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 Originally made in the last century, are still quoted as no reliable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.
Majority of bites
 Saw-scaled viper (Echis carinatus) Nearly 70-80%
Hemotoxin
 Russell’s viper (Daboia russelii) Vasculotoxin
 Common krait (Bungarus caeruleus)
 Indian cobra (Naja naja) Neurotoxic

1 2 3 4

YPB 13 mg 63 mg 23 mg 60 mg
FD 8 mg 15 mg 6 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 action
Beta-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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 OPHITOXEMIA
HEMOTOXICITY
NEUROTOXICITY  Starts late hence most of them
 Starts early- many die before reach hospitals
they reach hospitals  Many organ involvement hence
 Many reverse very well with MV is mostly supportive to buy
ASV if started early time for organs to recover
 Less number of cases  More number of cases

70-80%

20-30%

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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

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 Russell’s
Signs/Symptoms and Cobra Krait Saw Scaled
Viper Other Vipers
Potential Treatments Viper

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 & Atropine

Yes No? No? NO No
 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 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 paralysis
o 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 paralysis
 Unable 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

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Management of Snake Bite
 Blood grouping and typing
 Coagulation profile :PT, PTT, FDP and Clotting time.
 CBC- may show anemia , leucocytosis, thrombocytopenia.
 Peripheral smear - hemolysis and DIC.
 BUN , creatinine, electrolytes.
 Creatine kinase,SGOT,SGPT
 Urine 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.
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COMPRESSES LYMPHATIC CHANNELS AND INACTIVATES MUSCLE PUMP
LESSER AMOUNT OF VENOM REACHES CIRCULATION => “BUYS TIME”
 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 area
Incision and excision over the bite .
Tourniquet
Suction
Chemical application
Stimulants and Alcoholic beverages
Cauterization
Cryotherapy
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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 Supportive therapy
 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.

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 Supportive therapy
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.
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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 + Metronidazole
Blood and blood products – Fresh whole blood ideal
Volume expanders
Source control - Surgical debridement, Fasciotomies
Inotropes – Persistent shock
Dialysis 34
 Snake bite and Respiratory paralysis
Neurotoxic
MV for respiratory ASV
paralysis MV as Supportive care

Neuromuscular paralysis- Bulbar paralysis-Aspiration

blockade of neuromuscular
Sepsis,
transmission.
Cobra- post-synaptic DIC-shock
Krait- pre-synaptic ARF-Pulmonary edema

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 Anti Snake Venom
 Polyvalent /Monovalent
 Timing
 Repeat dose
 Hypersensitivity
 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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 Administration
 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

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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 administration
If 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 min
2. 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-
 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

5-day course of oral be temporarily
antihistamine/ suspended
Prednisolone.
Serum
 Adrenaline-0.1% Chlorpheniramine: 2 mg six hourly
sickness solution, 1 in 1,000, 1 mg/ml is the effective
Prednisolone:
treatment for early 5 mg six
anaphylactic hourly
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
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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

Causes

 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.
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 PROGNOSIS
 Long 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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 Summary
Snake bite
Majority is by non-venomous snakes

Venomous snakes
About 50% of bites are dry

Anti snake venom

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

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 Summary
ASV is the main stay in the treatment of snake bites
ASV must be initiated if indicated at the earliest
Not 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 hungry

Are The bottom
important line isinwe
elements theneed
food chain to
snakes
control to survive
the rodent population that destroy all
major crops.

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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
Surgical debridement beneficial
• Obvious
Earlytenseness
treatment of theantivenom
with compartment on palpation
remains the best
way of preventing irreversible muscle damage

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)

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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 anticholinesterase
Anticholinesterase (“Tensilon”/Edrophonium) test
 Record baseline parameters
 Give atropine IV
 Give anticholinesterase drug edrophonium chloride (adults
10 mg, children 0.25 mg/kg body weight)
Neostigmine given intravenously
25µg/kr/hr
overDose
3 orof
4 minutes
Neostigmine
Neostigmine 0.5 mg / 6 hr
IV atropine 0.5 mg / 12 hr
Observe
Negative response
Positive response Tearing, salivation,
Improvement in
ptosis, Respiratory muscle fasciculation,
distress, better cough abdominal cramp,
effort, decrease in bronchospasm,
RR bradycardia, cardiac
arrest Atropine IV
Neostigmine
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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 lactating
 Fetal 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.

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