snake bite management

snake bite management

1. SNAKE BITE GUIDE: Prof Dr. V. P. Pandey CANDIDATE: Dr. Naresh Patel

2. Introduction Snakebite is an acute life threatening time limiting medical emergency. A preventable public health hazard. Often faced by rural population with heavy rainfall and humid climate. WHO estimates number of bites to be 83,000 per annum with 11,000 deaths in India. No reliable National Statistics are available.

3. There are more than 2000 species of snakes in the world and about 300 species in India out of which 52 are venomous. Commonest type of snake bite is from → Russell’s viper followed by Hump nosed viper, Cobra, Krait and Cat snake. The commonest site → paddy fields followed by home and road.

4. The commonest location of the body → below the knees > hand Attributed to the fact that the snakes are crawling animals and the chances of the accidentally stepping on the snake are high. Sometime snake bite can be due to over enthusiastic

5. Cobras The venomous snakes found in India belong to three families Elapidae , Viperidae and Hydrophidae (Sea Snakes). Elapidae have short permanently erect fangs Includes Indian Cobra King cobra Kraits Sea snakes.

6. Viperidae have long fangs folded up against the upper jaw but are erected when the snake strikes. Two subgroups Typical vipers ( Viperinae ) & Pit vipers ( Crotalinae ).

7. Venomous sea-snakes have flattened paddle-like tails & tiny fangs.

8. Non-venomous: have no grooved or hollow teeth, no specialized venom glands, no venom storage lumens, or any kind of anatomical venom-delivery apparatus.

9. Approach to Snake Identification Tail Flat  sea snake[P] Round/ cylidrical  P /NP Ventral Scales Small belly scale  NP Incomplete  NP Complete  NP /P

10. Cobra : 3 rd supralabial touches the eye and nostril Cobra

11. Viper : Small scales on head and without shields. Body is massive, cylindrical, narrowing at both ends. Russel viper Saw-scaled viper

12. Krait : with enlarged hexagonal vertebral scales, uniform white or red belly and narrow white crossbars on the back.

13. Head of typical pit viper pit organ (red arrow)

14. Snake venoms Snake venoms contain more than 20 different constituents, Proteins, including enzymes and polypeptide toxins. Pro-coagulant enzymes ( Viperidae ) → activate different steps of the clotting cascade Formation of fibrin in the blood stream. Most of this is immediately broken down by the fibrinolytic system. DIC / Consumption coagulopathy.

15. Haemorrhagins → damage the endothelial lining of blood vessel walls → local and systemic swelling. Hyaluronidase → spread of venom through connective tissue. Pre-synaptic neurotoxins Elapidae and some Viperidae → Phospholipases A2 that damage nerve endings, initially releasing acetylcholine transmitter, then interfering with release. Post-synaptic neurotoxins Elapidae : These polypeptides compete with Ach. for receptors in the NM junction → curare like paralysis.

16. Management of snake bite First aid treatment. Rapid clinical assessment and resuscitation. Detailed clinical assessment and species diagnosis. Investigations/laboratory tests. Antivenom treatment. Observation of the response to antivenom. Treatment of the bitten part. Treatment of life threatening complication.

17. 1. First aid treatment Performed by the bystander or by snake bite victim himself/herself. Reassure the victim who may be very anxious. Avoid any interference with the bite wound as this may introduce infection, increase absorption of the venom and increase local bleeding. Immobilize the bitten limb with a splint or sling.

18. Pressure immobilization method Ideally, an elastic, crepe bandage, approximately 10 cm wide and at least 4.5 metre long should be used. The bandage is bound as tightly as for a sprained ankle, but not so tightly that the peripheral pulse (radial, posterior tibial , dorsalis pedis ) is occluded or that a finger cannot easily be slipped between its layers. Ideally applied by qualified medical personnel during transport to higher center.

19. The bandage is bound firmly around the entire bitten limb, starting distally around the fingers or toes and moving proximally, to include a rigid splint.

