SNAKE BITE MANAGEMENT AND

PROTOCOLS

DR SAMYEK NAPIT
IM RESIDENT
 Introduction
Important occupational hazard affecting farmers, plantation
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workers, herders and fishermen

In Nepal, WHO estimates that 20’000 people are bitten by snakes
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each year
Public health problem, medical emergency
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family elapidae: Cobra species, Krait species

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Viperidae: Russell’s Viper, Pit Viper species

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Non-venomous snakes
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 Components of the Management::
First aid Treatment
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Transport to hospital
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Rapid clinical assessment and resuscitation

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Detailed Clinical assessment and species diagnosis

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Investigations
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Antivenom Treatment
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Observation of the response to antivenom: and decision about

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need of further doses of antivenom

supportive/ancillary treatment
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 First Aid
Recommended
■Reassure the victim who may be very anxious
■Immobilise the bitten limb with a splint or sling (any movement or
muscular contraction increases absorption of venom into the
bloodstream and lymphatics)
■Consider pressure-immobilisation for some elapid bites
■Avoid any interference with the bite wound as this may introduce
infection, increase absorption of the venom and increase local
bleeding
■Remove rings, jewelries, tight fittings and clothing
Not recommended:
■making local incisions or pricks/punctures (“tattooing”) at the site of
the bite or in the bitten limb
■attempts to suck the venom out of the wound
■Tourniquets
■electric shock
■topical instillation or application of chemicals, herbs or ice packs.
The victim should be transported to the hospital where he can receive the medical care.
In-hospital management
RAPID CLINICAL ASSESSMENT AND RESUSCITATION
■Airway
■Breathing
■Circulation
■Disability of the nervous system
■Exposure and environmental control
 i. “In what part of your body have
you been bitten?”
II. “When and under what
■Thorough history (time of bite and were
circumstances any yousymptoms
bitten?” of
envenomation) iii. “Where is the snake that bit
you?”
iv. “How are you feeling now?”
■ Complete physical examination
■ Evaluation of the progression of local envenomation
■Victims of neurotoxic envenomation should be monitored
closely forevidence of cranial nerve dysfunction (e.g., ptosis)
that may precede more overt signs of impending airway
compromise (e.g., difficulty swallowing, respiratory
insufficiency)
fang marks
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local pain
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local bleeding
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bruising
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lymphangitis
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lymph node enlargement

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inflammation (swelling , redness, heat)

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blistering local infection, abscess formation

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necrosis
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 Systemic manifestations
Elapidae group of snakes
eneral manifestations: nausea, and vomiting, pain Note
Abdominal pain is par

domen (acute abdomen): krait bite, malaise, weakness, in suspected nocturna

envenoming.

owsiness, excessive salivation

eurotoxic manifestations: ptosis, ophthalmoplegia,

pillary dilation, inability/limitation to open mouth, inability
protrude the tongue beyond incisors teeth, Inability to
allow
● Broken neck sign-
● - cannot hold his/her neck straight when sitting up
(active or passive) from supine position
● Skeletal muscle weakness
● - limb weakness, flaccid paralysis and loss of deep
tendon reflexes.
● Loss of gag reflex
● - inability to produces gag on touching palate or
pharyngeal wall by cotton stick or throat swab.
●Paralysis of jaw and tongue that may lead to upper airway
obstruction and aspiration of pooled secretions

● Numbness around the lips and mouth.

●Hypoxia due to inadequate ventilation (breathing) can

cause cyanosis, altered sensorium and coma.
● 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.
Difference between cobra and krait
bite
Viperidae group of snakes
● Bleeding from
venipuncture site , gums
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nose (epistaxis)
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respiratory system (hemoptysis)

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gastrointestinal system (melaena, rectal bleeding)

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genitourinary system (hematuria, bleeding from vagina)

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● bleeding into the mucosae (subconjunctival hemorrhage)

