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Approach to a victim of snake bite

Snake Bite

Approach to a victim of snake bite

  1. 1. AN APPROACH TO A SNAKE BITE VICTIM Dr. Soumar Dutta. MD. DEM. MEM Consultant and Coordinator Department of Emergency Medicine Narayana Superspeciality Hospital, Guwahati
  2. 2. INTRODUCTION Snakebite is an acute life threatening time limiting medical emergency It is a preventable public health hazard often faced by rural population in tropical and subtropical countries with heavy rainfall and humid climate. 2
  3. 3. SNAKE BITE – AN OCCUPATIONAL DISEASE FishermanWorkers at site Farmers Snake Charmers Plantation work Hunter 3
  4. 4. STATISTICS • There is a huge gap between the number of snakebite deaths reported from direct survey and official data. • Only 7.23% snakebite deaths were officially reported Mohapatra,2011 Mazumdar,2014 49,500 deaths annually 5-6 lakhs bites annually but only 30% are venomous bites Mostly rural population Only 22.19% reaches hospital. Common in males than females Delay in first aid and unavailability of ASV Andhra Pradesh, Bihar, Tamil Nadu, West Bengal, Uttar Pradesh Majority of the bites being on the lower extremities 4
  5. 5. About 50% of bites are dry Majority (80%) is by non-venomous snakesSnake bite Venomous snakes FACTS 5
  6. 6. Features of poisonous & non-poisonous snakes Non Poisonous Snakes Head - Rounded Fangs - Not present Pupils - Rounded Anal Plate - Double row Bite Mark - Row of small teeths Poisonous Snakes Head - Triangle Fangs - Present Pupils - Elliptical pupil Anal Plate - Single row Bite Mark - Fang Mark 6
  7. 7. COMMON POISONOUS SNAKES IN INDIA • In India, >200 species of snakes; only 52 are poisonous. 1. Saw-scaled viper (Echis carinatus) 2. Russell’s viper (Daboia russelii) 3. Common krait (Bungarus caeruleus) 4. Indian cobra (Naja naja) Neurotoxic 20-30% of bites Majority of bites 70-80% Hemotoxin / Vasculotoxin 7
  8. 8. IS THERE ANY MEDICAL IMPLICATION FOR SNAKE IDENTIFICATION? 8
  9. 9. SPECIES: MEDICAL IMPLICATIONS 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 9
  10. 10. COMPOSITION OF SNAKE VENOM Procoagulant enzymes (Viperidae) Russell’s viper Haemorrhagins : Zinc metalloproteinases damage the endothelial lining. Cytolytic or necrotic toxins Haemolytic and myolytic: Phospholipases A2 damage cell membranes, endothelium, skeletal muscle, nerve and red blood cells. Pre-synaptic neurotoxins (Elapidae and some Viperidae) Post-synaptic neurotoxins (Elapidae) Highly Modified Saliva 10
  11. 11. SNAKE BITE TOXICITY PROFILE 11
  12. 12. HEMOTOXICITY • Starts late hence most of them reach hospitals • Many organ involvement hence MV is mostly supportive to buy time for organs to recover. • More number of cases. NEUROTOXICITY • Starts early- many die before they reach hospitals • Many reverse very well with ASV if started early • Less number of cases 70-80% 20-30% Overlap: Neuro-hemat 12
  13. 13. WHAT IS THE MODE OF NEUROTOXICITY IN KRAIT BITE 13
  14. 14. Beta-bungarotoxin- Phospholipases A2 1) Inhibiting the release of Ach from the presynaptic membrane 2) Presynaptic nerve terminals exhibit signs of irreversible physical damage and are devoid of synaptic vesicles 3) ASV & anticholinesterases have no effect • Paralysis lasts several weeks and frequently requires prolonged MV. • Recovery is dependent upon regeneration of the terminal axon. KRAIT- PRE-SYNAPTIC ACTION 14
  15. 15. WHAT IS THE MODE OF NEUROTOXICITY IN COBRA BITE 15
  16. 16. 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 Paralysis Anticholinesterases reverse the neuromuscular blockade 16
  17. 17. NEURO PARALYTIC MANIFESTATIONS STUDY Ptosis Repiratory Involvement Bulbar weakness N Sharma, S Chauhan, S Faruqi, P Bhat, S Varma, Emerg Med J 2005;22:118–120 Ophthalmoplegia 17
  18. 18. QUICK NEUROLOGICAL EXAMINATION ! 18
  19. 19. 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 paralyzed, giving the “broken neck sign 19
  20. 20. BUNGARUS NIGER(KRAIT) ENVENOMING 20 hr post-bite 20
  21. 21. 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. 21
