Snake Bite

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

2. INTRODUCTION
Snakebite is an acute life threatening time limiting medical emergency
It is a preventable public health hazard often faced by rural population
in tropical and subtropical countries with heavy rainfall and humid climate.
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3. SNAKE BITE – AN OCCUPATIONAL DISEASE
FishermanWorkers at site
Farmers Snake Charmers Plantation work
Hunter
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4. STATISTICS
• There is a huge gap between the number of snakebite deaths reported
from direct survey and official data.
• Only 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
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5. About 50% of bites are dry
Majority (80%) is by non-venomous snakesSnake bite
Venomous snakes
FACTS
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6. Features of poisonous & non-poisonous snakes
Non Poisonous Snakes
Head - Rounded
Fangs - Not present
Pupils - Rounded
Anal Plate - Double row
Bite Mark - Row of small teeths
Poisonous Snakes
Head - Triangle
Fangs - Present
Pupils - Elliptical pupil
Anal Plate - Single row
Bite Mark - Fang Mark
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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
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8. IS THERE ANY MEDICAL IMPLICATION
FOR SNAKE IDENTIFICATION?
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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
Procoagulant enzymes (Viperidae) Russell’s viper
Haemorrhagins :
Zinc metalloproteinases damage the endothelial
lining.
Cytolytic or necrotic toxins
Haemolytic and myolytic:
Phospholipases A2 damage cell
membranes, endothelium, skeletal
muscle, nerve and red blood cells.
Pre-synaptic neurotoxins (Elapidae
and some Viperidae)
Post-synaptic neurotoxins (Elapidae)
Highly Modified Saliva
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11. SNAKE BITE TOXICITY PROFILE
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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
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13. WHAT IS THE MODE OF
NEUROTOXICITY IN KRAIT BITE
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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
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15. WHAT IS THE MODE OF
NEUROTOXICITY IN COBRA BITE
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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
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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
Ophthalmoplegia
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18. QUICK NEUROLOGICAL
EXAMINATION !
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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
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20. BUNGARUS NIGER(KRAIT) ENVENOMING
20 hr post-bite
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21. NEUROTOXIC ENVENOMING-EXAMINATION
• Krait can cause fixed, dilated non reactive pupils simulating brain stem
death – however, it can recover fully
• Ask the patient to open their mouth wide and protrude their tongue; early
restriction often due to paralysis of pterygoid muscles.
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22. HOW TO IDENTIFY
FOR
BULBAR PALSY & EARLY
RESPIRATORY FAILURE
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23. BULBAR & RESPIRATORY PARALYSIS
• Impaired swallow or are secretions accumulating in
the pharynx- an early sign of bulbar paralysis.
• Objective measurement of ventilatory capacity is very useful. Use a peak
flow meter, spirometer (FEV1 and FVC)
• Ask the patient to blow into the tube of a sphygmomanometer to record
the maximum expiratory pressure (mmHg).
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24. PARADOXICAL RESPIRATION
• This is an abnormal pattern of breathing in which the abdominal wall is
sucked in during inspiration (it is usually pushed out).
• Due to paralysis of the diaphragm.
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25. HEMATOLOGICAL SIDE EFFECTS
• Venom induces bleeding.
• Venom induces clotting.
• Venom induces haemolysis.
• Haemorrhagin – causes direct endothelial damage by loosening the
gap between endothelial cells.
• Pro-coagulant factors.
• Anticoagulant factors.
• Fibrinonolytic factors.
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26. SNAKE VENOM AND THE COAGULATION CASCADE
RVV – Russel’s Viper
Venom ECV – Echis
carinatus Venom

27. PTT
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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
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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
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31. LOCAL NECROSIS
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32. WHAT ARE THE SYSTEMIC
MANIFESTATIONS OF THE
ENVENOMATION ?
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33. 33

34. MANAGEMENT
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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.
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36. 36

