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There are about 216 species of snakes identifiable in India, of which 52 are known poisonous. The major families of poisonous snakes in India are Elapidae which includes common cobra (Naja naja), king cobra and common krait (bungarus caerulus), viperidae includes Russell's viper, echis carinatus(saw scaled or carpet viper) and pit viper and hydrophidae (sea snakes). Fatal snake bites are common to feature in local news paper from taluka place ,headlines during monsoon season.
Snake venoms are not single toxins but cocktail of many components: enzymes, poly-nucleotides toxins, non-toxin proteins, carbohydrates, metals, lipids, free amino-acids, nucleotides and biogenic amines. The content and potency of venom in any snake varies with size, age, diet, climate and time of year. Potency of venom is reduced in a cold climate. More over small snake immature venom may not responds to routine anti-snake venom. The venom out put during summer months is more than winter.
Pro-coagulant enzymes is the major factor in viper venom, it stimulate blood clotting , subsequent fibrinolysis result in vicious cycle result in disseminated intravascular coagulation(DIC) result in incoagulable blood. Russell's viper venom contain several different pro-coagulants which activates varies steps of the clotting cascade. The result is formation of fibrin in the blood. Most of this is immediately broken down by the body's own fibrinolytic system. At times within 30 minutes of the Russell's viper bite, the levels of clotting factors have been so depleted that the blood remains incoaguable.
Haemorrhagins - It is zinc metalloproteinase , it damages the endothelial lining of the blood vessels causing of spurting of red blood cells and spontaneous systemic bleeding.
Cytolytic or necrotic toxins- These toxins damages the cell membranes, stimulates apoptosis . These digestive hydrolases , polypeptide toxins and other factors increase permeability resulting in local swelling and non-healing ulcers and gangrene of bitten part.
Haemolytic and myolytic phospholipases A2- These enzymes damage cell membranes, endothelium, skeletal muscle, nerve and red blood cells.
Pre-synaptic neurotoxins- These are phospholipids A2 that damage nerve endings, initially releasing acetylcholine transmitter, than interfering with its release. Venom of krait ( Bungarus ceruleus) is rich source of these enzymes. Similar systemic manifestation often reported due Russell's viper bite from northern part of India venom.
Post-synaptic neurotoxins - These polypeptides compete with acetyl choline for receptors in the neuromuscular junction and lead to curare-like paralysis (cobra venom).
The amount of venom injected at the time of bite depends on species and size of the snake and the mechanical efficiency of the bites. At times snake may be able to control whether or not venom to be injected at the time of bite. That is reasons many times irrespective of bite by poisonous snake did not result in systemic involvement i.e. dry bite. Repeat strikes by snake may result in additional envenomation, because snake's entire supply of venom is not usually exhausted with the first attack or after even several strikes. Snakes are no less venous after eating their prey.
Echis- carinatus or saw scaled viper or carpet viper
It is of size 1 to 3 feet long. Head of this snake is sub ovate with short rounded snout. Body is cylindrical, short and snout. Body is covered with rough, serrated flank scales, neck is distinctly constricted. Its color is pale brown, tawny with dark brown. A cruciform or trident or arrow type or just like the bird foot print shaped mark seen on head. It is flourished in hot and humid climate all over coastal region of India. It is an alert, diurnal in habit and capable of quick movement when necessary. It hibernates in the winter. It often climbs on to shrubs and other low vegetation. Readiness with which it bites on smallest provocation with extremely rapid strike makes it is one of the dangerous snakes. It forms a double coil in the form of figure of 8 with its head in the center a striking position. The coils keep moving against each other and serrated keels on the flank scales produce a hissing noise by friction. It is viviparous producing 3 to 15 young at a time. It injects 0.0046 gram venom at the time of bite.
Farmers, hunters, laborers and person walking bare foot at peddler or in jungle and rocky areas often bitten by this snake.
