinesterases Catalysis hydrolysis of Ach. But this is no longer thought to contribute to their neurotoxicity 5 nucleotidiase L aminoacid oxidase Specific hydrolysis of Phosphate mono-esterases which links with 5 position of DNA, RNA Catalysis of aminoacid oxidation gives colour of venom.
Thrombin like enzymes Depression of fibrinogen levels. Non-Enzymatic components in Snake Venom COMPONENT Neurotoxins (elapidae) Cobrotoxin Erabutoxin Alpha Bungarotoxin Cerelotoxin Beta Bungarotoxin Crotoxin Taipoxin Haemorrhagins (HR-1, HR-2) Viperidae, Crotalidae EFFECTS Post synaptic non depolarizing neuromuscular blockade of long duration, acting only on nicotinic acetyl choline receptors to some extend cardiotoxic Acetyl choline receptors to some extend cardiotoxic Haemotoxic and anticoaguland-blinds to receptors Similar post synaptic block but without binding to receptors
Pre-synaptic motor nerve end blockade
Direct disruption of vessel endothelium Procoagulant effects Factor IX activation by cleavage of peptide bond IX by Russells, Factor X activation by Ca++ binding to gammaglutamic residues in F.X with rapid change Xa, direct prothrombin activation by cleavage of peptide bonds by venom, producing an intermediate which quickly converts to thrombin. Prolonged defibrination without thrombocytopenia in Echis Carinatus bites. Contd.
Non-Enzymatic components in Snake Venom COMPONENT EFFECTS Anti coagulant effect Cardiotoxin (CTX) Inhibition of platelet aggregation, inhibition of clotting factors or their activation, direct fibrinolysis or fibrinogenolysis, by direct- action on plasminogen or its proactivator. Note : The venom can exhibit, pro, anticoagulation, fibrinolytic or fibrinogenolytic activity Neuromuscular blockade, haemolysis, cytotoxicity cardiac arrest
(Naja naga atra)
VENOM & BITE:

Most prey of snakes is warm-blooded mammals for which the venom has been designed. The normal temperature of humans is the optimum temperature at which most of the snake venom enzymes are most active and therefore devastating. The snake bites as a measure of self-defence when it perceives a threat, or when it is hurt or is accidently stepped upon etc. Usually the snake gives ample warning of its presence by various means, rubbing scales to produce a sound, loud hiss, swaying of the head, posturing etc. depending on the species. It is when the warning is not heeded that the snake usually bites. The amount of venom injected and its consequences depend on a number of factors. The most serious venomous bites are those in which the venom is directly injected into a blood vessel which is very rare. Bites on parts having large adipose tissue are less serious since adipose tissue delays venom absorption as it has a relatively poor blood supply as also because of loculation. Therefore, in bites over parts covered with fat. eg. Buttock, belly etc. the absorption of venom may be delayed. Bites in the scalp and face are the worst, as they have subcutaneous tissue and are richly vascular as also the proximity to the central circulation. The amount of venom injected by the snake would probably be the same irrespective of the size of the human victim. This being so, bites are more serious in children as the extent of distribution of the venom would be less with a lower body mass, also due to lesser fat in children. The more rapid circulation in children results in a more rapid absorption of venom when compared to adults. The bite characteristics are relevant i.e whether a full two-fanged one, a deflected bite or single-fanged one. Presence of teeth marks would suggest that the snake had bitten hard and also had probably clung on. Bites over bony prominences may be less serious. The size of the snake and the conditions of the fangs has relevance.
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A curious feature of the venom is that its composition not only differs from species to species, but may differ even among individuals of the same species representing different geographical races and surprisingly even among individuals of the same litter. There is significant difference in symptomatology amongst the snake species from area to area, which may have profound implications in the treatment aspect. For instance viper venom from South India and Sri Lanka can cause some serious neurotoxic effect also. The Haffkine Anti Snake Venom (ASV) is thought to be not as effective in envenomed patients in Burma and Sri Lanka as in India. The ASV is prepared from pooled samples of Venom. As the number of supplies of Venom is limited the chances of a sufficiently bio diverse pool are remote. This means that the ASV that shows a better result in victims from peninsular India may not show as good as result in the North East. Snakes shedding their skin are likely to be more irritable and, therefore, more dangerous due to the fact that they are partially blind at that time. Paradoxically enough, the new born and the very young have more potent venom than adults. This is natures way of compensating for the lesser quantity in the new born and the very young. Venom is absorbed from the bite site by way of the lymphatics and the venous system. The lower molecular weight fractions are carried from the capillaries into the venous system, whereas the relative larger molecular weight fractions are carried through the lymphatics. The Lymphatics are thin walled and easily compressible needing a few mm pressure for occlusion whereas a pressure of 25-35 mm Hg. would be required for venous compression. The venom delivery system: The venom delivery system consists of the fangs and the ducts which convey the venom from the glands to the fangs. The fangs are teeth modified to inject venom into prey and there are two one on either side. They are backward curved (All teeth are backward curved to prevent a pray seized by the mouth from escaping), hollow, with sharp, pointed ends. They may be very short 2 to 4 mm long as in Kraits & sea snakes, or 5-10 mm long as in Cobras or 8-10 mm long as in the King Cobra. A large Russell viper may have fangs 15 mm long. Fangs are of two types the fixed fangs and the movable, folding fangs. The fangs of the elapid like Cobra, Krait, Coral Snakes and hydrophids are fixed more or less immobile. The Viperidae Pit viper & Russells vipers have longer fangs and are kept folded backward & upward against the roof of the mouth. During the lifetime of the snake, the fangs like the other teeth, are shed and are replaced regularly. A series of 5 to 7 replacement fangs lie in the gums behind and above the functional fangs. If the functional fang wears out or is damaged or lost, it is replaced by the next fang and the process goes on through the snakes life time. The enzymes and other components have different destructive properties. Cytotoxins, damage the tissues Haemotoxins cause heavy bleeding internally and externally Neurotoxins impair the nervous system Cardiotoxins act directly on the heart Myotoxins damage the muscles
OCCUPATIONAL RISK AND OTHER ECOLOGICAL FACTORS:

The normal perception is that rural agricultural workers are most at risk and the bites occur first thing in the morning and last thing at night. However, this is of very little practical use to rural workers in preventing snake bite since it ignores the fact that : In rubber, coconut and arecanut plantations, clearing the base of the tree to place manure causes significant number of bites. Harvesting high growing crops like Millet which requires attention focused away from the ground. Rubber tapping in the early hours 03-00 a.m. to 06-00 a.m. Vegetable harvesting/fruit picking Tea and coffee plantation workers face the risk of arboreal and terrestial vipers when picking or tending bushes Clearing weeds, exposes workers to the same danger as their grass cutting colleagues. Walking at night without a torch, barefooted accounts for a significant number of bites. Bathing in ponds, streams and rivers, in the evening. It should not be assumed that because the victim is bitten in water that the species is non venomous. Cobras and other venomous species are good and may enter the water to hunt. Walking along the edge of water ways.
swimmers
PREVENTION:
Walk at night with sturdy foot wear and use a torch, walk with a heavy step as snakes can detect will move away. vibration and
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Carry a stick when grass cutting or picking fruit or vegetables or clearing the base of trees. Use the stick to move the grass or leaves first. Give the snake chance to move away. If collecting grass that has previously been cut and placed in a pile, disturb the grass with the stick before picking the grass up. Keep checking the ground ahead when cutting crops like Millet, which are often harvested at head height concentration is fixed away from the ground. Pay close attention to the leaves and sticks on the ground when wood collecting. Keep animal feed and rubbish away from your house. They attract rats and snakes will follow. Try to avoid sleeping on the ground. Keep plants away from your door and windows. Snakes like cover and plants help them climb up and windows During trekking etc. through forests or mountains stay on clearly marked tracks. Do not step or reach area where you cannot see the ground. Wear boots, long sleeved shirts & long pants. First Aid: When the snake bites its prey it usually let it go allowing for the venom to take effect after which it follows the prey by means of its scent trail. Therefore, it is also very likely that after biting a human, the snake is found in the Vicinity and it is no less dangerous after the first strike. So the Victim should be moved away to a safe distance. Increased activity would hasten the absorption of venom from the bite site. A bitten person should never run or indulge in any strenuous activity. This would hasten the blood circulation and venom distribution. The bitten part should be kept below the level of the heart. If it is above the level of the heart it would facilitate absorption. Application of a compression bandage should be done in all extremity bites. A compression bandage (NOT A TOURNIQUET) should be firmly tied from the bite site upwards. The idea is to compress the lymphatics and the venules but not retard arterial flow, if retarded could end up in gangrene or necrosis. The bandage should allow for the insinuation of one finger as is done for a fracture. A compressive bandage is a must in all elapidae envenomation as this would retard the entry of venom into the central circulation. The bandage should be released only 30 minutes after ASV has been infused. We had two cases of patient going into a respiratory paralysis on release of the compression bandage. However there are lots of differences of opinion about the pressure immobilization. The first aid thats currently recommended to be administered by self or the community volunteer is based around the mnemonic. Do it R.I.G.H.T The letter in the mnemonic stands for : R. Reassure the patient. 70% all snake bites are from non venomous species, from rest 30% half of it are bite (i.e 15%). I. Immobilise in the same way as a fracture limb. Use bandages or cloth to hold the splints. G.H. Get to Hospital immediately. Traditional remedies have no proven benefit in treating snake bite. T Tell the doctor of any systemic symptoms such as ptosis that manifest on the way to the hospital. The idea is to institute treatment as early as possible without wasting time in the hospital. The snake, if killed should be carefully taken to the hospital for identification by the doctor. No time should be wasted in attempting to kill the snake or capture the snake. This solely wastes time and can lead to other victims. Traditional Methods to be Discarded: Tourniquets The use of tight tourniquet made of rope, belt, string, cloth have been traditionally used to stop venom flow into the body following snake bite. However they have the following drawbacks and problem: Risk of Ischemia & loss of the limb Increased risk of necrosis with 4/5 of the medically significant snakes of India Increased risk of massive neurotoxic blockade when tourniquet is released. Risk of embolism if used in Viper bites. Procoagulant enzymes will cause clotting in distal blood. In the effect of the venom in causing vasodilation presents the danger of massive hypotension when released. They do not work ! Venom was not slowed by the tourniquet in several experimental studies as well as condition. They give patients a false sense of security, which encourages them to delay their journey to hospital. Cutting & Suction: Cutting a victim with in-coagulable blood increases the risk of severe bleeding as the clotting mechanism is no longer effective and increases the risk of infection. No venom is removed by this method. addition, tourniquet is dry into and
into an
in field
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Washing the wound: Victims and bystanders often want to wash the wound to remove any venom on the surface. This should not be done as the action of washing increases the flow of venom into the system by stimulating the lymphatic system. Electrical therapy & cryotherapy: Electric shock therapy for snake bite received a significant amount of press in the 1980s. The theory behind it stated that applying an electric current to the wound denatures the venom. Research showed however that the venom is not denatured. In addition it has been demonstrated that the electric shock has no beneficial effect and it has now been abandoned. Cryotherapy involving the application of ice to the bite site was proposed in 1950s. It was subsequently shown that this method has no benefit and merely increased the necrotic effect of the venom. Pressure Immobilisation Method (PIM): PIM was developed in Australia in 1974 by Sutherland. His research involved tying monkeys to wooden frames and injecting venom, then seeing if the pressure bandage would slow the absorption. He argued that a crepe bandage and an integral splint be applied over the wound to a pressure of 55 mm. of mercury. Further work done by Howarth (1994) demonstrated that the pressure, to be effective was 40-70 mm of mercury in the upper limb and the lower limb was 55-70 mm of mercury. Howarths work also showed that full immobilization was crucial. Work carried out by Norris (2005) showed that only 5% of lay people and 13% of doctors were able to correctly apply the technique!. In addition pressure bandages should not be used where there is a risk of local necrosis. There has been some initial research that has suggested that a Pressure pad or Monash technique may have some benefit in the first aid treatment of snake bite. In this method a hard pad of rubber or cloth is applied directly to the wound in an attempt to reduce venom entering the system. Creating awareness among the community about Dos & Donts Awareness should be created among community about the Dos & Donts of the snake bite. 1. Dos Reassure the victim that death is not imminent and that medical care is available. Reassure that most of the bites are non-venomous. Remain calm, make the victim comfortable. Control anxiety. Excitement may increase the heart rate blood circulation. This will help spread the venom through your body much faster. Lay down flat on the ground. Keep the bitten body part below heart level. Remove shoes, rings, watches, Jewellery and tight clothing from bitten areas. They may act as a tourniquet in the event swelling occurs. Immobilize the victims bitten limb. Bandage it using a cotton bandage (or using any clean cloth material). Remember, venom travels through the lymphatic system, so the spread of the venom can be slowed by a bandage. Wrap the limb from the bite site to above the elbow or knee. Finally apply a splint and do not allow the limb or the muscles in the area to be moved much. Be prepared to treat for shock and possibly administer CPR. Get the victim to the nearest hospital as soon as possible. The best possible tool for saving patient is watch and the available transport. 2. Donts Do not apply a tourniquet or constriction band. You could cut off blood flow to the limb causing more damage than the snakebite. Do not wash the bite site with water or any other solution to remove venom from the bite site. Action washing increase the flow of venom into the system by stimulating the lymphatic system. Do not make cuts or incisions on or near the bite site. You could cut nerves, tendons or block vessels. Do not apply cold, electro cautery, burns etc. to the bitten part. Do not apply any kind of potentially harmful herbal or folk remedies. Do not attempt to suck venom out with your mouth. You could have an ulcer or wound in your mouth, allowing venom to get into your blood stream. Do not give the victim drink, alcohol or other drugs as it may confound clinical examination. Do not attempt to capture, handle or kill a venomous snake. More people are bitten during these than in any other situation. Do not allow the victim to walk or run. Snake bite Diagnostic Phase Introduction: The first thing to be verified is whether it is a snake bite at all, and if so whether it was a venomous snake bite. The victim may be shown a chart with photographs of venomous snakes in the area to help identification. This has not really helped as most of the bites tend to be nocturnal or because the victim has not carefully noticed the details of the snake. Symptoms of pain out of activities of your and
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proportion to the extent of injury are typical of envenomation. If the pain seems proportional to the injury seen, it may not be a snake bite at all and could be an injury from other causes. Confusion arises most commonly when children are brought in. If a small wound is noticed on them by the parents even without any other definite history of a bite the parent may attribute it to snake bite. A diagnosis is particularly difficult when the victim comes with his vision and sense clouded by alcohol. The next big question is whether it is a venomous snake bite. The species can only be ascertained at the time of admission if the patient has come with the snake. Only 39 of our list of 860 patients (Little Flower Hospital, Angamaly) over the past seven years actually came with snakes. The species identification does not really change the medically management at present, as the ASV we use is polyvalent i.e ASV which neutralizes the venom of all the Big Four. The currently used polyvalent ASV would not cover king cobra bites, sea snake bites and would have nil or very minimal benefit in pit viper bite. Pit viper bites may also not need the present ASV. India still lacks an ELISA based kit which would reliably help us identify the venomous species. However, this does not make a significant difference in treatment since we are using polyvalent ASV at present. If the snake species can be reliably established, treatment could move from Polyvalent to monovalent ASV thereby decreasing the load of horse globulin. There is high incidence of allergic reactions to horse globulin which may range from allergic rashes to frank anaphylaxis. We had allergic reaction in 206 patients from 716 patients given ASV (L.F Hospital Communication). Top priority should be given to the development in India of an ELISA based kit. Patient assessment phase on arrival: Deal with any life threatening symptoms on presentation i.e. Airway, breathing and circulation. If there is evidence of a bite, where the skin has been broken, give Tetanus toxoid. Routine use of antibiotic is not necessary, although it should be considered if there is evidence of cellulitis or necrosis. Diagnosis Phase General principles: Where possible, identify the snake responsible. Snake colouration is a very unreliable means of determining species as is most of the advice given concerning pupil shape & scalation. Have the victim carefully bring the snake to the hospital if it has been killed. Bite marks are not of much use in identifying if a species is venomous or not. Many non venomous species leave just two fang like marks, eg. Wolf