Toxicology symposia Review Article

Snake bite poisoning

H. S. Bawaskar, P. H. Bawaskar
Abstract
Envenoming by venomous snake evokes a life-threatening response. Rapid diagnosis of acute hemorrhagic
disorders, neurorespiratory, renal, and hemodynamic failure subsequent to snake bite and their rapid interventions
saves life. Early administration of the appropriate dose of potent snake antivenom along with adjuvant treatment,
proper care of the wound, correcting electrolyte imbalance, tissue oxygenation, and maintenance of adequate
nutrition may help rapid recovery.

Keywords: Antisnake-venom, cobra, krait, snake bite, viper

Introduction Snake-venom antigen detection Kits should be made

Snake envenoming is a disease of poverty.[1]
Envenoming by poisonous animals (snakes, scorpions,
wasps, ants, and spiders) is an occupational hazard
often faced by farmers, farm laborers, hunters, and
shepherds of tropical and subtropical countries.
Poisoning by venomous snake bite is a common acute
life-threatening, time-limiting medical emergency. In
the rural area, snake bite poisoning is a leading cause
of death of young earning member of the family. More
than 2,000,000 snake bites are reported in the country,
and it is estimated that >50000 people die of snakebite
each year.[2,3] Newly posted or inexperienced doctors
and inadequate facilities at primary health center
(PHC), ignorance of conventional treatment of snake
bite by doctors; further delays appropriate treatment
of victims and contribute to increasing morbidity
and mortality.[4] It is the surprise to note that snake
bite poisoning is seldom mentioned as a priority for
health research in the developing country like India.
Access this article online
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DOI:
10.4103/0971-9903.151717
available. Mono-specific antivenom producers in India
should be encouraged to prepare antivenom from
venom obtained from snakes caught from relevant
areas of the country.[5,6]
Snakes
Of more than 3000 known species of snakes, only
about 300 are venomous and in India there are about
216 identifiable species of snakes, of which 52
are known to be poisonous. The major families of
poisonous snakes in India are Elapid which includes
common cobra (Naja naja), king cobra and common
krait (Bungarus caerulus, Banded krait, Sind krait),
viperidae (Russells viper), Echis carinatus (saw-
scaled or carpet viper), and pit viper and hydrophiidae
(sea snakes). Recently, venomous viper called hope
nosed viper is reported from Cochin region. During
monsoon season, fatal snake bites are common to
feature in local newspaper].[7] Table 1 highlights the
risk factors predisposing to snake bites. Table 2 gives
the characteristics of various snakes.
Biochemistry, Physiological, and
Pathology of Envenoming
Snakes are cold-blooded, highly specialized animals.
A pair of salivary glands secretes a powerful

Bawaskar Hospital and Clinical Research Center, Mahad, Raigad, Maharashtra, India

Address for correspondence:

Dr. H. S. Bawaskar, Bawaskar Hospital and Clinical Research Center, Mahad, Raigad, Maharashtra, India.
E-mail: himmatbawaskar@rediffmail.com

March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
6 Bawaskar and Bawaskar: Snake bite poisoning

Table 1: Risk factors involved in accidental snake envenoming

Conditions
Barefoot walking in the dark, sleeping on the floor, use of open toilets
Handling of rubbles blindly over attic, firewood, cattle shades, near
dwellings mud house with multiple groves, wattle, and daub houses
Chula (furnace made of mud use for cooking food at village)
Catching snake/handling snake
Predisposed individuals
All but mostly farmers, cattle grazers, school children
Housewives, laborers, young children
Housewives, housekeepers/cleaners
The ash remains in the Chula is warmer in winter and cold in summer a pleasant
environment to attract the snake-like krait
Untrained, unskilled snake catchers without proper instruments and requirement

Table 2: Characteristics of different snakes [Figure 1]

