Snake bite

Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.

1. MANAGEMENT OF SNAKE
BITE
Dr. Sachin Verma MD, FICM, FCCS, ICFC
Fellowship in Intensive Care Medicine
Infection Control Fellows Course
Consultant Internal Medicine and Critical Care
Web:- http://www.medicinedoctorinchandigarh.com
Mob:- [phone]

2. INTRODUCTION
•Poisoning by venomous snake bite is
a common acute life-threatening
medical emergency in India.

3. 61 507 bites and 1,124 deaths in 2006
76,948 bites and 1,359 deaths in 2007

[Government of India data:
pp 107–108 of http://cbhidghs.nic.in/writereaddata/mainlinkFile/Health%20
Status%20Indicators.pdf)

5. ETIOLOGY
There are about 216 species of
snakes identifiable in India, of
which 52 are known to be
poisonous.

6. ETIOLOGY
•Major families of poisonous
snake in India includes –
-Elapidae  Common cobra
(naja naja)
 King Cobra
 Common Krait
--

8. Viperidae
Russell’s viper
 Echis carinatus (Saw scaled or
carpet viper)
Pit viper

10. Colubridae
Largest snake family, and includes about
two-thirds of all current snake species.
most are nonvenomous and harmless, but
few groups can produce medically
significant bites, and have caused human
fatalities.

12. SNAKE VENOMS
•Snake venoms contain more than 20 different
constituents. Mainly proteins including enzymes &
polypeptide toxins.

13. SNAKE VENOMS
•Procoagulant enzymes
•Haemorrhagins
•Cytolytic or necrotic toxins
•Haemolytic and myolytic
phospholipases A2

14. SNAKE VENOMS
•Pre-synaptic neurotoxins
•
•Post-synaptic neurotoxins

16. SYMPTOMS & SIGNS OF
SNAKE BITE
WHEN VENOM HAS NOT BEEN INJECTED
•Anxiety
•Vaso-vagal shock

17. 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
WHEN VENOM HAS BEEN INJECTED

18. Fang marks made by Russell’s viper
SYMPTOMS & SIGNS OF SNAKE BITE

19. Local bleeding from fang marks made by pit viper
SYMPTOMS & SIGNS OF SNAKE BITE

20. Local swelling and blistering (a) with bruising,
following a bite by a pit viper (b) with early necrosis
following a bite by a cobra
SYMPTOMS & SIGNS OF SNAKE BITE

21. Tissue necrosis following a bite by a pit viper
SYMPTOMS & SIGNS OF SNAKE BITE

22. GENERALISED (SYSTEMIC)
SYMPTOMS AND SIGNS
General
•Nausea, vomiting, malaise, abdominal
pain, weakness, drowsiness, prostration
Cardiovascular (Viperidae)
•Visual disturbances, dizziness, faintness,
collapse, shock, hypotension, cardiac
arrhythmias, pulmonary oedema.

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

24. Neurological (Elapidae, Russell’s viper)
•Drowsiness, paraesthesiae,
•abnormalities of taste and smell,
•ptosis, external ophthalmoplegia,
•Muscle palsys
•aphonia,
•difficulty in swallowing secretions,
•respiratory and generalised flaccid paralysis

25. Skeletal muscle breakdown (sea snakes,
Russell’s viper)
•Generalised pain,
•stiffness and tenderness of muscles
trismus,
•myoglobinuria,
•hyperkalaemia,
• acute renal failure

26. Renal (Viperidae, sea snakes)
•Loin pain,
•haematuria,
• haemoglobinuria,
• myoglobinuria,
• oliguria/anuria,
• symptoms and signs of uraemia

27. Endocrine (acute pituitary/adrenal
insufficiency)
•Acute phase: shock, hypoglycaemia
•Chronic phase (months to years after
the bite):
•loss of secondary sexual hair
amenorrhoea,
•testicular atrophy
•hypothyroidism etc.

