SNAKE

BITE

ABHIJA BABUJI.
CRRI.
DEPARTMENT OF PEDIATRICS.
SMIMS.
Out line
INTRODUCTION
EPIDEMIOLOGY
TYPES OF SNAKE BITES
CLASSIFICATION
IDENTIFICATION FEATURES.
CLINICAL FEATURES OF SNAKE BITE
NATIONAL SNAKEBITE MANAGEMENT
PROTOCOL, INDIA.
INTRODUCTION
. Snake bite is one of the major public health
problems in the tropics. It is also emerging as
an occupational disease of agricultural workers.
In view of their strong beliefs and many
associated myths, people resort to magico
religious treatment for snake bite thus, causing
delay in seeking proper treatment.

Snake bites is a particularly important public

health problem in rural areas of tropical and
subtropical countries situated in Africa, Asia,
Oceania and Latin America.
INTRODUCTION
The 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 venom can be
introduced deep into the
tissues of their natural prey.
If a human is bitten, venom
is usually injected
subcutaneously or
intramuscularly.
epidemiology
The annual number of cases of snakebite worldwide is
about 5 million, among which there are some 100 000
to 200 000 deaths.

In addition to the deaths, there are an estimated

400000 snakebite-related amputations each year
around the world .

Children have both higher incidence rates and suffer

more severe effects than do adults, as a result of their
smaller body mass

SNAKE BITE INCIDENCES

Papua New Guinea has some of the highest snakebite

rates in the world, with the countrys rural central province
recording an annual incidence of 561.9 cases per 100 000
population

Snakebites are concentrated in mainly rural areas and

vary considerably by season, with the peak incidence
seen in the rainy and harvesting seasons
Snake bite deaths worldwide
india
India is estimated to have the highest
snakebite mortality in the world.
World Health Organization (WHO) estimates
place the number of bites to be 83,000 per
annum with 11,000 deaths

Males: Female::2:1.

Majority of the bites being on the lower

extremities.
SNAKES IN INDIA
There are about 236 species of snakes in India, most
of which are nonvenomous

Their bites, apart from causing panic reaction and

local injury, do not harm the patient.

13 known species that are venomous and of these

four, namely common cobra (Naja naja),
Russells viper (Dabiola russelii), saw-scaled
viper (Echis carinatus) and common krait
(Bungarus caeruleus) are highly venomous and
believed to be responsible for most of the poisonous
bites in India
 COMMONEST INDIAN venomous snakes

Cobra Krait

The venom is synthesized by the modified salivary glands

and injected through special channeled or grooved teeth
called fangs

Russels viper Saw-scaled viper

CLASSIFICATION
Worldwide, only about 15% of the more than 3000
species of snakes are considered dangerous to
humans.

The family Viperidae is the largest family of

venomous snakes, and members of this family can be
found in Africa, Europe, Asia, and the Americas.

The family Elapidae is the next largest family of

venomous snakes.
ELAPIDAE
Elapidae have short permanently erect fangs This family
includes the cobras, king cobra, kraits, coral snakes and
the sea snakes.

The most important species, from a medical point of view

include the following:
Cobras: Genus Naja
N naja(spectaled cobra all over in India )
N kaouthia (monocled West Bengal ,MP ,U.P,
Orissa)
N oxiana [Black cobra northern states - patternless]
N philippinensis
N atra
King cobra: Ophiophagus hannah
Short permanently erect fangs of a typical elapid
KRAITS (genus Bungarus)
KRAITS (genus Bungarus)
B caeruleus common krait [all over India ]
- paired white bands & large hexagonal scales in top
of the snakes
B fasciatus banded krait [black & yellow band
W.B,M.P,A.P,BIHAR ,ORRISSA]
B candidus Malayan krait
B multicinctus Chinese krait
Sea snakes (important genera include Enhydrina,
Lapemis and Hydrophis)
Blue spotted sea snake (Hydrophis cyanocinctus)
Common krait- key identification feature is PAIRED white bands.
VIPERIDAE
Have long fangs which are
Normally folded up against
the upper jaw but,when
the snake strikes,
are erected .

