snake bite ,bee sting and scorpian bite

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Snake Bite ,Bee sting and Scorpian Bite. Dr Pavan .M MD(A &EM), VMKVMC. 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 - PowerPoint PPT Presentation

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Dr Pavan .M MD(A &EM), VMKVMC

Epidemiology3 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 venomous97% of all snake bites are on the

extremities

Common Snakes - INDIA

Cobras(nagraj) –Naja naja,N.oxiana,

N.kabuthia

Neurotoxicity usually

predominates.

Common krait(karayat)-Bungarus caeruleus

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

Echis.carinatus(afai)-Saw scaled viper

                                                              

              

 

              Approximately 2500 different species of snakes are known. Approximately

Non Poisonous Snakes Head - Rounded

Fangs - 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  

Snake Venom

Snake venom is highly modified saliva

Mechanism of toxicityCytotoxic effects on tissuesHemotoxicNeurotoxicSystemic effects.Toxic dose. The potency of the venom

and the amount of venom injected vary considerably.

20% of all strikes are "dry" in which no venom is injected.

Snake Venom, Necrosis Proteolytic enzymes have 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

Contd..all these enzymes cause oedema,

blister formation and local tissue necrosis

Snake Venom ,Paralysis

block the stimulus transmission from nerve cell to muscle and cause paralysisdoes not penetrate the blood-brain barrier

Contd..postsynaptic effects are reversible with

antivenom and neostigmine.presynaptic nerve terminal, e.g. beta-

bungarotoxin and here neostigmine will not be effective.

Snake venom, Hemorrhagesactivate 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 CActivate or inhibit platelet aggregationHaemmorhagins- cause endothelial

damage

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

Syndrome 2

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

Syndrome 3 Local envenoming (swelling etc) with

paralysis=Cobra or king cobra

Syndrome 4

Paralysis with minimal or no local envenoming

Krait, Sea snake

Syndrome 5

Paralysis with dark brown urine and renal failure: Russle viper

Grade 0No evidence of envenomationSuspected snake biteFang mark may be presentPain and 1 inch edema & erythemaNo systemic signs- first 12 hoursNo lab changes

Grade 1Minimal envenomationSnake bite suspectedFang wound & moderate pain present1-5 inches of edema or erythemaNo systemic involvement in present after 12

hoursNo lab changes

Grade 3Severe envenomationWithin 12 hours edema spreads to the

extremities and part of trunk.Petechiae and ecchymosis may be

generalizedTachycardiaHypotensionSubnormal temperature

Grade 4Envenomation very severeSudden pain rapidlyProgressive swelling which leads to

ecchymosis all over trunk Bleb formation and necrosis

Grade 4 contd…Systemic manifestations within 15 min after

the bite.Nausea,vomitings,vertigo,Numbness,tingling lips and face, muscle

fasciculations,urinary incontinence,Weak pulseConvulsions, coma

What investigation to do?CBC RFT Coagulation studies Blood grouping & cross matchingSr.electrolytesUrinalysis

20 min whole blood clotting timeA few milliliters of fresh blood are placed in a

new, plain glass receptacle (e.g., test tube) and left undisturbed for 20 min.

Contd…The tube is then tipped once to 45° to

determine whether a clot has formed. If not, coagulopathy is diagnosed

Hess's testBlow 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.

First AidFirst Aid

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

When to use ASVHemostatic abnormalities(lab and clinical)progressive local findings Neurotoxicity Systemic signs and symptomsGeneralised rhabdomyolysis

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)

Contd..Lyophilised form: stored in a cool

dark place & may last for 5 yearsLiquid form: has to be stored at 4°c

with much shorter life spanEach 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

Guide for initial dose of antivenin

Grade Amount of

Antivenin Route

0 None None

1 None None

2 5 vials IV 1:10 dilutions

3 5-10 vials IV 1:10 dilutions

4 10-20 vials IV 1:10 dilutions

Skin testing- Done if patient is stable and time available0.02ml of 1:100 solution of serum is

injected sc

A positive reaction occurs within 5 to 30 mins.

Appearance of wheal & surrounding erythema

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.

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

What if the patient needs ASV following reactiondose 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

Serum SicknessCharacterised by fever, chills, urticaria,

myalgias, arthralgias, and possibly renal or neurologic dysfunction developing 1–2 weeks after antivenom administration

systemic glucocorticoids (e.g., oral prednisone, 1–2 mg/kg daily) until all findings resolve

dose is tapered over 1–2 weeks. Oral antihistamines (e.g., diphenhydramine in standard doses) provide additional relief of symptoms

When to stop using ASVBleeding subsidesLab values returns to baselineSigns of neurotoxicity reversesLocal effects halts progression

Supportive treatmentAnticholineesterase have variable but useful role

TrialAtropine sulphate 0.6 mgEdrophonium chloride 10 mg IV (or)

Neostigmine: 1.5–2.0 mg IM (children, 0.025–0.08 mg/kg)

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

Contd Hypotension

administration of crystalloid (20–40 mL/kg)

a trial of 5% albumin (10– 20mL/kg)

CVP guided fluids

Inotropic support and invasive monitoring

Contd..