Species Characteristics Factors predisposing to bite
Cobras Cobras are fast, graceful poisonous snakes that have a hood and raise the front part Cobra bite tends to occur during daytime
of their body off the ground in a distinctive way. The Indian cobra is favored by and early darkness while going to open the
snake charmers and measure 1.2-1.7 m (4-5 feet). toilet, while playing near the loose stones
or basement of the house, searching ball in
bushes, putting sticks in grooves and improper,
careless handling while rescuing the cobra.
Krait Krait is 1-4 feet long with enlarged hexagonal vertebral scales, uniform white or Most bite occurs during cooler months of June
red belly and narrow white crossbars on the back, more or less distinctly in pairs; to December, when snakes may, during the
the crossbars are typically absent near the head and neck region. The common krait course of hunting activity, linger on a persons
resides in the vicinity of human habitation, near the wattle and daub, mud, and bedding to take advantage of the warmth
small hut dwelling. Krait is nocturnal, terrestrial snake that enters human dwellings therein.
in search of prey such as rats, mice, and lizards. It eats even the small snakes Banded krait though is much active during the
(cannibalism). The common krait is regarded as the most dangerous species of night, but more reluctant to bite than common
venomous snake in Indian subcontinent krait.
Banded krait its head is slightly broader than the neck, tail is short and round tip.
Body is covered with equally spaced wide, yellow/pale brown/white and black
bands. It lives in termite mounds and rodent burrow close to the waterBanded
krait is seen West Bengal, Assam, Bihar, Orissa Madhya Pradesh, Andhra Pradesh,
Chandrapur district of Maharashtra
Sea snakes Sea snake bite cases are reported from the
coastal region. Fishermen accidentally handle
the sea snake result in envenoming
Russells viper or It is 3-5 feet long snake. Head is covered with small scales and without shields. While protecting the paddy, wheat by
Daboia or viper Body is massive, cylindrical, narrowing at both ends. Head is flat, triangular with containing the rodent (rats) population, it kills
Russell siamensis a short snout, large gold-flecked eyes with a vertical pupil and large open nostrils. many farmers unlucky enough to tread on it
Round belly with constricted neck. Typical rows of oval (Rudraksha) arranged in during harvest.
two rows is characteristic of Russells viper. Its natural prey includes mice, rats, Bite occurs while reaping or handling rice or
frogs, lizards, snakes and birds. Young are cannibalistic. Female produces 20-60 Jawar or sugar cane husk bundles. At times,
youngs usually around June or July. Length of fangs in adult snake is 16 mm long snake is trodden while walking in growing
and curved. The amount of venom injected at the time of the bite is 63+ - 7 mg. grass. Snake catcher often gets snake bite
It inhabits 10 South Asian countries. In Pakistan, India, Sri Lanka, Bangladesh, because of careless handling. Long sharp curve
Burma and Thailand, it ranks amongst the most important causes of snakebite fangs can bite through a simple cloth bag in
mortality. which temporarily caught snake is kept.
Echis cariniatus or It is of size 1-3 feet long. Head of this snake is sub ovate with short rounded Farmers, hunters, laborers, and person walking
saw scaled viper or snout. Body is cylindrical, short and snout. Body is covered with rough, serrated barefoot at peddler or in the jungle and rocky
carpet viper flank scales, neck is distinctly constricted. Its color is pale brown, tawny with areas often bitten by this snake
dark brown. A cruciform or trident or arrow type or just like the bird footprint
shaped mark seen on the head. It flourishes in hot and humid climate all over the
coastal region of India. It is an alert, active, diurnal in habit and capable of quick
movement when necessary. It hibernates in the winter. It often climbs onto shrubs
and other low vegetation. Readiness with which it bites on the smallest provocation
with extremely rapid strike makes it is one of the dangerous snakes. It forms a
double coil in the form of the figure of 8 with its head in the center a striking
position. The coils keep moving against each other, and serrated keels on the flank
scales produce a hissing noise by friction. It is viviparous producing 3-15 young at
a time. It injects 0.0046 g venom at the time of the bite
Green pit viper Pit viper victims report during the monsoon
and bamboo pit season.
(Trimeresurus)

multipurpose enzyme fluid (venom) that flow at the months with high morbidity and fatality. Snake is cold
time of envenoming through fine channeled or grooved blooded animal. Darker the snake, it secretes more
teeth called fangs. Venom secretion in all venomous venom as compared to a light colored. Because of the
snakes appears to vary in seasons; more in warmer rise in body temperature of dark skin (poor conductor

