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 Table of Contents  
TOXICOLOGY SYMPOSIA REVIEW ARTICLE
Year : 2015  |  Volume : 20  |  Issue : 1  |  Page : 5-14

Snake bite poisoning


Bawaskar Hospital and Clinical Research Center, Mahad, Raigad, Maharashtra, India

Date of Web Publication19-Feb-2015

Correspondence Address:
Dr. H S Bawaskar
Bawaskar Hospital and Clinical Research Center, Mahad, Raigad, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9903.151717

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  Abstract 

Envenoming by venomous snake evokes a life-threatening response. Rapid diagnosis of acute hemorrhagic disorders, neurorespiratory, renal, and hemodynamic failure subsequent to snake bite and their rapid interventions saves life. Early administration of the appropriate dose of potent snake antivenom along with adjuvant treatment, proper care of the wound, correcting electrolyte imbalance, tissue oxygenation, and maintenance of adequate nutrition may help rapid recovery.

Keywords: Antisnake-venom, cobra, krait, snake bite, viper


How to cite this article:
Bawaskar H S, Bawaskar P H. Snake bite poisoning. J Mahatma Gandhi Inst Med Sci 2015;20:5-14

How to cite this URL:
Bawaskar H S, Bawaskar P H. Snake bite poisoning. J Mahatma Gandhi Inst Med Sci [serial online] 2015 [cited 2018 Jan 20];20:5-14. Available from: http://www.jmgims.co.in/text.asp?2015/20/1/5/151717


  Introduction Top


Snake envenoming is a disease of poverty. [1] Envenoming by poisonous animals (snakes, scorpions, wasps, ants, and spiders) is an occupational hazard often faced by farmers, farm laborers, hunters, and shepherds of tropical and subtropical countries. Poisoning by venomous snake bite is a common acute life-threatening, time-limiting medical emergency. In the rural area, snake bite poisoning is a leading cause of death of young earning member of the family. More than 2,000,000 snake bites are reported in the country, and it is estimated that >50000 people die of snakebite each year. [2],[3] Newly posted or inexperienced doctors and inadequate facilities at primary health center (PHC), ignorance of conventional treatment of snake bite by doctors; further delays appropriate treatment of victims and contribute to increasing morbidity and mortality. [4] It is the surprise to note that snake bite poisoning is seldom mentioned as a priority for health research in the developing country like India. Snake-venom antigen detection Kits should be made available. Mono-specific antivenom producers in India should be encouraged to prepare antivenom from venom obtained from snakes caught from relevant areas of the country [5],[6]


  Snakes Top


Of more than 3000 known species of snakes, only about 300 are venomous and in India there are about 216 identifiable species of snakes, of which 52 are known to be poisonous. The major families of poisonous snakes in India are Elapid which includes common cobra (Naja naja), king cobra and common krait (Bungarus caerulus, Banded krait, Sind krait), viperidae (Russell's viper), Echis carinatus (saw-scaled or carpet viper), and pit viper and hydrophiidae (sea snakes). Recently, venomous viper called hope nosed viper is reported from Cochin region. During monsoon season, fatal snake bites are common to feature in local newspaper]. [7] [Table 1] highlights the risk factors predisposing to snake bites. [Table 2] gives the characteristics of various snakes [Figure 1].
Table 1: Risk factors involved in accidental snake envenoming

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Table 2: Characteristics of different snakes [Figure 1]

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Figure 1: Different types of snakes, (a) and (b) Cobra, (c) and (d) krait, (e) Russell's Viper, (f) and (g) is saw scaled viper and its fangs

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  Biochemistry, Physiological, and Pathology of Envenoming Top


Snakes are cold-blooded, highly specialized animals. A pair of salivary glands secretes a powerful multipurpose enzyme fluid (venom) that flow at the time of envenoming through fine channeled or grooved teeth called fangs. Venom secretion in all venomous snakes appears to vary in seasons; more in warmer months with high morbidity and fatality. Snake is cold blooded animal. Darker the snake, it secretes more venom as compared to a light colored. Because of the rise in body temperature of dark skin (poor conductor of heat) snake, the venom is in more fluid state and injected rapidly with high speed and maximum quantity in a short time during envenoming. As oppose to light colored skin because of low body temperature, the venom is thick and hence less amount is injected at the time of envenoming. [8]

It is quite clear that snake venom is not a substance evolved to attack man or any big vertebrates. Snake can bite and continue to secrete venom a number of times in succession. Most snakes inject 10% of the available venom in a single strike except the Russell's viper which injects 75% of stored venom in one bite due to big long sharp curved fangs. [7] At times snake only bite without envenoming called as "defence bite or dry bite" ;while the bite with envenoming is called as the "professional bite".

