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Bawaskar Hospital and Clinical Research Center, Mahad, Raigad, Maharashtra, India
March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
6 Bawaskar and Bawaskar: Snake bite poisoning
multipurpose enzyme fluid (venom) that flow at the months with high morbidity and fatality. Snake is cold
time of envenoming through fine channeled or grooved blooded animal. Darker the snake, it secretes more
teeth called fangs. Venom secretion in all venomous venom as compared to a light colored. Because of the
snakes appears to vary in seasons; more in warmer rise in body temperature of dark skin (poor conductor
Journal of Mahatma Gandhi Institute of Medical Sciences March 2015 | Vol 20 | Issue 1
Bawaskar and Bawaskar: Snake bite poisoning 7
Cobra venom
Cobra venom is of smaller molecular size and rapidly
absorbed into circulation. Absorption is further
e accelerated by threat of death, running and hence the
liberated catecholamine and running due to fear can
kill the victim within 8 min. Cobras unlike the krait
deposit its venom deeply. This in combination with
hyaluronidase allows spreading of the venom to occur
rapidly and symptoms to arise abruptly. Interestingly,
this rapidity of onset of symptoms prompts the rural
victim in India to seek care quickly after cobra
f g bite.[9] Severe, irreparable local tissue is lost at the
Figure 1: Different types of snakes, (a) and (b) Cobra, (c) and (d) krait, (e) bite site of cobra envenoming due to myocytolysis.
Russells Viper, (f) and (g) is saw scaled viper and its fangs Cobra venom is rich in postsynaptic neurotoxins
called alpha-bungarotoxin and cobratoxin. Cobra
of heat) snake, the venom is in more fluid state and venom binds especially to Ach receptors, prevents
injected rapidly with high speed and maximum the interaction between Ach and receptors on
quantity in a short time during envenoming. As oppose postsynaptic membrane result in neuromuscular
to light colored skin because of low body temperature, blockade. Cardio- toxin content of cobra venom has
the venom is thick and hence less amount is injected at direct action on skeletal, cardiac, smooth muscles,
the time of envenoming.[8] nerves and neuromuscular junction causes paralysis,
circulatory, respiratory failure, cardiac arrhythmias,
It is quite clear that snake venom is not a substance various heart block and cardiac arrest because
evolved to attack man or any big vertebrates. Snake can the venom releases calcium ions from the surface
bite and continue to secrete venom a number of times membrane to the myocardium.
in succession. Most snakes inject 10% of the available
venom in a single strike except the Russells viper which Common Indian krait (Bungarus caeruleus)
injects 75% of stored venom in one bite due to big long (Local names Kala gandait, kala taro, kandar,
sharp curved fangs.[7] At times snake only bite without manyar, chitti, kattu viriyan, valla pamboo)
envenoming called as defence bite or dry bite ;while the Common Indian krait venom contains both presynaptic
bite with envenoming is called as the professional bite. beta bungarotoxin and alpha bungarotoxin. These
toxins initially release Ach at the nerve endings,
Venom is a cocktail of 20 or more components at neuromuscular junction and then damage it
including proteins, enzymes, nonenzymatic subsequently preventing the release of Ach. Irrespective
polypeptide toxins, nontoxic nerve growth factors, of Krait, its venom is 10 times more lethal than cobra.
March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
8 Bawaskar and Bawaskar: Snake bite poisoning
But unfortunately unlike as in cobra bite, the victim endoplasmic reticulum, and separation of intracellular
reports too late due to delayed clinical manifestations. junction of the endothelial cells. Local loss of basement
Krait is nocturnal in habit. Its fangs are small size like membrane of the vessels leads to capillary leaking
that of insulin needle. It injects the venom into skin syndrome and a resistant shock [Table 3].[14-16,18]
or skin deep. It accidentally bites a person sleeping on
floor bed.[8,10-12] Though venom is of small molecular Management of Snake Bite
size it is absorbed slowly as skin has poor circulation
and reflexes are blunted during sleep.[11] Neuromuscular First aid (to be given at the time when bite
blockade by the short chain neurotoxin (cobra toxin, occurs)
alpha bungarotoxin) is more readily reversible than 1. If one can locate the bite site, remove the surface
with a long chain toxin (beta bungarotoxin). Beta deposited venom by clean cloth or cotton.
bungarotoxin in the krait venom bears similarity to 2. Keep the bitten part below heart level.
botulinum toxin.[6,9,13] Preserved tendon reflexes in 3. Crepe bandage from the distal end of the bite site
botulism differentiates it from krait bite. Krait venom with a pressure equal to that one can easily put and
has a great affinity towards presynaptic Ach receptors. remove the finger underneath the bandage.
Thus, the tissue having high concentration of this 4. One should not kill the time in search of the snake.
receptors are affected in the following order, such as If the snake is found or killed take it to hospital, it
sphincter pupillae, levator palpebral superioris, neck may help to doctor for diagnosis.
muscles, bulbar muscles, subsequently limbs and lastly 5. Victim should not be allowed to walk.
the diaphragm and intercostals muscles. Venom acts as 6. Do not incise at the site of the bite.
7. If the victim is found unconscious without
early as 30 min and till 18 h.[9] Envenoming by krait has
respiration, the relatives should start mouth to
an early phase profound paralysis which lasts for 30 to
mouth respiration and chest compressions.
60 minutes, followed by deep paralysis phase which
lasts for 2 to3 days and then recovery phase ranging
First response at the healthcare facility
from 2 to 3weeks.
(primary health center, hospital etc.)
