QMR Oct Dec 2009

FOR PRIVATE CIRCULATION For the use of a Registered Medical Practitioner only
QUARTERLY
MEDICAL REVIEW
Vol. 60, No. 4 October - December 2009
Management of Snake bite and

Scorpion Sting
CONTENTS
1. Snake bite .................................................................................................................. 4
2. Scorpion Sting .......................................................................................................... 26
Published and Issued by
RAPTAKOS, BRETT & CO. LTD., WORLI, MUMBAI 400 030.

QUARTERLY
MEDICAL REVIEW
Vol. 60, No. 4 October - December 2009
Management of Snake bite and

Scorpion Sting
*H.S.Bawaskar P.H.Bawaskar
*Bawaskar Hospital and Research Center
Mahad Dist- Raigad Maharashtra India 402301
Email:himmatbawaskar@rediffmail.com
4 Quarterly Medical Review
Snake bite
Snake bite is an acute life threatening medical emergency often faced by farmers and farm
labourers. Early diagnosis of envenoming by venomous snake and its rational and accurate
management may save life. Rural Indian victims of snake bite are reported earlier due to easily
available transport including auto and jeeps and constructed approachable roads to the majority of
villages. Irrespective of early reporting, the fatality in venomous snake envenoming is due to non-
availability of medical officers at primary health Center (PHC), inadequate facilities including anti-
snake venom (ASV), and resuscitation trolley: working laryngoscope, endo tracheal tubes, Ambu
bag, ventilator and other emergency medicine. Many times the medical officer is a freshly passed
graduate and has not seen and treated the venomous snake bites before. This adds to the morbidity
and mortality. Because of expensive ASV and it not being easily available to private hospitals,
many doctors avoid admitting the case due to threat of anaphylaxis. Moreover the poor rural
population cannot afford expensive ASV and treatment at private hospitals. Snake bite should be
declared as an occupational hazard. ASV should be available free of cost to victims admitted to
private hospitals. ASV is always in short supply. To avoid the crisis of ASV supply, peripheral
doctors should be trained regarding management of snake bite and indications of ASV. Availability
of snake venom antigen detection kit (ELISA Mono-specific) is a must. Antivenin producers in
India should be encouraged to prepare antivenom from venom obtained from snakes caught from
relevant areas of the country.
Introduction
Venomous snake bite is an important public health hazard in tropical and subtropical countries1, 2,
3. In rural areas snake bite poisoning is a leading cause of premature death of young earning
member of the family 4. In India 35,000-50,000 lives are lost per year due to venomous snake bite1,
3. More than 2000 deaths per year are reported from Maharashtra. This is the tip of the iceberg as
the majority of snake bite deaths go unreported as many villagers go to traditional healers like
mantriks and tantriks. Moreover snake bite is not a notified disease in medical fraternity. It is
surprising that, snake bite poisoning is seldom mentioned as a priority for health research in a
developing country like India. The grant allocated for snake bite is many times less than the grant
allocated to amoebic dysentery (with a negligible fatality as compared to snake bite). Unfortunately
public health authorities, nationally and internationally, have given little attention to this grave, life
threatening medical problem, relegating snake bite envenoming to the category of a major neglected
disease of the 21st century2. There should be more encouragement from government and other
funding agencies for conducting research. Moreover there are very few medical scientists taking
interest or carrying out research in this field.
Most of the venomous species of snakes are “sit and wait” predators wherein they lie camouflaged
lying in wait for their potential victim and they strike when the prey comes within their striking
distance. The snake usually then lets go allowing the venom to take effect after which they follow
their prey by following its scent trail. So after a human strike, it is very likely that the snake will be
found in the 30 foot radius and it should be remembered that they are no less dangerous after the
first strike. So victim should be moved away from the area 5,6.
Management of Snake bite and Scorpion Sting 5
Etiology
There are about 216 species of snakes identifiable in India, of which 52 are known to be venomous.
The major families of poisonous snakes in India are Elapidae (Cobra Naja naja, king cobra and
kraits) viperidae (Russell’s viper, Echis carinatus or saw scaled viper or carpet viper and pit
viper) and hydropidae (sea snake).7
Snake Venom
Snakes are highly specialized animals. Their gut secretes powerful fast acting digestive enzymes.
A pair of salivary glands secrete a powerful multipurpose enzyme fluid that flows at the time of
envenoming through fine channeled or grooved teeth called fangs. Venom immobilizes the prey
and facilitates its swallowing. It is quite clear that snake venom is not a substance evolved to
attack man or any big vertebrates. A snake can bite and continue to secrete venom a number of
times in succession. Dr PJ Deorus from India studied the average venom yield per bite in venomous
snakes
Cobra -0.2 gram of the dry weight of lypolized venom.

Krait- 0.022gram.
Russell’s viper-0.15 grams
Echis carnatus- 0.0046 grams.
Lethal dose of these venoms for man has been reported

Cobra-0.12grams
Krait-0.06 grams
Russell’s viper-0.15 grams
Echis carinatus -0.08 grams.
One ml of polyvalent antivenin neutralized

Cobra-0.6 mg
Krait-0.45 mg
Russel’s viper 0.6 mg
Echis carinatus -0.45 mg.
(Anti snake venom)ASV has a half life of 26-95 hours (8,9)
Venom secretion in all venomous snakes appears to vary in seasons. In warmer months the output
is more than in the cold season. Similarly darker the snake it secretes more venom as compared to
a light colored snake. While the venom is viscous and comes out in small quantity in winter and in
light colored snake. This explains the high fatality rate seen during summer and August, September
and October months due to high environmental temperature. Most snakes inject 10% of the available
venom in a single strike. Exception is the Russell’s viper which injects 75% of stored venom in one
bite and is responsible for high morbidity and mortality India. Venom is a cocktail made of 20 or
more components. It contains proteins, in form of enzymes, non-enzymatic polypeptide toxins and
non-toxic nerve growth factors. Enzymes are digestive hydrolase’s, hyaluronidase and various
activators and inactivators of physiological processes. Majority of venoms consist of l-amino acid
oxidase, phospho mono-and diesterases, 5’nucleotidase, DNAase, phospholipase A2, peptidase
and NAD-nucleosides. Krait and cobra venom also contains acetylcholine esterase, phospholipase
B and glycerophosphatase as against the vipers venoms which have endopeptidase, arginine ester
hydrolase, kininogenase and thrombin like (Echis carinatus), factor X and prothrombin activating
enzyme (Russell’ s viper) Lecithinase8,10 Phospholipase A2 is seen in majority of venoms extensively
studied. It destroys mitochondria, red blood cells, leucocytes, platelets, peripheral nerve endings,
skeletal muscle, vascular endothelium and other membranes, produces presynaptic neurotoxic
activity (krait), opiate –like sedative effects and autopharmacological release of
histamine(anaphylaxis). The acetylcholine esterase found in most krait and cobra venom does not
contribute to their neurotoxicity. Hyaluronidase promotes the spread of venom through tissue.
Proteolytic enzymes (endopeptidases or hydrolases) are responsible for local changes in permeability
leading to edema, blistering and bruising and local necrosis. Severe, irreparable local tissue loss
due to cobra venom is due to myocytolysis. Cobra venom is rich in postsynaptic neurotoxins called
alpha-bungarotoxin and cobratoxin. The acetyl choline receptors are primary signal transducers at
the neuromuscular junction. It is a multi-subunit, intrinsic membrane protein. Both short and long
acting toxins from cobra venom bind specially to acetyl choline receptors, preventing the interaction
between acetyl choline and receptors on postsynaptic membrane. This action subsequently prevents
the opening of the sodium channels associated with acetyl choline receptors and is responsible for
neuromuscular blockade. Treatment with appropriate anti-venom can result in rapid reversal of
paralysis. It is suggested that anti-venom accelerates the dissociation of the toxin-receptors complex,
which leads to a reversal of paralysis.8,10 Krait venom in India contains both pre-synaptic beta
bungarotoxin and pre-synaptic alfa-bungarotoxins11, 12. These toxins initially release acetylcholine
at the nerve ending at neuromuscular junction and then damage the nerve ending subsequently,
prevent the release of neurotransmitter acetyl choline. This explains the acute abdominal colicky
pain with salivation, vomiting and “gooseflesh” in krait bite (premonitory signs and symptom of
krait bite)8. Envenoming by kraits is associated with a syndrome of neuromuscular paralysis that
falls into three distinct phases. The first phase is a rapid onset phase leading to profound paralysis
within 30 to 60 minutes. The second is a stable phase of deep paralysis lasting 2 to 3 days. The
third is a recovery phase 2 to 3 weeks. This explains the prolonged period of ventilator support and
intensive care requirements essential for recovery13. Neuromuscular blockade by the short chain
neurotoxin (cobra toxin, alpha bungarotoxin) is more readily reversible than that with long chain
toxins (alpha –bungarotoxin). Beta bungarotoxin in the krait venom bears similarity to botulinum
toxin. The venom of cobra and krait is of smaller molecular size and is rapidly absorbed into
circulation. This is the reason why a victim of cobra bite can die within 8 minutes. Absorption is
further accelerated by threat of death and liberated catecholamine and running. Cobra unlike the
krait deposits it 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 prompts
the rural victim in India to seek care quickly after the cobra bite. While more insidious onset of
symptoms induced by the bite of the krait, more often results in a visit to the local traditional healer
(mantrik or tantrik) for natural curatives. Krait venom is ten times more lethal than cobra but the
victim reports too late (due to delayed absorption of venom as it usually bites a person sleeping on
the floor and it does not cause local effects, moreover reflexes in the sleep are blunted.) The
smaller sized fangs usually inject the venom skin deep where there is poor circulation14. Cardiotoxin
contents of cobra venom are extremely lethal to myocardium. Cardio -toxin has direct action on
skeletal, cardiac and smooth muscles, nerves and neuromuscular junction and is responsible for
paralysis, circulatory, respiratory failure, bradycardia, heart block and systolic cardiac arrest by
releasing calcium ions from the surface membrane to the myocardium.
Arginine –ester-hydrolase content of viper venom causes coagulation and release of bradykinin
responsible for sudden hypotension and anaphylaxis. It is similar to thrombin in its action. Viper
venoms interfere with blood clotting. This has been extensively studied. The prothrombinase causes
calcium dependent conversion of prothrombin to thrombin. Venoms exhibit both anti-coagulant and
coagulant effects on blood clotting mechanism resulting in defibrination syndrome or disseminated
intravascular fibrino-coagulopathy. The acute bleeding is due to hypocoagulopathy or incoagulability
due hypofibrinogenaemia as a result of massive consumption of fibrinogen and fibrinolysis of blood
clots. Microangiopathic haemolysis associated with disseminated intravascular coagulation, acute
renal failure and hypotension (due to acute tubular necrosis) occur with Russells viper venom.
Russell’s venom, is a rich source of enzymes that activate factor X to convert prothrombin to
thrombin in the presence of Calcium factor V and platelets, thus Russell’s venom contains several
different ‘pro-coagulants’ which activate different steps in the clotting cascade. The fibrinolytic
activity of the viper venom is so fast that sometimes within 30 minutes of the bite, the coagulation
factors are so depleted that blood does not clot. Russell’s viper venom activates the clotting system
of the snake’s natural prey with such speed that Macfarlane was “left feeling it is almost too
clever to be true”15. A protein in Echis Carinatus (saw scaled viper), found all over India except
in Bengal and Kashmir has the unique effect of enhancing fibrinolysis by plasminogen activation
by urokinase9, 16. Haemorrhagins -1and 2 and
metaloendopeptidase cause acute rapid bleeding
in brain, lungs, kidney, heart and gastrointestinal
tract. It causes severe vasoconstriction followed
by vasodilatation of the micro-vessels. It cause
endothelial gaps due to disintegration of the
endothelial cells with intracellular edema, swollen
mitochondria, and dilated endoplasmic reticulum
and separation of intercellular junction of the
endothelial cells and local loss of basement
membrane of the vessels leading to capillary and
venous hemorrhage. Cobra – Naja naja
Cobra
All Asiatic cobras can be considered as part of a single species, Naja naja. Four species are
found in India. Naja naja is seen throughout the country, naja kauthia in east and north east,
Naja axiana flourishes in the extreme north west and naja sagttifera often seen in the Andaman
islands 17 . Most adult cobra measure 100-150 cm,