Venom is a cocktail of 20 or more components including proteins, enzymes, nonenzymatic polypeptide toxins, nontoxic nerve growth factors, hyaluronidase, metalase, lipids, free amino acids, nucleotides, carbohydrates, biogenic amines, and various activators and in activators of physiological processes. [6] Krait and cobra venom contains acetylcholine (Ach) esterase, phospholipase B, and glycerophosphatase. Phospholipase A2 is found in the majority of venom and is extensively studied. It destroys mitochondria, red blood cells (RBCs), leukocytes, platelets, peripheral nerve endings, skeletal muscles, vascular endothelium, presynaptic neurotoxicity, opiate-like sedative effects, and auto pharmacological release of histamine (anaphylaxis). Hyaluronidase promotes the spread of venom through the tissue. Proteolytic enzymes are responsible for local changes in permeability leading to edema, blistering, bruising, and local necrosis. [6],[7]

Cobra venom

Cobra venom is of smaller molecular size and rapidly absorbed into circulation. Absorption is further accelerated by threat of death, running and hence the liberated catecholamine and running due to fear can kill the victim within 8 min. Cobras unlike the krait deposit its venom deeply. This in combination with hyaluronidase allows spreading of the venom to occur rapidly and symptoms to arise abruptly. Interestingly, this rapidity of onset of symptoms prompts the rural victim in India to seek care quickly after cobra bite. [9] Severe, irreparable local tissue is lost at the bite site of cobra envenoming due to myocytolysis. Cobra venom is rich in postsynaptic neurotoxins called alpha-bungarotoxin and cobratoxin. Cobra venom binds especially to Ach receptors, prevents the interaction between Ach and receptors on postsynaptic membrane result in neuromuscular blockade. Cardio- toxin content of cobra venom has direct action on skeletal, cardiac, smooth muscles, nerves and neuromuscular junction causes paralysis, circulatory, respiratory failure, cardiac arrhythmias, various heart block and cardiac arrest because the venom releases calcium ions from the surface membrane to the myocardium.

Common Indian krait (Bungarus caeruleus) - (Local names - Kala gandait, kala taro, kandar, manyar, chitti, kattu viriyan, valla pamboo)

Common Indian krait venom contains both presynaptic beta bungarotoxin and alpha bungarotoxin. These toxins initially release Ach at the nerve endings, at neuromuscular junction and then damage it subsequently preventing the release of Ach. Irrespective of Krait, its venom is 10 times more lethal than cobra. But unfortunately unlike as in cobra bite, the victim reports too late due to delayed clinical manifestations. Krait is nocturnal in habit. Its fangs are small size like that of insulin needle. It injects the venom into skin or skin deep. It accidentally bites a person sleeping on floor bed. [8],[10],[11],[12] Though venom is of small molecular size it is absorbed slowly as skin has poor circulation and reflexes are blunted during sleep. [11] Neuromuscular blockade by the short chain neurotoxin (cobra toxin, alpha bungarotoxin) is more readily reversible than with a long chain toxin (beta bungarotoxin). Beta bungarotoxin in the krait venom bears similarity to botulinum toxin. [6],[9],[13] Preserved tendon reflexes in botulism differentiates it from krait bite. Krait venom has a great affinity towards presynaptic Ach receptors. Thus, the tissue having high concentration of this receptors are affected in the following order, such as sphincter pupillae, levator palpebral superioris, neck muscles, bulbar muscles, subsequently limbs and lastly the diaphragm and intercostals muscles. Venom acts as early as 30 min and till 18 h. [9] Envenoming by krait has an early phase profound paralysis which lasts for 30 to 60 minutes, followed by deep paralysis phase which lasts for 2 to3 days and then recovery phase ranging from 2 to 3 weeks.

