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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 Wormsnakes10cm to KING COBRA6M.
.70% bites are from non-venomous species,5O%bites by venomous species doesnt cause envenomation.{dry bites}
COBRA
COMMON KRAIT
RUSSELS VIPER
ECHIS CARINATUS
Poisonous Snakes
Head Triangle Fangs Present Pupils - Elliptical pupil Anal Plate - Single row Bite Mark - Fang Mark
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.
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
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, 5nucleotidase,DNAase,NAD-nucleosidase, phospholipaseA2 & peptidases
Contd
Phospholipase A2(lecithinase) damages mitochondria,RBCs,WBCs,platelets, peripheral nerve endings,skeletal muscles, vascular
histamine
Contd
Proteolytic enzymes(endopeptidases & hydrolases) are responsible for local changes in vascular permeability leading to
through tissues
POLYPEPTIDE TOXINS
Postsynaptic () neurotoxins such as bungarotoxin and cobrotoxin,are bind to acetylcholine receptors at the motor endplate Presynaptic()neurotoxins such as bungarotoxin,crotoxin,& taipoxin release acetylcholine at the nerve endings at NMJs & then damage the endings,preventing furthur release of the transmitter
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
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
of systemic envenoming
Early syncope,vomiting,colic,diarrhoea, angioedema & wheezing may occur Local pain & bleeding from the fang punctures,swelling, bruising ,lymphangitis & regional lymphadenopathy
Bites by cobra
More of neurotoxic ,local effects
Neurotoxic Ptosis Ciliary mussle paralysis Partial/total opthalmoplegia Broken neck sign
Bulbar palsy
Locked-in syndrome
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
Bites by Viper
cytotoxic & hemotoxic Severe local effects Rapid devlopment of DIC Immediate shock Neuroparalysis-ptosis,respiratory paralysis Sheehans syndrome
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
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
Contd
Oliguria & loin pain indicate renal ischaemia
Generalised rhabdomyolysis
myoglobinuria Renal failure is a common mode of death Sawscaled viper doesnt causeneurological or renal complications
ecchymosis
Necrosis
Bite marks
Contd
Myoglobinuria appears 3 to 8hrs after the bite Myoglobin & potassium released from damaged skeletal muscle can cause renal failure
Investigations
CBC RFT Coagulation studies Blood grouping & cross matching Sr.electrolytes Urinalysis
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
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.
POLYVALENT ANTIVENIN
Manufactured by hyper immunizing horses against venoms of four standard snakes Cobra (naja naja) Krait (B.caerulus) Russels viper(V.russelli) Saw scaled viper(Echis carinatus)
Lyophilised form:stored in a cool dark place & may last for 5 years Liquid form:has to be stored at 4c 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
infusion with 5ml/kg of isotonic fluid ,all ASV has2be administered in 1hr
ROUTE OF ADMINISTRATION--IV
WHY NOT IM?
Contd
A histamine anti H1 blocker-chlorpheniramine 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
Contd
If patient goes for airway obstruction & respiratory paralysis MECHANICALVENTILATION
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
Contd
Hypotension & shock-a plasma expander, dopamine. Oliguria & renal failure-fluids,diuretics, dopamine-if no response,fluid restriction, dialysis Local infection-TT,antibiotics
Contd
Intracompartmental syn & fasciotomy Haemostatic disturbances-FFP,fresh whole blood,cryoprecipitates