SDE MGMT Snake-Bite

Guidelines
for the Clinical Management of

Snake bites in the South-East Asia Region
Common Krait
Saw Scaled Viper Spectacled Cobra Russells Viper

Guidelines
Snake Bite in the South-East Asia Region
Reprint of the 1999 edition written and edited for

SEAMEOTROPMED – Regional Centre for Tropical Medicine,
Faculty of Tropical Medicine, Mahidol University, Thailand.
Written and edited for SEAMEOTROPMED by David A Warrell with contributions

by an international panel of experts, first published as a Supplement to the Southeast
Asian Journal of Tropical Medicine & Public Health, Vol 30, Supplement 1, 1999
New Delhi
2005
© World Health Organization 2005
Publications of the World Health Organization enjoy copyright protection in accordance with the
provisions of Protocol 2 of the Universal Copyright Convention. For rights of reproduction or
translation, in part or in toto, of publications issued by the WHO Regional Office for South-East
Asia, application should be made to the Regional Office for South-East Asia, World Health House,
Indraprastha Estate, New Delhi 110002, India.
The designations employed and the presentation of material in this publication do not imply the
expression of any opinion whatsoever on the part of the Secretariat of the World Health Organization
concerning the legal status of any country, territory, city or area or of its authorities, or concerning
the delimitation of its frontiers or boundaries.
Guidelines for the Clinical Management

ii of Snake bite in the South-East Asia Region
Contents
Preface ............................................................................................... v
1. Introduction .................................................................................. 1
1.1 Venomous snakes of South-East Asia ..................................................... 1
1.2 Snake venoms ...................................................................................... 8
1.3 How common are snake bites? ............................................................. 9
1.4 How do snake bites happen? .............................................................. 11
1.5 How can snake bites be avoided? ....................................................... 11
2. Symptoms and Signs of Snake Bite ............................................. 13

2.1 When venom has not been injected ................................................... 13
2.2 When venom has been injected ......................................................... 13
2.3 Clinical pattern of envenoming by snakes in South-East Asia ................ 14
2.4 Clinical syndromes of snake bite in South-East Asia ............................. 18
2.5 Long term complications (sequelae) of snake bite ................................ 19
3. Symptoms and Signs of Cobra-spit Ophthalmia ........................ 21
4. Management of Snake Bites in South-East Asia .......................... 23

4.1 First aid treatment ............................................................................... 23
4.2 Transport to hospital ........................................................................... 26
4.3 Treatment in the dispensary or hospital ............................................... 26
4.4 Detailed clinical assessment and species diagnosis ............................... 27
4.5 Investigations/laboratory tests .............................................................. 30
4.6 Antivenom treatment .......................................................................... 32
4.7 Supportive/ancillary treatment ............................................................ 40
4.8 Treatment of the bitten part ................................................................ 46
4.9 Rehabilitation ..................................................................................... 47

of Snake bite in the South-East Asia Region iii
5. Management of Cobra Spit Ophthalmia..................................... 49
6. Conclusions and Main Recommendations ................................. 51
7. Further Reading .......................................................................... 55
Annex
1. Algorithm: Antivenom treatment of snakebite cases .................................... 61
2. Algorithm: Differentiating major asian snake
species by clincal symdrome ....................................................................... 62
3. Antivenoms for treatment of bites by South-East Asian snakes ...................... 63
4. Measurement of Central Venous Pressure ................................................... 66
5. Measurement of intracompartmental pressure in
tensely swollen snake-bitten limbs .............................................................. 67

iv of Snake bite in the South-East Asia Region
Preface
The geographical area specifically covered by this publication extends from Pakistan
and the rest of the Indian subcontinent in the west through to the Philippines and
Indonesia in the east, excluding Tibet, China, Taiwan, Korea, Japan, the eastern islands
of Indonesia and New Guinea and Australia (Figure 1, inside of front cover).
Figure 1: Map of Asia showing the area specifically covered by the guidelines
In many parts of this region, snake bite is a familiar occupational hazard of

farmers, plantation workers and others, resulting in tens of thousands of deaths each
year and innumerable cases of chronic physical handicap. Much is now known about

of Snake bite in the South-East Asia Region v
the species of venomous snakes responsible for these bites, the nature of their venoms
and the clinical effects of envenoming in human patients. This publication aims to
pass on a digest of this knowledge to medical doctors, nurses, dispensers and
community health workers who have the responsibility of treating victims of snake
bite.
Any recommendations must be continually reconsidered in the light of new

evidence and experience. Comments from readers are welcomed so that future
editions can be updated and improved.
The guidelines are intended to provide enough practical information to allow

any medicallytrained person to assess and treat a patient with snake bite at different
levels of the health service. Recommendations are based on clinical experience and,
where possible, on the results of clinical trials. The restrictions on the size of this
document prevented the inclusion of detailed references to the original publications
on which these recommendations were based. These can be found in the papers
and reviews listed in “Further Reading”.
I am grateful to the panel of experts who contributed to these Guidelines but I

must take responsibility for the writing and editing of the document.
I acknowledge the exellent help provided by Miss Eunice Berry (Centre for Tropical
Medicine, University of Oxford), who typed the several drafts of the manuscript, and
by Ms Vimolsri Panichyanon (Assistant Programme Coordinator, SEAMEOTROPMED
Network) and Drs Suvanee Supavej and Parnpen Viriyavejakul (Deputy Assistant
Deans for International Relations, Faculty of Tropical Medicine, Mahidol University)
who, under the overall direction of Professor Sornchai Looareesuwan, were
responsible for organising the meeting of the international panel of experts in Bangkok
on 29/30 November 1998.
David A Warrell
Oxford, December 1998

vi of Snake bite in the South-East Asia Region
Names and Addresses of the
International Panel of Experts
who Contributed to the Guidelines
Nepal* Mahidol University

Bishnu Bahadur Bhetwal 420/6 Rajvithi Road
Bangkok 10400
Bijalpura - 2 V.D.C.
Thailand
P.O. - Bijalpura
Dist - Mahottari
Nepal Myanmar
May-Mya-Win)
India Renal and Dialysing Units
Tingangyun Sanpya Hospital
Kirpal S Chugh
Kothi No 601, Sector 18B Yangon
Myanmar
Chandigarh - 160 018
India
Sri Lanka
Papua New Guinea Lena Sjöström
Therapeutic Antibodies Ltd
David G Lalloo
Nuffield Dept Clinical Medicine, Clinical Operations (UK)
14-15 Newbury Street
University of Oxford
London EC1A 7HU
John Radcliffe Hospital
Headington UK
Oxford OX3 9DU
UK Sri Lanka, Thailand
R David G Theakston
Thailand Alistair Reid Venom Research Unit
Sornchai Looareesuwan Liverpool School of Tropical Medicine
Pembroke Place
SEAMEOTROPMED Regional Centre
Liverpool L3 5QA
for Tropical Medicine
Faculty of Tropical Medicine UK

of Snake bite in the South-East Asia Region vii
Myanmar, Sri Lanka, Australia
Thailand, Viet Nam Julian White
David A Warrell State Toxinology Services
Centre for Tropical Medicine Poisons Information Centre
University of Oxford Adelaide Children’s Hospital
John Radcliffe Hospital King William Street
Headington North Adelaide
Oxford OX3 9DU SA 5006
UK Australia
Philippines, Thailand *indicates countries of clinical experience

with snake bite patients in the
George Watt South-East Asian region.
Dept of Medicine
AFRIMS
315/6 Rajvithi Road
Bangkok 10400
Thailand

viii of Snake bite in the South-East Asia Region
1
Introduction
1.1 Venomous snakes of South-East Asia
The venom apparatus (Fig 2)

Venomous snakes of medical importance have a pair of enlarged teeth, the fangs, at
the front of their upper jaw. These fangs contain a venom channel (like a hypodermic
needle) or groove, along which venom can be introduced deep into the tissues of
their natural prey. If a human is bitten, venom is usually injected subcutaneously or
intramuscularly. Spitting cobras can squeeze the venom out of the tips of their fangs
producing a fine spray directed towards the eyes of an aggressor.
Compressor
glandulae muscle Venom gland
Accessory
venom gland
Secondary
venom duct
Venom duct Venom canal
Figure 2: Venom apparatus of a saw-scaled viper (Copyright DA Warrell)

of Snake bite in the South-East Asia Region 1
Classification
There are two important groups (families) of venomous snakes in South-East Asia –
Elapidae have short permanently erect fangs (Fig 3). This family includes the cobras,
king cobra, kraits, coral snakes and the sea snakes. The most important species, from
a medical point of view, include the following:
cobras: N naja common spectacled Indian cobra (Fig 4)
(genus Naja) N oxiana North Indian or Oxus cobra (Fig 5)
N kaouthia monocellate cobra (Fig 6)
N philippinensis Philippine cobra
N atra Chinese cobra (Fig 7)
spitting cobras: N siamensis (Fig 8)
N sumatrana (Fig 9)
N sputatrix etc
king cobra: Ophiophagus hannah (Fig 10)
kraits: B caeruleus common krait (Fig 11)
(genus Bungarus) B candidus Malayan krait (Fig 12)
B multicinctus Chinese krait (Fig 13)
B fasciatus banded krait (Fig 14)
Sea snakes (important genera include Enhydrina, Lapemis and Hydrophis)
(Fig 15)
Figure 4: Short, permanently erect, fangs of

a typical elapid (Thai monocellate cobra –
Naja kaouthia (Copyright DA Warrell)
Figure 3: Short, permanently erect, fangs of a Figure 5: North Indian or Oxus cobra (Naja
typical elapid (Thai monocellate cobra – Naja oxiana) (Copyright DA Warrell) Viperdae
kaouthia) (Copyright DA Warrell) have long fangs

2 of Snake bite in the South-East Asia Region
Figure 6: (Left) Monocellate cobra (Naja kaouthia), (Right) Detail of hood (Copyright DA Warrell)
Figure 7: Chinese cobra (Naja atra) Figure 8(a): Indo-Chinese spitting cobra (Naja Saimensis)
(Copyright DA Warrell) (Copyright DA Warrell)

Figure 8(b): (Left) Brown coloured specimen with spectacle marking on hood. (Right) Black and
white specimen with ill-defined spectacle marking on the hood. (Copyright DA Warrell)
Figure 9: Sumatran spitting cobra Figure 10: King cobra or hamadryad (Ophiophagus
(Naja sumatrana) (a) black phase hannah). The famous king cobra dance in Yangon,
(b) golden phase (Copyright DA Myanmar (Copyright DA Warrell)
Warrell)
Figure 11: Common krait (Bungarus caeruleus) Figure 12: Malayan krait (Bungarus candidus)
(Copyright DA Warrell) (Copyright DA Warrell)

Figure 13: Chinese krait (Bungarus Figure 14: Banded krait (Bungarus fasciatus)
multicinctus) (Copyright DA Warrell) (Copyright DA Warrell)
Figure 15: Blue spotted sea snake (Hydrophis cyanocinctus) (Copyright DA Warrell)
Viperidae have long fangs which are normally folded up against the upper jaw
but, when the snake strikes, are erected (Fig 2). There are two subgroups, the typical
vipers (Viperinae) and the pit vipers (Crotalinae). The Crotalinae have a special sense
organ, the pit organ, to detect their warm-blooded prey. This is situated between the
nostril and the eye (Fig 16).
Medically important species in South-East Asia are:
typical vipers Daboia russelii Russell’s vipers (Fig 17)

Echis carinatus saw-scaled or carpet vipers
and E sochureki (Figs 18, 19)
pit vipers Calloselasma rhodostoma Malayan pit viper (Fig 20)

Hypnale hypnale hump-nosed viper (Fig 21)
green pit vipers or bamboo vipers (genus Trimeresurus)
T albolabris white-lipped green

pit viper (Fig 22)

T gramineus Indian bamboo viper
T mucrosquamatus Chinese habu (Fig 23)
T purpureomaculatus mangrove pit viper (Fig 24)
T stejnegeri Chinese bamboo viper
Figure 16: Head of a typical pit viper – white-lipped green pit viper (Trimeresurus albolabris)
showing the pit organ situated between the nostril and the eye (arrow head) (Copyright DA Warrell)
Figure 17(a): Russell’s vipers (Copyright DA Figure 17(b): Russell’s vipers (Copyright DA Warrell)
Warrell) Eastern subspecies (Daboia russelii specimen from India
siamensis); specimen from Myanmar
Figure 17(c): Russell’s vipers Figure 17(d): Russell’s vipers (Copyright DA Warrell)
(Copyright DA Warrell) Eastern specimen from Burma
subspecies (Daboia russelii
siamensis); specimen from Thailand

Figure 17(e): Russell’s vipers Figure 18: Saw-scaled viper (Echis carinatus) specimen
(Copyright DA Warrell) details of from Sri Lanka (Copyright DA Warrell)
fangs
Figure 19: Northern saw-scaled viper (Echis Figure 20: Northern saw-scaled viper (Echis
sochureki) (Copyright DA Warrell) sochureki) (Copyright DA Warrell)
Figure 21: Hump-nosed viper (Hynpale hypnale). Figure 22: White-lipped green pit viper
Specimen from Sri Lanka (Copyright DA Warrell) (Trimeresurus albolabris) (Copyright DA
Warrell)

Figure 23: Chinese habu (Trimeresurus microsquamatus) (Copyright DA Warrell)
How to identify venomous snakes