Local - Common bite site is left hand which goes blindly for to hold the grass while right hand hold the sickle while harvesting the grass for cattle. Soon after the bite within one hour there is development of swelling over the bitten part. Fang marks or abrasions with clotted blood seen. Swelling progress more than one segments. Venom content big molecular size toxins and being circulated through the lymphatic hence within 60-120 minute victim experience a painful lympnadenopathy at drainage area of the bitten part. If untreated swelling progressed to whole limb or to the chest wall. Ecchymosed seen over the bitten part or may spread over lymphatic drainage areas. Acute bleeding in form of gum bleeds or bleeding from abrasion on other part of body or from vene-puncure site seen within 90-120 minute of bite. At times patient remains untreated bleeding persisted for 1-2 weeks in form of blood stain sputum, haematuria and disappeared of its own. Such patients are markedly anemic and reported to hospital for weakness or non-healing cellulites with uncontrolled bleeding from cellulites. Natural immunity against the Echis carinatius venom developed in a case of repeated bite by same species in a endemic areas as minimum clinical involvement in subsequent bite reported in Jammu region. Renal failure due to Echis carinatus reported from Pondichery and Jammu areas. But rarely from Maharashtra.
Russell's viper or viper Russell siamensis
It inhabits ten south Asian countries. In Pakistan, India, Sri Lanka, Bangladesh, Burma and Thailand it ranks amongst the most important causes of snakebite mortality. While protecting the paddy, wheat by containing the rodent (rats) population, it kills many farmers unlucky enough to tread on it during harvest.
It is 3-5 feet long snake. Head is covered with small scales and without shields. Body is massive, cylindrical, narrowing at both ends. Head is flat, triangular with short snout, large gold flecked eyes with vertical pupil and large open nostrils. Round belly with constricted neck. Typical rows of oval arranged in two rows are characteristic of Russell's viper. Its natural prey includes mice, rats, frogs, lizards, snakes and birds. Young are cannibalistic. Females produces 20-60 young's usually around June or July. Length of fangs in adult snake is 16 mm long and curved. The amount of venom injected at the time of bite is 63+ - 7 MG.
Local- Bite usually to toes or fingers were bitten while reaping or carrying rice or Jawar or sugar cane husk bundles. At times victim remove the encircle snake to bitten limb.Victim experience severe local pain at the site of bite. Within 6-8 hours swelling progressed to whole limb. Active bleeding from the fangs marks without formation of blood clot. Subsequently Local ecchymosed, and blebs over bitten part occur. Because of edema of muscle and bleeding there is development of compartment syndrome characterized by swelling, pain full passive movement and loss of sensation over the nerve areas passing through the compartment if not treated in time lead to wet gangrene or non-healing ulcers. Common cause of disability. Lymph nodes proximal to the bite become enlarged and tender. Tenderness along Hunter's canal often noted, over bitten lower limb.
Soon after bite sudden giddiness and collapse due to hypotension, shock is due to sudden liberation of bradykinin in to circulation, bleeding and loss of fluid in swollen part, bleeding in to adrenal glands, or peritoneal or massive blood loss by hemetemesis or hemoptysis.
Pro-coagulant content of venom initiate rapid thrombosis, fibrinolysis result of consumption coagulopathy. This pro-coagulants, which activate the clotting system of the snake's natural prey with such speed and efficiency that Macfarlane was "left feeling it is almost too clever to be true". In human victims of Russell's viper bite, the injected dose of venom is insufficient to cause massive fatal intra-vascular coagulation within minute of bite. Once the patient's blood become defibrinated and incoagulable, accompanied with damage vascular endothelium by haemorrghins and platelet abnormalities may lead to the spontaneous systemic bleeding, haematuria, skin and pituitary. Victims with pulmonary tuberculosis with cavity, peptic ulcer and hypertension are more prone to developed life threatening bleeding.
Venom is rich source of tumor necrosis factor may cause recurrent ventricular arrhythmias.
Russell's bite victims subsequently developed amenorrhea, Sheehan's syndrome , loss of libido due hypo-pituitaries reported from south part of India . Enhanced capillary permeability seen in form of plural, pericardial effusion, ascities and conjunctivae hemorrhage or congestions and bilateral parotid swelling.
20-40% cases subsequently developed oliguria, anuria and acute renal failure. Renal angle tenderness is most important clinical sign for early diagnosis of renal failure. There is serial rise in blood urea and serum creatinine with acidosis and hyperkalaemia. Generalized anasarca, renal failure is due to interstitial nephritis, tubular damage by venom itself, hemoglobinuria, hypotension, micro thrombi in the kidney contribute to the acute tubular necrosis. Renal failure is a common cause of death due to Russell, envenoming.