20. Caution Release of a tight tourniquet or compression bandage may result in the dramatic development of severe systemic envenoming. Ideally, compression bandages should not be released until the patient is in hospital, resuscitation facilities are available and antivenom treatment has been started.

21. Useless or Dangerous Methods Making local incisions or pricks at the site of the bite or in the bitten limb. Attempts to suck the venom out of the wound. Use of snake stones. Electric shock. Topical instillation or application of chemicals, herbs or ice packs. Do not attempt to capture, handle or kill the snake.

22. Management of snake bite First aid treatment. Rapid clinical assessment and resuscitation. Detailed clinical assessment and species diagnosis. Investigations/laboratory tests. Antivenom treatment. Observation of the response to antivenom. Treatment of the bitten part. Treatment of life threatening complication

23. 2. Rapid clinical assessment and resuscitation Oxygen administration. IV access. Airway, breathing and circulation. The level of consciousness must be assessed. CPR, if needed.

24. Management of snake bite First aid treatment. Rapid clinical assessment and resuscitation. Detailed clinical assessment and species diagnosis. Investigations/laboratory tests. Antivenom treatment. Observation of the response to antivenom. Treatment of the bitten part. Treatment of life threatening complication.

25. 3. Detailed Clinical Assessment and Species Diagnosis History of the circumstances of the bite and the progression of local and systemic symptoms and signs is very important. Site of bite & Time of bite. Snake identification.

26. Clinical Presentation

27. Clinical presentation of snakebite victim depends upon Species of snake. Amount of venom injected. Season of the bite. Whether snake is fed or unfed. Dry or complete bite. Venom injection in vessel.

28. Occult snake bite Krait Neuroparalytic symptoms with no local sign. Severe abdominal pain Overt bite Non-poisonous(70%)/Poisonous (30%) Asymptomatic Dry bite Symptomatic Predominant symptoms manifestation Progressive painful Swelling, Viper, Cobra Neuroparalytic Cobra, Krait Vasculotoxic Russel viper Saw scaled viper Myotoxic Sea snake Suspected snake bite Local necrosis Ecchymosis Blister Painful swelling Compartment syndrome Ptosis, Diplopia Dysarthria, Dysphonia Dypnoea , Dysphagia paralysis Bleeding, DIC Shock, Acute kidney injury Muscle ache Muscle swelling Involuntary muscle contraction Compartment syndrome

29. Asymptomatic : (i.e. non-venom related) Non specific symptoms related to anxiety are Palpitation & Sweating. Tachycardia, tachypnoea , raised BP, cold extremities and paraesthesia. May have dilated pupils suggestive of sympathetic over activity. Dry bite : A proportion of bites do not result in the injection of venom. About 50% of bites by Pit vipers and Russell’s vipers, 30% of bites by cobras and 5-10% of bites by saw-scaled vipers are dry bites.

30. Occult snake bite: Krait bite victims often present in the early morning with paralysis with no local signs. Patient was healthy at night, in the morning gets up with severe epigastric/umbilical pain with vomiting persisting for 3 – 4 hours and followed by typical neuroparalytic symptoms within next 4- 6 hours. No history of snakebite.

31. Neuro-paralytic : Elapid envenomation Typical symptoms within 30 min - 6 hrs in cobra bite, and 6-24 hrs for Krait bite, as late as 36 hrs in case of Krait bite. In chronological order of appearance of symptoms : Heavy eyelid, P tosis f/b D iplopia D ysarthria D ysphonia D yspnoea D ysphagia Finally, P aralysis of intercostal and skeletal muscle occur in descending manner. Remembered as 5 Ds and 2 Ps.

32. Ptosis with neuro-paralytic snakebite

33. To identify the impending respiratory failure bedside PFT in adult via: Peak flow meter, if available Single breath count > 30 normal. Breath holding time > 45 sec in inspiration normal. Ability to complete one sentence in one breath. Cry in a child whether husky or loud can help in identifying impending respiratory failure. Bilateral dilated, poorly or a non-reacting pupil is not the sign of brain dead in elapid envenoming.

