This document provides guidance on snake bites in India. It discusses that snake bites are a major public health issue, killing over 11,000 people annually. The most common venomous snakes in India are Russell's viper, hump-nosed viper, cobra, and krait. It outlines the clinical presentation of envenomings from different snakes, including neuroparalytic effects from cobras and kraits, bleeding disorders from vipers, and muscle damage from sea snakes. The document emphasizes rapid assessment, resuscitation, detailed examination to identify the snake species, laboratory tests, and antivenom treatment for snake bites in India.

1. SNAKE BITE
GUIDE: Prof Dr. V. P. Pandey
CANDIDATE: Dr. Naresh Patel

2. Introduction
• Snakebite is an acute life threatening time limiting medical emergency.
• A preventable public health hazard.
• Often faced by rural population with heavy rainfall and humid climate.
• WHO estimates number of bites to be 83,000 per annum with 11,000
deaths in India.
• No reliable National Statistics are available.

3. • There are more than 2000 species of snakes in the
world and about 300 species in India out of which
52 are venomous.
• Commonest type of snake bite is from → Russell’s
viper followed by Hump nosed viper, Cobra, Krait
and Cat snake.
• The commonest site → paddy fields followed by
home and road.

4. The commonest location of the body → below the knees >
hand
Attributed to the fact that the snakes are crawling animals and
the chances of the accidentally stepping on the snake are high.
Sometime snake bite can be due to over enthusiastic

5. CobrasThe venomous snakes found in India belong to three
families
• Elapidae,
• Viperidae and
• Hydrophidae (Sea Snakes).
Elapidae have short permanently erect fangs
Includes
• Indian Cobra
• King cobra
• Kraits
• Sea snakes.

6. • Viperidae have long fangs folded up
against the upper jaw but are erected
when the snake strikes.
• Two subgroups
• Typical vipers (Viperinae) &
• Pit vipers (Crotalinae).

7. Venomous sea-snakes have flattened paddle-like tails & tiny fangs.

8. Non-venomous:
have no grooved or hollow teeth,
no specialized venom glands,
no venom storage lumens,
or any kind of anatomical venom-
delivery apparatus.

9. Approach to Snake Identification
Tail
• Flat sea snake[P]
• Round/cylidrical P /NP
Ventral Scales
• Small belly scale  NP
• Incomplete  NP
• Complete  NP /P

10. • Cobra : 3rd supralabial touches the eye and nostril
Cobra

11. • Viper : Small scales on head and without shields. Body is massive,
cylindrical, narrowing at both ends.
Russel viper Saw-scaled viper

12. Krait :with enlarged hexagonal vertebral scales, uniform white or
red belly and narrow white crossbars on the back.

13. Head of typical pit viper
pit organ (red arrow)

14. Snake venoms
Snake venoms contain more than 20 different constituents, Proteins,
including enzymes and polypeptide toxins.
Pro-coagulant enzymes (Viperidae) → activate different steps of the
clotting cascade
• Formation of fibrin in the blood stream.
• Most of this is immediately broken down by the fibrinolytic system.
• DIC / Consumption coagulopathy.

15. Haemorrhagins → damage the endothelial lining of blood vessel walls
→ local and systemic swelling.
Hyaluronidase → spread of venom through connective tissue.
Pre-synaptic neurotoxins
• Elapidae and some Viperidae → Phospholipases A2 that damage nerve
endings, initially releasing acetylcholine transmitter, then interfering with
release.
Post-synaptic neurotoxins
• Elapidae: These polypeptides compete with Ach. for receptors in the NM
junction → curare like paralysis.

16. Management of snake bite
1. First aid treatment.
2. Rapid clinical assessment and resuscitation.
3. Detailed clinical assessment and species diagnosis.
4. Investigations/laboratory tests.
5. Antivenom treatment.
6. Observation of the response to antivenom.
7. Treatment of the bitten part.
8. Treatment of life threatening complication.

17. 1. First aid treatment
• Performed by the bystander or by snake bite victim himself/herself.
• Reassure the victim who may be very anxious.
• Avoid any interference with the bite wound as this may introduce
infection, increase absorption of the venom and increase local
bleeding.
• Immobilize the bitten limb with a splint or sling.

18. Pressure immobilization method
• Ideally, an elastic, crepe bandage, approximately 10 cm wide and at
least 4.5 metre long should be used.
• The bandage is bound as tightly as for a sprained ankle, but not so
tightly that the peripheral pulse (radial, posterior tibial, dorsalis pedis)
is occluded or that a finger cannot easily be slipped between its
layers.
• Ideally applied by qualified medical personnel during transport to
higher center.