Rare complications of viper bite are acute myocardial and cerebral infarction.
Ptosis, bulbar palsy, inter-nuclear opthlamoplegia and respiratory paralysis due to presynaptic neuromuscular block in a Russell's viper bite poisoning often seen and reported from keral state and Sri Lanka.
Green pit viper and bamboo pit viper
Snakebite cases are reported from kerala characterized by local edema and rarely a systemic bleeding disorder. Edema persisted for many days. Regional lymphadenopathy is often absent
Coagulopathy and renal failure due to Hump-nosed pit viper snake bite have been reported from Keral state which was previously thought of a non-venomous snake.
Common Indian Krait (Bungarus caeruleus)
Local names - urdu Kala gandait, Gujarathi kala taro, Marathi Kandar , manyar, oria chitti, tamil kattu viriyan, Malayalam valla pamboo.
Krait is most poisonous snake among all its venom is ten times poisonous than cobra. It 1-4 feet long, with enlarged hexagonal vertebral scales, the entire subcudals, uniform white or red belly and the narrow white crossbars on the back, more or less distinctly in pairs, the crossbar are typically absent near the head and neck region. The common krait often flourish in the vicinity of human habitation. Near the wattle and daub, mud and small huts dwellings. Krait is a nocturnal, terrestrial snake that enter human dwelling in search of prey such as rats, mice and lizards. Even it eats the small snakes (cannibalism). The common krait is regarded as the most dangerous species of venomous snake in the Indian subcontinent. 35-50% fatality is due improper management and lack of artificial ventilator in the rural area has been reported. Villagers and adivasis (nomides) usually sleep on the floor of their huts, mud or wattle -and- daub houses which are often surrounded by dense vegetation. Krait may strike a person sleeping on the ground, if the person accidentally touches or rolls over onto the snake. Also snake could mistakenly identify an exposed body part as prey. Most bite occur during the cooler months June to December, when snakes may , during the course of their hunting activity, linger in a person's bedding to take advantage of the warmth therein.
Majority of cases are reported between 11pm - 5AM. The fangs of krait are small and sharp like a 24 size needle. During sleep the reflexes are blunted. Being sharp small fangs, krait injects maximum venom to a person who is in sound sleep. Usual bite site is any part of body, common site seen over neck, axilla, over knee or back. Victim might experience mild pain at the site of bite, parasthesia or numbness, without any local marks or swelling or bleed hence it is neglected and falsely initially attributed to ant or rat bite or no bite unfortunately this delays the reporting victim to hospital. Venom is small molecular size hence directly absorbed in the circulation. Initially venom causes of release of acetyl choline and than destruction of pre-synaptic receptors. The venom stimulates autonomic nervous system thus within 20-30 minute of bite, victim experience a transient abdominal colicky pain , brady-cardia, sweating , vomiting, persistent raised blood pressure with pulmonary edema . Subsequently venom within 30 minute to 8 hours attach block the the presynaptic acetyl choline receptors result in ptosis, pulling of saliva, nasal twang sound, unable to protrude the tongue beyond teeth margin, dysphagia, dysponea, inter-nuclearand external opthalmoplegia, weakness of neck muscle result in difficulty to raise the head from pillow or while lifting the both shoulder neck suddenly falls back ( broken neck sign) , respiratory muscle and lastly the diaphragm. Patient complaints of blurred vision, diplopia, respiratory paralysis , coma and anoxic cardiac arrest. Many times victims are brought dead with or without history of bite but taking details history is vital for suspected krait bite majority of cases of sudden unknown deaths in ashram schools are due to krait bite. Venom induced paralysis of pupillary muscle resulted in to non-reaction pupils is not the sign of irreversible brain damage. Recently myoneuropathy with reanl failure due to krait bite reported from Bangaldesh. After recovery few patient had signs and symptoms of peripheral neuropathy. Many times patients succumb to iatrogenic respiratory infection or adult respiratory distress syndrome.
Cobra bite also tend to occur during day time and early darkness , when the transportation is more readily available. More over because of known severity of envenoming patients and relative make hurry to report to hospital rather than killing time to go to village healer.
