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SNAKE BITE

CHAIRPERSON: Dr.Poornima Shankar

PRESENTER: Dr.Mohan.T.Shenoy

24.5.2010

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REFERENCES Medical emergencies in children - Meherban Singh Nelson Textbook of Pediatrics – 18th Edition Textbook of Pediatric and Neonatal emergencies -

Sachdev Textbook of forensic medicine and Toxicology by Reeddy

– 25th edition Indian National Snakebite Protocols 2007

Pediatric Management of Snakebite: The National Protocol INDIAN PEDIATRICS VOLUME 44__MARCH 17, 2007

WHO Guidelines for the Clinical Management of Snake bites in the South-East Asia Region

Management of Snake Bite - An Update Dr. S. Ghosh Journal of Physicians of india 2008 Vol. 18

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Epidemiology

India estimates in the region of 200,000 snake bites /year with 15-20,000 deaths .

Originally made in the last century, are still quoted as no reliable national statistics are available.

Males are bitten almost twice as often as females 50% of bites by venomous snakes are dry bites with

negligible envenomation

Majority of the bites being on the lower extremities. Mostly between age group 11-50 yrs. Only 7 to 15% are under 10 yrs age. .

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FAB FOUR In India, > 3500 species of snakes but only 200

are poisonous.

Saw-scaled viper (Echis carinatus) Russell’s viper (Daboia russelii) Common krait (Bungarus caeruleus) Indian cobra (Naja naja)

Majority of bitesNearly 70-80%HemotoxinVasculotoxin

Neurotoxic

1 2 43

YPB

FD

13 mg

8 mg

63 mg

15 mg

23 mg

6 mg

60 mg

8 mg

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Snake venom components

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Cobra

Hood bearing a single & double spectacle shaped mark on the dorsal aspect

White band in the region where the body touches the hood

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Cobra –post-synaptic Alpha-neurotoxins or

“Curare-mimetic toxins’’

Bind specifically to acetylcholine receptors, preventing the interaction between acetylcholine and receptors on postsynaptic membrane.

Prevents the opening of the sodium channel associated with the acetylcholine receptor and results in neuromuscular blockade.

ASV -rapid reversal of paralysis.

Dissociation of the toxin-receptor complex, which leads to a reversal of Paralysis

Anticholinesterases reverse the neuromuscular blockade

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Krait

Head is covered with large shield Steel blue often shining Has a single or double white band across the

back

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Krait- Pre-synaptic actionBeta-bungarotoxin- Phospholipases A2

1) Inhibiting the release of acetylcholine from the presynaptic membrane

2) Presynaptic nerve terminals exhibited signs of irreversible physical damage and are devoid of synaptic vesicles

3) Antivenoms & anticholinesterases have no effect

Paralysis lasts several weeks and frequently requires prolonged Mechanical ventilation.

Recovery is dependent upon regeneration of the terminal axon.

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Russell’s Viper

Flat triangular head with a white ‘V’ shaped mark 3 rows of diamond shaped black or brown spots

along the back

Hissing sound

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Determine whether the patient is actually bitten by the poisonous snake or not.

Look for fang marks , which are few mm to 4 cm. Depth of bite varies from 1 to 8 mm

Time of onset of poison may be as early as 5 min (cobra) to 10 hrs in krait bite. In viper mean duration of onset of symptom is 20 min. In sea snakes myotoxic features appear within 2 hrs.

