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Snake bite


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Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.

Published in: Health & Medicine

Snake bite

  1. 1. MANAGEMENT OF SNAKE BITE Dr. Sachin Verma MD, FICM, FCCS, ICFC Fellowship in Intensive Care Medicine Infection Control Fellows Course Consultant Internal Medicine and Critical CareWeb:- Mob:- +91-7508677495
  2. 2. INTRODUCTION• Poisoning by venomous snake bite is a common acute life-threatening medical emergency in India.
  3. 3. 61 507 bites and 1,124 deaths in 200676,948 bites and 1,359 deaths in 2007[Government of India data:pp 107–108 of
  4. 4. ETIOLOGYThere are about 216 species of snakes identifiable in India, of which 52 are known to be poisonous.
  5. 5. ETIOLOGY• Major families of poisonous snake in India includes – - Elapidae  Common cobra (naja naja)  King Cobra  Common Krait
  6. 6. ViperidaeRussell’s viper Echis carinatus (Saw scaled or carpet viper)Pit viper
  7. 7. ColubridaeLargest snake family, and includes abouttwo-thirds of all current snake species. most are nonvenomous and harmless, butfew groups can produce medicallysignificant bites, and have caused humanfatalities.
  8. 8. SNAKE VENOMS• Snake venoms contain more than 20 different constituents. Mainly proteins including enzymes & polypeptide toxins.
  9. 9. SNAKE VENOMS• Procoagulant enzymes• Haemorrhagins• Cytolytic or necrotic toxins• Haemolytic and myolytic phospholipases A2
  10. 10. SNAKE VENOMS• Pre-synaptic neurotoxins•• Post-synaptic neurotoxins
  12. 12. WHEN VENOM HAS BEEN INJECTEDLOCAL 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
  13. 13. SYMPTOMS & SIGNS OF SNAKE BITE Fang marks made by Russell’s viper
  14. 14. SYMPTOMS & SIGNS OF SNAKE BITELocal bleeding from fang marks made by pit viper
  15. 15. SYMPTOMS & SIGNS OF SNAKE BITELocal swelling and blistering (a) with bruising,following a bite by a pit viper (b) with early necrosis
  16. 16. SYMPTOMS & SIGNS OF SNAKE BITETissue necrosis following a bite by a pit viper
  17. 17. GENERALISED (SYSTEMIC) SYMPTOMS AND SIGNSGeneral• Nausea, vomiting, malaise, abdominal pain, weakness, drowsiness, prostrationCardiovascular (Viperidae)• Visual disturbances, dizziness, faintness, collapse, shock, hypotension, cardiac arrhythmias, pulmonary oedema.
  18. 18. Bleeding and clotting disorders (Viperidae)Bleeding from recent wounds (including fang marks, venepunctures etc) and from old partly-healed wounds.• Spontaneous systemic bleeding
  19. 19. Neurological (Elapidae, Russell’s viper)• Drowsiness, paraesthesiae,• abnormalities of taste and smell,• ptosis, external ophthalmoplegia,• Muscle palsys• aphonia,• difficulty in swallowing secretions,• respiratory and generalised flaccid paralysis
  20. 20. Skeletal muscle breakdown (sea snakes, Russell’s viper)• Generalised pain,• stiffness and tenderness of muscles trismus,• myoglobinuria,• hyperkalaemia,• acute renal failure
  21. 21. Renal (Viperidae, sea snakes)• Loin pain,• haematuria,• haemoglobinuria,• myoglobinuria,• oliguria/anuria,• symptoms and signs of uraemia
  22. 22. Endocrine (acute pituitary/adrenal insufficiency)• Acute phase: shock, hypoglycaemia• Chronic phase (months to years after the bite):• loss of secondary sexual hair amenorrhoea,• testicular atrophy• hypothyroidism etc.
