Snake Bite management

49
SNAKE BITE Dr.A. Sridhar Ist year pg

description

A clear and comphrensive discussion of snake bite and its management.

Transcript of Snake Bite management

Page 1: Snake Bite management

SNAKE BITE

Dr.A. Sridhar Ist year pg

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Snake bite• 3000 species of snakes, out of them only 10-15%

of snakes are venomous• 300 species are in India• .INDIAN snakes ranges from

Wormsnakes—10cm to

KING COBRA—6M.

.70% bites are from non-venomous species,5O%bites by venomous species doesn’t cause envenomation.{dry bites}

.

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Important species in INDIA

• Cobras(nagraj) –Naja naja,N.oxiana,

N.kabuthia

• Common krait(karayat)-Bungarus

caeruleus

• Russell’s viper(kander)-Daboia russelii

• Saw scaled viper - Echis.carinatus(afai)

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COBRA

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COMMON KRAIT

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RUSSEL’S VIPER

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ECHIS CARINATUS

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Approximately 2500 different species of snakes are known. Approximately

Poisonous Snakes Head – Triangle Fangs – Present Pupils - Elliptical pupil Anal Plate - Single row Bite Mark - Fang Mark Non Poisonous Snakes Head - Rounded

Fangs - Not presentPupils - RoundedAnal Plate - Double row Bite Mark - Row of small teeth.

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• How to identify a dead snake if it is brought to the ER

• Carefully handle the snake because even dead snake fangs can transmit poison

• Viper fangs are anterior,lengthy & loose• Elapidae have short,thick anterior fangs

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SNAKE VENOM

• Snakes that inject venom use glands, which are actually modified salivary glands.

• Venom is a modified form of saliva and probably evolved to aid in chemical digestion.

• Varying degrees of toxicity also make it useful in killing prey.

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VENOM APPARATUS

• The venom glands of elapidae & viperidae are situated behind the eyes & surrounded by compressor muscles

• Venom duct opens withinin the sheath at the base of the fang

• Venom is conducted to fang tip through a canal

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Venom properties

• Contain 20 or more components• >90% of the dry Wt of venom is protein- in

the form of enzymes,non enzymatic polypeptide toxins & non toxic proteins .

• Most venoms contain L-aminoacid oxidase, phosphomono & diesterases, 5-nucleotidase,DNAase,NAD-nucleosidase, phospholipaseA2 & peptidases

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Contd

• Phospholipase A2(lecithinase) damages

mitochondria,RBCs,WBCs,platelets, peripheral

nerve endings,skeletal muscles, vascular

endothelium & other membranes, produces

presynaptic neurotoxic activity & release of

histamine

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Contd

• Proteolytic enzymes(endopeptidases &

hydrolases) are responsible for local changes

in vascular permeability leading to

edema,blistering & bruising & to necrosis

• Hyaluronidase promotes the spread of venom

through tissues

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POLYPEPTIDE TOXINS• Postsynaptic () neurotoxins such as -

bungarotoxin and cobrotoxin,are bind to acetylcholine receptors at the motor endplate

• Presynaptic(β)neurotoxins such as β- bungarotoxin,crotoxin,& taipoxin release acetylcholine at the nerve endings at NMJs & then damage the endings,preventing furthur release of the transmitter

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PHARMACOLOGY

• Absorbed through the blood & lymphatics• Spitting cobra- venom can be absorbed

through the intact cornea• Most venoms are concentrated in the

kidneys & some are eliminated in urine• Bungarotoxin are tightly bound at the NMJ• Most venoms donot cross the blood brain

barrier

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Clinical features

• When venom not injected :• Anxious people-hyperventilation-stiffness,

tetany of hands and feet, dizzines• Vasovagal shock-few• First aid measures-constriction bands-pain,

swelling, congestion

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When venom injected

• Nausea & vomiting are common early symptoms

of systemic envenoming

• Early syncope,vomiting,colic,diarrhoea,

angioedema & wheezing may occur

• Local pain & bleeding from the fang

punctures,swelling, bruising ,lymphangitis &

regional lymphadenopathy

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Bites by cobra

• More of neurotoxic ,local effects• Neurotoxic-• Ptosis• Ciliary mussle paralysis• Partial/total opthalmoplegia• Broken neck sign• Bulbar palsy• Locked-in syndrome

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Bites by kraits

• Most poisonous snake in india• Local urticaria-rare• Delayed neuropathy of affected limb-rare• Bulbar palsy• Respiratory paralysis• Asphyxic cardiac arrest• No local pain or tissue damage

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Bites by Viper

• cytotoxic & hemotoxic

• Severe local effects• Rapid devlopment of DIC• Immediate shock• Neuroparalysis-ptosis,respiratory paralysis• Sheehans syndrome

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• Pain & tenderness in regional lymph nodes with bruising of overlying tissues & lymphangitic lines

• Bruising ,blistering & necrosis may appear in the next few days

• Compartment syn may develop

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Contd

• Haemostatic abnormalities are characteristic of envenoming by viperidae

• Hypotension & shock are common• Myocardial involvement may be present• Early collapse after bites has been attributed

to coronary & pulmonary thromboembolism

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Contd

• Oliguria & loin pain indicate renal ischaemia

• Generalised rhabdomyolysis

• myoglobinuria

• Renal failure is a common mode of death

• Sawscaled viper doesn’t causeneurological or

renal complications

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ecchymosis

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Necrosis Bite marks

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Bites by Sea snake

• Both myotoxic&haematotoxic

• Trismus is common

• Between 30mins to 3.5hrs,generalized

aching,stiffness & tenderness of the muscles.