Viper (Russel viper)

Viper venom interferes with blood clotting. Venoms contain serine proteases, metalloproteinases, C-type lectins, disintegrins, and phospholipases, and it exhibits both anticoagulant and procoagulant effects on blood clotting mechanism resulting in defibrination syndrome or disseminated intravascular fibrino-coagulopathy. [14],[15] Russell's venom is a rich source of enzymes that activates factor X to convert prothrombin to thrombin in presence of calcium factor V and platelets thus Russell's venom contains several different "pro-coagulants" which activate different steps in the clotting cascade. [14],[15],[16] The fibrinolytic activity of the viper venom is so fast that sometimes within 30 min of the bite, the coagulation factors are so depleted that blood does not clot. Russell's venom activates the clotting system of the snake's natural prey with such speed that Macfarlane a brilliant hematologist was "left feeling it is almost too clever to be true." [17] Haemorrhagins-1, 2 and metallo-endopeptidase causes acute rapid bleeding in brain, lungs, kidney, heart, and gastrointestinal tract. [16],[18] It causes severe vasoconstriction followed by vasodilatation of the microvessels. Endothelial gaps due to disintegration of the endothelial cells within intracellular edema, swollen mitochondria, dilated endoplasmic reticulum, and separation of intracellular junction of the endothelial cells. Local loss of basement membrane of the vessels leads to capillary leaking syndrome and a resistant shock [Table 3], [Figure 2], [Figure 3], [Figure 4]. [14],[15],[16],[18]
Table 3: Signs and symptoms of different snakes

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Figure 2: Characteristics of cobra bite (a) severe tissue damage at bite site (b) bilateral ptosis

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Figure 3: Characteristics of Russell's vipers bite (a) oedema with blood oozing from site of bite, (b) wet gangrene, (c) extensive oedema upto the groin, (d) gum bleed

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Figure 4: Characteristics of Echis carinatus bite (a) tense bleb at the site of bite, (b) active gum bleed, (c) active epistaxis

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  Management of Snake Bite Top


First aid (to be given at the time when bite occurs)

  1. If one can locate the bite site, remove the surface deposited venom by clean cloth or cotton.
  2. Keep the bitten part below heart level.
  3. Crepe bandage from the distal end of the bite site with a pressure equal to that one can easily put and remove the finger underneath the bandage.
  4. One should not kill the time in search of the snake. If the snake is found or killed take it to hospital, it may help to doctor for diagnosis.
  5. Victim should not be allowed to walk.
  6. Do not incise at the site of the bite.
  7. If the victim is found unconscious without respiration, the relatives should start mouth to mouth respiration and chest compressions.


First response at the healthcare facility (primary health center, hospital etc.)

  1. History - site of the bite, activity at the time of the bite, time of bite, visualization/recognition of the snake.
  2. Symptoms suggestive of neuromuscular palsy (ptosis, respiratory difficulty, dysphagia, weakness of limbs, etc.) should be specifically asked for.
  3. Initial clinical signs should be noted in detail such as heart rate, blood pressure, respiratory rate, one min counting test, oxygen saturation, bulbar palsy, muscle power, tendon reflexes, pooling of saliva, broken neck sign. These signs to be closely monitored every hour till clinical improvement. Electrocardiogram should be recorded for arrhythmias. Serum electrolytes and renal profile should be done.
  4. Give injection tetanus toxoid to all patients provided blood is clotted in 20WBCT.
  5. Intramuscular injection to be avoided in viper bite envenoming may result in huge hematoma.



  20 Minutes Whole Blood Clotting Time Top


Before the injection of anti-snake-venom (ASV) take 2-3 ml of patients' blood in a new dry glass test tube which is not irrigated by any detergents. Keep the tube undisturbed for 20 minutes and then tip it off, if blood did not clot, it confirms hypofibrinogenemia and that the venom action is persisting. This test should not be repeated before 6 h of the last dose of ASV as liver takes 6 h for regeneration of clotting factors. [34]


  Antisnake-venom Top


In India, we have polyvalent antivenom available which acts against krait, cobra, Russell's viper and Echis. It accelerates the dissociation of the toxin - receptors complexes and reverses the paralysis. On arrival of the patient, 100 ml (10 vials) ASV is added to 200 cc of normal saline and given to the patient over 30-50 min. One should sit by the side of the victim for early diagnosis and treatment of anaphylaxis. Within 30 min after initial dose of ASV if there is no improvement of neurological manifestations one can repeat dose of ASV and no more than total 20 vials of ASV to be administered. ASV neutralizes circulating venom and it has no action once the venom is attached to the receptor site. In krait bite, its venom destroys receptors thus neurological manifestation may persist for 2 to 3 weeks till there is regeneration of receptors. At this stage, administration of ASV is merely a waste. No amount of antivenom is going to reverse the ptosis or neuroparalysis till regeneration of receptors.