  23. 23. Bilateral conjunctival oedema (chemosis) after a
  24. 24. Bleeding from gingival sulci in a patient bitten by a saw-scaled viper
  25. 25. Subconjunctival haemorrhages in a patient bitten by a Russell’s viper
  26. 26. Bilateral ptosis (a) in a patient bitten by a common krait
  27. 27. LONG TERM COMPLICATIONS (SEQUELAE) OF SNAKE BITE• Chronic ulceration, infection, osteomyelitis or arthritis.• Malignant transformation in skin ulcers.• Chronic renal failure• Chronic panhypopituitarism or diabetes insipidus.• Chronic neurological deficit in patients of intracranial haemorrhages.
  28. 28. Patient with symptoms and signs of panhypopituitarismthree years after envenoming by Russell’s viper. There is loss ofsecondary sexual hair and testicular atrophy
  29. 29. (a) Deformity and dysfunction after a bite and subsequent necrosisof the calf
  30. 30. Squamous cell carcinoma arising at the site of a chronic skinulcer with osteomyelitis 8 years after the bite.
  31. 31. Clinical syndromes of snake-bite in South-East Asia Syndrome 1Local envenoming (swelling etc.) withbleeding/clotting disturbances =Viperidae (all species)
  32. 32. Syndrome 2Local envenoming with bleeding/clottingdisturbances, shock or AKI = Russell’s viper(hump-nosed pit viper in Sri Lankaand SW India)with conjunctival oedema and acute pituitaryinsufficiency =Russell’s viper, Myanmarwith ptosis, external ophthalmoplegia, facialparalysis etc and dark brown urine= Russell’s viper, Sri Lanka and South
  33. 33. Syndrome 3Local envenoming (swelling etc.)with paralysis = cobra or king cobra
  34. 34. Syndrome 4Paralysis with minimal or no localenvenomingBitten on land while sleeping on theground = kraitBitten in the sea, estuary and somefreshwater lakes = sea snake
  35. 35. Syndrome 5Paralysis with dark brown urine and AKI:Bitten on land (with bleeding/clotting disturbance)= Russell’s viper, SriLanka or South IndiaBitten on land while sleeping indoors = krait ,Bangladesh, ThailandBitten in sea, estuary and some freshwater lakes(no bleeding/clottingdisturbances) = sea snake
  36. 36. ASSESSMENT OF SEVERITYNo envenomation Absence of local or systemic reactions, Fang marks +/-Mild envenomation Fang marks (, moderate pain, minimal local oedema (0-15cms), erythema+, ecchymosis +/-, no systemic reactionsModerate Fang marks+, severe pain, moderate localenvenomation edema (15-30cms), erythema & ecchymosis +, systemic weakness, sweating, syncope, nausea, vomiting, anemia or thrombocytopeniaSevere envenomation Fang marks+, severe pain, severe local edema (>30cms), erythema & ecchymosis+, hypotension, parasthesia, coma, pulmonary edema, respiratory failure
  37. 37. MANAGEMENT OF SNAKE BITEFirst aid treatmentTransport to hospitalRapid clinical assessment and resuscitationDetailed clinical assessment and speciesdiagnosisInvestigations/laboratory testsAntivenom treatment
  38. 38. Observing the response to antivenomDeciding whether further dose(s) of antivenomare neededSupportive/ancillary treatmentTreatment of the bitten partRehabilitationTreatment of chronic complications
  39. 39. RECOMMENDED FIRST AID METHODS• Reassure the victim• Immobilise the bitten limb with a splint or sling• Consider pressure-immobilisation for some elapid bites• Avoid any interference with the bite wound as this may introduce infection, increase absorption of the venom and increase local bleeding.
  40. 40. •Application of a tourniquet to the bitten limb•Cuting open the bitten area•Sucking out venom, either by mouth or with a pump•Immersion in warm water or sour milk, followed by the apof snake-stones•.•Application of potassium permanganate.••Use of electroshock therapy•NOT RECOMMENDED
  42. 42. INVESTIGATIONS/LABORATORY TESTS20 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• Tip the vessel once• If the blood is still liquid (unclotted) and runs out, the patient has hypofibrinogenaemia
  43. 43. OTHER TESTS• haematocrit: a transient increase indicates haemoconcentration resulting from a generalised increase in capillary permeability (eg in Russell’s viper bite).• Decrease reflects blood loss or intravascular haemolysis.
