snake bite managment

1. Dr. ANIL KUMAR G
Moderator. Dr. A. K. Chaurasia (MD)

2.  In India, more than 200 species of snakes but
only 52 are poisonous.
 Saw-scaled viper (Echis carinatus)
 Russell’s viper (Daboia russelii)
 Common krait (Bungarus caeruleus)
 Indian cobra (Naja naja)
1 2 3 4
Majority of bites
Nearly 70-80%
Hemotoxin
Vasculotoxin
Neurotoxic

5.  Increasing local pain (burning, bursting,
throbbing) at the site of the bite
 Local swelling that gradually extends
proximally up the bitten limb and tender
painful enlargement of the Regional Lymph
nodes.
 However, bites by kraits and sea snakes may be
virtually painless.

6.  Local pain
 Local bleeding
 Bruising
 Lymphangitis
 LN Enlargement
 Blistering
 Local infection & Abscess
formation
 Necrosis
Fang marks

7. General
 Nausea
 Vomiting
 Malaise
 Abdominal pain
 Weakness
 Drowsiness
 Prostration

8.  Visual disturbances
 Dizziness
 Faintness
 Collapse
 Shock
 Hypotension
 Cardiac arrhythmias
 Pulmonary oedema
 Conjunctival oedema

9.  Bleeding from recent wounds (including fang
marks,venepunctures etc) and from old partly-
healed wounds
 Spontaneous systemic bleeding

10.  Drowsiness
 Paraesthesiae
 Abnormal taste and smell
 “Heavy” eyelids,Ptosis,Ext. ophthalmoplegia
 Facial paralysis
 Aphonia
 Difficulty in swallowing secretion
 Respiratory and generalised flaccid paralysis

11. Ptosis
RS
involvement
Ophthalmoplegia

12.  Generalised pain, stiffness and tenderness of
muscles, trismus, myoglobinuria,
hyperkalemia, cardiac arrest, acute renal failure
 Occur with sea snakes, Russell’s viper

13.  Loin (lower back) pain
 Haematuria
 Haemoglobinuria
 Myoglobinuria
 Oliguria / Anuria
 Symptoms and signs of Uraemia

14. Acute pituitary/adrenal insuff.
with Russell’s viper
Acute phase: Shock, Hypoglycaemia
Chronic phase (mnths to yrs after): Weakness,
Loss of 2ry sexual hair, Amenorrhoea,
Testicular atrophy, Hypothyroidism etc

16. Local envenoming (swelling etc) with
bleeding/clotting disturbances
 Viperidae (all species)

17.  Local envenoming with bleeding/clotting
disturbances, shock or renal failure
Russell’s viper +/-saw-scaled viper
 With conjunctival edema (chemosis) and acute
pituitary insufficiency
Russell’s viper
 With Ptosis , External Ophthalmoplegia, facial
paralysis etc and dark brown urine
Russell’s viper (Sri Lanka & South India)

18. Syndrome 3
 Local envenoming (swelling etc) with paralysis
Cobra or King Cobra
Syndrome 4
 Paralysis with minimal or no local envenoming
Krait,Sea snake

19. Paralysis with dark brown urine and renal failure:
 With bleeding/clotting disturbance)
Russell’s viper (Sri Lanka & South India)
 No bleeding/clotting disturbances
Sea snake

20.  The range of activities of a particular venom is
wide.
 Considerable overlap of clinical features caused
by venoms of different species of snake
 “Syndromic Approach” may still be useful,
especially when the snake has not been
identified and only monospecific antivenoms
are available.