There is no simple rule for identifying a
dangerous venomous snake. Some harmless
snakes have evolved to look almost identical
to venomous ones. However, some of the most
notorious venomous snakes can be recognised
by their size, shape, colour, pattern of markings,
their behaviour and the sound they make when
they feel threatened. For example, the
defensive behaviour of the cobras is well
known (Fig 8): they rear up, spread a hood,
hiss and make repeated strikes towards the
aggressor. Colouring can vary a lot. However,
some patterns, like the large white, dark
Figure 24: Mangrove pit viper rimmed spots of the Russell’s viper (Fig 17), or
(Trimeresurus purpureomaculatus) the alternating black and yellow bands of the
(Copyright DA Warrell)
banded krait (Fig 14), are distinctive. The
blowing hiss of the Russell’s viper and the
grating rasp of the saw-scaled viper are warning and identifying sounds.
1.2 Snake venoms

Composition of venom
Snake venoms contain more than 20 different constituents, mainly proteins, including
enzymes and polypeptide toxins. The following venom constituents cause important
clinical effects:
Procoagulant enzymes (Viperidae) that stimulate blood clotting but result in

incoagulable blood. Venoms such as Russell’s viper venom contain several different
procoagulants which activate different steps of the clotting cascade. The result is
formation of fibrin in the blood stream. Most of this is immediately broken down by

the body’s own fibrinolytic system. Eventually, and sometimes within 30 minutes of
the bite, the levels of clotting factors have been so depleted (“consumption
coagulopathy”) that the blood will not clot.
Haemorrhagins (zinc metalloproteinases) that damage the endothelial lining of

blood vessel walls causing spontaneous systemic haemorrhage.
Cytolytic or necrotic toxins - these digestive hydrolases (proteolytic enzymes

and phospholipases A) polypeptide toxins and other factors increase permeability
resulting in local swelling. They may also destroy cell membranes and tissues.
Haemolytic and myolytic phospholipases A2 - these enzymes damage cell

membranes, endothelium, skeletal muscle, nerve and red blood cells.
Pre-synaptic neurotoxins (Elapidae and some Viperidae) - these are

phospholipases A2 that damage nerve endings, initially releasing acetylcholine
transmitter, then interfering with release.
Post-synaptic neurotoxins (Elapidae) - these polypeptides compete with

acetylcholine for receptors in the neuromuscular junction and lead to curare-like
paralysis.
Quantity of venom injected at a bite

This is very variable, depending on the species and size of the snake, the mechanical
efficiency of the bite, whether one or two fangs penetrated the skin and whether
there were repeated strikes. The snake may be able to control whether or not venom
is injected. For whatever reason, a proportion of bites by venomous snakes do not
result in the injection of sufficient venom to cause clinical effects. About 50% of bites
by Malayan pit vipers and Russell’s vipers, 30% of bites by cobras and 5-10% of bites
by saw-scaled vipers do not result in any symptoms or signs of envenoming. Snakes
do not exhaust their store of venom, even after several strikes, and they are no less
venomous after eating their prey.
Although large snakes tend to inject more venom than smaller specimens of the
same species, the venom of smaller, younger vipers may be richer in some dangerous
components, such as those affecting haemostasis.
Bites by small snakes should not be ignored or dismissed. They should be taken
just as seriously as bites by large snakes of the same species.
1.3 How common are snake bites?

It is difficult to answer this question because many snake bites and even deaths from
snake bite are not recorded. One reason is that many snake bite victims are treated
not in hospitals but by traditional healers.

To remedy the deficiency in reliable snake bite data, it is strongly recommended
that snake bites should be made a specific notifiable disease in all countries in the
South East Asian region.
Bangladesh – a survey of 10% of the country in 1988-9 revealed 764 bites with
168 deaths in one year. Cobra bites (34% of all bites) caused a case fatality of 40%.
Bhutan – (no data available)
Cambodia – (no data available)
India – estimates in the region of 200,000 bites and 15-20,000 snake bite deaths
per year, originally made in the last century, are still quoted. No reliable national
statistics are available. In 1981, a thousand deaths were reported in Maharashtra
State. In the Burdwan district of West Bengal 29,489 people were bitten in one year
with 1,301 deaths. It is estimated that between 35,000 and 50,000 people die of
snake bite each year among India’s population of 980 million.
Indonesia – no reliable data are available from this vast archipelago. Snake bites
and deaths are reported from some islands, eg Komodo, but fewer than 20 deaths
are registered each year.
Lao DPR – (no data available)
Malaysia – bites are common, especially in northwest peninsular Malaysia, but

there are few deaths.
Myanmar (Burma) – snake bites and snake bite deaths have been reliably reported
from colonial times. Russell’s vipers are responsible for 90% of cases. In 1991, there
were 14,000 bites with 1,000 deaths and in 1997, 8,000 bites with 500 deaths.
Under-reporting is estimated at 12%. There are peaks of incidence in May and June
in urban areas and during the rice harvest in October to December in rural areas.
Nepal – there are estimated to be at least 20,000 snake bites with about 200
deaths in hospitals each year, mainly in the Terai region. One survey suggested as
many as 1,000 deaths per year. Among 16 fatalities recorded at one rural clinic
during a monsoon season, 15 had died on their way to seek medical care.
Pakistan – there are an estimated 20,000 snake bite deaths each year
Philippines – there are no reliable estimates of mortality among the many islands
of thearchipelago. Figures of 200-300 deaths each year have been suggested. Only
cobras cause fatal envenoming, their usual victims being rice farmers.
Sri Lanka – epidemiological studies in Anuradhapura showed that only two-

thirds of cases of fatal snake bite were being reported to the Government Agent

Statistical Branch. However, the Registrar General received reports of more than 800
deaths from bites and stings by venomous animals and insects in the late 1970s and
the true annual incidence of snake bite fatalities may exceed 1,000.
Thailand – between 1985 and 1989, the number of reported snake bite cases
increased from 3,377 to 6,038 per year, reflecting increased diligence in reporting
rather than a true increase in snake bites; the number of deaths ranged from 81 to
183 (average 141) per year. In 1991 there were 1,469 reported bites with five deaths,
in 1992, 6,733 bites with 19 deaths and, in 1994, 8,486 bites with eight deaths.
Deaths reported in hospital returns were only 11% of the number recorded by the
Public Health Authorities. In a national survey of dead snakes brought to hospital by
the people they had bitten, 70% of the snakes were venomous species, the most
commonly brought species being Malayan pit viper (Calloselasma rhodostoma) 38%,
white-lipped green pit viper (Trimeresurus albolabris) 27%, Russell’s viper (Daboia
russelii siamensis) 14%, Indo-Chinese spitting cobra (Naja siamensis) 10% and
monocellate cobra (N kaouthia) 7%. In an analysis of 46 fatal cases in which the
snake had been reliably identified, Malayan kraits (Bungarus candidus) and Malayan
pit vipers were each responsible for 13 cases, monocellate cobras for 12 and Russell’s
vipers for seven deaths.
Viet Nam – there are an estimated 30,000 bites per year. Among 430 rubber
plantation workers bitten by Malayan pit vipers between 1993 and 1998, the case
fatality was 22%, but only a minority had received antivenom treatment. Fishermen
are still occasionally killed by sea snakes but rarely reach hospitals.
1.4 How do snake bites happen?

In South-East Asia, snake bite is an occupational hazard of rice farmers; rubber,
coffee and other plantation workers; fishermen and those who handle snakes. Most
snake bites happen when the snake is trodden on, either in the dark or in undergrowth,
by someone who is bare-footed or wearing only sandals. The snake may be picked
up, unintentionally in a handful of foliage or intentionally by someone who is trying
to show off. Some bites occur when the snake (usually a krait) comes in to the home
at night in search of its prey (other snakes, lizards, frogs, mice) and someone sleeping
on the floor rolls over onto the snake in their sleep. Not all snake bites happen in
rural areas. For example, in some large cities, such as Jammu in India, people who
sleep in small huts (jhuggies) are frequently bitten by kraits.
1.5 How can snake bites be avoided?

Snake bite is an occupational hazard that is very difficult to avoid completely. However,
attention to the following recommendations might reduce the number of accidents.
• Education! Know your local snakes, know the sort of places where they like
to live and hide, know at what times of year, at what times of day/night or
in what kinds of weather they are most likely to be active.

Snake bite: an occupational disease in South East Asia
Farmers (rice)
Plantation workers (rubber, coffee)
Herdsmen
Hunters
Snake handlers (snake charmers and in snake restaurants and
traditional Chinese
pharmacies)
Fishermen and fish farmers
Sea snake catchers (for sea snake skins, leather)
• Be specially vigilant about snake bites after rains, during flooding, at harvest
time and at night.
• Try to wear proper shoes or boots and long trousers, especially when walking
in the dark or in undergrowth.
• Use a light (torch, flashlight or lamp) when walking at night.
• Avoid snakes as far as possible, including snakes performing for snake
charmers. Never handle, threaten or attack a snake and never intentionally
trap or corner a snake in an enclosed space.
• If at all possible, try to avoid sleeping on the ground.
• Keep young children away from areas known to be snake-infested.
• Avoid or take great care handling dead snakes, or snakes that appear to be
dead.
• Avoid having rubble, rubbish, termite mounds or domestic animals close to
human dwellings, as all of these attract snakes.
• Frequently check houses for snakes and, if possible, avoid types of house
construction that will provide snakes with hiding places (e.g. thatched rooves
with open eaves, mud and straw walls with large cracks and cavities, large
unsealed spaces beneath floorboards).
• To prevent sea snake bites, fishermen should avoid touching sea snakes
caught in nets and on lines. The head and tail are not easily distinguishable.
There is a risk of bites to bathers and those washing clothes in muddy water
of estuaries, river mouths and some coastlines.

2
Symptoms and
Signs of Snake Bite
2.1 When venom has not been injected

Some people who are bitten by snakes or suspect or imagine that they have been
bitten, may develop quite striking symptoms and signs, even when no venom has
been injected. This results from an understandable fear of the consequences of a real
venomous bite. Anxious people may overbreathe so that they develop pins and
needles of the extremities, stiffness or tetany of their hands and feet and dizziness.
Others may develop vasovagal shock after the bite or suspected bite – faintness and
collapse with profound slowing of the heart. Others may become highly agitated and
irrational and may develop a wide range of misleading symptoms. Another source of
symptoms and signs not caused by snake venom is first aid and traditional treatments.
Constricting bands or tourniquets may cause pain, swelling and congestion. Ingested
herbal remedies may cause vomiting. Instillation of irritant plant juices into the eyes
may cause conjunctivitis. Forcible insufflation of oils into the respiratory tract may
lead to aspiration pneumonia, bronchospasm, ruptured ear drums and pneumothorax.
Incisions, cauterisation, immersion in scalding liquid and heating over a fire can
result in devastating injuries.
2.2 When venom has been injected

Early symptoms and signs
Following the immediate pain of mechanical penetration of the skin by the snake’s
fangs, there may be increasing local pain (burning, bursting, throbbing) at the site of
the bite, local swelling that gradually extends proximally up the bitten limb and
tender, painful enlargement of the regional lymph nodes draining the site of the bite
(in the groin – femoral or inguinal, following bites in the lower limb; at the elbow
(epitrochlear) or in the axilla following bites in the upper limb). However, bites by
kraits, sea snakes and Philippine cobras may be virtually painless and may cause

negligible local swelling. Someone who is sleeping may not even wake up when
bitten by a krait and there may be no detectable fang marks or signs of local
envenoming.
2.3 Clinical pattern of envenoming by snakes

in South-East Asia
Symptoms and signs vary according to the species of snake responsible for the bite
and the amount of venom injected. Sometimes the identity of the biting snake can
be confirmed by examining the dead snake; it may be strongly suspected from the
patient’s description or the circumstances of the bite or from knowledge of the clinical
effects of the venom of that species. This information will enable the doctor to choose
an appropriate antivenom, anticipate the likely complications and therefore take
appropriate action. If the biting species is unknown, recognition of the emerging
pattern of symptoms, signs and results of laboratory tests (“the clinical syndrome”),
may suggest which species was responsible.
Local symptoms and signs in the bitten part

• fang marks (Fig 25)
• local pain
• local bleeding (Fig 26)
• bruising
• lymphangitis
• lymph node enlargement
• nflammation (swelling, redness, heat)
• blistering (Fig 27)
• local infection, abscess formation
• necrosis (Fig 28)
Figure 25: Fang marks made by Russell’s viper Figure 26: Local bleeding from
(Copyright DA Warrell) fang marks made by Malayan pit
viper (Copyright DA Warrell)

Figure 27 Local swelling and blistering (a) with bruising, following a bite by a Malayan pit viper
(Copyright DA Warrell), (Bottom) Local swelling and blistering (b) with early necrosis following a
bite by a monocellate cobra (Naja kaouthia) (Copyright DA Warrell)
Figure 28: Tissue necrosis following a bite by a Malayan pit viper (Copyright DA Warrell)
Figure 28(a): Tissue necrosis following a bite by an Indochinese spitting cobra (Naja siamensis)
(Copyright Sornchai Looareesuwan)
Generalised (systemic) symptoms and signs

General
Nausea, vomiting, malaise, abdominal pain, weakness, drowsiness, prostration
Cardiovascular (Viperidae)
Visual disturbances, dizziness, faintness, collapse, shock, hypotension, cardiac
arrhythmias, pulmonary oedema, conjunctival oedema (Fig 29)