19. The bandage is bound firmly around the entire bitten limb, starting distally
around the fingers or toes and moving proximally, to include a rigid splint.

20. Caution
• Release of a tight tourniquet or compression bandage may result in
the dramatic development of severe systemic envenoming.
• Ideally, compression bandages should not be released until the
patient is in hospital, resuscitation facilities are available and
antivenom treatment has been started.

21. Useless or Dangerous Methods
• Making local incisions or pricks at the site of the bite or in the bitten
limb.
• Attempts to suck the venom out of the wound.
• Use of snake stones.
• Electric shock.
• Topical instillation or application of chemicals, herbs or ice packs.
• Do not attempt to capture, handle or kill the snake.

22. Management of snake bite
1. First aid treatment.
2. Rapid clinical assessment and resuscitation.
3. Detailed clinical assessment and species diagnosis.
4. Investigations/laboratory tests.
5. Antivenom treatment.
6. Observation of the response to antivenom.
7. Treatment of the bitten part.
8. Treatment of life threatening complication

23. 2. Rapid clinical assessment and resuscitation
• Oxygen administration.
• IV access.
• Airway, breathing and circulation.
• The level of consciousness must be assessed.
• CPR, if needed.

24. Management of snake bite
1. First aid treatment.
2. Rapid clinical assessment and resuscitation.
3. Detailed clinical assessment and species diagnosis.
4. Investigations/laboratory tests.
5. Antivenom treatment.
6. Observation of the response to antivenom.
7. Treatment of the bitten part.
8. Treatment of life threatening complication.

25. 3. Detailed Clinical Assessment and Species
Diagnosis
• History of the circumstances of the bite and the progression of local
and systemic symptoms and signs is very important.
• Site of bite & Time of bite.
• Snake identification.

26. Clinical Presentation

27. Clinical presentation of snakebite victim
depends upon
• Species of snake.
• Amount of venom injected.
• Season of the bite.
• Whether snake is fed or unfed.
• Dry or complete bite.
• Venom injection in vessel.

28. Occult snake bite
Krait
Neuroparalytic
symptoms with no
local sign.
Severe abdominal painOvert bite
Non-poisonous(70%)/Poisonous (30%)
Asymptomatic Dry bite
Symptomatic
Predominant symptoms manifestation
Progressive painful
Swelling, Viper, Cobra
Neuroparalytic
Cobra, Krait
Vasculotoxic
Russel viper
Saw scaled viper
Myotoxic
Sea snake
Suspected
snake bite
Local necrosis
Ecchymosis
Blister
Painful swelling
Compartment syndrome
Ptosis, Diplopia
Dysarthria, Dysphonia
Dypnoea, Dysphagia
paralysis
Bleeding, DIC
Shock, Acute
kidney injury
Muscle ache
Muscle swelling
Involuntary muscle contraction
Compartment syndrome

29. Asymptomatic : (i.e. non-venom related)
• Non specific symptoms related to anxiety are
• Palpitation & Sweating.
• Tachycardia, tachypnoea, raised BP, cold extremities and paraesthesia.
• May have dilated pupils suggestive of sympathetic over activity.
• Dry bite :
• A proportion of bites do not result in the injection of venom.
• About 50% of bites by Pit vipers and Russell’s vipers, 30% of bites by
cobras and 5-10% of bites by saw-scaled vipers are dry bites.

30. Occult snake bite:
• Krait bite victims often present in the early morning with paralysis
with no local signs.
• Patient was healthy at night, in the morning gets up with severe
epigastric/umbilical pain with vomiting persisting for 3 – 4 hours and
followed by typical neuroparalytic symptoms within next 4- 6 hours.
• No history of snakebite.

31. Neuro-paralytic : Elapid envenomation
• Typical symptoms within 30 min - 6 hrs in cobra bite, and 6-24 hrs for Krait
bite, as late as 36 hrs in case of Krait bite.
• In chronological order of appearance of symptoms :
• Heavy eyelid, Ptosis f/b
• Diplopia
• Dysarthria
• Dysphonia
• Dyspnoea
• Dysphagia
• Finally, Paralysis of intercostal and skeletal muscle occur in descending manner.
• Remembered as 5 Ds and 2 Ps.