34. Vasculotoxic : cardiovascular ( viperidae ) Local Symptoms and Signs Local pain & swelling Local bleeding Bruising Tender LN Enlargement Blistering Local infection & Abscess formation Necrosis.

35. 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

36. Early stage of full thickness necrosis 5 days after russel viper bite.

37. Bleeding and clotting disorders ( Viperidae ) Bleeding from recent wounds (including fang marks, venepunctures etc ) and from old partly-healed wounds. Spontaneous systemic bleeding. Conjunctival chemosis

38. Thoroughly examine the gingival sulci, using a torch and tongue depressor, as these may show the earliest evidence of spontaneous systemic bleeding. Abdominal tenderness → gastrointestinal or retroperitoneal bleeding. Loin pain and tenderness → acute renal ischemia (Russell’s viper bites). Lateralizing neurological signs, asymmetrical pupils, convulsions or impaired consciousness → Intracranial hemorrhage.

39. Myotoxic : sea snakebite Generalized muscle ache, muscle swelling, involuntary contraction of muscle. Passage of dark brown urine. Compartment syndrome, cardiac arrhythmias due to hyperkalemia. Kidney injury due to myoglobinuria . Subtle neuroparalytic signs.

40. Management of snake bite First aid treatment. Rapid clinical assessment and resuscitation. Detailed clinical assessment and species diagnosis. Investigations/laboratory tests. Antivenom treatment. Observation of the response to antivenom. Treatment of the bitten part. Treatment of life threatening complication.

41. 4. Investigations/laboratory tests 20 minute whole blood clotting test (20WBCT) Place a few ml of freshly sampled venous blood in a small glass vessel. Leave undisturbed for 20 minutes at ambient temperature. If the blood is still liquid and runs out, the patient has hypofibrinogenaemia as a result of venom-induced consumption coagulopathy.

42. 20WBCT Contaminated glass tube may not stimulate clotting of the blood sample in the usual way and test will be invalid. If any doubt, repeat the test in duplicate, including a “control” (blood from a healthy person). The test should be carried out every 30 minutes from admission for 3 hours and then hourly after that.

43. Platelet count : may be decreased – viper. WBC cell count : Early neutrophil leucocytosis in systemic envenoming. Blood film : Fragmented RBC(“helmet cell”, schistocytes) are seen in microangiopathic hemolysis. Plasma/serum : may be pink or brownish if there is gross haemoglobinaemia or myoglobinaemia.

44. Biochemical Abnormalities Aminotransferases, creatine kinase elevated if there is severe local damage or particularly generalised muscle damage. Bilirubin is elevated following massive extravasation of blood. Creatinine, urea or blood urea nitrogen levels are raised in the renal failure.

45. Urine Examination For blood/myoglobin. Microscopy for erythrocytes in the urine. Red cell casts indicate glomerular bleeding. Massive proteinuria is an early sign of the generalized increase in capillary permeability in Russell’s viper envenoming.

46. Management of snake bite First aid treatment. Rapid clinical assessment and resuscitation. Detailed clinical assessment and species diagnosis. Investigations/laboratory tests. Antivenom treatment. Observation of the response to antivenom. Treatment of the bitten part. Treatment of life threatening complication.

47. 5. Anti-venom Treatment Antivenom is immunoglobulin (refined F(ab)2 fragment of IgG) purified from the serum or plasma of a horse or sheep that has been immunized with the venoms of one or more species of snake. Monovalent neutralizes the venom of only one species of snake. Polyvalent neutralizes the venoms of several species of snakes

48. Haffkine , Kasauli and Serum Institute of India produce “polyvalent anti-snake venom serum”. It is raised in horses using the venoms of the “ Big four ” in India (Indian Cobra, Indian Krait, Russell’s viper, Saw-scaled viper). Not included are venoms of King Cobra , Sea snakes and Pit vipers.