1. History site of the bite, activity at the time of the
Viper (Russel viper)
bite, time of bite, visualization/recognition of the
Viper venom interferes with blood clotting. Venoms
snake.
contain serine proteases, metalloproteinases, C-type
2. Symptoms suggestive of neuromuscular palsy
lectins, disintegrins, and phospholipases, and it exhibits
(ptosis, respiratory difficulty, dysphagia, weakness
both anticoagulant and procoagulant effects on blood
of limbs, etc.) should be specifically asked for.
clotting mechanism resulting in defibrination syndrome 3. Initial clinical signs should be noted in detail such
or disseminated intravascular fibrino-coagulopathy.[14,15] as heart rate, blood pressure, respiratory rate,
Russells venom is a rich source of enzymes that activates one min counting test, oxygen saturation, bulbar
factor X to convert prothrombin to thrombin in presence palsy, muscle power, tendon reflexes, pooling of
of calcium factor V and platelets thus Russells venom saliva, broken neck sign. These signs to be closely
contains several different pro-coagulants which monitored every hour till clinical improvement.
activate different steps in the clotting cascade.[14-16] The Electrocardiogram should be recorded for
fibrinolytic activity of the viper venom is so fast that arrhythmias. Serum electrolytes and renal profile
sometimes within 30 min of the bite, the coagulation should be done.
factors are so depleted that blood does not clot. 4. Give injection tetanus toxoid to all patients provided
Russells venom activates the clotting system of the blood is clotted in 20WBCT.
snakes natural prey with such speed that Macfarlane 5. Intramuscular injection to be avoided in viper bite
a brilliant hematologist was left feeling it is almost envenoming may result in huge hematoma.
too clever to be true.[17] Haemorrhagins-1, 2and
metallo-endopeptidase causes acute rapid bleeding 20 Minutes Whole Blood Clotting Time
in brain, lungs, kidney, heart, and gastrointestinal
tract.[16,18] It causes severe vasoconstriction followed Before the injection of anti-snake-venom (ASV) take
by vasodilatation of the microvessels. Endothelial gaps 2-3 ml of patients blood in a new dry glass test tube
due to disintegration of the endothelial cells within which is not irrigated by any detergents. Keep the tube
intracellular edema, swollen mitochondria, dilated undisturbed for 20 minutes and then tip it off, if blood
Journal of Mahatma Gandhi Institute of Medical Sciences March 2015 | Vol 20 | Issue 1
Bawaskar and Bawaskar: Snake bite poisoning 9
March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
10 Bawaskar and Bawaskar: Snake bite poisoning
Journal of Mahatma Gandhi Institute of Medical Sciences March 2015 | Vol 20 | Issue 1
Bawaskar and Bawaskar: Snake bite poisoning 11
March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
12 Bawaskar and Bawaskar: Snake bite poisoning
hyperkalemia, one can try potassium channel drug grown up grass hence victim may feel injury by thorn
oral glibenclamide provided one takes care of prick and failure of administration of ASV on wrong
hypoglycemia. history result in many amputation of limb,..Thus a
farmer or labourer with rapid development of swelling
Russells viper or Daboia or viper Russell within one hour while walking bare feet in grown of
siamensis grass or bund, attributed to a thorn, is often a case of
One of the most common and dreaded complication of Echis bite envenoming.
Russells vipers bite is DIC, which can be diagnosed by
thrombocytopenia, abnormal crenated RBCs in peripheral Green pit viper and bamboo pit (Trimeresurus)
blood smear. In addition to ASV, one has to try plasma The polyvalent ASV available in India does not cover
products and whole blood transfusion which is rare for envenomation with these two vipers. However,
required if ASV is administered in time with an adequate empirical treatment with polyvalent venom should
dose. Hypotension can be managed with fluid and inotropic be offered as paraspecificity may sometimes help to
agents. Severe hypotension due to bleeding in adrenal alleviate the envenoming.[44]
and pituitary glands and abdominal bleed and endothelial
dysfunction with capillary leak may need heavy doses of When there is doubt regarding species of snake in
intravenous methylprednisolone.[4,6,7] One should keep in such situation, one can manage the case on syndromic
mind and look for renal failure from time of admission. approach.[45]
Risk factors such as hypotension, hypovolemia should be
corrected. There are lot of controversies regarding early Conclusion
introduction of diuretic, acetylcysteine or allopurinol in
renal failure. However, in our experience, intravenous Scientists should make attempts to prepare venomous
frusemide 80-100 mg and oral acetylcysteine 600 mg 3 toxoid to immunize the farmers and risky population
times a day may help to arrest the renal damage, but this against venomous snake toxins. Toxicologists should
needs a randomized controlled trial. In a situation of renal make an attempt to prepare the pharmacological
failure with raised serum potassium, it may be treated antidote to venom actions. Antivenom producers in
with frusemide drip at rural areas or peritoneal dialysis or India should prepare ELISA kit for detection of venom
referred to higher center for hemodialysis.[4,18] Irrespective antigen in blood and prepare antivenom from venoms
of the standard dose of ASV many victims develop renal obtained from snakes caught from relevant areas of the
failure. This is particularly reported from Marathwada country. The attending doctor gets immense satisfaction
region. Thus venom procured from this region should be when the serious poor victim of snake bite recovers.
used to prepare antivenom against Russell s viper which
kills many farmers, sugarcane labors and deserts many References
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March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
14 Bawaskar and Bawaskar: Snake bite poisoning
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threatening envenoming by the hump-nosed pit viper bite poisoning. J Mahatma Gandhi Inst Med Sci 2015;20:5-14.
(Hypnale hypnale) in India. Trans R Soc Trop Med Hyg
Source of Support: Nil, Conflict of Interest: None declared.
2007;101:85-90.
Journal of Mahatma Gandhi Institute of Medical Sciences March 2015 | Vol 20 | Issue 1