• Later there is generalized flaccid paralysis

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Contd

• Myoglobinuria appears 3 to 8hrs after the bite

• Myoglobin & potassium released from

damaged skeletal muscle can cause renal

failure

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Investigations

• CBC • RFT • Coagulation studies • Blood grouping & cross matching• Sr.electrolytes• Urinalysis

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Contd

• 20 min whole blood clotting test• Sr.creatine kinase,myoglobin & potassium

levels• ECG-sinus bradycardia,ST-T changes,

various degrees of AV block & hyperkalaemic changes

• Immunodiagnosis

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MANAGMENT• “Do it R.I.G.H.T.” • It consists of the following: • R. = Reassure the patient. • I = Immobilise in the same way as a fractured

limb. Use bandages or cloth to hold the splints, Do not apply ligatures

• G. H. = Get to Hospital Immediately.. • T= Tell the doctor of any systemic symptoms

such as ptosis that manifest on the way to hospital.

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Antivenom ,antivenin,antivenene & antisnake serum

• POLYVALENT ANTIVENINS

• MONOVALENT ANTIVENINS: Highly effective

against a particular species & are available

only in some countries based on the

epidemicity of specific snakes

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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)

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• 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,2Yrs

• Each 1ml of reconstituted serum neutralise

• 0.6 mg of naja naja• 0.45 mg of Bungarus caerulus• 0.6 mg of V.russelli• 0.45 mg of Echis carinatus

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Approximate initial dose

• Common krait-100ml

• Russell’viper- 100ml

• Indian cobra-100ml

• Echis spp-100ml

• Given at the rate of 2ml/min IV push or as iv

infusion with 5ml/kg of isotonic fluid ,all ASV has2be administered in 1hr

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• ROUTE OF ADMINISTRATION--IV

• WHY NOT IM?

• WHEN TO GIVE IM?

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Indications for antivenom

• Local 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)

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Indications for antivenom

• Local envenoming• Rapid extension of swelling (for example

beyond the wrist or ankle within a few hours of bites on the hands or feet)

• Development of an enlarged tender lymph node draining the bitten limb

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Indications for antivenom

• Systemic envenoming• • Haemostatic abnormalities: spontaneous

systemic bleeding (clinical), coagulopathy (20WBCT or other laboratory) or thrombocytopenia (<100 x109/litre) (laboratory)

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Indications for antivenom

• • Neurotoxic signs: ptosis, external ophthalmoplegia, paralysis etc (clinical)

• • Cardiovascular abnormalities: hypotension, shock, cardiac arrhythmia (clinical), abnormal ECG

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Indications for antivenom

• • Acute renal failure: oliguria/anuria (clinical), rising blood creatinine/ urea

• • (Haemoglobin-/myoglobin-uria:) dark brown urine (clinical), urine dipsticks, other evidence of intravascular haemolysis or generalised rhabdomyolysis (muscle aches and pains, hyperkalaemia)

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Treatment of antivenom reactions

• Early (anaphylactic) reactions,occur within 10-180

min

Adrenaline 0.5 mg ,1:1000,IM

. If hypotension,severe bronchospasm or laryngeal

edema give 0.5 mg,1:10000of adrenaline IV

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Contd

• A histamine anti H1 blocker-chlorphenira- mine

maleate-10 mg IV

• Pyrogenic reactions-occurs 1-2hrs after treatment, give

antipyretics

• Late reactions-occur 1-12daysafter treatment respond

to CPM-2 mg, 6 hrly or oral prednisolone-5 mg 6 hrly

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Contd

• If patient goes for airway obstruction &

respiratory paralysis

MECHANICALVENTILATION

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Supportive treatment

• First do NEOSTIGMINE TEST• IF VICTIM RESPONDS CONTINUE WITH 0.5 mg

of neostigmine IM ,half hourly plus 0.6mg of atropine IV over an 8hr period by continuous infusion

• If there is no improvement after 1hr neostigmine should be stopped

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Contd

• Hypotension & shock-a plasma expander, dopamine.

• Oliguria & renal failure-fluids,diuretics, dopamine-if no response,fluid restriction, dialysis

• Local infection-TT,antibiotics

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Contd

• Intracompartmental syn & fasciotomy

• Haemostatic disturbances-FFP,fresh whole blood,cryoprecipitates

• Treatment of snake venom ophthalmia- topical antimicrobial,0.1% adrenaline relieves pain

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