Snakebite is a medical emergency that can be life-threatening. It most commonly affects rural populations in tropical areas. There are many species of poisonous snakes in India, with the "Big Four" being cobras, kraits, Russell's vipers, and saw-scaled vipers. Snake venom causes local and systemic effects through neurotoxins and hematoxins. Proper first aid and timely administration of antivenom are important for treatment. Hospital management involves monitoring for signs of envenoming, administration of antivenom, and supportive care.

1. AN APPROACH TO A SNAKEAN APPROACH TO A SNAKE
BITE VICTIMBITE VICTIM
Dr. Soumar Dutta. MD. DEM. MEM
Consultant and Coordinator
Department of Emergency Medicine
Narayana Superspeciality Hospital, Guwahati

2. INTRODUCTIONINTRODUCTION
Snakebite is an acute life threatening time limitinglife threatening time limiting medical emergency
It is a preventablepreventable public health hazard often faced by rural populationrural population
in tropical and subtropical countries with heavy rainfall and humid climate.
2

3. SNAKE BITESNAKE BITE – AN OCCUPATIONAL DISEASE– AN OCCUPATIONAL DISEASE
FishermanWorkers at site
Farmers Snake Charmers Plantation work
Hunter
3

4. STATISTICSSTATISTICS
• There is a huge gap between the number of snakebite deaths reportedThere is a huge gap between the number of snakebite deaths reported
from direct survey and official data.from direct survey and official data.
• Only 7.23% snakebite deaths were officially reportedOnly 7.23% snakebite deaths were officially reported
Mohapatra,2011 Mazumdar,2014
49,500 deaths annually 5-6 lakhs bites annually but only 30% are
venomous bites
Mostly rural population Only 22.19% reaches hospital.
Common in males than females Delay in first aid and unavailability of
ASV
Andhra Pradesh, Bihar, Tamil Nadu,
West Bengal, Uttar Pradesh
Majority of the bites being on the lower
extremities
4

5. About 50% of bites are dry
Majority (80%) is by non-venomous snakesSnake bite
Venomous snakes
FACTSFACTS
5

6. Features of poisonous & non-poisonous snakesFeatures of poisonous & non-poisonous snakes
Non Poisonous SnakesNon Poisonous Snakes
Head - Rounded
Fangs - Not present
Pupils - Rounded
Anal Plate - Double row
Bite Mark - Row of small teeths
Poisonous SnakesPoisonous Snakes
Head - Triangle
Fangs - Present
Pupils - Elliptical pupil
Anal Plate - Single row
Bite Mark - Fang Mark
6

7. COMMON POISONOUS SNAKES IN INDIA
• In India, >200 species of snakes; only 52 are poisonous.
1. Saw-scaled viper (Echis carinatus)
2. Russell’s viper (Daboia russelii)
3. Common krait (Bungarus caeruleus)
4. Indian cobra (Naja naja)
Neurotoxic
20-30% of bites
Majority of bites 70-80%
Hemotoxin / Vasculotoxin
7

8. IS THERE ANY MEDICAL IMPLICATIONIS THERE ANY MEDICAL IMPLICATION
FOR SNAKE IDENTIFICATION?FOR SNAKE IDENTIFICATION?
8

9. SPECIES: MEDICAL IMPLICATIONS
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 9

10. COMPOSITION OF SNAKE VENOM
Highly Modified Saliva
10

11. SNAKE BITE TOXICITY PROFILE
11

12. HEMOTOXICITY
•Starts late hence most of them reach hospitals
•Many organ involvement hence MV is mostly
supportive to buy time for organs to recover.
•More number of cases.
NEUROTOXICITY
•Starts early- many die before they reach
hospitals
•Many reverse very well with ASV if started
early
•Less number of cases
70-80%
20-30%
Overlap:
Neuro-hemat
12

13. WHAT IS THE MODE OFWHAT IS THE MODE OF
NEUROTOXICITY IN KRAIT BITENEUROTOXICITY IN KRAIT BITE
13

14. Beta-bungarotoxin- Phospholipases A2
1) Inhibiting the release of Ach
from the presynaptic membrane
2) Presynaptic nerve terminals
exhibit signs of irreversible
physical damage and are devoid of
synaptic vesicles
3) ASV & anticholinesterases have
no effect
• Paralysis lasts several weeks and frequently requires prolonged MV.
• Recovery is dependent upon regeneration of the terminal axon.
KRAIT- PRE-SYNAPTIC ACTION
14

