BITE

SNAKE BITE
- DR SUBIN JOLLY
■ INTRODUCTION
■ EPIDEMIOLOGY
■ TYPES OF SNAKE BITES
■ CLASSIFICATION
■ IDENTIFICATION FEATURES
■ CLINICAL FEATURES OF SNAKE BITES
■ SNAKEBITE MANAGEMENT PROTOCOL
Introduction
■ India bears the world's largest burden of death and disability
caused by snakebites

■ An estimated 46,000 deaths in India and at least thrice as

many people injured every year, snakebite has been a
complex but neglected problem. 

■ Emerging as an occupational disease of agricultural workers.

EPIDEMIOLOGY

■ Mostly in rural areas

■ Male : female ratio is 2:1.
■ Peaking ages 15-29 years.
■ Estimated 400,000 snakebite related amputations each year
around the world.
■ Children have both higher incidence and suffer more severe
effects than do adults, as a result of their smaller body mass.
■ There are about 236 species of snakes in India, most of
which are nonvenomous.

■ Common cobra (Naja naja), Russell’s Viper ( Dabiola

russelii), saw- scaled viper (Echis Carinatus) and common
krait (Bungarus caeruleus) are highly venomous and are
responsible for most of the poisonous bites in india.
■ The venom is synthesized by the modified salivary
glands and injected through specially channeled or
grooved teeth called Fangs.
CLASSIFICATION OF SNAKES
ELAPIDAE COBRA

COMMON KRAIT

VIPERIDAE RUSSELLS VIPER

SAW-SCALED VIPER

CROTALIDAE PIT VIPER

HYDROPHIDAE SEA SNAKES

FANGS
■ PUPIL
BODY SCALES
Snake venoms
Cobra Krait Viper Sea snake
R SS

Local effect ++ _ +++ _

Vasculotoxic _ _ +++ _

Neurotoxic ++ ++ _ ++

Cardiotoxic ++ ++ _ +

Myotoxic _ _ _ +++
Venom apparatus
■ Venomous snakes of medical importance have a pair of enlarged
teeth, the fangs, at the front of their upper jaw. These fangs
contain a venom channel or groove, along which the venom can
be introduced deep into the tissues of their natural prey. If a human
is bitten, venom is usually injected subcutaneously or
intramuscularly.
Venom composition
■ Each venom contains >100 different proteins: enzymes (constituting 80-
90% of viperid and 25-70% of elapid venoms), non enzymatic polypetptide
toxins, and nontoxic proteins such as nerve growth factor.

■ Non protein ingredients  carbohydrates and metals (often part of

glycoprotein metalloprotein enzymes), lipids, free amino acids,
nucleosides, and biogenic amines such as serotonin and Ach.
Venom enzymes

• Hydrolases, hyaluronidase and

activators or inactivators of
physiological processes, such as
kininogenases.
• Zinc metalloproteinases/
metalloproteinases (like disintegrin-
like cysteine – rich), hemorrhagins
(snake venom metalloproteinases
SVMPs).
Procoagulant enzymes
■ Thrombin like or activate factors like factor V, X, prothrombin and other
clotting factors. These enzymes stimulate blood clotting with formation of
fibrin in the blood stream.

■ Results in incoagulable blood because most of the fibrin clot is broken down
immediately by the bodys own plasmin fibrinolytic system.

1. Phospholipases A2 (lecithinase)

2. Proteolytic enzymes ( metalloproteinases, endopeptidases or hydrolases)

and polypeptide cytotoxins ( cardiotoxins)

3. Venom polypeptide toxins (neurotoxins)

Neurotoxic venom pathuphysiology
■ Venoms with neurotoxic activity produce paralysis and respiratory
distress by binding the nicotinic Ach receptors, thereby preventing
the depolarizing action of Ach.

■ Most important effect is to prevent the transmission of nerve

impulses in cholinergic synapses. ALFA neurotoxins interfere with
neurotransmitter release and cause muscle paralysis, respiratory
failure and death by asphyxiation.
Hemotoxic venom
■ Acts by lysing erythrocytes. Venoms of this kind have a proteolytic action.
They produce swelling, CVS damage and eventually necrosis. They
disrupt blood clotting and the in the process of destroying the blood’s
functionality, severely damage internal organs and other body tissues 
painful.

■ Immediate cause of death being hypovolaemic shock.