occasionally species of 210-220 cm are seen (but it is
very rare). The Indian spectacled cobra is very variable
in color. Often the color of cobra matches with the soil
Cobra bite of the regional areas as a natural gift for protection from
human enemies. It can be of grey, yellowish, tan, brown,
reddish or black. It is easily recognized by its hood and
can raise the hood more than 50% of its length. According
to hood marks it is named as ‘spectacled’ with two marks
or ‘monocled’ with one mark.
Cobra can be found in a variety of habitats including
agricultural areas in sugarcane, paddy, soybean or Jawar
growing crops. Many times in Maharashtra many cobra bite cases are reported in residence of old
mud houses, huts, recently built houses, blindly handling the rubble in the attic, fire wood, dry cow
dung. It is diurnal in habit. This species is shy and always attempts to escape, if it feels threatened.
It produces a loud, hollow sounding, explosive hiss. It generally bites only as a last resort or it may
just strike with mouth closed “head butting” its opponent. Many bites result in only little or no
venom injected - “dry bite”18. It feeds on small snakes, frogs, rats and lizards. Many times it enters
in the cages of hens often kept near the corner of the
Cobra bite
hut. Rats flourish in and near the grain bags in farms
and grain shops. Cobras follow the rats to hunt them
and accidentally bite humans handling the bags. Jawar
(Sorghum) breads or chapattis are kept in the small round
Local edema
baskets in the small open window in the mud walled
villages, where rats can enter in the basket and the cobra
may follow them and bite the house wife accidentally
when she blindly puts in her hand to lift up the bread.
Snake bite cases have increased recently in Mahrashtra
Respiratory Paralysis due to long periods of electric load shedding in
villages . Fangs of cobra are fixed and immobile1.
18,19
Bite without envenoming is dry (defence), bite with envenoming is called Professional bite.
**A Cobra found in school bag has been reported and child died at Cobra bite.
Clinical manifestations
Instantaneous death is due to thought or fear of threat of death. There is sudden pouring of
endogenous catecholamines resulting in cardiac (Ventricular) arrhythmias. Acute myocardial
infarction and cardiac arrest in such situation may occur just on sighting the hooded cobra and can
cause such an effect even without a bite11. Anxiety, tachycardia accelerated rapid absorption of
venom into circulation precipitates myocardial depression, heart block, bradycardia and cardiac
and respiratory arrest12,20,21. This phenomenon is not seen in children as they are unaware of
death11.
Local effects. Cobra bite usually occurs during the day and early darkness. Common site of the
bite is the extremities. Soon after bite the victims experience severe local pain, sudden development
of swelling, bleeding from fang marks and subsequently
clotted blood is seen over fangs abrasions. Local
ecchymoses develop. Venom is a rich source of cytotoxins
resulting in severe extensive edema followed by necrosis
and wound takes a long time to heal, at times leaving big
scars with contraction. Early skin grafting prevents the
contraction and subsequent consequences. The victim may
develop severe local necrosis without systemic
involvement11, 22.
Systemic involvement Open toilet – risk factor for snake bite
Foremost neurological manifestations include blurring of vision due to paralysis of ciliary muscles
of eyes and loss of accommodation. Signs of gradual development of bulbar palsy include difficulty
in deglutition, nasal twang in voice due to palatal palsy, broken neck sign i.e. unable to lift the neck
from pillow. Suffocation, partial or total opthalmoplegia and ptosis also may occur. Pupils are at
times dilated and not reacting to light. The victim may suddenly lapse into an acute respiratory
paralysis and shock.(11,14,19, 23,24,25).
Locked in syndrome - Few cases develop quadriplegia with total opthalmoplegia and dilated
pupils. The clinician may feel the patient is brain dead or comatose, but such victims recover
totally within 3-4 days if treated properly by maintaining oxygen saturation with proper ventilator
support and electrolytic balance and nutrition and care of infection. This phenomenon is due to
blocked postsynaptic acetyl choline receptors including the sphincter pupillary muscle which are
rich in acetyl choline receptors.(26).
Management - The victim should not be allowed to walk or run. The bitten part should be kept
below the heart level; no time should be wasted in search of the snake or application of tourniquet.
No local incision must be made, sucking, application of ice or any chemical must be avoided. Only
wound surface venom can be removed by clean cloth or tissue paper. The victim should be given
assurance that the good treatment of snake and antidote to the bite is available at hospital. And the
victim should be informed that all snakes are not poisonous and even poisonous snakes many a
times do not inject venom. Time should not be wasted by taking the victim to mantrik, tantrik or
village healer or temple or herbal remedies. The Victim should be removed at the earliest to the
nearest primary health center by any available vehicle or even over the back of a healthy person.
If the victim is transported on a motor bike (as may happen in villages) there must be another
person behind him to support him, as sudden paralyses may result in fall from a speedy motor bike.
At the hospital, the victim must be examined rapidly for any development of paralysis, vital functions
and local site. If the snake has been killed the specimen brought should be identified or if required,
the services of a snake catcher may be used.
Anti-snake venom (ASV) – To prepare ASV injection, dry powder in the ampoule of ASV is
dissolved by adding 10 ml of distilled water as dilutent. Each vial should be examined after dilution.
If it is turbid or some precipitate remains at bottom it should be discarded, (as allergic proteins may
cause severe anaphylaxis)1,22.
Test dose – A skin test dose need not be given as there is no guarantee that non sensitive victim
will not develop reaction or otherwise. Unnecessary time is wasted in testing the ASV 1,8. If not
contraindicated 0.3 ml of adrenaline can be given subcutaneously as prophylaxis against anaphylaxis
before injecting the ASV27. 100 (10 ampoules) ml of ASV to be added to 200 ml of normal saline
and given by intravenous route over 30-50 minutes. The physician should sit by the side of victim
to detect early signs and symptoms of anaphylaxis. 50 ml of ASV is repeated if there is no
improvement in neuroparalysis - mixed 50 ml in 500 ml of normal saline and infused over 24 hours
by micro drip. Administration of ASV by bolus should be avoided, as it may rapidly activate the
complement system and can cause severe anaphylaxis. The ASV will neutralize the venom that is
slowly absorbed from the bite site. Hypotension and bradycardia are treated with atropine or
isoprenaline drip. In case of shock, without cardiac block dopamine drip may be needed4.
Decrease in oxygen saturation or if the victim complaints of suffocation with loss of chest expansion,
decreased or poor expiratory nasal blow easily felt by the dorsum of hand, reduction in one breath
counting, reduction of muscle power grade 3/5, broken neck sign and pulling of saliva are indications
for endo tracheal intubations and ventilator support by the ambu bag or ventilator if available. At
the site of bite, if the victim develops respiratory paralysis mouth to mouth respiration can be
given.
Precipitated
proteins may
cause anaphylaxis
Neostigmine – 25 micrograms/kg neostigmine is given by intravenous route over the first hour
and then 50 micrograms/kg over next four hours can be repeated as per recovery. It can be
administered as 0.5 ml neostigmine every 30 minutes till recovery occurs. It usually requires 5-8
doses. Atropine must be given just to counteract the muscarinic action of neostigmine (salivation
and secretion)1,8,22,23,24, 28,29,30. Neostigmine can be give by subcutaneous route.
Reaction to antivenin- Anti-snake venom is a foreign protein and can cause mild to severe
reaction. It can occur between 10 to 180 minutes of administration of ASV 8. Mild reaction is
characterized by vomiting, flushing of face and skin, hot flushes from ear and forehead, itching
over scalp, and groins, urticaria, bronchospasm, cough, tachycardia, fever and palpitations
Severe reaction – ASV can cause sudden collapse with hypotension, shock low volume thready
pulse, disorientation, severe bronchospasm, cyanosis, cold extremities, swelling of tongue & lips
and difficulty in breathing and tracheal tug sound with angio oedema. Blood pressure may be 70 to
non recordable. The incidence and severity of these reactions “are directly proportional to the
speed and quantity with which the healing antiserum reaches target” (Lancet 1980).
Early reaction or immediate hypersensitivity reaction represents type IgE mediated hypersensitivity
to horse serum.
Treatment
Immediately the reaction is treated with adrenaline 0.3 to 0.5 ml (300 to 500 microgram) given by
intramuscular route8. It can be repeated within 3-5 minutes if necessary. Intravenous fluid,
aminophylline, antihistamine, and H2 blocker and hydrocortisone 100 mg are also given. If methyl
prednisolone is available, it can be given to tide over the emergency.
In case of severe anaphylaxis with poor circulation intravenous adrenaline may be given in a dose
100 microgram (1000 microgram i.e. one ml of adrenaline added to 9 ml of saline so one ml contain
100 microgram adrenaline), can be repeated every 5 minutes till there is improvement in circulation
and blood pressure.
Delayed reaction – may occur in the form serum sickness. It is seen after 5 to 24 days
characterized by fever, arthralgia, polyarteritis, radiculpathy (mono neuritis multiplex) or Guillain-
Barre syndrome, lymphadenopathy, amyotrophy. It responds to oral steroids. Serum sickness
depends upon the dose of ASV administered.
Local wound- Mouth of the snake is contaminated with pathogens such as Staphylococcus and
Clostridium tetani. Hence local wound must be treated with antibiotics. The victim should be
immunized for tetanus. Local necrosis with gangrene needs debridement. All victims should be
investigated for diabetes mellitus.
Showing cobra bite to snake catcher.