snakes. Some species like the Krait may leave no bite mark at all. Many venomous species have more than two fangs, as they grow reserve fangs in case the main one breaks off. Determine if any traditional medicines have been used, they can sometime cause confusing symptoms. Determine the exact time of the bite. This can give indications as to the progression of any symptoms. Ask questions as to what the victim was doing at the time of bite. Some activities such as grass cutting or feeding stock animals in the evening can be suggestive of snake bite. Non-poisonous resembling poisonous snakes a. Rat snake Common Cobra b. Common Cat Snake Saw Scaled Viper c. Striped keel back Baby Cobra d. Banded kurki banded krait e. Common Wolf Snake Common krait f. Checkered keel back- Cobra Water snake) g. Sand boa Russells Viper h. Vine snake Venomous green snake Diagnosis Phase Symptoms: Hemostatic abnormalities are prima facie evidence of a viper bite. Cobras & Krait do not cause haemostatic disturbances. All the vipers can cause renal failure. Russells Viper can also manifest neurotoxic symptoms in a wide area of India, especially southern Inida. This can sometimes cause confusion and further work is necessary to establish how wide this area might be. The neurotoxic symptoms of Russells Viper are believed to be pre-synaptic or krait like in nature. General Signs & Symptoms of Viperidae Envenomation: - Local pain & swelling and erythema over bitten part. - Tender enlargement of local lymphnodes, as large molecular weight viper venom molecules enter the system via lymphatic. - Local necrosis and or blistering - Vomiting, abdominal pain, Acute abdominal tenderness which may suggest gastro- intestinal or reteroperitoneal bleeding - Hypotension resulting from hypovolumia or direct vasodilatation. - Low back pain, loin pain indicative of an early renal failure or retroperitoneal bleeding. - The passing of reddish or dark brown urine or declining or no urine output. - Lateralising neurological symptoms and asymmetrical pupils maybe indicative of intracranial bleeding - Muscle pain indicating rhabdomyolysis - Bilateral Parotid swelling (Viper head) conjunctival edema, sub conjunctival haemorrhage - Metallic taste - Confusional State, ptosis - Jaundice - The victim may bleed from any orifice or organ, haemoptysis, epistaxis, hematuria, haemetemesis and malena, chemosis, macular bleed, excessive menstrual bleed, bleeding from bite site or the canula, bleeding into muscles, bleeding from gingival sulci, epistaxis. Bleeding into skin & mucous membrane may show evidence of petechiae, purpura, epistaxis. General signs and symptoms of Elapid envenomation:
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- Swelling and local pain (cobra) - Local necrosis and or blistering (Cobra) - Descending paralysis, initially of muscles innervated by the cranial nerves, commencing with ptosis,diplopia or ophthalmoplegia. The patient complains of difficulty in focusing and the eye lids feel heavy. - Dysphagia, dysguesia (tingling sensation in the tongue with a loss of taste) involvement of sense of smell, diaphoresis. Circum oral pallor and paraesthesia (a tingling sensation around the month which also looks pale). - Profound thirst, miosis, abdominal pain, vomiting - Painful lyphadenopathy - Palpitation, breathlessness, chest pain - Paralysis of jaw and tongue may lead to upper air way obstruction and aspiration of pooled secretions because of the patients inability to swallow. Bulbar paralysis and respiratory failure. - Hypoxia due to inadequate ventilation can cause cyanosis, altered sensorium and coma. This is a life threatening situation and needs urgent intervention. - Paradoxical respiration, as a result of the intercostal muscles becoming paralysed is a frequent sign. - Stomach pain which may suggest submucosal haemorrhage in the stomach (Krait). - Krait bite often present in the early morning with paralysis that can be mistaken for a stroke. Bite by Sea Snake The bite is usually painless and may not be noticed by the wader or swimmer. Teeth may be left in the wound. There is minimal or no local swelling and involvement of local lymph node is unusual. Generalised rhabdomyolysis is the dominant effect of envenoming by these snakes. Early symptoms include headache, a thick feeling of the tongue, thirst, sweating and vomiting, Generalised aching, stiffness and tenderness of the muscles become noticeable between 30 minutes to 3 hours after the bite. Trismus is common. Passive stretching of the muscle is painful, Later there is progressive flaccid paralysis starting with ptosis as in elapid envenoming. The patient remains conscious until the respiratory muscles are sufficiently affected to cause respiratory failure. Myoglobinemia and myoglobinuria develop 3 to 8 hours after the bite. These are suspected when the serum/plasma appears brownish & urine dark reddish coloured (Coco cola coloured). Myoglobin and Potassium released from damaged skeletal muscles may cause Acute renal failure, while hyperkalemia developing within 6-12 hours of the bite may precipitate cardiac arrest.. All species of sea snakes are deadly venomous and seldom exceed 3 m in length. As many as 50 species of sea snakes are known from Indian and Pacific oceans. Sea snakes are rarely aggressive and bites are uncommon. Factors effecting the severity of snake bite: Even when bitten by the same species of snake the severity of the effect will depend on a very large variety of factors and will differ from case to case. The factors are; i) The age, size, sex and state of health of victims. The larger the body mass, the lesser the effect. Since the venom gets distributed over a large area. - Men have greater resistance than women - Children more vulnerable, because of lower body mass, lesser fat and more rapid circulation of blood. ii) Even within the same species, the age, size, state of health of Snake will have a bearing on the quantity of venom produced. - Male snakes produce more venom than females. - A large sized snake (particularly with larger head and hence a larger venom gland) will have more venom. iii) There may be seasonal variations in the quantum and potency of the venom produced. During the summer month the output is more than in the winter, when the venom is viscous and comes out in small quantities. This may possibly explain the higher mortality rate by snake bites in the summer months including the monsoon. But not enough research has been done on this. iv) The venom is more toxic immediately after the snake moults. Conversely, if it is nearing its moult, the venom will be less toxic. v) The mental state and behavior of the victim. If he is agitated or runs in exerts himself after the bite, it will speed up the action of heart and lead to faster absorption of the venom in the blood. vi) Excessive movement of the bitten limb will lead to greater absorption of the venom. vii) Excessive fear and anxiety may have a direct effect on the victim even apart from the effect of venom. viii) The site of bite: A bite will be less dangerous in the fatty tissue or bony part, as the absorption will be less rapid. A bite near the vital organs or which punctures a blood vessel can be very serious. ix) If the snake has had a heavy meal recently, the quantity of venom in the gland is likely to be less. x) The intention of the snake, since the venom in an enzyme necessary for securing and digesting its prey, the snake does not expend it if it can help it. Experiment have shown that it can voluntarily control the quantity of venom injected. If the intention of snake is only to frighten a perceived enemy it may inflict a bite without injecting any venom dry bite or the venom discharged may be minimal. xi) The nature of bite whether it was full, direct strike or only a glancing blow or a scratch. xii) Whether the bite was on a bare part or through clothing or foot wear.
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xiii) The number of Bites: A snake if it is an extremely agitated state, may strike more than once, in which case the greater the quantity of venom injected. xiv) The duration, the snake hangs on: The fixed hang snakes like the Cobras, King Cobra, Krait and Sea Snakes (as distinct from the hinged fang snake like vipers) when they are highly agitated, are known to fang on to the victim and chew the flesh injecting large dose of venom. xv) The condition of fangs: Whether entire or broken, lately renewed or ready for shedding. If broken or ready for shedding, not much venom could have been injected. xvi) A snake may misjudge the distance while striking and to that extent the bite will be less serious. xvii) In the case of vipers, if the snake does not get the fangs fully erect at the time of bite, venom may not be injected at all or in adequate quantity or may spill outside.
INVESTIGATION
20 minute whole Blood clotting Test (20 WBCT) is considered the most reliable test of Coagulation in hematotoxic bite and can be carried out at the bedside without special training,. It is significantly superior to the capillary tube method. A few milliliters of fresh venous blood is placed in a new, clean, dry glass test tube and left at ambient temperature for 20 minutes. It is important that the tube is clean, glass and dry as the mechanism under review is the contact clotting mechanism. The use of plastic bottles, tubes or syringes will give false readings and should not be used The glass vessel should be left undisturbed for 20 minutes and then gently tilted, not shaken. If the blood is still liquid then the patient has in coagulable blood. The Test tube must not have been washed with detergent as this will inhibit the contact element of the clotting mechanism. The test should be carried out every 30 minutes from admission for three hours. If everything is normal, repeated at one hour interval till six hours after bite and twice more at 3 hour intervals the next 6 hours. If all reports are normal, no further triage would be needed. A normal 20 WBCT and Clot lysis would exclude viperidae species. But it occasionally happens that the parameters become abnormal only 24 hours after the bite especially in pit. Viper bites. Simultaneously, a single breath counting test is done in suspected elapidae bites and the same is repeated at 15 minutes interval over the first 2 hours. The onset of symptoms and sudden progression are more common with Elapidae bite rather than viperidae. Most sea snake, krait and cobra bite would show symptoms within the first 6hours, the shortest time frame being for the sea snakes. Similarly, the mortality due to elapidae bites is mostly in the first 24 hours. The victim is unlikely to die of Elapidae bite complication if alive 24 hours after the bite. The likelihood of a dry bite from among the big four is most with a cobra. Victims showing any signs or symptoms suggesting systemic envenomation are shifted to the ICU and have to be treated with ASV (Anti Snake venom). OTHER USEFUL TESTS (depending on availability). Haematological: Hemoglobin, PCV, Total Leucocyte count, Differential Leucocyte count, ESR, Peripheral smear. Platelet count- which is repeated 6 hourly the first 24 hours in viperidae bite. Coagulation Work up: CT, BT, APTT, PT DIC Work up: D-Dimer, FDP (Fibrin degradation product). Fibrinogen which is repeated on the third day. Renal function: Blood urea, serum creatinine Liver function: AST, ALT, Serum Bilirubin, Serum Protein & Albumin. Muscle Enzymes: Creatinine phosphokinase (CPK) Biochemistry: Na, K and Blood Sugar Urine: Checked for myoglobin, Haemoglobin & Protein Blood group : ABO, Rh (at the earliest as blood doesnt clot later) Oxygen saturation/BP/Postural Blood Pressure/PR/RR Arterial Blood gases (ABG) : if facilities are available. The same may have to be repeated depending on the clinical course of the patient. The tests repeated on a daily basis are : Hb, PCV, CBC, Urea, Creatinine, Platelets and Urine Protein The coagulation work up usually normalizes within 24 to 48 hours of treatment. Exceptions are in cases of certain pit viper species, where it may take up to 2-3 weeks to normalize. A peripheral smear is also sent for in which crenated RBC, schistocytes or burr cells are looked for. These suggest systemic envenomation and along with thrombocytopenia are markers for MAHA (microangiopathic haemolytic anaemia) The signs specifically looked for are: Regional lymphadenopathy Swelling of the bitten limb which is measured at 15 minutes intervals for the first hours and thereafter at 6 hourly intervals. An increase of 3 mm increases the circumference of the limb by 1 cm. As also the extent of spread of the swelling with time is kept. The upper limit of the spread of the swelling is marked and the time given and the same is repeated at 3 hourly interval for the first 24 hours.
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Discolouration of the Urine Look for gangrene or necrosis of the bitten part, especially, if a tight tourniquet has been tied. Urine output is measured and charted
SNAKE BITE TREATMENT PROTOCOL Treatment Phase