There are two subgroups,

the typical vipers (Viperinae)
and the pit vipers (Crotalinae).

The Crotalinae have a special sense organ, the pit

organ, to detect their warm-blooded prey. This is
situated between the nostril and the eye
Russells vipers details of fangs.
 RUSSELLS VIPER

Hemotoxic
. venom BUT can
also
Present neurotoxic symptoms

Key identification feature is the black

edged almond or chain shaped marks
on the back
 Key Identification
Feature- large plate
scales on the head
PIT VIPER
Haemotoxic venom.
Causes Renal failure
Late onset envenoming
 Saw-scaled or carpet vipers - Echis
carinatus and E sochureki
Most parts of India except Kerala Arrow
shaped mark in head & hoop like markings in
flanks
 India: Poisonous snakes

Elapidae Cobra, Kraits Neurotoxic

Viperidae Russells Vipers., Hemotoxic

(Vipers) Saw scaled Vipers.,
Pit Vipers.
Hydrophid Sea Snakes Myotoxic
ae

Krait and russells viper is much more toxic than that of cobra
IDENTIFICATION FEATURES
IDENTIFICATION FEATURES
 Snake Venom
Complex mixture of proteins including
Large enzymes-local tissue destruction.
Low molecular weight polypeptides-lethal systemic
effects
-Acidic.
-Sp Gravity: 1.030-1.070
-On drying Fine needle like crystals.
-Water Soluble.
-Lethal Dose:
Cobra-0.12gm, Krait0.06gm- Russells V-0.15gm
Healthy, angered and hungry snakes unload more venom
than a recently satiated and surprised snake .
Due to the venom, there is cell function degeneration and
the final outcome depends on the type of venom
injected.
Snake bite-venom injected

enters surrounding tissue

direct venom action
Capillary absorption

blood vessels lymphatics

Target organs-systemic effect

PATHOGENESIS
Snake venom is a mixture of
polypeptides, proteolytic
enzymes, and toxins, which
are species-specific.
Primarily neurotoxic
Hydrophidae - poisonous sea snakes

Elapidae - cobras, kraits, coral snakes

Venom have a curare-like effect by

blocking neurotransmission at
neuromuscular junction.

Death results from respiratory

depression.
Neurotoxic venom
Venoms with neurotoxic activity produce paralysis
and respiratory distress by binding the nicotinic
acetylcholine receptors, and preventing the
depolarizing action of acetylcholine.
The most important effect of neurotoxins 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.
PATHOGENESIS

Viperidae vipers
Primarily hemotoxic&
cytotoxic
Crotalidae (sub family of
viperidae) :

Tissue necrosis, vascular leak,

and coagulopathies.

Death from pit viper bites

results from hemorrhagic
shock, adult respiratory
distress syndrome, and renal
failure.
 HEMOTOXIC

VENOM
A hemotoxic venomthat acts bylysing erythrocytes. Venoms of
this kind have a proteolyticaction. They produce swelling,
cardiovascular damage, and eventualnecrosis. They also disrupt
blood clotting and, in the process of destroying the blood's
functionality, severely damage internal organs and other body
tissues, which can be extremely painful. The immediate cause of
death in such cases is usually hypovolemic shock.
envenomation increases capillary permeability that results in
blood and plasma loss from the intravascular to the extracellular
space, creating edema, which, in case of being sufficiently
important, may cause circulatory compromise and hypovolemic
shock.
Cytotoxic venom
snake venom has cytolytic properties, which
cause local necrosis and secondary infection,
which could result in sepsis and death
CLINICAL FEATURES.
When venom has not been injected;
Out of fear
Vasovagal attack
Collapse
Slowing of heart rate
Another source of misleading symptoms caused by
First aid and traditional treatments.
CLINICAL FEATURES
Following the immediate pain of the bite-increasing local
pain (burning, bursting, throbbing) at the site of the bite