15. WHAT IS THE MODE OFWHAT IS THE MODE OF
NEUROTOXICITY IN COBRA BITENEUROTOXICITY IN COBRA BITE
15

16. COBRA – POST-SYNAPTIC
Alpha-neurotoxins “curare -mimetic toxins’’
•Bind specifically to Ach receptors, preventing the
interaction between Ach and receptors on postsynaptic
membrane.
•Prevents the opening of the sodium channel associated
with the Ach receptor and results in neuromuscular
blockade.
• ASV -rapid reversal of paralysis.
•Dissociation of the toxin-receptor complex, which leads to
a reversal of Paralysis
Anticholinesterases reverse the neuromuscular blockade
16

17. NEURO PARALYTIC MANIFESTATIONS STUDY
Ptosis
Repiratory Involvement
Bulbar weakness
N Sharma, S Chauhan, S Faruqi, P Bhat, S Varma, Emerg Med J 2005;22:118–120
OphthalmoplegiaOphthalmoplegia
17

18. QUICK NEUROLOGICALQUICK NEUROLOGICAL
EXAMINATION !EXAMINATION !
18

19. NEUROTOXIC ENVENOMING EXAMINATION
• Ask the patient to look up and observe whether the
upper lids retract fully.
• Test eye movements for evidence of early external
ophthalmoplegia .
• Check the size and reaction of the pupils.
• The muscles flexing the neck may be paralyzed, giving
the “broken neck sign
19

20. BUNGARUS NIGER(KRAIT) ENVENOMINGBUNGARUS NIGER(KRAIT) ENVENOMING
20 hr post-bite
20

21. NEUROTOXIC ENVENOMING-EXAMINATIONNEUROTOXIC ENVENOMING-EXAMINATION
• Krait can cause fixed, dilated non reactive pupils simulating brain stemKrait can cause fixed, dilated non reactive pupils simulating brain stem
death – however, it can recover fullydeath – however, it can recover fully
• Ask the patient to open their mouth wide and protrude their tongue; earlyAsk the patient to open their mouth wide and protrude their tongue; early
restriction often due to paralysis of pterygoid muscles.restriction often due to paralysis of pterygoid muscles.
21

22. HOW TO IDENTIFYHOW TO IDENTIFY
FORFOR
BULBAR PALSY & EARLYBULBAR PALSY & EARLY
RESPIRATORY FAILURERESPIRATORY FAILURE
22

23. BULBAR & RESPIRATORY PARALYSISBULBAR & RESPIRATORY PARALYSIS
• Impaired swallow or are secretions accumulating inImpaired swallow or are secretions accumulating in
the pharynx- an early sign of bulbar paralysis.the pharynx- an early sign of bulbar paralysis.
• Objective measurement of ventilatory capacity is very useful. Use a peakObjective measurement of ventilatory capacity is very useful. Use a peak
flow meter, spirometer (FEV1 and FVC)flow meter, spirometer (FEV1 and FVC)
• Ask the patient to blow into the tube of a sphygmomanometer to recordAsk the patient to blow into the tube of a sphygmomanometer to record
the maximum expiratory pressure (mmHg).the maximum expiratory pressure (mmHg).
23

24. PARADOXICAL RESPIRATIONPARADOXICAL RESPIRATION
• This is an abnormal pattern of breathing in which the abdominal wall isThis is an abnormal pattern of breathing in which the abdominal wall is
sucked in during inspiration (it is usually pushed out).sucked in during inspiration (it is usually pushed out).
• Due to paralysis of the diaphragm.Due to paralysis of the diaphragm.
24

25. HEMATOLOGICAL SIDE EFFECTS
• Venom induces bleeding.Venom induces bleeding.
• Venom induces clotting.Venom induces clotting.
• Venom induces haemolysis.Venom induces haemolysis.
• Haemorrhagin – causes direct endothelial damage by loosening theHaemorrhagin – causes direct endothelial damage by loosening the
gap between endothelial cells.gap between endothelial cells.
• Pro-coagulant factors.Pro-coagulant factors.
• Anticoagulant factors.Anticoagulant factors.
• Fibrinonolytic factors.Fibrinonolytic factors.
25

26. SNAKE VENOM AND THE COAGULATION CASCADESNAKE VENOM AND THE COAGULATION CASCADE
RVV – Russel’s Viper
Venom ECV – Echis
carinatus
Venom

