|The Management of Snakebites in Malaysia|
Prof. Tan, Nget Hong
Department of Molecular Medicine
Faculty of Medicine, University of Malaya
Kuala Lumpur, Malaysia
|Back to Home Page|
Snakebite is a serious medical problem in Malaysia. During the year
1958 to 1980, there were 55000 cases of snakebites recorded in the
hospitals in Malaysia. The mortality rate of snakebite in Malaysia is only
0.3 per 100000 population but the local necrotic effects of some venoms
can cause prolonged morbidity or even crippling deformity.
Venomous Snakes of Malaysia
In Malaysia and the coastal waters of the region, there are at
least 18 different species of venomous front fanged land snakes and more
than 22 different species of sea snakes. These venomous snakes belong to
the following 5 subfamilies:
represented by the two genera Calloselasma
represented by the five genera Naja,
Bungarus, Ophiophagus, Maticora and Calliophis;
represented by the genus Laticauda
represented by the six genera Enhydrina,
Kerilia, Hydrophis, Thalassophis, Pelamis and Kolpophis
represented by the only genus Aipysurus.
Crotalinae and Elapinae subfamilies are land snakes whereas the other
three subfamilies are sea snakes.
Only a few of the Malaysian venomous snakes can be regarded as of
medical importance. Epidemiological studies showed that in Malaysia, bites
were mainly due to four species of land snakes (Table 1): Calloselasma
rhodostoma (Malayan pit viper), Naja
naja (Asian common cobra), Trimeresurus
purpureomaculatus (shore pit viper) and Trimeresurus
wagleri (Wagler’s pit viper). Other venomous snakes indigenous to
Malaysia that are potentially dangerous to human include Bungarus candidus (Malayan krait), Bungarus fasciatus (banded krait), Ophiophagus hannah (king cobra), Trimeresurus sumatranus (Sumatran pit viper), Trimeresurus
albolabris (white-lipped pit viper) and the sea snakes.
Table 1: Snakebites in West
from monthly statistics of 28 hospitals throughout Malaysia, 1965-1971.
Biochemical composition of Snake Venoms
Dried snake venom contains mainly proteins (70-90%) and small
amounts of metals, amino acids, peptides, nucleotides, carbohydrates,
lipids and biogenic amines. The protein components include enzymes and
The main toxins in the venoms of elapid snakes (cobras, kraits and
sea snakes) include: polypeptide postsynaptic neurotoxins, cardiotoxins
and phospholipases A that may exhibit presynaptic neurotoxicity or
myotoxicity. The main toxins of crotalid (pit viper) snake venoms, on the
other hand, are thrombin-like enzymes, hemorrhagic proteases and
Elapid Venom Poisoning
Elapid venoms (cobras, kraits and sea snakes) generally exhibit neurotoxicity and cardiotoxicity. The earliest symptom of systemic elapid poisoning is a feeling of drowsiness or intoxication, which starts from 15 min to 5 hr after cobra bites. Difficulty in opening the eyes (bilateral ptosis: eyelids may remain completely closed though the patient usually remains conscious until respiratory failure is advanced), speaking, opening the mouth, moving the lips and in swallowing follows within 1 to 4 hrs. Breathing becomes increasingly difficult. In severe poisoning, respiratory failure sets in rapidly.
One week after a cobra bite. Subcutaneous necrosis in cobra bites is always more extensive than visible skin changes would suggest.
ptosis in elapid venom poisoning
The neurotoxic effects are mainly at the postsynaptic level of the
neuromuscular junction where the neurotoxins block acetylcholine
receptors, thereby producing muscular paralysis and respiratory failure.
The major neurotoxins are usually basic polypeptides.
Cardiotoxicity is caused by polypeptide cardiotoxin that affects
both excitable and non-excitable cells, causing irreversible
depolarization of the cell membrane and consequently impairing the
structure and function of various cells, thus contributing to muscle
paralysis and leading to circulatory and respiratory failure and systolic
Cobra venom also causes extensive local necrosis, which requires
treatment. The local necrosis is presumably caused by the combine action
of cardiotoxin and phospholipase A2.