1. Managing Pain: Snake bite can often cause severe pain at the bite etc. This can be treated with pain killers such as Paracetamol. Adult dose 500 mg. To 1000 mg. 6 hourly orally Pediatric dose 10 mg/kg. body weight every 6 hourly orally Mild opiates like Ketorolol 50 mg. can be used orally for relief of severe pain. In cases of severe pain at a tertiary centre, Ketorolol can be given IV. 2. Handling tourniquets Though not recommended, the current practice being followed would see many snake bite victims reaching the emergency with tightly tied tourniquets. Care must be taken when removing tight tourniquets. Sudden removal can lead to a massive surge of venom leading to neurological paralysis, hypotension due to Vasodilation, etc. * Before removal of the tourniquet, check for the presence of pulse distal to the tourniquet. If the pulse distal to the tourniquet is absent ensure a doctor is present before removal. Be prepared to handle the complications such as sudden respiratory distress or hypotension. If the tourniquet has occluded the distal pulse, then a blood pressure cuff can be applied to reduce the pressure slowly Anti-Snake Venom (ASV) Anti Snake Venom (ASV) is the mainstay of treatment. The ASV available in India is polyvalent i.e it is effective against all the four common species; Russells Viper (Daboia Russeli) Common Cobra (Naja Naja) Common Krait (Bungarus caeruleus) and saw scaled Viper (Echis Carinatus). There are no current available monovalent ASVs primarily because there are no objective means of identifying the snake species, in the absence of the dead snake. It would be impossible for the physician to determine which type of Monovalent ASV to employ in treating the patient. There are known species such as the Hump-nosed pit viper (hypnale hypnale) where polyvalent ASV is known to be ineffective. In addition there are regionally specific species such as Sochureks saw scaled viper (Echis carinatus Sochureki) in Rajasthan, where the effectiveness of polyvalent ASV may be questionable. Further work is being carried out with ASV producers to address this issue. ASV is produced in both liquid and lyophilized forms. There is no evidence to suggest which form is more effective and many doctors prefer one or the other based purely on personal choice. Liquid ASV requires a reliable cold chain and refrigeration and has a 2 year shelf life. Lyophilized ASV, in powder form, has 5 year shelf life and requires only to be kept in cool. This is a useful feature in remote areas where power supply is inconsistent. ASV Administration Criteria: ASV is a scarce, costly commodity and should only be administered when there are definite signs of envenomation. Unbound, free flowing venom, can only be neutralized when it is in the blood stream or tissue fluid. In addition, Anti Snake Venom carries risks of anaphylactic reactions and should not therefore be used unnecessarily. The doctor should be prepared for such reactions. If a patient has evidence to suggest systemic envenoming or severe current local envenoming then only ASV will be administered. Evidence of Systemic Envenoming Evidence of coagulopathy: Primarily detected by 20 minute WBCT or visible spontaneous systemic bleeding from gums etc. Further laboratory tests for thrombocytopenia, Haemoglobin abnormalities, PCV, peripheral smear etc. provide confirmation, but 20 minute WBCT is paramount. Evidence of Neurotoxicity: Ptosis, external ophthalmoplegia, muscle paralysis, inability to lift head etc. The above two methods of establishing systemic envenomation are the primary determinants. They are simple to carry out, involving bedside tests or identification of visible neurological signs and symptoms. In the Indian context and in the vast majority of cases, one of these two categories will be the main determinants of whether ASV is administered to a patient. Other determinants are: Cardiovascular abnormalities, hypotension, shock cardiac arrhythmia, abnormal ECG Persistent and severe vomiting or abdominal pain Severe Current Local envenoming Severe current, local swelling involving more than half of the bitten limb (in the absence of a tourniquet). In case of (i) severe swelling after bites on the digits (toes and especially fingers) (ii) after a bite from a known necrotic species (iii) rapid extension of swelling (for example beyond the wrist or ankle within a few hours of bite on the hands or feet).
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If a tourniquet or tourniquets have been applied, these themselves can cause swelling, once they were been removed for 1 hour and the swelling continues, then it is unlikely to be as a result of the tourniquet and ASV may be applicable. Prevention of ASV Reactions - Prophylactic Regimen There is no statistical, trial evidence of sufficient statistical power to show that prophylactic regimes are effective in the prevention of ASV reaction. Micro studies either show no benefit or modest benefit. These studies are not powered to detect the true outcome effect. Well designed clinical trials are needed to conclude that the prophylactic treatment is beneficial. Two regimens are normally recommended. 100 mg. of hydrocortisone and H anti-histamine (10 mg. Cholripheneramine maleate; 22.5 mg IV pheneramine maleate IV or 25 mg. Promethazine H.Cl. 1 M). 5 minutes before ASV administration. 0.25 0.3 mg adrenaline 1 : 1000 given subcutaneously & (deep im) If the victim has a known sensitivity to ASV pre-medication with adrenaline, hydrocortisone and anti histamine may be advisable, in order to prevent severe reactions Test dose of ASV Test dose have been shown to have no predictive value in detecting anaphylactoid or late serum reaction and should not be used. These reactions are not IgE mediated but complement activated. They may also pre-sensitise the patient and thereby create greater risk. ASV administration - Dosage Symptoms and signs being not a useful guide for deciding the degree of envenomation and having no diagnostic methods to determine the level of Venom in blood or tissue, any ASV regimen adopted could only be an estimate. 1 ml. of ASV neutralizes 0.6 mg. of Russel Viper venom 0.6 mg. of Cobra venom 0.45 mg. of krait venom 0.45 mg. of saw-scaled viper venom Russell Viper (Hemato toxic bite) Russel Viper injects on an average 63 mg. (5 to 147 mg. + 7) of venom 1 ml. of ASV neutralizes 0.6 mg. of Russells Viper Venom So 1 vial i.e 10 ml. of ASV neutralisen 6 mg. of Russells viper venom So the total required dose will be between 100 mg. (10 Vial) to 250 mg. (25 vials) So starting with 10 vial ensures sufficient neutralizing power Not all victims will require 10 vials as some may be injected with less than 63 mg. Not all victims will require 25 vials as very few are injected with a dose that is an outlier. However, starting with 10 vials ensures that there is sufficient neutralizing power to neutralize the average amount of venom injected and during the next 12 hours to neutralize any remaining free flowing venom. Start IV Normal Saline with wide bore needle. Begin with 10 vials of ASV in 100 ml. of Normal Saline and to start with 10-15 drops per minutes for 15 minutes and watch for reactions. If the patient is not having signs and symptoms of anaphylactic shock continue the ASV drip in one hour period. All ASV are to be administered over 1 hour period at constant speed. Continue to monitor the vital signs at 5 minutes interval for first 30 minutes and then at 15 minutes interval for 2 hours. Repeat dose in haematotoxic envenomation As already explained, initial blood test reveals coagulation abnormality 10 vials of ASV given. No additional ASV until next 6 hours (Liver unable to replace clotting factors in under 6 hours). After initial 6 hours, another 20 WBCT is done. If there is evidence of abnormality of 20 WBCT (continued coagulation disturbance) another 8-10 vials of ASV administered in one hour time. Repeat 20 WBCT and repeat ASV 6 hourly until coagulation is restored, unless a species is identified as one against which polyvalent ASV is not effective. (Usually in majority of cases 20 vial ASV is enough). Neurotoxic Envenomation Neostigmine is an anti cholinesterase that prolongs the life of acetylcholine and can therefore reverse respiratory failure and neurotoxic symptoms. It is particularly effective for Post synaptic neurotoxins such as those of the Cobra. There is some doubt over its usefulness against pre-synaptic neurotoxin such as those of the Krait and the Russells Viper. However it is worth trying in these cases. Neostigmine Test: In the case of neurotoxic envenomation the Neostigmine Test will be administered. This test involves administration of 1.5 to 2 mg. of Neostigmine IM together with 0.6 mg. of Atropine IV. The paediatric neostigmine dose is 0.04 mg/kg IM and the dose of atropine is 0.05 mg/kg.