■ Blood and plasma loss from the intravascular to the extracellular space,
creating oedema  circulatory compromise and hypovolaemic shock.
Various snakebites, their fatal dose, quantity
of venom injected, and time to fatality.
Snake Fatal dose in Average dose Average fatal
humans delivered per bite period

Indian cobra 12mg 60mg 8 hours

Common Krait 6mg 20mg 18 hours

Russell's viper 15mg 63mg 4 days

Saw scaled viper 8mg 13-40mg 41 days

Clinical features
■ Dry bites – 20% Pit viper and 43% Cobra bites
■ Local features

• Fang marks
• Pain
• Swelling
• Blistering & necrosis
• Lymphangitis,
lymphadenopathy
• Venom ophthalmia
• Secondary infection
General features
■ Flushing
■ Sweating
■ Breathlessness, palpitation
■ Tightness in chest
■ Nausea and vomiting
■ Acroparaesthesia
■ Hypersalivation, blurring of vision( Cobra)
■ Abdominal colic, diarrhea, collapse (krait)
Neuroparalytic ( Elapid envenomation)
■ Symptoms  2 Ps & 5Ds

DYSNOEA
PTOSIS DYSPHONIA
DYSARTHRIA
PARALYSIS DIPLOPIA
DYSPHAGIA
Chronological order of appearance of symptoms
■ Furrowing of forehead & ptosis
■ Diplopia
Related to 3rd, 4th, 6th
■ Dysarthria and lower cranial nerve
■ Dysphonia (pitch of voice becomes less) paralysis.
■ Dyspnea
■ Dysphagia
■ Intercostal
■ And skeletal muscle weakness occurs in descending manner
Other signs

1. Impending respiratory failure

2. Absent deep tendon reflexes
3. Head lag
4. Stridor
5. Ataxia
6. Hypertension and tachycardia may be
present due to hypoxia
How to identify impending respiratory failure?
■ Cry in a child whether loud or husky can help in identifying
impending respiratory failure.

IMPORTANT

■ Bilateral dilated, poorly or a non reacting pupil is not a sign of brain dead
in elapid envenoming…
Vasculotoxic (Hemotoxic or bleeding)
■ Bleeding and clotting disorders (Vipieridae)
■ Visible systemic bleeding from the action of hemorrhagins.
■ Gingival bleeding
■ Epistaxis
■ Ecchymotic patches
■ Hemetemesis
■ Hemoptysis
■ Bleeding per rectum
■ Subconjunctival hemorrhages

■ Continous bleeding from the bite site

■ Bleeding from pre exsisting conditions

■ Compartment syndrome

■ GI or retroperitoneal bleeding

■ Intracranial bleeding

■ Life threatening complications  AKI

 AKI in snake bite additional
causes being
• Hypotension
• Hypovolemia
• Direct vasodilatation
• Direct cardiotoxicity

■ Long term sequelae 

1. Pituitary insufficiency with Russells viper
2. Sheehans syndrome
3. Amenorrhea in females
Skeletal muscle breakdown( sea snakes, Russells
Viper)

Generalized pain
Stiffness
Tenderness of muscles
Trismus
Hyperkalaemia
Myoglobinuria
Cardiac arrest
Renal (Viperidae, Sea snakes)
■ Loin pain
■ Hematuria
■ Hemoglobinuria
■ Myoglobinuria
■ Oliguria/anuria
■ Symptoms and signs of uremia  Acidotic breathing, hiccups,
nausea, pleuritic chest pain etc.
FIRST AID TREATMENT PROTOCOL
■ Recommended based on the mnemonic
■ CARRY NO R.I.G.H.T
■ Carry – do not allow the patient to walk even for a short distance.
Children can be carried.
■ NO tourniquet
■ NO electrotherapy
■ NO cutting
■ NO pressure immobilization
■ Nitric oxide donor (Nitrogesic ointment/ Nitrate Spray)
■ R.= Reassure the patient. 70% of all snakebites are from
nonvenomous species. Only 50% of bites by venomous species
actually envenomate the patient
■ I = Immobilize in the same way as a f r a c t u r e d limb. Use
bandages or cloth to hold the splints, not to block the blood supply
or apply pressure. Do not apply any compression in the form of
tight ligatures, they don’t work and can be dangerous!
■ GH= Get to Hospital Immediately.
■ Traditional remedies have NO P R O V E N benefit in treating
snake bites.
■ T= Tell the Doctor of any systemic symptoms that manifest on the
way of hospital like ptosis.
Critical assessment

• Airway
• Breathing
• Circulation
• Deal with any life
threatening symptoms
on presentation
• Bite site local • Blood pressure
swelling • Pulse rate
• Painful tender • Bleeding (gums, nose,
• Enlarged local vomit, urine or stool)
lymph glands • Level of consciousness
• Persistent bleeding • Drooping eyelids
from the bite (ptosis) and other signs
wound of paralysis
Check for and monitor the following

• HR, BP, RR and Spo2 every 20

minutes.