  44. 44. • Platelet count: this may be decreased in victims of viper bites.• White blood cell count: an early neutrophil leucocytosis is evidence of systemic envenoming from any species.• Blood film: fragmented red cells (“helmet cell”, schistocytes) are seen when there is microangiopathic haemolysis.
  45. 45. INVESTIGATIONS/LABORATORYOTHER TESTS TESTS• Plasma/serum may be pinkish or brownish if there is gross haemoglobinaemia or myoglobinaemia.•• Biochemical abnormalities: aminotransferases and muscle enzymes (creatine kinase, aldolase etc) will be elevated if there is severe local damage or, particularly, if there is generalised muscle damage (Russell’s viper bites, sea snake bites).
  46. 46. Bilirubin is elevated following massiveextravasation of blood.Renal function tests are raised in the renalfailure (Russell’s viper , saw-scaled viperand sea snake bites.)Hyperkalaemia may be seen followingextensive rhabdomyolysis in sea snakebites.
  47. 47. OTHER TESTS• Arterial blood gases• Arterial oxygen Saturation•• Urine examination: the urine should be tested for blood/ haemoglobin/myoglobin.
  48. 48. Snake Bite Treatment Protocol
  49. 49. On arrival.Deal with any life threatening symptoms onpresentation. i.e. Airway, Breathing andCirculation.If there is evidence of a bite, where the skinhas been broken, give Tetanus ToxoidRoutine use of anti-biotic is not necessary,although it should be considered if there isevidence of cellulitis or necrosis
  50. 50. Diagnosis Phase: General PrinciplesWhere possible identify the snake responsible.keep under observation for a minimum of 24 hours.Determine if any traditional medicines have been usedDetermine the exact time of the bite.Question what the victim was doing at the time of bite.
  51. 51. ANTIVENOM TREATMENT• Antivenom is immunoglobulin (usually the enzyme refined F(ab)2 fragment of IgG) purified from the serum or plasma of a horse or sheep that has been immunised with the venoms of one or more species of snake.• Monovalent or monospecific antivenom neutralises the venom of only one species of snake. Polyvalent or polyspecific antivenom neutralises the venoms of several different species of snakes
  52. 52. INDICATIONS Systemic envenoming• Haemostatic abnormalities•• Neurotoxic signs• Cardiovascular abnormalities:
  53. 53. INDICATIONS• Acute renal failure• Haemoglobinuria/myoglobinuria•• Supporting laboratory evidence of systemic envenoming.
  54. 54. INDICATIONSLocal envenoming• Local swelling involving more than half of the bitten limb (in the absence of a tourniquet)• Swelling after bites on the digits (toes and especially fingers).• Rapid extension of swelling• Development of an enlarged tender lymph node draining the bitten limb.
  55. 55. SELECTION OF ANTIVENOM• Liquid antivenoms that have become opaque should not be used as precipiated of protein indicates loss of activity & increased risk of reaction.• Polyspecific/polyvalent antivenoms are preferred in many countries because of difficulty in identifying species responsible for bites.
  56. 56. • 1 ml of polyvalent antivenom will neutralise• 0.6 mg of dried cobra venom• 0.45 mg of dried krait venom• 0.6 mg of dried Russel’s viper venom• 0.45 mg of dried saw-scales viper venom.
  57. 57. DOSE OF ANTIVENOM• Children must be given exactly the same dose of antivenom as adults.• Test dose of ASV is not essential because even if victim is sensitive to ASV, does not preclude its use. Because there is no guarantee that victim would not develop anaphylaxis reaction after administration.