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The patient should be closely observed for 1 hour to determine if the neostigmine is effective. The following measures are useful objective methods to assess this. Single breath count MM of Iris uncovered (amount covered by the descending eye lid) Inter incisor distance (measured distance between the upper & lower incisors) Length of time upward gaze can be maintained FEV1 or FVC (if available) For example, if single breath count or inter incisor distance is selected, the breath count or distance between the upper and lower incisors are measured and recorded. Every 10 minutes the measurement is repeated. The average blood plasma time for neostigmine is 20 minutes, so by T + 30 minutes any improvement should be visible by an improvement in the measure. Some authors have suggested that it may be possible to treat patient with anticholinesterase drugs solely, in the case of elapid bites. However, this approach ignores the value of neutralizing the free flowing venom before it can attach and carry out its task. Neurotoxic Envenomation: Treat the patient with 10 vial of ASV initially as in the case of hematotoxic envenomation. If the Neostigmine test is positive, 0.5 mg of Neostigmine IM and 0.6 mg. Atropine IV at half hourly intervals for 5 injection, followed by repeating the same dose at increasing intervals of 2 to12 hours. If there is no improvements in symptoms after 1 hour, Neostigmine should be stopped. The ASV regime relating to neurotoxic envenomation has caused considerable confusion. If the initial dose has been unsuccessful in reducing the symptoms, or if the symptoms have worsened or if the patient has gone into respiratory failure, then a further dose should be administered, after 1-2 hours. At this point the patient should be re-assessed. Repeat dose Neurotoxic envenomation: Initial dose of 10 vials given and if symptomic persist or worsen or in respiratory failure repeat 10 more vials of ASV after 1-2 hours as a second dose and discontinue ASV. 20 vials is the maximum dose of ASV that should be given to a neurotoxically envenomed patient. Once the patient in respiratory failure, has received 20 vials of ASV and is supported on a ventilator, ASV therapy should be stopped. This recommendation is due to the assumption that all circulating venom would have been neutralized by this point. Therefore, further ASV serves no useful purpose. Evidence suggests that reversibility of post synaptic neurotoxic envenoming is only possible in the first few hours. After that the body recovers by using its own mechanism. Large doses of ASV, over long period, have no benefit in reversing envenomation. Confusion has arisen due to some medical text books suggesting that massive doses of ASV can be administered and that there need not necessarily be a clear and upper limit to ASV. These texts are talking about snakes which inject massive amounts of venom, such as King Cobra or Australian Elapids. There is no justification for massive doses of 50 + vials in India, which usually result from the continued use of ASV whilst the victim is on a Ventilator. No further doses of ASV are required, unless a proven recurrence of envenomation is established. Additional vials to prevent recurrence is not necessary. ASV in Children: Children receive the same ASV dosage as adults. The ASV is targeted at neutrlising the venom. Snake inject the same amount of venom into adults and children. Recovery signs: If an adequate dose of appropriate antivenom has been administered, the following response may be seen: Spontaneous systemic bleeding such as gum bleeding, bleeding from Vene puncture sites etc. usually stops within 15 to 30 minutes. Blood coagulability is usually restored in 6 hours. Principal test is 20 WBCT. Post-synaptic neurotoxic envenoming such as the Cobra may begin to improve as early as 30 minutes after Pre-synaptic neurotoxic envenoming such as the krait usually takes a considerable time to improve. Active hemolysis and Rhabdomyolysis may cease within few hours and urine return to its normal colour. In patient with shock, blood pressure may increase after 30 minutes. Recurrent Envenomation: When coagulation has been restored no further ASV should be administered, unless proven recurrence of a coagulation abnormality is established. Indian ASV a F(ab)2 product and has a half life of 90 hours and therefore is not required in a prophylactic dose to prevent re-envenomation Anti Heamostalic Maximum ASV Dosage guidance: The normal guidelines are to administer ASV every 6 hours until coagulation has been restored. However, what should the clinician do after say, 30 vials have been administered and the coagulation abnormally persists?
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There are a number of questions that should be considered. Firstly, is the envenoming species one for which polyvalent ASV is effective? For example it has been established that envenomation by the Humpnosed Pit Viper (Hypnale Hypnale) does not respond to normal ASV. This may be a cause as, in the case of Hypnale, Coagulopathy can continue upto 3 weeks. The next point to consider is whether the coagulopathy is resulting from the action of the venom. Published evidence suggest that the maximum venom yield from say a Russells Viper is 147 mg. which will reduce the moment the venom enters the system and starts binding to tissues. If 30 vials of ASV have been administered that represents 180 mg. of neutralizing capacity. This should certainly be enough to neutralize free flowing venom. At this point the clinician should consider whether the continued administration of ASV is serving any purpose, particularly in the absence of proven systemic bleeding. At this stage the use of fresh frozen plasma (F.F.P) or factors can be considered if available. ASV in Special Situation: Victims Requiring Life Saving Surgery: In very rare cases, symptoms may develop which indicate that life saving surgery is required in order to save the victim. An example would be a patient who presents with signs of an intracranial bleed. Before surgery can take place, coagulation must be restored in the victim in order to avoid catastrophic bleeding. In such cases a higher initial dose of ASV is justified (upto 25 vials) solely on the basis on guaranteeing a restoration of coagulation after 6 hours. Snake bite in Pregnancy: There is very little definitive data published on the effects of snake bite during pregnancy. There have been cases reported when spontaneous abortion of foetus has been reported, although this is not the outcome in majority of cases. It is not clear if venom can pass the placental barrier. Pregnant women are treated in exactly the same way as other victims. The same dosage of ASV is given. Victims who arrive late: A frequent problem witnessed in our country is victims who arrive late after the bite, often after several days, usually with Acute Renal failure. The key determining factor to decide on ASV treatment is to look for signs of current venom activity Venom can only be neutralized if it is unattached. Perform a 20 WBCT and determine if any coagulatopathy is present. If coagulopathy is present administer ASV. If no coagulopathy is evident treat renal failure. In case of neurotoxic envenoming where the victim is evidencing symptoms such as ptosis, respiratory failure etc, it is probably wise to administer one dose of 8 to 10 vials of ASV to ensure that no unbound venom is present. ASV Reactions: Anaphylaxis with ASV may be life threatening. Anaphylaxis can be rapid onset and can deteriorate into a life threatening emergency very rapidly. Adrenaline should always be immediately available. The patient should be monitored closely for urticaria, itching, fever, shaking chills, nausea, vomiting diarrhoea, abdominal cramps, tachycardia, hypotension, bronchospasm and angio-oedema of lips mucous membrane, larynx (lump in throat hoarseness) and peri-orbital. If anyaphylaxis is evident then. ASV will be discontinued temporarily 0.5 mg of 1 :1000 adrenaline will be given IM for adults. Children are given 0.01 mg/kg. of body weight of adrenaline 1 M. In addition to provide long term protection against anaphylactoid reaction, 100 mg. of hydro cortisone and an H antihistamine can be given. If after 10-15 minutes the patient condition has not improved or is worsening a second dose of 0.5 mg. of adrenaline 1 : 1000 IM is given. This can be repeated for a third and final occasion, but in the vast majority of reaction 2 doses of adrenaline will be sufficient. If there is hypotension or hemodynamic instability IV fluids should be given. In persistent hypotension and life threatening anaphylaxis adrenaline 0.1 mg. 1 : 10,000 dilution IV bolus given over 5 minutes. If hypotension refractory to bolus dose, start an adrenaline infusion. There is better patient outcome if adrenaline is used early. Pyrogen reactions (endotoxin) - 1 - 2 hours after treatment - Chills and rigors - Fever - Vasodialation and hypotension - Febrile convulsion in children These are due to pyrogen contamination during the manufacturing process. Adrenaline infusion: - add 1 mg. of adrenaline to 500 ml. of 5% dextrose (2 microgram/ml.). Infuse at 1 ml/min. titrate upwards to 4 ml/min. 2 to 8 mg./min.
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Can cause life threatening arrhythmia. Cardiac monitoring is necessary Late serum sickness reaction: 1 - 12 days after treatment Fever, arthralgia myalgia. Nausea vomiting diarrhoea, lymphadenopathy, proteinuria with immune complex nephropathy Can be easily be treated with an oral sterioids such as prednisolone oral, Antihistamine provide additional symptomatic relief. When to restart the ASV after a reaction : Once the patient has stabilized Once BP is under control Once the manifestation of the reaction have subsided. In severe reactions ASV can be restarted under cover of an adrenaline infusion Rate of ASV infusion can be decreased initially Patient should be under strict monitoring Poor Prognostic indicators in Viper bite: Low Platelets < 20,000 Polymorphonuclear leucocytosis with presence of band form Crenated RBC Haemo concentration at presentation indirectly denotes capillary leak Raised D Dimer Low Fibrinogen Low Serum Protein and Albumin Haemoglobinuria Bilateral Parotid swelling Viper Head appearance Giddiness, syncope immediately following a snake bite Agitated behaviour Cerebral Anoxia Profound thirst Drugs not to be used in Viper bites: Heparin & Botropase Heparin has been proposed as a means of reducing fibrin deposit in DIC. However heparin use is controversial. Trial evidence has shown that it has no benefical effect. Venom induced thrombin is resistant to Heparin. The effect of Heparin on Anti thrombin III are negated due to the elimination of Anti-thrombin III by the time heparin is administered and heparin can cause bleeding by its own action. Botropase is a procoagulant compound derived from one of the two South American Pit Viper. It should not be used as a coagulant in viper bites as it simply prolongs the coagulation abnormality by causing consumption coagulatopathy in the same way as the Indian Viper Venom currently affecting the victim.
COMPLICATIONS AND TREATMENT:

Hypotension: Hypotension can have a number of causes, particularly loss of circulating volume due to haemorrhage, vasodilation due to the action of venom or direct effects on the heart. Test for hypovolemia by examining the blood pressure lying down & sitting up to establish a postural drop. It should be treated by infusing plasma expanders preferably fresh whole blood if the patient has features of anemia or fresh frozen plasma if the patient has hemoconcentration due to Capillary leak. Central venous pressure or pulmonary arterial catheter monitoring is the safest way to control volume replacement. Russell viper is known to cause an acute pituitary adrenal insufficiency. This condition may contribute to shock. Follow up checks on known Russells viper victims need to ensure that no long term pituitary sequelae are evident. Surgical Intervention: Whilst there is undoubtedly a place for a surgical debridement of necrotic tissue, the use of fasciotomy is highly questionable. The appearance of : Pain on passive stretching Pain out of proportion Pulselessness Pallor
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Parasthesia Paralysis and significant swelling in the limb can lead to the conclusion that the intra compartmental pressure is above 40 mm of mercury and this requires a fasciotomy. Fasciotomy is required if the intra compartmental pressure is sufficiently high to cause a blood vessels to collapse and lead to ischemia. Fasciotomy does not remove or reduce any envenomation. There is little objective evidence that the intracompartmental pressure due to snake bite in India, ever reaches the prescribed limit for a fasciotomy. What is important is that the intra-compartmental pressure should be measured objectively using saline manometers or newer specialized equipment such as the Stryker Intra-compartmental pressure monitoring equipment. Visual impression is a highly unreliable guide to estimating intra-compartmental pressure. Persistent or Severe bleeding: In the majority of cases the timely use of ASV will stop systemic bleeding. However in some cases the bleeding may continue to a point when further treatment should be considered. The major point to note is that clotting must have been re-established before additional measures are taken. Adding clotting factors FFP, cryoprecipitate or whole blood in the presence of unneutralised venom will increase the amount of degradation products with the accompanying risk to renal function. Renal failure: Renal failure is a common complication of Russells Viper, Saw scaled Viper & Hump nosed Pit viper bites. As mentioned previously, loin or lumbar pain in the first 12 24 hours is a predictor of the likelihood of the victim going on to develop renal failure. Acute Renal Failure (ARF) is the most frequent and clinically important effect of envenomation on the kidneys. The majority of cases are seen after viper bites and the incidence varies with the distribution of viperidae snakes in different geographic regions. About 13% to 32% of those bitten by Russells Viper or Echis carinatus, Hypnale-hypnale develops ARF in India. The reported incidence from other countries varies between 1% to 27%. The symptoms depend on the dose of venom injected. Renal failure in a Viperidae bite is multifactorial DIC, acute tubular necrosis resulting from shock, intravascular hemolysis, hemoglobinuria and myoglobinuria from rhambdomyalysis being the likely causes. Bleeding into the kidneys and perinephric capsule could be another reason. Apart from blood loss, hypotension and circulatory collapse can result from release of Kinins or depression of medullary vasomotor centre or myocardium. Kininogenases are present in crotalid venom. To this could be added the possibility of immune complex deposits related to the venom anti venom complex getting deposited in the glomerulus and causing injury. In view of the typical loin pain especially with Rusell Viper we believe that there could be a direct toxic effect of venom component. The onset of renal failure is signaled by a decrease in urine output. This may occur within one hour to as late as 4 days after the bite. Renal damage can develop very early in case of Rusells viper bite and even when the patient arrives at hospital soon after bite the damage may already have been done. Studies have shown that even when ASV is administered within in 2 hours of the bite, it was incapable of preventing ARF. About half the patients give a history of passage of Cola-coloured urine, indicating intravascular hemolysis. Fibrin degradation products can be detected in the urine, indicating disseminated intravascular coagulation. Life threatening hyperkalemia may develop in patients with haemolysis or myonecrosis. Renal failure is non-oliguric in less than 10% cases. Persistance of oliguria of more than one month indicates the possibility of acute cortical necrosis which may be confirmed by Renal Biopsy. Acute Cortical necrosis due to snake bite is the second most common cause of acute cortical necrosis in India. Elevated urinary excretion of N-acetyl glucosamine (NAG) is an early marker of Renal damage in bitten patient. Other causes of ARF include glomerulonephritis, direct nephrotoxicity of venom, tubulo interstitial nephritis and rarely papillary necrosis. In patients with established Acute Renal failure, the treatment of choice is Dialysis. Indications of Dialysis: Clinical: Anuria of > 48 hours Deterioration of general condition Severe metabolic Acidosis Hyperkalemia Pulmonary oedema Biochemical: Blood urea >120 mg/dl. Ser creatinine > 5 mg./dl Ser. potassium > 6 meq./litre Daily rise of blood urea > 50 mg/dl
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Daily rise of serum creatinine > 1 mg/dl Daily fall of bicarbonates > 2 meq./dl Hemodialysis is preferred in those who are haemodynamically stable. In those who are haemodynamically unstable CAVH, CAVHD, CVVH or CVVHD can be employed. Peritoneal dialysis which is less effective, has a role in children, those with hemodynamically unstable state. Phospholipase A and a basic protein called Direct Lytic Factor, present in Russells viper and Echis carinatus venom can lead to intra vascular hemolysis. The viper venom activates the coagulation cascade at a number of sites leading to rapid thrombin formation. Acute Respiratory Distress Syndrome (ARDS): The other major complication of venomous Snake bite is the acute respiratory distress syndrome or acute lung syndrome. This too is multifactorial, the possible explanations being toxin related, DIC related, aspiration related. Components of the venom are known to cause, a capillary leak and could thereby directly cause ARDS. The other possibility is an immune complex deposition resulting from venom antivenom complex getting deposited in the capillaries of the lung. Nervous system complications: This could range from a catastrophic intracerebral bleed in case of viperidae bites to cerebral infarcts from DIC. Elapidae bites could lead to paralysis and cranial nerve palsies. Rarely pituitary infarcts are known to occur, which present a few months after the bite with symptoms of fatigue, lassitude, somnolence, loss of secondary sexual characteristics as a consequance of hypopitutarism. Peripheral sensory neuropathies are known to follow an Elapidae bite, more commonly seen with a krait bite. Uncommonly, victims of a venomous snake bite have developed an acute demyclinating poly neuropathy (GBS). Cardiac Complications: Myocarditis can develop secondary to an Elapidae bite, commonly so with the Sea Snake species. The symptoms are that of Cardiac failure. Venomous hematotoxic bite is related to DIC, the manifestation of which could be as a prothrombotic phenomenon, victims could develop an acute coronary syndrome. Myocardial infarction which is very uncommon. Rhythm disturbances are common with bradycardia, first degree heart block or a tachy arrhythmic in which PSVT and AF have been most common. Hepato-Biliary system: A two to three fold increase in serum transferase has been seen in most envenomed cases. Jaundice has been noted with severe viperidae bite, mostly due to hemolysis which carried a bad prognosis. Serum Albumin and total proteins fall in viperidae bite more are consequence of capillary leak and proteinuria. Muscle: Rhabdomyolysis is common with elapidae bite more so with sea snake species. This could lead to muscle pain, tenderness, renal shut down & hyperkalemia. Secondary infections: These range from infection at the bite site introduced from the snakes mouth to an aspiration. Aspiration pneumonia in an unconscious state secondary to an Elapidae bite. Osteomyelitis