Age/sex Snake Bite to Total ASV Clinical Results
Hospital in in ML
minutes
35F Cobra 30 —- Fangs marks Dry bite
only
35M Cobra 30 100 Blurred vision. No progression
Fangs marks to
with blood clot neuroparalysis
Local swelling+
Pain +
53M Cobra 45 50 Fangs++ Ventilator -1
Swelling++ day
Ptosis++
28/M Cobra 30 - Fang marks only Dry bite
25/M Cobra 10 100 Fangs ++ blood No progression
clot Swelling,
pain+
30/M Cobra 30 100 Fang++ No progression
Blood clot,
Swelling+
Pain+
Krait
Local names- Urdu: kala gandait, gugrathi : kala taro, Marathi:kandar or manyar or kaner Tamil:
kattu viriasn; Malayalam: valla pamboo.
Krait is the most poisonous among all species of snakes seen in India. Its venom is ten times more
poisonous than cobra venom. The head is slightly broader than the neck with a black eye with
round pupil. Its color is glossy black, bluish gray or dark brownish black with narrow (at times
paired) white bands that continue towards the pointed tip of the short tail. These bands are absent
on fore body and they are replaced by white vertebral spots. Whereas in the non venomous wolf
snake there are complete bands from beginning of the head and absent in the narrow long tail18.
Kraits are active during night hours. During day time they take shelter in termite mounds, rodent
burrows, piles of brick, dry coconut, cow dung, rubble and at times in a corner underneath beddings
or under pillow covers. Thus the common krait is found in the vicinity of human habitation, near
wattle and daub houses, mud and small huts. It is a terrestrial snake that enters in human dwelling
in search of prey. The Krait eats small kraits (cannibalism), rodents, lizards and frogs. It is oviparous.
It is 1-4 feet long; it is not an active or aggressive snake. Even in pucca concrete house kraits
enter through the outlet pipe of bathroom if its inlet is not packed with tight iron mesh. It is interesting
to note in our study majority of victims are Hindus and few Muslims because muslims, irrespective
of place and poverty, always sleep on a cot while Hindus prefer floor bed31.
Mechanism of envenoming - High incidence of krait bite occurs during monsoon months. Because
of heavy rain the holes of rats and other rodents are filled with water. There is no grain for the rats
to eat in the surrounding farm hence rats enter the house. The krait may follow to hunt for the rat.
Fang of the krait is sharp and short and fixed to the upper jaw. The Krait may strike a person
sleeping on the ground. Also, the snake could mistakenly identify an exposed body part as prey.
Most bites occur during months of June to December when snakes may, during the course of their
hunting activity, linger in a person’s bedding to take advantage of warmth therein12. Majority of the
cases are bitten between 11 PM to 5 AM. During sleep the reflexes are blunted and with small
sharp fangs the krait injects maximum venom in a person who is in sound sleep1,4,11,19,21,32,33,34
Local manifestations. The Venom is injected in skin deep or in subcutaneous tissue. It causes
little local tissue damage, little or no pain and is absorbed slowly due to poor and sluggish circulation
to the skin and tissue in sleep. At times the victim may forget the local pain or may give history of
ant bite, rat bite or no bite. Local mild urtcaria, swelling and pin head skin bleed may be noted. No
subsequent local tissue damage is noted. (Except delayed neuropathy which also rare).
Systemic involvement – The Victim experiences heaviness, itching at the bite site, parasthesias
and weakness in the bitten part of the body. Sudden vomiting, giddiness and pain in the abdomen
occur within 10-30 minutes of the bite wrongly attributed to indigestion31. Usually these symptoms
are neglected and the victim goes to sleep and subsequently the venom is absorbed into the circulation.
Krait venom is rich in beta bungarotoxin and irreversibly blocks the presyanptic acetyl choline
receptors. In Indian krait, the venom has properties to block both pre and post-synaptic acetyl
choline receptors. Initially there is release of acetyl choline resulting in autonomic stimulation
characterized by vomiting, mild sweating, gooseflesh, hypertension and staring look. The mechanism
for autonomic dysfunction due to snake bite is not fully understood. It is plausibly due to the
blockade of the receptor site such as presynaptic alpha-2 adrenergic receptor by krait neurotoxin
thereby inhibiting the inhibition of neural mediated release of nor epinephrine with resultant
sympathetic over activity. It could be also due to reduction in parasympathetic activity 8, 11, 35, 36.
After 30 minutes to 8 hours and at times even after 14 hours subsequently there is development of
neuroparalysis characterized by ptosis which occurs first as levator papillae muscle is rich in
acetyl choline receptor. Extra ocular muscles are quite sensitive to neuromuscular blockade by
elapid venom because each motor neuron innervates only 6 to 12 muscle fibers in eye muscles,
compared with large proximal limb muscles where the ratio may reach 1:2000. Blurring of vision,
heaviness in eyelids followed by ptosis, dilated non reacting pupils, paralysis of facial muscles
resulting in myasthenia look and loss of naso-labial fold are the other symptoms Paralysis of Neck
muscles, dysphagia, difficulty in deglutition, paralysis of palatal muscles, pooling of saliva,
opthalmoplegia, suffocation, quadriplegia with presence of tendon reflexes are the other signs.
The diaphragm is the last to undergo paralysis. Death is due to respiratory paralysis and asphyxic
cardiac arrest or iatrogenic or hospital respiratory infection and acute respiratory distress syndrome
due to artificial ventilation.
Management – The Victim usually reports late due to absence of local signs and poor transport
during night. The Bite may occur in any part of the body, Usually the neck, scalp, ear lobules, chest
wall, popliteal fossae, axilla etc. Application of crepe bandage if bite occurs to limbs is helpful in
delaying the venom absorption and respiratory paralysis37. At the hospital, initial clinical signs,
muscle power, respiration, oxygen saturation and intensity of expiratory nasal blow should be
noted. The ASV and respiratory care and other management is same as described in cobra bite
except, in krait bite the victim requires prolonged ventilator support for 3-10 days. If there is
hypertension, intravenous nitroglycerine drip is given35. At times the victim may land in pulmonary
edema.
Many times the victims are
admitted to surgical ward
with pain in the abdomen
for appendicitis or sent
home as labelled functional
pain. Even the admitted
victims may suddenly
relapse and manifest acute
respiratory failure and
doctor may face an acute
emergency for which
neither he himself or the
ward staff are prepared.
“Thus a person reported
in mid night or early in the morning with history that he woke from floor bed due pain in
abdomen, with or without history of bite coming from village or farm and bulbar palsy
should be diagnosed as krait bite and closely observed unless until proved otherwise.
During transport of victim to the big hospital the doctor should accompany the patient
and follow the progress. This may also help the doctor to learn and gain experience to
manage the next case at his center or hospital”.
Russell’s viper
Russell’s viper (daboia, viper russelli) snake inhabits ten South Asian countries including Pakistan,
Sri Lanka, Bangladesh, Burma and Thailand. It ranks amongst the most important causes of
morbidity and mortality due to snake bite. While protecting the paddy and wheat by controlling the
rodent (rats) population, it kills many farmers unlucky enough to tread on it during harvest and
watering the crops especially sugarcane and horticulture plants in night, due to electricity load
shedding during daytime in Maharashtra.
It is 3-5 feet long snake, body is stout and has a rough appearance. The head is Triangular and
broader than the neck. Nostrils are very large. The eye has a vertical pupil. It has a short and thin
tail. Brown - yellow brown, with three longitudinal series prominent, large brown, black oval round
spots. The spots may have pointed ends, to form a chain like pattern or may have narrow white or
cream margins. The Top of head usually has narrow inverted v shaped mark. It is nocturnal. It is
often found in grassy areas, scrub jungle, forest edges, rocky hillocks, dense throne hedgerows
and in and around mangroves. It preys on rodents, frogs, lizard, snakes and birds. The female
produces 20-60 young (viviparous) usually around June or July. The Fangs are big and semicircular
mobile and attached to upper jaw. The length of the fangs in adult snake is 16 mm and they are
curved. The amount of venom injected at the time of bite is 63+7 mg. When disturbed, hisses
loudly “like a pressure cooker” and only bites as a last resort. It is the most aggressive snake18.
Local manifestations – soon after the bite, the victim experiences severe local pain, giddiness
and may often collapse. Sudden development of rapid progressive swelling may occur within 5-15
minutes of bite. The swelling may attain a length equal to the length of culprit snake. Active
persistent bleeding of cuts from the fang marks seen Ecchymoses and big blebs appear in next
few days on the bitten part. Subsequent ulceration or gangrene may develop. Lymph nodes proximal
to the bite become enlarged and tender. There is bruising of overlying tissues and lymphangitis.
Tenderness along the Hunter’s canal is often noted, over the bitten lower limb. Because of edema
of muscles and bleeding there is development of compartment syndrome characterized by swelling,
pain on full passive movement, tenderness over affected muscles, hypoesthesia over the areas of
the nerve passing through the compartment. Ischemic damage is common if the snake injects
venom at tight compartments such as pulp space of digits or the anterior tibial compartments.
Absence of swelling 2 hours after the bite exclude, the envenoming or it may be a dry bite.
Systemic involvement
Haemorraghic manifestations -Acute bleeding is due to rapid development of DIC (Disseminated
Intravascular coagulation) due to consumption coagulaopathy due to conversion of procoagulant
to coagulant and
fibrinolysis, damage of
vascular endothelium and
p l a t e l e t
abnormalities10,19. Active
bleeding is seen within 30
minutes to few hours
from gums. Epistaxis
occurs, skin is
e c c h y m o s e d ,
subconjuctival
hemorrhages can occur.
These may be
h a e m a t u r i a ,
hematemesis, bleeding in
peritoneal cavity,
intracranial bleed and
active bleeding from
postpartum uterus, active
uncontrolled bleed from
wound, abrasion or
punctured site. Hence no
intramuscular injection
should be given to a viper
bite patient as it may
result in a big
haematoma. Epigastric
pain often precedes acute
bleeding.
Shock- Immediate shock is
due to sudden liberation of
bradykinin in the content of
viper venom with
angioedema and anaphylaxis
due to the venom.
Subsequent shock is due to
massive bleeding from
gums, bleeding in
peritoneum and from the
uterus. Intracranial bleeding
may occur.
Acute bleeding in the adrenal and pituitary gland may result in hypotension and hypoglycemia.
Haemorrhagic pituitary infarction results in hypogonadism, amenorrhea, Sheehan syndrome, of
loss of libido38.
Neuroparalysis- Ptosis gradually occurs within 6-8 hours and persists for one week. Paralysis
progresses to broken neck sign. Respiratory paralysis due to Russell’s viper bite in Maharashtra is
not often reported from Vidharbha region. Respiratory paralysis due to Russell’s viper is common
in southern part of India and Sri Lanka. Russell’ s venom causes presyanptic neuromuscular block
like krait venom and resistance to anticholinesterase. Artificial ventilatory support is required for
respiratory failure 19,39.
Table- 5-Neuroparalysis due to Russell’s viper envenoming
Age/sex month Bite To Snake 20WBCT Bite to ASV Recovery

Hospital Neuroparalysis ML In days
hours in hours
17 F September 2 RV + 3 100 3
27F September 2 RV + 4 100 3
30F September 4 RV + 4 100 3
40F September 2 RV + 2.5 100 Died of
renal failure
12 M October 2.5 RV + 2 100 4
32F September 2.5 RV + 2 100 7
Renal failure – The common cause of morbidity and mortality due to Russell’s viper bite is
acute renal failure. 20 - 40% hospitalized cases of Russell’s viper bite subsequently developed
anuria, oliguria and acute renal shut down within few hours to as late as 96 hours. Direct
nephrotoxic action of venom, heavy
proteinuria with red cell casts suggestive
of glomerular damage and glomerular
capillary fibrin deposition has been
reported following Russell’s viper bite.
In all snake bite cases close monitoring
of urine output should be strictly
observed so as to diagnose earlier or
impending renal failure. The foremost
sign of renal failure is bilateral tenderness
over renal angles. Many times vomiting,
anorexia is attributed to drug induced
gastritis by the newly posted medical
Recovery from haemahune Russell’s viper bite
officer and the victim is discharged if there is no active bleeding. Many such victims are readmitted
to other hospitals in acute renal failure19. Renal failure occurs due to the direct action of the
venom on renal tubules resulting in acute tubular necrosis, interstitial nephritis, patchy cortical
necrosis and hypovolemic pre-renal failure due to acute blood loss and hypotension. Early
administration of ASV, mannitol and diuretic may help to delay or prevent the acute renal failure.
In early phase of renal failure if urine output improves with 80-100 mg of frusemide, it indicates
minimum renal damage. Renal tissue responding to diuretics will further improve with slow
intravenous diuretic (frusemide or toresemide) drip. Early dialysis on the verge of impending
renal failure may salvage the kidney. Many times victims are reported in full blown case of renal
failure with generalized anasarca, raised serum potassium and blood urea and creatinine. Often
there is conjunctival edema accompanied by renal failure. There may be a capillary leak
syndrome10,40,41,42,43.
Table -6 Renal failure due to Russell’ viper envenoming
Age/sex Bite BP ASV Bite BUL S.Cre- Hb Dialysis Result
month To To RF atinine
Hospital In
Hours hours
40/F/Nov 2.5 80/60 150 30 176 8.6 7 NA* Fatal-3day
55/M/May 3 110/80 120 24 130 4.8 8 +++ Recovery
-3rd day
32/M/Sep. 3.5 150/90 170 24 107 5.33 5 +++ Fatal
-7th day
*Not available
Middle cerebral artery thrombosis with cerebral infarction, acute myocardial infarction and
ventricular tachycardia have been reported due to Russell’s viper bite 44,45,46,47.
20WBCT test –This is the most important simple gold standard bedside blood test. Before injecting
the ASV from the same vein puncture 2-3 ml of blood is withdrawn and added to a dry new glass
test tube (not washed or cleaned with detergent) kept undisturbed and observed after 20 minutes,
at the end of 20 minutes tipped of the blood, if the blood did not clot it confirms hypofibrinogenemia.
This test should not be repeated within 6 hours of the last dose of ASV administered, as the liver
takes six hours for synthesis of coagulant factors to be replaced into circulation. 20WBCT test
decides the further requirement of ASV. This is an important test for diagnosis and indicates
improvement48.
Management
Initially 100 ml of ASV must be administered on arrival in 5% dextrose over 30-40 minutes. If
external bleeding persists after 30-40 minutes of administration of ASV it is repeated. Another 50
ml of ASV added to 50-100 ml of 5% dextrose can be given over 24 hours by slow drip to
neutralize the venom absorbed from the bite site which acts as depot. However if the 20WBCT
shows non clotting blood, further dose of ASV may be added. In addition to this the victim may
require blood and blood

products transfusion,
renal dialysis and
ventilator support in case
of neuroparalysis, which
is rare. Local wound
care with early skin
grafting and mobility will
prevent subsequent
contractures and
debility.
Echis carinatus or saw scaled viper

The saw scaled viper is 1-3 feet long. Head of echis carinatus is sub-ovate with short rounded
snout. Body is cylindrical, short and stout. It has a large eye with vertical pupil. The tail is very
short. The Body is covered with rough, serrated flank scales and the neck is distinctly constricted.
Its color is pale brown, tawny with dark brown, brick red, gray or sand colored with zigzag patterns
on back. A cruciform or trident or arrowhead type or bird foot like print mark is seen on the head.
It is mainly nocturnal. The snake is mostly found in open dry, sandy, rocky plains and hills. It often
flourishes in heavy rainfall areas. It rests under the rocks, behind bark, at the base of thorny plants
during the day. It climbs well. It is often found on the warm road or path in night. Its prey is mice,
lizards, frogs, scorpions and insects. High incidence of saw scaled viper is seen in Deogad and
Ratanagiri district as there is a hot humid climate. It hibernates in the winter18. The quickness with
which it bites on smallest provocation with an extremely rapid strike makes it one of the most
dangerous snakes. It forms a double coil in the form of figure 8 with its head in the center in a
striking position (looks like chumbal a rough cloth with round folded cushion is kept below the
heavy pot on the head to support the head and scalp. Hence lay persons in Marathwada call it as
chumbal snake). The coils keep moving against each other and serrated keels on the flank scales
produce a hissing noise by friction. It is viviparous and produces 3-15 young ones at a time. It
injects 0.0046 grams of venom at the one strike.
Local manifestations
Soon after the envenoming within one hour the victims experience mild pain and swelling at the
bite site. Fangs marks or abrasions with clotted blood are seen and no active oozing of blood
occurs like that of Russell’s viper bite. Swelling gradually progresses to more than one segment.
The Echis Carinatus venom is of a bigger molecular size and is circulated by lymphatics, hence
within 60-120 minutes the victim experiences a painful regional lymphadenopathy. Untreated swelling
progresses to the whole limb or even to the chest wall. Ecchymoses are seen over the bitten part
or may spread over lymphatic drainage area. Acute bleeding from the gum margins or from abrasion
or old unhealed wound or from venepuncture site is seen within 90-120 minutes of the bite or may
be delayed by few hours to days.