Cobra venom is potent cardiotoxic, neurotoxic, haematotoxic , cytotoxic. The fangs are small and sharp. Its venom is small molecular size hence rapidly absorbed in to circulation.
Soon after bite victim experience severe pain at the site of bite with fangs marks covered with blood clots. Rapid development of swelling over the bitten part, ecchymosed, blebs and massive damage of skin and subcutaneous tissue due to myocytolysis. If the victim saw the bitten hooded cobra may die of cardiac lethal ventricular arrhythmias or cardiogenic shock due to massive myocardial infarction. As a result of massive liberation of endogenous catecholamine in to circulation due to threat of death feeling this phenomenon is absent in children having no ideas of death. Sinus bradycardia, A-V block and hypotension are due to cardio-depressant action of venom. Sudden respiratory arrest without any other neurological manifestations can occur resulting in anoxic cardiac arrest. Then rapid ptosis and bulbar palsy accompanied with respiratory depression occurred. Rarely hematotoxic effects are seen. Blurring of vision and loss of accommodation is earliest most sign of neurological envenoming. Victim may be seen in locked in syndrome.
Are seen all over coastal region as sea snake is accidentally handle by fishermen during fishing. Its venom is neurotoxin, myotoxic and haematotoxic, Soon after bite victim experience pain in throat , swelling of tongue ,severe muscle pain, marked tenderness all over muscles, truisms ,muscular paralysis, respiratory arrest , without local manifestations at the site of bite. Due to myotoxic effects of venom resulting in liberation of potassium in to circulation followed by tented T waves, widened QRS complexes and diastolic cardiac arrest. Massive liberation myoglobin in to circulation, it blocks the renal tubules and acute renal shut down.
Confirmation of diagnosis - victim is envenomed by venomous snake can be diagnosed by noting the above signs and symptoms. Most important is the history in krait bite that victim woke due to pain in abdomen from floor bed.
At times relatives and victim brought the killed specimen which help for further management. If snake is seen but did not killed of killed but did not bring to hospital in such situation one can show the photographs of varies venomous snakes or hospital preserved specimen.
In case if snake is not seen or unable to identify on photographs and specimen in such situation one can go ahead with syndromic approach.
Both are confusing because Russell viper and cobra got both neurological and haemostatic manifestation .however following short view to confirm clinically.
Local pain , edema , ecchymosed and rapidly development of neuroparalysis or respiratory arrest is cobra bite.
No local manifestations, rat bite, ant bite or no bite often reported during night hours with pain in abdomen , floor bed and ptosis confirms krait bite.
Soon after bite giddiness, collapse , rapid swelling and active blood oozing from fangs marks is Russell's viper bite.
Slow developing edema no active oozing and fangs marks clntent clotted blood is Echis bite.
Soon after bite victim is anxious and feels threat of death can be reduced by reassurance. Removing him from bite site to prevent repeat bite. Taking patient to ventilated room. Local incision, tight tourniquet or suction, electric shock or application of herbal remedies to be discouraged. Patient to be removed to near primary health center. Patient is not allowed to walk and the bitten part should be kept below the heart level, if available can be immobilized by loose splint. Crebb bandage starting from distal to bitten site with a pressure enough that one can easily introduce the finger between skin and bandage. It is worthy to apply crepe bandage to krait bite case if victim took >30 minute but less than 2-3 hours to reach the hospital. This help to delay the absorption of venom and more over may prevent rapid development of respiratory paralysis. If victim is carried over motor bile he should be between driver and another person to avoid fall from bike due to neuroparalysis. During transport be aware victim should not get injury in form of abrasion or trauma by the branches of road side trees as in case of viper bite victim may die due to uncontrolled bleeding. If snake is killed one can carefully put by fork of two sticks in the bags and not handle because sheared head of snake can inject the venom . An it should be shown to medical officer or doctor who is treating the case.
Treatment of circulating venom- at primary health center where the victim reach earlier before full-blown systemic involvement occur.
Treatment with Anti-snake venom (ASV)
History of snake bite or evidence of fangs marks should not be the indication of antisnake venom. At times snake may not inject venom (dry bite). There should be signs and symptoms suggestive of envenoming.
