Bites and Stings

1. Bites and Stings Dr Pavan .M MD(A &EM), VMKVMC

2. Epidemiology 3 million bites and 1,50,000 deaths/year from venomous snake worldwide. Bites highest in temperate and tropical regions. 3000 species of snakes, out of them only 10-15% of snakes are venomous 97% of all snake bites are on the extremities

3. Common Snakes - INDIA Cobras(nagraj) –Naja naja,N.oxiana, N.kabuthia Neurotoxicity usually predominates.

4. Common krait(karayat)-Bungarus caeruleus

5. Russell’s viper(kander)-Daboia russelii Heat-sensing facial pits (hence the name "pit vipers").

6. Echis.carinatus(afai)-Saw scaled viper

7. Features of poisonous & non-poisonous snakes Non Poisonous Snakes Head - RoundedFangs - Not presentPupils - RoundedAnal Plate - Double row Bite Mark - Row of small teeth. Poisonous Snakes Head – Triangle Fangs – Present Pupils - Elliptical pupil Anal Plate - Single row Bite Mark - Fang Mark Approximately 2500 different species of snakes are known. Approximately

8. Snake Venom Snake venom is highly modified saliva

9. Mechanism of toxicity Cytotoxic effects on tissues Hemotoxic Neurotoxic Systemic effects. Toxic dose. The potency of the venom and the amount of venom injected vary considerably. 20% of all strikes are "dry"

10. Snake Venom, Necrosis Proteolytic enzymeshave a trypsin-like activity. Hyaluronidase splits acidic mucopolysaccharides and promotes the distribution of venom in the extracellular matrix of connective tissue. Phospholipases A2-break down membrane phospholipids -causes cellular membrane damage

11. Contd.. All these enzymes cause oedema, blister formation and local tissue necrosis

12. Snake Venom ,Paralysis Blocks the stimulus transmission from nerve cell to muscle and cause paralysis Does not penetrate the blood-brain barrier

14. Contd.. Postsynaptic effects are reversible with antivenom and neostigmine. Presynaptic nerve terminal, e.g. beta-bungarotoxin and here neostigmine will not be effective.

15. Snake venom, Hemorrhages Activate prothrombin (e.g. ecarin from Echis carinatus) Effect on fibrinogen and convert it into fibrin -thrombin-like activity, such as crotalase (rattlesnake venom) Activate factor 5, factor 10 , Protein C Activate or inhibit platelet aggregation Haemmorhagins- cause endothelial damage

17. Clinical syndromic approachSyndrome 1 Local envenoming (swelling etc) with bleeding/clotting disturbances VIPERIDAE

18. Syndrome 2 Ptosis, external opthalmoplegia, facial paralysis etc and dark brown urine=Russell's viper, Sri Lanka and South India

19. Syndrome 3 Local envenoming (swelling etc) with paralysis=Cobra or king cobra

20. Syndrome 4 Paralysis with minimal or no local envenoming Krait, Sea snake

21. Syndrome 5 Paralysis with dark brown urine and renal failure: Russle viper

22. Grade 0 No evidence of envenomation Suspected snake bite Fang mark may be present Pain and 1 inch edema & erythema No systemic signs- first 12 hours No lab changes

23. Grade 1 Minimal envenomation Fang wound & moderate pain present 1-5 inches of edema or erythema No systemic involvement in present after 12 hours No lab changes

24. Grade 2 • Moderate envenomation • Severe pain • Edema spreading towards trunk • Petechiae and ecchymosis limited area • Nausea,vomiting,giddiness • Mild temperature

25. Grade 3 Severe envenomation Within 12 hours edema spreads to the extremities and part of trunk. Petechiae and ecchymosis may be generalized Tachycardia Hypotension Subnormal temperature

26. Grade 4 Envenomation very severe Sudden pain rapidly Progressive swelling which leads to ecchymosis all over trunk Bleb formation and necrosis

27. Grade 4 contd… Systemic manifestations within 15 min after the bite Weak pulse,N&V,vertigo Convulsions, coma

28. What investigation to do? CBC RFT Coagulation studies Blood grouping & cross matching Sr.electrolytes Urinalysis

29. 20 min whole blood clotting time A few milliliters of fresh blood are placed in a new, plain glass receptacle (e.g., test tube) and left undisturbed for 20 min.