Journal of Mahatma Gandhi Institute of Medical Sciences March 2015 | Vol 20 | Issue 1
Bawaskar and Bawaskar: Snake bite poisoning
a b
c d
e accelerated by threat of death, running and hence the
f g
Figure 1: Different types of snakes, (a) and (b) Cobra, (c) and (d) krait, (e)
Russells Viper, (f) and (g) is saw scaled viper and its fangs
of heat) snake, the venom is in more fluid state and
injected rapidly with high speed and maximum
quantity in a short time during envenoming. As oppose
to light colored skin because of low body temperature,
the venom is thick and hence less amount is injected at
the time of envenoming.[8]
It is quite clear that snake venom is not a substance
evolved to attack man or any big vertebrates. Snake can
bite and continue to secrete venom a number of times
in succession. Most snakes inject 10% of the available
venom in a single strike except the Russells viper which
injects 75% of stored venom in one bite due to big long
sharp curved fangs.[7] At times snake only bite without
envenoming called as defence bite or dry bite ;while the
bite with envenoming is called as the professional bite.
Venom is a cocktail of 20 or more components
including proteins, enzymes, nonenzymatic
polypeptide toxins, nontoxic nerve growth factors,
March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
7
hyaluronidase, metalase, lipids, free amino acids,
nucleotides, carbohydrates, biogenic amines, and
various activators and in activators of physiological
processes.[6] Krait and cobra venom contains
acetylcholine (Ach) esterase, phospholipase B, and
glycerophosphatase. Phospholipase A2 is found in
the majority of venom and is extensively studied.
It destroys mitochondria, red blood cells (RBCs),
leukocytes, platelets, peripheral nerve endings,
skeletal muscles, vascular endothelium, presynaptic
neurotoxicity, opiate-like sedative effects, and auto
pharmacological release of histamine (anaphylaxis).
Hyaluronidase promotes the spread of venom through
the tissue. Proteolytic enzymes are responsible for
local changes in permeability leading to edema,
blistering, bruising, and local necrosis.[6,7]
Cobra venom
Cobra venom is of smaller molecular size and rapidly
absorbed into circulation. Absorption is further
liberated catecholamine and running due to fear can
kill the victim within 8 min. Cobras unlike the krait
deposit its venom deeply. This in combination with
hyaluronidase allows spreading of the venom to occur
rapidly and symptoms to arise abruptly. Interestingly,
this rapidity of onset of symptoms prompts the rural
victim in India to seek care quickly after cobra
bite.[9] Severe, irreparable local tissue is lost at the
bite site of cobra envenoming due to myocytolysis.
Cobra venom is rich in postsynaptic neurotoxins
called alpha-bungarotoxin and cobratoxin. Cobra
venom binds especially to Ach receptors, prevents
the interaction between Ach and receptors on
postsynaptic membrane result in neuromuscular
blockade. Cardio- toxin content of cobra venom has
direct action on skeletal, cardiac, smooth muscles,
nerves and neuromuscular junction causes paralysis,
circulatory, respiratory failure, cardiac arrhythmias,
various heart block and cardiac arrest because
the venom releases calcium ions from the surface
membrane to the myocardium.
Common Indian krait (Bungarus caeruleus)
(Local names Kala gandait, kala taro, kandar,
manyar, chitti, kattu viriyan, valla pamboo)
Common Indian krait venom contains both presynaptic
beta bungarotoxin and alpha bungarotoxin. These
toxins initially release Ach at the nerve endings,
at neuromuscular junction and then damage it
subsequently preventing the release of Ach. Irrespective
of Krait, its venom is 10 times more lethal than cobra.
8 Bawaskar and Bawaskar: Snake bite poisoning
But unfortunately unlike as in cobra bite, the victim
reports too late due to delayed clinical manifestations.
Krait is nocturnal in habit. Its fangs are small size like
that of insulin needle. It injects the venom into skin
or skin deep. It accidentally bites a person sleeping on
floor bed.[8,10-12] Though venom is of small molecular
size it is absorbed slowly as skin has poor circulation
and reflexes are blunted during sleep.[11] Neuromuscular
blockade by the short chain neurotoxin (cobra toxin,
alpha bungarotoxin) is more readily reversible than