can occur at the bite site. We had this rare complication in two patient, one of whom needed a talo-navicular fusion procedure. Persistent swelling or infection at the bite site may be due to an embedded fang which can be picked up on x-ray of the bitten part. Worsening of proteinuria after initial improvement, arthralgia and fever about 7 to 10 days after envenomation could be due to a serum sickness related to antivenom complex for which steroids are indicated. Snake Venom Ophthalmia: The spat venom should be washed from the eye or mucous membrane as soon as possible using large volumes of water or other bland fluid. Our Hospital experience: Snake bites are common in males in a series of 933 envenomed patients admitted at Little Flower Hospital over the past eight years. Of the admitted patients 618 (66%) were males and 315 (34%) were females. The age distribution was as follows; 138 Victims (14.79%) were less than 20 years of age 335 Victims (36%) were between 21- to 40 years of age 343 Victims (37%) were between 41-60 years of age 117 Victims (13.21%) were more than 60 years of age Of the 933 victims the overwhelming majority, 716 (77%) reached the hospital within 6 hours of bite 104 (11%) reached between 13 24 hours of the event. Only 5 (1%) reached 24 hours after the bite. A tourniquet or a bandage had been applied in 828 (89%) of the victims while it had not been used in 105 (11%) of the victims. The puncture, fang marks or an abrasion was present in 714 (87%) victims, while there were no fang marks in 139 (13%) of the victims. 89 (10%) of the victims had
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undergone some modality of traditional care prior to hospitalization. 378 (41%) of the victims needed less than 10 vials of ASV, 377 (40%) needed between11 to 20 vials. There were no signs of local reaction in 172 victims (18%). Mild signs equating to swelling, discoloration and signs of inflammation not extending beyond the proximal joint line or less than 5 cm. from the bite site Mild signs were seen in 539 (58%) of the victims. Moderate swelling involved inflammation beyond the proximal joint without any signs of limb ischemia. This was seen in 67 (7%) of the victim. The site of bite was foot in 717(77%) of cases, leg 56 (6%) of cases, hand 124 (13%) of cases, arm 18 (2%) of cases and others 16 (2%) of cases. Others include face, breast, buttock, fore-head, back & scalp. 306 of the Victims were of hematotoxic envenomation (33%) Russels Viper 162 (20.5%),Cobra 30 (3%), Krait 11 (1%), unknown bites 366 (30%). Neurological manifestations were seen in 352 victims which included ptosis, weakness, incoherent speech, respiratory paralysis, diplopia blurring of vision and coma. Gastro-intestinal symptoms with nausea, vomiting abdominal pain, loin pain & ileus were observed in 824 of the victims. Bleeding manifestation by way of persistant bleed from bite/1V cannula or from viscera was seen in 122 victims. The other common general symptoms included, severe pain at the bite site, painful nodes, transient giddiness with a fall early after the bite (this group of victims in our series have had a bad prognosis). Reactions to ASV have been seen in upto 321 Victms (34%) of patients which ranged from hypo/hypertension vomiting after institution of ASV, rashes & hives to more severe anaphylaxis which had warranted stopping ASV in 3 victims. Local complications at the bite site included gangrene which was observed in 39 victims,necrosis, was observed in 87 victims and cellulitis were observed in 170 victims. Death occurred in 23 victims (2%) ventilation support was needed in 22 victims (2%) and dialysis was needed in 87 victims (9%) ARDS was seen in 13 victims. From among patient with ARF diagnosed a subset of them needed dialysis and some did not need. Comparing between the two groups of ARF. Lymphadenopathy was observed in 28 of 98 subjects in the dialysed group (29%) as compared to 26% of 79 in the non dialysed group (33%). (crenated RBCs were seen in 30 of 98 victims the dialysis group (31.%) as compared to 18 of 79 victims in the non dialysed group (23%). A low Hb value <10 g% was seen in 66 victims in the dialysed group and in 19 victims in the non dialysed group. Haemo concentration with a Hb >15 g% was observed in 16 victims in the dialysed group and 13 victims of the non dialysed group. Elevated D - dimer.between 251 20000 Hg./ml were seen in 14 of the dialysed group and in 7 victims in the non dialysed group very high D dimer, raised liver enzymes raised total leucocyte count (TLC) band form were more common in the dialysed group compared to the non dialysed group. Low platelet counts strongly correlated to dialysis in patients with ARF. 77 of the 98 patients who needed dialysis had a platelet count < 1 lakh To summarise our finding, poor prognostic factors in Viperidae envenomation include. Low platelets Prolonged clotting time Presence of band forms Polymorphonuclear leucocytosis Crenated RBCs Haemoconcentration at presentation Poor prognosis factors on biochemical analysis include ; Raised D-dimer Low fibrinogen Low serum protein and Albumin Hemoglobinuria Poor prognostic factors from symptom complex are : Bilateral parotid swelling the so called Viper head appearance Giddiness or syncope immediately following the bite Skin necrosis and lymphadenopathy Agitated behaviour secondary to cerebral anoxia. Profound thirst Less pain first few hours after the bite or renal angle tenderness (most of such victims have ended up in renal failure) Besides the obvious benefits of snake venom to produce antivenom, have there been any other breakthrough in medical research ? There have been many early results from research that gives promise on many medical fronts. In France, an enzyme derived from copperhead venom may hold an answer to treatment for breast cancer. Ingredients from the venom of a Malayan pit viper have shown promise in breaking blood clots that would be very beneficial in treating stroke victims. Enzymes from Cobra venom may hold the keys to finding cures for Parkinsons disease and Alzheimers disease. Some viper venom seems to hold the secrets to curing osteoporosis and promoting tumour reduction. Several venom extracts have shown possibilities that could lead to the production of anticoagulants that would be helpful in treating heart disease. Proteins from
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certain rattle snakes have produced blood pressure medicine. Ingredients from the red-necked spitting cobra have provided clues to breaking down cell membranes that would provide treatment for leukemia and cancer. It is obvious that these very complex enzymes derived from snake venom could produce potentially huge medical benefits for mankind. Besides protecting these unique creatures as part of a responsible effort to preserve our natural heritage, it seems increasingly clear that protecting venomous snakes is in our own best medical and health interest.
FUTURE:
Treatment of snake bite has essentially remained the same over the past 35 years. There are no doubts as to the efficacy of ASV, but at what costs. We would have to shift to monovalent ASV for a more effective and a less costly and treatment with a significantly better side effect profile (the dose of ASV would be of what is now given in a standard snake bite). Before developing monovalent ASV one should have the means to diagnose the species of snake for which ASV could then be developed. The most accurate means for the same would be an ELISA based kit for the diagnosis of snake bite which would reliably tell us as to the species of snake. If one were able to identify the toxic elements in the more than 55-70 enzyme fraction in the individual venom, one would be able to target the same. Of the 55-70 different groups in individual venom it only 15-20 enzyme groups which are lethal. A further refinement to the monovalent ASV would be developing antibodies targeting only the specific lethal groups. This should make it a targeted pin point therapy. The same could probably be done on a mass scale from duck or chick embryo. The present stumbling block to harvest from the chick embryo has been that because of the large load of antigen (enzymes in the snake venom) the antibody harvest in the chick embryo has not been consistent to all enzyme groups. By decreasing the venom enzyme fraction injected one hopes for a more consistent response in the chick embryo. This would tremendously decrease the cost of therapy if successful. One hopes with successful research and development one is able to match the Americas and Australia in the management of snake bite in