Snake Bite Vch

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    Snake Bite

    Dr.Vemuri Chaitanya

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    Epidemiology

    > 5 million bites annually by venomous snakesworld wide

    With > 1,25,000 deaths

    Age : 1150 yrs

    Sex : males

    Mc site : lower limbs 40 %

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    Classification of snakes

    Colubridae

    Elapidae

    Viperidae

    Hydrophidae

    Most non venomoussnakes eg : grass snake

    Cobras, krait, mambas,

    coral snake American rattlesnake,

    Asian pitviper, Russelsviper, aders

    Sea Snake

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    Snake venom

    It is complex mixture ofenzymes, low.mol.wtpolypeptides,

    glycoproteins, metal ions.

    Component Action

    Serineproteases

    haemolysis

    Otherproteases

    haemolysis

    Phospholipase

    A2

    Myotoxic

    CardiotoxicNeurotoxic

    Increases

    vascularermeabilit

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    Component Action/effect

    Hyaluronidase Local tissue destruction

    Neurotoxins

    Alpha Bungarotoxin

    Cobrotoxin

    Post synaptic inhibition

    Beta bungarotoxin

    Crotoxin

    Pre synaptic inhibition

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    Poisonous Snakes

    Neurotoxiccobra,krait & coral

    Haemotoxicvipers

    Myotoxicsea snake

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    Common Indian venomous snakes

    ELAPIDAE Common CobraNaja Naja, Indian Cobra

    Common KraitBangarus Caeruleus

    VIPERIDAE Saw Scaled ViperEchis Carinatus

    Russells Viper Vipera Russelli

    OTHER SNAKES King CobraNaja Bangarus, Hamadryad Banded KraitBangarus Fasciatus

    Sea Snakes

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    Poisonous Non poisonous

    Head scales : small

    Large and opening / pitb/w eye & nostril (pit

    viper) Third labial touches eye

    and nostril shield (cobra)

    No pit or third labialtouches eye & nostrilshield( krait )

    large

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    Poisonous Non poisonous

    Fangs : hollow likehypodermic needles

    Teeth : 2 long fangs

    Tail : compressed

    Short and solid

    Several small teeth

    Not much compressed

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    Non poisonous snake

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    INDIAN COBRA COMMON KRAIT

    Neurotoxic NeurotoxicFatal period8 h Fatal period : 18 h

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    Indian cobra King cobra

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    Coral snake

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    Saw Scaled Viper Russels Viper

    (Echis Carinata) ( Vipera russeli )

    Venom: Vasculo & Venom: Vasculo & Haemato

    Haematotoxic toxic

    Fatal period : 3 days Fatal period : 5 days

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    Banded Krait Common Krait

    ( Bungarus Fasciatus )

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    Diagnosislook for fang marks

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    & Identify the snake

    Features of poisonous snakes

    Usually dull coloured (Brown, Black, Grey)

    Stout body with abruptly compressed and tapering tail

    Broad belly scales extending entire width of belly

    Small scales on triangular head

    Pit between eye and nostril

    Presence of hood with or without markings

    Presence of fangs

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    Clinical features

    Flushing, palpitations, sweating, anxiety & fearprominent features in any snake bite victim (even if snake is non-venomous )

    Specific features of venomous snakesdependupon type of snake and consists of local &systemic features of envenomation.

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    Grades of envenomation

    GRADE FEATURES

    Non-envenomated (dry)bites

    Presence of fang markswithout local / systemic

    reactionsMild envenomation Local swelling & pain

    without systemic reaction

    Moderate envenomation Extensive local effects withmin.sys.effects / mild localeffects with markedsys.effects , mild lab.abn

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    Grades of envenomation

    GRADE FEATURES

    Severe envenomation Extensive local effects &systemic effects & marked

    lab.abn

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    Bites by Elapids

    Generally cause minimal local effects Swelling, local pain & local necrosis ( cobra ) Descending paralysis, initially of muscles innervated by

    cranial nerves commencing with PTOSIS, DIPLOPIA,OPHTHALMOPLEGIA

    Numbness around lips & mouth, progressing topooling of secretions, bulbar paralysis & resp.failure

    Paradoxical respintercostal muscle paralysis Stomach pain ( Krait )submucosal hage in stomach Krait bitespresent in early morning with paralysis

    can be mistaken for STROKE .