with a long chain toxin (beta bungarotoxin). Beta
bungarotoxin in the krait venom bears similarity to
botulinum toxin.[6,9,13] Preserved tendon reflexes in
botulism differentiates it from krait bite. Krait venom
has a great affinity towards presynaptic Ach receptors.
Thus, the tissue having high concentration of this
receptors are affected in the following order, such as
sphincter pupillae, levator palpebral superioris, neck
muscles, bulbar muscles, subsequently limbs and lastly
the diaphragm and intercostals muscles. Venom acts as
early as 30 min and till 18 h.[9] Envenoming by krait has
an early phase profound paralysis which lasts for 30 to
60 minutes, followed by deep paralysis phase which
lasts for 2 to3 days and then recovery phase ranging
from 2 to 3weeks.
Viper (Russel viper)
Viper venom interferes with blood clotting. Venoms
contain serine proteases, metalloproteinases, C-type
lectins, disintegrins, and phospholipases, and it exhibits
both anticoagulant and procoagulant effects on blood
clotting mechanism resulting in defibrination syndrome
or disseminated intravascular fibrino-coagulopathy.[14,15]
Russells venom is a rich source of enzymes that activates
factor X to convert prothrombin to thrombin in presence
of calcium factor V and platelets thus Russells venom
contains several different pro-coagulants which
activate different steps in the clotting cascade.[14-16] The
fibrinolytic activity of the viper venom is so fast that
sometimes within 30 min of the bite, the coagulation
factors are so depleted that blood does not clot.
Russells venom activates the clotting system of the
snakes natural prey with such speed that Macfarlane
a brilliant hematologist was left feeling it is almost
too clever to be true.[17] Haemorrhagins-1, 2and
metallo-endopeptidase causes acute rapid bleeding
in brain, lungs, kidney, heart, and gastrointestinal
tract.[16,18] It causes severe vasoconstriction followed
by vasodilatation of the microvessels. Endothelial gaps
due to disintegration of the endothelial cells within
intracellular edema, swollen mitochondria, dilated
Journal of Mahatma Gandhi Institute of Medical Sciences March 2015 | Vol 20 | Issue 1
endoplasmic reticulum, and separation of intracellular
junction of the endothelial cells. Local loss of basement
membrane of the vessels leads to capillary leaking
syndrome and a resistant shock [Table 3].[14-16,18]
Management of Snake Bite
First aid (to be given at the time when bite
occurs)
1. If one can locate the bite site, remove the surface
deposited venom by clean cloth or cotton.
2. Keep the bitten part below heart level.
3. Crepe bandage from the distal end of the bite site
with a pressure equal to that one can easily put and
remove the finger underneath the bandage.
4. One should not kill the time in search of the snake.
If the snake is found or killed take it to hospital, it
may help to doctor for diagnosis.
5. Victim should not be allowed to walk.
6. Do not incise at the site of the bite.
7. If the victim is found unconscious without
respiration, the relatives should start mouth to
mouth respiration and chest compressions.
First response at the healthcare facility
(primary health center, hospital etc.)
1. History site of the bite, activity at the time of the
bite, time of bite, visualization/recognition of the
snake.
2. Symptoms suggestive of neuromuscular palsy
(ptosis, respiratory difficulty, dysphagia, weakness
of limbs, etc.) should be specifically asked for.
3. Initial clinical signs should be noted in detail such
as heart rate, blood pressure, respiratory rate,
one min counting test, oxygen saturation, bulbar
palsy, muscle power, tendon reflexes, pooling of
saliva, broken neck sign. These signs to be closely
monitored every hour till clinical improvement.
Electrocardiogram should be recorded for
arrhythmias. Serum electrolytes and renal profile
should be done.
4. Give injection tetanus toxoid to all patients provided
blood is clotted in 20WBCT.
5. Intramuscular injection to be avoided in viper bite
envenoming may result in huge hematoma.
20 Minutes Whole Blood Clotting Time
Before the injection of anti-snake-venom (ASV) take
2-3 ml of patients blood in a new dry glass test tube
which is not irrigated by any detergents. Keep the tube
undisturbed for 20 minutes and then tip it off, if blood
Bawaskar and Bawaskar: Snake bite poisoning 9