32. Ptosis with neuro-paralytic snakebite

33. • To identify the impending respiratory failure bedside PFT in adult via:
• Peak flow meter, if available
• Single breath count > 30 normal.
• Breath holding time > 45 sec in inspiration normal.
• Ability to complete one sentence in one breath.
• Cry in a child whether husky or loud can help in identifying impending
respiratory failure.
• Bilateral dilated, poorly or a non-reacting pupil is not the sign of brain
dead in elapid envenoming.

34. Vasculotoxic : cardiovascular (viperidae)
Local Symptoms and Signs
• Local pain & swelling
• Local bleeding
• Bruising
• Tender LN Enlargement
• Blistering
• Local infection & Abscess formation
• Necrosis.

35. Characteristics of
Russell’s vipers bite
(a) oedema with
blood oozing from site
of bite,
(b) wet gangrene,
(c) extensive oedema
upto the groin,
(d) gum bleed

36. • Early stage of full thickness
necrosis 5 days after russel viper
bite.

37. Bleeding and clotting disorders (Viperidae)
• Bleeding from recent wounds (including fang marks,
venepunctures etc) and from old partly-healed wounds.
• Spontaneous systemic bleeding.
• Conjunctival chemosis

38. • Thoroughly examine the gingival sulci, using a torch and tongue
depressor, as these may show the earliest evidence of spontaneous
systemic bleeding.
• Abdominal tenderness → gastrointestinal or retroperitoneal bleeding.
• Loin pain and tenderness → acute renal ischemia (Russell’s viper
bites).
• Lateralizing neurological signs, asymmetrical pupils, convulsions or
impaired consciousness → Intracranial hemorrhage.

39. Myotoxic : sea snakebite
• Generalized muscle ache, muscle swelling, involuntary contraction of
muscle.
• Passage of dark brown urine.
• Compartment syndrome, cardiac arrhythmias due to hyperkalemia.
• Kidney injury due to myoglobinuria.
• Subtle neuroparalytic signs.

40. Management of snake bite
1. First aid treatment.
2. Rapid clinical assessment and resuscitation.
3. Detailed clinical assessment and species diagnosis.
4. Investigations/laboratory tests.
5. Antivenom treatment.
6. Observation of the response to antivenom.
7. Treatment of the bitten part.
8. Treatment of life threatening complication.

41. 4. Investigations/laboratory tests
• 20 minute whole blood clotting test (20WBCT)
• Place a few ml of freshly sampled venous blood in a small glass vessel.
• Leave undisturbed for 20 minutes at ambient temperature.
• If the blood is still liquid and runs out, the patient has hypofibrinogenaemia as
a result of venom-induced consumption coagulopathy.

42. 20WBCT
• Contaminated glass tube may not stimulate clotting of the blood
sample in the usual way and test will be invalid.
• If any doubt, repeat the test in duplicate, including a “control” (blood
from a healthy person).
• The test should be carried out every 30 minutes from admission for 3
hours and then hourly after that.

43. • Platelet count : may be decreased – viper.
• WBC cell count : Early neutrophil leucocytosis in systemic
envenoming.
• Blood film : Fragmented RBC(“helmet cell”, schistocytes) are seen in
microangiopathic hemolysis.
• Plasma/serum : may be pink or brownish if there is gross
haemoglobinaemia or myoglobinaemia.

44. Biochemical Abnormalities
• Aminotransferases, creatine kinase elevated if there is severe local
damage or particularly generalised muscle damage.
• Bilirubin is elevated following massive extravasation of blood.
• Creatinine, urea or blood urea nitrogen levels are raised in the renal
failure.

45. Urine Examination
• For blood/myoglobin.
• Microscopy for erythrocytes in the urine.
• Red cell casts indicate glomerular bleeding.
• Massive proteinuria is an early sign of the generalized increase in
capillary permeability in Russell’s viper envenoming.

46. Management of snake bite
1. First aid treatment.
2. Rapid clinical assessment and resuscitation.
3. Detailed clinical assessment and species diagnosis.
4. Investigations/laboratory tests.
5. Antivenom treatment.
6. Observation of the response to antivenom.
7. Treatment of the bitten part.
8. Treatment of life threatening complication.

47. 5. Anti-venom Treatment
• Antivenom is immunoglobulin (refined F(ab)2 fragment of IgG)
purified from the serum or plasma of a horse or sheep that has been
immunized with the venoms of one or more species of snake.
• Monovalent neutralizes the venom of only one species of snake.
• Polyvalent neutralizes the venoms of several species of snakes

48. • Haffkine, Kasauli and Serum Institute of India produce “polyvalent
anti-snake venom serum”.
• It is raised in horses using the venoms of the “Big four” in India
(Indian Cobra, Indian Krait, Russell’s viper, Saw-scaled viper).
• Not included are venoms of King Cobra , Sea snakes and Pit vipers.

