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1. Management
of Snakebite:
A clinical
perspective

2. 12/04/2025 2

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General condition: intubated
Vitals: HR: 170/min. RR: 20/min BP: 110/80 mm of hg
Shifted to PICU
Kept under MV at PAC mode with PIP 16, PEEP 7, Fio2 60%
Spo2: 98%, GRBS: 124mg/dl
On Examination at ER

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Systemic examination:
Respi: decreased air entry on left side of chest, no added sound
CVS: S1S2Mo
P/A: soft, not distended, no organomegaly
Et tube was repositioned and confirmed by auscultation.

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Whole blood clotting test: Negative
CBC:
PT/INR:
APTT:
CK- MB:
Troponin I:
Investigations

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Pro BNP:
Calcium:
Mg:
RFT:
ABG: pH: 7.40, pCO2: 34, pO2: 130, Hco3: 21

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• Treated with iv antibiotics inj Meropenam and vancomycin
• Was under Ionotrope support Epinephrine and Dopamine
which was gradually tapered and stopped.
• Inj Hydrocortisone was added.

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• On 3rd
day of admission: GCS: E4VtM6
• She was extubated and kept under HFNC> CPAP> Nasal Prongs
• Proximal muscle weakness gradually improved
Discharged on 7th
day of admission

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How common is this scenario?

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• Globally, snakebite results in 1.8 to 2.7 million envenomings and 81,000 to
138,000 deaths annually.
• The highest incidence of snakebite envenomings and deaths occurs in South
Asia, particularly in India and Pakistan.
• In Nepal, 20,000 to 37,661 people are bitten by snakes resulting in 1,000 to
3,225 deaths annually.
Source: 1. World Health Organization (1987) Zoonotic disease control: baseline epidemiological study
on snakebite treatment and management. Weekly Epidemiological Record 42: 319–320.
2. Alcoba G, Sharma SK, Bolon I, Ochoa C, Martins SB, et al. (2022) Snakebite epidemiology in humans
and domestic animals across the Terai region in Nepal: a multicluster random survey. Lancet Global
Health 10: e398–e408.

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Source: Analysis of News Media-Reported Snakebite Envenoming in Nepal during 2010–2022. PLoS
Negl Trop Dis 17(8): e0011572.

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Total- 89 species
Poisonous- 17 species
Subdivided into two groups: Elapidae and Viperidae
Medically Important snakes in Nepal

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1. Cobra species
Elapidae

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2. Krait species

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Other species

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Venum composition and its action
• A complex mixture of enzymes, low molecular wt. polypeptides, glycoproteins
and metal ions.
• Enzymes: Proteases, Phospholipase A, amino acid esterases, Hyaluronidase

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1. Hemotoxic venoms act on the heart and cardiovascular system: vascular
leaking, local and systemic bleeding
2. Neurotoxic venom acts on the nervous system and brain, pre or post
synaptically to inhibit nerve impulse
3. Cytotoxic venom has a localized action at the site of the bite: local tissue
necrosis

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No clinical manifestation except bite mark. (Dry bite)
Due to bite by non-venomous snakes or bite by venomous snake without
injection of venom.
Consequences of snake bite

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Local signs and symptoms
• Fang mark may be obvious as single puncture, dual puncture or marks of
multiple tooth marks.
• Bite in the arm or lower limb occurs to victim who unintentionally steps on or
otherwise disturbs a snake while working in the filed or walking.

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Cobra- swelling and local pain with or without erythema or discoloration at the
bite site.
Krait- Usually do not cause signs of local envenoming and can be virtually
painless.
Viper- persistent bleeding from fang marks, wounds or any injured parts of the
body due to venom induced coagulopathy.
Swelling or tenderness of regional lymph node denotes venom spread.

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General manifestation of snake envenoming are:
nausea, and vomiting pain abdomen malaise weakness drowsiness
prostration excessive salivation, etc.
Systemic Manifestations

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Elapidae group
Neurotoxic features

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• Ophthalmoplegia
• Pupillary dilatation
• Skeletal muscle weakness
• Loss of gag reflex
• Paradoxical breathing
• Respiratory failure

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Viperidae group

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1. ELISA tests: to identify species based on Ag in venom,expensive,not
freely available and thus have limited value in diagnosis.
2. Neurotoxic envenoming: no lab investigation in Nepal that can help
diagnose neurotoxic manifestation.
Diagnosis

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3. Hematotoxic envenoming due to vipers:
• BT and CT : Prolonged.
• PT and INR: Increased.
• 20-minute whole blood clotting test (20WBCT): Positive (Bedside test to see
the incoagulability of the blood to detect venom induced coagulopathy.)

32. • 2-3 ml of freshly sampled
venous blood in a small, new,
dry, glass tube.
• Tube standing undisturbed for
20 minutes at ambient
temperature.
• Blood still liquid (unclotted) and
runs out, the pt has
uncoagulable blood.