ASV is the only specific treatment of snake bite. It neutralizes the free circulating venom and it has minimum or no action once the venom attached the receptor site such as neuromuscular junction, platelets , RBCs, endothelium , muscles and renal tissue. In India polyvalent antivenom is available it includes antibodies against cobra, krait, Echis and Russell's viper venom. It available in powder and liquid form potency of both are same. Dissolve solution should be clear and turbid solution should be discarded as it will give more reaction due to precipitate of proteins. ASV should be administered by intravenous route and not by intramuscular route. The treating doctor should know that emergency treatment of venomous bite is antivenom only. Clinical out come depends upon the time lapsed between bite to needle time. The initial dose of ASV is decided by the total venom injected in one bite and neutralizing property of one ML of ASV. On this background and available knowledge .
Initial 100( 10 ampoules) ml ASV to be added 200 ml of crystalloid solution administered over 60 minute by intravenous route in a victim of krait, cobra and Russell's viper envenoming. It neutralizes the circulating venom, while the venom absorbed slowly from the site of bite which act as depot can be neutralized by subsequent 20- 50Ml of ASV subsequently.
While the total initial dose required for echis carinatus envenoming is 20-40 ML over one hour and 20 ML over next 24 hours. Due lack of scientific randomized trial the dose of ASV administered empirically .
If after initial 100 ML ASV there is no improvement in neurological manifestation within 30 minute than one can repeat 50 ML ASV not more than that in case of cobra and krait bite. One should not go on pouring expensive ASV till neurological manifestations persist.
Indication of intubations
Pooling of saliva
Broken neck sign
Grade III power
5 - Tidal volume below 200 ml.
At the site of bite or d during transport if victim develop respiratory repression on give mouth -mouth respiration and at primary health center ambu bag ventilation should be started.
Though it is reported that the krait venom is purely presynptic blocker and resistant to anti-choline estarse we found in Indian krait both receptors are blocked however one can see the rapid response to neostigamine or by putting ice contain glove finger over eyelids that cold test if there is improvement in ptosis such victim will be benefited by ACEI.
Dose of neostigmine 25micrigam/kg in one hour followed by 50micrgram/kg every four over by intravenous drip or 0.5 mg intravenously every hourly . Atropine to neutralize the muscarinic action of neostigmnie.
Cobra victim usually recover very fast within 24 -72hours. Because cobra venom reversible block the post synaptic neuromuscular receptors.
However krait venom destroys the presynaptic receptors hence required prolonged ventilation till new receptors are generated may be 7 days to few weeks.
Mortality was 40-50% before advent of ventilation facilities at present which is almost negligible. Provided victim reach earlier and has not suffered of prolonged hypoxia to brain and hypoxic brain death. Basal ganglia thalamus and lentiform nucleus is more susceptible to transient hypoxia.
ASV may be administered even after 12-14 days after viper bite if systemic toxicity present. Thus you are never late to administer the ASV in a viper bite with systemic involvement.
After initial dose of anti-venom the active bleeding such as hemetemesis, haematuria, bleeds from wound do not disappeared within 20-30 minute particularly in viper bite one can repeat 20-50 ml antivenom a addition extra bolus.
20 minute whole blood clotting test (20WBCT) this is most gold standard bed side test can be performed by unskilled staff. Before injecting ASV from same vein-puncture 2-3 ml of blood is withdrawn and added to a dry glass tube ( not washed with detergent) is kept standstill and observed after 20 minute, tipped of the blood did not clot confirmed hypofibrinogenemia. This test should not be repeated with 6 hours after the dose of ASV, as liver took six hours for synthesis of coagulants factors. 20WBCT test decides the further requirement of ASV. This test is important for diagnosis and also indicates the improvement.
Refractory shock due to capillary leak syndrome seen in Russell's viper bite with conjunctivae congestions and edema need intensive care management and inotropic support close monitoring , fluid replacement and 1000 mg methyl prednisolone.
Renal failure - Close monitoring of urine out is crucial important. Early detection of renal failure in Russell's viper bite. Early failure treated by intravenous frusemide 200-500 mg or torasemide by continuous intravenous drip and dopamine drip with fluid restriction. Rise in serum creatinine and hyperkalemia need renal or peritoneal dialysis.
