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"Snake Bite Management in Indian Context" by Dr Subhash Ranjan NM,VSM

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I have summed up this presentation with practical point of view. I have shot myself majority of the snakes and feel they should be understood by the community. Some of them are venomous (not …

I have summed up this presentation with practical point of view. I have shot myself majority of the snakes and feel they should be understood by the community. Some of them are venomous (not poisonous)! The management is syndromic approach and I feel this ppt would be beneficial to medical students.

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  • Nerve cells in the pit organ contain an ion channel called TRPA1 — an infrared receptor transient receptor potential family of protein ; that detects infrared radiation as heat, rather than as light, thus confirming theories of pit-organ function long held by behavioural ecologists. The receptors are also found inside the heads of mammals, where TRPA1 channels, also known as wasabi receptors, detect pungent irritants from mustard plants or other sources. The pit organ is part of the snake's somatosensory system — which detects touch, temperature and pain — and does not receive signals from the eyes, confirming that snakes 'see' infrared by detecting heat, not photons of light. Infrared radiation heats up the pit membrane tissue, and TRPA1 channels open when a threshold temperature is reached, allowing ions to flow into the nerve cells and triggering an electrical signal.
  • Refer http://emedicine.medscape.com/article/771804-treatment Figure 1, Apply a broad-pressure bandage over the bite site as soon as possible. Do not take off jeans because the movement of doing so assists venom to enter the bloodstream. Keep the bitten leg still. Figure 2, The bandage should be as tight as would be applied to a sprained ankle. Figure 3, Extend the bandage as high as possible. Figure 4, Apply a splint to the leg. Figure 5, Bind the splint firmly to as much of the leg as possible. If the bandages and splint are applied correctly, they will be comfortable and may be left on for several hours. They should not be taken off until the patient has reached medical care. The doctor will decide when to remove the bandages. If venom has been injected, it will move into the bloodstream quickly once the bandages are removed. The doctor should leave the bandages and splint in position until he or she has assembled appropriate antivenom and drugs that may need to be used when the dressings and splint are removed. Figure 6, For bites on a hand or forearm, bind to the elbow with bandages, use a splint to the elbow, and use a sling.
  • Transcript

    • 1. SNAKE BITE PROF. SUBHASH RANJAN
    • 2. INTRODUCTION India estimates approx 2,00,000 bites and 35- 50,000 snake bite deaths/year No reliable national statistics are available. Males bitten almost twice as often as females Majority of the bites being on the lower extremities. 50% of bites by venomous snakes are dry bites, result in negligible envenomation.
    • 3. What are Indian FAB FOUR?
    • 4. FAB FOUR In India, >200 species of snakes; only 52 are poisonous. Saw-scaled viper (Echis carinatus) Majority of bites 70-80% Hemotoxin / Vasculotoxin Russell’s viper (Daboia russelii) Common krait (Bungarus caeruleus) Neurotoxic 20-30% Indian cobra (Naja naja) 1 2 3 4
    • 5. COMMON INDIAN SNAKES
    • 6. COBRA (Naja naja)
    • 7. King Cobra (Ophiophagus hannah)
    • 8. Saw-scaled Viper(Echis carinatus)
    • 9. Green Vine Snake (Ahaetulla nasuta)MildVenomous;ASV notrequired
    • 10. Indian Russells Viper
    • 11. Russell’s Viper
    • 12. Green Pit ViperInfrared Vision TRPA1/Wasabi Receptor
    • 13. Indian Green Pit Viper
    • 14. Asian Sand Viper(Eristicophis macmahonii)
    • 15. Hump Nosed Viper
    • 16. Hump Nosed Viper
    • 17. Common Indian Krait(Bungar us caer uleus )
    • 18. Common Indian Krait(Bungar us caer uleus )
    • 19. The Greater Black Krait (Bungarus niger)
    • 20. T he Greater Black Krait(Bungar us niger)
    • 21. MildVenomous;ASV not Indian Cat Snakerequired
    • 22. MildVenomous;ASV not Wolf Snakerequired
    • 23. Sea Snake
    • 24. Trinket SnakeMildVenomous; ( ElapheASV notrequired helena monticollaris)
    • 25. MildVenomous;ASV not Montane Trinketrequired
    • 26. Non Venomous; Indian Rat SnakeASV not required
    • 27. Indian Rock Python
    • 28. Varie gated KukriNon Venomous;ASV not required (Oligodon taeniolatus)
    • 29. Non Venomous;ASV not required KEELBACK http://animalrescuesquadgoa.com/Non%20venemous.html
    • 30. FACTS Snake biteMajority (80%) is by non-venomous snakes Venomous snakes About 50% of bites are dry
    • 31. Is there any medicalimplication for snake identification?
