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Snake bite is one of the major public health problems in the tropics. It is also emerging as an occupational disease of agricultural workers. In view of their strong beliefs and many associated myths, people resort to magico –religious treatment for snake bite thus, causing delay in seeking proper treatment.

Snake bites is a particularly important public health problem in rural areas of tropical and subtropical countries situated in Africa, Asia, Oceania and Latin America.

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  3. 3. INTRODUCTION • . Snake bite is one of the major public health problems in the tropics. It is also emerging as an occupational disease of agricultural workers. In view of their strong beliefs and many associated myths, people resort to magico –religious treatment for snake bite thus, causing delay in seeking proper treatment. • Snake bites is a particularly important public health problem in rural areas of tropical and subtropical countries situated in Africa, Asia, Oceania and Latin America.
  4. 4. INTRODUCTION The venom apparatus Venomous snakes of medical importance have a pair of enlarged teeth, the fangs, at the front of their upper jaw. These fangs contain a venom channel or groove, along which venom can be introduced deep into the tissues of their natural prey. If a human is bitten, venom is usually injected subcutaneously or intramuscularly.
  5. 5. epidemiology • The annual number of cases of snakebite worldwide is about 5 million, among which there are some 100 000 to 200 000 deaths. • In addition to the deaths, there are an estimated 400000 snakebite- related amputations each year around the world . • Children have both higher incidence rates and suffer more severe effects than do adults, as a result of their smaller body mass •
  6. 6. SNAKE BITE INCIDENCES • Papua New Guinea has some of the highest snakebite rates in the world, with the country’s rural central province recording an annual incidence of 561.9 cases per 100 000 population • Snakebites are concentrated in mainly rural areas and vary considerably by season, with the peak incidence seen in the rainy and harvesting seasons
  7. 7. Snake bite deaths worldwide
  8. 8. india • India is estimated to have the highest snakebite mortality in the world. • World Health Organization (WHO) estimates place the number of bites to be 83,000 per annum with 11,000 deaths • Males: Female::2:1. • Majority of the bites being on the lower extremities.
  9. 9. SNAKES IN INDIA • There are about 236 species of snakes in India, most of which are nonvenomous • Their bites, apart from causing panic reaction and local injury, do not harm the patient. • 13 known species that are venomous and of these four, namely common cobra (Naja naja), Russell’s viper (Dabiola russelii), saw-scaled viper (Echis carinatus) and common krait (Bungarus caeruleus) are highly venomous and believed to be responsible for most of the poisonous bites in India
  10. 10. COMMONEST INDIAN venomous snakes – The venom is synthesized by the modified salivary glands and injected through special channeled or grooved teeth called fangs Cobra Krait Russel’s viper Saw-scaled viper
  11. 11. CLASSIFICATION • Worldwide, only about 15% of the more than 3000 species of snakes are considered dangerous to humans. • The family Viperidae is the largest family of venomous snakes, and members of this family can be found in Africa, Europe, Asia, and the Americas. • The family Elapidae is the next largest family of venomous snakes.
  12. 12. ELAPIDAE • Elapidae have short permanently erect fangs This family includes the cobras, king cobra, kraits, coral snakes and the sea snakes. • The most important species, from a medical point of view include the following: • Cobras: Genus Naja N naja(spectaled cobra –all over in India ) N kaouthia (monocled – West Bengal ,MP ,U.P, Orissa) N oxiana [Black cobra – northern states - patternless] N philippinensis N atra King cobra: Ophiophagus hannah
  13. 13. Short permanently erect fangs of a typical elapid
  14. 14. KRAITS (genus Bungarus) KRAITS (genus Bungarus) • B caeruleus common krait [all over India ] - paired white bands & large hexagonal scales in top of the snakes • B fasciatus banded krait [black & yellow band – W.B,M.P,A.P,BIHAR ,ORRISSA] • B candidus Malayan krait • B multicinctus Chinese krait • Sea snakes (important genera include Enhydrina, Lapemis and Hydrophis) • Blue spotted sea snake (Hydrophis cyanocinctus)
  15. 15. Common krait- key identification feature is PAIRED white bands.