Antivenom should be administered as soon as signs of systemic or severe local swelling are noted. The mean times between envenoming and death are 8 h (12 min to 120 h) in cobra, 18 h (3-63 h) in Bungarus caeruleus, 3 days (15 min to 264 h) in Russell's viper and 5 days (25-41 days) for Echis cariniatus. The approximate serum half-life of antivenom in envenomed victims ranges from 26 to 95 h. Before discharge, envenomed victims should be closely observed daily for minimum 3-4 days. [6],[9]


  Antivenom Reaction and its Management Top


No skin test should be performed before giving ASV as it does not give any surety regarding reaction. It is merely killing vital time. Antivenom should not be given intramuscularly. It should be administered by a qualified person who has knowledge of the anaphylaxis reaction and its management. However, snake catchers or trekkers should take with them few ampoules of ASV in case of an accident, so as to make is readily available to a doctor. [4]

Reaction of ASV can develop within 10-180 min. The incidence is increased with dose of antivenom and speed of administered. Bolus dose may give rapid reaction. A turbid solution of ASV may precipitate severe reaction and hence should be thrown away

Earliest symptoms are hotness in ears, scalp, itching over scalp, urticaria, sudden onset of intractable cough, nausea, vomiting, goose skin, giddiness often complained of uneasiness, suffocation, and irrelevant behavior. Febrile reactions due to contamination of ASV with endotoxin like compounds may cause fever, rigors, vasodilatation, and hypotension which can occur within 1-2 h of treatment. Children get febrile convulsions.

Systemic anaphylaxis

Sudden onset of projectile profound vomiting, sphincter relaxation, hypotension, bronchospasm, foreign body sensation in throat and angioedema. These reactions are due to complement activation by immune complexes or aggregates of immune globulin.

Delayed reaction serum sickness can develop between 5 and 24 days of ASV therapy. Incidence of this depends upon the dose of ASV but is rare. This delayed reaction is clinically characterized by pyrexia of unknown origin, itching, arthralgia, lymphadenopathy, joint swellings, mononeuritis multiplex, albuminuria, and rarely encephalopathy. Low dose of adrenaline, promethazine, and hydrocortisone can be used as prophylaxis against anaphylaxis reaction. [35]


  Management of Reaction Top


In case of reaction, injection adrenalin 0.5 ml of 0.1% to be administered by intramuscular route on the lateral aspect of the thigh. Dose can be repeated if not controlled. In a situation where life is at stake, that is, severe hypotension, bronchospasm, laryngeal edema adrenalin to be given in the dose of 1000 μg (1 ml) diluted in 9 cc of normal saline. A total of 10 cc of this solution can be given 1 ml intravenously every 3-5 min till reaction is reduced. In addition to this, intravenous aminophylline, head low position, intravenous normal saline, H1 blocker, chlorpheniramine maleate, intravenous methyl prednisolone, nasal oxygen may be helpful. Sometimes, patient may require endotracheal intubation and ventilation. Irrespective of due care and when reaction is over; during re-administration of ASV, the patient can develop re-reaction. In such situation, one can select ASV from another batch and try. Patient should not die of reaction and so also not due to snake bite envenoming. One should not be afraid of administration of ASV in a severe venomous bite provided one is fully prepared to treat any severe reaction. Many victims are referred from PHC to rural or district hospital without giving ASV and succumb on way to the hospital.


  Emergency Management Top


Basic cardiopulmonary resuscitation

All patients found unconscious at home and not breathing should start receiving chest compressions and mouth to mouth respiration en-route to the hospital.

Endotracheal intubation and ventilation

Indicated if victim has pooling of saliva, unable to lift the neck from pillow, muscle power <3/5, reduction in oxygen saturation, signs of respiratory failure like abdominal-thoracic respiration, signs of cerebral hypoxia. At the periphery, one can do endotracheal intubation, or if not possible a laryngeal mask can be put directly over larynx and ambu bag ventilation.


  Management of Specific Snake Bites Top


Cobra bite

Cobra venom is reversibly attached to postsynaptic receptors. Acetylcholinesterase inhibitor (AChEI) like neostigmine 50 μg/kg over 1 st h and then 25 μg/kg next four hours preceded by atropine (to counter the muscarinic action of AChEI). Or alternatively, 0.5 mg neostigmine half hourly proceeded by atropine, may help the majority of victim to recover within 24 h. This cycle may not be required more than 5-6 times. [4],[5],[8],[9],[19],[20],[21],[36] In our experience, a victim diagnosed "dead" by the peripheral doctor only by absence of respiration and nonreacting pupils was recovered with artificial ventilation, cardiopulmonary resuscitation, and AChEI. [4],[37] Local wound care is done by intravenous antibiotic, daily dressing and may require plastic surgery. One should always rule out diabetes mellitus in a non-healing wound in any snake bite.