Bleeding and clotting disorders (Viperidae)
• bleeding from recent wounds (including fang marks (Fig 26), venepunctures
etc) and from old partly-healed wounds
• spontaneous systemic bleeding – from gums (Fig 30), epistaxis, bleeding
into the tears, haemoptysis, haematemesis, rectal bleeding or melaena,
haematuria, vaginal bleeding, bleeding into the skin (petechiae, purpura,
ecchymoses) and mucosae (eg conjunctivae [Fig 31]), intracranial
haemorrhage (meningism from subarachnoid haemorrhage, lateralising signs
and/or coma from cerebral haemorrhage)
Neurological (Elapidae, Russell’s viper)

Drowsiness, paraesthesiae, abnormalities of taste and smell, “heavy” eyelids, ptosis
(Fig 32), external ophthalmoplegia (Fig 33), paralysis of facial muscles and other
muscles innervated by the cranial nerves, aphonia, difficulty in swallowing secretions,
respiratory and generalised flaccid paralysis
Skeletal muscle breakdown (sea snakes, Russell’s viper)

Generalised pain, stiffness and tenderness of muscles, trismus, myoglobinuria
(Fig 34), hyperkalaemia, cardiac arrest, acute renal failure
Renal (Viperidae, sea snakes)

Loin (lower back) pain, haematuria, haemoglobinuria, myoglobinuria, oliguria/anuria,
symptoms and signs of uraemia (acidotic breathing, hiccups, nausea, pleuritic chest
pain....)
Endocrine (acute pituitary/adrenal insufficiency) (Russell’s viper)

Acute phase: shock, hypoglycaemia
Chronic phase (months to years after the bite): weakness, loss of secondary sexual
hair, amenorrhoea, testicular atrophy, hypothyroidism etc (Fig 35)
Figure 29: Bilateral conjunctival oedema (chemosis) after a bite by a Burmese Russell’s viper

Figure 30: Bleeding from gingival sulci in a patient bitten by a saw-scaled viper
Figure 31: Subconjunctival haemorrhages in a patient bitten by a Burmese Russell’s viper

Figure 32: Bilateral ptosis (a) in a patient bitten by a common krait (Copyright DA Warrell),
Bilateral ptosis (b) in a patient bitten by a Sri Lankan Russell’s viper (Copyright DA Warrell)

Figure 33: External ophthalmoplegia in a patient Figure 34: Patient bitten by a Sri Lankan
bitten by a Russell’s viper in Sri Lanka. The Russell’s viper who began to pass dark
patient is attempting to look to his right. The brown urine containing myoglobin and
eyes are held open because of the bilateral haemoglobin 8 hours after the bite
ptosis (Copyright DA Warrell) (Copyright DA Warrell)
Figure 35: (a) Haemorrhagic infarction of the anterior pituitary (Sheehan’s-like syndrome) after a
bite by a Burmese Russell’s viper, (b) Patient bitten by a Burmese Russell’s viper three years
previously, showing clinical signs of panhypopituitarism: loss of secondary sexual hair and
testicular atrophy (Copyright DA Warrell)
2.4 Clinical syndromes of snake bite in South-East Asia

Limitations of syndromic approach
The more carefully the clinical effects of snake bites are studied, the more it is realised
that the range of activities of a particular venom is very wide. For example, some
elapid venoms, such as those of Asian cobras, can cause severe local envenoming

(Fig 28), formerly thought to be an effect only of viper venoms. In Sri Lanka and
South India, Russell’s viper venom causes paralytic signs (ptosis etc) (Fig 32), suggesting
elapid neurotoxicity, and muscle pains and dark brown urine (Fig 34), suggesting sea
snake rhabdomyolysis. Although thre may be considerable overlap of clinical features
caused by venoms of different species of snake, a “syndromic approach” may still be
useful, especially when the snake has not been identified and only monospecific
antivenoms are available (see Annex 1 & 2).
Syndrome 1
Local envenoming (swelling etc) with bleeding/clotting disturbances = Viperidae
(all species)
Syndrome 2
Local envenoming (swelling etc) with bleeding/clotting disturbances, shock or renal
failure = Russell’s viper (and possibly saw-scaled viper – Echis species – in some
areas)
with conjunctival oedema (chemosis) and acute pituitary insufficiency = Russell’s
viper, Burma
with ptosis, external ophthalmoplegia, facial paralysis etc and dark brown urine =
Russell’s viper, Sri Lanka and South India
Syndrome 3
Local envenoming (swelling etc) with paralysis = cobra or king cobra
Syndrome 4
Paralysis with minimal or no local envenoming
Bite on land while sleeping, outside the Philippines = krait
in the Philippines = cobra (Naja philippinensis)
Bite in the sea = sea snake
Syndrome 5
Paralysis with dark brown urine and renal failure:
Bite on land (with bleeding/clotting disturbance) = Russell’s viper, Sri Lanka/South
India
Bite in the sea (no bleeding/clotting disturbances) = sea snake
2.5 Long term complications (sequelae) of snake bite

At the site of the bite, loss of tissue may result from sloughing or surgical débridement
of necrotic areas or amputation: chronic ulceration, infection, osteomyelitis or arthritis
may persist causing severe physical disability (Fig 36). Malignant transformation may
occur in skin ulcers after a number of years (Fig 37).

Figure 36: (a) and (b) Chronic physical handicap resulting from necrotic envenoming by Malayan
pit vipers (Copyright DA Warrell)
Chronic renal failure occurs after

bilateral cortical necrosis (Russell’s
viper bites) and chronic
panhypopituitarism or diabetes
insipidus after Russell’s viper bites in
Myanmar and South India (Fig 35b).
Chronic neurological deficit is seen
in the few patients who survive
Figure 37: Squamous cell carcinoma developing at intracranial haemorrhages
the site of a chronic skin ulcer with osteomyelitis 8 (Viperidae).
years after a bite by a Malayan pit viper (Copyright
DA Warrell)

3
Symptoms and Signs of

Cobra-spit Ophthalmia
(Eye injuries from spitting cobras) (Fig 38)
If the “spat” venom enters the eyes, there is immediate and persistent intense burning,
stinging pain, followed by profuse watering of the eyes with production of whitish
discharge, congested conjunctivae, spasm and swelling of the eyelids, photophobia
and clouding of vision. Corneal ulceration, permanent corneal scarring and secondary
endophthalmitis are recognised complications of African spitting cobra venom but
have not been described in Asia.
Figure 38: Bilateral conjunctivitis in a patient who had venom spat into both eyes by an Indo-
Chinese spitting cobra (Naja siamensis) (Copyright DA Warrell)

4
Management of Snake
Bites in South-East Asia
The following steps or stages are often involved
Management of snake bite
• First aid treatment

• Transport to hospital
• Rapid clinical assessment and resuscitation
• Detailed clinical assessment and species diagnosis
• Investigations/laboratory tests
• Antivenom treatment
• Observation of the response to antivenom: decision about the need for further
dose(s) of antivenom
• Supportive/ancillary treatment
• Treatment of the bitten part
• Rehabilitation
• Treatment of chronic complications
4.1 First aid treatment

First aid treatment is carried out immediately or very soon after the bite, before the
patient reaches a dispensary or hospital. It can be performed by the snake bite victim
himself/herself or by anyone else who is present.

Aims of first aid
• attempt to retard systemic absorption of venom

• preserve life and prevent complications before the patient can receive medical
care (at a dispensary or hospital)
• control distressing or dangerous early symptoms of envenoming
• arrange the transport of the patient to a place where they can receive medical
care (4.2)
• Above all, do no harm!
Unfortunately, most of the traditional, popular, available and affordable first aid
methods have proved to be useless or even frankly dangerous. These methods include:
making local incisions or pricks/punctures (“tattooing”) at the site of the bite or in the
bitten limb, attempts to suck the venom out of the wound, use of (black) snake
stones, tying tight bands (tourniquets) around the limb, electric shock, topical
instillation or application of chemicals, herbs or ice packs.
Local people may have great confidence in traditional (herbal) treatments, but
they must not be allowed to delay medical treatment or to do harm.
Most traditional first aid methods should be discouraged:

They do more harm than good !
Recommended first aid methods
• Reassure the victim who may be very anxious

• Immobilise the bitten limb with a splint or sling (any movement or muscular
contraction increases absorption of venom into the bloodstream and lymphatics)
• Consider pressure-immobilisation (Fig 39) for some elapid bites
• Avoid any interference with the bite wound as this may introduce infection,
increase absorption of the venom and increase local bleeding
As far as the snake is concerned – do not attempt to kill it as this may be dangerous.
However, if the snake has already been killed, it should be taken to the dispensary or
hospital with the patient in case it can be identified. However, do not handle the
snake with your bare hands as even a severed head can bite!
The special danger of rapidly developing paralytic envenoming after

bites by some elapid snakes: use of pressure-immobilisation
Bites by cobras, king cobras, kraits or sea snakes may lead, on rare occasions, to the
rapid development of life-threatening respiratory paralysis. This paralysis might be

delayed by slowing down the absorption of venom from the site of the bite. The
following technique is currently recommended:
Pressure immobilisation method (Fig 39). Ideally, an elasticated, stretchy, crepe

bandage, approximately 10 cm wide and at least 4.5 metres long should be used. If
that it not available, any long strips of material can be used. The bandage is bound
firmly around the entire bitten limb, starting distally around the fingers or toes and
moving proximally, to include a rigid splint. The bandage is bound as tightly as for a
sprained ankle, but not so tightly that the peripheral pulse (radial, posterior tibial,
dorsalis pedis) is occluded or that a finger cannot easily be slipped between its layers.
Figure 39: Pressure immobilisation method. Recommended first-aid for bites by neurotoxic
elapid snakes (by courtesy of the Australian Venom Research Unit, University of Melbourne)
Pressure immobilisation is recommended for bites by neurotoxic elapid snakes,

including sea snakes but should not be used for viper bites because of the danger
of increasing the local effects of the necrotic venom.
Ideally, compression bandages should not be released until the patient is under
medical care in hospital, resuscitation facilities are available and antivenom treatment
has been started (see Caution below).
Caution: Release of a tight tourniquet or compression bandage may result

in the dramatic development of severe systemic envenoming.
Tight (arterial) tourniquets are not recommended!

Traditional tight (arterial) tourniquets. To be effective, these had to be applied around
the upper part of the limb, so tightly that the peripheral pulse was occluded. This
method was extremely painful and very dangerous if the tourniquet was left on for
too long (more than about 40 minutes), as the limb might be damaged by ischaemia.
Many gangrenous limbs resulted!

Viper and cobra bites
The pressure-immobilisation method as described above will increase
intracompartmental pressure and, by localising the venom, might be expected to
increase the locally-necrotic effects of viper venoms and some cobra venoms.
Pressure bandaging is not recommended for bites by vipers and cobras whose
venoms cause local necrosis.
The use of a local compression pad applied over the wound, without pressure
bandaging of the entire bitten limb, has produced promising results in Myanmar and
deserves further study.
Arterial tourniquets are not recommended
4.2 Transport to hospital

The patient must be transported to a place where they can receive medical care
(dispensary or hospital) as quickly, but as safely and comfortably as possible. Any
movement, but especially movement of the bitten limb, must be reduced to an
absolute minimum to avoid increasing the systemic absorption of venom. Any muscular
contraction will increase this spread of venom from the site of the bite. A stretcher,
bicycle, cart, horse, motor vehicle, train or boat should be used, or the patient should
be carried.
4.3 Treatment in the dispensary or hospital

Rapid clinical assessment and resuscitation
Cardiopulmonary resuscitation may be needed, including administration of oxygen
and establishment of intravenous access. Airway, respiratory movements (Breathing)
and arterial pulse (Circulation) must be checked immediately. The level of
consciousness must be assessed.
The following are examples of clinical situations in which snake bite victims
might require urgent resuscitation:
• Profound hypotension and shock resulting from direct cardiovascular effects

of the venom or secondary effects such as hypovolaemia or haemorrhagic
shock.
• Terminal respiratory failure from progressive neurotoxic envenoming that
has led to paralysis of the respiratory muscles.
• Sudden deterioration or rapid development of severe systemic envenoming
following the release of a tight tourniquet or compression bandage (see
Caution above).

• Cardiac arrest precipitated by hyperkalaemia resulting from skeletal muscle
breakdown (rhabdomyolysis) after sea snake bite.
• Late results of severe envenoming such as renal failure and septicaemia
complicating local necrosis.
4.4 Detailed clinical assessment and species diagnosis

History
A precise history of the circumstances of the bite and the progression of local and
systemic symptoms and signs is very important. Three useful initial questions are:
“In what part of your body have you been bitten?”

The doctor can see immediately evidence that the patient has been bitten by a
snake (eg fang marks) and the nature and extent of signs of local envenoming.
“When were you bitten?”

Assessment of the severity of envenoming depends on how long ago the patient was
bitten. If the patient has arrived at the hospital soon after the bite, there may be few
symptoms and signs even though a large amount of venom may have been injected.
“Where is the snake that bit you?”

If the snake has been killed and brought, its correct identification can be very helpful.
If it is obviously a harmless species (or not a snake at all!), the patient can be quickly
reassured and discharged from hospital.
Early clues that a patient has severe envenoming:
• Snake identified as a very dangerous one

• Rapid early extension of local swelling from the site of the bite
• Early tender enlargement of local lymph nodes, indicating spread of venom in
the lymphatic system
• Early systemic symptoms: collapse (hypotension, shock), nausea, vomiting,
diarrhoea, severe headache, “heaviness” of the eyelids, inappropriate
(pathological) drowsiness or early ptosis/ophthalmoplegia
• Early spontaneous systemic bleeding
• Passage of dark brown urine
Patients who become defibrinogenated or thrombocytopenic may begin to bleed

from old, partially-healed wounds as well as bleeding persistently from the fang marks.
The patient should be asked how much urine has been passed since the bite and
whether it was a normal colour.

