I have summed up this presentation with practical point of view. I have shot myself majority of the snakes and feel they should be understood by the community. Some of them are venomous (not poisonous)! The management is syndromic approach and I feel this ppt would be beneficial to medical students.

1. SNAKE BITE
PROF. SUBHASH RANJAN

2. INTRODUCTION
 India estimates approx 2,00,000 bites and 35-
50,000 snake bite deaths/year
 No reliable national statistics are available.
 Males bitten almost twice as often as females
 Majority of the bites being on the lower
extremities.
 50% of bites by venomous snakes are dry bites,
result in negligible envenomation.

3. What are Indian FAB FOUR?

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

5. COMMON INDIAN SNAKES

6. COBRA (Naja naja)

7. King Cobra (Ophiophagus
hannah)

8. Saw-scaled Viper
(Echis carinatus)

9. Green Vine Snake
(Ahaetulla nasuta)
Mild
Venomous;
ASV not
required

10. Indian Russell's Viper

11. Russell’s Viper

12. Green Pit Viper
Infrared Vision
TRPA1/Wasabi
Receptor

13. Indian Green Pit Viper

14. Asian Sand Viper
(Eristicophis macmahonii)

15. Hump Nosed Viper

16. Hump Nosed Viper

17. Common Indian Krait
(Bungar us caer uleus )

18. Common Indian Krait
(Bungar us caer uleus )

19. The Greater Black Krait
(Bungarus niger)

20. T he Greater Black
Krait
(Bungar us niger)

21. Mild
Venomous;
ASV not Indian Cat Snake
required

22. Mild
Venomous;
ASV not Wolf Snake
required

23. Sea Snake

24. Trinket Snake
Mild
Venomous;
( Elaphe
ASV not
required helena monticollaris)

25. Mild
Venomous;
ASV not Montane Trinket
required

26. Non Venomous;
Indian Rat Snake
ASV not required

27. Indian Rock Python

28. Varie gated Kukri
Non Venomous;
ASV not required
(Oligodon taeniolatus)

29. Non Venomous;
ASV not required
KEELBACK
http://animalrescuesquadgoa.com/Non%20venemous.html

30. FACTS
Snake bite
Majority (80%) is by non-venomous snakes
Venomous snakes
About 50% of bites are dry

31. Is there any medical
implication for snake
identification?

32. Species: Medical Implications
Signs/Symptoms Russell’s
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

33. What is syndromic approach &
its significance in Indian
scenario?
Desired when snake is unidentified

34. SYNDROMIC APPROACH
Syndrome 1
Local envenoming (swelling etc) with bleeding/clotting
disturbances = Viperidae (all species)
Syndrome 2
Local envenoming (swelling etc) with bleeding/clotting
disturbances, shock or renal failure = Russell’s viper (and
possibly saw-scaled viper – Echis species)
With conjunctival oedema (chemosis) and acute
pituitary insufficiency = Russell’s viper
With ptosis, external ophthalmoplegia, facial paralysis etc
and dark brown urine = Russell’s viper

35. SYNDROMIC APPROACH
Syndrome 3
Local envenoming (swelling etc) with paralysis = cobra or
king cobra
Syndrome 4 : Paralysis with minimal or no local
envenoming
Bite on land while sleeping= krait
Bite in the sea = sea snake
Syndrome 5 : Paralysis with dark brown urine and renal
failure:-
Bite on land (with bleeding/clotting disturbance) =
Russell’s viper
Bite in the sea (no bleeding/clotting disturbances) = sea
snake

36. Composition of Snake
Venom
 Pr ocoa gulant enzymes  Haemol ytic and myol ytic
( Viperidae) Russell’s viper phospholipases A2
damage cell membranes,
 Haemor rha gins endothelium, skeletal
muscle, nerve and red blood
(zinc metalloproteinases) cells.
damage the endothelial
lining.
 Pr e-synaptic neur otoxins
(Elapidae and some
 Cytol ytic or necr otic
Viperidae)
toxins
 Post-synaptic
neur otoxins (Elapidae)

37. Snake Bite Toxicity Profile ?

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

39. What is the mode of
Neurotoxicity in Krait Bite?

40. Krait- Pre-synaptic action
Beta-bungarotoxin- Phospholipases A2
1) Inhibiting the release of Ach
from the presynaptic
membrane
2) Presynaptic nerve terminals
exhibited 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.