Oliguria & renal failure- fluids,diuretics, dopamine

no response-fluid restriction, Dialysis

Local infection- TT,antibiotics

Haemostatic disturbances-FFP,fresh whole blood,cryoprecipitates

Cobra spit opthalmiatopical antimicrobial0.1% adrenaline relieves painNo need for ASV

Compartment syndrome If signs of compartment syndrome are

present and compartment pressure > 30 mm Hg:

Elevate limbAdminister Mannitol 1-2 g/kg IV over 30

minSimultaneously administer additional

antivenom, 4-6 vials IV over 60 min If elevated compartment pressure persists

another 60 min, consider fasciotomy

Bee StingHoney bee belong Family- Hymenoptera Sub Family-Apidaeonly the females have adapted a stinger from the

ovipositor on the posterior aspect of the abdomen

VenomHistamine.Melittina –membrane active polypeptide that can

cause degranulation of basophils and mast cells, constitutes more than 50 percent of the dry weight of bee venom

Venom commonly causes pain, slight erythema, edema, and pruritus at the sting site

PresentationsLocal reactionToxic manifestation and anaphylaxisDelayed reaction –Serum sickness

Treatment

Immediate removal is the important principle and the method of removal is irrelevant.

sting site should be washed thoroughly with soap and water to minimize the possibility of infection.

Intermittent ice packs at the site- diminish swelling and delay the absorption of venom while limiting edema.

Oral antihistamines and analgesics may limit discomfort and pruritus.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can be effective in relieving pain

Severe systemic reactionEpinephrine 0.3 to 0.5 mg (0.3 to 0.5 mL of

1:1000 concentration) in adults and 0.01 mg/kg in children (never more than 0.3 mg).

Injected IM and the injection site massaged to hasten absorption

If hypotension,severe bronchospasm or laryngeal edema give 0.5 ml of adrenaline diluted in 20 ml of isotonic saline over 20 mins

Observation for 24 hours in ICU

Contd…Parenteral antihistamines (diphenhydramine 25

to 50 mg IV, IM, or PO) and H2-receptor antagonists (ranitidine 50 mg IV)

Steroids (methylprednisolone 125 mg) -to limit ongoing urticaria and edema and may potentiate the effects of other measures.

Bronchospasm is treated with -agonist

nebulization.

Contd..Hypotension -massive crystalloid infusion, and central

venous pressure monitoring may be helpful in these patients.

-Persistent hypotension require dopamine. -If dopamine is ineffective, an intravenous

infusion of epinephrine can be used

Preventive CareEvery patient who has had a systemic reaction -

insect sting kit containing premeasured epinephrine and be carefully instructed in its use.

patient must inject the epinephrine at the first sign of a systemic reaction.

Medic alert tag

Scorpion sting- C. exilicauda Scorpions have a world-wide distribution.

Highly toxic species are found in the Middle East, India, North Africa, South America, Mexico, and the Caribbean island of Trinidad.

Mechanism of actionVenom can open neuronal sodium channels and

cause prolonged and excessive depolarization

Symptoms and signsomatic and autonomic nerves may be affected

Initial pain and paresthesia at the stung extremity that becomes generalised

Cranial nerve- abnormal roving eye movements, blurred vision, pharyngeal muscle incoordination and drooling and respiratory compromise

Contd…Excessive motor activity

Nausea, vomiting, tachycardia, and severe agitation can also be present.

Cardiac dysfunction, pulmonary edema, pancreatitis, bleeding disorders, skin necrosis, and occasionally death can occur

TreatmentPain Management• Ice pack• Immobilization of limb• Local anaesthetics are better than opiates

Tetanus prophylaxis, wound care and antibiotics

Benzodizepines for motor activity.

Contd..Stabilize Airway Breathing and Circulation

Hyperdynamic circulation• always combination of alpha blocker with beta blocker to

prevent unopposed alpha action causing tachycardia• Nitrates for Hypertension/MI

Contd..Hypodynamic Circulation:• CVP guided fluids• Decrease preload with furosemide (not hypovolumic)• Reduction of afterload improves outcome-Prazosin,

nitroprusside, hydralizine, ACE inhibitor

Dobutamine is the best inotrope, avoid Dopamine

Noradrenaline can be used

Newer modalityInsulin has shown to improve cardiopulmonary status in

case of scorpion envenomation

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