An important early symptom of sea snake envenoming that may develop as soon
as 30 minutes after the bite is generalised pain, tenderness and stiffness of muscles
and trismus.
Physical examination
This should start with careful assessment of the site of the bite and signs of local
envenoming.
Examination of the bitten part

The extent of swelling, which is usually also the extent of tenderness to palpation,
should be recorded. Lymph nodes draining the limb should be palpated and overlying
ecchymoses and lymphangitic lines noted.
A bitten limb may be tensely oedematous, cold, immobile and with impalpable
arterial pulses. These appearances may suggest intravascular thrombosis, which is
exceptionally rare after snake bite, or a compartmental syndrome, which is
uncommon. If possible, intracompartmental pressure should be measured (see
Annex 5) and the blood flow and patency of arteries and veins assessed (eg by doppler
ultrasound).
Early signs of necrosis may include blistering, demarcated darkening (easily

confused with bruising) or paleness of the skin, loss of sensation and a smell of
putrefaction (rotting flesh).
General examination
Measure the blood pressure (sitting up and lying to detect a postural drop indicative
of hypovolaemia) and heart rate. Examine the skin and mucous membranes for
evidence of petechiae, purpura, ecchymoses and, in the conjunctivae, chemosis.
Thoroughly examine the gingival sulci, using a torch and tongue depressor, as these
may show the earliest evidence of spontaneous systemic bleeding. Examine the nose
for epistaxis. Abdominal tenderness may suggest gastrointestinal or retroperitoneal
bleeding. Loin (low back) pain and tenderness suggests acute renal ischaemia (Russell’s
viper bites). Intracranial haemorrhage is suggested by lateralising neurological signs,
asymmetrical pupils, convulsions or impaired consciousness (in the absence of
respiratory or circulatory failure).
Neurotoxic envenoming
To exclude early neurotoxic envenoming, ask the patient to look up and observe
whether the upper lids retract fully (Fig 40). Test eye movements for evidence of
early external ophthalmoplegia (Fig 33). Check the size and reaction of the pupils.
Ask the patient to open their mouth wide and protrude their tongue; early restriction
in mouth opening may indicate trismus (sea snake envenoming) or more often paralysis
of pterygoid muscles (Fig 41). Check other muscles innervated by the cranial nerves
(facial muscles, tongue, gag reflex etc). The muscles flexing the neck may be paralysed,
giving the “broken neck sign” (Fig 42).

Bulbar and respiratory paralysis
Can the patient swallow or are secretions accumulating in the pharynx, an early sign
of bulbar paralysis? Ask the patient to take deep breaths in and out. “Paradoxical
respiration” (abdomen expands rather than the chest on attempted inspiration)
indicates that the diaphragm is still contracting but that the intercostal muscles and
accessory muscles of inspiration are paralysed. Objective measurement of ventilatory
capacity is very useful. Use a peak flow metre, spirometer (FEV1 and FVC) or ask the
patient to blow into the tube of a sphygmomanometer to record the maximum
expiratory pressure (mmHg). Remember that, provided their lungs are adequately
ventilated, patients with profound generalised flaccid paralysis from neurotoxic
envenoming are fully conscious. Because their eyes are closed and they do not move
or speak, they are commonly assumed to be unconscious. They may still be able to
flex a finger or toe and so simple communication is possible.
Figure 40: Examination for ptosis, Figure 41: Inability to open the mouth and protrude the
usually the earliest sign of neurotoxic tongue in a patient with neurotoxic envenoming from
envenoming (Copyright DA Warrell) the Malayan krait (Copyright DA Warrell)
Figure 42: Broken neck sign in a child envenomed by a cobra in Malaysia (Copyright the late
HA Reid)

Do not assume that patients have irreversible brain damage because they are
areflexic, unresponsive to painful stimuli, or have fixed dilated pupils.
Generalised rhabdomyolysis
In victims of envenoming by sea snakes and Russell’s vipers in Sri Lanka and South
India, muscles, especially of the neck, trunk and proximal part of the limbs, may
become tender and painful on active or passive movement and later may become
paralysed. In sea snake bite there is pseudotrismus that can be overcome by sustained
pressure on the lower jaw. Myoglobinuria may be evident 3 hours after the bite.
Examination of pregnant women

There will be concern about fetal distress (revealed by fetal bradycardia), vaginal
bleeding and threatened abortion. Monitoring of uterine contractions and fetal heart
rate is useful. Lactating women who have been bitten by snakes should be encouraged
to continue breast feeding.
Species diagnosis
If the dead snake has been brought, it can be identified. Otherwise, the species
responsible can be inferred indirectly form the patient’s description of the snake and
the clinical syndrome of symptoms and signs (see above and Annex 1 & 2). This is
specially important in Thailand where only monospecific antivenoms are available.
4.5 Investigations/laboratory tests

20 minute whole blood clotting test (20WBCT)
This very useful and informative bedside test requires very little skill and only one
piece of apparatus - a new, clean, dry, glass vessel (tube or bottle).
20 minute whole blood clotting test (20WBCT)
• Place a few mls of freshly sampled venous blood in a small glass vessel
• Leave undisturbed for 20 minutes at ambient temperature
• Tip the vessel once
• If the blood is still liquid (unclotted) and runs out, the patient has hypo-
fibrinogenaemia (“incoagulable blood”) as a result of venom-induced
consumption coagulopathy
• In the South East Asian region, incoagulable blood is diagnostic of a viper bite
and rules out an elapid bite
• Warning! If the vessel used for the test is not made of ordinary glass, or if it
has been used before and cleaned with detergent, its wall may not stimulate
clotting of the blood sample in the usual way and test will be invalid
• If there is any doubt, repeat the test in duplicate, including a “control” (blood
from a healthy person)

Other tests
Haemoglobin concentration/haematocrit: a transient increase indicates
haemoconcentration resulting from a generalised increase in capillary permeability
(eg in Russell’s viper bite). More often, there is a decrease reflecting blood loss or, in
the case of Indian and Sri Lankan Russell’s viper bite, intravascular haemolysis.
Platelet count: this may be decreased in victims of viper bites.
White blood cell count: an early neutrophil leucocytosis is evidence of systemic

envenoming from any species.
Blood film: fragmented red cells (“helmet cell”, schistocytes) are seen when
there is microangiopathic haemolysis.
Plasma/serum may be pinkish or brownish if there is gross haemoglobinaemia

or myoglobinaemia.
Biochemical abnormalities: aminotransferases and muscle enzymes (creatine

kinase, aldolase etc) will be elevated if there is severe local damage or, particularly, if
there is generalised muscle damage (Sri Lankan and South Indian Russell’s viper
bites, sea snake bites). Mild hepatic dysfunction is reflected in slight increases in
other serum enzymes. Bilirubin is elevated following massive extravasation of blood.
Creatinine, urea or blood urea nitrogen levels are raised in the renal failure of Russell’s
viper and saw-scaled viper bites and sea snake bites. Early hyperkalaemia may be
seen following extensive rhabdomyolysis in sea snake bites. Bicarbonate will be low
in metabolic acidosis (eg enal failure).
Arterial blood gases and pH may show evidence of respiratory failure (neurotoxic
envenoming) and acidaemia (respiratory or metabolic acidosis).
Warning: arterial puncture is contraindicated in patients with haemostatic

abnormalities (Viperidae)
Desaturation: arterial oxygen desaturation can be assessed non-invasively in

patients with respiratory failure or shock using a finger oximeter.
Urine examination: the urine should be tested by dipsticks for blood/

haemoglobin/myoglobin. Standard dipsticks do not distinguish blood, haemoglobin
and myoglobin. Haemoglobin and myoglobin can be separated by immunoassays
but there is no easy or reliable test. Microscopy will confirm whether there are
erythrocytes in the urine. Red cell casts indicate glomerular bleeding. Massive
proteinuria is an early sign of the generalised increase in capillary permeability in
Russell’s viper envenoming.

4.6 Antivenom treatment
Antivenom is the only specific antidote to snake venom. A most important decision
in the management of a snake bite victim is whether or not to give antivenom.
What is antivenom?
Antivenom is immunoglobulin (usually the enzyme refined F(ab)2 fragment of IgG)
purified from the serum or plasma of a horse or sheep that has been immunised with
the venoms of one or more species of snake. “Specific” antivenom, implies that the
antivenom has been raised against the venom of the snake that has bitten the patient
and that it can therefore be expected to contain specific antibody that will neutralise
that particular venom. Monovalent or monospecific antivenom neutralises the venom
of only one species of snake. Polyvalent or polyspecific antivenom neutralises the
venoms of several different species of snakes, usually the most important species,
from a medical point of view, in a particular geographical area. For example, Haffkine,
Kasauli, Serum Institute of India and Bengal “polyvalent anti-snake venom serum” is
raised in horses using the venoms of t he four most important venomous snakes in
India (Indian cobra, Naja naja; Indian krait, Bungarus caeruleus; Russell’s viper, Daboia
russelii; saw-scaled viper, Echis carinatus). Antibodies raised against the venom ofone
species may have cross-neutralising activity against other venoms, usually from closely
related species. This is known as paraspecific activity. For example, the manufacturers
of Haffkine polyvalent anti-snake venom serum claim that this antivenom also
neutralises venoms of two Trimeresurus species.
Indications for antivenom treatment (see also Annex 1 & 2)
Antivenom treatment carries a risk of severe adverse reactions and in most countries
it is costly and may be in limited supply. It should therefore be used only in patients
in whom the benefits of antivenom treatment are considered to exceed the risks.
Indications for antivenom vary in different countries.
Inappropriate use of antivenom

In some parts of the world, antivenom is given to any patient claiming to have been
bitten by a snake, irrespective of symptoms or signs of envenoming. Sometimes the
local community are so frightened of snake bite that they compel the doctor to give
antivenom against medical advice. These practices should be strongly discouraged
as they expose patients who may not need treatment to the risks of antivenom
reactions; they also waste valuable and scarce stocks of antivenom.

Indications for antivenom
Antivenom treatment is recommended if and when a patient with proven or

suspected snake develops one or more of the following signs
Systemic envenoming
• Haemostatic abnormalities: spontaneous systemic bleeding (clinical),
coagulopathy (20WBCT or other laboratory) or thrombocytopenia (<100 x
109/litre) (laboratory)
• Neurotoxic signs: ptosis, external ophthalmoplegia, paralysis etc (clinical)
• Cardiovascular abnormalities: hypotension, shock, cardiac arrhythmia (clinical),
abnormal ECG
• Acute renal failure: oliguria/anuria (clinical), rising blood creatinine/ urea
(laboratory)
• (Haemoglobin-/myoglobin-uria:) dark brown urine (clinical), urine dipsticks, other
evidence of intravascular haemolysis or generalised rhabdomyolysis (muscle
aches and pains, hyperkalaemia) (clinical, laboratory)
• Supporting laboratory evidence of systemic envenoming (see 4.5, page 30)
Local envenoming
• Local swelling involving more than half of the bitten limb (in the absence of a
tourniquet) Swelling after bites on the digits (toes and especially fingers)
• Rapid extension of swelling (for example beyond the wrist or ankle within a
few hours of bites on the hands or feet)
• Development of an enlarged tender lymph node draining the bitten limb
How long after the bite can antivenom be expected to be

effective?
Antivenom treatment should be given as soon as it is indicated. It may reverse systemic
envenoming even when this has persisted for several days or, in the case of haemostatic
abnormalities, for two or more weeks. However, when there are signs of local
envenoming, without systemic envenoming, antivenom will be effective only if it
can be given within the first few hours after the bite.
Prediction of antivenom reactions
Skin and conjunctival “hypersensitivity” tests may reveal IgE mediated Type I
hypersensitivity to horse or sheep proteins but do not predict the large majority of
early (anaphylactic) or late (serum sickness type) antivenom reactions. Since they
may delay treatment and can in themselves be sensitizing, these tests should not
be used.