Sea snake venoms contain both polypeptide neurotoxins (homologous to elapid neurotoxins) and myotoxins, which are basic phospholipase A2. The venom causes respiratory failure (neurotoxic effect), myonecrosis, myoglobinemia and acute renal failure.
Pit Viper Venom Poisoning
The venom of pit vipers causes local swelling, necrosis and
Swelling in Malayan pit viper bite Ecchymoses in Malayan pit viper bite
Blisters in Malayan pit viper bite Local necrosis in finger bite by Malayan pit viper
In Malayan pit viper bite, the clotting defect is primarily due to
thrombocytopenia aggravated by defibrination syndrome.
Thrombocytopenia is presumably due to the actions of platelet aggregation inducers. Aggregoserpentin, a non-enzymatic protein with molecular weight of 28160 has been purified, it activates platelets through the activation of endogenous phospholipase A2 or C. Anti-platelet protease may be also be involved.
Defibrination syndrome is
due mainly to the action of ancrod and partly to the activation of
fibrinolysis causing fibrinogenolysis. Ancrod is a thrombin-like enzyme
that acts directly on fibrinogen, releasing only fibrinopeptide A and
fibrin monomers that form microclots.
The microclots formed are easily lysed by plasmin digestion. Thus,
ancrod causes continual microcoagulation of fibronogen but the microclots
are virtually simultaneously lysed. In the presence of sufficient amount
of ancrod, the rate of consumption of fibrinogen may exceeed its rate of
synthesis in the liver, resulting in defibrination syndrome characterized
by non-clotting blood.
Right: Clot-quality observation test in systemic Malayan pit viper venom poisoning. This is a simple test useful for assessing defibrination and the severity of systemic poisoning. The clot quality is graded according to the size of the remaining clot, after 1 hour at room temperature.
Grade 1: Normal
Grade 2: Slight defect, clot size is slightly diminished.
Grade 3: Moderate defect, clot size is about half the size of a contracted normal clot
Grade 4: Severe defect, clot is only a small speck.
Death Times and Recovery Times
Generally speaking, deaths are most rapid after cobra bites and most protracted after viper bites:
In the absence of necrosis, pain after viper bites rarely exceeds 2
weeks. When necrosis develops (in about 10% of cases) pain may remain
severe for a month. Swelling usually resolves completely in 2-3 weeks.
Healing time of local necrotic lesions varies greatly according to the
extent of the lesion and the treatment given, but may requires 1-6 months
In patients who do not receive specific antivenin, systemic
symptoms generally subside more quickly than local symptoms. Neurotoxic
symptoms usually resolve in 2-3 days. Hemorrhagic effects in viper bites
are also short-lived and rarely exceed a week but the coagulation defect
may persist for 3-4 weeks.
First-Aid Measure in Snake Venom Poisoning
not panic and keep calm, reassure the individual as complete recovery is
the rule. Lie the patient down to ensure minimum activity
the bitten part at rest, immobilize the bitten limb with splints
bite with care because washing might disfigure or deface the original bite
marks. Do not attempt to cut the
wound and suck out the venom. This will introduce infection.
a broad and firm bandage to cover the bitten area using any flexible
material. Arterial tourniquets can be dangerous
patients with snake bites must be brought to the hospital for treatment
the snake has been killed, bring it to the hospital for identification.
8. Diagnosis of Snakebite Poisoning
Two major questions in the diagnosis of snakebite poisoning are:
the identity of the snake inflicting the bite and the severity of
of the snake if the patient brings the snake to the hospital
this is costly and can be performed only in a well-equipped laboratory.
Presently not available in Malaysian hospitals
observation and inquiring circumstances of bite:
viper venom poisoning is characterized by non-clotting blood and other hemorrhagic syndrome
accompanied by rapid local swelling after the bite
venom poisoning (due to cobras, kraits): characterized by neurotoxic effects including
ptosis, glossopharyngeal palsy, respiratory paresis and sometime cardiac
snake venom poisoning is characterized by myotoxic effects such as myaligia on moving,
paresis, myoglobinuria, hyperkalaemia.