27. PTT
27

28. 20 MIN WHOLE BLOOD CLOTTING TEST
• Take 2 ml fresh blood in glass vessel
• Leave undisturbed for 20 minutes
• If blood is still liquid – incoagulable blood – Hypofibrinogenaemia/DIC
• Repeat the test periodically if positive – Normal WBCT is 6-8 min
28

29. LOCAL SYMPTOMS & 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 29

30. Russell’s Viper
Bite
30

31. LOCAL NECROSIS
31

32. WHAT ARE THE SYSTEMICWHAT ARE THE SYSTEMIC
MANIFESTATIONS OF THEMANIFESTATIONS OF THE
ENVENOMATION ?ENVENOMATION ?
32

33. 33

34. MANAGEMENTMANAGEMENT
34

35. FIRST AID/PRE HOSPITAL CARE
• Reassure the victim
• Immobilize the bitten limb with a splint or sling
• Avoid any interference with the bite wound as this may introduce
infection, increase venom absorption & local bleeding
• All rings, watches, constricting clothing should be removed.
35

36. 36

37. COMPLICATIONS OF ARTERIAL TOURNIQUET
 Congestion & swelling
 Ischaemia & gangrene
 Damage to peripheral nerves
 Increased bleeding from bite site
37

38. TOURNIQUET GANGRENE
38

39. INCISION & SUCTION
No!No!
39

40. HOSPITAL MEASURES FOR ASYMPTOMATIC PATIENTS
a) OBSERVATION for 24 hours b) MONITOR:
• PR, RR, BP
• CBC-TLC , Platelets↑ ↓
• Urine output
• BUN, Creatinine
• PT, aPTT, INR
• CPK (>600 IU/L)
• Vomiting, diarrhoea
• Abnormal bleeds
• Local swelling necrosis
• Continuous ECG monitoring
• Blood gas analysis
40

41. MEDICOLEGAL
41

42. HOSPITAL MANAGEMENT, IF TOURNIQUET IS A
ALREADY IN PLACE
•Limb is ischemic – remove immediately
•Limb is not ischemic:
1) Snake (unknown) or neurotoxic – Don’t remove until definite
treatment (ASV) is initiated
2) Snake is viper – remove the tourniquet
42

43. ANTI SNAKE VENOMANTI SNAKE VENOM
43

44. INDIAN NATIONAL SNAKE BITE PROTOCOL
• Systemic envenomation
• Evidence of coagulopathy
• Evidence of neurotoxicity
• Cardiovascular abnormalities
• Persistent and severe vomitting
• Local envenomation
• Local swelling involving half of
the limb
• Rapid extension of swelling
Start ASV 45

45. ANTI SNAKE VENOMANTI SNAKE VENOM
• ASV is Ig purified from the serum/plasma of a horse/sheep immunizedASV is Ig purified from the serum/plasma of a horse/sheep immunized
with the venoms of one or more species of snake.with the venoms of one or more species of snake.
• Monovalent/PolyvalentMonovalent/Polyvalent
• The ASV in India is a polyvalent type which is active against theThe ASV in India is a polyvalent type which is active against the
commonly found snakes in India - FAB Four.commonly found snakes in India - FAB Four.
46

46. Polyvalent antivenoms from India
raised against venom from:
•Cobra
•Krait
•Russel’s viper
•Saw scaled viper
No monovalent vaccine in India
ANTI SNAKE VENOMANTI SNAKE VENOM
47

47. ANTI SNAKE VENOMANTI SNAKE VENOM
• ASV comes in two forms lyophilised powdered and liquid.
• Lyophilised ASV is simply liquid ASV freeze-dried.
48

48. ANTI SNAKE VENOMANTI SNAKE VENOM
• Always to be given only by slow IV route only.
• Never give IM route : poor bioavailability , painful and may increase
intra-compartmental pressure.
• Rate of infusion can be increased gradually in absence of reaction until
full starting dose is administered(0ver ~ 1 hour)
• Epinephrine (adrenaline) should always be drawn up in
readiness before ASV is administered
49

49. ANTI SNAKE VENOMANTI SNAKE VENOM
Each ml neutralizeEach ml neutralize
 0.6 mg of cobra0.6 mg of cobra
 0.6 mg of rusells viper0.6 mg of rusells viper
 0.45 mg of krait0.45 mg of krait
 0.45 mg of saw-scaled viper0.45 mg of saw-scaled viper
Average yield / biteAverage yield / bite
 Cobra- 60 mg
 Rusells- 63 mg
 Krait- 20 mg
 Saw-scaled- 13 mg
50