Contraindications to antivenom
There is no absolute contraindication to antivenom treatment, but patients who
have reacted to horse (equine) or sheep (ovine) serum in the past (for example after
treatment with equine anti-tetanus serum, equine anti-rabies serum or equine or
ovine antivenom) and those with a strong history of atopic diseases (especially severe
asthma) should be given antivenom only if they have signs of systemic envenoming.
Prophylaxis in high risk patients

In the absence of any prophylactic regimen that has proved effective in clinical trials,
these high risk patients may be pre-treated empirically with subcutaneous epinephrine
(adrenaline), intravenous antihistamines (both anti-H1, such as promethazine or
chloramphenicol; and anti- H2, such as cimetidine or ranitidine) and corticosteroid.
In asthmatic patients, prophylactic use of an inhaled adrenergic ∃2 agonist such as
salbutamol may prevent bronchospasm.
Selection of antivenom
Antivenom should be given only if its stated range of specificity includes the species
known or thought to have been responsible for the bite. Liquid antivenoms that have
become opaque should not be used as precipitation of protein indicates loss of
activity and an increased risk of reactions.
Expiry dates quoted by manufacturers are often very conservative. Provided that
antivenom has been properly stored, it can be expected to retain useful activity for
many months after the stated “expiry date”.
If the biting species is known, the ideal treatment is with a monospecific/

monovalent antivenom, as this involves administration of a lower dose of antivenom
protein than with a polyspecific/ polyvalent antivenoms. Polyspecific/polyvalent
antivenoms are preferred in many countries because of the difficulty in identifying
species responsible for bites. Polyspecific antivenoms can be just as effective as
monospecific ones, but since they contain specific antibodies against several different
venoms, a larger dose of antivenom protein must be administered to neutralise a
particular venom.
Administration of antivenom
• Epinephrine (adrenaline) should always be drawn up in readiness before

antivenom is administered.
• Antivenom should be given by the intravenous route whenever possible.
Freeze-dried (lyophilised) antivenoms are reconstituted, usually with 10 ml of sterile

water for injection per ampoule. The freeze-dried protein may be difficult to dissolve.
Two methods of administration are recommended:

(1) Intravenous “push” injection: reconstituted freeze-dried antivenom or neat
liquid antivenom is given by slow intravenous injection (not more than 2
ml/minute). This method has the advantage that the doctor/nurse/dispenser
giving the antivenom must remain with the patient during the time when
some early reactions may develop. It is also economical, saving the use of
intravenous fluids, giving sets, cannulae etc.
(2) Intravenous infusion: reconstituted freeze-dried or neat liquid antivenom is
diluted in approximately 5-10 ml of isotonic fluid per kg body weight (ie
250-500 ml of isotonic saline or 5% dextrose in the case of an adult patient)
and is infused at a constant rate over a period of about one hour.
Local administration of antivenom at the site of the bite is not

recommended!
Although this route may seem rational, it should not be used as it is extremely painful,
may increase intracompartmental pressure and has not been shown to be effective.
Intramuscular injection of antivenom

Antivenoms are large molecules (F(ab )2 fragments or sometimes whole IgG) which,
after intramuscular injection, are absorbed slowly via lymphatics. Bioavailability is
poor, especially after intragluteal injection and blood levels of antivenom never reach
those achieved rapidly by intravenous administration. Other disadvantages are the
pain of injection of large volumes of antivenom and the risk of haematoma formation
in patients with haemostatic abnormalities.
Antivenom must never be given by the intramuscular route if it could be given

intravenously.
Situations in which intramuscular administration might be considered :

• at a peripheral first aid station, before a patient with obvious envenoming is
put in an ambulance for a journey to hospital that may last several hours;
• on an expedition exploring a remote area very far from medical care;
• when intravenous access has proved impossible.
Although the risk of antivenom reactions is less with intramuscular than intravenous
administration, epinephrine (adrenaline) must be readily available. Patients must be
closely observed for at least one hour after starting intravenous antivenom
administration, so that early anaphylactic antivenom reactions can be detected and
treated early with epinephrine (adrenaline).
Under these unusual circumstances, the dose of antivenom should be divided

between a number of sites in the upper anterolateral region of both thighs. A maximum
of 5-10 ml should be given at each site by deep intramuscular injection followed by
massage to aid absorption. Local bleeding and haematoma formation is a problem in
patients with incoagulable blood.

Finding enough muscle mass to contain such large volumes of antivenom is
particularly difficult in children.
Antivenom should never be injected into the gluteal region (upper outer quadrant
of the buttock) as absorption is exceptionally slow and unreliable and there is
always the danger of sciatic nerve damage when the injection is given by an
inexperienced operator.
Dose of antivenom
Snakes inject the same dose of venom into children and adults. Children must
therefore be given exactly the same dose of antivenom as adults.
Manufacturers’ recommendations are usually based on inappropriate animal tests in

which venom and antivenom are incubated before being injected into the test animal.
The recommended dose is often the amount of antivenom required to neutralise the
average venom yield when captive snakes are milked of their venom. In practice, the
choice of an initial dose of antivenom is usually empirical.
Antivenom manufacturers, health institutions and medical research organisations

should encourage and promote the proper clinical testing of antivenoms as with
other therapeutic agents. This is the only reliable guide to the initial dose (and
safety) of an antivenom.
Since the neutralising power of antivenoms varies from batch to batch, the results
of a particular clinical trial may soon become obsolete if the manufacturers change
the strength of the antivenom.
Antivenom reactions
A proportion of patients, usually more than 20%, develop a reaction either early
(within a few hours) or late (5 days or more) after being given antivenom.
Early anaphylactic reactions: usually within 10-180 minutes of starting antivenom,

the patient begins to itch (often over the scalp) and develops urticaria, dry cough,
fever, nausea, vomiting, abdominal colic, diarrhoea and tachycardia. A minority of
these patients may develop severe life-threatening anaphylaxis: hypotension,
bronchospasm and angio-oedema. Fatal reactions have probably been under-reported
as death after snake bite is usually attributed to the venom.
In most cases, these reactions are not truly “allergic”. They are not IgE-mediated
type I hypersensitivity reactions to horse or sheep proteins as there is no evidence of
specific IgE, either by skin testing or radioallergosorbent tests (RAST). Complement
activation by IgG aggregates or residual Fc fragments or direct stimulation of mast
cells or basophils by antivenom protein are more likely mechanisms for these reactions.

Pyrogenic (endotoxin) reactions usually develop 1-2 hours after treatment.
Symptoms include shaking chills (rigors), fever, vasodilatation and a fall in blood
pressure. Febrile convulsions may be precipitated in children. These reactions are
caused by pyrogen contamination during the manufacturing process. They are
commonly reported.
Late (serum sickness type) reactions develop 1-12 (mean 7) days after treatment.
Clinical features include fever, nausea, vomiting, diarrhoea, itching, recurrent urticaria,
arthralgia, myalgia, lymphadenopathy, periarticular swellings, mononeuritis multiplex,
proteinuria with immune complex nephritis and rarely encephalopathy. Patients who
suffer early reactions and are treated with antihistamines and corticosteroid are less
likely to develop late reactions.
Treatment of early anaphylactic and pyrogenic antivenom

reactions
Epinephrine (adrenaline) is given intramuscularly (into the deltoid muscle or the
upper lateral thigh) in an initial dose of 0.5 mg for adults, 0.01 mg/kg body weight for
children. Severe, life-threatening anaphylaxis can evolve very rapidly and so
epinephrine (adrenaline) should be given at the very first sign of a reaction, even
when only a few spots of urticaria have appeared or at the start of itching, tachycardia
or restlessness. The dose can be repeated every 5-10 minutes if the patient’s condition
is deteriorating.
At the earliest sign of a reaction:

• Antivenom administration must be temporarily suspended
• Epinephrine (adrenaline) (0.1% solution, 1 in 1,000, 1 mg/ml) is the effective
treatment for early anaphylactic and pyrogenic antivenom reactions
Additional treatment
After epinephrine (adrenaline), an anti H1 antihistamine such as chlorpheniramine
maleate (adults 10 mg, children 0.2 mg/kg by intravenous injection over a few minutes)
should be given followed by intravenous hydrocortisone (adults 100 mg, children
2 mg/kg body weight). The corticosteroid is unlikely to act for several hours, but may
prevent recurrent anaphylaxis.
There is increasing evidence that anti H2 antihistamines such as cimetidine or

ranitidine have a role in the treatment of severe anaphylaxis. Both drugs are given,
diluted in 20 ml isotonic saline, by slow intravenous injection (over 2 minutes).
Doses: cimetidine – adults 200 mg, children 4 mg/kg;
ranitidine – adults 50 mg, children 1 mg/kg.
In pyrogenic reactions the patient must also be cooled physically and with
antipyretics (for example paracetamol by mouth or suppository). Intravenous fluids
should be given to correct hypovolaemia.

Treatment of late (serum sickness) reactions
Late (serum sickness) reactions usually respond to a 5-day course of oral antihistamine.
Patients who fail to respond in 24-48 hours should be given a 5-day course of
prednisolone.
Doses: Chlorpheniramine: adults 2 mg six hourly, children 0.25 mg/kg /day
in divided doses
Prednisolone: adults 5 mg six hourly, children 0.7 mg/kg/day in divided doses for
5-7 days
Observation of the response to antivenom

If an adequate dose of appropriate antivenom has been administered, the following
responses may be seen.
• General: the patient feels better. Nausea, headache and generalised aches
and pains may disappear very quickly. This may be partly attributable to a
placebo effect.
• Spontaneous systemic bleeding (eg from the gums) usually stops within 15-
30 minutes.
• Blood coagulability (as measured by 20WBCT) is usually restored in 3-9
hours. Bleeding from new and partly healed wounds usually stops much
sooner than this.
• In shocked patients, blood pressure may increase within the first 30-60
minutes and arrhythmias such as sinus bradycardia may resolve.
• Neurotoxic envenoming of the post-synaptic type (cobra bites) may begin
to improve as early as 30 minutes after antivenom, but usually take several
hours. Envenoming with presynaptic toxins (kraits and sea snakes) is unlikely
to respond in this way.
• Active haemolysis and rhabdomyolysis may cease within a few hours and
the urine returns to its normal colour.
Recurrence of systemic envenoming

In patients envenomed by vipers, after an initial response to antivenom (cessation of
bleeding, restoration of blood coagulability), signs of systemic envenoming may recur
within 24-48 hours.
This is attributable to:
(1) continuing absorption of venom from the “depot” at the site of the bite,
perhaps assisted by improved blood supply following correction of shock,
hypovolaemia etc, after elimination of antivenom (range of elimination half-
lives: IgG 45 hours; F(ab)2 80-100 hours; Fab 12-18 hours);
(2) a redistribution of venom from the tissues into the vascular space, as the
result of antivenom treatment.
Recurrent neurotoxic envenoming after treatment of cobra bite has also been
described.

Criteria for repeating the initial dose of antivenom
Criteria for giving more antivenom
• Persistence or recurrence of blood incoagulability after 6 hr of bleeding after

1-2 hr
• Deteriorating neurotoxic or cardiovascular signs after 1-2 hr
If the blood remains incoagulable (as measured by 20WBCT) six hours after the
initial dose of antivenom, the same dose should be repeated. This is based on the
observation that, if a large dose of antivenom (more than enough to neutralise the
venom procoagulant enzymes) is given initially, the time taken for the liver to restore
coagulable levels of fibrinogen and other clotting factors is 3-9 hours.
In patients who continue to bleed briskly, the dose of antivenom should be

repeated within 1-2 hours.
In case of deteriorating neurotoxicity or cardiovascular signs, the initial dose

of antivenom should be repeated after 1-2 hours, and full supportive treatment must
be considered.
Conservative treatment when no antivenom is available

This will be the situation in many parts of the region, where supplies of antivenom
run out or where the bite is known to have been inflicted by a species against whose
venom there is no available specific antivenom (for example for bites by the Malayan
krait (Bungarus candidus), coral snakes - genera Calliophis and Maticora), sea snakes,
the mangrove/shore pit viper T purpureomaculatus and the mountain pit viper Ovophis
monticola.
The following conservative measures are suggested:

Neurotoxic envenoming with respiratory paralysis: assisted ventilation. This
has proved effective, and has been followed by complete recovery, even after being
maintained for periods of more than one month. Manual ventilation (anaesthetic
bag) by relays of doctors, medical students, relatives and nurses has been effective
where no mechanical ventilator was available. Anticholinesterases should always be
tried (see below Trial of anticholinesterase, p 41).
Haemostatic abnormalities – strict bed rest to avoid even minor trauma;

transfusion of clotting factors and platelets; ideally, fresh frozen plasma and
cryoprecipitate with platelet concentrates or, if these are not available, fresh whole
blood. Intramuscular injections should be avoided.
Shock, myocardial damage: hypovolaemia should be corrected with colloid/

crystalloids, controlled by observation of the central venous pressure. Ancillary pressor

drugs (dopamine or epinephrine-adrenaline) may also be needed. Patients with
hypotension associated with bradycardia should be treated with atropine.
Renal failure: conservative treatment or dialysis (see Oliguria and renal failure,
page 42).
Dark brown urine (myoglobinuria or haemoglobinuria): correct hypovolaemia

and acidosis and consider a single infusion of mannitol (see Prevention of renal damage
in patients with myoglobinuria or haemoglobinuria, page 45 ).
Severe local envenoming: local necrosis, intracompartmental syndromes and

even thrombosis of major vessels is more likely in patients who cannot be treated
with antivenom. Surgical intervention may be needed but the risks of surgery in a
patient with consumption coagulopathy, thrombocytopenia and enhanced fibrinolysis
must be balanced against the lifethreatening complications of local envenoming.
Prophylactic broad spectrum antimicrobial treatment is justified (see Bacterial
infections, page 46).
4.7 Supportive/ancillary treatment

Antivenom treatment can be expected to neutralise free circulating venom, prevent
progression of envenoming and allow recovery. However, these processes take time
and the severely envenomed patient may require life support systems such as assisted
ventilation and renal dialysis until the severely damaged organs and tissues have had
time to recover.
Dangers of venepuncture in patients with haemostatic

abnormalities
In patients with incoagulable blood, any injection (subcutaneous, intramuscular) and,
particularly venepuncture, carries a risk of persistent bleeding and haematoma
formation. Arterial puncture is contraindicated in such patients.
Repeated venepuncture can be avoided by using an indwelling cannula and three-

way tap system. When blood coagulability has been restored, the dead space should
be filled with heparinised saline, but beware! If this is not flushed out before blood
sampling, misleading results will be obtained in clotting tests, including the 20WBCT.
In patients with coagulopathy, sites of venous access and placement of intravenous

cannulae or catheters should be chosen where haemostasis by external pressure is
most likely to be effective, eg the antecubital fossa. If possible, avoid jugular, subclavian
and femoral vein puncture. A pressure pad must be applied at the site of any
venepuncture.
Neurotoxic envenoming
Antivenom treatment alone cannot be relied upon to save the life of a patient with
bulbar and respiratory paralysis.