49. Neutralization of Venom
1 cc of ASV neutralises
0.60 mg of Cobra venom &
Russel’s Viper venom.
0.45 mg of Saw scaled viper
venom & Krait venom.

50. Indications for Antivenom
Systemic Envenoming
• Haemostatic abnormalities:
• Spontaneous systemic bleeding
• Coagulopathy
• Thrombocytopenia (<100 x 109/L).
• Neurotoxic signs:
• Ptosis, external ophthalmoplegia, paralysis.

51. • Cardiovascular abnormalities:
• Hypotension, shock, cardiac arrhythmia.
• Acute renal failure:
• Oliguria/anuria, rising serum creatinine/urea.
• Haemoglobinuria/myoglobinuria:
• Dark brown urine, evidence of intravascular haemolysis or
generalised muscle aches and pains.

52. • Local swelling involving more than half of the bitten limb (in the
absence of a tourniquet).
• Rapid extension of swelling (for example beyond the wrist or ankle
within a few hours of bites on the hands or feet).
• Swelling after bites on the digits (toes and especially fingers).
• Development of an enlarged tender lymph node draining the bitten
limb.

53. Contraindications to antivenom
• There is no absolute contraindication to antivenom treatment.
• Patients who have reacted to horse (equine) or sheep (ovine) serum
in the past and those with a strong history of atopic diseases
(especially severe asthma) should be given antivenom only if they
have signs of systemic envenoming.
• Test dose is not recommended.

54. Administration of Antivenom
• Intravenous Infusion
• Reconstituted freeze-dried or neat liquid antivenom is diluted in
approximately 5-10 ml of isotonic fluid per kg body weight (i.e. 250-500
ml of isotonic saline or 5% D in the case of an adult patient).
• Infused at a constant rate over a period of about one hour.
• IV “push” Injection
• Antivenom is given by slow IV inj. (<2 ml/min)
• This method has the advantage that the doctor/nurse/dispenser giving
the antivenom remain with the patient during the time when some
early reactions may develop.

55. • Adrenaline should always be in readiness before antivenom is
administered.
• Local administration of antivenom at the site of the bite is not
recommended.
• Although this route may seem rational, it should not be used as it is
extremely painful, may increase compartment pressure and has not
been shown to be effective.

56. • Dose of ASV for neuroparalytic snake bite:
• ASV 10 vials stat as infusion over 1 hour followed by 2nd dose of
10 vials after 1 hour if no improvement within 1st hour.
• Dose of ASV for vasculotoxic snake bite:
• 10 vials of polyvalent ASV stat over 1 hour as infusion, followed by
6 vials 6 hourly till clotting time normalizes and/or local swelling
subsides.
• Children & pregnant women should receive the same ASV dosage as
adults.

57. Repeat dose of ASV
Repeat dose: neuroparalytic or neurotoxic envenomation-
• Repeat ASV when there is worsening neurotoxic or cardiovascular
signs even after 1-2 hrs.
• Maximum dose 20 vials ASV for neurotoxically envenomed patients.
Repeat dose: in Vasculotoxic or hemotoxic envenomation-
• Repeat clotting test every 6 hrs and administer ASV every 6 hrs until
coagulation is restored.
• If coagulation abnormality persists, give FFP or cryoprecipitate
(fibrinogen, factor VIII), fresh whole blood, if FFP not available or
platelet concentrate.

58. Management of snake bite
1. First aid treatment.
2. Rapid clinical assessment and resuscitation.
3. Detailed clinical assessment and species diagnosis.
4. Investigations/laboratory tests.
5. Antivenom treatment.
6. Observation of the response to antivenom.
7. Treatment of the bitten part.
8. Treatment of life threatening complication.

59. Observation of the response to antivenom
• Nausea, headache and generalised aches and pains may disappear
very quickly.
• Spontaneous systemic bleeding (eg from the gums) usually stops
within 15-30 minutes.
• In shocked patients, blood pressure may increase within the first 30-
60 minutes and arrhythmias such as sinus bradycardia may resolve.