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    Bites by Viperidae

    Severe local effectsas early as within 15 min of bite Extensive swellingspreading quickly to involve whole

    limb. Asso with blistering , necrosis & regional tender

    lymphadenopathy. Hemostatic abnpersistant ooze & bleeding from

    venepuncture sites, fang marks & later bleeding fromgums, epistaxis, petechiae, purpura & ecchymoses

    Abdominal tendernessgi / retroperitoneal bleed Passage of reddish / dark brown urine / diminishing /

    nil urine output.

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    Bites by Viperidae

    Lateralising neurological symptoms like asymmetricalpupilsintracranial bleed

    Hypotensionresulting from hypovolemia / directvasodilation

    Low back pain , indicative of early renal failure Muscle painrhabdomyolysis Parotid swelling, conj.edema, sub.conj.hage Renal failurerussels viper, hump nosed pit viper . Long term comp : hypopituitarism & cardiotoxicity Saw scaled viper doesnt cause renal failure generally

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    Hydrophid bites

    Stiffness, ache, tenderness in muscles

    Later, rhabdomyolysis, myoglobinuriaresulting in acute renal failure .

    FEATURE Russels Saw Hump

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    FEATURE

    Cobra Krait

    Russels

    viper

    Saw

    scaled

    viper

    Hump

    nosed

    viper

    Local pain /tissue damage

    YES NO YES YES YES

    Ptosis/Neurological signs

    YES YES YES NO NO

    Hemostatic abn NO NO YES YES YES

    Renal Comp NO NO YES NO YES

    Response toNeostigmine

    YES NO? NO? NO NO

    Response to ASV YES YES YES YES NO

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    First Aid- Do it R.I.G.H.T

    RReassure the patient . 70 % snake bitesnonvenomous species. Only 50 % of bites by

    venomous species actually envenomate the pt.

    IImmobilise in the same way as # limb. Usebandages / cloth to hold splints, not to block bloodsupply / apply pressure. Do not apply any compressionin the form of tight ligatures

    GHGet to the hospital immediately T- Tell the doctor of any systemic symptoms that

    manifest on way to the hosp

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    Traditional Methods to be

    DISCARDED

    Tourniquets traditionally used to stop venom flow. (increased risk of ischemia , loss of limb, necrosis,massive neurotoxic blockade when tourniquet is

    released, embolismviper , false sense of security ) Incision & Suctionincreases risk of severe bleeding as

    clotting mech is ineffective & infection . No venom isremoved by this method

    Washing the woundit increases the flow of venominto system by stimulating the lymphatic system.

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    Treatment protocol

    Attend toAIRWAY , BREATHING, CIRCULATION

    Tetanus toxoid

    Routine antibiotic is not necessary

    Identify the snake responsible

    All patients should be kept under observation for a minperiod of 24 hrs.

    Determine the exact time of bite Ask the victim as to what he was doing at the time of

    bite

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    investigations

    20 minute whole blood clotting testconsidered most reliable test of coagulation

    Single breath count

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    investigations

    Urine for RBCViper BiteHematuria,Proteinuria, Hemoglobinuria, Myoglobinuria

    ECGNormal, Bradycardia with ST elevationor depression, T inversion, QT prolongation

    ABGHypoxemia with Respiratory Acidosis,

    Metabolic / lactic Acidosis Chest X- rayNormal, Pulmonary Oedema,

    Intrapulmonary Hemorhages, Pleural Effusion

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    Monitor vital signs

    Observe every patient for minimum 24 hours

    Pulse, BP, Respiration

    Urine output

    Blood urea, Creatinine

    Bleeding tendency

    Local swelling

    Vomiting

    Diplopia, Ptosis, Muscle Weakness, Breathlessness

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    Anti Snake Venom

    ASV is prepared by hyperimmunising horsesagainst venoms of snake

    It neutralises the free, unbound venom & tosome extent also dissociates the bound toxin

    ASV is manufactured in India by the HaffkineCentral Research Institute, Kasauli & Serum

    Institute of India, Pune & both arePOLYVALENT.