Death may result from aspiration, airway obstruction or respiratory failure. A
clear airway must be maintained. Once there is loss of gag reflex and pooling of
secretions in the pharynx, failure of the cough reflex or respiratory distress, a cuffed
endotracheal tube should be inserted. If this is impossible for any reason, a
tracheostomy should be performed and a snugly-fitting or cuffed tracheostomy tube
inserted.
Although artificial ventilation was first suggested for neurotoxic envenoming 125
years ago, patients continue to die of asphyxiation because some doctors believe
that antivenom is sufficient treatment.
Anticholinesterase drugs have a variable, but potentially very useful effect in

patients with neurotoxic envenoming, especially those bitten by cobras.
A trial of anticholinesterase (eg “Tensilon test”) should be performed in every

patient with neurotoxic envenoming, as it would be in any patient with suspected
myasthenia gravis.
Trial of anticholinesterase
Anticholinesterase (eg “Tensilon”/edrophonium) test
• Baseline observations
• Give atropine intravenously
• Give anticholinesterase drug
• Observe effect
• If positive, institute regular atropine and (long acting) anticholinesterase
Ideally, a short acting anticholinesterase, such as edrophonium (“Tensilon”), should

be used. Baseline observations or measurements are made against which to assess
the effectiveness of the anticholinesterase. Atropine sulphate (adults 0.6 mg, children
50 µg/kg body weight) is given by intravenous injection (to prevent the undesirable
muscarinic effects of acetylcholine such as increased secretions, sweating, bradycardia
and colic) followed immediately by edrophonium chloride (adults 10 mg, children
0.25 mg/kg body weight) given intravenously over 3 or 4 minutes. The patient is
observed over the next 10-20 minutes for signs of improved neuromuscular
transmission. Ptosis may disappear (Fig 43) and ventilatory capacity (peak flow, FEV1
or maximum expiratory pressure) may improve.
If edrophonium chloride is not available, any other anticholinesterases

(neostigmine – “Prostigmine”, distigmine, pyridostigmine, ambenomium) can be used
for this assessment but a longer period of observation will be needed (up to 1 hour).
Patients who respond convincingly can be maintained on a longer-acting

anticholinesterase such as neostigmine methylsulphate combined with atropine.

Figure 43: (a) before and (b) after intravenous atropine followed by intravenous edrophonium
chloride in a patient envenomed by a Malayan krait (Bungarus candidus) (Copyright DA Warrell)
Hypotension and shock
Snake bite: causes of hypotension and shock

(1) Anaphylaxis (2) Antivenom reaction
Vasodilatation Respiratory failure
Cardiotoxicity Acute pituitary adrenal insufficiency
Hypovolaemia Septicaemia
This is usually the result of hypovolaemia (from loss of circulating volume into the
swollen limb, or internal/external haemorrhage), venom-induced vasodilatation or
direct myocardial effects with or without arrhythmias. Ideally, treatment with plasma
expanders (colloids or crystalloid) should be controlled by observation of the central
venous pressure (jugular venous pressure or direct measurement of pressure in the
superior vena cava via a catheter connected to a saline manometer, see Annex 4).
Excessive volume replacement may cause pulmonaryoedema when plasma
extravasated in the bitten limb and elsewhere is reabsorbed into the circulation.
In patients with evidence of a generalised increase in capillary permeability, a

selective vasoconstrictor such as dopamine may be given by intravenous infusion,
preferably into a central vein (starting dose 2.5-5 µg/kg/minute).
In victims of Russell’s viper bites in Myanmar and South India, acute pituitary
adrenal insufficiency resulting from haemorrhagic infarction of the anterior pituitary
may contribute to shock. Hydrocortisone is effective in these cases.
Oliguria and renal failure

Detection of renal failure
• Dwindling or no urine output
• Rising blood urea/creatinine concentrations
• Clinical “uraemia syndrome”
nausea, vomiting, hiccups, fetor, drowsiness, confusion, coma, flapping tremor,
muscle twitching, convulsions, pericardial friction rub, signs of fluid overload

In patients with any of these features, the following should be monitored
• pulse rate
• blood pressure, lying and sitting, to detect postural hypotension
• respiratory rate
• temperature
• height of jugular venous pulse
• auscultation of lung bases for crepitations
Oliguric phase of renal failure

Most, but not all, patients with acute renal failure are oliguric, defined as a urine
output of less than 400 ml/day or less than 20 ml/hour. Conservative management
may tide the patient over, avoiding the need for dialysis. If the patient is hypovolaemic,
indicated by supine or postural hypotension, empty neck veins, sunken eyeballs, loss
of skin turgor and dryness of mucosae, proceed as follows:
(1) Establish intravenous access
(2) Insert a urethral catheter (full sterile precautions!)
(3) Determine the central venous pressure. This can be achieved either by
observing the vertical height of the jugular venous pulsation above the sternal
angle with the patient propped up on pillows at 45 o; or by direct
measurement of central venous (superior vena caval) pressure through a
long catheter preferably inserted at the antecubital fossa (see Annex 4). The
catheter is connected to a saline manometer, the 0 point of which must be
placed at the same level as the right atrium (that is, at the sternal angle
when the patient is propped up at 45o). In someone who is obviously volume-
depleted, resuscitation should start immediately, and not be delayed until a
central venous line has been inserted.
(4) Fluid challenge: depending on the initial state of hydration/dehydration,
an adult patient can be given two litres of isotonic saline over one hour or,
until the jugular venous pressure/central venous pressure has risen to 8-10
cm above the sternal angle (with the patient propped up at 45o). The patient
must be closely observed while this is being done. The fluid challenge must
be stopped immediately if pulmonary oedema develops. If the urine output
does not improve, try furosamide challenge.
(5) Furosamide (frusemide) challenge: 100 mg of furosamide is injected slowly
(4-5 mg/minute). If this does not induce a urine output of 40 ml/hour, give
a second dose of furosamide, 200 mg. If urine output does not improve, try
mannitol challenge.
(6) Mannitol challenge: 200 ml of 20% mannitol may be infused intravenously
over 20 minutes but this must not be repeated as there is a danger of
inducing dangerous fluid and electrolyte imbalance. An improvement in
urine output to more than 40 ml/hr or more than 1 litre/day is considered
satisfactory.
(7) Conservative management: If the urine output does not improve, despite
these challenges, no further diuretics should be given and fluid intake should

be restricted to a total of the previous day’s output plus “insensible losses”
(500-1000 ml/day). If possible, the patient should be referred to a renal
unit. The diet should be bland, high in calories (1700/day), low in protein
(less than 40g/day), low in potassium (avoid fruit, fruit juices and potassium-
containing drugs) and low in salt. Infections will cause tissue breakdown
and increase urea levels. They should be prevented or treated promptly
with non-nephrotoxic antibiotics (ie avoid aminoglycosides such as
gentamicin).
(8) Biochemical monitoring: Serum potassium, urea, creatinine and, if possible,
pH, bicarbonate, calcium and phosphate should be monitored frequently.
If this is not possible the electrocardiogram (ECG) should be examined for
evidence of hyperkalaemia, especially following bites by sea snakes, or Sri
Lankan or South Indian Russell’s vipers or if the patient is passing dark
brown urine, indicating rhabdomyolysis or intravascular haemolysis.
ECG evidence of hyperkalaemia: tall peaked T waves, prolonged P-R
interval, absent P waves, wide QRS complexes.
Emergency treatment of hyperkalaemia

(serum potassium >6.5 mmol/l or ECG changes)
• give 10 ml of 10% calcium gluconate intravenously over 2 minutes

(with ECG monitoring if possible) repeated up to three times
• give 50 ml of 50% dextrose with 10 units of soluble insulin intravenously
• sodium bicarbonate (40 ml of 8.4%) by slow intravenous infusion and
a â2 agonist aerosol by inhaler (eg salbutamol – “Ventolin” 5-10 mg)
may also be used
These emergency treatments will control hyperkalaemia for 3-6 hours

only. If the patient is hypotensive and profoundly acidotic (deep sighing
“Kussmaul” respirations, very low plasma bicarbonate concentration or very
low pH - <7.10), 40 ml of 8.4% sodium bicarbonate (1 mmol/ml) may be
infused intravenously over 30 minutes. If this leads to circulatory
improvement, the dose can be repeated.
Caution: Intravenous bicarbonate may precipitate profound
hypocalcaemia and fitting, especially in patients with rhabdomyolysis.
(9) Dialysis
Indications for dialysis

• Clinical uraemia
• Fluid overload
• Blood biochemistry – one or more of the following
creatinine >6 mg/dl (500 µmol/l)
urea >200 mg/dl (400 mmol/l)
potassium >7 mmol/l (or hyperkalaemic ECG changes)
symptomatic acidosis

Prevention of renal damage in patients with myoglobinuria or
haemoglobinuria
To minimise the risk of renal damage from excreted

myoglobin and/or haemoglobin:
• correct hypovolaemia (see above) and maintain saline diuresis (if possible)
• correct severe acidosis with bicarbonate (see above)
• give a single infusion of mannitol (200 ml of 20% solution over 20 minutes)
Diuretic phase of renal failure

Urine output increases following the period of anuria. The patient may become
polyuric and volume depleted so that salt and water must be carefully replaced.
Hypokalaemia may develop, in which case a diet rich in potassium (fruit and fruit
juices) is recommended.
Renal recovery phase

The diuretic phase may last for months after Russell’s viper bite. In Myanmar and
South India, hypopituitarism may complicate recovery of Russell’s viper bite victims.
Corticosteroid, fluid and electrolyte replacement may be needed in these patients.
Persisting renal dysfunction

In Myanmar, persistent tubular degenerative changes were observed in Russell’s viper
bite victims who showed continuing albuminuria, hypertension and nocturia for up
to 11 months after the bite, despite apparent recovery in renal function. In India, 20-
25% of patients referred to renal units with acute renal failure following Russell’s
viper bite suffered oliguria for more than 4 weeks suggesting the possibility of bilateral
renal cortical necrosis. This can be confirmed by renal biopsy or contrast enhanced
CT scans of the kidneys. Patients with patchy cortical necrosis show delayed and
partial recovery of renal function but those with diffuse cortical necrosis require
regular maintenance dialysis and eventual renal transplantation.
Haemostatic disturbances
Bleeding and clotting disturbances usually respond satisfactorily to treatment with
specific antivenom, but the dose may need to be repeated several times, at six hourly
intervals, before blood coagulability (assessed by the 20WBCT) is finally and
permanently restored.
In exceptional circumstances, such as severe bleeding or imminent urgent surgery,

once specific antivenom has been given to neutralise venom procoagulants and other
antihaemostatic toxins, restoration of coagulability and platelet function can be
accelerated by giving fresh frozen plasma, cryoprecipitate (fibrinogen, factor VIII),
fresh whole blood or platelet concentrates.

Heparin is ineffective against venom-induced thrombin and may cause bleeding
on its own account. It should never be used in cases of snake bite.
Antifibrinolytic agents are not effective and should not be used in victims of
snake bite.
4.8 Treatment of the bitten part

The bitten limb, which may be painful and swollen, should be nursed in the most
comfortable position, preferably slightly elevated, to encourage reabsorption of
oedema fluid. Bullae may be large and tense but they should be aspirated only if
they seem likely to rupture.
Bacterial infections
Infection at the time of the bite with organisms from the snake’s venom and buccal
cavity is a problem with some species such as the Malayan pit viper. In this case, a
prophylactic course of penicillin (or erythromycin for penicillin-hypersensitive patients)
and a single dose of gentamicin or a course of chloramphenicol, together with a
booster dose of tetanus toxoid is recommended. Interference with the wound
(incisions made with an unsterilised razor blade/knife etc) creates a risk of secondary
bacterial infection and justifies the use of broad spectrum antibiotics (eg amoxycillin
or a cephalosporin plus a single dose of gentamicin plus metronidazole).
Compartmental syndromes and fasciotomy

The appearance of an immobile, tensely-swollen, cold and apparently pulseless snake-
bitten limb may suggest to surgeons the possibility of increased intracompartmental
pressure, especially if the digital pulp spaces or the anterior tibial compartment are
involved. Swelling of envenomed muscle within such tight fascial compartments could
result in an increase in tissue pressure above the venous pressure, resulting in
ischaemia. However, the classical signs of an intracompartmental pressure syndrome
may be difficult to assess in snake bite victims.
Clinical features of a compartmental syndrome

• Disproportionately severe pain
• Weakness of intracompartmental muscles
• Pain on passive stretching of intracompartmental muscles
• Hypoaesthesia of areas of skin supplied by nerves running through the
compartment
• Obvious tenseness of the compartment on palpation
Detection of arterial pulses by palpation or doppler ultrasound probes, does not

exclude intracompartmental ischaemia. The most reliable test is to measure

Figure 44: Disastrous results of unnecessary fasciotomy in snake bite victims (a) profuse
bleeding in a patient with mild local envenoming but severe coagulopathy following a bite by a
green pit viper (Trimeresurus albolabris) (Copyright Sornchai Looareesuwan). Disastrous results
of unnecessary fasciotomy in snake bite victims (b) Persistent bleeding for 10 days, resulting in
haemorrhagic shock despite transfusion of 20 unites of blood, in a victim of Malayan pit viper
bite in whom fasciotomy was performed before adequate antivenom treatment had been given to
correct the coagulopathy (Copyright DA Warrell). (Right) Disastrous results of unnecessary
fasciotomy in snake bite victims (c) Residual skin loss and exposure of tendons following
fasciotomy for mild local envenoming in a patient bitten by a green pit viper (Trimeresurus
albolabris) (Copyright Sornchai Looareesuwan)
intracompartmental pressure directly through a cannula introduced into the

compartment and connected to a pressure transducer or manometer (Annex 5). In
orthopaedic practice, intracompartmental pressures exceeding 40 mmHg (less in
children) may carry a risk of ischaemic necrosis (eg Volkmann’s ischaemia or anterior
tibial compartment syndrome). However, fasciotomy should not be contemplated
until haemostatic abnormalities have been corrected, otherwise the patient may
bleed to death (Fig 44). Animal studies have suggested that muscle sufficiently
envenomed and swollen to cause intracompartmental syndromes, may already be
irreversibly damaged by the direct effects of the venom. Early treatment with
antivenom remains the best way of preventing irreversible muscle damage.
Criteria for fasciotomy in snake-bitten limbs

Haemostatic abnormalities have been corrected (antivenom with or without clotting
factors)
• clinical evidence of an intracompartmental syndrome
• intracompartmental pressure >40 mmHg (in adults)
4.9 Rehabilitation
Restoration of normal function in the bitten part after the patient has been discharged
from hospital is not usually supervised. Conventional physiotherapy may well
accelerate this process. In patients with severe local envenoming, the limb should be
maintained in a functional position. For example, in the leg, equinus deformity of
the ankle should be prevented by application of a back slab.