At times the patient remains
untreated and bleeding persists in the
form of blood stained sputum,
haematuria and disappears without
any ASV. Such victims report a few
weeks later due to severe weakness,
severe anemia or non healing
cellulitis is with active blood oozing.
Natural immunity against the Echis
carinatus venom develops in a
cases of repeated bite by same
species in endemic areas with
minimum clinical involvement in
16
subsequent bite as reported in Jammu region . Renal failure due to echis bite is reported from
Pondicherry and Jammu areas and rarely from Maharashtra41, 49.
Management
The ASV requirement in the Maharashtra is 20-70 ml (average 50) ml19. However the requirement
is very high up to 420 ml in Pondicherry9. Prolonged defibrinating syndrome due to echis bite have
been reported 50,51. There is controversy regarding use of heparin or low molecular weight
heparin52,53. Other management is similar to Russell’ viper bite.
Green pit viper (Trimeresurus).

It is usually found in hill forest like
Mahabaleshwar, near sea level. It often
flourishes on low bushes, near stream edges.
Accidental bite occurs while plucking the
flowers or berries. Green pit viper cases are
reported from Kerala, characterized by local
edema and rarely systemic bleeding as the
venom has thrombin – like effects and may
cause defibrinating syndrome (54).
Coagulopathy and renal failure due to hump-nosed pit viper snake bite have been reported from
Kerala state which was previously thought to be a non- venomous snake.
Sea snakes
Sea snakes are seen allover the coastal region. Sea snake is accidentally handled by fishermen
during fishing. Its venom content includes neurotoxin, both myotoxic and hematotoxic. Soon after
the bite the victim develops headache, heaviness in tongue, sweating and vomiting. Within 30
minutes to 3.5 hours after envenoming there is generalized muscle pain, stiffness and marked
tenderness over the muscles. Trismus is common. Subsequently there is generalized and flaccid
paralysis. Myogobinuria appears within 30-38 hours of bite. Myoglobinuria and hyperkalaemia due
to venom damaged skeletal muscle causes renal failure. Hyerkalaemia causes tented T waves,
widened QRS, prolonged QTC and cardiac arrest.
Antivenin against the pit viper and sea snake is not available but routine polyvalent serum may be
administered.
Treatment of hyperkalemia
1. Intravenous calcium gluconate
2. Intravenous diuretics
3. Glucose –insulin drip (50ml 50% glucose and 50 units of plain insulin)
4. Salbutamol inhalers
5. Dialysis
What are reasons of high morbidity and mortality due to snake bite in India?
Delay in reporting due to attending mantrik or trantrik is one of the main reasons. Herbal
administration causes gastritis. Induction of forceful vomiting in case of neuroparalytic victims due
to elapid bite results in aspiration and death. Tight tourniquet may lead to necrosis and gangrene.
Absence of medical officers is another common problem. Failure to diagnose the early krait bite
(pain in abdomen, floor bed, unknown bite, ants or rat bite, minimum local signs).
Delay or failure to administer the ASV in adequate dose.
Non- availability of intubation facilities, non functional batteries or laryngoscope, ambu bag.
Failure of intubation by untrained medical officer.
Failure to closely monitor neurological, hemorrhagic and renal profile.
Non-availability of ventilator at rural hospital or non- functioning ventilator due to want of trained
doctors.
Prevention
Fire wood, dry cow dung, cattle shed and rubble should be kept away from residential area. Old
storage rubble particularly in an old
house should be handled in full
sunlight. Rubble in the attic should not
be handled blindly. Bare foot walking
in darkness, in grown grass should be
avoided or one should go out with a
torch and big stick so as to vibrate
the place before stepping. Proper care
of rats, mice and lizards must be
taken. No attempt should be made to
catch the snake or to kill it. Killed
snake should not be handled; even
sheared head of snake may inject
venom. Thick electrician rubber
gloves with rubber shoes should be worn at

the time of handling the Jowar (sorghum) or
paddy or sugarcane husk. Everybody should
sleep on a cot with mosquito net, which will
prevent snake, scorpion and mosquito bites
alike55.
45 year old man reported within 30 minutes of
cobra bite in conscious state to primary health
center. Medical officer noted bulbar palsy but
did not administer the anti snake venom and
victim was referred to rural hospital. Victim
died on way to hospital. Thus referring victim
with venomous envenoming without giving ASV to big hospital contributed to their death.
Training in appropriate use of antivenin and protocol of indications for its use should be arranged at
general hospital level. Mere history of snake bite should not be the indication for administration of
expensive and risky anti snake venom. ELISA test of venom detection should be prepared and
then monospecfic antivenom will be of much more use. Neuroparalytic victim should be given
semi-prone position to avoid aspiration till intubated.
Attempts should be made to prepare venomous snake toxoid to immunize the farmers against
venomous snake toxins in endemic areas. Many times ASV is in short supply, it can give rise to
severe life threatening anaphylaxis reaction, is expensive and needs natural resources (an animal,
laboratory) for its preparation. Toxicologists should make an attempt to synthesize the
pharmacological antidote to venom actions or should prepare a chemical receptors product so that
the venom might attack the external injected receptors and protect the natural receptors. Anti
venom producers in India should be encouraged to prepare antivenom from venoms obtained from
snakes caught from relevant areas of country, Regional snake park and snake venom banks should
be encouraged31.
Snake bite is a life threatening unnoticed sudden onset accident like earhquake in the family of
poor farmer or farm labourers. Young and earning member of farmer family is prone to this
accident. Victim should be provided all possible help (money, transfer and treatment) and facilities
whatever required saving his life at private or government hospital. It is our moral duty to save the
honest sons of soil.
The attending doctor gets immense satisfaction when the serious poor victim of snake
bite recovers. Scorpion and Snake envenoming should be included in graduate and post
graduate medical training.
References
1. Warrell DA. The clinical management of snake bite in southeast Asian region. Southeast
Asian J.Tropical Medicine and public health.1999;30:1-84.
2. Gutierrez JM, Theakston RDG and Warrell DA. Comforting the neglected problem of snake
bite envenoming : The need for a global partnership. PLOS Medicine 2006;3:0727-31.
3. Rabies and envenoming: a neglected Public Health Issue. Report of consultative meeting
WHO 10th January 2007 :3-11.
4. Punde DP. Management of snake bite in rural Maharashtra: A 10 - year experience. The
National Medical J Of India. 2005;18:71-5.
5. Menon JM, Joseph JK and Kulkarni K. Over view of snake bite in India (personal
communication).
6. Borron SW, Chase PB and Walter FG. Elapidae: North American and selected non-native
species. Biological toxins. 2006; 26-34.
7. Mathew JL. Snake –bite Pediatrics today 1999;11:36-44.
8. Warrell DA. Injuries, envenoming, poisoning, and allergic reactions caused by animals. Oxford
text book of Medicine 2006. Chapt 8.2 in 4th edition Page 923-46.
9. Vijeth SR, Dutta TK, Shahapurkar J and Sahai A. Dose and frequency of anti-snake venom
injection in treatment of Echis cainatus (saw scaled viper) bite. JAPI 2000;48:187-9.
10. Win M, Phillips RE, Pe-Tun, Warrell DA, Swe TN and Lay MM. Bites by Russell’s viper in
Burma : haemostatic, vascular and renal disturbances and response to treatment. Lancet
1985;1259-64.
11. Bawaskar HS and Bawaskar PH. Envenoming by the common krait (bungarus caeruleus)
and Asian cobra (naja naja) : Clinical manifestations and their management in a rural setting.
Wilderness and environmental medicine.2004; 15:257-66.
12. Bawaskar HS and Bawaskar PH. Snake bite, cocktails, and a girl with stomach ache. Lancet
2008;371:696.
13. Dixon RW and Haris JB. Nerve terminal damage by beta Bungarotoxin. American Journal of
Pathology.1999;154:447-54.
14. Bawaskar HS. Snake bite poisoning. Chap 59 in Medicine update.
15. Macfarlane RG. Russell’s viper venom 1934-64. Br.J.Haematol 1967;13:437-51
16. Bhat RN. Viperine snake bite poisoning in Jammu. J Ind. Med. Assoc. 1974;63:383-91.
17. Wuster W. The cobras of the genus Naja In India. Hamadryad 1998;2315-32.
18. Romulus Whitaker and captain Ashok. Snakes of India. The field guide. reprinted 2008.
19. Bawaskar HS, Bawaskar PH, Punde DP. Inamdar MK, Dongar RB and Bhoite RR. Profile
of snake bite envenoming in rural Maharashtra, India. JAPI 2008;56:88-95.
20. Achyuthan KC and Ramchandran L. Cardiotoxin of the Indian Cobra (Naja naja) is a
Pyrophosphate. J.biosci.1982;3:149-56.
21. Bawaskar HS and Bawaskar PH. Snake bite (a clinical observations) Bombay Hospital Journal.
1992; 34:190-94.
22. Banerjee RN. Poisonous snakes and their venoms, symptomatology and treatment. Progress
in Clinical medicine, second series, Ahuja MMS (editor) India :1978 Heinemann pp 136-79.
23. Theakston RDG, Phillips RE, Warrell DA Galagedera Y, Abeysekera DTDJ, Dissanayaka P,
de siva A and Aloysius DJ. Envenoming by the common krait (bungarus caeruleus) and
Sri Lankan cobra (Naja naja) : Efficacy and complications of therapy with Haffkine antivenom.
Trans.Roy.Soc. Trop.Med.Hyg 1990;84:301-8.
24. Watt G, Theakston RDG, Hayes C, Yambao ML Sangalang R, Raoa CP, Alquizalas E and
Warrell DA. Positive response to endrophonium in patients with neurotoxic envenoming by
cobras naja naja Philippinesis) NEJM 1986;315:1444-8.
25. Amin MR, Mamun SMH, Chowdhury NH, Rahman M, Ghose AL, Hasan A and faiz MA.
Consecutive bites on two persons by the same cobra: a case report. J VAT and TS 2008;
14:725-37.
26. Agarwal R, Singh and Gupta D. Is the patient brain-dead? Emergency Medicine 2006;
23: 23-25
27. Premawardhena AP, de Silva CE, Fonseka MMD, Gunatilake SB and de Silva HD. Low dose
subcutaneous adrenaline to prevent acute adverse reactions to antivenom serum in people
bitten by snakes: randomized placebo controlled trial. BMJ 1999;318: 1041-43.
28. Banerjee RN, Aahni AL, Chacko KA and Kumar V. Neostigmine in the treatment of elapidae
bite. API 1972;20:503-9.
29. Pande AK, Singh AN and Sinha BN. Neostigmine in the neuroparalytic effects of snake bite
JIMA 1979;73:86-88.
30. Warrell DA, Looarressuwan S, White N, Theakston RDG, Warrell MJ, Kosakaran W and
Reid HA. Severe neurotoxic envenoming by the Malayan krait Bungarus candidus (Linnaeus)
: response to antivenom and anticholinesterase. BMJ 1983;286:678-80.
31. Bawaskar HS and Bawaskar PH. Profile of snakebite envenoming in western Maharashtra,
India. Roy.SOC.Trop.Med,Hyg.2002;96:79-84
32. Kularatne SANM. Common krait (bungarus caeruleus) bite in Anuradhapura, Sri Lanka : a
prospective clinical study 1996-98. Postgraduate medical journal 2002;78:276-80.
33. Prakash S, Mathew C and Bhagat S locked in syndrome in snake bite. JAPI.2008;56: 121-3.
34. Harish R, Digra SK. Sanke bite neurotoxicity : Reversal after 84 hours. Indian Pediatrics
2007;44:233.
35. Agarwal R, Aggarwal AN, Gupta D. Elapid snakebite as a cause of severe hypertension. The
J. Emer. Med.2006;30:319-20.
36. Laothong c, Sitprija V. decreased parasympathetic activities in Malayan krait (bungarus
candidus) envenoming. Toxicon 2001;39:1353-7.
37. Sutherland SK, Coulter AR and Harris RD. Rationalization of first-aid measures for elapid
snakebite. Lancet 1979; i:183-86.
38. PE- T, Warrell DA, Swe N, Phillips RE, Moore RA and Lwin M. Acute and chronic pituitary
failure resembling Sheehan’s syndrome following bites by Russell’s viper in Burma. Lancet
1987;ii:763-7.
39. Kulatane SAM. Epidemiology and clinical picture of the Russell’s viper bite in Anuradhapuram,
Sri Lanka: a prospective study of 336 patients. Southeast Asian J Trop. Med. public
health.2003;34:855-62.
40. Athappan G, Balaji MV, Navaneethan U and Thirumalikolundusubramanian P. Acute Renal