Table 3: Signs and symptoms of different snakes

Snake Signs and symptoms
Cobra [Figure 2] Regional lymphadenopathy is often absent
Victim experiences severe pain at bite site having a fangs marks
Rapid progression of swelling
Skin at and around the bite site is ecchymosed. Subsequently developed tense blebs and massive damage of skin and subcutaneous
tissue due to myocytolysis result in huge nonhealing ulcers
Victim may die of cardiac lethal ventricular arrhythmias or cardiogenic shock due to massive myocardial infarction, due to a surge of
catecholamines because of the threat of death
Sinus bradycardia, A-V block and hypotension due to cardio-depressant action of venom
Sudden respiratory arrest without any other neurological manifestations can occur resulting in anoxic cardiac arrest. Rapid ptosis and
bulbar palsy accompanied with respiratory depression can occur
Rarely hematotoxic effects are seen
Blurring of vision and loss of accommodation is earliest most sign of neurological envenoming[4,11,19-21]
Common Indian Acute abdominal pain (due to cholecystokinin release),[8,9,22] vomiting, staring look, blurring of vision, gooseflesh, salivation,
krait hypertension, pulmonary edema (autonomic symptoms)
A syndrome of neuromuscular paralysis that falls into three distinct phases. The first phase is rapid onset phase leading profound
paralysis within 30-60 min. The second phase is a stable phase of deep paralysis lasting 2-3 days. The third phase is a recovery phase
2-3 weeks.[13] This explains the prolonged period of ventilators support and intensive care requirements essential for recovery[10-12]
Envenoming by different species of krait in addition can cause resistant neuroparalysis[23] hyponatremia[24] renal failure,[25]
hyperkalemia, myocytolysis, myocardial damage with lethal arrhythmias, pulmonary edema, hypertension.[26-28]
T wave inversion in electrocardiograph due to hypoxia, accompanied with vague chest discomfort due to respiratory muscle weakness
and dysphasia
Bradycardia, sweating, raised blood pressure, pulmonary edema, starring look, blurring of vision or at times photophobia
Ptosis, pulling of saliva, difficult to protrude the tongue beyond teeth margin, slurred or nasal twang speech, aphasia dysphagia,
dyspnea, external ophthalmoplegia, weakness of neck muscle, respiratory muscle and lastly the diaphragm
Quadriplegia with aphasia and dilated pupils locked in syndrome may be diagnosed as brain death. Patient can only communicate by flicker
of toes and fingers or pelvic girdle. Frontalis muscle has dual nerve supply may be spared in locked in syndrome, patient attempt to move
this muscle on command movement can be felt by putting palm over forehead confirm patient is conscious hence it is called pseudo-coma.
Venom induced paralysis of pupillary muscle causing nonreactive dilated pupils should not be taken as a sign of irreversible brain damage
Viper (Russells Acute renal failure due to viper bite is attributed to hypotension due to raised circulating bradykinin, hypovolemia due to blood
viper) [Figure 3] loss either by external bleed or accumulation in compartment severe ongoing edema. Renal tubular blockade by free hemoglobin,
myoglobulin, hyperkalemia, tubular damage, interstitial nephritis
Victim experience severe local pain at the site of the bite
Within 6-8 h rapid swelling progresses to the whole limb may extend to abdominal or chest wall
Local ecchymosis and tense blebs over bitten part
Within 1 h, there is regional lymphangitis
Rapid development of edema of muscles, bleeding result in the development of compartment syndrome, characterized by swelling, pain
full passive movements, and loss of sensation over the nerve areas passing through the compartment. Subsequently, the development of
wet gangrene or nonhealing ulcer. If untreated the bitten part usually toe or finger results in auto amputations
Lymph nodes proximal to the bite become enlarged and tender. Tenderness along hunters canal often noted, over bitten lower limb
Hemostatic failure
Pro-coagulant content of venom causes initiate rapid thrombosis, hypofirbinogenelmia as result of consumption coagulopathy
Hematuria, bleeding in the skin, and pituitary hemorrhage
Russells bite victims subsequently developed amenorrhea, Sheehans syndrome, loss of libido due hypopituitarism reported from south
part of India.[29-31]
Enhanced capillary permeability seen in the form of pleural, pericardial effusion, ascites and conjunctival hemorrhage or congestions
resistant shock syndrome responsible for a high fatality (capillary leaking syndrome)
Ptosis, bulbar palsy, internuclear ophthalmoplegia and respiratory paralysis due to presynaptic neuromuscular block in a Russells viper
bite poisoning often seen and reported from Kerala and Sri Lanka[32]
Sea snakes Headache, sweating, vomiting tingling numbness, foreign body sensation in the throat and swelling of the tongue
Within 30 min to 3 h after bite victim experience severe muscle pain, marked tenderness all over muscles, trismus, muscular paralysis,
respiratory arrest, without local manifestations at the site of the bite
Due to myotoxic effects of the venom resulting in liberation of potassium into circulation followed by tented T waves, widened QRS
complexes and diastolic cardiac arrest
Massive liberation myoglobin into circulation, it blocks the renal tubules, and acute renal shut down. Brown colored urine a diagnostic
of myoglobinuria
Echis cariniatus or Soon after the bite within 1 h there is development of swelling over the bitten part
saw scaled viper Swelling progress more than one segments
or carpet viper Within 60-120 min victim experience a painful lymphadenopathy at drainage area of the bitten part
[Figure 4] If untreated swelling progressed to the whole limb or the chest wall
Ecchymosis seen over the bitten part or may spread over lymphatic drainage areas
Acute bleeding in the form of gum bleeds or bleeding from abrasion on the other part of the body or from the venipuncture site seen
within 90-120 min of bite. At times, patient remains untreated bleeding persisted for 1-2 weeks in the form of blood stain sputum,
hematuria and disappeared of its own
Natural immunity against the echis carinatus venom developed in cases of repeated bite by same species in an endemic areas as
minimum clinical involvement in subsequent bite reported in Jammu region
Renal failure due to echis carinatus reported from Pondicherry and Jammu areas but not from Maharashtra.[33]
Green pit viper/ Rarely victim manifests external bleeding or renal failure. Snake bite cases are reported from Kerala characterized by local edema and
bamboo viper rarely a systemic bleeding disorder
Coagulopathy and renal failure due to hump-nosed pit viper snakebite have been reported from Kerala state which was previously
thought of a nonvenomous snake