  16. 16. VIPERIDAE Have long fangs which are Normally folded up against the upper jaw but,when the snake strikes, are erected . There are two subgroups, • the typical vipers (Viperinae) • and the pit vipers (Crotalinae). • The Crotalinae have a special sense organ, the pit organ, to detect their warm-blooded prey. This is situated between the nostril and the eye
  17. 17. Russell’s vipers details of fangs.
  18. 18. RUSSELL’S VIPER .Hemotoxic venom BUT can also Present neurotoxic symptoms Key identification feature is the black edged almond or chain shaped marks on the back
  19. 19. Key Identification Feature- large plate scales on the head PIT VIPER Haemotoxic venom. Causes Renal failure Late onset envenoming
  20. 20. •Saw-scaled or carpet vipers - Echis carinatus and E sochureki Most parts of India except Kerala – Arrow shaped mark in head & hoop like markings in flanks
  21. 21. India: Poisonous snakes Elapidae Cobra, Kraits Neurotoxic Viperidae (Vipers) Russell’s Vipers., Saw scaled Vipers., Pit Vipers. Hemotoxic Hydrophidae Sea Snakes Myotoxic Krait and russell’s viper is much more toxic than that of cobra
  24. 24. Snake Venom Complex mixture of proteins including Large enzymes-local tissue destruction. Low molecular weight polypeptides-lethal systemic effects -Acidic. -Sp Gravity: 1.030-1.070 -On drying Fine needle like crystals. -Water Soluble. -Lethal Dose: Cobra-0.12gm, Krait0.06gm- Russell’s V-0.15gm
  25. 25. Healthy, angered and hungry snakes unload more venom than a recently satiated and surprised snake . Due to the venom, there is cell function degeneration and the final outcome depends on the type of venom injected. Snake bite-venom injected enters surrounding tissue direct venom action blood vessels lymphatics Target organs-systemic effect Capillary absorption
  26. 26. PATHOGENESIS • Snake venom is a mixture of polypeptides, proteolytic enzymes, and toxins, which are species- specific. Primarily neurotoxic • Hydrophidae - poisonous sea snakes’ • Elapidae - cobras, kraits, coral snakes • Venom have a curare-like effect by blocking neurotransmission at neuromuscular junction. • Death results from respiratory depression.
  27. 27. Neurotoxic venom • Venoms with neurotoxic activity produce paralysis and respiratory distress by binding the nicotinic acetylcholine receptors, and preventing the depolarizing action of acetylcholine. • The most important effect of neurotoxins is to prevent the transmission of nerve impulses in cholinergic synapses. ALFA neurotoxins interfere with neurotransmitter release and cause muscle paralysis, respiratory failure and death by asphyxiation.
  28. 28. PATHOGENESIS • Viperidae – vipers Primarily hemotoxic& cytotoxic • Crotalidae (sub family of viperidae) : • Tissue necrosis, vascular leak, and coagulopathies. • Death from pit viper bites results from hemorrhagic shock, adult respiratory distress syndrome, and renal failure.
  29. 29. • A hemotoxic venom that acts by lysing erythrocytes. Venoms of this kind have a proteolytic action. They produce swelling, cardiovascular damage, and eventual necrosis. They also disrupt blood clotting and, in the process of destroying the blood's functionality, severely damage internal organs and other body tissues, which can be extremely painful. The immediate cause of death in such cases is usually hypovolemic shock. envenomation increases capillary permeability that results in • blood and plasma loss from the intravascular to the extracellular space, creating edema, which, in case of being sufficiently important, may cause circulatory compromise and hypovolemic shock. HEMOTOXIC VENOM
  30. 30. Cytotoxic venom • snake venom has cytolytic properties, which cause local necrosis and secondary infection, which could result in sepsis and death
  31. 31. CLINICAL FEATURES. When venom has not been injected; • Out of fear Vasovagal attack Collapse Slowing of heart rate • Another source of misleading symptoms caused by First aid and traditional treatments.