Krait bite

Indian common krait venom contains both pre and postsynaptic blocker. Whether the victim will respond to AChEI or not can be tested by putting an ice-filled glove finger over eyelid. Hypothermia sensitizes the Ach receptors. [38] If there is a slight improvement in ptosis, one can try AChEI. [39],[40],[41],[42] Recently, we found envenoming by kokan krait (light coppery color) respond to AChEI. [4]

Sea snakes

Patient may require a ventilator for respiratory failure. Electrolyte imbalance especially hyperkalemia needs to be corrected (diuretic, glucose-insulin, salbutamol inhalation, calcium gluconate). In case of resistant hyperkalemia, one can try potassium channel drug oral glibenclamide provided one takes care of hypoglycemia.

Russell's viper or Daboia or viper Russell siamensis

One of the most common and dreaded complication of Russell's vipers bite is DIC, which can be diagnosed by thrombocytopenia, abnormal crenated RBCs in peripheral blood smear. In addition to ASV, one has to try plasma products and whole blood transfusion which is rare required if ASV is administered in time with an adequate dose. Hypotension can be managed with fluid and inotropic agents. Severe hypotension due to bleeding in adrenal and pituitary glands and abdominal bleed and endothelial dysfunction with capillary leak may need heavy doses of intravenous methylprednisolone. [4],[6],[7] One should keep in mind and look for renal failure from time of admission. Risk factors such as hypotension, hypovolemia should be corrected. There are lot of controversies regarding early introduction of diuretic, acetylcysteine or allopurinol in renal failure. However, in our experience, intravenous frusemide 80-100 mg and oral acetylcysteine 600 mg 3 times a day may help to arrest the renal damage, but this needs a randomized controlled trial. In a situation of renal failure with raised serum potassium, it may be treated with frusemide drip at rural areas or peritoneal dialysis or referred to higher center for hemodialysis. [4],[18] Irrespective of the standard dose of ASV many victims develop renal failure. This is particularly reported from Marathwada region. Thus venom procured from this region should be used to prepare antivenom against Russell' s viper which kills many farmers, sugarcane labors and deserts many families.

Local wound care is most important to avoid disability. Once the clotting mechanism is reversing (20 min whole blood clotting time), the edematous limb can be elevated with rest on the pillow below the knee. Glycerin Magsulf dressing, aspiration of tense blebs by sterile needle and syringe, debridement of dead tissues, intravenous antibiotics and avoiding surgical decompression unless absolute essential remain the mainstay of treatment here.

Echis cariniatus or saw-scaled viper or carpet viper

Due to the possibility of renal failure and bleeding due to this snake envenomation more ASV is required in states of Jammu and Pondicherry (ASV >100 ml) to correct bleeding disorder as compared to Maharashtra (ASV approx 30-50 ml). [43] This snake runs rapidly in a grown up grass hence victim may feel injury by thorn prick and failure of administration of ASV on wrong history result in many amputation of limb,..Thus a farmer or labourer with rapid development of swelling within one hour while walking bare feet in grown of grass or bund, attributed to a thorn, is often a case of Echis bite envenoming.

Green pit viper and bamboo pit (Trimeresurus)

The polyvalent ASV available in India does not cover for envenomation with these two vipers. However, empirical treatment with polyvalent venom should be offered as paraspecificity may sometimes help to alleviate the envenoming. [44]

When there is doubt regarding species of snake in such situation, one can manage the case on syndromic approach. [45]


  Conclusion Top


Scientists should make attempts to prepare venomous toxoid to immunize the farmers and risky population against venomous snake toxins. Toxicologists should make an attempt to prepare the pharmacological antidote to venom actions. Antivenom producers in India should prepare ELISA kit for detection of venom antigen in blood and prepare antivenom from venoms obtained from snakes caught from relevant areas of the country. The attending doctor gets immense satisfaction when the serious poor victim of snake bite recovers.

 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]


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Abstract
Introduction
Snakes
Biochemistry, Ph...
Management of Sn...
20 Minutes Whole...
Antisnake-venom
Antivenom Reacti...
Management of Re...
Emergency Management
Management of Sp...
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