41. What is the mode of
Neurotoxicity in Cobra Bite?

42. 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

43. Neuroparalytic Manifestations Study
Ptosis
Ophthalmoplegia
RS
r
Bulba ss involvement
e
weakn
N Sharma, S Chauhan, S Faruqi, P Bhat, S Varma, Emerg Med J 2005;22:118–120

44. Quick Neurological
Examination !

45. 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 paralysed, giving
the “broken neck sign

46. Bungarus niger envenoming
20 hr post-bite

47. 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.

48. How to identify for bulbar palsy
& early resp failure?

49. Bulbar & Resp Paralysis
 Can the patient swallow or are secretions accumulating
in the pharynx- an early sign of bulbar paralysis.
 Ask the patient to take deep breaths in and out.
“Paradoxical respiration”.
 Objective measurement of ventilatory capacity is very
useful. Use a peak flow metre, spirometer (FEV1 and
FVC)
 Ask the patient to blow into the tube of a
sphygmomanometer to record the maximum expiratory
pressure (mmHg).

50. Paradoxical Respiration
 This is an abnormal pattern of breathing in which the
abdominal wall is sucked in during inspiration (it is
usually pushed out).
 Paradoxical respiration is due to paralysis of the
diaphragm.

51. Hematological Side Effects
Venom induces bleeding
Venom induces clotting
Venom induces haemolysis
Haemorrhagin – causes direct endothelial damage by
loosening the gap between endothelial cells
Procoagulant factors
Anticoagulant factors
Fibrinonolytic factors

52. Snake Venom and the Coagulation Cascade
RVV – Russel’s Viper
Venom ECV – Echis
carinatus
Venom

53. PTT

54. PT

55. 20 min W hole Blood
Clotting Test (20-WBCT)
 Place a few ml of freshly sampled venous
blood in a small glass vessel
 Leave undisturbed for 20 minutes at ambient
temp & tip the vessel once
 If the blood is still unclotted and runs out, the
patient has hypofibrinogenaemia/DIC
 In the SE Asia, incoagulable blood is
diagnostic of a viper bite and rules out an
elapid bite

56. 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

57. Russell’s Viper
Bite

58. Venomous Non-venomous

59. LOCAL NECROSIS

60. What are the systemic
manifestations of the
envenomation ?

61. Systemic Symptoms & Signs
 General
 Nausea, vomiting, malaise, abdominal pain, weakness, drowsiness,
prostration, conjunctival oedema
 Cardiovascular (Viperidae)
 Visual disturbances, dizziness, faintness, collapse, shock,
hypotension, cardiac arrhythmias, pulmonary oedema
 Neurological (Elapidae, Russell’s viper)
 Drowsiness, paraesthesiae, abnormalities of taste and smell,
“heavy” eyelids, ptosis
 external ophthalmoplegia, paralysis of facial muscles and other
muscles innervated by the cranial nerves, aphonia, difficulty in
swallowing secretions,
 respiratory and generalised flaccid paralysis

62. Systemic Symptoms & Signs
 Bleeding & Clotting Disorders
 Bleeding from recent wounds (including fang marks), venepunctures
and from old partly-healed wounds
 Spontaneous systemic bleeding – from gums, epistaxis, bleeding
into the tears
 haemoptysis, haematemesis, hematochezia or melaena,
haematuria, bleeding P/V, bleeding into the skin (petechiae,
purpura, ecchymoses) and mucosae (eg conjunctivae)
 Intracranial haemorrhage (meningism from SAH, lateralising signs
and/or coma from cerebral haemorrhage)

