This document discusses snake venom poisoning and its management. It begins by classifying snakes and identifying the 5 families that contain venomous species. It then describes the differences between poisonous and non-poisonous snakes. The document outlines the components of snake venom and their effects. Signs and symptoms of envenomation are provided for different snake families. Diagnosis involves identifying the snake species based on symptoms, circumstances, or antigen detection. Treatment primarily involves administering antivenom, with dosages varying based on severity of symptoms. Adjuvant treatments like neostigmine may also be used depending on the neurotoxin involved.
2. SNAKES
Snakes belong to the Class Reptilia. All snakes are placed in the
Suborder Serpentes. All snakes share the common characteristics
separating them from the lizards namely: Lack of eyelids & Lack
of visible external ears.
3. CLASSIFICATION OF SNAKES
There are approximately 3,000 species of snakes globally, but only
about 600 species are venomous and all of these are found in just 5
snake Families:
15. SNAKE VENOM
• Snake venoms are generally produced in specific venom glands,
derived from salivary glands.
• The venom, once produced, is delivered by a duct to the fang
base, where it is transported into the victim either by a groove in
the fang, or through a fang duct.
16. Contnd.
Medical classification of snake venom activities.
Toxin activity type Clinical effects
Neurotoxin Flaccid paralysis
Presynaptic - Resistant to late antivenom
therapy
Postsynaptic - Often reversal with
antivenom therapy
Anticholinesterase - Fasciculation
Myotoxin Systemic skeletal muscle
damage
Haemostatic system toxins Interfere with normal haemostasis,
causing either bleeding or
thrombosis
17. Contnd.
Haemorrhagin Damage vascular wall,
causing bleeding
Nephrotoxin Direct renal damage
Cardiotoxin Direct cardiotoxicity
Necrotoxin Direct tissue injuryat
the bite site/bitten limb
18. Snake venom• Procoagulant enzymes
– DIC-“consumption coagulopathy”
–non clotting blood
– Viperidae
• Zinc metalloproteinase
haemorrhagins
– Damage vascular endothelium –
bleeding
• Hyaluaronidase
– Promotes the spread of
venom through tissues.
• Proteolytic enzymes
(metalloproteinases, endopeptidases
or hydrolases) & polypetide
cytotoxins (“cardiotoxins”)
– ↑ vascular permeability causing
oedema, blistering, bruising and
necrosis at the site of the bite
• Phospholipase A2
(lecithinase )
– damages mitochondria, red
blood cells, leucocytes,
platelets, peripheral nerve
endings
– damages skeletal muscle,
vascular endothelium
– produces presynaptic
neurotoxic activity
• Venom polypeptide
toxins (“neurotoxins”)
– Postsynaptic (α) neurotoxins
such as α-bungarotoxin and
cobrotoxin,
– Presynaptic (β) neurotoxins
such as β-bungarotoxin,
crotoxin and taipoxin,
20. Generalized (systemic) symptoms and signs
General
• Nausea, vomiting
• Abdominal pain
• Malaise, weakness
• Drowsiness
• Prostration
21. Local symptoms and signs in
the bitten part:
• Fang marks
• Local pain
(burniang, bursting, throbbing)
• Lymph node enlargement
(femoral /inguinal , epitrochlear,
axilla)
• Local bleeding
• Inflammation
(swelling, redness, heat)
• Blisters
• Necrosis
Bites by kraits & sea
snakes
-virtually painless
-negligible local swelling
-no detectable fang
marks
22. Neurological (Elapidae,
Russell’s viper)
• Drowsiness, paraesthesiae
• Abnormalities of taste and smell
• “Heavy” eyelids, ptosis
• External ophthalmoplegia
Diplopia
• Descending paralysis of facial
muscles and other muscles
innervated by the cranial nerves
• Nasal regurgitation
• Difficulty in swallowing
secretions
• Respiratory and generalised
flaccid paralysis.