● skin (petechiae, purpura)
●bleeding into internal organs like brain and cranium, lungs or
abdomen
●bleeding and hypotension may lead to acute kidney injury (acute
renal failure) and other organ dysfunctions
● prolonged bleeding time (BT) and clotting time (CT)
● increased prothrombin time and INR
thrombotic strokes
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 Diagnosis
■Severe envenomation is suggested by one or more of the
following findings
■Confirmation of a bite from a dangerous snake
■Rapidly progressive swelling from the bite site
■Rapid development of local blistering or bruising
■Persistent oozing of blood from bite marks and other
wounds
■Enlarged, painful lymph nodes draining the region of the
bite
 Investigations
■Complete blood count : degree of hemorrhage or hemolysis and
thrombocytopenia; septicemia
■PBS
■Blood type and cross-matching;
■Assessment of renal and hepatic function
■Coagulation studies to diagnose consumptive coagulopathy;
■Measurement of creatine kinase for suspected rhabdomyolysis;
■ Testing of urine for blood or myoglobin ( urine dipstick test)
■ABG
■Radiological test
 Treatment of bitten part
■Nurse painful swollen limb in most comfortable position
■Avoid excessive elevation, leave blisters
■Aerobic and anaerobic antibiotic prophylaxis
■Tetanus toxoid booster
■Surgical debridement of necrotic tissue
■Look for compartment syndrome
■Compartment syndrome are often misdiagnosed, and fasciotomy are
performed unnecessarily
■Measurement of intercompartmental pressure is mandatory
 Antivenom treatment
■Antivenom is immunoglobulin (usually the enzyme refined F(ab)2
fragment of IgG) purified from the serum or plasma of a horse or
sheep that has been immunised with the venoms of one or more
species of snake.
■‘’Specific” antivenom, implies that the antivenom has been raised
against the venom of the snake that has bitten the patient and that it
can therefore be expected to contain specific antibody that will
neutralise that particular venom
■Monovalent or monospecific antivenom neutralises the venom of
only one species of snake.
■Polyvalent or polyspecific antivenom neutralises the venoms of
 Antivenom treatment
■The currently available antivenom in Nepal is imported from India
and is polyvalent.
■It is effective against Russell's Viper (Daboia russelii), Common
Cobra (naja naja), Common Krait (Bungarus caeruleus) and Saw
Scaled Viper (Echis carinatus).
■Antivenom should be used as early as possible when indicated i.e.
when patient develops systemic feature of envenoming.
■ The venom which is not attached to receptor and freely flowing in
blood stream (and tissue) is neutralized by antivenom.
■Administration of antivenom carries risk of anaphylactic reactions
and should not therefore be used unnecessarily. It is also costly and
Indications of ASV: National guideline
Evidence of Ptosis, external ophthalmoplegia, broken neck sign, respiratory difficulty, etc.
Neurotoxicity
Evidence of Evidence of coagulopathy primarily detected by 20 WBCT or visible
Coagulopathy spontaneous systemic bleeding, bleeding gums, etc., including myoglobinuria
and hemoglobinuria. Rapid extension of local swelling (more than half of
limb) which is not due to pit vipers or tight tourniquet application.
Evidence of Shock and hypotension (in case of Russell’s viper bite).
Cardiovascular
Collapse
Evidence Of Traditionally AKI is an indication for antivenom therapy.
Acute Kidney
Injury However, AKI in absence of hematotoxic manifestation is
highly unlikely.
WHO GUIDELINE
How long after the bite can antivenom be expected
to be effective?
■Antivenom treatment should be given as soon as it is indicated.
■It may reverse systemic envenoming even when this has persisted
for several days or, in the case of haemostatic abnormalities, for two
or more weeks.
■However, when there are signs of local envenoming, without
systemic envenoming, antivenom will be effective only if it can be
given within the first few hours after the bite.
Administration of ASV
■Freeze-dried (lyophilised) antivenoms are reconstituted, usually with 10 ml
of sterile water for injection per ampoule.
■Prophylactic adrenaline: (0.25 ml/mg of 0.1% solution sc) used before
initiation of antivenom (Exception: older patients with evidence or suspicion
of underlying ischemic heart disease or cerebrovascular disease). Dose:
IV Infusion Adult
Reconstituted antivenom is diluted in 5-10ml/kg
body
weight (approximately 250 to 500ml) of isotonic
saline or
glucose and administered as
infusion@2ml/minute.
Children
Reconstituted antivenom is diluted in 3-5ml/kg
body weight of isotonic saline or dextrose water
and
administered as infusion @ 2ml/min.
IV Injection Reconstituted antivenom is administered
No by slow IV @2ml/
Intram IV Injection minute. However, this route is
uscula
not practiced commonly.
r
 Neurotoxic envenoming
Initial Dose 10 vials (100 ml) is further diluted or mixed with
dextrose
water or saline (100 ml to 400 ml). Then it is
administered
Initial dose
with intravenous infusion at the rate of 2ml/minute (40-
60
min @60-70 drops/min).
Repetition of the antivenom dose in If neurological sign/s deteriorates (or neurological
score
neurotoxic worsen, if score calculated at baseline and thereafter
envenoming every hour) an IV push of 5 vials of antivenom (50 ml
reconstituted antivenom) should be administer @
2ml/min
Note: Do not repeat antivenom even if neurological sign
persists. It should be repeated only if neurological sign/s
deteriorates.
 Hematotoxic envenoming (Russell’s viper envenoming)
Initial dose Same as dose for neurotoxic
envenoming.
Repetition of dose Persistence or recurrence of blood
incoagulability after
every 6 hours of antivenom dose. Repeat
20WBCT (or other
test for coagulation) after 6 hours. If
20WBCT is abnormal
(incoagulable blood) or other coagulation
test are abnormal
repeat 5 vials of antivenom (50 ml
reconstituted antivenom)
IV push @ 2ml/min.
Snakes inject the same dose of venom into children and adults.
Therefore, the dose of antivenom for children is same as adult dose.
Response to treatment
■spontaneous bleeding ceases by 20 mins
■coagulation test normalize: by 6-8 hours
■hypotension, cardiotoxicity: Improve within 20-30min
■neurotoxicity: detectable improvement within 30min with complete
reversal in several hrs (only postsynaptic type)
Reasons for failure to respond to
antivenom
■Excessive delay in administration of antivenom after envenoming
(specially in case of krait envenoming)
■Patient with established respiratory failure who need artificial
ventilation and antivenom alone will not suffice.
■if antivenom administered does not contain neutralizing antibodies
against the venom of biting species.
■Insufficient dose of antivenom. Clinical trial in Nepal has shown that
the mean dose of antivenom required to treat neurotoxic envenoming
is 12.5 ± 3.9 vial per patients. However, it may range from as low as
five vials to 20 vials, rarely, as high as 30 vials.
Indication for intubation
■Imminent respiratory arrest
■Neck muscle weakness with shallow respiration or paradoxical
breathing
■Secretion pooling in pharynx with loss of gag reflex
■Upper airway obstruction ,stridor and angioedema
■SPo2 <90% despite high flow 02
■Respiratory acidosis with Pa C02 >45mmhg
Observation and monitoring