• Whole blood clotting test (20

WBCT) every hour for first 3
hours and every 6 hours for
remaining 24 hours.

• Distal pulse and signs of

compartment syndrome.
Vasculotoxic patients

Bleeding from multiple 1. Need urgent attention

orifices with hypotension, 2. ICU care
reduced urine output, 3. Volume replacement
obtunded mentation 4. Pressor support
(drowsy, confused), cold 5. Dialysis
extremities. 6. Infusion of blood and
blood products
Neuroparalytic patients

1. Need urgent
Respiratory paralysis,
ventilator
tachypnoea or bradypnea or
paradoxical respiration, management.
obtunded mentation and 2. Endotracheal
peripheral skeletal muscle intubation
paralysis. 3. Ventilator
assistance.
Other cases
■ Establish large bore IV access.

■ Start NS infusion.

■ Before removal of tourniquets/ ligatures, test for the

presence of a pulse distal to the tourniquet.
Diagnosis and testing
■ Bite marks to distinguish between venomous or non venomous is of no use.

The 20 Minute Whole Blood Clotting Test (20

WBCT) was adopted as the standard test for
coagulopathy.
Simple to carry out but crucially requires a clean,
new and dry test tube. A few mL of fresh venous
blood is left undisturbed for 20 minutes, and then
gently tilted. If the blood is still liquid this is
evidence of coagulopathy and confirms that the
biting species is Viperine.
Cobras or Kraits do not cause anti-hemostatic
symptoms
Other useful tests
■ Hb/platelet count/peripheral smear/ PT and APTT.

■ Urine examination for proteinuria/RBC/ hemoglobinuria

■ Myoglobinuria

■ Biochemistry for serum creatinine, urea, potassium.

■ ECH/CXR/CT/USG

■ Oxygen saturation/ ABG

■ ELISA to confirm snake species.

ANTI SNAKE VENOM (ASV)
■ ASV is the mainstay of treatment.
■ Anti venom is an immunoglobulin purified from the plasma of a
horse, mule or donkey, or sheep that has been immunized with the
venoms of one or more species of snake.
■ In India, polyvalent ASV, is effective against all the four common
species, Russell’s viper, cobra, common Krait, saw scaled Viper,
and no monovalent ASV’s are available.
■ ASV is produced in both liquid and lyophilized forms.

■ Liquid ASV requires a cold chain and has 2 year shelf life.

■ Lyophilized ASV in powder form has 5 year shelf life and requires
to be stored in a cool place.
Route?
■ Lyophilized forms of anti venom are reconstituted using 10ml sterile
water for injection per ampoule.

■ 2 methods of administration are recommended.

■ Intravenous “push” injection  given by slow intravenous injection

( not more than 2ml/min).

■ Intravenous infusion  diluted in 5-10ml/kg of isotonic fluid and

infused over a period of 1 hour.

■ W/O for anaphylactic antivenom reactions after ASV has been

initiated so that reactions can be detected and epinephrine can be
administered.
Indications for ASV
■ Evidence of systemic toxicity

■ Hemodynamic /respiratory instability (hypotension, respiratory distress)

■ Haemotoxicity ( clinically significant bleeding or abnormal coagulation

studies)

■ Neurotoxicty (CNS abnormalities and progressing to descending

paralysis including diaphragm).

■ Evidence of local toxicity (progressive soft tissue swelling).

Initial dose
■ In practice, the choice of an initial dose of antivenom is usually
empirical.
■ As each vial of polyvalent ASV neutralises 6 mg of Russells viper
venom, each vial is 10 ml of reconstituted ASV.
■ The initial dose is 8-10 vials for both adults and children.
■ Common krait- 100ml ASV
■ Russell’s viper -100ml ASV
■ Saw scaled viper- 50 ml
■ Indian cobra- 100ml
Response to initial dose of ASV
GENERAL Pt feels better, nausea, headache,
generalized aches and pains subsides.