Local swelling that gradually extends proximatelly up the

bitten limb and tender, painful enlargement of the regional
lymph nodes draining the site of the bite

Bites by kraits, sea snakes may be virtually painless and

may cause negligible local swelling. Someone who is
sleeping may not even wake up when bitten by a krait and
there may be no detectable fang marks or signs of local
envenoming
Local symptoms and signs in the bitten part
Fang marks
Local pain
Local bleeding
Bruising
Lymphangitis
Lymph node enlargement
Inflammation (swelling, redness, heat)
Blistering
Local infection, abscess formation
Necrosis
 Fang marks
Persistent bleeding from
fang marks 40min after
bite of pit viper

Blistering at
site of bite
SYSTEMIC SYMPTOMS & SIGNS

Generalised (systemic) symptoms and signs

Nausea, vomiting, malaise, abdominal pain, weakness,
drowsiness, prostration

Cardiovascular (Viperidae)
Dizziness, faintness, collapse, shock, hypotension,
cardiac arrhythmias, pulmonary oedema, cardiac arrest
Cont.
Bleeding and clotting disorders (viperidae)
Bleeding from recent wounds (including fang
marks,venepunctures etc) and from old partly-healed
wounds.

Spontaneous systemic bleeding from gums, epistaxis,

bleeding into the tears, haemoptysis, haematemesis,
rectal bleeding or melaena, haematuria, vaginal bleeding,
bleeding into the skin (petechiae, purpura, ecchymoses)
and mucosae
Cont.
Neurological(Elapidae, Russellss viper)
Drowsiness, paraesthesiae, abnormalities of taste and
smell, heavy eyelids, ptosis, external ophthalmoplegia,
paralysis of facial muscles ,difficulty in opening mouth and
showing tongue and weakness of other muscles
innervated by the cranial nerves, aphonia, difficullty in
swallowing secretions, respiratory and generalised flaccid
paralysis
Cont.
Skeletal muscle breakdown(sea snakes, Russells
viper)
Generalised pain, stiffness and tenderness of
muscles, trismus, myoglobinuria hyperkalaemia,
cardiac arrest
Renal(Viperidae, sea snakes)
Loin (lower back) pain, haematuria,
haemoglobinuria, myoglobinuria, oliguria/anuria,
symptoms and signs of uraemia (acidotic breathing,
hiccups, nausea, pleuritic chest pain etc
 Bleeding from
gingival sulci

Broken neck
sign in a
child
envenomed
by krait
Species: Signs and Symptoms
Signs/Symptoms Russells
Cobra Krait Saw Scaled Other
and Potential Viper
Viper Vipers
Treatments

Local pain/ Tissue

Damage Yes No Yes Yes Yes

Ptosis/Neurotoxicity Yes Yes Yes! NO No

Coagulation No No Yes Yes Yes

Renal Problems No No Yes NO Yes

Neostigmine &
Atropine Yes No? No? NO No
 National snakebite management
protocol, India.
FIRST AID
The first aid recommended is based around the mnemonic:

"Do it R.I.G.H.T."
It consists of:
R. = Reassure the patient. Seventy per cent of all snakebites are from non
venomous species. Only 50% of bites by venomous species actually enveno-
mate the patient
I = Immobilize in the 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. Do not apply any compression in the form of tight ligatures, they do not
work and can be dangerous!
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 that manifest on
the way to hospital.
 PRESSURE IMMOBILISATION

Its purpose is to retard the

movement of venom from
bite site into circulation,
thus buying time for the
patient to reach
medical care.
Cont.
Be prepared to treat the shock and provide
cardiopulmonary resuscitation (CPR).

Get the victim to the nearest secondary or tertiary care

hospital where antivenom can be provided
DO NOTS IN FIRST AID
Do not apply a tourniquet.

