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.

1. SNAKE
BITE
ABHIJA BABUJI.
CRRI.
DEPARTMENT OF PEDIATRICS.
SMIMS.

2. Out line
INTRODUCTION
EPIDEMIOLOGY
TYPES OF SNAKE BITES
CLASSIFICATION
IDENTIFICATION FEATURES.
CLINICAL FEATURES OF SNAKE BITE
NATIONAL SNAKEBITE MANAGEMENT PROTOCOL, INDIA.

3. 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.

4. 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.

5. 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
•

6. SNAKE BITE INCIDENCES
• Papua New Guinea has some of the highest snakebite
rates in the world, with the country’s 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

7. Snake bite deaths worldwide

8. 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.

9. 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), Russell’s 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

10. COMMONEST INDIAN venomous snakes
–
The venom is synthesized by the modified salivary glands and injected
through special channeled or grooved teeth called fangs
Cobra Krait
Russel’s viper Saw-scaled viper

11. 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.

12. 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

13. Short permanently erect fangs of a typical elapid

14. 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)

15. Common krait- key identification feature is PAIRED white bands.

16. 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

17. Russell’s vipers details of fangs.

18. RUSSELL’S VIPER
.Hemotoxic venom BUT can
also
Present neurotoxic symptoms
Key identification feature is the black
edged almond or chain shaped marks
on the back

19. Key Identification
Feature- large plate
scales on the head
PIT VIPER
Haemotoxic venom.
Causes Renal failure
Late onset envenoming

20. •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

21. India: Poisonous snakes
Elapidae Cobra, Kraits Neurotoxic
Viperidae
(Vipers)
Russell’s Vipers.,
Saw scaled Vipers.,
Pit Vipers.
Hemotoxic
Hydrophidae Sea Snakes Myotoxic
Krait and russell’s viper is much more toxic than that of cobra

22. IDENTIFICATION FEATURES

23. IDENTIFICATION FEATURES

24. 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- Russell’s V-0.15gm

25. 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
blood vessels lymphatics
Target organs-systemic effect
Capillary absorption

26. 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.

27. 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.

28. 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.

29. • A hemotoxic venom that acts by lysing erythrocytes. Venoms of this
kind have a proteolytic action. They produce swelling,
cardiovascular damage, and eventual necrosis. 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.
HEMOTOXIC
VENOM

30. Cytotoxic venom
• snake venom has cytolytic properties, which cause local
necrosis and secondary infection, which could result in sepsis
and death

31. 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.

32. 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

33. 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

34. Fang marks
Persistent bleeding from
fang marks 40min after
bite of pit viper
Blistering at
site of bite

35. 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

36. 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

37. Cont.
Neurological(Elapidae, Russells’s 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

38. Cont.
Skeletal muscle breakdown(sea snakes, Russell’s
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

39. Broken neck
sign in a
child
envenomed
by krait
Bleeding from
gingival sulci

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

41. •National snakebite management
protocol, India.

42. 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.
•

43. 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.

44. 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

45. 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.
• .

46. 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.

47. SNAKE BITE TREATMENT PROTOCOL
• The initial management includes dealing with airway,
breathing and treatment of shock.
• Administer tetanus toxoid

48. 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.

49. 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
venom effects.

50. 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 6–12 hours

51. 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.

52. 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.

53. Treatment Phase
• Pain can be relieved with oral paracetamol or tramadol.
• Aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs)
should not be administered

54. Severity of envenomation.

55. 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; Russell’s viper, common cobra, common
Krait and saw-scaled Viper and no monovalent ASVs are
available

56. • 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.

57. 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.
HOW LONG ASV CAN BE GIVEN?

58. 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)

59. 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

60. 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

61. 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
• .

62. 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
• Russell’s viper-100ml
• Saw scaled viper-50 ml
• Indian cobra-100ml

63. 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

64. 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.

65. 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.

66. 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

67. 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 μg/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.

68. 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).

69. • 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

70. 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.

71. 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 patient’s 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.

72. 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 protein.

73. 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 5–10 days

74. 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), Russell’s 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.

75. REFERENCES
• WHO Fact Sheet On Snake Bite .Geneva.WHO.last accessed on 19th
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

76. THANK
YOU