antivenom reaction
■Early anaphylactic reactions (EAR): Anaphylaxis usually develops
within 3 hours of antivenom initiation
■Pyrogenic reaction: Usually develops 1-2 hrs. after treatment
initiation. Features include, chills, rigors, fever, fall of blood pressure,
febrile convulsion may develop in children.
■Late reaction (serum sickness type): May develop 1- 12 (mean 7)
days after treatment. Features include fever, itching, recurrent
urticaria, arthralgia, myalgia, lymphadenopathy, proteinuria etc.
Management when ASV is not
available
Neuroparalysis
■Cobra:
- Post synaptic (α) neurotoxin produces a curare-like non-depolarizing, competitive
post synaptic block by binding to acetylcholine receptors at the motor endplate.
- Blockade can be antagonized by neostigmine.

■Krait:
- Presynaptic neurotoxins (β –bungarotoxin) damages the nerve endings.
- Neuromuscular paralysis is prolonged in krait envenoming and does not respond to
treatment by neostigmine.
- Therefore, in case of neurotoxic paralysis by krait bite, assisted ventilation is
Use of acetylcholinesterase inhibiters in envenomation by
neurotoxic snake
 Coagulopathy
■Strict bed rest
■Avoid injuries including IM injection, avoiding straining.
■Transfusion of fresh frozen plasma or cryoprecipitate with platelet concentrates is
only indicated in cases of life-threatening hemorrhage in conjunction with
antivenom administration or, when antivenom is not available and the patient has
major bleeding.
■However, in absence of neutralizing antivenom and in presence of circulating
venom procoagulant toxins, the clotting factors administered is rapidly consumed
and it may lead to formation of microthrombi in the circulation.
Rhabdomyolysis
■Antivenom may prevent development of muscle toxicity but does not
reverse established rhabdomyolysis.

■Initial therapy: Rapid infusion of NS to establish urine output of 200-

300 ml/hr.

Renal Failure
■May result from hypotension, rhabdomyolysis and/or DIC.
● Criteria for fasciotomy

Haemostatic abnormalities have been corrected (antivenom

with or without
● clotting factors)
● Clinical evidence of an intracompartmental syndrome
● Intracompartmental pressure >40 mmHg (in adults)
Management of cobra spit ophthalmia*

(1) urgent decontamination by copious irrigation

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●(2) analgesia by vasoconstrictors with weak mydriatic activity (e.g.

epinephrine) and limited topical administration of local anesthetics
(e.g. tetracaine)
●(3) exclusion of corneal abrasions by fluorescein staining with a
slit lamp examination and application of prophylactic topical
Antibiotics
4) prevention of posterior synechiae, ciliary spasm and discomfort
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with topical cycloplegics and

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(5) antihistamines
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Reference
■National guidelines for snakebite management in nepal
■WHO guidelines for management of snakebites