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by: lokeshagchopra

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1 : Venomous snakebite Dr. Lokesh A.C
2 : Venomous snakes 5 major snake families: Atractaspididae: Burrowing asps , Stiletto ,Natal black Colubridae: Boomslang , Australian brown tree snake Viperidae: Russell’s viper , Euro. addler Subfamily Crotalidae: Pit vipers, Rattle snakes, Moccasins Elapidae: Cobras, Coral snakes, Krait, Mamba, Aust. snakes Hydrophidae: Sea snakes
3 : Scenario in India Indian subcont. home to 230+ species of snakes; about 50 are venomous 4 considered: most snake bite related deaths These are Elapidae: Cobras, Kraits Viperidae: Russell’s viper, Saw-scaled viper° Few deaths related to sea snakes, Hump nosed and other pit vipers Snake identification not possible*/unreliable No monovalent antivenom available
4 : (L)Saw scaled viper (T)Naja Naja (RTop)Com. Krait (RBot)Russell’s viper
5 : Rare venomous bites Very, very rarely by King cobra Rarely in South India by Bamboo Pit viper Sometimes in South India by Hump-nosed Pit  viper
6 : Profile: Saw scaled/Russell’s viper Saw-scaled viper constitutes about 80% of the total venomous bites in some geographical areas. Usu. severe pain, quick onset of local swelling and tender regional lymph nodes Bleeding from fang marks, blistering and necrosis well established <24h Bleeding may be obvious from gums, nose, GIT, genitourinary system, sometimes tissue planes. Hypovolaemia and shock may be observed.ECG changes also. Russell’s viper bites are also known to cause acute infarction of pituatary with adrenal insufficiency(panhypopituatarism).Also Rhabdomyolysis ,ARF are seen. Presynaptic neuroparalysis in South-Indian Russell’s
7 : Profile:Cobra Often Sev. Local reaction, pain, blister formation & tissue necrosis. Postsynaptic neurotoxin: responds to Achase enzyme inhibitors Neuroparalysis:- 6-12hr; b/l ptosis,palatal muscles, tongue, jaw, larynx, deglutition, neck & respiration later gen paralysis. Preparalytic stage: Vomiting, blurred vision, drowsiness, heaviness of eyes & tingling sensation around mouth
8 : Profile: Common Krait Bites are most often nocturnal, indoor, unprovoked and painless Systemic symptoms and abdominal pain are the distinctive features of a Krait envenomation, along with hypokalemia. The neurotoxins in the Krait venom are prominently pre-synaptic and prevent release of acetylcholine at the neuromuscular junctions. Krait bites akin to cobra bites except the absence of local pain, swelling and necrosis Preparalytic stage is marked by rapid onset of paralysis Time to toxicity is usu 4-12h
9 : Profile: Sea snakes A distinctive trait of a sea snake is a flat, paddle-shaped tail that land snakes do not possess. Venom is 2-10 times more toxic than that of the cobra, however~75% bites fail Don’t produce local tissue necrosis Variable local pain Hallmark: Gen. muscle pain and stiffness Envenomed pts develop rhabdomyolysis, myoglobinaemia, myoglobinuria, ARF & hyperkalaemia Also neurotoxicity known. Time to toxicity: 2-4h(unlikely after 6-8h) The yellow-lipped sea krait is a timid but highly venomous sea snake common throughout Indo-Pacific oceanic waters.
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11 : Significant envenoming occurs in ~50% However even no envenomation occurs, symptoms attributable to fear/ anxiety develop. Pain,cold clamy skin, palpitations, vaso vagal shock are common without significant envenomation.