  22. 22. HOW TO IDENTIFY FOR BULBAR PALSY & EARLY RESPIRATORY FAILURE 22
  23. 23. BULBAR & RESPIRATORY PARALYSIS • Impaired swallow or are secretions accumulating in the pharynx- an early sign of bulbar paralysis. • Objective measurement of ventilatory capacity is very useful. Use a peak flow meter, spirometer (FEV1 and FVC) • Ask the patient to blow into the tube of a sphygmomanometer to record the maximum expiratory pressure (mmHg). 23
  24. 24. PARADOXICAL RESPIRATION • This is an abnormal pattern of breathing in which the abdominal wall is sucked in during inspiration (it is usually pushed out). • Due to paralysis of the diaphragm. 24
  25. 25. HEMATOLOGICAL SIDE EFFECTS • Venom induces bleeding. • Venom induces clotting. • Venom induces haemolysis. • Haemorrhagin – causes direct endothelial damage by loosening the gap between endothelial cells. • Pro-coagulant factors. • Anticoagulant factors. • Fibrinonolytic factors. 25
  26. 26. SNAKE VENOM AND THE COAGULATION CASCADE RVV – Russel’s Viper Venom ECV – Echis carinatus Venom
  27. 27. PTT 27
  28. 28. 20 MIN WHOLE BLOOD CLOTTING TEST • Take 2 ml fresh blood in glass vessel • Leave undisturbed for 20 minutes • If blood is still liquid – incoagulable blood – Hypofibrinogenaemia/DIC • Repeat the test periodically if positive – Normal WBCT is 6-8 min 28
  29. 29. 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 29
  30. 30. Russell’s Viper Bite 30
  31. 31. LOCAL NECROSIS 31
  32. 32. WHAT ARE THE SYSTEMIC MANIFESTATIONS OF THE ENVENOMATION ? 32
  33. 33. 33
  34. 34. MANAGEMENT 34
  35. 35. FIRST AID/PRE HOSPITAL CARE • Reassure the victim • Immobilize the bitten limb with a splint or sling • 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. 35
  36. 36. 36
  37. 37. COMPLICATIONS OF ARTERIAL TOURNIQUET  Congestion & swelling  Ischaemia & gangrene  Damage to peripheral nerves  Increased bleeding from bite site 37
  38. 38. TOURNIQUET GANGRENE 38
  39. 39. INCISION & SUCTION 39
  40. 40. HOSPITAL MEASURES FOR ASYMPTOMATIC PATIENTS a) OBSERVATION for 24 hours b) MONITOR: • PR, RR, BP • CBC-TLC ↑, Platelets ↓ • Urine output • BUN, Creatinine • PT, aPTT, INR • CPK (>600 IU/L) • Vomiting, diarrhoea • Abnormal bleeds • Local swelling necrosis • Continuous ECG monitoring • Blood gas analysis 40
  41. 41. MEDICOLEGAL 39 Code of Criminal Procedure under Constitution of India Article 21 MLC to be initiated 41
  42. 42. HOSPITAL MANAGEMENT, 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 42
  43. 43. ANTI SNAKE VENOM 43
  44. 44. INDIAN NATIONAL SNAKE BITE PROTOCOL • Systemic envenomation • Evidence of coagulopathy • Evidence of neurotoxicity • Cardiovascular abnormalities • Persistent and severe vomitting • Local envenomation • Local swelling involving half of the limb • Rapid extension of swelling Start ASV 45
  45. 45. ANTI SNAKE VENOM • ASV is Ig purified from the serum/plasma of a horse/sheep immunized 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 - FAB Four. 46
  46. 46. Polyvalent antivenoms from India raised against venom from: • Cobra • Krait • Russel’s viper • Saw scaled viper No monovalent vaccine in India ANTI SNAKE VENOM 47
  47. 47. ANTI SNAKE VENOM • ASV comes in two forms lyophilised powdered and liquid. • Lyophilised ASV is simply liquid ASV freeze-dried. 48
  48. 48. ANTI SNAKE VENOM • Always to be given only by slow IV route only. • Never give IM route : poor bioavailability , painful and may increase intra-compartmental pressure. • Rate of infusion can be increased gradually in absence of reaction until full starting dose is administered(0ver ~ 1 hour) • Epinephrine (adrenaline) should always be drawn up in readiness before ASV is administered 49
  49. 49. ANTI SNAKE VENOM Each ml neutralize  0.6 mg of cobra  0.6 mg of rusells viper  0.45 mg of krait  0.45 mg of saw-scaled viper Average yield / bite  Cobra- 60 mg  Rusells- 63 mg  Krait- 20 mg  Saw-scaled- 13 mg 50
  50. 50. ANTI SNAKE VENOM Neuroparalytic snakebite ASV 10 vials stat as infusion over 30 minutes followed by 2nd dose of 10 vials after 1 hour if no improvement within 1st hour. 51