Do not wash the bite site with soap or any other solution to
remove the venom.

Do not make cuts or incisions on or near the bitten area.

Do not use electrical shock.

Do not freeze or apply extreme cold to the area of bite.

Do not apply any kind of potentially harmful herbal or folk

remedy.
.
Cont.
Do not attempt to suck out venom with your
mouth.

Do not give the victim drink, alcohol or other

drugs.

Do not attempt to capture, handle or kill the snake

and patients should not be taken to quacks.
SNAKE BITE TREATMENT PROTOCOL
The initial management includes dealing with
airway, breathing and treatment of shock.

Administer tetanus toxoid

Emergency care

Try to identify the snake responsible.

Snake colouration, its pupil shape and bitemarks

Ask the victim relatives to carefully bring the snake to

hospital if it has been killed and then use the snake
identification material in protocol to identify it.

Determine if any traditional medicines have been used as

they can sometimes lead to confusing symptoms.

Determine the exact time of bite which helps in determining

progression of signs and symptom.
Cont.
Iv access established in unaffected
extremity
CBC, coagulation profile, fibrinogen
concentration, should be assessed.
Tourniquets placed in field should be
carefully removed.
The bitten extremity should be marked at 2
or more sites proximal to the bite and the
circumference at these locations should be
assessed every 15min to monitor for
progressive edema-indicative of ongoing
Cont.
All the patients should be kept under observation
for a minimum of 24 hours.

Many species, particularly the Krait and the hump-

nosed pit viper are known for delayed appearance
of symptoms which can develop after 612 hours
Investigations
Twenty-minute whole blood clotting test (20WBCT) reliable
test of coagulation which can be carried out by bedside
and is considered to be superior to capillary tube
method for establishing clotting capability in snake bite.

A few milliliters of fresh venous blood should be placed

in a fresh, clean and dry glass vessel preferably test tube
and left undisturbed at ambient temperature for 20
minutes.

After that tube should be gently tilted to detect whether

blood is still liquid and if so then blood is incoagulable.The
test should be carried out every 30 minutes from
admission for 3 hours and then hourly after that.
Other Useful Tests (If Facilities Available
Hb/platelet count/peripheral smear prothrombin time (PT)/activated
partialthromboplastin time

Urine examination for proteinuria/RBC/hemoglobinuria

Myoglobinuria

Biochemistry for serum creatinine/Urea/Potassium

ECG/X-ray/CT/Ultrasound(The use of X-ray and ultrasound, area

of unproven benefit, apart from identification of clot in viperine bite)

Oxygen saturation/arterial blood gas (ABG)

Enzyme-linked immunosorbent assay (ELISA) to confirm

snakespecies.
Treatment Phase

Pain can be relieved with oral paracetamol or

tramadol.

Aspirin or nonsteroidal anti-inflammatory drugs

(NSAIDs) should not be administered
Severity of envenomation.
Anti-snake venom (ASV)
Anti-snake venom (ASV)is the mainstay of
treatment.
Antivenom is immunoglobulin [usually pepsin-
refined F(ab)2 fragment of whole IgG] purified from
the plasma of a horse, mule or donkey (equine) or
sheep (ovine) that has been immunized with the
venoms of one or more species of snake.
In India, polyvalent ASV, i.e. effective against
all the four common species; Russells viper,
common cobra, common Krait and saw-scaled
Viper and no monovalent ASVs are available
 ASV is produced both in Liquid and Lyophilized forms.

There is no evidence to suggest which form is more

effective.

Liquid ASV requires a reliable cold chain and has 2-

year shelf life.