5
Management of Cobra
Spit Ophthalmia
First aid consists of irrigating the affected eyes and other mucous membranes with
liberal quantities of water or any other available bland liquid. Instillation of 0.5%
adrenaline drops relieves pain and inflammation. In view of the risk of corneal abrasion,
fluorescein staining or slit lamp examination is essential. Otherwise, topical
antimicrobials (tetracycline or chloramphenicol) should be applied to prevent
endophthalmitis or blinding corneal opacities. Some ophthalmologists recommend
the use of a dressing pad to close the eye.
The instillation of diluted antivenom may cause local irritation and is of uncertain
benefit. It is not recommended.

6
Conclusions and Main

Recommendations
1. It is clear that in many parts of the South East Asian region, snake bite is an
important medical emergency and cause of hospital admission. It results in the
death or chronic disability of many active younger people, especially those
involved in farming and plantation work. However, the true scale of mortality
and acute and chronic morbidity from snake bite remains uncertain because of
inadequate reporting in almost every part of the region.
To remedy this deficiency, it is strongly recommended that snake bite should be

made a specific notifiable disease in all countries in the South East Asian region.
2. Snake bite is an occupational disease of farmers, plantation workers, herdsmen,

fishermen and other food producers. It is therefore a medical problem that has
important implications for the nutrition and economy of the countries where it
occurs commonly.
It is recommended that snake bite should be formally recognised as an important

occupational disease in the South East Asian region.
3. Despite its importance, there have been fewer proper clinical studies of snake
bite than of almost any other tropical disease. Snake bites probably cause more
deaths in the region than do Entamoeba histolytica infections but only a small
fraction of the research investment in amoebiasis has been devoted to the study
of snake bite.
It is recommended that governments, academic institutions, pharmaceutical,

agricultural and other industries and other funding bodies, should actively encourage
and sponsor properly designed clinical studies of all aspects of snake bite.

4. Some ministries of health in the region have begun to organise training of doctors
and other medical workers in the clinical management of snake bite patients.
However, medical personnel throughout the region would benefit from more
formal instruction on all aspects of the subject. This should include the
identification of medically-important species of snake, clinical diagnosis and the
appropriate use of antivenoms and ancillary treatments.
It is recommended that education and training on snake bite should be included

in the curriculum of medical schools and should be addressed specifically through
the organisation of special training courses and other educational events.
5. Community education on snake bite is outside the terms of eference of this

publication. However, it is clear that this is an essential component of any
community programme for prevention of snake bite.
Community education about venomous snakes and snake bite is strongly

recommended as the method most likely to succeed in preventing bites.
6. Most of the familiar methods for first-aid treatment of snake bite, both western
and “traditional/herbal”, have been found to result in more harm (risk) than
good (benefit). Their use should be discouraged and they should never be allowed
to delay the movement of the patient to medical care at the hospital or dispensary.
Recommended first-aid methods emphasise reassurance, immobilisation of the

bitten limb and movement of the patient to a place where they can receive medical
care as soon as possible.
7. Diagnosis of the species of snake responsible for the bite is important for optimal
clinical management. This may be achieved by identifying the dead snake or by
inference from the “clinical syndrome” of envenoming.
A syndromic approach should be developed for diagnosing the species responsible

for snake bites in different parts of the region.
8. Antivenom is the only effective antidote for snake venom. However, it is usually
expensive and in short supply and its use carries the risk of potentially dangerous
reactions.
• It is recommended that antivenom should be used only in patients in whom

the benefits of treatment are considered to exceed the risks. Indications for
antivenom include signs of systemic and/or severe local envenoming.
• Skin/conjunctival hypersensitivity testing does not reliably predict early or late
antivenom reactions and is not recommended.

• It is recommended that whenever possible antivenom should be given by slow
intravenous injection or infusion.
• Epinephrine (adrenaline) should always be drawn up in readiness in case of an
early anaphylactic antivenom reaction.
• Subcutaneous epinephrine (adernaline) may reduce the incidence of early
antivenom reactions if given immediately before the start of antivenom
treatment.
9.
When no antivenom is available, judicious conservative treatment can in many

cases save the life of the patient.
10.
In the case of neurotoxic envenoming with bulbar and respiratory paralysis,

antivenom alone cannot be relied upon to prevent early death from asphyxiation.
Artificial ventilation is essential in such cases.
11.
Conservative management and, in some cases, dialysis, is an effective supportive

treatment for acute renal failure in victims of Russell’s viper, saw-scaled viper and
sea snake bites.
12.
Fasciotomy should not be carried out in snake bite patients unless or until
haemostatic abnormalities have been corrected, clinical features of an
intracompartmental syndrome are present and a high intracompartmental pressure
has been confirmed by direct measurement.

7
Further Reading
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383-392.
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Bon C, Goyffon M (1996). Envenomings and their treatments. Editions Fondation

Marcel Mérieux, Lyon.
Bücherl W, Buckley EE & Deulofeu V (eds) (1968, 1971). Venomous animals and
their venoms. Vols 1 and 2. Academic Press, New York.
Chugh KS (1989). Snake-bite-induced acute renal failure in India. Kidney International

35: 891-907.
Gans C & Gans KA (eds) (1978). Biology of the reptilia. Vol 8. Academic Press, London.
Gopalakrishnakone P (ed) (1994). Sea snake toxinology. National University of

Singapore Press.
Gopalakrishnakone P & Chou LM (eds) (1990). Snakes of medical importance (Asia-

Pacific region). National University of Singapore Press.
Ho M et al (1986). Clinical significance of venom antigen levels in patients envenomed

by the Malayan pit viper (Calloselasma rhodostoma). American J Trop Med Hyg 34:
579-587.
Ho M et al (1990). Pharmacokinetics of three commercial antivenoms in patients

envenomed by the Malayan pit viper (Calloselasma rhodostoma) in Thailand. American
J Trop Med Hyg 42: 260-66.

Hutton RA et al (1990). Arboreal green pit vipers (genus Trimeresurus) of South East
Asia: bites by T albolabris and T macrops in Thailand and a review of the literature.
Transactions Roy Soc Trop Med Hyg 84: 866-874.
Junghanss T & Bodio M (1995). Notfal-Handbuch Gifttiere. Diagnose-Terapie-Biologie.

Georg Thieme Verlag, Stuttgart.
Lee C-Y (ed) (1979). Snake venoms. Handbook of experimental pharmacology. Vol
52. Springer-Verlag, Berlin.
Looareesuwan S, Viravan C, Warrell DA (1988). Factors contributing to fatal snake

bite in the rural tropics: analysis of 46 cases in Thailand. Trans Roy Soc Trop Med Hyg
82: 930-4.
Malasit P et al (1986). Prediction, prevention and mechanism of early (anaphylactic)

antivenom reactions in victims of snake bites. British Medical Journal 292: 17-20.
Matsen FA (1980). Compartmental syndromes. New York: Grune & Stratton. May
Mya Win (1996). Snake bite control for primary health care providers. 1st edition.
WHO Snake Bite control Project, Myanmar.
Myint-Lwin et al (1985). Bites by Russell’s viper (Vipera russelli siamensis) in Burma:

haemostatic, vascular and renal disturbances in response to treatment. Lancet ii:
1259-64.
Phillips RE et al (1988). Paralysis, rhabdomyolysis and haemolysis caused by bites of

Russell’s viper (Vipera russelli pulchella) in Sri Lanka: failure of Indian (Haffkine)
antivenom. Quarterly Journal Medicine 68: 691-716.
Reid HA, Thean PC, Chan KE, Baharom AR (1963). Clinical effects of bites by Malayan
viper (Ancistrodon rhodostoma). Lancet i: 617-21.
Reid HA (1964). Cobra bites. BMJ 2: 540-545.
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India and South East Asia. In: Venomous Animals and their Venoms [Bücherl W,
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Reid HA (1975). Epidemiology of sea snake bites. J Trop Med Hyg 78: 106-113.
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Reid HA & Lim KJ (1957). Sea snake bite. A survey of fishing villages in northwest
Malaya. BMJ 2: 1266-1272.
Reid HA, Thean PC & Martin WJ (1963). Specific antivenene and prednisone in
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Saini RK et al (1986). Snake bite poisoning presenting as early morning neuroparalytic
symptoms in jhuggi dwellers. J Assoc Physns India 34: 415-417.
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test (WBCT20) as an indicator of low plasma fibrinogen concentration in patients
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Sitprija V, Boonpucknavig V (1979). Snake venoms and nephrotoxicity. In: Lee C-Y
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for elapid snake bite. Lancet i: 183-186.
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viper bite in Burma. British J Haematology 65: 193-198.
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Acta Tropica, Basel 46: 23-38.
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Roy Soc Trop Med Hyg 84: 875-879.
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currently available for the treatment of envenoming by bites and stings. Toxicon 29:
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and Sri Lankan cobra (Naja naja naja): efficacy and complications of theray with
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Thein-Than et al (1991). Development of renal function abnormalities following

Russell’s viper (Vipera russelli siamensis) bite in Myanmar. Trans Roy Soc Trop Med
Hyg 85: 404-409.
Thorpe RS, Wüster W, Malhotra A (eds) (1997). Venomous snakes. Ecology, evolution
and snake bite. Symposia of the Zoological Society of London No 70, Clarendon
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in Myanmar. Trans Roy Soc Trop Med Hyg 87: 678-681.

Tin-Myint et al (1991). Bites by the king cobra (Ophiophagus hannah) in Myanamar:
successful treatment of severe neurotoxic envenoming. QJM 80: 751-762.
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Warrell DA (1995). Clinical toxicology of snake bite in Asia. In: Clinical Toxicology of
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envenoming by cobras (Naja naja philippinensis): a placebo-controlled study. New
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important cause of death among rice farmers. Am J Trop Med Hyg 37(3): 636-639.
Watt G et al (1988). Tourniquet application after cobra bite: delay in the onset of
neurotoxicity and the dangers of sudden release. American J Trop Med & Hyg 38:
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cobra-bite paralysis. Trans Roy Soc Trop Med Hyg 83: 570-3.
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widely overlooked spitting cobra from South East Asia: geographic variation, medical
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Annex
1
Algorithm: Antivenom
Treatment of Snakebite Cases
Patient presents with
history of snakebite
No Snake brought Yes

into hospital
Signs of No Snake clearly

envenoming
present identified
No Yes
Treatment*
observe in hospital Yes Snake defintely
for 24 hours non-venomous
No Yes
Treatment
Signs diagnostic of
envenoming by a Signs of Reassure, give
envenoming tetanus toxoid
particular species present then discharge
found in this
geographical area Yes No
(see algorithm 2) Treatment*
Signs meet criteria No Observe in hospital
Yes
for antivenom
No treatment for 24 hours
Yes
Signs meet criteria Appropriate
for antivenom monospecific or
treatment polyspecific
antivenom available No
No Yes
Yes
Treatment* Treatment* Treatment* Treatment*
Give polyspecific Give appropriate Treat conservatively
Observe in hospital
antivenom covering monospecific or (refer to section
for 24 hours
medically important polyspecific 5.6.16)
species in this antivenom
geographical area
Check response
Treatment* Treatment*
observe in No Signs of persisting Yes Repeat intial dose

hospital systemic of antivenom
envenoming
*Patients must be assessed carefully for signs of emerging or recurrent

envenoming and appropriate action taken.