failure in snake envenomation: a large prospective study. Saudi journal of Kidney disease and
Transplantation 2008;19:40-10.
41. Chugh KS. Snake –bite –induced acute renal failure in India. Kidney International.1989;35;
891-07.
42. Soe P. Russell’s viper bite: Correlation of different clinical criteria to peritoneal dialysis and
clinical outcome. Regional health forum.2005;9:37-42.
43. Sitprija V. Extra capillary proliferate glomerulonephritis in Russell’s viper bite. BMJ.1980;1417.
44. Maheshwari M, Mittal Sr. Acute myocardial infarction complicating snake bite. JAPI.2004;
52;63-4.
45. Saadesh a. Case report; Acute myocardial infarction complicating a viper bite.
AM.J.Trop.Med.Hyg 2001;64:280-2.
46. Hoskote SS, Iyer VR, Kothari VM, Sanghvi DA. Bilateral anterior cerebral artery infarction
following viper bite JAPI.2009;57:67-69.
47. Thewjitcharoen Y, Poopitaya. Ventricular tachycardia, a rare manifestation of Russell’s viper
bite : case report. J.med.assoc.Thai. 2005;88:1931-33.
48. San-Martins IS, fan HW, Castro SCB, Tomy SC, Franca FOS, Jorge MT, Kamiguti As, Warrell
Da, Theakston RDG and BIASG. Reliability of the simple 20 minute whole blood clotting test
920WBCT) as an indicator of low plasma fibrinogen concentration in patients envenomed by
bothrops snakes. Toxicon 1994;32:1045-50.
49- Kak GA, Kumar SK, Tak SI, Hassan G, Wadhawa MB. Acute renal failure following echis
carinatus envenomation. Indian J.Nephrol 2004;14: 177-81.
50. Jacob J. Viper bite with continuous drfibrination despite adequate treatment with
antivenom.JAPI 2006;54:733-34.
51. Reid HA. Prolonged defibrination syndrome after bite by carpet Echis carinatus. BMJ 1977;
126-27.
52. Paul V, Udoor A, Earali J, John B, Kumar A and Anthony T. Trial of low molecular weight
heparin in the treatment of Viper bites. JAPI 2007;55:338-42.
53. Paul v, Prahld, Earali J, Francis S and Lewis F. Trial of Heparin in viper bites. JAPI.2003;
51:163-66.
54. Roinuckrin P, Intraquimtornchai T, Sattapiboon R, Muanpasitporn C,Pakmanee N,khow O,
Swasdikul D. The effects of green pt viper venom on the fibrinolytic system in human.
Toxicon;1999;37:743-55.
55. Bawaskar HS and Bawaskar PH. Malaria vaccine (letter). Lancet.1996;348:1329.
Scorpion Sting
Scorpion envenomation is a public health problem in tropical and subtropical countries,
especially in Africa, Middle East, Latin America and India. At times it poses a significant
life threatening acute time limiting cardiovascular emergency. Irrespective of different
species of scorpion similar cardiovascular effects are reported. Scientists working on
this problem have tried to understand the pathophysiology of severe scorpion sting by
various investigations including, neurotransmitter study, radioisotope study,
echocardiography, haemodynamic pattern and clinical manifestations. Various regimen
including vasodilators, antivenin, platelet activating inhibitors, inotropic support, and
metabolic rectifier such as insulin and L-carnitine have been tried. Irrespective of the
understanding of detailed pathophysiology and its management, the fatality remains high
in rural areas due to non-approachable medical facilities and faith in village healers which
delays hospitalization. Scorpion envenoming has been underestimated as this problem
is faced by the majority of underdeveloped and developing countries. Moreover the
medical attendee from poor countries may not be aware of western line of treatment of
scorpion sting. Since the advent of prazosin therapy the fatality is dropped to <1% from
29%. Recently addition of scorpion antivenom within 1-2 hours of envenoming has
hastened the recovery as compared to prazosin alone.
Introduction
Scorpion envenomation is a public health problem, common in certain areas of the world including
Middle East, Latin America, Africa and India 1,2,3. Mesobuthus Tamulus (Indian red scorpion)
scorpion venom is a potent sodium channel activator 4. The clinical manifestations of scorpion
envenomation appear to be secondary to activation of both the sympathetic and parasympathetic
nervous system. In 2/3rd of victims, the main clinical manifestations of scorpion sting are local
severe excruciating pain only, which radiates along with corresponding dermatomes accompanied
by mild edema and local sweating at
the site of sting. Systemic
manifestations (vomiting, sweating,
salivation, cold extremities, priapism
hyper or hypotension, brady or
tachycardia and ventricular premature
beats or at times non-sustained
ventricular tachycardia) are not
uncommon due to envenoming by the
lethal scorpion species Mesobuthius
tamulus, Leiurus quinquestriatus,
Androctonus mauretanicus, Buthus
occitanus, Centruroides,A
crassicauda, Tityus zulianus Tityus
serrulatus1,3,4. Similar cardiovascular Geographical distribution of venomous scorpions
manifestations have been reported irrespective of different species of scorpion4. Morbidity and
mortality due to scorpion sting is related to acute pulmonary edema, cardiogenic shock and multi
organ failure. 434 cases were studied during ten years period at the national guard hospital in
Riyadh. They showed 92% had local pain, 25.6% had systemic involvement. Hypertension was
seen in 17%, Tachycardia in 4% cases5. We from Western Maharashtra reported 526 cases
studied between 1984-1991, of these 236 (45%) had hypertension, 27(5%) had hypertension with
pulmonary edema, 139(27%) had pulmonary edema, 96(27%) demonstrated tachycardia and 28(5%)
died. Similar report has been obtained from Israel 6. 13223 cases were recorded in the Ministry of
Health in Colina state of Mexico in the year 2000-2001, of these 49% had a mild clinical, 33.8%
had moderate and 17% had severe manifestations, children are more in severe group 7. Tityus
Zulianus scorpion found in the Merida state, Venezuela. It was reported that children had high
fatality 8. 13 out of 78 cases died due to scorpion sting a report from Mahad region9. At rural
hospitals from western Maharashtra, India, 3546 scorpion sting cases reported in one year of
these 542 had systemic involvement10. Similar report has been received from Pondicherry, Andhra
Pradesh and Karnataka states of India10.11.12. Opinions differ regarding correct treatment of scorpion
envenomation7.
Recently WHO reported that the truth of scorpion sting envenoming is not known because many
cases do not seek medical attention. Moreover scorpion envenoming accidents occur in villages of
tropical and subtropical countries and in many countries including India it was not a notifiable
disease hence actual statistical data is scarce, moreover majority of victims go to the village
healers or tantriks or quacks and remain unregistered. It has been estimated that there are
approximately 1 million stings per year. In Mexico alone, 250000 scorpion stings are reported
yearly, in Tunisia 40000 stings, 1000 hospital admissions and 100 deaths are reported each year.
There is a high incidence in other parts of North Africa, the Middle East Iran, India13, and Latin
America. In Khuzestan, Southwest Iran, scorpion stings is the fourth leading cause of death
attributed to Hemi scorpion lepturus14. In Brazil 37000 scorpion stings and 50 deaths were reported
in 200513. This incidence indicates envenoming by scorpion sting is an important, yet neglected,
health issue in affected parts of world13. Scientists are more keen on treating reporting and studying
the snake bite than scorpion envenoming. However the clinical research done in tropical countries
is often neglected by health authority and unfortunately yet there is no consensus regarding
management of scorpion sting similar to snake bite (WHO personal communication).
Scorpion antivenin is widely used in many countries such as Brazil, Saudi Arabia, Mexico, India
15,16,17,18,19, 20,21,22,13,24,25,26. The acceptance of scorpion antivenin as an effective treatment in
scorpion sting and is based mainly on its efficacy in experimental studies. Scorpion antivenin is no
better than placebo as reported from Tunisia, Israel (23, 24). The beneficial effects of antivenin in
protecting victims against severe scorpion sting are still questionable 27,28,29.
Scorpion
Scorpions have been recognized by a sting with severe excruciating pain which is long lasting but
rarely a threat to the life. They are one of the oldest known terrestrial arthropods. Fossils of
scorpions found in Paleozoic strata 430 million year old appear very similar to the present species30.
They have been able to survive heat, drought, can withstand freezing conditions for weeks, desert
conditions and starvation for months, total immersion in water for days, this remarkable power of
adaptation, makes them independent of ecological condition and gives the species an unbroken
continuity. They are strictly carnivorous, feeding for the most part on insects. Scorpions are viviparous
and give birth directly to young ones and sometimes the mother tries to eat the young, but more
often, the young ones nibble the mother to death (cannibalism)31. Scorpions belong to venomous
arthropods in the class Arachnida. Scorpions take shelter under bark of trees, dry firewood or cow
dung, in the piles of bricks, paddy husk, beddings, loose tiles of huts at times in the shoe left empty
over night and in pockets of trousers and shirt, carvings, crevices of window and doors. In a
tropical country the sparrow
usually brings small scorpion
along with the dried grass to
build a nest over the window
of a pucca concrete house.
Farmers and farm labourers
are often stung by the scorpion
during handling of paddy husk,
harvesting grass over bund in
the months of September to
November 3,32 . Traveler’s
while walking barefoot in the
desert are more prone to these
painful life threatening
accidents.
There are around 1400 species of scorpions but only 46-50 of these are potentially lethal to humans33.
Lethal species belongs to Androctonus (Morocco and Senegal eastwards to India, Buthus
(Mediterranean, middle East and east Africa), Hottentotta (northern Africa and middle east),
Leiurus (East Africa and Middle East), parabuthus (Sudan to south Africa), Mesobuthus (India,
Southern and central Asia), Tityus (south America), Centruoides (USA, Mexico, and central
America). Hemiscorpion lepturus ( family scorpiodae) is a dangerous species seen in Iran.
Palmaneus garvimanus a cactoid species scorpion is of bigger size as compared to other species
black in color and it causes severe pain with mild sweating 3,33
Venom
Tail end of the scorpion contains two telson glands which actively secret the venom at the time of
sting which is injected into the prey by sharp stinger. All scorpion species secret venom. Venom is
a mixture of various active substances, of these, neurotoxins are the most important34. Neurotoxins
consist of different small size proteins with sodium and potassium cations which interfere with the
neurotransmitters in the victim. Venom action on neurotransmitter is rapid and fast. It contains a
peptide neurotoxin that opens the Na + channels (B–toxin). Sodium is primarily an extra cellular
ion maintaining electric voltage difference across the cell membrane. The Scorpion venom depolarizes
the cell membrane, in addition it also inhibits the deactivation of Na+ channels (alpha- toxin).
There is massive release of endogenous catecholamine into the circulation due to delayed inactivation
of sodium neuronal channel by the venom4. Thus venom of the Mesobuthus Tamulus (an Indian
red scorpion), Buthus Martensi (Chinese scorpion) and Leiurus Quinquestriatius (Israel scorpion)
causes autonomic storm by stimulating both sympathetic and parasympathetic nervous system.
Charybdotoxine another component of the venom inhibits the calcium dependent K+ channels,
similarly iberiotoxin isolated from Mesobuthus Tamulus has similar action on K + channels35,36.
The venom of leiurus
species includes chlorotoxin
which acts on Chloride —
channels. Scorpion venom
also contains serotonin,
which causes local pain at
the site of sting. The venom
of Tityus species a
kallikrenin inhibitor causes
raised bradykinin37. Venom
of Tityus Serrulatus from
Trinidad is pancreotoxic
responsible for development
of acute pancreatitis. Hemi
scorpion leptirus is the most
dangerous scorpion of
Khuzestan, south west, hot and humid province of Iran 13. Venom causes severe local tissue
necrosis, renal failure and cardio respiratory arrest13.
Scorpion sting - Clinical Features

• Local pain without systemic involvement is benign
• Vomiting, sweating, salivation, priapism in male, cold extremities suggestive of autonomic
storm. Needs close monitoring
• Hypertension, hypotension, bradycardia , tachycardia, ventricular entopic and acute
myocardial infarction like pattern seen in ECG
• Pulmonary edema, hypotension and tachycardia with respiratory failure seen within 30
minute to 10 hours of sting
• Massive life threatening pulmonary edema needs rapid intervention
• Tachycardia >125 per minute with warm extremities, with or without pulmonary edema
with cadaver pallor with convulsions suggestive of poor prognosis.
Clinical manifestations
Clinical effects of the envenoming depend upon the species of scorpion and dose of venom injected
at the time of sting. The severity of envenoming is related to age, size of the scorpion and season.
High incidence of pulmonary edema and fatality is seen in the month June, September and October
3,9,38 .
Irrespective of different species with few exceptions (Iran and Trinidad) the cardiovascular
manifestations due to envenoming are similar1,3,6,17,24,39. The early or premonitory clinical
manifestations as result of autonomic storm are characterized by vomiting 34%, profuse sweating
allover body 45%, priapism in males 28%, cold extremities 71% and mild tolerable pain which
becomes severe. When extremities become warm it is a sign of recovery 40.
On the basis of clinical presentations or course the hospitalized patients may be