  32. 32. CLINICAL FEATURES • Following the immediate pain of the bite-increasing local pain (burning, bursting, throbbing) at the site of the bite • Local swelling that gradually extends proximatelly up the bitten limb and tender, painful enlargement of the regional lymph nodes draining the site of the bite • Bites by kraits, sea snakes may be virtually painless and may cause negligible local swelling. Someone who is sleeping may not even wake up when bitten by a krait and there may be no detectable fang marks or signs of local envenoming
  33. 33. Local symptoms and signs in the bitten part • Fang marks • ™Local pain • ™Local bleeding • ™Bruising • ™Lymphangitis • ™Lymph node enlargement • ™Inflammation (swelling, redness, heat) • ™Blistering • ™Local infection, abscess formation • ™Necrosis
  34. 34. Fang marks Persistent bleeding from fang marks 40min after bite of pit viper Blistering at site of bite
  35. 35. SYSTEMIC SYMPTOMS & SIGNS Generalised (systemic) symptoms and signs • Nausea, vomiting, malaise, abdominal pain, weakness, drowsiness, prostration Cardiovascular (Viperidae) • Dizziness, faintness, collapse, shock, hypotension, cardiac arrhythmias, pulmonary oedema, cardiac arrest
  36. 36. Cont. Bleeding and clotting disorders (viperidae) • Bleeding from recent wounds (including fang marks,venepunctures etc) and from old partly-healed wounds. • Spontaneous systemic bleeding – from gums, epistaxis, bleeding into the tears, haemoptysis, haematemesis, rectal bleeding or melaena, haematuria, vaginal bleeding, bleeding into the skin (petechiae, purpura, ecchymoses) and mucosae
  37. 37. Cont. Neurological(Elapidae, Russells’s viper) • Drowsiness, paraesthesiae, abnormalities of taste and smell, “heavy” eyelids, ptosis, external ophthalmoplegia, paralysis of facial muscles ,difficulty in opening mouth and showing tongue and weakness of other muscles innervated by the cranial nerves, aphonia, difficullty in swallowing secretions, respiratory and generalised flaccid paralysis
  38. 38. Cont. Skeletal muscle breakdown(sea snakes, Russell’s viper) • Generalised pain, stiffness and tenderness of muscles, trismus, myoglobinuria hyperkalaemia, cardiac arrest Renal(Viperidae, sea snakes) • Loin (lower back) pain, haematuria, haemoglobinuria, myoglobinuria, oliguria/anuria, symptoms and signs of uraemia (acidotic breathing, hiccups, nausea, pleuritic chest pain etc
  39. 39. Broken neck sign in a child envenomed by krait Bleeding from gingival sulci
  40. 40. Species: Signs and Symptoms Signs/Symptoms and Potential Treatments Cobra Krait Russell’s Viper Saw Scaled Viper Other Vipers Local pain/ Tissue Damage Yes No Yes Yes Yes Ptosis/Neurotoxicity Yes Yes Yes! NO No Coagulation No No Yes Yes Yes Renal Problems No No Yes NO Yes Neostigmine & Atropine Yes No? No? NO No
  41. 41. •National snakebite management protocol, India.
  42. 42. FIRST AID • The first aid recommended is based around the mnemonic: • "Do it R.I.G.H.T." • It consists of: • R. = Reassure the patient. Seventy per cent of all snakebites are from non venomous species. Only 50% of bites by venomous species actually enveno-mate the patient • I = Immobilize in the same way as a fractured limb. Children can be carried. Use bandages or cloth to hold the splints, not to block the blood supply or apply pressure. Do not apply any compression in the form of tight ligatures, they do not work and can be dangerous! • G.H. = Get to Hospital immediately. Traditional remedies have NO PROVEN benefit in treating snakebite. • T = Tell the doctor of any systemic symptoms such as ptosis that manifest on the way to hospital. •
  43. 43. PRESSURE IMMOBILISATION Its purpose is to retard the movement of venom from bite site into circulation, thus buying time for the patient to reach medical care.
  44. 44. Cont. • Be prepared to treat the shock and provide cardiopulmonary resuscitation (CPR). • Get the victim to the nearest secondary or tertiary care hospital where antivenom can be provided
  45. 45. DO NOTS IN FIRST AID • Do not apply a tourniquet. • Do not wash the bite site with soap or any other solution to remove the venom. • Do not make cuts or incisions on or near the bitten area. • Do not use electrical shock. • Do not freeze or apply extreme cold to the area of bite. • Do not apply any kind of potentially harmful herbal or folk remedy. • .