21. Summary of Manifestations
LOCAL NEURO BLEED MISC.
COBRA + ++ Nil Shock +/-
KRAIT Nil + Nil Pupils –
dilated,
fixed
VIPER +++ + / - ++ Renal
failure,
Shock

22.  First aid treatment
 Transport to hospital
 Rapid clinical assessment and resuscitation
 Detailed clinical assessment and species
diagnosis
 Investigations/laboratory tests

23.  Antivenom treatment
 Observation of the response to antivenom:
decision about the need for further dose(s) of
antivenom
 Supportive/ancillary treatment
 Treatment of the bitten part
 Rehabilitation
 Treatment of chronic complications

24.  To retard systemic absorption of venom
 Preserve life and prevent complications before
receiving medical care
 Control distressing early symptoms
 Arrange the transport to a place where they can
receive medical care

25.  Reassure the victim who may be very anxious
 Immobilise the bitten limb with a splint or sling
(any movement or muscular contraction
increases absorption of venom into the
bloodstream and lymphatics)
 Consider Pressure-Immobilisation for some
elapid bites

26.  Pressure immobilisation is recommended for
bites by neurotoxic elapid snakes, including sea
snakes but should not be used for viper bites
because of the danger of increasing the local
effects of the necrotic venom.

27.  Quickly, but as safely and comfortably as
possible
 Any movement, especially of the bitten limb,
must be reduced to an absolute minimum to
avoid increasing the systemic absorption of
venom
 Any muscular contraction will increase this
spread of venom from the site of the bite.

28.  Oxygen administration
 IV access.
 ABC
 The level of consciousness must be assessed.
 CPR may be needed

29.  Snake identified as a very dangerous one.
Rapid early extension of local swelling.
 Early tender enlargement of local LN.

30.  Early systemic symptoms (hypotension, shock),
nausea, vomiting, diarrhoea, severe headache,
“heaviness” of the eyelids, inappropriate
drowsiness or early ptosis/ophthalmoplegia
 Early spontaneous systemic bleeding
 Passage of dark brown urine
 Patients who become defibrinogenated or
thrombocytopenic.

31.  20 minute whole blood clotting test (20WBCT)
 Place a few mls 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 and runs out, the patient
has hypofibrinogenaemia as a result of venom-
induced consumption coagulopathy.

32.  Platelet count : may be decreased – viper
 WBC cell count : Early neutrophil leucocytosis in
systemic envenoming from any species.
 Blood film : Fragmented RBC(“helmet cell”,
schistocytes) are seen in microangiopathic
haemolysis.
 Plasma/serum : may be pink or brownish if there
is gross haemoglobinaemia or myoglobinaemia.

33.  Aminotransferases, creatine kinase, aldolase
elevated if there is severe local damage or,
particularly generalised muscle damage.
 Bilirubin is elevated following massive
extravasation of blood.
 Creatinine, urea or blood urea nitrogen levels
are raised in the renal failure.

34.  Early hyperkalaemia may be seen following
extensive rhabdomyolysis in sea snake bites.
Bicarbonate will be low in metabolic acidosis
(eg renal failure).
 Arterial blood gases and pH may show
evidence of respiratory failure (neurotoxic
envenoming) and acidaemia (respiratory or
metabolic acidosis).

35.  Arterial puncture is contraindicated in patients
with bleeding disorder.
 Arterial oxygen desaturation can be assessed
non-invasively in patients with respiratory
failure or shock using a finger oximeter.

36.  Dipsticks for blood/ Hb./myoglobin
 Microscopy for erythrocytes in the urine
 Red cell casts indicate glomerular bleeding
 Massive proteinuria is an early sign of the
generalised increase in capillary permeability in
Russell’s viper envenoming.

37.  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


38.  Haffkine, Kasauli, and Serum Institute of India
produce “polyvalent anti-snake venom serum”
 It is raised in horses using the venoms of the
“Big four” in India (Indian Cobra,Indian Krait,
Russell’s viper,Saw-scaled viper).
 Not included are venoms of King Cobra , Sea
snakes and Pitvipers and coral snakes.

39. Systemic Envenoming
 Haemostatic abnormalities:
 Spontaneous systemic bleeding
 Coagulopathy
 Thrombocytopenia
 Neurotoxic signs:
 Ptosis, external ophthalmoplegia, paralysis…

40.  Cardiovascular abnormalities:
 Hypotension, shock, cardiac arrhythmia,
abnormal ECG
 Acute renal failure:
 Oliguria/anuria, rising blood creatinine/urea
 Haemoglobinuria/myoglobinuria:
 dark brown urine, evidence of intravascular
haemolysis or generalised rhabdomyolysis
(muscle aches and pains)