1. Severe local pain only or grade I
2. systemic involvement
Local pain or grade I – severe excruciating pain is the only clinical manifestation seen in 35% of
cases. In 57%, 33%, 11% cases lower, upper extremities and other parts of the body are the site
of sting respectively. Severe pain radiates along the corresponding dermatomes. Due to intolerable
pain, inconsolable crying in a child which is of sudden onset is a diagnostic sign (especially in
darkness when one can not find the culprit). Children are confused and anxious due to pain. Local
edema, urticaria, fasciculation and spasm of underlying muscles are seen at the site of sting due
persistent stimulation of pain conducting receptors and liberated serotonin29,30. Due to pain there is
transient bradycardia, transient rise in blood pressure and mild sweating but extremities are warm3.
Sudden tap at the site of sting induces severe pain and sudden withdrawal of the part is diagnostic
of scorpion sting called TAP sign.
Systemic manifestations
All cases have premonitory signs and
symptoms of autonomic storm.Clinical
manifestations depend upon time lapse
between sting and hospitalization or
treatment received at periphery 32 .
According to clinical manifestations they
are divided into grades II, III and IV. All
cases had initial sign and symptoms
suggestive of autonomic storm 3.
Grade II – Profuse sweating,
hypertension or transient hypotension,
Tachycardia, bradycardia, premature
ventricular ectopics, and cold extremities.
Grade III – hypertension, hypotension, tachycardia and pulmonary edema or Massive pulmonary
edema, respiratory failure.
Grade IV- tachycardia, hypotension, pulmonary edema with warm extremities called warm shock.
Hypertension
45% of victims with systemic involvement have raised blood pressure soon after the sting. Blood
pressure ranges between 140/90 to 180/130 mm Hg. Children look agitated confused and have
propped up eyes and puffy face38. Hypertension is noted in the victim. It has been reported 15
minutes to 11 hours after the sting. Majority of the cases have headache, chest discomfort, and
perioral pareasthesia.
Transient initial hypotension is due to dehydration caused by excessive sweating, salivation and
vomiting which is further aggravated by hot

climatic condition of tropical and subtropical
countries, while post adrenergic
hypotension (24 to 36) hours is due to
depletion of catecholamine due to over
stimulated alpha-1 receptors 32,41,42.
Pulmonary edema
Pulmonary edema occurs in 27-30% cases,
with respiratory failure. Pulmonary edema
develops within 30 minutes to maximum
10 hours after the sting. 8 % cases are
reported with an acute life threatening
massive pulmonary edema. Rapid onset of pulmonary edema within two hours of envenoming is
often accompanied by severe hypertension. Parasternal sustained systolic lift due to sudden rise in
pulmonary pressure with right ventricular after load occurs3,32. Sudden onset of breathlessness,
intractable cough, poor peripheral oxygenation, ice cool extremities, tachycardia with low volume
thready pulse are present. Central cyanosis, bilateral moist rales heard all over chest, with loud
summation gallops and transient systolic murmur with mitral valve incompetence auscultation over
pre-cordium are the other signs. Intractable cough, with massive expectoration of blood mixed
froth from mouth and nostril, with central cyanosis, hypo or hypertension and loud death rattle
sounds heard few feet away from the patient are suggestive of massive pulmonary edema43.
Victims reported late i.e. after 6-10 hours had persistence pulmonary edema or if treated by
peripheral doctors with excessive intravenous fluids, steroids, antihistamines, atropine diuretics
such victims develop hypotension, tachycardia, air hunger. Prolonged poor tissue circulation with
accumulation of anoxic metabolites in the circulation resulted in paralysis of capillary sphincter
(vasodilatation) and cadaver like appearance. Patients are irritable, disoriented with or without
pulmonary edema suggestive of warm shock44,45,46.
58% who reported within 8 hours of
sting had heart rate 110-200 (mean
143) per minute with mean blood
pressure 60-113 (mean 85) with cold
extremities with or without pulmonary
edema, 42% cases reported later with
marked tachycardia 140-200 (mean
165) with hypotension systolic blood
pressure 50-90 mm Hg with warm
extremities with or without pulmonary
edema (warm shock) 46 .
Reappearance of local pain at the site
of sting which is mild or absent on
arrival is suggestive of recovery40. Hemiplegia, cerebral edema, disseminated intravascular

coagulation, due to scorpion sting have been reported. Fatality is high once neurological complications
such as coma, convulsions, miosis, mydriasis occur47,48,51,49,50,51,52.
Abdominal pain, nausea, vomiting common signs and symptoms of scorpion envenomation in older
children and adults were also attributed to acute pancreatitis with raised level of plasma immunoactive
cationic trypsin seen due to envenoming by Tityus Trinitatatis and Leiurus Quinquestritus53 and
uncommon due to Mesobuthus Tamulus envenoming. Scorpion envenoming rarely causes acute
renal failure. However ill-treated, delayed reporting of a case may result in death due to multi-
organs failure54.
Investigations
Leukocytosis 11,000- 26,000 per/cu.mm
Increased in troponin 1 and other cardiac enzymes
Raised interleukin, tumor necrosis factor, platelet activating factor. Renin, angiotensin II,
55,56,57
and urinary and serum catecholamine levels .
X- Ray chest - showed typical picture of pulmonary edema with batwing appearance. At
times unilateral distribution of pulmonary edema with air bronchogram and
17,44,58
cardiomegaly .
Electrocardiogram (ECG) - ECG is the most important diagnostic and easily available tool in
rural setting. Not a single victim with systemic involvement had normal ECG. Sinus bradycardia
was seen in early hypertensive cases with heart rate of 42- 60 per minute which persisted for 3-4
hours, ventricular premature contraction, couplets, transient runs of ventricular tachycardia and
rarely fatal lethal ventricular arrhythmias, sinus tachycardia, injury to conducting system in the
form of left anterior hemiblock, right bundle branch block, left bundle branch block, complete heart
block, marked tented T waves mimicking an acute myocardial infarction pattern, ST elevated with
non Q wave infarction pattern, PQRST alternans have been reported. Subsequent broad wide
base with round top T wave suggestive of delayed depolarization with prolonged QTc 450 – 650
Ms accompanied with asymptomatic bradycardia and hypotension was observed 36 -48 hours of
hospitalization and persisted for next five days. T wave inversion persists for more than four
weeks. Despite good clinical condition of the victim, ECG showed marked changes 59,60,61,62,63,64.
Echocardiography changes - showed poor global contractility 12-15 hours after the sting, with low
ejection fraction, decreased systolic left ventricular performance and mitral incompetence. Abnormal
diastolic filling persisted for 5 days to four weeks. Diminished or hypokinetic left ventricular global
movement with decreased systolic function was seen in a scintigraphic study. But
echocardiographically there is good correlation between clinical improvement and the return of the
left ventricular wall motion towards normal58,60,61,62.
Haemodynamics-It is difficult to perform haemodymic study in severely ill scorpion sting case.
Karnad DR from India studied the haemodynamic pattern in a patient with Mesobuthus tamulus
envenoming from western Maharashtra India. He reported that mild envenomation causes severe
vasoconstriction and hypertension while predominant left ventricular dysfunction with normal
systemic vascular resistance with pulmonary edema is seen in severe scorpion sting, however
severe hypotension depends upon the fluid balance. While hypotension and shock with warm
extremities occurs terminally due to biventricular dysfunction and terminal vasodilatation (warm
shock). Similar haemodymic pattern has been reported from Tunisia, Brazil and Israel48,64,65,66,67,68.
Pathophysiology
Delayed inactivation of neuronal sodium channels results in acute autonomic storm. Sudden liberation
of endogenous catecholamine resulted in initial transient rise in blood pressure, bradycardia and
increased vascular resistance. Alpha-1 receptor stimulation plays an important part in the pathogenesis
of acute pulmonary edema due to scorpion sting69. Accumulation of Calcium in the heart is caused
by the action of a liberated catecholamine resulting in increased requirement of oxygen to
myocardium with systolic and diastolic dysfunction63,69. There is also experimental evidence of
impaired coronary perfusion70. In addition to this coronary circulation is further compromised due
to raised level of renin and angiotensin II. There is no significant evidence of direct effects of
venom on the myocardium71. Reversible cardiomyopathy is attributed to catecholamines67,72,73.
Pulmonary edema is due to myocardial dysfunction. However acute lung injury pattern or adult
respiratory distress like syndrome attributed to secretory or non cardiogenic pulmonary edema has
been reported from Brazil16. Myocardial and lung parenchyma injury is due to raised level of
interleukin 6, tumor necrosis factor and kallikrenin and platelet activating factors37.
Histopathology study showed accumulation of fluid in the alveoli and contraction band necrosis in
the myocardium and hyaline membrane in the lung in a fatal scorpion sting case74,75. The
pathophysiology, clinical and histological pattern is similar to that of a patient suffering from
pheochromocytoma41,76.
On the basis of pathophysiology the therapeutic effort should be directed against the clinical
manifestations of the over stimulated autonomic nervous system and after effects of excessive
catecholamine and correction of hypovolemia43,65,77,79.
Scorpion sting - Management

• If victim reports within hour of sting with autonomic storm if available scorpion antivenin
in dose of 30 to 100 ml to be administered by intravenous route. After one hour it has
negligible action to neutralize the venom. Even after giving antivenin victim should be
closely monitored for possibility of development of pulmonary edema.
• Oral prazosin 250 microgram in children below 5 year and 500 microgram above five
year to be administered every three hour interval till extremities are cold.
• Single dose of 20-30 mg frusemide, aminophylline , oxygen, in addition to prazosin to be
given to pulmonary edema case .
• Intravenous sodium nitroprusside 3 -10 microgram/kg / minute or nitroglycerine drip 5
microgram per minute raised to 15 microgram per minute in case of massive pulmonary
edema.
• Dobutamine 5-15 microgram / kg / min in case of warm shock
• BiPaP or non-invasive ventilator is useful for refractory pulmonary edema with
respiratory failure.
Scorpion Sting - Management

• Repeat xylocaine for local pain to be avoided local pain can be well managed with oral
NSAID, Diazepam and local cold therapy.
• Atropine, steroids digoxin, antihistamines and excessive diuretic to be avoided
Search strategy and selection criteria
We are studying and treating scorpion sting cases since 1977 till today. We have collection
of articles from request reprints obtained from authors since 1977, before electronic media.
Extensive search made by scorpion sting, pulmonary edema, catecholamine on pub med and
Google.
Management
Scorpion sting is an unnoticed sudden onset accident. Majority of victims are healthy before the
sting. There is sudden onset myocardial injury with normal sized heart and liberated free fatty
acids, increased myocardial contraction where digoxin is no more beneficial46. While excessive
diuretics are hazardous80, reduction of preload by applying rotating tourniquet to periphery did help
in three out of four victims of severe scorpion sting with pulmonary edema 81.
Alpha blocking properties of chlorpromazine-one of the constituents of lytic cocktail is responsible
in reducing the fatality in children, however out of 100 children with severe scorpion sting treated
with lytic-cocktail 22 died as stated in a report from Pondicherry, India. Pethidine and antihistamine
(promethazine) enhances the venom toxicity and should be avoided in scorpion sting82. Insulin
therapy was advocated by Waterman from Trinidad in 193883. Inotropic support is required in
admitted patients with scorpion sting in a intensive care unit irrespective of treatment with insulin
glucose drip84. Recently Gupta V from India reported hypoglycemia in 30%,pulmonary edema in
40% and fatality in 35% victims of scorpion sting given insulin glucose drip, while in prazosin
treated group fatality was
6.2% 85 . Negative inotropic
effects of calcium channel
blocker (nifedipine) and beta-
blocker enhances myocardial
failure86. Steroids enhance the
necrotizing effects of circulating
catecholamine and should be
avoided in scorpion sting
victims 87,88 . Antihistamines
inhibit calcium dependent
potassium channels like that of
Scorpion venom action and
should be
avoided38, 89.
In experimental pharmacokinetic studies with radioactively labeled scorpion venom given