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4. RFT: to detect AKI
5. CBC, blood group: Increased TLC indicate systemic envenoming, platelet
count may decrease viper envenoming.
6. CPK: raised in rhabdomyolysis
7. Urine examination for albumin and RBCs

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Management
Steps for the snakebite management

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First Aid Treatment
• Do ‘s
R= Reassure the patient. Only 50% of bites by venomous species actually envenomate the patient
I= Immobilise the limb in the same way as for a fracture, not to block the blood supply or apply pressure.
G. H.= Get to Hospital Immediately. Traditional remedies have NO PROVEN benefit in treating snakebite.
T=Tell the doctor of any systemic symptoms that manifest on the way.
Remove tight clothing, shoes, watch, rings
Keep affected limb as low level as possible
Identification of snake

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Interfere with bitten area
Suck by mouth
Apply chemicals or electricity
Use arterial tourniquets
Cooling agents on the bitten area
Make incision on the wound
Walking of patient is contraindicated
Don’t’s

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• Secure ABC
• Assess vitals and secure I.V. Line: large bore cannula inserted on an
unaffected limb
• History should be quickly obtained
• Rapid, thorough physical examination
• Look for signs of envenomation
• Even if absent- admit and observe for 24 hours,
Rapid clinical assessment and resuscitation

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• Close monitoring ~ hourly for vital signs, cardiac rhythm, oxygen
saturation, urine output, ptosis, local swelling, diplopia, bleeding.
• Fluid resuscitation with isotonic saline if clinical shock.
• Species diagnosis
• Investigation and laboratory tests

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1. A critical moment for the patient, doctor and attendants. Possibility of sudden collapse
2. Do not take the bandages off until IV is established, other resuscitation facilities and
ASV are ready to use.
3. If an arterial tourniquet: first apply another bandage or tourniquet at venous
obstructing pressure above the arterial tourniquet. Release it for a few moments at a
time.
4. If rapid deterioration, re-apply a pressure immobilisation bandage until the situation
stabilizes.
Removal of torniquets

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• The bitten limb may be swollen and painful
 nursed in the most comfortable position.
• Elevation of limb with rest.
• Simple washing with antiseptic solution - chlorhexidine, povidone iodine
• Broad-spectrum antibiotic - if features of infection.
Treatment of the bitten part

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• Local necrosis and gangrene: surgical debridement, skin grafting
 Broad spectrum antibiotic is indicated if there is feature of
infection.
• Tetanus toxoid IM injection should be given.
 If coagulopathy postponed until after resolution of coagulopathy.

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Indication of Antivenom, Nepal

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• Each vial is diluted with 10 ml of
sterile water
• Reconstituted antivenom is
diluted in 3-5 ml/kg body weight
of isotonic saline or dextrose
water
• Infusion at 2ml/min
Antivenom route and dose
Prophylactic Adrenaline (0.1%) subcutaneously
Age (years) Dose (mcg) Volume (ml)
>13 250 0.25
>10-12 200 0.20
>5-10 125 0.12

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Initial dose
 10 vials(100ml) is further diluted or mixed with dextrose water or saline
(100-400ml)
 Administered at rate of 2ml/min(40-60 min at 70 drops/min)
Repetition of dose
 If neurological signs deteriorate (DO NOT REPEAT IF PERSIST)
Neurotoxic envenoming

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Initial dose
 Same as dose for neurotoxic envenoming
Repetition of dose
 Persistence or recurrence of blood incoagulability afer every 6 hours of
antivenom dose.
 Repeat 20 WBCT is abnormal or other coagulation test are abnormal repeat 5
vials of antivenom at 2ml/min
Hematotoxic envenoming

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All patients with features of envenoming may not respond to antivenom administered.
• Excessive delay in administration of antivenom – esp karaits.
• Patient with established respiratory failure.
• need artificial ventilation and antivenom alone will not suffice.
• If antivenom administered does not contain neutralizing antibodies against
biting species.
• Insufficient dose of antivenom.
• Inactive or poor quality antivenom.
Reasons for failure to respond to antivenom

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• Mean dose of antivenom for treat neurotoxic envenoming -12.5 ± 3.9
vials.
• May range from five vials to 20 vials, rarely, as high as 30 vials.
• Do not use more than 20 vials of antivenom.
• Administration of higher dose antivenom is unlikely to be useful, not
responding to initial bolus or around 20 vials of antivenom.
Clinical trial in Nepal

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•Clinical assessment for appearance of signs and symptoms of antivenom
reaction should be performed.
•The anaphylaxis reaction may be life threatening.
• no time may be available to draw adrenaline from ampule.
• adrenaline (epinephrine) must be ready, drawn up in a syringe, prior
to antivenom.
Observation and monitoring

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•Antivenom reactions
• Significant number of patients develops reaction to antivenom.
• Around 80% developed some reactions to antivenom in clinical
trial conducted in Nepal
• Rarely IgE-mediated Type I reaction person previously exposed
to animal serum (e.g. Tetanus toxoid injection)- dose related.

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Early anaphylactic reactions (EAR):
• a serious allergic reaction - rapid in onset and may cause death.
• usually develops within 3 hours of antivenom initiation.
• Common features - itching, urticaria, fever, angio-edema,
dyspnea due to bronchospasm, laryngeal edema, hypotension,
abdominal pain, vomiting, diarrhea etc.