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    1 ml of ASV neutralises

    Cobra0.6 mg

    Common krait0.45mg

    Russels viper0.6 mg Saw scaled viper0.45 mg

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    Indications

    As perW.H.O Guidelines ONLY if a pt devoleps one/ more of the following signs/symptoms ASV shouldbe administered :

    SYSTEMIC ENVENOMING

    Evidence of coagulopathy: detected by 20WBCT orvisible spontaneous systemic bleeding

    Evidence of neurotoxicity : ptosis, ext.ophthalmoplegia CVS abn : hypotension, shock, arrhythmias ARF Hemoglobinuria / myoglobinuria Persistant severe vomiting / abd.pain

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    LOCAL ENVENOMING :

    Local swelling > of involved limb

    Rapid extension of swelling Enlarged tender lymph nodes draining the bitten

    limb.

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    ASV administration

    NO ASV TEST DOSE MUST BEADMINISTERED .

    Recommended initial dosages are 100 ml( 10vials) of polyvalent ASV for adults & childrenbased on published research that russells viperinjects on an avg of 63 mg of venom.

    Our initial dose must be calculated to neutralizethe avg dose of venom injected.

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    Range of venom inj = 5mg147 mg

    Sugg ASV dose = 100 -250 ml

    Initial dose of 100 ml must be diluted in 100 mlof NS & given over 1 hour.

    Pt should be carefully monitored for 2 hrs.

    Local adm of ASV, near the bite siteineffective, painful, raises intracompartmentalpressure.SHOULD NOT BE DONE.

    Victim who arrives late ?

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    Victim who arrives late ?

    Often after several days , usually with ARF

    Are there any signs of current venom activity ?

    Perform 20WBCT & determine if anycoagulopathy is +, if + adm ASV.If - , treat ARFdialysis

    Neurotoxic envenominglook for ptosis, respfailure , + adm 1 dose of ASV , resp support

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    ASV reactions

    Pt should be monitored closely

    First sign of any one of the following :

    1. Utricaria 6. Vomiting 11.Bronchospasm

    2. Itching 7. Diarrhoea 12.Angioedema3. Fever 8. Abd.cramps

    4. Chills 9. Tachycardia

    5. Nausea 10. Hypotension

    Discontinue ASV & give 0.5 mg of 1 :1000 adrenalineIM

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    ASV reactions

    Long term protection :100 mg Hydrocortisone IV

    10 mg H1 Antihistaminic IVAfter 10 -15 min , pt not improved /worsened :

    give 2 nd dose of 0.5 mg of 1:1000 adrenaline

    IM Once pt has recovered , restart ASV slowly for

    10-15 min , close observation & later normally.

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    Repeat doses of ASV

    HEMATOTOXIC POISONING :

    20 WBCTabninitial dose given over 1 hr.

    Repeat 20WBCT after 6 hrs

    Abnanother dose to be given. Repeat samedose again.

    20WBCT & Repeat doses of ASVto becontinued on 6 hrly manner untill coagulation isrestored.

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    Repeat doses of ASV

    NEUROTOXIC POISONING :

    Assess the pt 1-2 hrs after the initial dose

    If symptoms persist / worsen , 2 nd dose whichis same as 1st dose is to be given & then ASVcan be discontinued.

    R l f N i i i N i

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    Role of Neostigmine in Neurotoxic

    poisoning

    Anticholinestrase & prolongs life of Ach - which canreverse resp.failure & neurotoxic symptoms ( postsynaptic )

    Neostigmine test : 1.5 -2.0 mg IM preceeded by 0.6 mgatropine IV

    Observe for 1 hr

    If victim responds , continue 0.5 mg Neostigmine IM

    hrly with 0.6 mg Atropine IV over 8 hrs If no improvement in symptoms after 1 hr ,

    stop Neostigmine

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    Supportive Therapy

    RESPIRATORY FAILURE :

    ABG

    Intubate & Ventilate

    Neostigmine & Atropine

    HYPOTENSION :

    Plasma expanders Dopamine 2.55 micrograms/Kg/min

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    Supportive Therapy

    PERSISTANT / SEVERE BLEEDING :

    Majoritytimely use of ASV will stop sys.bleed

    ASV + Blood Transfusion

    RENAL FAILURE

    Hemodialysis / peritoneal dialysis

    COMPARTMENT SYNDROME :

    Fasciotomy

    SURGICAL DEBRIDEMENT OF WOUND

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    Thank You