23. Bleeding
(Viperidae)
• Traumatic bleeding
– fang marks /venipunctures
Spontaneous systemic bleeding
– gums
– epistaxis
– haemoptysis , haematemesis,
haematuria
– bleeding into the mucosae (e.g.
conjunctivae )
– bleeding into the skin (petechiae,
purpura, discoid haemorrhages and
ecchymoses)
– bleeding into the retina
– intracranial haemorrhage
– rectal bleeding or melaena
– vaginal bleeding
– ante-partum haemorrhage in pregnant
women
24. Cerebral arterial thrombosis
(Russell’s viper)
• Thrombotic strokes,
confirmed by angiography
or imaging, are reported
rarely after envenoming by
D. russelii
25. Skeletal muscle breakdown
(Rhabdomyolysis)
• Generalized pain
• Stiffness and tenderness of
muscles
• Trismus
• Myoglobinuria (Coca-
Cola-coloured)
• Acute renal failure
• Hyperkalaemia
• Cardiac arrest
• Sea snakes
• Russell’s viper ( Daboia russelii )
• Krait species –Bungarus niger
and B. candidus
30. Aims of first-aid
• Attempt to retard systemic absorption of venom.
• Preserve life and prevent complications before the patient can
receive medical care
• Arrange the transport of the patient to a place where they can
receive medical care.
32. Do not panic
• Reassure
– 70% of all snakebites-
non-venomous
– only 50% of bites from
venomous snakes
envenomate the patient
( So only 15% of all
snake bites
envenomate the
patient)
33. Tight (arterial)
Tourniquets
• Severe pain
• Risk of ischemia, necrosis & loss of
limb
• Increased risk of massive neurotoxic
blockade when tourniquet is released
• Hypotension
• False sense of security – delay to
reach the hospital
34. Incising the wound
• Do not cut into the flesh around the fang marks.
• Muscles, nerves, and
blood vessels may all
be in the area and you
can damage them,
sometimes permanently
• Increased risk of bleeding –
Incoagulable blood
• Increased risk of infection
Unless you really know what you are doing
you may do more damage than the snake did
35. Oral Suction
• Sucking venom by mouth is unlikely to be of any benefit, risks
venom getting into your bloodstream via an open sore
• More likely to be a source of infection for the wound
36. Washing
• The bite site should not be washed so that the area can be
swabbed for venom detection.
• Act of washing accelerates lymphatic flow
37. First aid “Do’s”• Reassure
• Lay flat on the ground
• Immobilize the bitten
limb with splint or
sling
• Get to Hospital fast
• Tell the doctor about
signs such as bleeding,
shock or drooping
eyelids that develop
on way to hospital
• Do it R. I. G. H. T
• Remove shoes, rings,
watches, jewelry & tight
clothing's from the
bitten part of the body
40. Diagnosis
• Diagnosis is crucial in effective
management of snake bites
• “Is this a snake bite or some other
condition?”
• If it’s a snake bite;
– What type of snake was responsible
– Is there significant envenoming
present?
– To what extent?
41. Species diagnosis
• Dead snake
• Circumstances
• ‘Syndrome approach’ – clinical symptoms
• Antigen detection by ELISA technique
42. Diagnosis cont….
HISTORY :
• Time and place of definite or possible exposure to a snake.
• Description of a snake, if seen (colour, size).
• Number of times bitten (multiple bites are usually more
severe).
• Was the bite through clothing, which might make the bite less
effective
43. Patient presents with a Hx of snake bite BUT no dead snake and
little / no description of the snake
Acute Renal
Failure
YES
Early
blistering /
necrosis
NO
Cobra bite Russell’s Viper
bite
Marked local
swelling
Neurotoxic signs
YES Non clotting blood /
spontaneous systemic
bleeding
YES
Neurotoxic signs
NO
Bitten in
sea
Krait
bite
Sea Snake
bite
Bitten on land,
sleeping on
floor of house
YES
Hump
Nosed Viper
bite
YES
Saw Scaled
Viper bite
NO
Acute Renal
Failure
YES
Non clotting blood /
spontaneous systemic
bleeding
YES
44. Diagnosis cont….
LABORATORY TESTS
• Twenty-minute whole blood clotting test (20WBCT) is
considered as reliable test of coagulation which can be carried out
by bedside and is considered to be superior to ‘capillary tube’
method for establishing clotting capability in snake bite.