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NEUROTOXICITY Starts early- many die before

they reach hospitals Many reverse very well with

ASV if started early Less number of cases

HEMOTOXICITY Starts late hence most of

them reach hospitals Many organ involvement

hence MV is mostly supportive to buy time for organs to recover

More number of cases

70-80%

20-30%

OPHITOXEMIA

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No local signs with Neurotoxicity- Krait

With or without local signs and Neurotoxicity-Cobra With or without Neurotoxicity and local signs,

hemotoxicity- Russell’s Viper

Local signs with hemotoxicity-Saw Scaled Viper

Signs/Symptoms and Potential Treatments

Cobra Krait Russell’s Viper Saw Scaled

Viper Other Vipers

Local pain/ Tissue Damage Yes No Yes Yes Yes

Ptosis/Neurotoxicity Yes Yes Yes! NO No

Coagulation No No Yes Yes Yes

Renal complications No No Yes NO Yes

Neostigmine & AtropineYes No? No? NO No

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Local examination Starts within 6-8 min

During the initial evaluation, the bite site should be examined for signs of local envenomation (edema, petechiae, bullae, oozing from the wound, etc) and for the regional lymphadenopathy.

The bite site and at least two other, more proximal, locations should be marked and the circumference of the bitten limb should be measured every 15 min thereafter, until the swelling is no longer progressing.

Gangrene – Early wet ( ELAPID) – SLOWER DRY (Viper)

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Neurological manifestationsNeurological manifestations

Mostly seen in bite like cobra and krait

o Ptosis is the earliest foll by external opthalmoplegia.o Weakness of muscles of palate, jaw , tongue larynx,

neck and muscles of deglutition.o Generally cranial nerves are involved earlier followed

by drowsiness, coma and respiratory paralysiso Muscle cramps,hyperacusis o Paraesthesia, Fasciculations, Perioral Numbness.o Pupils remain reactive to light till terminal stages

where Diaphragm is affected with resultant respiratory failure.

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Neurological Examination

•Ask the patient to look up and observe whether the upper lids retract fully. •Test eye movements for evidence of early external ophthalmoplegia•Check the size and reaction of the pupils.•Krait can cause fixed, dilated non reactive pupils simulating brain stem death – however, it can recover fully•Ask the patient to open their mouth wide and protrude their tongue; early restriction often paralysis of pterygoid muscles.• The muscles flexing the neck may be paralysed, giving the “broken neck sign”

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Bulbar paralysisUnable to swallow => secretions accumulating

in the pharynx- an early sign Ask the patient to take deep breaths in and out.

“Paradoxical respiration”. Objective measurement of ventilatory capacity

by single breath count is very useful.Use a peak flow meter, spirometer (FEV1 and

FVC) Ask the patient to blow into the tube of a

sphygmomanometer to record the maximum expiratory pressure (mmHg).

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Bleeding manifestations

Seen in bites by vipers

Characterized by

•Prolonged clotting time,

•Bleeding at the site of bite,

•echymosis, purpura,epistaxis & bleeding from the gums, GIT, urinary tract, and cerebral hemorrhages

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Acute renal failure

may occur in russell viper bite due to

• Prolonged hypotension• Intravascular hemolysis• DIC• HUS

Muscle necrosis and myoglobinuria occur in sea snake bite which may also lead on to acute tubular necrosis.

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Cardiovascular Changes Arrhythmias, Hypotension, Shock ECG changes

Other Changes

Parotid swelling,conjunctival oedema,subconjunctival haemorrhage

Low back pain – retroperitoneal bleeding / early renal failure

Stomach Pain – Krait bite ( Submucosal hemorrhages)

Muscle pain – Sea snake bite ( Rhabdomyolysis )

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Recurrent manifestations of poisoning occur due to ongoing action of venom especially in Viper which has half life of 26- 96 hrs

Venom being released from local blebs which acts as a venom depots not accessible to antivenom.

Redistribution of venom from tissues into vascular space as result of ASV.

So frequent evaluation of patient is essential for 3-4 days

Delayed manifestation in an initially stabilized patient can occur even after 3 weeks

Management of Snake Bite

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Blood grouping and typingCoagulation profile :PT, PTT, FDP and Clotting time.CBC- may show anemia , leucocytosis,

thrombocytopenia. Peripheral smear - hemolysis and DIC. BUN , creatinine, electrolytes.Creatine kinase,SGOT,SGPTUrine analysis - hematuria, proteinuria,

myoglobinuria.