intravenously, it was observed that the half life of venom distribution and its excretion were 5.6
minutes and 6.4 hours respectively90. Other similar studies using antivenin showed that the half life
of distribution was 1-9 hours with the result of these studies, it is concluded that antivenin therapy
was inefficient because no interaction could occur between scorpion toxin and antitoxin, justified
the use of prazosin and dobutamine91. IgG distribution half life was tenfold longer than that of
venom which was short (32 min). In comparison to immunoglobins, venom distributes fast and
achieves greater concentration with a shorter time needed to achieve its maximum concentration71.
Severe clinical manifestations due to scorpion sting are alleviated in victim if the antivenin is given
within one hour of sting92. However delayed administration of scorpion antivenin did not prevent
pulmonary edema93. All the ten cases had severe cardiovascular manifestations, irrespective of
administration of scorpion antivenin. Of these 5 recovered with prazosin and four required inotropic
support and one died (a report from western Maharashtra India)94. The persistence of signs and
symptoms of envenoming after neutralization of circulating venom could be explained by the inability
of antivenin to neutralize scorpion toxins bound to their receptors on the sodium channel95. A
number of specific scorpion antivenins are available but their efficacy is uncertain. Ancillary
treatment with vasodilators is crucial in severely envenomed patients78. Administration of scorpion
antivenin after one hour of sting did not prevent the development of pulmonary edema8,27 and
cerebral edema, cardiac arrest.
Captopril, angiotensin converting enzyme inhibitor did help to alleviate the diuretic induced pulmonary
edema in Scorpion sting80. Though the result of captopril therapy is similar to other vasodilators, an
author reported 5 deaths out of 38 studied cases treated in intensive care unit in tertiary care
hospital80.
In retrospective study of scorpion sting cases, Rajasekhar D et al from cardiology department
from Andhra Pradesh reported the use of L-carnitine to reverse myocardial dysfunction following
scorpion envenomation especially in patients with hypotension and severe LV dysfunction95.
Aprotinin was advocated in the
treatment of pulmonary
edema to inhibit the platelet
activating factor 95 . Recent
study by Mangano DT et al
confirmed that aprotinin is not
free from toxicity and can
result in acute renal failure,
strokes and myocardial
infarction 97. Moreover it is
expensive, not easily available
and can cause severe
anaphylaxis.
Prazosin, a post-synaptic
alpha blocker, reduces preload, causes left ventricular impendence without raising heart rate. It
reverses the metabolic syndrome evoked due to excessive catecholamines86,87. Prazosin is a
pharmacological and physiological antidote to venom action98,99. Three victims developed severe
pulmonary edema irrespective of 5 ampoules of scorpion antivenin and recovered with oral prazosin,
according to a recent report from Saudi Arabia28. Similar observations are reported from Tunisia98.
Morbidity and mortality depend upon the time lapsed between sting and administration of prazosin,
since the advent of prazosin the fatality is reduced to 1%41. Massive life threatening pulmonary
edema is due to severe hypertension or delayed reporting of victim to health center or if the
attending doctor fails to administer prazosin or inadequate dose of prazosin (which is advocated
three hourly intervals) or giving excessive diuretics, IV fluids, atropine, steroids and antihistamines.
These cases should be treated with intravenous nitroglycerine or sodium nitroprusside drip. 7-10%
pediatric cases developed marked tachycardia, hypotension with warm extremities called “warm
shock”. This necessitates dobutamine drip45,47,99.
Many toxins from scorpion venoms activate sodium channels, thereby enhancing neurotransmitter
release. On this basis, Fantail et al in experimental study showed beneficial effects of intravenous
lidocaine, a sodium channel blocker100.
Seven young patients admitted with history of scorpion sting presented with pulmonary edema
which was successfully managed with positive pressure ventilation with PEEP, cardiac support
with inotropic and fluid balance, a report from Nepal101.
Thus management strategy for severe scorpion sting depends upon the understanding of patho-
physiology and proper diagnosis of clinical manifestations and their rational and timely interventions
with appropriate therapeutic agents.
Scorpion antivenin is available for clinical use. Scorpion venom is a potent neuronal sodium channel
activator resulting in transient cholinergic (vomiting, sweating, salivation, priapism, ventricular ectopic
and bradycardia) and prolonged sympathetic (hypertension, tachycardia, cold extremities, pulmonary
edema, hypotension, shock or warm extremities with pulmonary edema and death) stimulation.
Ongoing cholinergic phenomenon is suggestive of free circulating scorpion venom, which can be
neutralized by antivenin. While sympathetic stimulation suggests after effects and fatality due to
sympathetic over activity. We treated 30 cases of severe scorpion sting with scorpion anti venom
30-50 ml and oral prazosin. We found that if the victim reported earlier, within 1-2 hours of sting
the recovery time in a group treated with scorpion antivenin and prazosin is shorter than the cases
treated with prazosin alone. But the cost of one ampoule of scorpion antivenin is more than Rs.350
and at times 100 ml (10Ampoules) of antivenin is advocated. While one mg prazosin cost is Rs 32
for ten tablets. Prazosin is easily available while scorpion antivenin is often in short supply as its
preparation involves natural resources including scorpion, horse and laboratory with scientists.
References
1. Ismail M. The scorpion envenoming syndrome. Toxicon 1995, 33:825-58.
2. Gueron M, Ilia R and Sofer S. The cardiovascular system after scorpion envenomation :A
review. Clinical Toxicology; 1992, 30:245-58.
3. Bawaskar HS. Diagnostic cardiac premonitory sings and symptoms of red scorpion sting
Lancet 1982; ii: 552-54.
4. Gwee MCE, Nirtthanan S, Khoo H, Gopalkrishnakone P, Kini Mr,Cheah LS. Autonomic effects
of some scorpion venoms and toxins.Clinical experimental pharmacology and physiology 2002;
29:795-801.
5. Dittrich K, Power AP and smith NA. Scorpion sting syndrome – A ten year experience.
http:// www.kfshrc.edu.sa/annals/152/94139ar.html.
6. Gueron M, llia R and sofer S. the cardiovascuilar system after scorpion envenomation:a review.
Clinical toxicology 1992,30(2),245-258
7. Chowell G, Diaz-duenas P, Bustos-saldana, Mireles AA and Fet v. Epidemiological and clinical
characteristics of scorpionism in Colina, mexico (2000-2001) toxicon 2006:1-6.
8. Mazzei de Davila CA, Davila DF, Donis JH, de Bellabarba AD, Villarreal V and Barboza JS.
Sympathetic nervous system activation, antivenin administration and cardiovascular
manifestations of scorpion envenomation. Toxicon 2002;40:1339-46.
9. Mundle PM. Scorpion sting. BMJ 1961 1042.
10. Bawaskar HS and Bawaskar PH. Peripheral doctors form backbone for management of
acute life threatening medical emergency evoked due to envenoming by Indian Red scorpion:
Mesobuthus tamulus. Bombay Hospital Journal 1997;39:71014.
11. DAS S, Nalini P,Ananthakrishnan S, Sethuraman KR et al cardiac involvement and scorpion
envenomation in children. J. Trop. O Peditr 1995;41:338-40.
12. Mahadevan S. Scorpion sting. Indian peditr. 2000;37:504-14.
13. WHO. Rabies and envenoming : a neglected public health issue. Report of a consultative
th
meeting WHO Geneva 10 January 2007 Page 1-32.
14. Pipelzadeh MH, Jalali A, Tarz M, Pourabhaa s R and zaremirakabadi A. An epidemiological
and clinical survey of scporpionism Iranian scorpion Hescorpion Leptus. Toxicon 2007;
50:984-92.
16. De-Rezende NL, dias MM, Campolina d, Olortegui CC, Diniz CR and Amaral CFS. Efficacy
of antivenom therapy for neutralizing circulating venom antigen in patients stung by tityus
serrulatus scorpion. The Amer.J.Trop.Med.Hyg. 1995; 52:277080.
16. Amral CFS, De-rezende NV, and Freire-Maia. acute pulmonaryedema after Tityus serrulatus
scorpion sting in children. Amer.J.Cardiol 1993;71:242-45.
17. Mahaba HM, Sayed SE. Scorpion sting, is it a health problem in Saudi Arabia? Evaluation of
management of 620 cases. Saudi Medical Journal 1996;17:315-21.
18. Ismail M. The treatment of the scorpion envenoming syndrome: the Saudi experience with
serotherapy. Toxicon 1994;32:1019-26.
19. Ghalim N, El-Hafny B, Sebti F, Heikel J, Lazar N,Moustanir R and Benslimane A.. Scorpion
envenomation and serotherapy in Morocco. Am.J. Trop. Med. Hyg. 2000;62(2):277-83.
20. El-gawad Abd TA, Ibrahim HMM, El-sahrigy SAF, Sherif HA. Study of cardiac changes in
Egyptian children with scorpion envenomation before and after antivenin. J.Medical Sciences.
2006;6:1033-38.
21. Dehesa –davila M and Possani LD. Scorpionism and serotherapy in México. Toxicon
1994;32:1015-18.
22. Mazzei de Davila C, Davila DF, Donis DJ et al sympathetic nervous system activation, antivenin
administration and cardiovascular manifestations of scorpion envenomation. Toxicon
2002;40:1339-46.
23. Abroug F, Elatrous S, Nouira S, Hagiuga H, Touzi N, Bouchoucha S.. Serotherapy in scorpion
envenomation; A randomized controlled trial. Lancet 1999;359:906-9.
24. Sofer S, Shahak E and Gueron M. scorpion envenomation and antivenin therapy. J. pediatr
1994;124:973-8.
25. Al-asmari AK and Al-saif AA. Scorpion sting syndrome in general hospital in Saudi Arabia.
Saudi. Med. J. 2004;25:64-70.
26. Bawaskar HS and Bawaskar PH. Utility of scorpion antivenin Vs Prazosin in the management
of severe Mesobuthus tamulus (Indian red scorpion) envenoming at rural setting.
J.asso.Pysicians India 2007;55:14-21.
27. White J, Warrell DA, eddlestom M, Currie BJ, Wyte IM and Isbister GK. Clinical Toxicology
–Where are we now?. Clinical toxicology 2003;41:263-76.
28. Al-asmari AK, Al-seif AA, Hassen MA and Abdulmakssod NA. role of Prazosin on
cardiovascular manifestations and pulmonary edema following severe scorpion sting in Saudi
Arabia. Saudi Med. J. 2008;29 : 1296-99.
29. Bawaskar HS and Bawaskar PH. Treatment of cardiovascular manifestations of human
scorpion envenoming : is serotherapy essential? J.Trop.med.and Hyg 1991;94:156-58.
30. Scorpions. http: //www.kingsnake.com/toxinology/old/archnid/scorpions.html
31. Deoras PJ. A study of scorpions. Probe 1961;1:45-54.
32. Bawaskar HS and Bawaskar PH. Sting by red scorpions ( Buthotus tamulus) in Maharashtra
stae, india : a clinical study. Trans.Rpy.soc.trop.med.hyg 1989; 83:858-60.
33. Bawaskar HS and Bawaskar PH. Scorpion sting : Review of 121 cases. Journal Wilderness
Medicine 1991;2:164 - 74.
34. Cruz NAV, Batista CV, Zamudio FZ, Bosmans F, Tytgat J and Possani LD. Phaiodotoxin, a
novel structural class of insect –toxin isolated from the venom of the Mexican scorpion
Anuroctonus Phaiodactylus. Eur. J. Biochem 2004;271:4753-61.
35. Xu CQ, Brone B, Wicher D, Bozkurt O etal BMBKTx1,a vovel Ca+ activated K+ channel
blocker purified from the Asian scorpion N Buthus martensi Karsch. J. biological chemistry;
2004;279:34562-69.
36. Pedarzani P, D’hoedt D, Doorty KB, Wadsworth JDF, Joseph JS etal Tamapin, a venom
peptide from the Indian red scorpion ( Mesobuthus tamulus) that target small conductance
Ca+ activated K+ channels and afterhyperpolarization current in central neurons. J.Biochemical
Chemistry 2002;277:46101-109.
37. Sofer S, Gueron M, White RM, Lifshitz M and apte RN. Interleukin -6 release following
scorpion sting in children. Toxicon 1996;34:489-92.
38. Bawaskar HS and Bawaskar PH. cardiovascular manifestations of severe scorpion sting in
India( review of 34 children). Annal trop.Peditr1991;11:381-87.
39. Bawaskar HS and Bawaskar PH. Management of the cardiovascular manifestations of
poisoning by the Indian red scorpion (mesobuthus tamulus). British Heart.J 1992; 68:478-80
40. Bawaskar HS and Bawasakar PH. Prazosin for vasodilator treatment of acute pulmonary
edema due to scorpion sting. Annals of Trop. Med. Parasitol. 1987;81:719-23.
41. Mcmanus BM, Fleury TA and Roberts WC. Fatal catecholamine crisis in pheochromocytoma:
curable causes of cardiac arrest. Amer.Heart J 1881:930-33.
42. Kobal SL, Paran E, Jamaili A, Mizrahi S, Siegel RJ and Leor j. Pheochromocytoma: cyclic
attacks of hypertension alternating with hypotension. Nature 2008;5:53-57.
43. Bawaskar HS and Bawaskar PH.(1986). Prazosin in management of cardiovascular
manifestations of scorpion sting. Lancet;ii:510-11.
44. Bawaskar HS and Bawaskar PH. Indian red scorpion envenoming. Indian J.Pediatr
1998;65:383-91.
45. Bawaskar Hs and Bawaskar PH. Clinical profile of severe scorpion envenomation in children
at rural setting. Indian pediatrics2003;40:1072-81.
46. Karnad DR. haemodynamic pattern in patients with scorpion envenomation. Heart 1998;
79 : 485-89.
47. Sira - Devi C, Reddy CN, Devi SL, etal. Defibrination syndrome due to scorpion venom
poisoning. BMJ1970,I: 345-47.
48. Bisarya BN, Vasa vada JP, Bhatt A, Nair PNR and Sharma VK. Hemiplegia and myocarditis
following scorpion bite Indian heart J 1977;29:97-100.
49. Kothari UR, Shah SS, Doshi HV and Vasa NT. Myocarditis from scorpion sting :a clinical and
electrocardiographic study of 50 cases. Indian Heart J 1976;28:88-92.
50. Jammihal JH, Srinivas HV. Hemiplegia following scorpion sting. Indian Peditr1972;X:337-38.
51. Udayakumar N, Jendiran C and Srinivasan AV. Cerebrovascular manifestations in scorpion
sting :a case series. Indain J. Med.Sci 2006;60: 243-44.
52. Bahloul M, Rekik N, Chabchoub I, Chaari A etal. Neurological complications secondary to
severe scorpion envenomation. Med. Sci. Monit. 2005;11:cr196-202.
53. Sofer S, Shalev H, weizman Z, Shahak E and Gueron M. Acute Pancreatitis in children
following envenomation by the yellow scorpion Leiurus quinquestriatus. Toxicon 1991;
29:125-28.
54. Krkic. Dautovics S, Begovic B. Acute renal insufficiency and toxic hepatitis following scorpion
sting. Med. Arh 2007;61:123-4.
55. Meki AR, Mohamed ZM, Mohey EL-deen NM. Significant of assessment of serum cardiac
troponin 1 and interleukin-8 in scorpion envenomed children. Toxicon 2003;41:129-37.
56. Gueron M, Iliaa R, Shahak E and Sofer s. rennin and aldosterone levels and hypertension
following envenomation in humans by the yellow scorpion Leiurus quinquestriarus.
Toxicon;1992;30:765-67
57. Gueron M, Weizman S Catecholamines and myocardial damage in scorpion sting. American
Heart J. 1968;25:716-17.
58. Rahav G, Weiss T. scorpion sting induced pulmonary edema (scintigraphic evidence of cardiac
dysfunction) Chest 1990;97:1478-80.
59. Gueron M, stern J and Cohen W. severe myocardial damage and heart failure in scorpion
sting. Ame. J.Cardiol 1967;19:719-26.
60. Amaral CFS, Lopes JG, magalhaes RA and de-rezende N. Electrocardigraphic. enzymatic
and echocardiographic evidence of myocardial damage after Tityus serrulatus scorpion
poisoning. Amer.J.Cardiol 1991;67:655-57.
61. Diaz p, Chowell G, Ceja G, Anuria TCD, Lioyd RC and Chavez Cc. pediatric electrocardiograph
abnormalities following centruoides limpidus tecomanus scorpion envenomation. Toxicon
2004; 1-5
62. Sharifkazemi MB, Rezeaian GR, zamirian M and Hashemi SAR. Prolonged atrio-ventricular
block following scorpion bite: a case report. IJMS. 2003;28:96-97.
63. Gueron M and Margulis G and Sofer s. Echocardiographic and radionuclide angiographic
observations following scorpion envenomation by Leiurus quinquestriatus. Toxicon
1990;28:1005-9.
64. Poon-king T. myocarditis from scorpion sting BMJ;1963:374-77.
65. Sofer S Scorpion envenomation (editorial) intensive care medicine 1995;21:626-28.
66. Nouira S, Abroug F, Haguiga H, Jaafoura M, Boujdaria R and Bouchoucha S. Right ventricular
dysfunction following severe scorpion envenomation. Chest 1995;108:682-87
67. Kumar S, Hamdani AA,and Shimy NE. scorpion venom cardiomyopathy. Ame. Heart
j.1992;123:725-29.
68. Hearing SE, Jurca M, Vichi FL Azevedo-Marques MM and Cupo P. reversible cardiomypathy
in patients withsevere scorpion envenoming by Tityus serrulatus : evolution of enzymatic,
electrocardiographic and echocardiographic alterations. Ann.Trop.Paediatr. 1993;13:173-82
69. Frire –Maia L and campos JA. Pathophysiology and treatment of scorpion poisoning. In natural
toxins edited by Ownby C and Odell G. pergamon press 1989; 1-159.
70. Margulis G, sofer s, zalstein E, Zunker E, Zunker R, Ilia R and gueron M. abnormal coronary
perfusion in experimental scorpion envenomation. Toxicon 1994;32: 1675-78
71. Abroug F, nouria S, Atrous SE et al. A canine study of immunotherapy in scorpion envenomation.
Intensive care med 2003;29:2266-76.
72. Spall HGV, Robert JD,Sawka AM,Swallow CJ and Mak S. Not a broken heart. Lancet
2007;370:628
73. Wittstein IS. Apical –Ballooning syndrome Lancet 2007;370:545-47
74. Benvenuti LA, Dpouetts KV and Cardoso JLC. Myocardial necrosis after envenomation by
the scorpion tityus serrulatus. Trans.roy.soc.trop.med.hyg 2002;96:275-75.- Reddy CRRM
and Suvarnakumar. pathophysilogy of scorpion venom poisoning. J.Trop.Med.Hyg 1972;75:98-
100.
76. Gueto L, Arriaga J and zinser J. Echocardiographic changes in pheochromocytoma. Chest
1979;76:600-01.78-
77. Warrell DA. Venomous bites and stings. Saudi Arabia. Saudi Medical Journal 1993; 14:196-
01.
78. Krishnan A Sonawane RV and Karnad DR. Captopril in the treatment of cardiovascular
manifestations of Indian red scorpion(Mesobuthus tamulus) envenomation. J.Assoc.Physician.
India 2007; 55:2226.
79. Bawaskar HS and Bawaskar PH. Role of atropine in management of cardiovascular
manifestations of scorpion envenoming in humans. J.Trop.med and Hyg. 19992;95:30-35.
80. Karnad DR, Deo AM, Apte N, Lohe AS, Thatte S and Tilve GH. Captopril for correcting
diuretic induced hypotension in pulmonary edema after scorpion sting.BMJ 1989; 293:1430-1.
81. Bawaskar HS. Scorpion sting and cardiovascular complications. Indian heart J1977; 29:228.
82. Mahadevan S, chudhury P, Puri RK and Srinivasan S. Scorpion envenomation and the role of
lytic cocktail in its management. Indian J. Pediatr 1981;48:757-61.
83. Waterman JA. Some notes on scorpion poisoning in Trinidad. TransRroy.Soc.Trop.Med.Hyg
1938. 31:607-24.
84. Murthy KRK (1991). Insulin reverses hemodynamic changes and pulmonary edema in children
stung by the Indian red scorpion mesobuthus tamulus concanesis,pocock.