60. • Neurotoxic envenoming of the post-synaptic type (cobra bites) may begin
to improve as early as 30 minutes after antivenom, but usually take several
hours.
• Envenoming with presynaptic toxins (kraits and sea snakes) is unlikely to
respond in this way.
• Blood coagulability (as measured by 20WBCT) is usually restored in 3-9
hours. Bleeding from new and partly healed wounds usually stops much
sooner than this.
• Active haemolysis and rhabdomyolysis may cease within a few hours and
the urine returns to its normal colour.

61. Management of snake bite
1. First aid treatment.
2. Rapid clinical assessment and resuscitation.
3. Detailed clinical assessment and species diagnosis.
4. Investigations/laboratory tests.
5. Antivenom treatment.
6. Observation of the response to antivenom.
7. Treatment of the bitten part.
8. Treatment of life threatening complication.

62. 7. Treatment of the bitten part
• Keep slightly elevated, to encourage reabsorption of edema fluid.
• Prophylactic broad spectrum antimicrobial treatment is justified
• Bullae may be large and tense but they should be aspirated only if they
seem likely to rupture.
• Its worthy to wait 5-7 days for debridement of necrotic tissue in order to
specify line of demarcation between viable and non-viable tissue.
• Skin grafting and amputation of a necrotic digit may be required.

63. Management of snake bite
1. First aid treatment.
2. Rapid clinical assessment and resuscitation.
3. Detailed clinical assessment and species diagnosis.
4. Investigations/laboratory tests.
5. Antivenom treatment.
6. Observation of the response to antivenom.
7. Treatment of the bitten part.
8. Treatment of life threatening complication.

64. 8. Life threatening complications:
• Neuroparalytic envenomation.
• Renal involvement.
• Shock.

65. Management Neuroparalytic Envenomation
As ASV cannot be relied upon to save life of a patient with respiratory
paralysis, administer following in addition:
• Oxygen
• Assisted ventilation-
• Neuroparalysis recovers quickly with ASV, so duration of mechanical
ventilation is shorter.
• Manual ventilation is effective in absence of mechanical ventilator.
• Administer Atropine Neostigmine (An) schedule.

66. Atropine neostigmine (AN) dosage schedule
• Patients with clear evidence of neurotoxicity should receive test dose
of neostigmine.
• Atropine 0.6mg followed by neostigmine 1.5 mg to be given IV stat.
• If objective improvement evident after 5 minutes in ptosis, repeat
dose of neostigmine 0.5mg with atropine every 30 mins for 5 doses.
• Majority of patients improve within first 5 doses.
Stop AN dosage schedule if:
• Patient has complete recovery from neuroparalysis.
• If there is no improvement after 3 doses.

67. Forced Alkaline Diuresis
• If the patient has oliguria or dipstick positive for blood give a trial of
forced alkaline diuresis (FAD) within first 24 hours of the bite to avoid
nephropathy leading to acute tubular necrosis (ATN).
• Delayed FAD has no role.
• Sequence of FAD in adults is as follows:
• Inj. Frusemide 40 mg IV stat
• Inj. Normal saline 500 ml + 20 ml of NaHCO3 over 20 minutes
• Inj. Ringer’s lactate 500 ml + 20 ml of NaHCO3 over 20 minutes
• Inj. 5% dextrose 500 ml + 10 ml of Potassium Chloride over 90 minutes
• Inj. Mannitol 150 ml over 20 min

68. • Whole cycle completes in 2 h 30 min and urine output of 3 ml/min is
expected.
• If patient responds to first cycle continue for 3 cycles.
• FAD converts oliguria into polyuria and avoid ATN and acute kidney
injury needing dialysis reduce up to >75% patients.
• If there is no response discontinue FAD and consider for dialysis.

69. Indications for dialysis are:
• Absolute value
• Blood urea >130 mg/dl,
• Sr. Creatinine > 4 mg/dl
• OR evidence of hypercatabolism
• rise in blood urea 30 mg/dL (BUN > 15),
• Sr. Creatinine > 1 mg/dL,
• Sr. Potassium > 1 mEq/L and fall in bicarbonate >2 mmol/L
• Fluid overload leading to pulmonary oedema.
• Hyperkalaemia (>7 mmol/l or hyperkalaemic ECG changes).
• unresponsive to conservative management.
• Uremic encephalopathy & uremic pericarditis.

70. Shock
• Hypovolaemia should be corrected with colloid/crystalloids,
controlled by observation of the central venous pressure.
• IV ionotropics (dopamine or nor-adrenaline).
• Hypotension associated with bradycardia should be treated with
atropine.