    • 32. Species: Medical ImplicationsSigns/Symptoms Russell’s Cobra Krait Saw Scaled Otherand Potential Viper Viper VipersTreatments Local pain/ Tissue Damage Yes No Yes Yes YesPtosis/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
    • 33. What is syndromic approach & its significance in Indian scenario? Desired when snake is unidentified
    • 34. SYNDROMIC APPROACHSyndrome 1Local envenoming (swelling etc) with bleeding/clottingdisturbances = Viperidae (all species)Syndrome 2Local envenoming (swelling etc) with bleeding/clottingdisturbances, shock or renal failure = Russell’s viper (andpossibly saw-scaled viper – Echis species)With conjunctival oedema (chemosis) and acutepituitary insufficiency = Russell’s viperWith ptosis, external ophthalmoplegia, facial paralysis etcand dark brown urine = Russell’s viper
    • 35. SYNDROMIC APPROACHSyndrome 3Local envenoming (swelling etc) with paralysis = cobra orking cobraSyndrome 4 : Paralysis with minimal or no localenvenomingBite on land while sleeping= kraitBite in the sea = sea snakeSyndrome 5 : Paralysis with dark brown urine and renalfailure:-Bite on land (with bleeding/clotting disturbance) =Russell’s viperBite in the sea (no bleeding/clotting disturbances) = seasnake
    • 36. Composition of Snake Venom Pr ocoa gulant enzymes  Haemol ytic and myol ytic ( Viperidae) Russell’s viper phospholipases A2 damage cell membranes, Haemor rha gins endothelium, skeletal muscle, nerve and red blood(zinc metalloproteinases) cells. damage the endothelial lining.  Pr e-synaptic neur otoxins (Elapidae and some Cytol ytic or necr otic Viperidae) toxins  Post-synaptic neur otoxins (Elapidae)
    • 37. Snake Bite Toxicity Profile ?
    • 38. NEUROTOXICITY HEMOTOXICITY Starts early- many die before  Starts late hence most of them they reach hospitals reach hospitals Many reverse very well with  Many organ involvement hence ASV if started early MV is mostly supportive to buy Less number of cases time for organs to recover  More number of cases 70-80% Overlap: Neurohemat 20-30%
    • 39. What is the mode ofNeurotoxicity in Krait Bite?
    • 40. Krait- Pre-synaptic action Beta-bungarotoxin- Phospholipases A2 1) Inhibiting the release of Ach from the presynaptic membrane 2) Presynaptic nerve terminals exhibited signs of irreversible physical damage and are devoid of synaptic vesicles 3) ASV & anticholinesterases have no effectParalysis lasts several weeks and frequently requiresprolonged MV. Recovery is dependent upon regenerationof the terminal axon.
    • 41. What is the mode ofNeurotoxicity in Cobra Bite?
    • 42. Cobra – post-synaptic  alpha-neurotoxins “Curare -mimetic toxins’’ Bind specifically to Ach receptors, preventing the interaction between Ach and receptors on postsynaptic membrane. Prevents the opening of the sodium channel associated with the Ach receptor and results in neuromuscular blockade.  ASV -rapid reversal of paralysis.  Dissociation of the toxin-receptor complex, which leads to a reversal of ParalysisAnticholinesterases reverse the neuromuscular blockade
    • 43. Neuroparalytic Manifestations Study PtosisOphthalmoplegia RS r Bulba ss involvement e weakn N Sharma, S Chauhan, S Faruqi, P Bhat, S Varma, Emerg Med J 2005;22:118–120
    • 44. Quick Neurological Examination !