  46. 46. Cont. • Do not attempt to suck out venom with your mouth. • Do not give the victim drink, alcohol or other drugs. • Do not attempt to capture, handle or kill the snake and patients should not be taken to quacks.
  47. 47. SNAKE BITE TREATMENT PROTOCOL • The initial management includes dealing with airway, breathing and treatment of shock. • Administer tetanus toxoid
  48. 48. Emergency care Try to identify the snake responsible. • Snake colouration, its pupil shape and bitemarks • Ask the victim relatives to carefully bring the snake to hospital if it has been killed and then use the snake identification material in protocol to identify it. • Determine if any traditional medicines have been used as they can sometimes lead to confusing symptoms. • Determine the exact time of bite which helps in determining progression of signs and symptom.
  49. 49. Cont. • Iv access established in unaffected extremity • CBC, coagulation profile, fibrinogen concentration, should be assessed. • Tourniquets placed in field should be carefully removed. • The bitten extremity should be marked at 2 or more sites proximal to the bite and the circumference at these locations should be assessed every 15min to monitor for progressive edema-indicative of ongoing venom effects.
  50. 50. Cont. • All the patients should be kept under observation for a minimum of 24 hours. • Many species, particularly the Krait and the hump-nosed pit viper are known for delayed appearance of symptoms which can develop after 6–12 hours
  51. 51. Investigations • Twenty-minute whole blood clotting test (20WBCT) reliable test of coagulation which can be carried out by bedside and is considered to be superior to ‘capillary tube’ method for establishing clotting capability in snake bite. • A few milliliters of fresh venous blood should be placed in a fresh, clean and dry glass vessel preferably test tube and left undisturbed at ambient temperature for 20 minutes. • After that tube should be gently tilted to detect whether blood is still liquid and if so then blood is incoagulable.The test should be carried out every 30 minutes from admission for 3 hours and then hourly after that.
  52. 52. Other Useful Tests (If Facilities Available • Hb/platelet count/peripheral smear prothrombin time (PT)/activated partialthromboplastin time • • Urine examination for proteinuria/RBC/hemoglobinuria • Myoglobinuria • Biochemistry for serum creatinine/Urea/Potassium • • ECG/X-ray/CT/Ultrasound(The use of X-ray and ultrasound, area of unproven benefit, apart from identification of clot in viperine bite) • Oxygen saturation/arterial blood gas (ABG) • • Enzyme-linked immunosorbent assay (ELISA) to confirm snakespecies.
  53. 53. Treatment Phase • Pain can be relieved with oral paracetamol or tramadol. • Aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) should not be administered
  54. 54. Severity of envenomation.
  55. 55. Anti-snake venom (ASV) • Anti-snake venom (ASV)is the mainstay of treatment. Antivenom is immunoglobulin [usually pepsin-refined F(ab’)2 fragment of whole IgG] purified from the plasma of a horse, mule or donkey (equine) or sheep (ovine) that has been immunized with the venoms of one or more species of snake. • In India, polyvalent ASV, i.e. effective against all the four common species; Russell’s viper, common cobra, common Krait and saw-scaled Viper and no monovalent ASVs are available
  56. 56. • ASV is produced both in Liquid and Lyophilized forms. • There is no evidence to suggest which form is more effective. • Liquid ASV requires a reliable cold chain and has 2-year shelf life. • Lyophilized ASV in powder form,has 5-year shelf life and requires only to be kept cool. • Only free unbound fraction of venom can be neutralized by anti snake venom.
  57. 57. Antivenom treatment should be given as soon as it is indicated. It may reverse systemic envenoming even when this has persisted for several days or, in the case of haemostatic abnormalities, for two or more weeks. It is,therefore, appropriate to give antivenom for as long as evidence of the coagulopathy persists. HOW LONG ASV CAN BE GIVEN?