Lyophilized ASV in powder form,has 5-year shelf life

and requires only to be kept cool.
Only free unbound fraction of venom can be
neutralized by anti snake venom.
 HOW LONG ASV CAN BE GIVEN?
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. It is,therefore, appropriate to give
antivenom for as long as evidence of the
coagulopathy persists.
ROUTE?
Freeze-dried (lyophilized) antivenoms are reconstituted,
usually with 10ml of sterile water for injection per ampoule.
Two methods of administration are recommended:
(1) Intravenous push injection: Reconstituted freeze-
dried antivenom is given by slow intravenous injection(not
more than 2 ml/minute).
(2) Intravenous infusion: Reconstituted freeze-dried
antivenom is diluted in approximately 5-10 ml of isotonic
fluid per kg body weight) and is infused at a constant rate
over a period of about one hour
Patients must be closely observed for at least one hour after
starting intravenous antivenom administration, so that early
anaphylactic antivenom reactions can be detected and treated
early with epinephrine(adrenaline)
Cont.
Local administration of ASV is not recommended as
it is extremely painful and can raise the
intracompartmental pressure.
Intramuscular inj are not recommended .Antivenoms
are large molecules (F(ab)2 fragments or
sometimes whole IgG) which, after intramuscular
injection, are absorbed slowly via lymphatics.
Bioavailability is poor, especially after intragluteal
injection, and blood levels of antivenom never
reach those achieved rapidly by intravenous
administration. Other disadvantages are the pain
of injection of large volumes of antivenom and the
risk of haematoma formation
Anti-snake Venom Administration
INDICATIONS
Evidence of systemic toxicity.
Hemodynamic or respiratory instability
Hypotension, respiratory distress
Hemotoxicity
Clinically significant bleeding or
abnormal coagulation studies
Neurotoxicity
Any evidence of toxicity usually beginning with CN
abnormalities and progressing to descending
paralysis including diaphragm
Evidence of local toxicity
Progressive soft tissue swelling
TEST DOSE
Anti-snake Venom Test Dose
Test doses have not been shown to have predictive
value in predicting anaphylactic reaction or late
serum sickness and not recommended
.
INTIAL DOSE.
The recommended dose is often the amount of
antivenom required to neutralize the average
venom yield when captive snakes are milked of
their venom. In practice, the choice of an initial
dose of antivenom is usually empirical.
Each vial is 10 ml of reconstituted ASV

Initial dose is 8-10 vials for

both adults and children.
Common krait- 100ml ASV
Russells viper-100ml
Saw scaled viper-50 ml
Indian cobra-100ml
Response to intial dose of ASV
: If an adequate dose of appropriate antivenom has been administered,
the following responses may be observed.
(a) General: The patient feels better. Nausea, headache and
generalised
aches and pains may disappear very quickly. .
(b) Spontaneous systemic bleeding (e.g. from the gums): This
usually stops within 15-30 minutes.
(c) Blood coagulability (as measured by 20WBCT): This is usually
restored in 3-9 hours.
(d) In shocked patients: Blood pressure may increase within the first
30-60 minutes and arrhythmias such as sinus bradycardia may
resolve.
(e) Neurotoxic envenoming (cobra bites)
may begin to improve as early as 30 minutes after antivenom, but
usually takes several hours.
(f) Active haemolysis may cease within a few hours and the urine
returns to its normal colour
REPEAT DOSES
Criteria for giving more antivenom
Persistence or recurrence of blood incoagulability
after 6 hours(measured by 20WBCT) or of bleeding
after 1-2 hours.
Deteriorating neurotoxic or cardiovascular signs
after 1-2 hours of administering intial dose of ASV
Range of venom injected is about 5mg-147mg
Maximum dose of ASV is
around 25 vials.
ASV should be administered over a
period of 1hour.
In hemotoxic envenomation;

Once 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. If the blood remains incoagulable (as
measured by 20WBCT) six hours after the initial dose of
antivenom, the same dose should be repeated. This is based
on the observation that, if a large dose of antivenom (more
than enough to neutralize the venom procoagulant enzymes)
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 a patient with bulbar and
respiratory paralysis