Annex
2
Algorithm: Differentiating
Major Asian Snake Species
by Clincal Syndrome
Patient presents with a history
of snakebite but no dead snake and
little/no description of the snake
Neurotoxic Yes Marked local No Neurotoxic

signs swelling signs
No Yes Yes No
Treatment*
Non-clotting Observe in
In Sri Lanka or Bitten on
blood (20WBCT) hospital for
South India the land
or spontaneous 24 hours
systemic bleeding
Yes No Yes
No Yes No
Non-clotting Myalgia and/or

Early bistering Cobra or king In the
Viper bite blood (20WBCT) black urine or
or necrosis cobra bite Philippines
or spontaneous renal failure
systemic bleeding Yes No
Treatment* No
or black urine Treatment Treatment Treatment
Oberve in Sea snake bite:
Local necrosis Philippine Krait bite:
hospital for Renal failure give appropiate
Yes cobra bite: give
24 hours evident
give anti- appropriate anitvenom
Yes Yes No cholinesterase antivenom
Treatment Yes
Cytotoxic cobra Russell’s viper and
No Bite by very large appropiate
bite: give present in this
snake and king antivenom
appropriate area
No cobra occurs in
antivenom
the area
No Yes Yes
No
Treatment Treatment Treatment
Patient describes Russell’s viper Cobra bite: give King cobra bite:
green snake or bite: give anticholinesterase give appropriate
tree snake appropriate and appropriate antivenom
antivenom antivenom
Yes No
Treatment
Malayan pit Probable Malayan Blood still non-
Yes
viper present pit viper bite: clotting after four
in this area give appropriate 6 hourly doses of
antivenom Malayan pit viper
No antivenom
Yes No
Treatment Treatment
Russell’s viper
No Try green pit Observe in
present in this
viper antivenom hospital
area
Yes
Treatment Treatment
Green pit viper bite: Try Russell’s
give appropriate viper antivenom
antivenom or *Observe patient closely for emerging signs of envenoming and
conservative treatment take appropriate action.

Annex
3
Antivenoms for Treatment of
Bites by South-East Asian Snakes
(List by Country of Manufacture)
1. China
Shanghai Institute of Biological Products, Ministry of Health, 1262 Yan An Road (W),
Shanghai 200052, China (Tel ++ 8621-62803189; Fax ++ 8621-62801807).
Contact: Ms Minzhi Lu, Manager, International Affairs & Trade Department
(Tel ++ 8621-62805234)
(liquid antivenoms, 10-15 ml/ampoule)

• Agkistrodon acutus antivenin (purified) (= Deinagkistrodon acutus, found in
North Viet Nam). Recommended dose 8,000 IU (= 4 ampoules)
• “Agkistrodon halys” antivenin (purified) (said to be active against venoms of
Trimeresurus mucrosquamatus and T stejnegeri). Recommended dose 6,000
IU (= 1 ampoule)
• Bungarus multicinctus antivenin (purified) (said to be effective against the
venom of Ophiophagus hannah). Recommended dose for bites by both
species 10,000 IU (= 1.25 ampoules)
• “Naja naja” antivenom (purified) (= Naja atra). Recommended dose 2,000
IU (= 2 ampoules)
2. Germany
Knoll AG, Postfach 21 08 05, 67008 Ludwigshafen, Germany (Tel ++ 49621-
5892688; Fax ++ 49621-5893707). Contact: Mr Lok, Managing Director
(liquid antivenom, 10 ml/ampoule)
• Cobra monospecific antivenom (Naja naja sputatrix = Malaysian N sumatrana)
3. India
(a) Bengal Chemicals & Pharmaceuticals, 6 Ganesh Chunder Avenue, Calcutta
(Fax ++91 33 2257697)
(liquid antivenom)
• Polyvalent (Bungarus caeruleus, Naja naja, Vipera russelli, Echis carinatus)

(b) Central Research Institute (Simla Hills), 173 204 (HP) Kasauli (Tel ++ 91-
17932060; Fax ++ 91-179272049)
(liquid and lyophilised antivenoms, 10 ml/ampoule)
• Polyvalent (B caeruleus, N naja, V russelli, E carinatus)
(c) Haffkine Biopharmaceutical Company Ltd, Acharya Donde Marg, Parel, Bombay
400012 (Tel ++ 91-224129320 and 234129224; Fax ++ 91 41 68578; Telex
11.71427 HBPC IN)
(lyopholised antivenoms, 10 ml/ampoule)
• Polyvalent anti-snake venom serum (B caeruleus, E carinatus, N naja, V russelli)
(d) King’s Institute of Preventive Medicine, Guindi, Madras NA5

• Polyvalent
(e) Serum Institute of India Ltd, 212/2 Hadapsar, Pune-411 028 (Tel ++ 91-
212672016; Fax ++ 91-212672040; Telex 145-7317 SERA IN, 145-7216 SEAL
IN) Contact: Dr SS Jadhav, Executive Director (QA)
(lyopholized antivenoms)
• Polyvalent (B caeruleus, N naja, V russelli, E carinatus)
• Bivalent (E carinatus, V russelli)
4. Indonesia
Perum Bio Farma (Pasteur Institute), Jl Pasteur 28, Post Box 1136, Bandung 40161
(Tel ++ 6222-83755; Fax ++ 6222-210299; Telex 28432 BIOFAR IA)
(liquid antivenom, 5 ml/ampoule)
• Polyvalent antivenom serum (Calloselasma rhodostoma, B fasciatus, N
sputatrix)
5. Iran
State Serum & Vaccine Institute, Razi Hessarek, bP 656, Teheran
(Tel ++ 98 2221 2005)
(liquid antivenoms, 10 ml/ampoule)
• Polyvalent snake antivenom (equine) (said to neutralise the venoms of two
South-East Asian species – Naja oxiana and Echis carinatus (probably E sochureki),
Vipera lebetina (= Macrovipera lebetina) and Pseudocerastes persicus
6. Myanmar (Burma)
Myanmar Pharmaceutical Factory, Yangon
(lyophilized and liquid antivenoms, 10 ml/ampoule)
• Viper antivenom (V russelli)
• Cobra antivenom (N kaouthia)

7. Pakistan
National Institute of Health, Biological Production Division, Islamabad (Tel ++ 9251-
240946; Fax ++ 9251-20797; Telex 5811-NAIB-PK) Contact: Shahid Akhtar
(liquid and lyophilized antivenoms, 10 ml/ampoule)
• Polyvalent anti-snake venom serum (B caeruleus, E carinatus, N naja, V
lebetina, V russelli)
8. Philippines
Biologicals Production Service, Dept of Health, Los Baños, Laguna
(liquid antivenom)
• Philippine cobra antivenin (Naja philippinensis)
9. Taiwan
National Institute of Preventive Medicine, 161 Kun-Yang Street, Nan-Kang, Taipei,
ROC 11513 (Tel ++ 8862-7859215; Fax ++ 8862-7853944). Contact: Dr Gong-
Ren Wang, Director
(lyophilised antivenoms, 10 ml/ampoule)
• Bungarus multicinctus and N atra bivalent antivenom
• Trimeresurus muquosquamatus and Trimeresurus grammineus (= T stejnegeri)
bivalent antivenom
• Agkistrodon acutus (= Deinagkistrodon acutus) antivenom
10. Thailand
The Thai Red Cross Society, Queen Saovabha Memorial Institute, 1871 Rama VI
Road, Bangkok 10330 (Tel ++ 662-2520161-4; Fax ++ 662-2540212; Telex 82535
THRESCO TH)
(freeze dried monovalent antivenoms, 10 ml/ampoule)
• Cobra antivenom
• King cobra antivenin
• Banded krait antivenin
• Russell’s viper antivenin
• Malayan pit viper antivenin
• Green pit viper antivenin

Annex
4
Measurement of
Central Venous Pressure
In seriously ill patients with shock or renal failure in whom clinical assessment of the
jugular venous pressure is difficult or considered inaccurate, a central venous catheter
should be inserted percutaneously. In those with no haemostatic problems, a catheter
may be inserted into the jugular or subclavian vein provided adequate facilities for a
sterile procedure and subsequent nursing are available. However, patients who have
been bitten by vipers may have obvious haemostatic problems or may develop
coagulopathy. In these cases, the antecubital approach is by far the safest as
haemostasis can be achieved by local pressure. A long catheter (at least 50-70 cm for
an adult) is required (Fig 45). The catheter is connected via a three-way tap and
pressure tubing to a manometer. The whole system is filled with sterile isotonic saline.
Before readings can be taken, the zero on the manometer must be aligned as
accurately as possible with the horizontal plane of the left atrium. A simple spiritlevel
(eg a 20 ml glass ampoule with bubble, taped to a ruler) can be used to locate the
manometer zero at the same height as an appropriate chest-wall landmark, such as
the midaxillary line, in the supine patient (Fig 46) or the sternal angle in a patient
sitting up at 45o. There should be strict attention to asepsis. Infection and thrombosis
are potential complications; especially if the catheter remains in place for a long time.
Figure 45: Central venous pressure Figure 46: Adjusting the zero point of the central
monitoring in a patient with shock after venous pressure manometer to the mid-axillary
Russell’s viper bite, in a township hospital line, using a home-made ruler-plus-glass-ampoule
in rural Myanmar. A 70 cm long catheter “spirit level” (Copyright DA Warrell)
was inserted into an antecubital vein
(Seldinger percutaneous guidewire
technique) and advanced until its tip was
in the superior vena cava. An extension
tube connects with a simple saline
manometer whose zero point is at the
level of the mid-axillary line (Copyright
DA Warrell)

Annex
5
Measurement of
Intracompartmental Pressure in
Tensely Swollen Snake-bitten Limbs
To confirm a clinical suspicion of intracompartmental syndrome (see Compartmental

syndromes and fasciotomy, page 46) the pressure inside the particular compartment
should be measured directly. The threshold pressure required to initiate the flow of
liquid into the fascial compartment is a measure of the tissue pressure inside that
compartment. With full sterile precautions and after infiltrating local anaesthetic, a
21 or 22 gauge cannula, approximately 3-4 cm long, is inserted into the compartment
through or around an introducing 20 or 21 gauge needle. The cannula is connected
through narrow pressure tubing to a syringe or low speed infusion pump. Through a
three-way tap, the system is connected, through a side arm to a blood pressure
transducer or saline or mercury manometer (Fig 47). The system is filled with sterile
isotonic saline. If a syringe-type infusion pump and arterial blood pressure transducer
with monitor is used, the pressure can be measured continuously at a very slow rate
of infusion (eg 0.7 ml/day). If a saline or mercury manometer is used, a much higher
rate of infusion is required to initiate flow into the compartment. These systems are
not suitable for continuous intracompartmental pressure monitoring.
Alternatively, the simple but expensive Stryker pressure monitor can be used (Fig
48). Whatever system is employed, the zero point in the pressure measuring device
must be aligned to the level at which the cannula enters the fascial compartment.
Figure 47: Infusion pump, saline manometer Figure 48: Stryker pressure monitor in use
system in use for measuring the tissue pressure for measurement of intracompartmental
inside the anterior tibial compartment (Copyright pressure (Copyright DA Warrell)
DA Warrell)

Guidelines
Snake bites in the South-East Asia Region
Common Krait
Russells Viper
Saw Scaled Viper Spectacled Cobra

SDE MGMT Snake-Bite

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What are some of the venomous snakes found in Southeast Asia?

What are some of the venomous snakes found in Southeast Asia?

What are some common symptoms of snake envenomation?

What are some common symptoms of snake envenomation?

Guidelines

for the Clinical Management of

Saw Scaled Viper Spectacled Cobra Russells Viper

Reprint of the 1999 edition written and edited for

Written and edited for SEAMEOTROPMED by David A Warrell with contributions

Guidelines for the Clinical Management

2. Symptoms and Signs of Snake Bite ............................................. 13

3. Symptoms and Signs of Cobra-spit Ophthalmia ........................ 21

4. Management of Snake Bites in South-East Asia .......................... 23

Guidelines for the Clinical Management

6. Conclusions and Main Recommendations ................................. 51

7. Further Reading .......................................................................... 55

Guidelines for the Clinical Management

In many parts of this region, snake bite is a familiar occupational hazard of

Guidelines for the Clinical Management

Any recommendations must be continually reconsidered in the light of new

The guidelines are intended to provide enough practical information to allow

I am grateful to the panel of experts who contributed to these Guidelines but I

Guidelines for the Clinical Management

Nepal* Mahidol University

Guidelines for the Clinical Management

Philippines, Thailand *indicates countries of clinical experience

Guidelines for the Clinical Management

1.1 Venomous snakes of South-East Asia

The venom apparatus (Fig 2)

Venom duct Venom canal

Figure 2: Venom apparatus of a saw-scaled viper (Copyright DA Warrell)

Guidelines for the Clinical Management

Figure 4: Short, permanently erect, fangs of

Guidelines for the Clinical Management

Guidelines for the Clinical Management

Guidelines for the Clinical Management

Medically important species in South-East Asia are:

typical vipers Daboia russelii Russell’s vipers (Fig 17)

pit vipers Calloselasma rhodostoma Malayan pit viper (Fig 20)

green pit vipers or bamboo vipers (genus Trimeresurus)

T albolabris white-lipped green

Guidelines for the Clinical Management

Guidelines for the Clinical Management

Guidelines for the Clinical Management

How to identify venomous snakes

1.2 Snake venoms

Procoagulant enzymes (Viperidae) that stimulate blood clotting but result in

Guidelines for the Clinical Management

Haemorrhagins (zinc metalloproteinases) that damage the endothelial lining of

Cytolytic or necrotic toxins - these digestive hydrolases (proteolytic enzymes

Haemolytic and myolytic phospholipases A2 - these enzymes damage cell

Pre-synaptic neurotoxins (Elapidae and some Viperidae) - these are

Post-synaptic neurotoxins (Elapidae) - these polypeptides compete with

Quantity of venom injected at a bite

1.3 How common are snake bites?

Guidelines for the Clinical Management

Bhutan – (no data available)

Cambodia – (no data available)

Lao DPR – (no data available)