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Pyrogenic reaction:
• Usually develops 1-2 hrs. after treatment initiation.
• chills, rigors, fever, hypotension, febrile convulsion - children.
Late reaction (serum sickness type):
• May develop 1- 12 (mean 7) days after treatment.
• fever, itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy,
proteinuria etc.

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• Both usually occurs within 3 hours after initiation of antivenom
administration.
• Symptoms and signs that are consistent with EAR or PAR should be
identified;
• some common to both (fever, hypotension)
Detection of early anaphylaxis (EAR) and pyrogenic
reactions (PR)

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• Following associated features help to identify EAR.
• itching, urticaria, swollen lips or tongue
• respiratory symptoms - dry cough, wheezing, stridor, hoarse voice,
‘lump in throat’
• digestive symptoms - nausea, vomiting, abdominal colic, diarrhea
• identify symptoms and signs of life-threatening anaphylaxis/EAR
• airway- obstruction/compromise

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• breathing- tachypnoea, wheezing
• circulation- hypotension or shock +/- poor peripheral
circulation
• Urticaria should be regarded as early sign of anaphylaxis &
treated as ‘full blown’ anaphylaxis.
• Itching alone is not life threatening but requires close
monitoring.

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• Treatment of neurotoxic envenoming:
• Antivenom treatment alone cannot always prevent respiratory
paralysis.
• should be artificially ventilated to avoid asphyxiation
• Complete recovery observed in the absence of treatment with
antivenom after 36 to 72 hours of artificial ventilation.
• Russell’s viper
• may lead to renal failure (dialysis support).
• Shock
Supportive/ancillary treatment

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Management of snakebite envenoming when no
antivenom is available

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Neuroparalysis
• The most important venom component of cobra is post synaptic (α)
such as α -bungarotoxin,
• produces a curare-like non-depolarizing, competitive post synaptic
block by binding to acetylcholine receptors at the motor endplate.
• This blockade can be antagonized by neostigmine.
• must be given together with atropine to block muscarinic side
effects.
• Assisted ventilation may still be required.

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Krait venom
• neuromuscular paralysis by presynaptic neurotoxins, β –
bungarotoxin- damages nerve endings
• pre-synaptic toxicity - depletion of synaptic vesicles, destruction of
motor nerve terminals, axonal degeneration followed by
reinnervation preventing further release of transmitter.
• neuromuscular paralysis prolonged in krait envenoming and does
not respond to neostigmine.

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• Activation of clotting pathway by procoagulant snake toxins and consumption
of clotting factors.
• Antivenom, containing antibodies against envenoming species - standard
treatment
• Antivenom will neutralize the circulating venom and stop the consumption
coagulopathy process.
• Takes another 24 to 48 hours for liver to produce clotting factors for full
recovery of clotting
Venom-induced consumption coagulopathy (VICC)

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Transfusion of fresh frozen plasma (FFP) or cryoprecipitate with platelet
concentrates
• only indicated in cases of life-threatening hemorrhage with antivenom
administration,
• in absence of neutralizing antivenom and in presence of circulating
venom procoagulant toxins,
• clotting factors administered is rapidly consumed and
• may lead to formation of microthrombi in the circulation.
• when antivenom not available and the patient has major bleeding.

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In absence of specific antivenom
• strict bed rest, avoiding injuries including intramuscular
injection,
• avoiding straining and constipation- useful to prevent
bleeding in vital organ

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The pediatric management of
snakebite

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• Bite marks to determine whether species was venomous or non venomous
are of no use
• Cobras or kraits donot cause antihemostatic symptoms
• Each vial of polyvalent ASV neutralizes 6 mg of Russel vipers venom
• Initial dose is 8-10 vials for both adults and children
• There is no good evidence to suggest children should receive either more
ASV because of body mass or less in order to avoid adverse reactions

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• ASV should be administered over 1hour.
• At the first sign of any of symptoms i,e urticaria, itching, fever, shaking chills,
nausea, vomiting, diarrhea, abdominal pain,tachycardia, hypotension,
bronchospasm and angioedema  ASV will be discontinued
• 0.5 mg of 1:1000 adrenaline given IM (0.01mg/kg)
• To provide longer protection, 0.2 mg/kg of antihistamine IV and 2mg/kg of
hydrocortisone will be administered
• If adverse reaction persists 10-15 minutes , second dose give, can be repeated.
Usually 2 doses will suffice

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• In anti- hemostatic bites, once the initial dose is administered over1 hour, no further
ASV is given for 6 hours.
• 20-WBCT every 6 hours will determine if additional ASV required
• In case of neurotoxic bites, once the first dose has been administered and a
Neostigmine test given,the victim is closely monitored . If after 1-2 hours the victim
has not improved or has worsened then the second and final dose should be given At
this point, the victim will have received suffiecient neutralizing capacity from the ASV,
and will either recover or require MV, in either event further ASV will achieve
nothing.
Repeat doses of ASV

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Updates

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• PSCS is a critical
problem that
requires multiple
surgical
interventions.
• Elevated WBC and
AST upon ED arrival
are highly likely to
be risk factors for
the development of
PSCS and may be
useful as clinical
markers.

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