March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
10
a b
Figure 2: Characteristics of cobra bite (a) severe tissue damage at bite site
(b) bilateral ptosis
a b
c d
Figure 3: Characteristics of Russells vipers bite (a) oedema with blood
oozing from site of bite, (b) wet gangrene, (c) extensive oedema upto the
groin, (d) gum bleed
a
b c
Figure 4: Characteristics of Echis carinatus bite (a) tense bleb at the site of
bite, (b) active gum bleed, (c) active epistaxis
did not clot, it confirms hypofibrinogenemia and that
the venom action is persisting. This test should not be
repeated before 6 h of the last dose of ASV as liver
takes 6 h for regeneration of clotting factors.[34]
Antisnake-venom
In India, we have polyvalent antivenom available
which acts against krait, cobra, Russells viper and
Journal of Mahatma Gandhi Institute of Medical Sciences March 2015 | Vol 20 | Issue 1
Bawaskar and Bawaskar: Snake bite poisoning
Echis. It accelerates the dissociation of the toxin
receptors complexes and reverses the paralysis. On
arrival of the patient, 100 ml (10 vials) ASV is added
to 200 cc of normal saline and given to the patient over
30-50 min. One should sit by the side of the victim
for early diagnosis and treatment of anaphylaxis.
Within 30 min after initial dose of ASV if there is no
improvement of neurological manifestations one can
repeat dose of ASV and no more than total 20 vials of
ASV to be administered. ASV neutralizes circulating
venom and it has no action once the venom is
attached to the receptor site. In krait bite, its venom
destroys receptors thus neurological manifestation
may persist for 2 to 3 weeks till there is regeneration
of receptors. At this stage, administration of ASV is
merely a waste. No amount of antivenom is going to
reverse the ptosis or neuroparalysis till regeneration
of receptors.
Antivenom should be administered as soon as signs of
systemic or severe local swelling are noted. The mean
times between envenoming and death are 8 h (12 min
to 120 h) in cobra, 18 h (3-63 h) in Bungarus caeruleus,
3 days (15 min to 264 h) in Russells viper and 5 days
(25-41 days) for Echis cariniatus. The approximate
serum half-life of antivenom in envenomed victims
ranges from 26 to 95 h. Before discharge, envenomed
victims should be closely observed daily for minimum
3-4 days.[6,9]
Antivenom Reaction and its Management
No skin test should be performed before giving ASV
as it does not give any surety regarding reaction. It
is merely killing vital time. Antivenom should not be
given intramuscularly. It should be administered by a
qualified person who has knowledge of the anaphylaxis
reaction and its management. However, snake catchers
or trekkers should take with them few ampoules of
ASV in case of an accident, so as to make is readily
available to a doctor.[4]
Reaction of ASV can develop within 10-180 min. The
incidence is increased with dose of antivenom and
speed of administered. Bolus dose may give rapid
reaction. A turbid solution of ASV may precipitate
severe reaction and hence should be thrown away
Earliest symptoms are hotness in ears, scalp, itching
over scalp, urticaria, sudden onset of intractable
cough, nausea, vomiting, goose skin, giddiness often
complained of uneasiness, suffocation, and irrelevant
Bawaskar and Bawaskar: Snake bite poisoning
behavior. Febrile reactions due to contamination of
ASV with endotoxin like compounds may cause fever,
rigors, vasodilatation, and hypotension which can
occur within 1-2 h of treatment. Children get febrile
convulsions.
Systemic anaphylaxis
Sudden onset of projectile profound vomiting,
sphincter relaxation, hypotension, bronchospasm,
foreign body sensation in throat and angioedema.
These reactions are due to complement activation
by immune complexes or aggregates of immune
globulin.
Delayed reaction serum sickness can develop
between 5 and 24 days of ASV therapy. Incidence
of this depends upon the dose of ASV but is rare.