28. Bilateral conjunctival oedema (chemosis) after a
bite by a Russell’s viper

29. Bleeding from gingival sulci in a patient bitten
by a saw-scaled viper

30. Subconjunctival haemorrhages in a patient
bitten by a Russell’s viper

31. Bilateral ptosis (a) in a patient bitten by a common krait
Bilateral ptosis (b) in a patient bitten by a Russell’s viper

32. LONG TERM COMPLICATIONS
(SEQUELAE) OF SNAKE BITE
•Chronic ulceration, infection, osteomyelitis or
arthritis.
•Malignant transformation in skin ulcers.
•Chronic renal failure
•Chronic panhypopituitarism or diabetes
insipidus.
•Chronic neurological deficit in patients of
intracranial haemorrhages.

33. Patient with symptoms and signs of panhypopituitarism
three years after envenoming by Russell’s viper. There is loss of
secondary sexual hair and testicular atrophy

34. (a) Deformity and dysfunction after a bite and subsequent necrosis
of the calf

35. Squamous cell carcinoma arising at the site of a chronic skin
ulcer with osteomyelitis 8 years after the bite.

36. Clinical syndromes of
snake-bite in South-East
Asia
Syndrome 1
Local envenoming (swelling etc.) with
bleeding/clotting disturbances =
Viperidae (all species)

37. Syndrome 2
Local envenoming with bleeding/clotting
disturbances, shock or AKI = Russell’s viper
(hump-nosed pit viper in Sri Lanka
and SW India)
with conjunctival oedema and acute pituitary
insufficiency =
Russell’s viper, Myanmar
with ptosis, external ophthalmoplegia, facial
paralysis etc and dark brown urine
= Russell’s viper, Sri Lanka and South
India

38. Syndrome 3
Local envenoming (swelling etc.)
with paralysis = cobra or king cobra

39. Syndrome 4
Paralysis with minimal or no local
envenoming
Bitten on land while sleeping on the
ground = krait
Bitten in the sea, estuary and some
freshwater lakes = sea snake

40. Syndrome 5
Paralysis with dark brown urine and AKI:
Bitten on land (with bleeding/clotting disturbance)
= Russell’s viper, Sri
Lanka or South India
Bitten on land while sleeping indoors = krait ,
Bangladesh, Thailand
Bitten in sea, estuary and some freshwater lakes
(no bleeding/clotting
disturbances) = sea snake

41. ASSESSMENT OF SEVERITY
No envenomationAbsence of local or systemic reactions, Fang
marks +/-
Mild envenomationFang marks (, moderate pain, minimal local
oedema (0-15cms), erythema+, ecchymosis
+/-, no systemic reactions
Moderate
envenomation
Fang marks+, severe pain, moderate local
edema (15-30cms), erythema & ecchymosis +,
systemic weakness, sweating, syncope,
nausea, vomiting, anemia or thrombocytopenia
Severe envenomationFang marks+, severe pain, severe local edema
(>30cms), erythema & ecchymosis+,
hypotension, parasthesia, coma, pulmonary
edema, respiratory failure

42. MANAGEMENT OF SNAKE BITE
First aid treatment
Transport to hospital
Rapid clinical assessment and resuscitation
Detailed clinical assessment and species
diagnosis
Investigations/laboratory tests
Antivenom treatment

43. Observing the response to antivenom
Deciding whether further dose(s) of antivenom
are needed
Supportive/ancillary treatment
Treatment of the bitten part
Rehabilitation
Treatment of chronic complications

44. RECOMMENDED FIRST AID
METHODS
•Reassure the victim
•Immobilise the bitten limb with a splint or
sling
•Consider pressure-immobilisation for some
elapid bites
•Avoid any interference with the bite wound as
this may introduce infection, increase
absorption of the venom and increase local
bleeding.

45. •Application of a tourniquet to the bitten limb
•Cuting open the bitten area
•Sucking out venom, either by mouth or with a pump
•Immersion in warm water or sour milk, followed by the application
of snake-stones
• .
•Application of potassium permanganate.
•
•Use of electroshock therapy
•NOT RECOMMENDED

46. PRESSURE IMMOBILISATION
METHOD.

47. 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
•Tip the vessel once
•If the blood is still liquid (unclotted) and runs
out, the patient has hypofibrinogenaemia

49. OTHER TESTS
•haematocrit: a transient increase
indicates haemoconcentration resulting
from a generalised increase in capillary
permeability (eg in Russell’s viper bite).
•Decrease reflects blood loss or
intravascular haemolysis.