  51. 51. ANTI SNAKE VENOM Vasculotoxic snakebite Low Dose infusion therapy – 10 vials stat as infusion over 30 minutes followed by 2 vials every 6 hours as infusion in 100 ml of normal saline till clotting time normalizes or for 3 days whichever is earlier. High dose intermittent bolus therapy - 10 vials of polyvalent ASV stat over 30 minutes as infusion, followed by 6 vials 6 hourly as bolus therapy till clotting time normalizes and/or local swelling subsides. 52
  52. 52. ANTI SNAKE VENOM • Each vial of AVS be dissolved in 10 ml of distilled water and added to an infusion medium such as normal saline 10 vials + 100 ml of distilled water + 400ml of normal saline Given over 30-60 mins NO Test Dose 53
  53. 53. PAEDIATRIC ASV DOSE • Snakes inject the same dose of venom into children and adults. • Children must therefore be given exactly the same dose of antivenom as adults. 54
  54. 54. MONITORING PATIENT ON ASV All patients should be watched carefully every 5 min for first 30 min, then at 15 min for 2 hours for manifestation of a reaction. At the earliest sign of an adverse reaction suspend temporarily. Maintain a strict intake output chart and note colour of urine to detect acute kidney injury early. 55
  55. 55. LIMITATIONS OF ASV X Reverse necrotic action of the venom on tissue X Reverse local swelling X Reverse renal failure X Reverse coagulopathy; the liver does this. X Reverse pre synaptic envenoming; the nerve damage is structural and large quantities of ASV are ineffective, the body must regenerate synaptic vesicles 56
  56. 56. THERAPEUTIC ENDPOINT • Neuro /paralytic effect abolished – Presynaptic Only • Coagulation profile restored – repeat tests q6H • Restoration of hemodynamics. • Signs of local and systemic envenomation disappears • Active haemolysis and rhabdomyolysis ceases within a few hours and the urine returns to its normal colour • Patient improves clinically 57
  57. 57. ADVERSE ASV REACTION • Early anaphylactic reactions occurs within 10–180 min of start of therapy and is characterized by itching, urticaria, dry cough, nausea and vomiting, abdominal colic, diarrhoea, tachycardia, and fever. • Some patients may develop severe life-threatening anaphylaxis characterized by hypotension, bronchospasm, and angioedema 58
  58. 58. ADVERSE ASV REACTION • Pyrogenic reactions usually develop 1–2 h after treatment. Symptoms include chills and rigors, fever, and hypotension. • Late (serum sickness–type) reactions develop 1–12 (mean 7) days after treatment. Clinical features include fever, nausea, vomiting, diarrhea, itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy, immune complex nephritis and, rarely, encephalopathy 59
  59. 59. NEUROTOXIC ENVENOMATION • Antivenom treatment alone cannot be relied upon to save the life of a patient with bulbar and respiratory paralysis. • Neostigmine is an anticholinesterase that prolongs the life of acetylcholine and can therefore reverse respiratory failure and neurotoxic symptoms • Effective for post synaptic neurotoxins – Cobra • In all cases of neurotoxic envenomation the 'AN challenge Test' to be performed 60
  60. 60. “AN CHALLENGE TEST” Atropine 0.6 mg followed by neostigmine (1.5mg) to be given IV stat and repeat dose of neostigmine 0.5 mg with atropine every 30 minutes for 5 doses In children, Inj. Atropine 0.05 mg/kg followed by Inj.Neostigmine 0.04 mg/kg IV and repeat dose 0.01 mg/kg every 30 minutes for 5 doses A fixed dose combination of Neostigmine and glycopyrolate IV can also be used. 61
  61. 61. SUPPORTIVE CARE Close monitoring Analgesics – no aspirin Volume replacement Broad spectrum antibiotics Tetanus prophylaxis Renal replacement therapy Fasciotomy/ wound debridement Blood or blood products MV support 62
  62. 62. TAKE HOME MESSAGE • Identify early signs of envenomation • Manage as per “ABC” approach • Start ASV early • Prepare for anaphalytic reaction • Surgical intervention • Prevent multi organ failure • Create public awareness 63
  63. 63. Thank You 64

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