41.  Supporting laboratory evidence of systemic
envenoming
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)

42.  Rapid extension of swelling (for example
beyond the wrist or ankle within a few hours of
bites on the hands or feet)
 Development of an enlarged tender lymph
node draining the bitten limb
 Antivenom treatment is recommended if and
when a patient with proven or suspected snake
develops one or more of the signs

43.  Skin and conjunctival “hypersensitivity” tests
may reveal IgE mediated Type I
hypersensitivity to horse or sheep proteins but
do not predict the large majority of early
(anaphylactic) or late (serum sickness type)
antivenom reactions
 Since they may delay treatment and can in
themselves be sensitizing, these tests should
not be used.

44.  There is no absolute contraindication to
antivenom treatment
 Patients who have reacted to horse (equine) or
sheep (ovine) serum in the past and those with
a strong history of atopic diseases (especially
severe asthma) should be given antivenom
only if they have signs of systemic
envenoming.

45.  No drug proved effective in clinical trials
 High risk patients may be pre-treated
empirically with s/c adrenaline, i/v
antihistamines (both anti-H1 anti- H2) and
corticosteroid.
 In asthmatic patients, prophylactic use of an
inhaled adrenergic Beta2 agonist may prevent
bronchospasm.

46.  Should be given only if its stated range of
specificity includes the species responsible for the
bite.
 Liquid antivenoms that have become opaque
should not be used.
 Provided that antivenom has been properly
stored, it can be expected to retain useful activity
for many months after the stated “expiry date”.

47.  Ideal treatment is monovalent antivenom, as
this involves administration of a lower dose of
antivenom protein than with a polyvalent
antivenoms.
 Polyspecific antivenoms can be as effective as
monospecific ones, but a larger dose of
antivenom protein must be administered to
neutralise a particular venom.

48.  Adrenaline should always be in readiness before
antivenom is administered.
 Antivenom should be given by the intravenous
route whenever possible.
 Freeze-dried (lyophilised) antivenoms are
reconstituted, usually with 10 ml of sterile water
for injection per ampoule. The freeze-dried
protein may be difficult to dissolve.

49. Initial
AV dose
LabsSystemic
effects
Local
effects
Grade
0 - 3
NoneNormalNoneNone
Dry 0
NoneNormalNoneConfined to
bite areaMild 1
5-10
As needed
Mild changes:
Thrombocytopenia
Hypofibrinogenemia
High CK
Mild: vomiting
Metabolic taste
fasciculations
Extends beyond
immediate bite
area but not all
part
Moderate
2
15 or
more as
needed
Marked:
Rhabdomyolysis
Coagulopathies
Severe:
Shock, bleeding
CNS changes
Lethargy, RD ,
ARF
Involves
entire partSevere
3
Grades of Envenomation and
Antivenom Treatment Guidelines

50.  Antivenom is given by slow IV inj. (<2 ml/min)
 This method has the advantage that the
doctor/nurse/dispenser giving the antivenom
must remain with the patient during the time
when some early reactions may develop

51.  Reconstituted freeze-dried or neat liquid
antivenom is diluted in approximately 5-
10 ml of isotonic fluid per kg body
weight (ie 250-500 ml of isotonic saline or
5% D in the case of an adult patient) and
is infused at a constant rate over a period
of about one hour.

52.  Local administration of antivenom at the site of
the bite is not recommended!
 Although this route may seem rational, it
should not be used as it is extremely painful
may increase intracompartmental pressure and
has not been shown to be effective.
 Antivenom must never be given by the
intramuscular route if it could be given
intravenously.

53.  Early anaphylactic reactions: usually within 10-
180 minutes of starting antivenom
 the patient begins to itch (often over the scalp)
and develops urticaria, dry cough,fever, nausea,
vomiting, abdominal colic, diarrhoea and
tachycardia

54.  develop 1 - 12 (mean 7) days after treatment.
 Clinical features include fever, nausea,
vomiting, diarrhoea, itching, recurrent
urticaria, arthralgia, myalgia,
lymphadenopathy, periarticular swellings,
mononeuritis multiplex.