  58. 58. ROUTE? Freeze-dried (lyophilized) antivenoms are reconstituted, usually with 10ml of sterile water for injection per ampoule. Two methods of administration are recommended: (1) Intravenous “push” injection: Reconstituted freeze-dried antivenom is given by slow intravenous injection(not more than 2 ml/minute). (2) Intravenous infusion: Reconstituted freeze-dried antivenom is diluted in approximately 5-10 ml of isotonic fluid per kg body weight) and is infused at a constant rate over a period of about one hour Patients must be closely observed for at least one hour after starting intravenous antivenom administration, so that early anaphylactic antivenom reactions can be detected and treated early with epinephrine(adrenaline)
  59. 59. Cont. • Local administration of ASV is not recommended as it is extremely painful and can raise the intracompartmental pressure. • Intramuscular inj are not recommended .Antivenoms are large molecules (F(ab’)2 fragments or sometimes whole IgG) which, after intramuscular injection, are absorbed slowly via lymphatics. Bioavailability is poor, especially after intragluteal injection, and blood levels of antivenom never reach those achieved rapidly by intravenous administration. Other disadvantages are the pain of injection of large volumes of antivenom and the risk of haematoma formation
  60. 60. Anti-snake Venom Administration INDICATIONS Evidence of systemic toxicity. Hemodynamic or respiratory instability  Hypotension, respiratory distress Hemotoxicity  Clinically significant bleeding or abnormal coagulation studies Neurotoxicity  Any evidence of toxicity usually beginning with CN abnormalities and progressing to descending paralysis including diaphragm Evidence of local toxicity  Progressive soft tissue swelling
  61. 61. TEST DOSE • Anti-snake Venom Test Dose • Test doses have not been shown to have predictive value in predicting anaphylactic reaction or late serum sickness and not recommended • .
  62. 62. INTIAL DOSE. The recommended dose is often the amount of antivenom required to neutralize the average venom yield when captive snakes are milked of their venom. In practice, the choice of an initial dose of antivenom is usually empirical. • Each vial is 10 ml of reconstituted ASV Initial dose is 8-10 vials for both adults and children. • Common krait- 100ml ASV • Russell’s viper-100ml • Saw scaled viper-50 ml • Indian cobra-100ml
  63. 63. Response to intial dose of ASV : If an adequate dose of appropriate antivenom has been administered, the following responses may be observed. (a) General: The patient feels better. Nausea, headache and generalised aches and pains may disappear very quickly. . (b) Spontaneous systemic bleeding (e.g. from the gums): This usually stops within 15-30 minutes. (c) Blood coagulability (as measured by 20WBCT): This is usually restored in 3-9 hours. (d) In shocked patients: Blood pressure may increase within the first 30-60 minutes and arrhythmias such as sinus bradycardia may resolve. (e) Neurotoxic envenoming (cobra bites) may begin to improve as early as 30 minutes after antivenom, but usually takes several hours. (f) Active haemolysis may cease within a few hours and the urine returns to its normal colour
  64. 64. REPEAT DOSES Criteria for giving more antivenom • Persistence or recurrence of blood incoagulability after 6 hours(measured by 20WBCT) or of bleeding after 1-2 hours. • Deteriorating neurotoxic or cardiovascular signs after 1-2 hours of administering intial dose of ASV Range of venom injected is about 5mg-147mg Maximum dose of ASV is around 25 vials. ASV should be administered over a period of 1hour.
  65. 65. In hemotoxic envenomation; • Once initial dose has been administered over one hour, no further ASV is given for 6 hours. • Twenty WBCT test every 6 hours will determine if additional ASV is required. If the blood remains incoagulable (as measured by 20WBCT) six hours after the initial dose of antivenom, the same dose should be repeated. This is based on the observation that, if a large dose of antivenom (more than enough to neutralize the venom procoagulant enzymes) is given initially, the time taken for the liver to restore coagulable levels of fibrinogen and other clotting factors is 3-9 hours • This reflects the period the liver requires to restore clotting factors.