49. Neutralization of Venom 1 cc of ASV neutralises 0.60 mg of Cobra venom & Russel’s Viper venom. 0.45 mg of Saw scaled viper venom & Krait venom.

50. Indications for Antivenom Systemic Envenoming Haemostatic abnormalities: Spontaneous systemic bleeding Coagulopathy Thrombocytopenia (<100 x 10 9 /L). Neurotoxic signs: Ptosis, external ophthalmoplegia, paralysis.

51. Cardiovascular abnormalities: Hypotension, shock, cardiac arrhythmia. Acute renal failure: Oliguria/anuria, rising serum creatinine/urea. Haemoglobinuria / myoglobinuria : Dark brown urine, evidence of intravascular haemolysis or generalised muscle aches and pains.

52. Local swelling involving more than half of the bitten limb (in the absence of a tourniquet). Rapid extension of swelling (for example beyond the wrist or ankle within a few hours of bites on the hands or feet). Swelling after bites on the digits (toes and especially fingers). Development of an enlarged tender lymph node draining the bitten limb.

53. Contraindications to antivenom There is no absolute contraindication to antivenom treatment. Patients who have reacted to horse (equine) or sheep (ovine) serum in the past and those with a strong history of atopic diseases (especially severe asthma) should be given antivenom only if they have signs of systemic envenoming. Test dose is not recommended.

54. Administration of Antivenom Intravenous Infusion Reconstituted freeze-dried or neat liquid antivenom is diluted in approximately 5-10 ml of isotonic fluid per kg body weight (i.e. 250-500 ml of isotonic saline or 5% D in the case of an adult patient). Infused at a constant rate over a period of about one hour. IV “push” Injection Antivenom is given by slow IV inj. (<2 ml/min) This method has the advantage that the doctor/nurse/dispenser giving the antivenom remain with the patient during the time when some early reactions may develop.

55. Adrenaline should always be in readiness before antivenom is administered. Local administration of antivenom at the site of the bite is not recommended. Although this route may seem rational, it should not be used as it is extremely painful, may increase compartment pressure and has not been shown to be effective.

56. Dose of ASV for neuroparalytic snake bite: ASV 10 vials stat as infusion over 1 hour followed by 2nd dose of 10 vials after 1 hour if no improvement within 1 st hour. Dose of ASV for vasculotoxic snake bite: 10 vials of polyvalent ASV stat over 1 hour as infusion, followed by 6 vials 6 hourly till clotting time normalizes and/or local swelling subsides. Children & pregnant women should receive the same ASV dosage as adults.

57. Repeat dose of ASV Repeat dose: neuroparalytic or neurotoxic envenomation- Repeat ASV when there is worsening neurotoxic or cardiovascular signs even after 1-2 hrs. Maximum dose 20 vials ASV for neurotoxically envenomed patients. Repeat dose: in Vasculotoxic or hemotoxic envenomation- Repeat clotting test every 6 hrs and administer ASV every 6 hrs until coagulation is restored. If coagulation abnormality persists, give FFP or cryoprecipitate (fibrinogen, factor VIII), fresh whole blood, if FFP not available or platelet concentrate.

58. Management of snake bite First aid treatment. Rapid clinical assessment and resuscitation. Detailed clinical assessment and species diagnosis. Investigations/laboratory tests. Antivenom treatment. Observation of the response to antivenom. Treatment of the bitten part. Treatment of life threatening complication.

59. Observation of the response to antivenom Nausea, headache and generalised aches and pains may disappear very quickly . Spontaneous systemic bleeding ( eg from the gums) usually stops within 15-30 minutes . In shocked patients, blood pressure may increase within the first 30-60 minutes and arrhythmias such as sinus bradycardia may resolve.

60. Neurotoxic envenoming of the post-synaptic type (cobra bites) may begin to improve as early as 30 minutes after antivenom, but usually take several hours. Envenoming with presynaptic toxins (kraits and sea snakes) is unlikely to respond in this way. Blood coagulability (as measured by 20WBCT) is usually restored in 3-9 hours . Bleeding from new and partly healed wounds usually stops much sooner than this. Active haemolysis and rhabdomyolysis may cease within a few hours and the urine returns to its normal colour .