    • 45. Neurotoxic Envenoming-Examination Ask the patient to look up and observe whether the upper lids retract fully. Test eye movements for evidence of early external ophthalmoplegia . Check the size and reaction of the pupils. The muscles flexing the neck may be paralysed, giving the “broken neck sign
    • 46. Bungarus niger envenoming 20 hr post-bite
    • 47. Neurotoxic Envenoming-Examination Krait can cause fixed, dilated non reactive pupils simulating brain stem death – however, it can recover fully Ask the patient to open their mouth wide and protrude their tongue; early restriction often due to paralysis of pterygoid muscles.
    • 48. How to identify for bulbar palsy & early resp failure?
    • 49. Bulbar & Resp Paralysis Can the patient swallow or are secretions accumulating in the pharynx- an early sign of bulbar paralysis. Ask the patient to take deep breaths in and out. “Paradoxical respiration”. Objective measurement of ventilatory capacity is very useful. Use a peak flow metre, spirometer (FEV1 and FVC) Ask the patient to blow into the tube of a sphygmomanometer to record the maximum expiratory pressure (mmHg).
    • 50. Paradoxical Respiration This is an abnormal pattern of breathing in which the abdominal wall is sucked in during inspiration (it is usually pushed out). Paradoxical respiration is due to paralysis of the diaphragm.
    • 51. Hematological Side EffectsVenom induces bleedingVenom induces clottingVenom induces haemolysisHaemorrhagin – causes direct endothelial damage byloosening the gap between endothelial cellsProcoagulant factorsAnticoagulant factorsFibrinonolytic factors
    • 52. Snake Venom and the Coagulation CascadeRVV – Russel’s ViperVenom ECV – Echis carinatus Venom
    • 53. PTT
    • 54. PT
    • 55. 20 min W hole Blood Clotting Test (20-WBCT) Place a few ml of freshly sampled venous blood in a small glass vessel Leave undisturbed for 20 minutes at ambient temp & tip the vessel once If the blood is still unclotted and runs out, the patient has hypofibrinogenaemia/DIC In the SE Asia, incoagulable blood is diagnostic of a viper bite and rules out an elapid bite
    • 56. Local Symptoms & 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
    • 57. Russell’s ViperBite
    • 58. Venomous Non-venomous
    • 59. LOCAL NECROSIS
    • 60. What are the systemicmanifestations of the envenomation ?
    • 61. Systemic Symptoms & Signs General Nausea, vomiting, malaise, abdominal pain, weakness, drowsiness, prostration, conjunctival oedema Cardiovascular (Viperidae) Visual disturbances, dizziness, faintness, collapse, shock, hypotension, cardiac arrhythmias, pulmonary oedema Neurological (Elapidae, Russell’s viper) Drowsiness, paraesthesiae, abnormalities of taste and smell, “heavy” eyelids, ptosis external ophthalmoplegia, paralysis of facial muscles and other muscles innervated by the cranial nerves, aphonia, difficulty in swallowing secretions, respiratory and generalised flaccid paralysis
    • 62. Systemic Symptoms & Signs Bleeding & Clotting Disorders Bleeding from recent wounds (including fang marks), venepunctures and from old partly-healed wounds Spontaneous systemic bleeding – from gums, epistaxis, bleeding into the tears haemoptysis, haematemesis, hematochezia or melaena, haematuria, bleeding P/V, bleeding into the skin (petechiae, purpura, ecchymoses) and mucosae (eg conjunctivae) Intracranial haemorrhage (meningism from SAH, lateralising signs and/or coma from cerebral haemorrhage)
    • 63. Systemic Symptoms & Signs Skeletal muscle breakdown (sea snakes, Russell’s viper) Generalised pain, stiffness and tenderness of muscles, trismus, myoglobinuria hyperkalaemia, cardiac arrest, acute renal failure 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) Endocrine (acute pituitary/adrenal insufficiency) (Russell’s viper) Acute phase: shock, hypoglycaemia Chronic phase (months to years after the bite): weakness, loss of secondary sexual hair, amenorrhoea, testicular atrophy, hypothyroidism etc
    • 64. Myoglobinuria after Bungarus niger envenoming
    • 65. PleuropericardialHaemorrhagic EffusionManoj Lakhotia et al JIACM 2002; 3(4): 392-4
    • 66. TreatmentFirst AidPrimary/Secondary Care LevelTertiary Care Level
    • 67. Fir st Aid Reassure the victim Immobilise the bitten limb with a splint or sling Consider pressure-immobilisation for some elapid bites; AVOID IN COBRA Avoid any interference with the bite wound as this may introduce infection, increase venom absorption & local bleeding All rings, watches, constricting clothing should be removed.