63. Systemic Symptoms & Signs
 Skeletal muscle breakdown (sea snakes, Russell’s
viper) Generalised pain, stiffness and tenderness of muscles, trismus,
myoglobinuria hyperkalaemia, cardiac arrest, acute renal failure
 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)
 Endocrine (acute pituitary/adrenal insufficiency)
(Russell’s viper)
 Acute phase: shock, hypoglycaemia
 Chronic phase (months to years after the bite): weakness, loss of
secondary sexual hair, amenorrhoea, testicular atrophy, hypothyroidism
etc

65. Myoglobinuria after Bungarus niger
envenoming

66. Pleuropericardial
Haemorrhagic Effusion
Manoj Lakhotia et al JIACM 2002; 3(4): 392-4

67. Treatment
First Aid
Primary/Secondary Care Level
Tertiary Care Level

68. Fir st Aid
 Reassure the victim
 Immobilise the bitten limb with a splint or sling
 Consider pressure-immobilisation for some elapid
bites; AVOID IN COBRA
 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.

69. Pressure Immobilization
(Elapidae bite)
 Developed in 1970 by late Struan Sutherland,
Australia
 Bandaging entire limb using a long crepe
bandage – starting from toe or finger as tightly
as for a sprained ankle incorporating a splint.

71. Pressure
Immobilisation
 Pr immobilisation is recommended for bites by
neurotoxic elapid snakes, including sea snakes.
 Caries risk of sudden envenomation after release –
neurotoxic snakes.
 Should not be used for viper bites because of the
danger of increasing the local effects of the necrotic
venom.

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

73. Tour niquet Gangrene

74. INCISION & SUCTION
No!


75. TREATMENT
CRYOTHERAPY:
No!
Incr eases tendency to necr osis

76. TREATMENT
HOSPITAL MEASURES FOR ASYMPTOMATIC
PTS
a) OBSERVATION FOR 24 HOURS
b) MONITOR:
 PR, RR, BP
 CBC-TLC ↑, Platelets ↓
 Urine output
 BUN, Creatinine
 PT, aPTTK, INR
 CPK (>600 IU/L)
 Vomiting, diarrhoea
 Abnormal bleeds
 Local swelling necrosis
 ECG
 Blood gas analysis

77. MEDICOLEGAL
39 Code of Criminal Procedure under
Constitution of India Article 21
MLC to be initiated

78. Hospital mngt, 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

79. What is ASV?

80. ASV
 ASV is Ig (usually the enzyme refined F(ab)2 fragment of
IgG) purified from the serum/plasma of a horse/sheep
immunised 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 including
the FAB Four.

81. Antivenom
Polyvalent antivenoms
from India raised
against venom from:
•Bungarus caeruleus
•Naja naja
•Echis carinatus
•Daboia russelii
No monovalent
vaccine in India

82. ASV
 Average dry weight of venom injected =
63 +/- 7mg by Russell’s Viper or Cobra.
 Each vial neutralises venoms of
6 mg Cobra
6 mg Russell's Viper
4.5 mg of Krait
4.5 mg of Saw Scaled Viper
 Initial dose should be 8-12 vials.
 Snake inject same amount of venom into
children, dose of ASV is same as adult .
http://cbcreatures.webs.com/snakeantivenom.htm

83. What are the indications for
ASV use?

84. Indications for Antivenom
 Shock UseSevere GI Symptoms

 Resp distress /failure  Myoglobinuria
 Extensive Local Swelling  Elevated creatine kinase
level (>600 IU/l)
 Ptosis
 Altered level of
 Generalized myalgias consciousness
 Hyperkalemia
 Trismus
 Mod-to-severe pain with  ECG Changes
passive movement of
extremities  Leukocytosis.

85. Antivenom
Reconstitution
 Freeze-dried (lyophilised) ASV is reconstituted
with 10 ml of sterile DW per vial.

86. TREATMENT OF
SNAKEBITE
PROCEDURE OF ADMINISTRATION
Test Dose?
No!
 Has no predictive value in detecting
anaphylactoid or late serum
reactions and should not be used.
 Not IgE mediated, but complement -
activated. May also pre-sensitise
the patient, and create greater risk.