ECG changes are non specific and include bradycardia and AV block with ST elevation or depression.

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A simple bed side test is adequate for clinical purpose

Useful to monitor the effectiveness of ASV therapy when more sensitive tests for coagulation are not easily available

2-3 ml of blood is kept in a new clean, dry, test tube undisturbed for 20 minutes, and then gently tilted. If the blood is still liquid, it is evidence of coagulopathy.

In South eastern countries, suggestive of Viper bite and rules out Elapid bites.

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R. = Reassure the patient. Moral support.

70% of all snakebites are from non-venomous species. Dry bites - Only 50% of bites by venomous species actually

envenomate the patient.

I = Immobilize in the neutral position (same way as a fractured limb)

Children can be carried. Use bandages or cloth to hold the splints, not to block the

blood supply or apply pressure.

COMPRESSES LYMPHATIC CHANNELS AND INACTIVATES MUSCLE PUMP

LESSER AMOUNT OF VENOM REACHES CIRCULATION => “BUYS TIME”

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G.H. = Get to Hospital immediately.

Traditional remedies have NO PROVEN benefit in treating snakebite.

T = Tell the doctor of any systemic symptoms such as ptosis, gum bleeds or abdominal pain that manifest on the way to hospital. Exact time of bite can give indication of progression.

Take a blood sample Tetanus toxoid vaccine if the immunisation is incomplete

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Manipulation of bitten areaIncision and excision over the bite .

TourniquetSuction

Chemical application Stimulants and Alcoholic beverages

CauterizationCryotherapy

Electric shock

As these may cause more tissue bleeding , gangrene and uncontrolled bleeding .

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Supportive therapy Admit for observation – 24 hrs Reassure the patient Take care of ABC Monitor vitals, urine for hematuria and

clotting time

Monitor HR, RR , chest expansion and sensorium periodically

Close observation for early neurotoxic effects such as ptosis , opthalmoplegia, speech and swallowing difficulty periodically

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Avoid IM injections

Vascular access should be obtained in the unbitten limb for treatment of shock.

Keep pressure immobilization/ constriction bands in place till anti venom is administered

Anticonvulsant for seizures

Ventilator support may be needed for respiratory failure or unstable airway.

Supportive therapy

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Sedation and analgesic for pain. (Paracetamol,

Pethidine).

Neostigmine is given in Indian cobra and krait bite with neurological manifestations.

Dose

0.05-0.1 mg/kg IV / 4TH hourly with atropine ( 0.02mg/kg) IV 5 min prior.

Supportive therapy

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Treatment issues in non Neurotoxic respiratory paralysis

Mechanical ventilation is instituted to buy time till the organs recover

Aspiration can complicate MV Respiratory paralysis due to Shock, ARF, Sepsis, etc.. Treatment is directed towards the cause

ASV Broad Spectrum Antibiotics - Chloramphenicol +

MetronidazoleBlood and blood products – Fresh whole blood ideal Volume expandersSource control - Surgical debridement, FasciotomiesInotropes – Persistent shockDialysis

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Snake bite and Respiratory paralysis

Neuromuscular paralysis-blockade of neuromuscular transmission.Cobra- post-synapticKrait- pre-synaptic

Bulbar paralysis-AspirationSepsis,

DIC-shockARF-Pulmonary edema

NeurotoxicMV for respiratory paralysis

ASV

MV as Supportive care

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Anti Snake Venom Polyvalent /MonovalentTiming Repeat doseHypersensitivity Mechanical ventilation

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The decision to treat a snake bite with antivenin is largely based on clinical parameters.

Haffkine institute,Mumbai and Central Research institute,Kasauli manufacture it by hyperimmunising horse with venoms of the 4 common poisonous snakes.

ASV is polyvalent Syndromic approach helps in examination and investigations and outcome predictions

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There is no consensus as to the outer limit of time of administration of antivenom.