55. At the earliest sign of a reaction:
 Antivenom administration must be
temporarily suspended
 Epinephrine (adrenaline) (0.1%
solution, 1 in 1,000, 1 mg/ml) is
effective

56.  Doses: Chlorpheniramine: adults 2 mg six
hourly, children 0.25 mg/kg in divided doses
In those who fail to respond
 Prednisolone: adults 5 mg six hourly, children
0.7 mg/kg/day in divided doses
 5-7 days

57.  Nausea, headache and generalised aches and
pains may disappear very quickly.
 Spontaneous systemic bleeding (eg from the
gums) usually stops within 15-30 minutes.
 In shocked patients, blood pressure may
increase within the first 30-60 minutes and
arrhythmias such as sinus bradycardia may
resolve.

58.  Blood coagulability (as measured by
20WBCT) is usually restored in 3-9 hours.
Bleeding from new and partly healed
wounds usually stops much sooner than
this.
 Active haemolysis and rhabdomyolysis
may cease within a few hours and the
urine returns to its normal colour.

59. Signs of systemic envenoming may recur in
24-48 hrs
This is attributable to:
(1) continuing absorption of venom from
the “depot” at the site of the bite,
(2) a redistribution of venom from the
tissues into the vascular space, as the result
of antivenom treatment.

60. Persistence or recurrence of
blood incoagulability after 6 hr
Deteriorating neurotoxic or
cardiovascular signs after 1-2
hr.

61.  If the blood remains incoagulable (as
measured by 20WBCT) six hours after
the initial dose of antivenom, the same
dose should be repeated.
 This is based on the observation that, if a
large dose of antivenom given initially,
the time taken for the liver to restore
coagulable levels of fibrinogen and other
clotting factors is 3-9 hours.

62.  In patients who continue to bleed briskly,
the dose of antivenom should be
repeated within 1-2 hours.
 In case of deteriorating neurotoxicity or
cardiovascular signs, the initial dose of
antivenom should be repeated after 1-2
hours, and full supportive treatment
must be considered.

63.  When antivenom is unavailable
 Bite by a species against whose venom
there is no available specific antivenom
(for example coral snakes - genera, sea
snakes)

64. Assisted ventilation has proved
effective
 Anticholinesterases should always
be tried

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

66.  Neostigmine methylsulphate, 0.5-2.5 mg every
1-3 hours up to 10 mg/24 hours maximum for
adults or 0.01-0.04 mg/kg every 2-4 hours for
children by intramuscular, intravenous or
subcutaneous
 Together with atropine to block muscuranic
side effects.
 maintained on atropine 0.6 mg twice each day,
neostigmine 15 mg four times each day or
pyridostigmine 60 mg four times each day.

67.  If patient has respiratory distress or bulbar
paralysis-intubate and ventilate.
 If delayed can cause aspiration or hypoxia and
cardiac arrest.
 Even if the facility for MV is not available
Ambuing can save the day.
 This helps even during transport.
 MV is not complicated is like ventilating a
patient with curare over-dosage

68.  Strict bed rest to avoid even minor
trauma
 transfusion of clotting factors and
platelets; ideally, fresh frozen plasma
with platelet concentrates or, if these are
not available, fresh whole blood.
 Intramuscular injections should be
avoided.

69.  Hypovolaemia should be corrected with
colloid/crystalloids, controlled by
observation of the central venous pressure
 Ancillary pressor drugs (dopamine or
epinephrine-adrenaline)
 Hypotension associated with bradycardia
should be treated with atropine.

70.  Renal failure: conservative treatment
or dialysis
 Myoglobinuria or haemoglobinuria:
correct hypovolaemia and acidosis
and consider a single infusion of
mannitol

71.  Keep slightly elevated, to encourage
reabsorption of oedema fluid
 Bullae may be large and tense but they should
be aspirated only if they seem likely to rupture.

72.  Prophylactic course of penicillin (or
erythromycin for penicillin-hypersensitive
patients)and a single dose of gentamicin or a
course of chloramphenicol
 Booster dose of tetanus toxoid is
recommended.