  66. 66. In Neurotoxic envenomation • Antivenom treatment alone cannot be relied upon to save the life of a patient with bulbar and respiratory paralysis • Death may result from aspiration, airway obstruction or respiratory failure.A clear airway must be maintained. Once there is loss of gag reflex and pooling of secretions in the pharynx, failure of the cough reflex or respiratory distress,a cuffed endotracheal tube or laryngeal mask airway should be inserted
  67. 67. Neostigmine test. • A trial of anticholinesterase (eg “Tensilon test”) should be performed in every patient with neurotoxic envenoming • Atropine sulphate (0.6 mg for adults; 50 μg/kg for children) or glycopyrronium is given by intravenous injection followed by neostigmine bromide . in appropriate doses) by intramuscular injection 0.02 mg/kg for adults, 0.04 mg/kg for Children. • The patient is observed over the next 30-60 minutes (neostigmine) or 10-20 minutes (edrophonium) for signs of improved neuromuscular transmission. Ptosis may disappear and ventilatory capacity (peak flow, FEV-1 or maximum expiratory pressure) may improve. • If positive institute regular atropine & neostigmine.
  68. 68. Treatment of hypotension and shock Snake bite causes of hypotension and shock. • Anaphylaxis • Vasodilatation • Cardiotoxicity • Hypovolaemia • Antivenom reaction • Respiratory failure • Acute pituitary adrenal insufficiency • Septicaemia Treatment- a selective vasoconstrictor such as dopamine may be given by intravenous infusion, preferably into a central vein (startingdose 2.5-5mcg/kg/minute).
  69. 69. • Adverse reactions to anti-snake venom • Fear of potentially life threatening adverse reactions causes reluctance amongst some to treat snakebite. • However, if handled early and with the primary drug of choice, these reactions are easily managed. • Patients should be monitored closely as there is evidence that many anaphylactoid reactions go unnoticed
  70. 70. Adverse reactions to anti-snake venom At the first sign of any of the following: Urticaria, itching, fever, shaking chills, nausea, vomiting, diarrhea, abdominal cramps, tachycardia, hypotension, bronchospasm and angio-oedema: 1. ASV should be discontinued 2. 0.5 mg. of 1:1000 adrenaline should be given IM The pediatric dose is 0.01 mg/kg body weight of adrenaline IM. Evidence shows that adrenaline reaches necessary blood plasma levels in 8 minutes via the IM route, but up to 34 minutes in the subcutaneous route.
  71. 71. Adverse reactions to anti-snake venom 100 mg of hydrocortisone and 10 mg of H1 antihistamine will be administered IV. The dose for children is 0.2 mg/kg of antihistamine IV and 2 mg/kg . If after 10 to 15 minutes the patient’s condition has not improved or is worsening, 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 reactions, 2 doses of adrenaline will be sufficient.
  72. 72. Once the patient has recoverd ASV can be restarted Given slowly for 10-15 minutes (underclose monitoring) Then the normal drip rate should be resumed ASV test doses have been abandoned: Have no predictive value in anaphylactoid or late serum reactions. May pre-sensitise the patient to the protein.
  73. 73. FOLLOW-UP • After discharge from hospital, victim should be followed. • If discharged within 24 hours, patient should be advised to return if there is any worsening of symptoms such as bleeding, pain or swelling at the site of bite, difficulty in breathing, altered sensorium, etc. • The patients should also be explained about serum sickness which may manifest after 5–10 days
  74. 74. SUMMARY • Snake bites is a particularly important public health problem in rural areas of tropical and subtropical countries situated in Africa, Asia, Oceania and Latin America • The annual number of cases of snakebite worldwide is about 5 million, among which there are some 100 000 to 200 000 deaths. • common cobra (Naja naja), Russell’s viper (Dabiola russelii), saw-scaled viper (Echis carinatus) and common krait (Bungarus caeruleus) are highly venomous and believed to be responsible for most of the poisonous bites in India.
  75. 75. REFERENCES • WHO Fact Sheet On Snake Bite .Geneva.WHO.last accessed on 19th january 2015. • National snakebite management protocol, India. (2008). [online] Avaialable at www:// (Directorate General of Healthand Family Welfare, Ministry of Health and Family Welfare, India). • Simpson ID. Snakebite Management in India, the first few hours: A guide forprimary care physicians.J Indian Med Assoc. 2007;105:324-35. • .Snake Bite Guidelines INDIAN PEDIATRICS, VOLUME 44 -MARCH 17, 2007. • NELSON TEXTBOOK OF PEDIATRICS
  76. 76. THANK YOU