Best effects are observed within four hours of bite

It has been noted to be effective in symptomatic patients even when administered up to 48 hours after bite.

Reports suggest that antivenom is efficacious even 6-7 days after the bite from vipers

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5 vials(50ml)

5-10 vials(50-100ml)

10-20 vials(100-200ml)

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ASV and children Snakes inject the same dose of venom into children and adults but children

fare worser due to greater amt of toxins injected per unit body mass.

Children must be given exactly the same dose of antivenom as adults.

No absolute contraindication

Use ASV cautiously in those with High-risk for reactions Prev. history of allergic reaction to antitetanus/antirabies serum Strong history of atopic diseases and severe asthma

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Mix one vial of anti venom with 10 ml of injection water or saline or dextrose - between palms of the hand till dissolved ie.. it appears clear.

Don’t shake vigorously

If foam appears , turbid or milky , it indicates denatured protein and there is a great risk of anaphylaxis if this is used.

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Epinephrine ALWAYS kept ready at hand before.

Intravenous “push” injection @ 2ml/min in places with less facility

Intravenous infusion [ reconstituted ,diluted in 5-10 ml/kg isotonic saline or glucose]

Avoid IM and local administration at bite site

Administration

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Observation of the response to Antivenom

Cobra bites-Post synaptic

May begin to improve as early as 30 minutes after anti-venom, but usually take several hours.

Krait and sea snakes- Pre synaptic

Depends on the timing of ASV administrationIf delayed may not produce any action or Minimal delayed action

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Antivenom reactions 20%, of patients, usually more than develop a reaction

Complement activation by IgG aggregates or residual Fc fragments or direct stimulation of mast cells or basophils by antivenom protein are more likely mechanisms for these reactions.

Types 1. Early anaphylactic reactions- within 10-180 min2. Pyrogenic (endotoxin) reactions- develop 1-2 hours 3. Late (serum sickness type) - develop 1-12 days (mean 7)

Fatal reactions have probably been under-reported as death after snake bite is usually attributed to the venom.

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Treatment of anaphylaxis

0.01ml/kg of 1:1000 IM/IV Adrenaline ( Max dose 0.5ML)

Hydrocortisone-6-10mg/kg/dose IV Volume replacement for shock CPM 0.2mg/kg /dose IV

If patient found sensitive to equine ASV, desensitization may be necessary by administering graded dose of antivenin at a regular interval .

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Sensitivity test-Sensitivity test- Inject intradermal over forearm with 0.02ml of

antivenin diluted 1:10 with other forearm as control

Observe the patient for local or general symptoms of hypersensitivity.

Appearance of erythema or wheal > 10mm within 30 min is positive test

Needs desensitisation with 0.01 ml of 1:100 solution increasing concentration at 15 min interval till 1 ml given subcutaneously given over 2 hrs.

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Antivenom reactions At the earliest sign of a reaction:

Antivenom administration must be temporarily suspended

Adrenaline-0.1% solution, 1 in 1,000, 1 mg/ml is the effective treatment for early anaphylactic reactions.

IV hydrocortisone (adults 100 mg, children 2 mg/kg body weight). The corticosteroid is unlikely to act for several hours, but may prevent recurrent anaphylaxis

There is increasing evidence for anti H2 antihistamines-Ranitidine – adults 50 mg, children 1 mg/kg.

Pyrogenic reactions require- antipyretics. In case of circulatory collapse- start fluids, inotropes along

with IV adrenaline

5-day course of oral antihistamine/ Prednisolone.Chlorpheniramine: 2 mg six hourly Prednisolone: 5 mg six hourly

Serumsickness

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Repeat dose

Signs of systemic envenoming may recur within 24-48 hrs

Criteria for repeating the initial dose of antivenom Persistence / recurrence of blood incoagulability after 1-2 hr Deteriorating neurotoxic or cardiovascular signs after 1-2 hr

Continuing absorption- due to improved blood supply following correction of shock, hypovolaemia etc,

After elimination of antivenom A redistribution of venom from the tissues into the vascular

space.