73.  Pregnant patient is treated the same manner as
the nonpregnant patient. Spontaneous
abortion, bleeding, fetal death & malformations
are common.
 Lactating mothers can continue lactating.
 Generally speaking, the severity of the mother's
clinical course seems to be the best indicator of
the fetal survival.

74.  Anker RL, StraffonWG, Loiselle DS, Anker KM. Retarding the uptake
of “mock venom” in humans: comparison of three first-aid treatments
.med J Aust.1982 mar 6;1(5):212-4.
 Ariaratnam Ca et al. Distinctive epidemiologic and clinical features of
common krait (Bungarus caeruleus) bites in srilanka. Am J Trop Med
Hyg.2008; 79: 458-62.
 Banreji RN , Sahin AL , Chacko KA. Neostigmine in the treatment of
Elapidae bites. J Assoc physicians India.1972;20: 503-9
 Bon C, Goyffon M. Envenomings and their treatments. Lyon: Editions
Fondation Marcel Merieux, 1996.
 Caron EJ et al. Apparent marked reduction in early antivenom
reactions compared to historical controls ; was it prophylaxis or
method of administration Toxicon.2009.54: 779-83.
 Chugh KS. Snake –bite –induced acute renal failure in india. Kidney
International. 1989;35: 891-907.
 Currie BJ, Canale E. snake-bite-induced acute renal failure in india.
Kidney International. 1989; 35:: 891-907.

75.  Currie BJ, Canale , Isbister GK. Effectiveness of pressure-
immobilization first aid for snakebites requires further
study. Emerg Med Australas. 2008 Jun ; 20(3): 267-70.
 Dassanayake AS et ai. Prevention of acute adverse reactions
to snake antivenom serum in snakebite. Ceylon Med J. 2002;
47: 48-9.
 De silva, H.A et al. Preventiion of acute adverse reactions to
snake antivenom after snakebite: multicenter, randomized,
controlled clinical trial. In: Presented at the Global Issues in
clinical toxinology 2008 Conference, 23-28 November 2008,
University of, Melbourne, Australia.
 Lallo DG et al. Snake bites by the papuan taipan (oxyuranus
scutellatus canni). Paralysis, hemostatic and
electrocardiographic abnormalities, and effects of
antivenom. American J trop med hyg. 1995 ; 52: 525-31.

76. THANK YOU.

77. Five Key Focus Areas
• Prevention, Community Education & Pre-hospital Care
– Low cost per capita interventions
• Surveillance & Reporting, Clinical & Lab. Research
– Informing debate & resource allocation and deploying
technology
• Education & Training, Improved Medical Management
– Getting maximum value from therapeutic care
• Immunotherapeutics
– Establishing simple, cheap methods of immunodiagnosis
– Optimising antivenom production, ensuring safety &
efficacy
• Rehabilitation from Disability
– Repairing shattered lives, advocating basic human
rights, restoring opportunity, human dignity and
independence

80.  Avoid any interference with the
bite wound as this may
introduce infection, increase
absorption of the venom and
increase local bleeding

81. Krait- Pre-synaptic action
Beta-bungarotoxin- Phospholipases A2
1) Inhibiting the release of
acetylcholine from the presynaptic
membrane
2) Presynaptic nerve terminals
exhibited signs of irreversible physical
damage and are devoid of synaptic
vesicles
3) Antivenoms &
anticholinesterases
have no effect
Paralysis lasts several weeks and frequently requires prolonged MV.
Recovery is dependent upon regeneration of the terminal axon.

82.  alpha-neurotoxins
“Curare-mimetic toxins’’
Bind specifically to acetylcholine
receptors, preventing the interaction
between acetylcholine and receptors
on postsynaptic membrane.
Prevents the opening of the
sodium channel associated with the
acetylcholine 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

83.  Neostigmine methylsulphate, 0.5-2.5 mg every
1-3 hours up to 10 mg/24 hours maximum for
adults or 0.01-0.04 mg/kg every 2-4 hours for
children by intramuscular, intravenous or
subcutaneous
 Together with atropine to block muscuranic
side effects.
 maintained on atropine 0.6 mg twice each day,
neostigmine 15 mg four times each day or
pyridostigmine 60 mg four times each day.

84. THANK YOU.