    • 68. Pressure Immobilization (Elapidae bite) Developed in 1970 by late Struan Sutherland, Australia Bandaging entire limb using a long crepe bandage – starting from toe or finger as tightly as for a sprained ankle incorporating a splint.
    • 69. Pressure Immobilisation Pr immobilisation is recommended for bites by neurotoxic elapid snakes, including sea snakes. Caries risk of sudden envenomation after release – neurotoxic snakes. Should not be used for viper bites because of the danger of increasing the local effects of the necrotic venom.
    • 70. COMPLICATIONS OF ARTERIAL TOURNIQUET Congestion & swelling Ischaemia & gangrene Damage to peripheral nerves Increased bleeding from bite site
    • 71. Tour niquet Gangrene
    • 72. INCISION & SUCTION No!
    • 73. TREATMENTCRYOTHERAPY: No! Incr eases tendency to necr osis
    • 74. TREATMENTHOSPITAL MEASURES FOR ASYMPTOMATIC PTSa) OBSERVATION FOR 24 HOURSb) MONITOR:  PR, RR, BP  CBC-TLC ↑, Platelets ↓  Urine output  BUN, Creatinine  PT, aPTTK, INR  CPK (>600 IU/L)  Vomiting, diarrhoea  Abnormal bleeds  Local swelling necrosis  ECG  Blood gas analysis
    • 75. MEDICOLEGAL39 Code of Criminal Procedure under Constitution of India Article 21MLC to be initiated
    • 76. Hospital mngt, if tourniquet is a already in place•Limb is ischemic – remove immediately•Limb is not ischemic:- 1) Snake (unknown) or neurotoxic – Don’t remove until definite treatment (ASV) is initiated 2) Snake is viper – remove the tourniquet
    • 77. What is ASV?
    • 78. ASV ASV is Ig (usually the enzyme refined F(ab)2 fragment of IgG) purified from the serum/plasma of a horse/sheep immunised with the venoms of one or more species of snake. Monovalent/Polyvalent The ASV in India is a polyvalent type which is active against the commonly found snakes in India including the FAB Four.
    • 79. AntivenomPolyvalent antivenomsfrom India raisedagainst venom from:•Bungarus caeruleus•Naja naja•Echis carinatus•Daboia russeliiNo monovalentvaccine in India
    • 80. ASV Average dry weight of venom injected = 63 +/- 7mg by Russell’s Viper or Cobra. Each vial neutralises venoms of 6 mg Cobra 6 mg Russells Viper 4.5 mg of Krait 4.5 mg of Saw Scaled Viper Initial dose should be 8-12 vials. Snake inject same amount of venom into children, dose of ASV is same as adult . http://cbcreatures.webs.com/snakeantivenom.htm
    • 81. What are the indications for ASV use?
    • 82. Indications for Antivenom Shock UseSevere GI Symptoms  Resp distress /failure  Myoglobinuria Extensive Local Swelling  Elevated creatine kinase level (>600 IU/l) Ptosis  Altered level of Generalized myalgias consciousness  Hyperkalemia Trismus Mod-to-severe pain with  ECG Changes passive movement of extremities  Leukocytosis.
    • 83. Antivenom Reconstitution Freeze-dried (lyophilised) ASV is reconstituted with 10 ml of sterile DW per vial.