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13 : 40-70 mm or 55-70 mmhg Full immobilisation crucial Start distally,move proximal Include splint Not too tight Not suitable in Indian context
14 : Hospital care Rapidly assess and resuscitate -airway and resp movements -circulation/B.P. -Level of consciousness(risk of asp) Detailed clinical assessment & special diagnosis History(what, when and where) -urine :output, dark colored -gen pain, stiffness of Muscles, trismus, tenderness -bleeding, double vision, ptosis, head lift
15 : Examination: Local: Extent of swelling & tenderness(M).Palpate LN, note ecchymosis Early signs of necrosis may include blistering, demarcated darkening (easily confused with bruising) or paleness of the skin, loss of sensation and a smell of putrefaction Tensely edematous,cold immobile limb with no peripheral pulse: intravascular thrombosis/ compartment syndrome General: B.P./pulse/heart rate-hypotension/circulatory failure Examine skin/mucous membrane/conjunctiva/gingival sulci/nose Abd tenderness/loin pain Lateralising neuro signs/asy pupils/convulsion/impaired consciousness
16 : Neuro: Upper eyelids retract on up gaze? Eye movts? size &reaction of pupils? Open mouth & protrude tongue? Cranial nerves? Head lift? broken neck sign? Paradoxical resp? Gen rhabdomyolysis: Neck, trunk & prox parts of limbs Myoglobinuria(3hr) Pregnancy: Monitor FHS/contractions, vaginal bleeding Lactation to be continued Special diagnosis: If snake can be identified
17 : INVESTIGATIONS: 20 minute whole blood clotting test (20WBCT):Every 30 minutes from admission for three hours and then hourly after that. If incoagulable blood is discovered, the 6 hourly cycle will then be adopted to test for the requirement for repeat doses of ASV. Haemoglobin concentration/haematocrit:ˆ Capillary permeability ? bleed/hemolysis Platelet count White blood cell count Blood film: Fragmented RBC Biochemical abnormalities: Bl.urea, S.creatinine, S. potassium Muscle: CPK/aldolase ABG & pH(Avoid in coaugulapaty):Resp failure Urine examination: Hb/Mb/red cell casts/massive proteinuria ECG/CXR/doppler studies/USG
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19 : Polyvalent antivenom Same dose for adults and children Each ml of polyvalent anti-snake venom can neutralize 0.6mg of Cobra, 0.6mg of Russell’s viper, 0.45mg of Krait and 0.45mg of Saw-scaled viper venom NO ASV TEST DOSE MUST BE ADMINISTERED! NO LOCAL ASV!
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21 : ASV reactions: usually more than 20%, develop a reaction either early(within a few hours) or late (5 days or more) after being given antivenom. Early anaphylactic reactions: Usually within 10-180 minutes of starting antivenom, itch (often over the scalp), urticaria, dry cough, fever, nausea, vomiting, abdominal colic, diarrhoea and tachycardia. A minority may develop severe life-threatening anaphylaxis: hypotension, bronchospasm and angio-oedema. If the patient develops an acute reaction to antivenom, the infusion should be temporarily stopped and the reaction immediately treated with IM epinephrine and IV antihistamine and steroids Not truly “allergic”. Complement activation or direct stimulation of mast cells or basophils by antivenom protein are more likely.
22 : Prevention of ASV reaction: Prophylactic regimes*
23 : Dose of ASV: To neutralize avg venom injected Observe for response/monitor pt: Spon bleed/20wbct Neurotoxicity may improve in 30 min(usu sev hrs);if worsens in 1 hr repeat dose of ASV; if no improvement in 2 hrs repeat dose Active hemolysis/rhabdomyolysis usu take hrs to respond:urine If coagulopathy continues after 6hrs, rpt ASV.Again observe and repeat 20WBCT 6hrs later to know if further ASV is reqired(final dose)
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25 : The following conservative measures are suggested whenever necessary: Neurotoxic envenoming with respiratory paralysis: Assisted ventilation. Anticholinesterases should always be tried. Haemostatic abnormalities Strict bed rest to avoid even minor trauma; transfusion of clotting factors and platelets; ideally, fresh frozen plasma and cryoprecipitate with platelet concentrates or, if these are not available, fresh whole blood. Intramuscular injections should be avoided. Shock, myocardial damage: Hypovolaemia should be corrected with colloid/crystalloids, controlled by observation of the central venous pressure. Ancillary pressor drugs (dopamine) may also be needed. Patients with hypotension associated with bradycardia should be treated with atropine.
26 : Renal failure: Conservative treatment or dialysis. Dark brown urine (myoglobinuria or haemoglobinuria): Correct hypovolaemia and acidosis and consider a single infusion of mannitol. Severe local envenoming: Local necrosis, intracompartmental syndromes and even thrombosis of major vessels is more likely in patients who cannot be treated with antivenom. Surgical intervention may be needed but the risks of surgery in a patient with consumption coagulopathy, thrombocytopenia and enhanced fibrinolysis must be balanced against the lifethreatening complications of local envenoming. Prophylactic broad spectrum antimicrobial treatment is justified
27 : General care: Min 24 hr stay Monitor pt with respect to vitals, bleeding tendency & sys envenomation, during ASV use Use of analgesics Application of dry sterile dressings Splinting of extremity with padding between digits Elevate limb once ASV is initiated TT vaccination Prophylactic antibiotic* Muscle compartment syndrome:Mannitol Wound care(once coagulation’s restored) Physical therapy(loss of func. probably >30%) Discharge warnings

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