37. COMPLICATIONS OF ARTERIAL TOURNIQUET
 Congestion & swelling
 Ischaemia & gangrene
 Damage to peripheral nerves
 Increased bleeding from bite site
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38. TOURNIQUET GANGRENE
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39. INCISION & SUCTION
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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
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41. MEDICOLEGAL
39 Code of Criminal Procedure
under Constitution of India Article 21
MLC to be initiated
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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
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43. ANTI SNAKE VENOM
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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 VENOM
• ASV is Ig purified from the serum/plasma of a horse/sheep immunized
with the venoms of one or more species of snake.
• Monovalent/Polyvalent
• The ASV in India is a polyvalent type which is active against the
commonly found snakes in India - FAB Four.
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46. Polyvalent antivenoms from India
raised against venom from:
• Cobra
• Krait
• Russel’s viper
• Saw scaled viper
No monovalent vaccine in India
ANTI SNAKE VENOM
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47. ANTI SNAKE VENOM
• ASV comes in two forms lyophilised powdered and liquid.
• Lyophilised ASV is simply liquid ASV freeze-dried.
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48. ANTI 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
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49. ANTI SNAKE VENOM
Each ml neutralize
 0.6 mg of cobra
 0.6 mg of rusells viper
 0.45 mg of krait
 0.45 mg of saw-scaled viper
Average yield / bite
 Cobra- 60 mg
 Rusells- 63 mg
 Krait- 20 mg
 Saw-scaled- 13 mg
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50. ANTI 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.
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51. ANTI 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 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
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53. PAEDIATRIC 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.
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54. MONITORING PATIENT ON ASV
All patients should be watched carefully every 5 min for first 30
min, then at 15 min for 2 hours for manifestation of a reaction.
At the earliest sign of an adverse reaction suspend temporarily.
Maintain a strict intake output chart and note colour of urine to
detect acute kidney injury early.
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55. LIMITATIONS OF ASV
X Reverse necrotic action of the venom on tissue
X Reverse local swelling
X Reverse renal failure
X Reverse coagulopathy; the liver does this.
X Reverse pre synaptic envenoming; the nerve damage is structural and large quantities of ASV are
ineffective, the body must regenerate synaptic vesicles
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56. THERAPEUTIC ENDPOINT
• Neuro /paralytic effect abolished – Presynaptic Only
• Coagulation profile restored – repeat tests q6H
• Restoration of hemodynamics.
• Signs 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 clinically
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57. ADVERSE 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
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58. ADVERSE ASV REACTION
• Pyrogenic reactions usually develop 1–2 h after treatment. Symptoms
include chills and rigors, fever, and hypotension.
• Late (serum sickness–type) reactions develop 1–12 (mean 7) days
after treatment. Clinical features include fever, nausea, vomiting, diarrhea,
itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy,
immune complex nephritis and, rarely, encephalopathy
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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 acetylcholine
and can therefore reverse respiratory failure and neurotoxic symptoms
• Effective for post synaptic neurotoxins – Cobra
• In all cases of neurotoxic envenomation the 'AN challenge Test' to be
performed 60

60. “AN CHALLENGE TEST”
Atropine 0.6 mg followed by neostigmine (1.5mg) to be given IV stat and repeat
dose of neostigmine 0.5 mg with atropine every 30 minutes for 5 doses
In children, Inj. Atropine 0.05 mg/kg followed by Inj.Neostigmine 0.04 mg/kg IV
and repeat dose 0.01 mg/kg every 30 minutes for 5 doses
A fixed dose combination of Neostigmine and glycopyrolate IV can also be used. 61

61. SUPPORTIVE CARE
Close monitoring
Analgesics – no aspirin
Volume replacement
Broad spectrum antibiotics
Tetanus prophylaxis
Renal replacement therapy
Fasciotomy/ wound debridement
Blood or blood products
MV support
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62. TAKE 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
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63. Thank You
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