Causes

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PROGNOSISLong term effects

Hypopituitarism, bilateral thalamic hematoma Usually swelling resolves within 2-3 weeks ;

Sometimes may persist upto 3 months or permanent.

Necrosis,Gangrene and resultant cosmetic defects Rarely clotting defects and neurotoxicity persist.

Overall mortality – 10% but 50-70% children may eventually succumb despite ASV administration .

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RECENT ADVANCES Snake Venom Detection Kit Rapid 2-step enzyme immunoassay employed preferably over bite site. Available only in Australia

Role of Steroids – delays necrosis , no effect on severity of outcome

Role of IVIg – eliminates need to repeat antivenom for envenomations asso with

coagulopathy.

R 2-hydroxy-4 methoxy benzoic acid – from Indian medicinal plant Hemidesmus indicus - effective against Russel’s viper venom

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Snake bite

Venomous snakes

Anti snake venom

Majority is by non-venomous snakes

ASV -severe adverse reactions, Costly, Limited supply.Used- benefits of ASV treatment is considered to exceed the risks.

About 50% of bites are dry

Summary

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Summary

ASV is the main stay in the treatment of snake bites

ASV must be initiated if indicated at the earliestNot all snake bites require ASV

Respiratory paralysis can be because of different reasons-Neurotoxicity, shock, sepsis, ARF

MV may be main stay of treatment or just supportive depending on the cause of failure.

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How to prevent snake bites? A world free of snakes

Nearly a quarter of us would go hungryAre important elements in the food

chain to control the rodent population that destroy all major crops.

The bottom line is we need snakes to survive

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Clinical features of a compartmental syndrome

• Disproportionately severe pain

• Weakness of intracompartmental muscles

• Pain on passive stretching of intracompartmental muscles

• Hypoaesthesia of areas of skin supplied by nerves running

through the compartment

• Obvious tenseness of the compartment on palpation

Criteria for fasciotomy in snake-bitten limbs

Haemostatic abnormalities have been corrected (antivenom, with or without clotting factors)• Clinical evidence of an intracompartmental syndrome• Intracompartmental pressure >40 mmHg (in adults)

Surgical debridement beneficial Early treatment with antivenom remains the best way of preventing irreversible muscle damage

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Mechanical ventilation

If patient has respiratory distress or bulbar paralysis-intubate and ventilate.

If delayed can cause aspiration or hypoxia and cardiac arrest.

Even if the facility for MV is not available

Ambuing can save the day.This helps even during transport.MV is not complicated is like ventilating a patient with

curare over-dosage

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Trial of anticholinesteraseAnticholinesterase (“Tensilon”/Edrophonium) test Record baseline parameters Give atropine IV Give anticholinesterase drug edrophonium chloride (adults

10 mg, children 0.25 mg/kg body weight) given intravenously over 3 or 4 minutes

Observe

Improvement in ptosis, Respiratory distress, better cough effort, decrease in RR

Tearing, salivation,muscle fasciculation, abdominal cramp,bronchospasm, bradycardia, cardiac arrest

Neostigmine

Positive response

Atropine IV

Negative response

Dose of Neostigmine

Neostigmine 25µg/kr/hr Neostigmine 0.5 mg / 6 hr IV atropine 0.5 mg / 12 hr

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Pregnancy and snake bite

Pregnant patient is treated the same manner as the nonpregnant patient. Spontaneous abortion, bleeding, fetal death & malformations are common.

Lactating mothers can continue lactatingFetal demise is difficult to predict because of

associated symptoms, such as coagulopathy or hypotension, and complications of treatment including anaphylaxis.

Generally speaking, the severity of the mother's clinical course seems to be the best indicator of the fetal survival.