  58. 58. • Initial dose should depend on an estimate of amount of envenomation.• 5 vials given if signs are mild -primarily local manifestations. (Minimal envenomination)• 10 vials if signs are moderate -bleeding from gums, ptosis. (Moderate envenomination)• 15 vials if signs are severe -vascular collapse, progressive paralysis. (Severe
  59. 59. ADMINSITRATION OF ANTIVENOMASV diluted in 100ml of isotonic saline orglucose or 5-10 ml / kg body wt of isotonicsaline or glucose as an infusion. All ASV to be administered over 1 Hour atconstant speed. The patient should beclosely monitered for two hours.• Local administration of antivenom at the site of bite is not
  60. 60. Observation of the response to antivenom:(a) General: The patient feels better. Nausea,headache and pains disappear very quickly.(b) Spontaneous systemic bleeding (e.g. fromthe gums): stops within 15-30 minutes.(c) Blood coagulability (as measured by20WBCT):restored in 3-9 hours. Bleeding from new andpartly healed wounds usually stops muchsooner than this.
  61. 61. (d) In shocked patients: Blood pressure mayincrease within the first 30-60 minutes andarrhythmias may resolve.(e) Neurotoxic envenoming of the post-synaptictype (cobra bites) begin to improve as early as30 minutes after antivenom, but usually takesseveral hours.(f) Active haemolysis and rhabdomyolysis maycease within a few hours and the urine returns toits normal colour.
  62. 62. Criteria for giving more antivenom:Persistence or recurrence of bloodincoagulability after 6 hours or of bleedingafter 1-2 hours.Deteriorating neurotoxic or cardiovascularsigns after 1-2 hours.
  63. 63. CONTRAINDICATIONS TO ANTIVENOM• No absolute contraindication
  64. 64. ANTICHOLINESTERASE THERAPY• Post synaptic neurotoxins compete with acetylcholine for available nicotinic Ach receptor sites on adjacent skeletal muscle cell synaptic clefts. This process tend to be reversible.• Anticholinesterases are the drugs that inhibit the process of acetylcholine breakdown & re-uptake.
  65. 65. LIMITATIONS• No value in the treatment of presynaptic neurotoxicity.• No substitute for antivenom therapy and mechanical ventilation.• Only an adjunct treatment
  66. 66. CONTRAINDICATIONS TO USE• If there is positive 20WBCT (incoagulable blood).• Previous allergy to the drug.
  67. 67. ASSESSMENT OF SUITABILITY• “Neostigmine Test”.
  68. 68. Neostigmine test1.5 to 2 mg of neostigmine  I M together with0.6 mg  of atropine I V . The patient should be closely observed for 1 houMethods to asses effectiveness of neostigmine are1.      single breath count2.      mm of iris uncovered3.      Inter incisor distance4.    Length of time upwards gaze can be maintain5.      FEVi or FVC
  69. 69. • If the victim responds to neostigmine test• 0.5 mg of neostigmine IM half hourly plus 0.6 mg atropine IV for 5 doses• then 2 to 12 hourly according to recovery.  • If there is no improvement in symptoms after 1 hr, neostigmine should be stopped.
  70. 70. • Can be given in the form of interavenous infusion at the rate of 25 µg/kg/hour until the neuroparalysis is reversed.
  71. 71. No incision, suction, tourniquet, Splint + crepe bandage On site Ressure, transport in lateral decubitus Hospital Tetanus toxoid, IV line, lateral position, anxiolytic Mandatory observation 24 hrs Local Systemic Cobra Krait Viper Sea snake Swelling Local pain, swelling + - ++ - Blisters Local bleeding + - ++ - Necrosis Pain in regional nodes + + + - Vomiting + + + + Hypotension + + + -Clean dressing
  72. 72. Vomiting, diarrhoea Oozing Headache, thirst CompartmentMajor defect Abdominal pain Nonclotting Thick tongue syndrome Paraesthesiae Blood MyalgiaDebride Graft Fasciotomy Antivenom infusion 5- 15 vials Pooled secretions Neuroparalysis Retest blood Myoglobin damage 6 hrs. Suction Neostigmine test Intubation Positive No Clot Repeat Antivenom Renal failure Neostigmine Respiratory Paralysis Retest 6 hrs. Dialysis Clots Mechanical ventilation Observe 48-72 hrs.