• Extended coagulation studies; prothrombin time/international
normalised ratio (PT/INR), activated partial thromboplastin time
(apt), fibrinogen level, cross linked or d-dimer degradation
products of fibrin/ fibrinogen degradation products (XDP/FDP).
ii) Complete blood picture; especially platelet and absolute
lymphocyte counts.
iii) Electrolytes, urea, creatinine.
iv) Creatinine phosphokinase
v) Where appropriate, arterial blood gas estimation.
vi) Examination of peripheral blood smear
46. Cont…..
• Anti-snake venom (ASV) is the mainstay of treatment. In
India, polyvalent ASV, i.e. effective against all the four
common species; Russell’s viper, common cobra, common
Krait and saw-scaled viper and no monovalent ASVs are
available
47. Cont…..
• Anti-snake Venom Administration
1. Anti-snake venom should be administered only when
there are definite signs of envenomation, i.e.
coagulopathy or neurotoxicity.
2. Only unbound, free flowing venom in bloodstream or
tissue fluid, can be neutralized by it.
3. It carries the risk of anaphylactic reaction and doctors
should be prepared to handle such reactions.
48. Cont…..
• Prophylaxis for Anti-snake Venom Reactions
There are no systematic trials of sufficient power to show that
prophylactic regimes are effective in preventing ASV
reactions.
Two regimens are normally recommended, i.e. hydrocortisone
(100 mg) + antihistamine or 0.25–0.3 mg adrenaline
subcutaneously
49. Cont…..
Mild envenomation (systemic
symptoms manifest > 3 hours after
bite) neurotoxic/hemotoxic 8–10
Vials
Severe envenomation (systemic
symptoms manifest < 3 hours after
bite) neurotoxic or hemotoxic 8
Vials
Each vial is 10 ml of reconstituted
ASV. Children should receive the
same ASV dosage as adults.
Initial Dose
50. Cont…..
• Further Doses
It will depend on the response to the initial dose. ASV
should be administered either as intravenous infusion (5–
10 mL/kg body weight) or as slow intravenous (IV)
injection i.e. 2 mL/min).
ASV should be administered over 1 hour at constant
speed and patient should be closely monitored for 2
hours.
51. Cont…..
Repeat Doses of Anti-snake Venom
After initial ASV dose, no
additional ASV should be given
until the next clotting test at 6
hours
After initial ASV dose, no
additional ASV should be given
until the next clotting test at 6
hours
repeat dose of 5–10 vials of ASV,
i.e. 1/2 1 full dose, should continue‒
6 hourly till coagulation is restored
or species is identified against
which polyvalent ASV is
ineffective.
repeat dose of 5–10 vials of ASV,
i.e. 1/2 1 full dose, should continue‒
6 hourly till coagulation is restored
or species is identified against
which polyvalent ASV is
ineffective.
If WBCT more than 20 minutesHemotoxic bite
52. Cont…..
Repeat Doses of Anti-snake Venom
After 1–2 hours of initial
dose, patient should be
reassessed and if symptoms
have worsened or have not
improved, a second dose of
ASV should be given.. and
should have if required.
After 1–2 hours of initial
dose, patient should be
reassessed and if symptoms
have worsened or have not
improved, a second dose of
ASV should be given.. and
should have if required.
This dose should be the same
as the initial dose, i.e. 10
vials and then discontinued
This dose should be the same
as the initial dose, i.e. 10
vials and then discontinued
Once the patient develops
respiratory failure, has
received 20 vials, ASV
therapy should be
discontinued assuming that all
the circulating venom is
neutralized
Once the patient develops
respiratory failure, has
received 20 vials, ASV
therapy should be
discontinued assuming that all
the circulating venom is
neutralized
assisted ventilationassisted ventilation
Neurotoxic
53. Cont…..
Neostigmine is an
anticholinesterase,
which is particularly
effective in
postsynaptic
neurotoxins such as
those of cobra and is
not useful against
presynaptic neurotoxin
i.e. common Krait and
the Russell’s viper.
Neostigmine is an
anticholinesterase,
which is particularly
effective in
postsynaptic
neurotoxins such as
those of cobra and is
not useful against
presynaptic neurotoxin
i.e. common Krait and
the Russell’s viper.
Neostigmine test should be
performed by administering 0.5–2
mg IV and if neurological
improvement occurs, it should be
continued 1/2 hourly over next 8
hours with atropin.
Neostigmine test should be
performed by administering 0.5–2
mg IV and if neurological
improvement occurs, it should be
continued 1/2 hourly over next 8
hours with atropin.
Neostigmine