50. •Platelet count: this may be decreased in
victims of viper bites.
•White blood cell count: an early neutrophil
leucocytosis is evidence of systemic
envenoming from any species.
•Blood film: fragmented red cells (“helmet
cell”, schistocytes) are seen when there is
microangiopathic haemolysis.

51. INVESTIGATIONS/LABORATORY
TESTSOTHER TESTS
•Plasma/serum may be pinkish or
brownish if there is gross
haemoglobinaemia or myoglobinaemia.
•
•Biochemical abnormalities :
aminotransferases and muscle enzymes
(creatine kinase, aldolase etc) will be
elevated if there is severe local damage
or, particularly, if there is generalised
muscle damage (Russell’s viper bites, sea
snake bites).
•

52. Bilirubin is elevated following massive
extravasation of blood.
Renal function tests are raised in the renal
failure (Russell’s viper , saw-scaled viper
and sea snake bites.)
Hyperkalaemia may be seen following
extensive rhabdomyolysis in sea snake
bites.

53. OTHER TESTS
•Arterial blood gases
•Arterial oxygen Saturation
•
•Urine examination: the urine should be
tested for blood/ haemoglobin/myoglobin.

54. Snake Bite Treatment
Protocol

55. On arrival.
Deal with any life threatening symptoms on
presentation. i.e. Airway, Breathing and
Circulation.

If there is evidence of a bite, where the skin
has been broken, give Tetanus Toxoid

Routine use of anti-biotic is not necessary,
although it should be considered if there is
evidence of cellulitis or necrosis

56. Diagnosis Phase: General Principles

Where possible identify the snake responsible.

keep under observation for a minimum of 24 hours.

Determine if any traditional medicines have been used

Determine the exact time of the bite.

Question what the victim was doing at the time of bite.

57. ANTIVENOM TREATMENT
•Antivenom is immunoglobulin (usually the
enzyme refined F(ab)2 fragment of IgG)
purified from the serum or plasma of a horse or
sheep that has been immunised with the
venoms of one or more species of snake.
•Monovalent or monospecific antivenom
neutralises the venom of only one species of
snake. Polyvalent or polyspecific antivenom
neutralises the venoms of several different
species of snakes

58. INDICATIONS
Systemic envenoming
•Haemostatic abnormalities
•
•Neurotoxic signs
•Cardiovascular abnormalities :

59. INDICATIONS
•Acute renal failure
•Haemoglobinuria/myoglobinuria
•
•Supporting laboratory evidence of
systemic envenoming.

60. INDICATIONS
Local envenoming
•Local swelling involving more than half of
the bitten limb (in the absence of a
tourniquet)
•Swelling after bites on the digits (toes and
especially fingers).
•Rapid extension of swelling
•Development of an enlarged tender lymph
node draining the bitten limb.

61. SELECTION OF ANTIVENOM
•Liquid antivenoms that have become opaque
should not be used as precipiated of protein
indicates loss of activity & increased risk of
reaction.
•Polyspecific/polyvalent antivenoms are
preferred in many countries because of
difficulty in identifying species responsible for
bites.

62. •1 ml of polyvalent antivenom will
neutralise
•0.6 mg of dried cobra venom
• 0.45 mg of dried krait venom
• 0.6 mg of dried Russel’s viper venom
•0.45 mg of dried saw-scales viper venom.

63. DOSE OF ANTIVENOM
•Children must be given exactly the
same dose of antivenom as adults.
•Test dose of ASV is not essential
because even if victim is sensitive to
ASV, does not preclude its use.
Because there is no guarantee that
victim would not develop anaphylaxis
reaction after administration.