    • 84. TREATMENT OF SNAKEBITE PROCEDURE OF ADMINISTRATIONTest Dose? No! Has no predictive value in detecting anaphylactoid or late serum reactions and should not be used. Not IgE mediated, but complement - activated. May also pre-sensitise the patient, and create greater risk.
    • 85. Methods of AdministrationIV “push” injection: recons freeze-dried ASV is given by slow iv inj (not more than 2ml/min).IV infusion: recons freeze - dried ASV is diluted in approx 5-10 ml of isotonic fluid per kg BW (ie 250-500 ml of N/S or 5% Dex in adult pt) and infused at a constant rate over a period of about 1h.
    • 86. Antivenom Administration Adrenaline drawn up in readiness before ASV is administered. ASV should be given by the IV route whenever possible. I/M may be given when no i/v access, expeditions with limited med facilities.
    • 87. Prophylaxis in High Risk patients Pre-treated empirically with s/c epinephrine (adrenaline) IV antihistamines anti-H1 + anti- H2 (Ranitidine) IV Hydrocortisone 100 mg
    • 88. IM Antivenom A maximum of 5-10 ml should be given at each site by deep IM inj followed by massage to aid absorption ASV should never be injected into the gluteal region (upper outer quadrant of the buttock) as absorption is exceptionally slow and unreliable and there is always the danger of sciatic N damage by an inexperienced operator.
    • 89. Dose 5 vials(50ml) 5-10 vials (50-100ml) 10-20 vials (100-200ml)
    • 90. Large vs Small dose •High dose group 100ml stat and 100 ml every 6 hrs •Low dose group 100ml stat and 50 ml every 6 hrs Until recovery of neurological signsLow dose of snake antivenom is as effective as high dose inpatients with severe neurotoxic snakeenvenomingAgarwal, Aggarwal, Gupta, et al Emerg Med J 2005;22:397–399 .
    • 91. Timing of ASV There is no consensus as to the window period of administration of ASV. Best effects are observed within 4 h of bite . It has been noted to be effective in symptomatic pts even when administered up to 48 h after bite. ASV is efficacious even 6-7 days after the bite from vipers
    • 92. At the Ear liest Sign of a Reaction : ASV administration must be temporarily suspended Adrenaline (0.1% solution, 1 in 1,000; 1 mg/ml) is the effective treatment for early anaphylactic and pyrogenic ASV reactions
    • 93. Ear ly reaction to ASV Anaphylaxis Adrenaline (SC or IM) 0.3 to 0.5ml 1:1000 (1mg/ml). Repeated at 5 to 20 min interval if severe. Adrenaline (IV) - in intractable reaction 2.5 ml iv; 1:10,000 (0.1mg/ml). Volume resuscitation
    • 94. Case scenario……. 34 yr old male shifted from Periph Hosp with H/O snake bite 6 hrs back has ptosis, respiratory distress, RR 35/mt, BP 120/60, oral secretions present, absent gag and cough reflex shifted to ICU for tertiary care. On ASV 100ml stat, & 50ml in NS over 6 hrs Oxygen 3l/mt Patient is comfortable, vitals stable No ptosis, distress Patient received in casualty: 2 situations Patient is dead –what do you think went wrong ?