India. We too should be able to bring down the mortality due to snake bites in our country to a three digit number. A venomous Snake Bite is one of the most preventable forms of death. MAY THE SNAKES LIVE IN PEACE! References: 1) R.N Banerjee Poisonous snakes of India, their venoms, symptomatology and treatment of envenomation Progress in Clinical medicine in India, edited by MSS Ahuja, Arnold Heinemann Publishers (India) Pvt. Ltd., 1978 2) Kochva Elazar The origin of snakes and evaluation of the venom apparatus. Toxicon Vol. 25 No. 1 pp 65 106, 1957 3) Schaeffer Richard C. Jr. Heterogeneity of Echis Venoms from different sources Toxicon. Vol. 25 No. 12, 11 B 43 1346, 1987 4) Sharma, Budhdev Snakes in India a Source book An Indispensible book on Indian Snakes, their ecology, conservation & clinical study 5) Chug K.S Snake bite induced Acute Renal failure in India Nephrology forum, Kidney International Vol. 35, 1998 PP 891917 6) Fry Brian.G From Genome to venom molecular origin and evaluation of the snake venom proteome inferred from Phyllogenetic analysis of toxin sequences and related body protein Geneme Research, Vol. 15, PP 403 420, 2005 7) Riviere Gilles, choumet valarie etal Absorption and elimination of viper venom after antivenom administration Journal of Pharmacology and experimental therapeutics, Vol. 285, issue 2, PP 490 495; 1998. 8) Jayanthi G.P, Gowda T.V, Georgraphed variation in India in the composition and lethal potency of Russeth Viper Venom, Toxicon Vol. 26, No. 3, PP 257-264, 1988 9) Whitaker Romulus and Captain Ashok, Snakes of India, DRACO Books, Chennai 2004 10) Nephropathy associated with Animal, Plant and Chemical Toxins in the Tropics. Jha Vivekanand and Chug K.S Seminars in Nephrology, Vol. 23 No. 1, pp 49 65, 2003 11) Warrell, DA, Animal toxins, Mansonia Tropical Diseases, 21st Edition, 2003 12) Ian D. Simpson, Snake bite arrangement in India, the first few hours : A guide for primary care physicians, JIMA, Vol. 103 006 pp 324-335, 2007. 13) Vijayaraghavan .B, snakebite, a book for India Publication of the Chennai Snake Part Trust, 2007 14) Pillay V.V Irritants of animal origin, Modern Medical Toxicology Text book, 3rd edition, Jaypee brothers, New Delhi 120153, 2005. 15) Barry S Gold, Richard CD, & Robert A. Barish, Bites of Venomous snakes, NEJM, Vol. 347, pp 347-355, 2002 16) Joseph K. Joseph, computerized data bank of envenomed patients in Little Flower Hospital, Angamaly. Souvenier, Conference on Snakes, Venom & Snake bite, National and International perspective, PP 73-75, 2008 17) Warrel, D.A, 1988 (Ed.) WHO/SEARO Guidelines for the Clinical Management of Snake bite in the Southeast Asian Region. SE Asian J. Trop. Med. Pub. Hlth, 30, Suppl. 1, 1-85
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18) Simpson ID 1988 Snakebite: Recent Advances in Medicine Update Ed. Sahay BK. The Association of Physicians of India 2006 639-643 19) White J. Snake venoms and Coagulopathy, 2005 Toxicon 45; 951-967 20) Joseph JK, Simpson ID, Menon NCS et al, First Authenticated cases of life-threatening envenoming by the Hump-nosed pit viper (Hypnate hypnale) in India Trans R. Soc. Trop. Med. Hyg: 2007, 101, 85-90. 21) Rosner F. Medical writings of Moses Maimonides, Arch Intern Med. 1974: Vol 133: 318-319 22) Watt. G, Padre L. Tuazon L. Theakston RDG, Laughlin L. 1988, Tourniquet Application after Cobra Bite: Delay in the Onset of Neurotoxicity and the Dangers of Sudden Release. Am J Trop Med Hyg 87 618-622 23) Tun Pe, Tin-Nu-Swe, Myint-Lwin, Warrel DA, Than-Win 1987. The efficacy of trouniquets as a first aid measure for Russells Viper bites in Burma Trans. R. Soc. Trop Med. Hyg. 81 403-405 24) Amaral CF, Campolina D, Dias MB, Bueno CM, Rezende NA, 1998, Tourniquet ineffectiveness to reduce the severity of envenoming after Crotalus durissus snake bite in Belo Horizonte, Minas Gerais, Brazil, Toxicon, May: 36(5):805-8. 25) Sutherland Coulter AR, Harris RD, 1979 Rationalisation of first aid methods for elapid snakebite Lancet 1: 183-186. 26) Howarth DM, Southee A.S, Whytx IM, 1994 Lymphatic flow rates and first aid in simulated peripheral snake or spider envenomation, Medical Journal of Australia: 161 695-700 27) Norris RL, Ngo J, Nolan K, Hooker G, 2005 Physicians and lay people are unable to apply Pressure Immobilisation properly in a simulated snakebite scenario Wilderness and Environmental Medicine 16, 16-21 28) Bush SP, 2004 Snake bite suction devices dont remove venom: They just suck. Ann Emerg Med. Feb; 43(2): 181-186 29) Gray, S, 2003 Pressure Immobilisation of Snakebite. Wilderness and Environmental Medicine : Vol. 14 No. I, pp, 73-73. 30) Anker RL, Staffon WG, Loiselle DS, Anker KM, 1982. Retarding the uptake of mock venom in humans. Comparison of three first aid treatments Medical Journal of Australia I 212-214. 31) Warrell, D.A., Davidson, N. McD., Greenwood, B.M., Ormerod, L.D., Pope, H.M, Walkins, B.J Prentice, C.R.M 1982. Poisoning by bites of the saw-scaled or carpet viper (Echis carinatus) in Nigeria Quart. J. Med. 46, 33-62. 32) Ho M, Warrell MJ, Warrell DA, Bidwell D, Voller A, 1982. A critical reappraisal of the use of enzyme-linked immunosorbent assays in the study of snakebite : Toxicin : 24: 211-221. 33) Tun P. Khin Aung Cho. 1986 Amount of Venom injected by Russells Viper (Viper russelli) Toxicon: 24(7): 730-733. 34) Paul V. Pratibha S. Prahlad K.A, Earali J, Francis S, Lewis F, 2004 High-Dose Anti-Snake Venom versus low dose antisnake venom in the treatment of poisonous snakebites A critical study Journal of the Associations of Physicians of India 1417. 35) Agarwal R, Agarwal AN, Gupta D. Behera D, Jindal SK. 2005 Low dose of snake antivenom is as effective as high dose in patients with severe neurotoxic snake envenoming. 36) Watt G, Theakston RD, Hayes CG, Yambao ML, Sangalang R, Ranao CP, Alquizalas.E, Warrell DA, 1986 Positive response to edrophonium in patients with neurotoxic envenoming by Cobras (Naja Naja Philippinensis). The New England Journal of Medicine 23 1444-1448. 37) Warrel DA, Looareesuwan.S, White NJ, Theakston RD, Warrel MJ, Kosakarn W. Reid HA, Severe neurotoxin envenoming by the Malayam Krait Bungarus candidus (Linnaeus) response to anticholinesterase. 1983 BMJ 286 670-680. 38) Simons FE, Gu X, Simons KJ, 2001 Epinephrine absorption in adults : intramuscular versus subcutaneous injection. J Allergy Clin Immunol; 108:871-3 39) Sampson HA, Mendelson L, Rosen JP. 1992 Fatal and near fatal anaphylactic reactions to food in children and adolescents, N. Engl. J Med:327:380-4. 40) American Association of Allergy, Asthma and Immunology. Media resources: position statement 26. The use of epinephrine in the treatment of anaphylaxis. www.aaai.org/media/resources/advocacy-statements/ps26.stm (accessed Apr. 2003) 41) Wen Fan H, Marcopito LF, Cardoso JLC, Franca FOS, Malaque CMS, Ferrari RA, Theakston RD, Warrel DA, 1999 Sequential randomized and double blind trial of Promethazine prophylaxis against early anaphylactic reactions to antivenom for Bothrops snake bites. BMJ (318) 1451-1453. 42) Premawardenha A, de Silva CE, Fonseka MMD, Gunatilakee SB, de Silva HJ, Low dose subcutaneous adrenaline to prevent acute adverse reactions to antiveom serum in people bitten by snakes randomized, placebo controlled trial BMJ 318 1041-1043. 43) Gawarammana IB, Kularante M, Abeysinga.S, Dissarayake WP, Kumarasri RPV, Seranayake N, Ariyasena H, 2004 Parallel infusion of hydrocortisone + Chlorpheniramine bolus injection to prevent acute adverse reactions to antivenom for snake bites. Med. Journal of Australia. Jan. 5: 180 (1) 20-3. 44) Tin Na Swe, Myint Lwin, Myint-Aye-Mu, Than Than, Thein Than, Tun Pediatrics, 1992 Heparin Therapy in Russells Viper bite victims with disseminated intravascular coagulation: a controlled trial. Southeast Asian J. Trop Med. Public Helth 23(2) 282287.
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SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

Risk and Other Ecological Factors Prevention

ANATOMY & PHYSIOLOGY

and Treatment Future

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

name="Introduction" id="A4" class="articlesubtitle_txt">TABLE Enzymatic components in Snake Venom ENZYME EFFECTS

Pre-synaptic motor nerve end blockade

(Naja naga atra)

VENOM & BITE:

SNAKES, VENOM & SNAKE BITE

OCCUPATIONAL RISK AND OTHER ECOLOGICAL FACTORS:

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKE BITE TREATMENT PROTOCOL Treatment Phase

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

COMPLICATIONS AND TREATMENT:

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

SNAKES, VENOM & SNAKE BITE

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