87. Methods of
Administration
IV “push” injection: recons
freeze-dried ASV is given by slow iv
inj (not more than 2ml/min).
IV infusion: recons freeze - dried
ASV is diluted in approx 5-10 ml of
isotonic fluid per kg BW (ie 250-500
ml of N/S or 5% Dex in adult pt) and
infused at a constant rate over a
period of about 1h.

88. Antivenom
Administration
 Adrenaline drawn up in readiness before ASV is
administered.
 ASV should be given by the IV route whenever
possible.
 I/M may be given when no i/v access,
expeditions with limited med facilities.

89. Prophylaxis in High Risk
patients
 Pre-treated empirically with s/c
epinephrine (adrenaline)
 IV antihistamines anti-H1 + anti- H2
(Ranitidine)
 IV Hydrocortisone 100 mg

90. IM Antivenom
 A maximum of 5-10 ml should be given at
each site by deep IM inj followed by massage
to aid absorption
 ASV should never be injected into the gluteal
region (upper outer quadrant of the buttock)
as absorption is exceptionally slow and
unreliable and there is always the danger of
sciatic N damage by an inexperienced
operator.

91. Dose
5 vials(50ml)
5-10 vials
(50-100ml)
10-20 vials
(100-200ml)

92. Large vs Small dose
•High dose group 100ml stat and 100 ml every 6 hrs
•Low dose group 100ml stat and 50 ml every 6 hrs
Until recovery of neurological signs
Low dose of snake antivenom is as effective as high dose inpatients with severe neurotoxic snake
envenoming
Agarwal, Aggarwal, Gupta, et al Emerg Med J 2005;22:397–399 .

93. Timing of ASV
 There is no consensus as to the window period of
administration of ASV.
 Best effects are observed within 4 h of bite .
 It has been noted to be effective in symptomatic
pts even when administered up to 48 h after bite.
 ASV is efficacious even 6-7 days after the bite
from vipers

94. At the Ear liest Sign of a
Reaction :
 ASV administration must be
temporarily suspended
 Adrenaline (0.1% solution, 1 in 1,000; 1
mg/ml) is the effective treatment for
early anaphylactic and pyrogenic ASV
reactions

95. Ear ly reaction to ASV
Anaphylaxis
 Adrenaline (SC or IM) 0.3 to 0.5ml
1:1000 (1mg/ml). Repeated at 5 to 20
min interval if severe.
 Adrenaline (IV) - in intractable reaction
2.5 ml iv; 1:10,000 (0.1mg/ml).
 Volume resuscitation

96. Case scenario…….
 34 yr old male shifted from Periph Hosp with H/O snake
bite 6 hrs back has ptosis, respiratory distress, RR
35/mt, BP 120/60, oral secretions present, absent gag
and cough reflex shifted to ICU for tertiary care.
 On ASV 100ml stat, & 50ml in NS over 6 hrs
 Oxygen 3l/mt
Patient is comfortable, vitals stable
No ptosis, distress
Patient received
in casualty: 2 situations
Patient is dead –what do you think
went wrong ?

97. Patient is dead –what do you think went wrong ?
 What could have been done better ?
 Bulbar signs-probably aspirated and died
 Endotracheal intubation could have been placed on T-
piece Ambuing or Transport Ventilator
 Anticholienesterases
 Neostigmine with atropine

98. Trial of Anticholinesterase
Anticholinesterase (“Tensilon”/Edrophonium) test
 Record baseline parameters
 Give atropine IV
 Give anticholinesterase drug edrophonium chloride
(adults 10 mg, children Neostigmine 25µg/kg/hr
0.25 mg/kg body weight) given
Dose of
intravenously over 3 or Neostigmine 0.5 mg / 6 hr
4 minutes
Neostigmine
IV atropine 0.5 mg / 12 hr
Observe
Negative response
Positive response Tearing, salivation,
Improvement in
ptosis, Respiratory muscle fasciculation,
distress, better cough abdominal cramp,
effort, decrease in bronchospasm,
RR bradycardia, cardiac
arrest Atropine IV
Neostigmine