This delayed reaction is clinically characterized
by pyrexia of unknown origin, itching, arthralgia,
lymphadenopathy, joint swellings, mononeuritis
multiplex, albuminuria, and rarely encephalopathy.
Low dose of adrenaline, promethazine, and
hydrocortisone can be used as prophylaxis against
anaphylaxis reaction.[35]
Management of Reaction
In case of reaction, injection adrenalin 0.5 ml of
0.1% to be administered by intramuscular route on
the lateral aspect of the thigh. Dose can be repeated
if not controlled. In a situation where life is at
stake, that is, severe hypotension, bronchospasm,
laryngeal edema adrenalin to be given in the dose
of 1000 g (1 ml) diluted in 9 cc of normal saline.
A total of 10 cc of this solution can be given 1 ml
intravenously every 3-5 min till reaction is reduced.
In addition to this, intravenous aminophylline,
head low position, intravenous normal saline, H1
blocker, chlorpheniramine maleate, intravenous
methyl prednisolone, nasal oxygen may be helpful.
Sometimes, patient may require endotracheal
intubation and ventilation. Irrespective of due care
and when reaction is over; during re-administration
of ASV, the patient can develop re-reaction. In such
situation, one can select ASV from another batch
and try. Patient should not die of reaction and so
also not due to snake bite envenoming. One should
not be afraid of administration of ASV in a severe
venomous bite provided one is fully prepared to treat
any severe reaction. Many victims are referred from
PHC to rural or district hospital without giving ASV
and succumb on way to the hospital.
March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
11
Emergency Management
Basic cardiopulmonary resuscitation
All patients found unconscious at home and not
breathing should start receiving chest compressions
and mouth to mouth respiration en-route to the
hospital.
Endotracheal intubation and ventilation
Indicated if victim has pooling of saliva, unable to lift
the neck from pillow, muscle power <3/5, reduction
in oxygen saturation, signs of respiratory failure like
abdominal-thoracic respiration, signs of cerebral
hypoxia. At the periphery, one can do endotracheal
intubation, or if not possible a laryngeal mask can be
put directly over larynx and ambu bag ventilation.
Management of Specific Snake Bites
Cobra bite
Cobra venom is reversibly attached to postsynaptic
receptors. Acetylcholinesterase inhibitor (AChEI)
like neostigmine 50 g/kg over 1st h and then 25 g/
kg next four hours preceded by atropine (to counter the
muscarinic action of AChEI). Or alternatively, 0.5 mg
neostigmine half hourly proceeded by atropine, may help
the majority of victim to recover within 24 h. This cycle
may not be required more than 5-6 times.[4,5,8,9,19-21,36]
In our experience, a victim diagnosed dead by
the peripheral doctor only by absence of respiration
and nonreacting pupils was recovered with artificial
ventilation, cardiopulmonary resuscitation, and
AChEI.[4,37] Local wound care is done by intravenous
antibiotic, daily dressing and may require plastic surgery.
One should always rule out diabetes mellitus in a non-
healing wound in any snake bite.
Krait bite
Indian common krait venom contains both pre and
postsynaptic blocker. Whether the victim will respond
to AChEI or not can be tested by putting an ice-filled
glove finger over eyelid. Hypothermia sensitizes the
Ach receptors.[38] If there is a slight improvement in
ptosis, one can try AChEI.[39-42] Recently, we found
envenoming by kokan krait (light coppery color)
respond to AChEI.[4]
Sea snakes
Patient may require a ventilator for respiratory failure.
Electrolyte imbalance especially hyperkalemia needs
to be corrected (diuretic, glucose-insulin, salbutamol
inhalation, calcium gluconate). In case of resistant
12
hyperkalemia, one can try potassium channel drug
oral glibenclamide provided one takes care of
hypoglycemia.
Russells viper or Daboia or viper Russell