Profuse bleeding - Due to DIC and thrombocytomia can be treated by blood transfusion.
Shock due to accumulation of fluid in compartmental syndrome or muscles damage can be prevented by surgical decompression but following criteria should be fulfilled before surgical procedure
Marked tenderness over muscles
Pain during passive movement of muscles.
Loss of sensation or hypo-aesthesia over in the supply of a nerve passing through the compartment
Local wound care - If the blebs are tense they can be aspirated by sterile needle. Higher antibiotic as snake mouth is contaminated with varies bacteria. In case of non healing wound victim should be investigated for diabetes and hypertension. At times because of huge tissue necrosis due to myocytolysis need skin graft for recovery.
Is test dose of ASV essential? NO because if victim is sensitive to ASV does not preclude its use nor if not sensitive did not give guarantee that victim did not develop anaphylaxis reaction. Recently it is reported that subcutaneous adrenaline, antihistamine and steroid can be used as prophylaxis before starting ASV.
How to recognized the anaphylaxis- Most earlier symptoms is vomiting sensation, warm sensation in ears or head, itching behind ears, urticaria, itching all over body, hypotension , tachycardia , bronchospasm, dysphagia , swelling of tongue and lip. Feeling of obstruction in throat.
ASV should not be given by rapid intravenous bolus may activate complements and gives more severe reaction. One should keep watch for appearance of anaphylaxis for 10 to 180 minutes after administration of ASV.
Treatment of anaphylaxis
Intravenous clorphenarmine maleate, hydrocortisone, intramuscular adrenaline , to be repeated every 5-7 minutes or if not responding than intravenous adrenaline drip or 1 ml 1:1000 adrenaline diluted in 20 ML of saline to be administered over 20 minutes by slow drip.
Late serum sickness - developed 5-24 ( mean 7) days after antivenom. Characterized by fever, body ache, Itching,arthralgia and mononeuritis multiplex.
At times involvement of serous membrane, lymphadenopathy. This serum sickness responds to steroids.
Intra muscular injection should be avoided till blood fail to clot.
Total requirement of ASV dose can be reduced by preparing mono-specific ASV or purified F(ab)2 ASV.
ELISA kit for detection of venom antigen help for a treating doctor to know the exact species of snake and even help to monitor the circulating venom antigen thus the dose of ASV.
Prevention- fire wood, cow dung, cattle shade and rubbles should be kept away from residential house. Old storage rubble particularly in old house should be handling with full sunlight. Bare foot walking in darkness, in grown up grass should be avoided or go with torch. Proper care of rats, mice and lizards, they can be killed by rat poison. No attempt should be made to catch snake or to kill.
Thick electrician gloves with rubber shoe should be wearing at the time of handling the Jawar or paddy or sugar cane husk.
Routine use of cot with mosquito net or simple mosquito net with properly tugged net margins under bed prevents krait bite.
Training in appropriate use of antivenom and protocol of indications for its use should be arranged at general hospital level to ease the crisis of supply of antisnake venom and mere history of snake bite should not be the indication of administration of antisnake venom.
Medical officer should be trained how to do endotrachael intubations and ambu bag respiration. Ambu bag with necessary requirement must be made available at any dispensary including primary health centers and facilities of ventilator and renal dialysis should be mandatory at rural, cottage and districts hospital, if we want to reduce the fatality of snake bite in agricultural country India.
ASV causes severe reaction, it is expensive hence toxicologists should made attempt to synthesis the pharmacological antidote to venom action or should prepared a chemical receptors so as the venom might attack the external injected receptors and protect the natural receptors.
* Young male (15-29 years) farmers are most highly affected, making snake bite envenoming a truly occupational disease.
* unfortunately ,global health authority given little attention to this life threatening problem, relegating snake bite envenoming to the category of major neglected disease of 21st century
* There is one snake bite death for every two AIDS deaths in India
* Doctors working at periphery should be trained for endo- tracheal intubations, how to diagnose a venomous bite and initial dose of ASV
* ventilator facilities with trained staff for operating ventilator should be made available at rural hospital.
* Doctor should accompany during transfer of case to higher center.