61. Management of snake bite First aid treatment. Rapid clinical assessment and resuscitation. Detailed clinical assessment and species diagnosis. Investigations/laboratory tests. Antivenom treatment. Observation of the response to antivenom. Treatment of the bitten part. Treatment of life threatening complication.

62. 7. Treatment of the bitten part Keep slightly elevated, to encourage reabsorption of edema fluid. Prophylactic broad spectrum antimicrobial treatment is justified Bullae may be large and tense but they should be aspirated only if they seem likely to rupture. Its worthy to wait 5-7 days for debridement of necrotic tissue in order to specify line of demarcation between viable and non-viable tissue. Skin grafting and amputation of a necrotic digit may be required.

63. Management of snake bite First aid treatment. Rapid clinical assessment and resuscitation. Detailed clinical assessment and species diagnosis. Investigations/laboratory tests. Antivenom treatment. Observation of the response to antivenom. Treatment of the bitten part. Treatment of life threatening complication.

64. 8. Life threatening complications: Neuroparalytic envenomation. Renal involvement. Shock.

65. Management Neuroparalytic Envenomation As ASV cannot be relied upon to save life of a patient with respiratory paralysis, administer following in addition: Oxygen Assisted ventilation- Neuroparalysis recovers quickly with ASV, so duration of mechanical ventilation is shorter. Manual ventilation is effective in absence of mechanical ventilator. Administer Atropine Neostigmine (An) schedule.

66. Atropine neostigmine (AN) dosage schedule Patients with clear evidence of neurotoxicity should receive test dose of neostigmine. Atropine 0.6mg followed by neostigmine 1.5 mg to be given IV stat. If objective improvement evident after 5 minutes in ptosis, repeat dose of neostigmine 0.5mg with atropine every 30 mins for 5 doses. Majority of patients improve within first 5 doses. Stop AN dosage schedule if: Patient has complete recovery from neuroparalysis . If there is no improvement after 3 doses.

67. Forced Alkaline Diuresis If the patient has oliguria or dipstick positive for blood give a trial of forced alkaline diuresis (FAD) within first 24 hours of the bite to avoid nephropathy leading to acute tubular necrosis (ATN) . Delayed FAD has no role. Sequence of FAD in adults is as follows: Inj. Frusemide 40 mg IV stat Inj. Normal saline 500 ml + 20 ml of NaHCO3 over 20 minutes Inj. Ringer’s lactate 500 ml + 20 ml of NaHCO3 over 20 minutes Inj. 5% dextrose 500 ml + 10 ml of Potassium Chloride over 90 minutes Inj. Mannitol 150 ml over 20 min

68. Whole cycle completes in 2 h 30 min and urine output of 3 ml/min is expected. If patient responds to first cycle continue for 3 cycles . FAD converts oliguria into polyuria and avoid ATN and acute kidney injury needing dialysis reduce up to >75% patients . If there is no response discontinue FAD and consider for dialysis.

69. Indications for dialysis are: Absolute value Blood urea >130 mg/dl, Sr. Creatinine > 4 mg/dl OR evidence of hypercatabolism rise in blood urea 30 mg/ dL (BUN > 15), Sr. Creatinine > 1 mg/dL, Sr. Potassium > 1 mEq/L and fall in bicarbonate >2 mmol/L • Fluid overload leading to pulmonary oedema. • Hyperkalaemia (>7 mmol /l or hyperkalaemic ECG changes). • unresponsive to conservative management. • Uremic encephalopathy & uremic pericarditis.

70. Shock Hypovolaemia should be corrected with colloid/crystalloids , controlled by observation of the central venous pressure. IV ionotropics (dopamine or nor-adrenaline). Hypotension associated with bradycardia should be treated with atropine.

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