siamensis
One of the most common and dreaded complication of
Russells vipers bite is DIC, which can be diagnosed by
thrombocytopenia, abnormal crenated RBCs in peripheral
blood smear. In addition to ASV, one has to try plasma
products and whole blood transfusion which is rare
required if ASV is administered in time with an adequate
dose. Hypotension can be managed with fluid and inotropic
agents. Severe hypotension due to bleeding in adrenal
and pituitary glands and abdominal bleed and endothelial
dysfunction with capillary leak may need heavy doses of
intravenous methylprednisolone.[4,6,7] One should keep in
mind and look for renal failure from time of admission.
Risk factors such as hypotension, hypovolemia should be
corrected. There are lot of controversies regarding early
introduction of diuretic, acetylcysteine or allopurinol in
renal failure. However, in our experience, intravenous
frusemide 80-100 mg and oral acetylcysteine 600 mg 3
times a day may help to arrest the renal damage, but this
needs a randomized controlled trial. In a situation of renal
failure with raised serum potassium, it may be treated
with frusemide drip at rural areas or peritoneal dialysis or
referred to higher center for hemodialysis.[4,18] Irrespective
of the standard dose of ASV many victims develop renal
failure. This is particularly reported from Marathwada
region. Thus venom procured from this region should be
used to prepare antivenom against Russell s viper which
kills many farmers, sugarcane labors and deserts many
families.
Local wound care is most important to avoid disability.
Once the clotting mechanism is reversing (20 min
whole blood clotting time), the edematous limb can
be elevated with rest on the pillow below the knee.
Glycerin Magsulf dressing, aspiration of tense blebs
by sterile needle and syringe, debridement of dead
tissues, intravenous antibiotics and avoiding surgical
decompression unless absolute essential remain the
mainstay of treatment here.
Echis cariniatus or saw-scaled viper or carpet
viper
Due to the possibility of renal failure and bleeding due
to this snake envenomation more ASV is required in
states of Jammu and Pondicherry (ASV >100 ml) to
correct bleeding disorder as compared to Maharashtra
(ASV approx 30-50 ml).[43] This snake runs rapidly in a
Journal of Mahatma Gandhi Institute of Medical Sciences March 2015 | Vol 20 | Issue 1
Bawaskar and Bawaskar: Snake bite poisoning
grown up grass hence victim may feel injury by thorn
prick and failure of administration of ASV on wrong
history result in many amputation of limb,..Thus a
farmer or labourer with rapid development of swelling
within one hour while walking bare feet in grown of
grass or bund, attributed to a thorn, is often a case of
Echis bite envenoming.
Green pit viper and bamboo pit (Trimeresurus)
The polyvalent ASV available in India does not cover
for envenomation with these two vipers. However,
empirical treatment with polyvalent venom should
be offered as paraspecificity may sometimes help to
alleviate the envenoming.[44]
When there is doubt regarding species of snake in
such situation, one can manage the case on syndromic
approach.[45]
Conclusion
Scientists should make attempts to prepare venomous
toxoid to immunize the farmers and risky population
against venomous snake toxins. Toxicologists should
make an attempt to prepare the pharmacological
antidote to venom actions. Antivenom producers in
India should prepare ELISA kit for detection of venom
antigen in blood and prepare antivenom from venoms
obtained from snakes caught from relevant areas of the
country. The attending doctor gets immense satisfaction
when the serious poor victim of snake bite recovers.
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How to cite this article: Bawaskar HS, Bawaskar PH. Snake
bite poisoning. J Mahatma Gandhi Inst Med Sci 2015;20:5-14.
Source of Support: Nil, Conflict of Interest: None declared.