50. ANTI SNAKE VENOMANTI SNAKE VENOM
Neuroparalytic snakebite
ASV 10 vials stat as infusion over 30 minutes followed by 2nd dose of 10 vials after 1
hour if no improvement within 1st hour.
51

51. ANTI SNAKE VENOMANTI SNAKE VENOM
Vasculotoxic snakebite
Low Dose infusion therapy –
10 vials stat as infusion over 30
minutes followed by 2 vials every 6
hours as infusion in 100 ml of
normal saline till clotting time
normalizes or for 3 days whichever
is earlier.
High dose intermittent bolus
therapy - 10 vials of polyvalent
ASV stat over 30 minutes as
infusion, followed by 6 vials 6
hourly as bolus therapy till clotting
time normalizes and/or local
swelling subsides. 52

52. ANTI SNAKE VENOMANTI SNAKE VENOM
• Each vial of AVS be dissolved in 10 ml of distilled water and added to an
infusion medium such as normal saline
10 vials + 100 ml of distilled water + 400ml of normal saline
Given over 30-60 mins
NO Test Dose
53

53. PAEDIATRIC ASV DOSEPAEDIATRIC ASV DOSE
• Snakes inject the same dose of venom into children and adults.
• Children must therefore be given exactly the same dose of antivenom as
adults.
54

54. MONITORING PATIENT ON ASVMONITORING PATIENT ON ASV
55

55. LIMITATIONS OF ASVLIMITATIONS OF ASV
56

56. THERAPEUTIC ENDPOINTTHERAPEUTIC ENDPOINT
• Neuro /paralytic effect abolished – Presynaptic OnlyNeuro /paralytic effect abolished – Presynaptic Only
• Coagulation profile restored – repeat tests q6HCoagulation profile restored – repeat tests q6H
• Restoration of hemodynamics.Restoration of hemodynamics.
• Signs of local and systemic envenomation disappearsSigns of local and systemic envenomation disappears
• Active haemolysis and rhabdomyolysis ceases within a few hours and the urine
returns to its normal colour
• Patient improves clinicallyPatient improves clinically
57

57. ADVERSE ASV REACTIONADVERSE ASV REACTION
• Early anaphylactic reactions occurs within 10–180 min of start of
therapy and is characterized by itching, urticaria, dry cough, nausea and
vomiting, abdominal colic, diarrhoea, tachycardia, and fever.
• Some patients may develop severe life-threatening anaphylaxis
characterized by hypotension, bronchospasm, and angioedema
58

58. ADVERSE ASV REACTIONADVERSE ASV REACTION
• Pyrogenic reactionsPyrogenic reactions usually develop 1–2 h after treatment. Symptomsusually develop 1–2 h after treatment. Symptoms
include chills and rigors, fever, and hypotension.include chills and rigors, fever, and hypotension.
• Late (serum sickness–type) reactionsLate (serum sickness–type) reactions develop 1–12 (mean 7) daysdevelop 1–12 (mean 7) days
after treatment. Clinical features include fever, nausea, vomiting, diarrhea,after treatment. Clinical features include fever, nausea, vomiting, diarrhea,
itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy,itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy,
immune complex nephritis and, rarely, encephalopathyimmune complex nephritis and, rarely, encephalopathy
59

59. NEUROTOXIC ENVENOMATION
• Antivenom treatment alone cannot be relied upon to save the life of a patient
with bulbar and respiratory paralysis.
• Neostigmine is an anticholinesterase that prolongs the life of acetylcholineNeostigmine is an anticholinesterase that prolongs the life of acetylcholine
and can therefore reverse respiratory failure and neurotoxic symptomsand can therefore reverse respiratory failure and neurotoxic symptoms
• Effective for post synaptic neurotoxins – Cobra
• In all cases of neurotoxic envenomation theIn all cases of neurotoxic envenomation the 'AN challenge Test''AN challenge Test' to beto be
performedperformed
60

60. ““AN CHALLENGE TEST”AN CHALLENGE TEST”
61

61. SUPPORTIVE CARESUPPORTIVE CARE
62

62. TAKE HOME MESSAGETAKE HOME MESSAGE
• Identify early signs of envenomation
• Manage as per “ABC” approach
• Start ASV early
• Prepare for anaphalytic reaction
• Surgical intervention
• Prevent multi organ failure
• Create public awareness
63

63. Thank YouThank You
64