30. Contd… The tube is then tipped once to 45° to determine whether a clot has formed. If not, coagulopathy is diagnosed

31. Hess's test Blow up a blood pressure cuff to 80 mm Hg and leave it on for 5 minutes. If a crop of purpuric spots appears below the cuff, the test is positive.

32. First Aid First Aid

33. Donts • No Tornique • No Suction apparatus to be used(Sawyers) • Do not run • No role of Ice application

34. ASV When to use ASV? How much to use? What if a reaction occurs? When to stop ASV?

35. When to use ASV Hemostatic abnormalities(lab and clinical) Progressive local findings Neurotoxicity Systemic signs and symptoms Generalised rhabdomyolysis

36. Polyvalent antivenin Manufactured by hyper immunizing horses against venoms of four standard snakes Cobra (naja naja) Krait (B.caerulus) Russel’s viper(V.russelli) Saw scaled viper(Echis carinatus)

37. Contd.. Lyophilised form: stored in a cool dark place & may last for 5 years Liquid form: has to be stored at 4°c with much shorter life span Each 1ml of reconstituted serum neutralise0.6 mg of naja naja0.45 mg of Bungarus caerulus0.6 mg of V.russelli0.45 mg of Echis carinatus

38. Guide for initial dose of antivenin

39. Dose in Paediatric • Same as adult as the amount of venom does not change-hence the dose of antivenom should be the same • Only the dilution changes

40. Skin testing- Done if patient is stable and time available 0.02ml of 1:100 solution of serum is injected sc A positive reaction occurs within 5 to 30 mins. Appearance of wheal & surrounding erythema

41. What to do in case of anaphylactic reaction to ASV Adrenaline 0.5 to 1ml IM If hypotension,severe bronchospasm or laryngeal edema give 0.5 ml of adrenaline diluted in 20 ml of isotonic saline over 20 mins iv.

42. contd.. A histamine anti H1 blocker-chlorpheniramine maleate-10 mg IV Pyrogenic reactions-antipyretics Late reactions-respond to CPM-2 mg, 6 hrly or oral prednisolone-5 mg 6 hrly

43. What if the patient needs ASV following reaction Dose should be further diluted in isotonic saline and restarted as soon as possible. Concomitant IV infusion of epinephrine may be required to hold allergic sequelae at bay while further antivenom is administered

44. When to stop using ASV Bleeding subsides Lab values returns to baseline Signs of neurotoxicity reverses Local effects halts progression

45. Supportive treatment Anticholineesterase have variable but useful role Trial Atropine sulphate 0.6 mg Edrophonium chloride 10 mg IV (or) Neostigmine: 1.5–2.0 mg IM (children, 0.025–0.08 mg/kg)

46. Contd.. If objective improvement is evident at 5 min continue neostigmine at a dose of 0.5 mg (children, 0.01 mg/kg) every 30 min as needed with atropine by continuous infusion of 0.6 mg over 8 h -children, 0.02 mg/kg over 8 h

47. Contd Hypotension Administration of crystalloid (20–40 mL/kg) Trial of 5% albumin (10– 20mL/kg) CVP guided fluids Inotropic support and invasive monitoring

48. Contd.. Oliguria & renal failure- fluids,diuretics, dopamine no response-fluid restriction- Dialysis Local infection- TT,antibiotics Haemostatic disturbances-FFP,fresh whole blood,cryoprecipitates

49. Cobra spit opthalmia Topical antimicrobial 0.1% adrenaline relieves pain No need for ASV

50. Compartment syndrome If signs of compartment syndrome are present and compartment pressure > 30 mm Hg: Elevate limb Administer Mannitol 1-2 g/kg IV over 30 min Simultaneously administer additional antivenom, 4-6 vials IV over 60 min If elevated compartment pressure persists another 60 min, consider fasciotomy