    • 95. Patient is dead –what do you think went wrong ? What could have been done better ? Bulbar signs-probably aspirated and died Endotracheal intubation could have been placed on T- piece Ambuing or Transport Ventilator Anticholienesterases Neostigmine with atropine
    • 96. Trial of AnticholinesteraseAnticholinesterase (“Tensilon”/Edrophonium) test Record baseline parameters Give atropine IV Give anticholinesterase drug edrophonium chloride (adults 10 mg, children Neostigmine 25µg/kg/hr 0.25 mg/kg body weight) given Dose of intravenously over 3 or Neostigmine 0.5 mg / 6 hr 4 minutes Neostigmine IV atropine 0.5 mg / 12 hr Observe Negative response Positive response Tearing, salivation, Improvement in ptosis, Respiratory muscle fasciculation, distress, better cough abdominal cramp, effort, decrease in bronchospasm, RR bradycardia, cardiac arrest Atropine IV Neostigmine
    • 97. Case scenario…….34 yr old male shifted from Periph Hosp with H/Osnake bite 6 hrs back has ptosis, respiratory distress,RR 35/mt, BP 120/60, oral secretions present, absentgag and cough reflex shifted to ICU for tertiary care.On ASV 100ml stat, & 50ml in NS over 6 hrsOxygen 3l/mtRecd neostigmine 0.6mg and 0.6 mg atropine iv You can have alive but a sicker patient Cobra You can have dead patient Krait
    • 98. Alive but a sicker patientShifted to ICU placed on a Ventilator lot of secretionsDo we continue anticholinesterases ?Issues to considerIncreased secretionsIncreased incidence of VAP ?We rarely use these drugs once the patient is in theICU under observation
    • 99. Observation of the Response to AntivenomCobra bites-Post synaptic May begin to improve as early as 30 minutes after anti-venom, but usually take several hours.Krait and sea snakes- Pre synaptic Depends on the timing of ASV administration If delayed may not produce any action or Minimal delayed action
    • 100. Repeat Dose Signs of systemic envenoming may recur within 24-48 hrs Criteria for repeating the initial dose of antivenom Persistence/recurrence of blood incoagulability after 1-2 h Deteriorating neurotoxic or cardiovascular signs after 1-2 h Causes Continuing absorption- due to improved blood supply following correction of shock, hypovolaemia etc After elimination of antivenom a redistribution of venom from the tissues into the vascular space.
    • 101. How to Know ASV DoseAdministered is Suf ficient?a) Spontaneous systemicbleeding stops in 15-30 min.b) Blood coagulability isusually restored in 6 hour s.c) Post synaptic neurotoxicenvenoming be gins to improvein 30 min, but can take severalhour s.
    • 102. How to Know ASV DoseAdministered is Suf ficient?d) Presynaptic neurotoxic envenoming usually takes a considerably more time to improve.e) Active haemolysis & rhabdomyolysis may cease within a few hour s & urine retur ns to its nor mal colour.f) In shocked pts, BP may improve in 30 min.
    • 103. W hat is the Max Dose of ASV?25 – 30 vialsQ. If symptoms per sist despite giving max dose, w hat must be done? Ans. Suppor tive measur es & tr eatment of complications:  Ventilation – Elapid bite  Dialysis, tr ansfusions, etc – V iperid bite  Fasciotomy, wound sur ger y, amputation, etc, as per need.
    • 104. Pregnancy and Snake Bite Pregnant pt is treated the same manner as the nonpregnant . Spontaneous abortion, bleeding, fetal death & malformations are common. Lactating mothers can continue lactating
    • 105.  A 25 yr old male with snake bite has signs of compartment syndrome and the pressure is 60 mmHg, is undergoing surgery, has a Hb of 6 gm%, is hypotensive 100/60, on noradrenalin, acidotic, coagulation profile is normal Blood is started After 15 mts of surgical time patient develops Dark colored urine Treatment BP drops to 80/60 with ARF Fluids, Mannitol, Alkalinize the urine, What are the possibilities ? Manage electrolytes Fasciotomy RRT Rhabdomyolysis (Viper Bite)
    • 106. Other RxAntibioticsHydrationTetanus prophylaxisWound debridementFasciotomy for compartment syndromeHaemodialysis for acute renal failureMechanical ventilationDIC; related mngt
    • 107. Criteria for Fasciotomy in Snake-Bitten LimbsClinical evidence of an intracompartmental syndromeIntracompartmental pr >40 mmHg (in adults)
    • 108. Disposition (Dr y bite)* Viper BiteNo local and systemic envenomationat 8 to 12h by repeated lab tests – ‘Dry Bite’.* Neurotoxic snakeObservation period 12-24hr.Neurotoxicity can be delayed .
    • 109. References N Engl J Med, Vol. 347, No. 5 August 1, 2002 www.nejm.org Page 347-356 WHO Guidelines for the Clinical Mana gement of Snake Bites in the South-East Asia Re gion
    • 110. THANK YOU Happy Year of the Snake! 新年快乐!