SPONTANEOUS SYSTEMIC Stops within 15-30 minutes

BLEEDING
BLOOD COAGULABILITY ( as Usually restored in 3-9 hours
measured by 20WBCT)
PTs IN SHOCK BP increases within the first 30-60 minutes
and arrhythmias such as sinus
bradycardia may resolve.

NEUROTOXIC ENVENOMING Begins to improve by 30 minutes, but can

(COBRA BITES) take up to several hours.

ACTIVE HEMOLYSIS May cease within a few hours and the

urine returns to its normal colour.
Criteria for giving more antivenom
■ Persistence or recurrence of blood incoagulability after 6 hours.
■ Bleeding after 1-2 hours
■ Deteriorating neurotoxic or cardiovascular signs after 1 hour.
Range of venom injected is about 5mg-147mg

Maximum dose of ASV is around

25 vials.
ASV should be administered over
a period of 1 hour.
In hemotoxic envenomation

■ Initial dose administered over 1 hour, no further dose of ASV is given for
6 hours.

■ 20 WBCT every 6 hours will determine if additional ASV is required. If

the blood remains uncoagulable 6 hours after the initial dose, the same
dose should be repeated.

■ Based on the observation  if a large dose of antivenom is given

initially, the time taken for the liver to restore coagulable levels of
fibrinogen and other clotting factors is 3-9 hours.

■ This reflects the period the liver requires to restore clotting factors.
In Neurotoxic envenomation
■ Antivenom treatment alone cannot be relied upon to save the life
of the patient with bulbar and respiratory paralysis.
■ Death may result from

Aspiration
Airway obstruction
Respiratory paralysis

■ Once there is loss of gag reflex and pooling of secretions in the

pharynx, failure of cough or respiratory distress, a cuffed ETT or a
laryngeal mask airway should be inserted.
Indications for intubation

1. Imminent respiratory arrest ( breathing is absent

or inadequate)
2. Neck muscle weakness with shallow respiration
or paradoxical breathing.
3. Upper airway obstruction
4. Oxygen saturation <90% (equivalent to Pa02 <
60 mmhg) despite high flow oxygen.
5. Blood gas measurement showing respiratory
acidosis ( hypoxia Pa02 < 60 mmhg, PaC02
>45mmhg)
Neostigmine test
■ A trial of anticholinesterase (eg Tensilon test) should be performed in every patient
with neurotoxic envenoming.

■ Atropine sulphate (50microgram/kg for children) or glycopyrronium is given by IV

injection followed by neostigmine IM injection of 0.04mg/kg or edrophonium
0.25mg/kg

■ Patient is observed for the next 30-60 minutes (neostigmine) or 1—20 minutes
(edrophonium) for signs of improved neuromuscular transmission. Ptosis may
disappear and ventilatory capacity may improve.

■ If positive institute regular atropine and neostigmine. 0.01-0.04mg/kg neostigmine every

2-4hours
Treatment of hypotension and shock
■ Snake bite causes of hypotension and shock are as follows:
1. Anaphylaxis
2. Vasodilatation
3. Cardiotoxicity
4. Hypovolemia
5. Antivenom reaction
6. Respiratory failure
7. Acute pituitary adrenal insufficiency
8. Septicemia
■ Treatment  selective vasoconstrictor such as dopamine can be
given IV, preferably into a central vein (2.5-5mcgs/kg/min)
Other managements in Snake bites

• Mechanical ventilation
• Volume replacement
• Forced alkaline diuresis
• Management of
hyperkalaemia
• Management of severe
acidosis
• Dialysis
• Management of shock and
myocardial damage
• Management of local severe
envenoming
Indication for Dialysis in Snake bite

• Clinical uremia
• Fluid overload not responding to diuretics
• Hyperkalemia >7mmol/l or ecg changes
• Symptomatic acidosis
• 1 or more of - 1. creatinine >4mg/dl
2.urea >130mg/dl
Surgical procedures in snake bite
■ Debridement of necrotic tissues

■ Fasciotomy in compartment syndrome

Antivenom reactions
■ Early anaphylactic reactions

1. Seen within minutes and up to 180 minutes after starting antivenom.

2. Patient begins to itch and develops urticaria.

3. Minority may present with life threatening anaphylactic reactions like

hypotension, bronchospasm and angio-oedema.