99. Case scenario…….
34 yr old male shifted from Periph Hosp with H/O
snake bite 6 hrs back has ptosis, respiratory distress,
RR 35/mt, BP 120/60, oral secretions present, absent
gag and cough reflex shifted to ICU for tertiary care.
On ASV 100ml stat, & 50ml in NS over 6 hrs
Oxygen 3l/mt
Recd neostigmine 0.6mg and 0.6 mg atropine iv
You can have alive but a sicker patient Cobra
You can have dead patient Krait

100. Alive but a sicker patient
Shifted to ICU placed on a Ventilator lot of secretions
Do we continue anticholinesterases ?
Issues to consider
Increased secretions
Increased incidence of VAP ?
We rarely use these drugs once the patient is in the
ICU under observation

101. Observation of the Response to
Antivenom
Cobra bites-Post synaptic
May begin to improve as early as 30 minutes
after anti-venom, but usually take several hours.
Krait and sea snakes- Pre synaptic
Depends on the timing of ASV administration
If delayed may not produce any action or
Minimal delayed action

102. Repeat Dose
 Signs of systemic envenoming may recur within 24-48 hrs
 Criteria for repeating the initial dose of antivenom
 Persistence/recurrence of blood incoagulability after 1-2 h
 Deteriorating neurotoxic or cardiovascular signs after 1-2 h
Causes
 Continuing absorption- due to improved blood supply
following correction of shock, hypovolaemia etc
 After elimination of antivenom a redistribution of venom from
the tissues into the vascular space.

103. How to Know ASV Dose
Administered is Suf ficient?
a) Spontaneous systemic
bleeding stops in 15-30 min.
b) Blood coagulability is
usually restored in 6 hour s.
c) Post synaptic neurotoxic
envenoming be gins to improve
in 30 min, but can take several
hour s.

104. How to Know ASV Dose
Administered is Suf ficient?
d) Presynaptic neurotoxic
envenoming usually takes a
considerably more time to
improve.
e) Active haemolysis &
rhabdomyolysis may cease
within a few hour s & urine
retur ns to its nor mal colour.
f) In shocked pts, BP may improve
in 30 min.

105. W hat is the Max Dose of
ASV?
25 – 30 vials
Q. If symptoms per sist despite giving max
dose, w hat must be done?
Ans. Suppor tive measur es & tr eatment
of complications:
 Ventilation – Elapid bite
 Dialysis, tr ansfusions, etc – V iperid
bite
 Fasciotomy, wound sur ger y,
amputation, etc, as per need.

106. Pregnancy and Snake Bite
 Pregnant pt is treated the same manner as the
nonpregnant .
 Spontaneous abortion, bleeding, fetal death &
malformations are common.
 Lactating mothers can continue lactating

107.  A 25 yr old male with snake bite has signs of
compartment syndrome and the pressure is 60 mmHg,
is undergoing surgery, has a Hb of 6 gm%, is
hypotensive 100/60, on noradrenalin, acidotic,
coagulation profile is normal
 Blood is started
 After 15 mts of surgical time patient develops
 Dark colored urine Treatment
 BP drops to 80/60 with ARF Fluids, Mannitol,
Alkalinize the urine,
 What are the possibilities ? Manage electrolytes
Fasciotomy
RRT
Rhabdomyolysis
(Viper Bite)

108. Other Rx
Antibiotics
Hydration
Tetanus prophylaxis
Wound debridement
Fasciotomy for compartment syndrome
Haemodialysis for acute renal failure
Mechanical ventilation
DIC; related mngt

109. Criteria for Fasciotomy in
Snake-Bitten Limbs
Clinical evidence of an
intracompartmental syndrome
Intracompartmental pr >40
mmHg (in adults)

110. Disposition (Dr y bite)
* Viper Bite
No local and systemic envenomation
at 8 to 12h by repeated lab tests – ‘Dry Bite’.
* Neurotoxic snake
Observation period 12-24hr.
Neurotoxicity can be delayed .

111. References
 N Engl J Med, Vol. 347, No. 5 August 1, 2002
www.nejm.org Page 347-356
 WHO Guidelines for the Clinical
Mana gement of Snake Bites in the
South-East Asia Re gion

112. THANK YOU
Happy Year of the Snake! 新年快乐！