Death may result from aspiration, airway

obstruction or respiratory failure.A clear airway
must be maintained. Once there is loss of gag
reflex and pooling of secretions in the pharynx,
failure of the cough reflex or respiratory distress,a
cuffed endotracheal tube or laryngeal mask
airway should be inserted
Neostigmine test.
A trial of anticholinesterase (eg Tensilon test) should be
performed in every patient with neurotoxic envenoming
Atropine sulphate (0.6 mg for adults; 50 g/kg for
children) or
glycopyrronium is given by intravenous injection followed
by
neostigmine bromide . in appropriate doses) by
intramuscular injection 0.02 mg/kg for adults, 0.04
mg/kg for Children.
The patient is observed over the next 30-60 minutes
(neostigmine) or 10-20 minutes (edrophonium) for signs of
improved neuromuscular transmission. Ptosis may
disappear and ventilatory capacity (peak flow, FEV-1 or
maximum expiratory pressure) may improve.
If positive institute regular atropine & neostigmine.
Treatment of hypotension and shock
Snake bite causes of hypotension and shock.
Anaphylaxis
Vasodilatation
Cardiotoxicity
Hypovolaemia
Antivenom reaction
Respiratory failure
Acute pituitary adrenal insufficiency
Septicaemia
Treatment- a selective vasoconstrictor such as dopamine
may be given by intravenous infusion, preferably into a
central vein (startingdose 2.5-5mcg/kg/minute).
 Adverse reactions to anti-snake venom

Fear of potentially life threatening adverse reactions

causes reluctance amongst some to treat snakebite.

However, if handled early and with the primary drug of

choice, these reactions are easily managed.

Patients should be monitored closely as there is evidence

that many anaphylactoid reactions go unnoticed
Adverse reactions to anti-snake venom

At the first sign of any of the following:

Urticaria, itching, fever, shaking chills, nausea, vomiting,

diarrhea, abdominal cramps, tachycardia, hypotension,
bronchospasm and angio-oedema:

1. ASV should be discontinued

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

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

Evidence shows that adrenaline reaches necessary blood

plasma levels in 8 minutes via the IM route, but up to 34
minutes in the subcutaneous route.
Adverse reactions to anti-snake venom

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

. If after 10 to 15 minutes the patients condition

has not improved or is worsening, 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 recoverd

ASV can be restarted

Given slowly for 10-15 minutes

(underclose monitoring)

Then the normal drip rate

should be resumed

ASV test doses have been abandoned:

Have no predictive value in anaphylactoid
or late serum reactions.
May pre-sensitise the patient to the
FOLLOW-UP
After discharge from hospital, victim should be
followed.

If discharged within 24 hours, patient should be

advised to return if there is any worsening of
symptoms such as bleeding, pain or swelling at the
site of bite, difficulty in breathing, altered
sensorium, etc.

The patients should also be explained about serum

sickness which may manifest after 510 days
SUMMARY
Snake bites is a particularly important public health
problem in rural areas of tropical and subtropical countries
situated in Africa, Asia, Oceania and Latin America
The annual number of cases of snakebite worldwide is
about 5 million, among which there are some 100 000 to
200 000 deaths.
common cobra (Naja naja), Russells viper (Dabiola
russelii), saw-scaled viper (Echis carinatus) and
common krait (Bungarus caeruleus) are highly
venomous and believed to be responsible for most of the
poisonous bites in India.
REFERENCES
WHO Fact Sheet On Snake Bite .Geneva.WHO.last accessed on 19 th
january 2015.

National snakebite management protocol, India. (2008). [online]

Avaialable at www://mohfw.nic.in (Directorate General of Healthand
Family Welfare, Ministry of Health and Family Welfare, India).

Simpson ID. Snakebite Management in India, the first few hours: A guide
forprimary care physicians.J Indian Med Assoc. 2007;105:324-35.

.Snake Bite Guidelines INDIAN PEDIATRICS, VOLUME 44 -MARCH 17,

2007.

NELSON TEXTBOOK OF PEDIATRICS

THANK
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