4. Not IgE mediated.

5. Complement activation by IgG aggregates or direct stimaulation of

mast cells or basophils by antivenom proteins are most likely
mechanism.
■ Pyrogenic (endotoxin) reactions:

1. Develops 1-2 hours after treatment.

2. Symptoms include shaking chills, fever, vasodilatation, and a fall

in BP.

3. Febrile convulsions are seen in children.

4. Caused by pyrogenic contamination during the manufacturing

process.

5. Commonly reported.
■ Late (serum sickness type) reactions.

1. Develops 1- 12 days after treatment.

2. Clinical features include fever, nausea, vomiting, diarrhea, itching,

recurrent urticaria, arthralgia, myalgia, lymphadenopathy,
periarticular swellings, mononeuritis multiplex, proteinuria with
immune complex nephritis and rarely encephalopathy.
Adverse reactions to anti snake venom
■ At the first sign of any of the following :

■ Urticaria, itching, fever, chills, nausea, vomiting, diarrhea,

abdominal pain, tachycardia, hypotension, bronchospasm and
angio-oedema.

1. ASV should be discontinued

2. 0.5mg of 1:1000 adrenaline should be given IM

3. The pediatric dose is 0.01 mg/kg body weight of adrenaline IM

■ 100 mg of hydrocortisone and 10 mg of H1 antihistamine will be
administered IV.

■ The dose for children is 0.2 mg/kg of antihistamine IV and 2 mg/kg of

hydrocortisone IV.

■ If after 10 to 15 minutes the patient’s condition has not improved or is

worsening, a second dose of 0.5 mg of adrenaline 1:1000 IM is given.

■ This can be repeated for a third and final occasion but in the vast
majority of reactions, 2 doses of adrenaline will be sufficient.
 Once the patient has recovered

ASV can be restarted

Given slowly for 10-15 minutes (under close monitoring)

Then the normal drip rate should be resumed

■ Adrenaline reaches necessary blood plasma levels in 8 minutes via the
IM route, but up to 34 minutes in the subcutaneous route.
Repeat dose of ASV
■ In Anti-hemostatic bites, once the initial dose has been administered over one
hour, no further ASV is given for 6 hours.

■ Twenty WBCT test every 6 hours, will determine if additional ASV is required.
This reflects the period the liver requires to restore clotting factors. I

■ 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 a second and final dose should
be given. At this point the victim will have received sufficient neutralising
capacity from the ASV, and will either recover or require mechanical ventilation;
in either event further ASV will achieve nothing
Supportive care

■ Antivenom treatment can be expected to neutralize free circulating

venom, prevent progression of envenoming and allow recovery.

■ Patient may require life support systems such as treatment of

shock, assisted ventilation and dialysis until the severely damaged
organs and tissues have had time to recover.
Airway, Breathing, Circulation, Disability, Exposure
Connect cardiac monitors, start IV line, remove tourniquet
carefully.
1) Systemic envenomation 3. AKI
• Oliguria
1. Neurotoxic • Raising blood urea, 2) Local envenomation
• Ptosis creatinine, • Local swelling involving more
• Ophthalmoplegia • Rhabdomyolysis
than half of the bitten limb.
• Paralysis • DIC
• Rapid extension of swelling within
few hours of bite.
2. Hematotoxic • Development of an enlarged tender
• Spontaneous systemic
bleeding 4. Cardiovascular system lymph node draining the bitten
• Coagulopathy (WBCT > • Hypotension limb.
20mins) • Cardiac arrhythmia
• Thrombocytopenia < • ECG abnormalities
1,00,000
• Deranged PT/INR
Infusion ASV 10 vials diluted in 500ml NS/5D Inj Augmentin 1.2g IV
Administer over 1 hour +
Closely monitor the patient for 2 hours Inj Metronidazole 500mg IV
W/O for anaphylaxis +
Inj T.T IM stat.

Hemotoxic
Neurotoxic
Initial 10 vials of ASV over 1 hour
Give an initial dose of 10 vials
If neurotoxicity persists after 2 hours give 10
Repeat PT 6hours later, if deranged give
more vials (max 20 vials).
2nd dose of ASV (10 vials)
If respiratory failure still persists, continue
Repeat PT every 6 hours and give ASV if
ventilation.
indicated (upto maximum of 25 vials).
THANKYOU…!!!