Annal.Trop.Med.parasitol 1991.;85:651-7
85. Gupta V. Prazosin: a pharmacological antidote for scorpion envenomation.. J.Trop.Pediatr
2006.;52:150-1.
86. Bawaskar HS and Bawaskar PH. severe envenoming by the Indian red scorpion Mesobuthus
tamulus; the use of parzosin therapy. QJM 1996;89:701-4.
87. Raab W. Key position of catecholamines in functional and degenerative cardiovascular
pathology. Amer.J.Cardiol 1960;5:571-78.
88. Abroug F, Nouira S, Haguiga H et al randomized clinical trial of high dose hydrocortisone
hemisuccinate in scorpion envenomation. Ann Emerg. Med 1997;30;245-58.
89. Rankin AC.Non-sedating antihistamines and cardiac arrhythmias. Lancet 1997;350:1115-16.
90. Ismail M, Abdullah ME, Morad A, Ageel AM. Pharmacokinetics of 125I-labelled venom from
the scorpion androctonus amoreixi (and&sar). Toxicon 1980; 18:301-08.
91. Ismail M, Shibl AM, Morad AM, Abdullah ME. Pharmacokinetics of 125I-labelled antivenin
to the venom from scorpion androctonus amoreuxi.Toxicon 1983;21:47-56.
92. Ghalim N, El-Hafny B, Sebti F, Heikel J, Lazar N,Moustanir R and Benslimane A. Scorpion
envenomation and serotherapy in Morocco. Am.J.trop. Med.hyg 2000.;62(2):277-83.
93. Ismail M. The treatment of the scorpion envenoming syndrome : The Saudi experience with
serotherapy. Toxicon 1994;32:1019-26.
94. Patil SN, Dhavalikar S, Khedekar a. Role of 2D-echocardiography in scorpion sting (2007).
http://www.swamisamarth.com
95. Rajesekar D and Mohan A. Clinical and echocardiographic findings in patients with myocardial
toxicity due to scorpion sting. National Medical Journal 2004;17:207-9
96. Pande R and Deshpande SB. Protecuve effects of aprotinin on respiratory and cardiac
abnormalities induced by Mesobuthus tamulus venom in adult rat. Toxicon 2004;44:201-5.
97. Mangano DT, Tudor IC and Dietzel C. The risk associated with aprotinin in cardiac surgery
2006. New.Eng.J.Med; 354:353-65
98. Koseoglu Z, Koseoglu A. Use of prazosin in the treatment of scorpion envenomation.
Amer.J.Therap 2006;13:285-87.
99. Bawaskar HS and Bawaskar Ph. Vasodilators : scorpion envenoming and the heart ( an
Indian experience ) Toxicon;32:1031-40.
100. Fatani AJ, Harvey AL, furman BL and Rowan EG. The effects of lignocaine on actions of the
venom from the yellow scorpion”leiurus quinquestriatus’ in vivo and vitro. Toxicon 2000;
38:1767-01.
101. Bhadani UK, Tripathi M, Sharma S, Pandey R. scorpion sting envenomation presenting with
pulmonary edema in adults: a report of seven cases from Nephal. Indian J.Med.Sci.2000;
60:19-23.
102. Boyer LV, Theodorou A, Berg RA and Mallie J. Antivenom for critically ill children with
neurotoxicity from scorpion sting. New.Eng.J.med. 2009;360:2090-8.
103. Sofer S, Bawaskar HS and Gueron M. Antivenom for Critically Ill Children with Neurotoxicity
from Scorpion Stings. NEJM (inpress)
Brief resume
Dr. H. S. Bawaskar, MD
Bawaskar Hospital and Research Center Mahad,

Dist. Raigad, Maharashtra, India.
Phone : 02145 222398 • Cell : 9422594794
E-mail : himmatbawaskar@rediffmail.com
RESEARCH
Published >50 papers in national and international journals The Lancet, Heart, Tropical
Doctor, Transaction of Royal Society, Tropical Medicine, JAPI, Q.J.Med. Toxicon,
etc. on Scorpion sting, Snake bite, Hypothyroidism, Acute Myocardial Infarction,
Chloroquine toxicity; HIV, BCG vaccine, etc.
Contributed Chapter in Medicine Update.
Contributed Complete chapter on Scorpion sting in the 7th EDITION API TEXT
BOOK OF MEDICINE 2003.
Written a Book - SCORPION STING published by popular Prakashan Mumbai.
Trained >30,000 peripheral doctors on management of Scorpion sting in rural areas
Invited as Guest speaker for discussion at the meeting on Scorpion envenoming

held in London in 1993. Guest speaker at various national conferences, IMA
conferences and CME.
Mortality due scorpion sting is reduced to <1% which was >45% all over
Maharashtra.
Dr. Bawasker’s research on treatment of severe scorpion sting with the help of
Prazosin is of importance. The death rate due severe scorpion sting is reduced to
<1% (which was >6% before his research). He managed the cases without use of
scorpion antivenom which is expensive, needs laboratory, animals and not free from
severe anaphylaxis reactions. His research is helpful to not only India but also all over
tropical and subtropical countries like Israel, Trinidad, Brazil, Saudi Arabia, Turkey,
etc.
Dear Doctor,
It has been our endeavour to provide the medical fraternity, the latest thinking on a variety of
8
medical topics, a tradition that we have been following for over 60 years through out Quarterly
Medical Reviews.
This booklet is presented to you by Raptakos Brett, & Co. Ltd.
We would very much like to have your valuable suggestions and comments to make our future
issues more meaningful to you.
We will appreciate if you could spend a few minutes to fill in your comments and mail the same
to us.
Thanking You,
General Manager (Medical)
General Manager
FEED BACK Oct. - Dec. 2009
General Manager (Medical)

RAPTAKOS, BRETT & CO. LTD.
Dr. Annie Besant Road, Worli,
Munbai 400 030.

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Management of Snake bite and

1. Snake bite .................................................................................................................. 4

2. Scorpion Sting .......................................................................................................... 26

Published and Issued by

RAPTAKOS, BRETT & CO. LTD., WORLI, MUMBAI 400 030.

Management of Snake bite and

Cobra -0.2 gram of the dry weight of lypolized venom.

Lethal dose of these venoms for man has been reported

One ml of polyvalent antivenin neutralized

islands 17 . Most adult cobra measure 100-150 cm,

Systemic involvement Open toilet – risk factor for snake bite

Showing cobra bite to snake catcher.

Table- 5-Neuroparalysis due to Russell’s viper envenoming

Age/sex month Bite To Snake 20WBCT Bite to ASV Recovery

require blood and blood

Echis carinatus or saw scaled viper

be delayed by few hours to days.

Green pit viper (Trimeresurus).

gloves with rubber shoes should be worn at

40. Athappan G, Balaji MV, Navaneethan U and Thirumalikolundusubramanian P. Acute Renal

Scorpion sting - Clinical Features

On the basis of clinical presentations or course the hospitalized patients may be

vomiting which is further aggravated by hot

arrival is suggestive of recovery40. Hemiplegia, cerebral edema, disseminated intravascular

Scorpion sting - Management

Scorpion Sting - Management

In experimental pharmacokinetic studies with radioactively labeled scorpion venom given

stung by the Indian red scorpion mesobuthus tamulus concanesis,pocock.

Bawaskar Hospital and Research Center Mahad,

Contributed Chapter in Medicine Update.

Written a Book - SCORPION STING published by popular Prakashan Mumbai.

Trained >30,000 peripheral doctors on management of Scorpion sting in rural areas

Invited as Guest speaker for discussion at the meeting on Scorpion envenoming

FEED BACK Oct. - Dec. 2009

General Manager (Medical)

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