Evaluation of severity of
In mild cases, there are minimal local signs, no swelling except in
immediate vicinity of the wound, no significant systemic symptoms,
no laboratory abnormalities.
In severe cases, pain is great, swelling is massive.
9. Management Principles in Snake Venom Poisoning
General management of snakebite
General management of snakebite poisoning includes the following
Antivenom is the only specific treatment for snake venom poisoning
that is of proved value. If used correctly, it can reverse systemic
poisoning even when given hours and even days after the bite. However, it
should not be given routinely in all cases of snakebite because it is very
expensive and can cause reactions. Antivenom, however, is generally
ineffective in preventing or lessening local effects of snake venom
Monospecific (monovalent) antivenoms are more effective and less
likely to cause reactions than polyspecific (polyvalent) antivenoms.
At present, however, monospecific antivenoms are available only
against the three common types of Malaysian poisonous snakes (anti-Malayan
pit viper, anti-Malayan cobra and anti-Enhydrina schistosa). Some
commercially available polyvalent antivenoms (in particular, polyvalent Trimeresurus
antivenom and polyvalent Elapid antivenom from National Institite of
Preventive Medicine, Taiwan, R.O.C.) may be useful for the treatment of
snake venom poisoning caused by other Malaysian poisonous snakes. However,
these have not been evaluated clinically.
Early (anaphylactic), pyrogenic and late (serum sickness) reactions
can occur after antivenom treatment. Reported incidence of early reactions
following intravenous antivenom ranges from 3 to 5%. About 40% of these
reactions involve severe systemic anaphylaxis (bronchospasm, hypotension
or angioneurotic oedema), though few fatal cases have been reported. Most authorities have recommended that antivenom should be
diluted in isotonic fluid and given by slow intravenous infusion.
H.A. (1964). Cobra bites. Br. Med.
J. 2, 540-545.
H.A., Chan, K.E. and Thean, P.C. (1963). Prolonged coagulation defect (defibrination
syndrome) in Malayan viper bite. Lancet, i, 621-626.
H.A., Thean, P.C., Chan, K.E. and Baharom, A.R. (1963). Clinical effects
of bites by Malayan viper. Lancet
H.A. and Lim, K.J. (1957). Sea-snake bite. Br.
Med. J. 2, 1266-1272.
H.A., Theakston, R.D.S. (1983) The management of snake bite. Bull.
W.H.O., 61, 885-895.
C. (1973). Effects of green pit viper venoms on blood coagulation,
platelets and the fibrinolytic enzyme systems: studies in vivo and in
vitro. Am. J. clin. Pathol. 60,
D.A., Looareesuwan, S., White, N.J., Theakston, R.D.G., Warrell, M.J.,
Kosakarn, W., and Reid, H.A. (1983). Severe neurotoxic envenoming by the
Malayan krait, Bungarus candidus: response to antivenom and
anti-cholinesterase. Br. Med. J.
D.A., Theakston, R.D.G., Phillips, R.E., Chanthavanich, P., Viravan, C.,
Supanaranond, W., Karbwang, J., Ho, M., Hutton, R.A. and Vejcho, S.
(1986). Randomized comparative trial of three monospecific antivenoms for
bites by the Malayan pit viper (Calloselasma rhodostoma) in southern
Thailand: clinical and laboratory correlations. Am.
J. Trop. Med. Hyg. 35,
B.L. (1982) Poisonous Snakes of Peninsular Malaysia. 2nd Ed. Malayan
Nature Society, Kuala Lumpur, 72pp.
H.A. (1968) Symptomatology, pathology and treatment of land snake bites in
India and Southeast Asia. In: Venomous
Animals and Their Venoms. Vol.1. (Buckely, E.D., Bucheri, W., and
Deulofeu, V. Eds.), Academic Press, New York. Pp. 611-642.
N.H. (1991) The biochemistry of venoms of some venomous snakes of
Malaysia. – A Review. Tropical
Biomedicine 8, 91-103.
|Back to Home Page|