64. •Initial dose should depend on an estimate
of amount of envenomation.
•5 vials given if signs are mild -primarily
local manifestations. (Minimal
envenomination)
•10 vials if signs are moderate -bleeding
from gums, ptosis. (Moderate
envenomination)
•15 vials if signs are severe -vascular
collapse, progressive paralysis. (Severe
envenomination)

65. ADMINSITRATION OF ANTIVENOM
ASV diluted in 100ml of isotonic saline or
glucose or 5-10 ml / kg body wt of isotonic
saline or glucose as an infusion.
 All ASV to be administered over 1 Hour at
constant speed. The patient should be
closely monitered for two hours.
•Local administration of antivenom
at the site of bite is not
recommended.

66. Observation of the response to antivenom:
(a) General: The patient feels better. Nausea,
headache and pains disappear very quickly.
(b) Spontaneous systemic bleeding (e.g. from
the gums): stops within 15-30 minutes.
(c) Blood coagulability (as measured by
20WBCT):
restored in 3-9 hours. Bleeding from new and
partly healed wounds usually stops much
sooner than this.

67. (d) In shocked patients: Blood pressure may
increase within the first 30-60 minutes and
arrhythmias may resolve.
(e) Neurotoxic envenoming of the post-synaptic
type (cobra bites) begin to improve as early as
30 minutes after antivenom, but usually takes
several hours.
(f) Active haemolysis and rhabdomyolysis may
cease within a few hours and the urine returns to
its normal colour.

68. Criteria for giving more antivenom:
Persistence or recurrence of blood
incoagulability after 6 hours or of bleeding
after 1-2 hours.
Deteriorating neurotoxic or cardiovascular
signs after 1-2 hours.

69. CONTRAINDICATIONS TO
ANTIVENOM
•No absolute
contraindication

70. ANTICHOLINESTERASE THERAPY
•Post synaptic neurotoxins compete with
acetylcholine for available nicotinic Ach
receptor sites on adjacent skeletal muscle
cell synaptic clefts. This process tend to be
reversible.
•Anticholinesterases are the drugs that
inhibit the process of acetylcholine
breakdown & re-uptake.

71. LIMITATIONS
•No value in the treatment of
presynaptic neurotoxicity.
•No substitute for antivenom therapy
and mechanical ventilation.
•Only an adjunct treatment

72. CONTRAINDICATIONS TO USE
•If there is positive 20WBCT
(incoagulable blood).
•Previous allergy to the drug.

73. ASSESSMENT OF
SUITABILITY
•“Neostigmine Test”.

74. Neostigmine test
1.5 to 2 mg of neostigmine  I M together with
0.6 mg  of atropine I V .
The patient should be closely observed for 1 hour
Methods to asses effectiveness of neostigmine are
1.      single breath count
2.      mm of iris uncovered
3.      Inter incisor distance
4.    Length of time upwards gaze can be maintained.
5.      FEVi or FVC

76. •If the victim responds to neostigmine test
• 0.5 mg of neostigmine IM half hourly
plus 0.6 mg atropine IV for 5 doses
• then 2 to 12 hourly according to
recovery.  
• If there is no improvement in symptoms
after 1 hr, neostigmine should be stopped.

77. •Can be given in the form of
interavenous infusion at the rate of 25
µg/kg/hour until the neuroparalysis is
reversed.

78. Local pain, swelling+ - ++ -
Local bleeding + - ++ -
Pain in regional nodes+ + + -
Vomiting + + + +
Hypotension + + + -
On site
Hospital
Mandatory observation 24 hrs
LocalSystemic Cobra Sea snakeKraitViper
Swelling
Blisters
Necrosis
Clean dressing
No incision, suction, tourniquet, Splint + crepe bandage
Ressure, transport in lateral decubitus
Tetanus toxoid, IV line, lateral position, anxiolytic

79. Major defect
Mechanical ventilation
Compartment
syndrome
Vomiting, diarrhoea
Abdominal pain
Paraesthesiae
Oozing
Nonclotting
Blood
Headache, thirst
Thick tongue
Myalgia
Antivenom infusion 5- 15 vials
Debride GraftFasciotomy
Pooled secretionsNeuroparalysisRetest blood
6 hrs.
Myoglobin damage
Renal failure
Dialysis
Observe 48-72 hrs.
Clots
Retest 6 hrs.
Repeat Antivenom
No Clot
Neostigmine
Neostigmine test
Suction
Positive
Intubation
Respiratory Paralysis