Management of

Snake Bites
 FINAL DRAFT
SEPTEMBER 2010

With particular acknowledgement to

Emeritus Professor David A. Warrell of the University of Oxford, UK
for his helpful review of the protocol

2
 Table of contents

1. Snake Bites...................................................................................................................................... 4
1.0 Introduction .................................................................................................................................................... 4
1.1 Epidemiology of venomous snake bites ..................................................................................................... 4
1.2 Identification of venomous snakes ............................................................................................................. 4
2. Medical Effects of Venom .............................................................................................................. 6
2.0 Venom.............................................................................................................................................................. 6
2.1 Neurotoxic effects.......................................................................................................................................... 6
2.2 Haemotoxic effects ........................................................................................................................................ 6
2.3 Cytotoxic effects ............................................................................................................................................. 6
2.4 Myotoxic effects ............................................................................................................................................. 6
3. Symptoms of Snake Bites ............................................................................................................... 7
3.0 Signs and symptoms of venomous bites .................................................................................................... 7
3.1 Non venomous ............................................................................................................................................... 7
3.2 Venomous ....................................................................................................................................................... 7
3.2.1 Local signs and symptoms .............................................................................................................. 7
3.2.2 Systemic signs and symptoms ........................................................................................................ 7
4. Principles of Snake Bite Management ........................................................................................... 9
4.0 Introduction .................................................................................................................................................... 9
4.1 Pressure immobilisation (PI) and pressure pad ......................................................................................... 9
4.2 Anti-venom ..................................................................................................................................................... 9
4.2.1 Supply of anti-venom..................................................................................................................... 10
4.2.2 Storage of anti-venom ................................................................................................................... 10
5. First Aid and Transport ................................................................................................................. 11
5.0 First aid after snake bite .............................................................................................................................. 11
5.1 Transport of patients ................................................................................................................................... 11
6. Clinical Management of Snake Bites ............................................................................................ 12
6.0 Rapid assessment and resuscitation........................................................................................................... 12
6.1 History ........................................................................................................................................................... 12
6.2 Physical examination.................................................................................................................................... 12
6.2.1 Local ................................................................................................................................................. 13
6.2.2 Systemic............................................................................................................................................ 13
6.3 Laboratory testing ........................................................................................................................................ 13
6.4 Therapy decision: anti-venom or not? ...................................................................................................... 14
6.4.1 Indications for anti-venom ........................................................................................................... 14
6.4.2 Timing of administration .............................................................................................................. 15
6.4.3 Side effects - general and managing ............................................................................................ 15
6.4.5 Dosages ............................................................................................................................................ 17
6.4.6 Additional treatment ...................................................................................................................... 17
6.4.7 Conservative treatment without anti-venom ............................................................................. 18
6.5 Admission and follow up/monitoring ...................................................................................................... 18
7. Complications................................................................................................................................ 19
7.0 Local complications ..................................................................................................................................... 19
7.1 Systemic complications ............................................................................................................................... 19
8. Special cases ................................................................................................................................. 20
8.0 Pregnant (and lactating) women ................................................................................................................ 20
8.1 Spitting cobra ................................................................................................................................................ 20
9. Prevention ..................................................................................................................................... 20
References ........................................................................................................................................................ 21
Annex I Snake families and species ......................................................................................................... 22
Annex II A simple anti-venom administration algorithm ................................................................. 26
Annex III Mission Snake Bite inventory list ......................................................................................... 27
Annex IV Clotting Test for Snake venom............................................................................................... 28

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 1. Snake Bites

1.0 Introduction
This document is designed to aid medical staff with prevention and treatment measures for venomous
and non-venomous snake bites. In particular it addresses the critical decision of whether or not to
administer anti-venom to a patient bitten by a snake. Anti-venom, like most drugs, is potentially
dangerous and so the risk/benefit of its use must be seriously considered.

The key information – patient management – can be found in chapters 5 and 6. However, it is
recommended that the whole guideline is read and adapted to the local situation. It is the responsibility of
the Medical Coordinator to ensure that the local situation (with respect to species of snakes present) is
investigated and documented.
Snake bites in our missions are rare but the potential medical consequences of their attack are severe;
therefore prevention is imperative and should be included in the staff health policy of each mission. A
detailed list of prevention measures is given in chapter 9.

Recommendations provided are based on a literature review and input from international experts.

1.1 Epidemiology of venomous snake bites

Venomous snakes exist on all continents, except Antarctica. It is estimated that at least 421,000
envenomings and 20,000 deaths (figures may be as high as 1,841,000 and 94,000 resp.)1 occur annually
worldwide. The highest burden of snakebites is in South Asia, Southeast Asia, and sub-Saharan Africa.
People most at risk are agricultural workers and children.

The majority of snake-bite victims seek traditional treatment and may die at home unrecorded.2 The
amount of disability (permanent sequelae due to snakebites) is unknown and underreported. Although it
is more common in rural areas, snakes can be present in town areas (e.g. in India). Snake bites have
recently been recognized as a neglected disease by WHO.

1.2 Identification of venomous snakes

Over 600 snake species are known to be venomous. It is important to know which snakes are where, as
there is a certain correlation between snake-family and pathology.

In Central and South America, pit vipers are the primary subfamily responsible for human envenoming;
rattlesnakes and the Bothrops species (B. jararaca, fer-de-lance) are responsible for the high morbidity and
mortality. The largest venomous snake in the Americas is the bushmaster (Lachesis muta muta). Africa is
home to a large number of venomous species. Elapids (e.g. cobras and mambas) and the Old World vipers
(e.g., saw-scaled viper, puff adder) are among the most prevalent and dangerous of all the world's snakes.
In India and Southeast Asia, Elapids and Viperids are prominent. Cobras, kraits, pit vipers, and saw-scaled
and Russell's vipers are responsible for most of the injuries.3

The following groupings (though rough and incomplete) can be made of medically important, dangerous
snakes.4 For a longer list, see Annex I.

1 Kasturiratne et al. The global burden of snakebite: a literature analysis and modeling based on regional estimates of envenoming
and deaths. PLoS Medicine Nov 2008 Volume 5 Issue 11 e 218
2 WHO/SEARO (2010) Guidelines for the Clinical Management of Snake Bite in the South-East Asia Region 2nd Ed. WHO

Website: http://www.searo.who.int/EN/Section10/Section17.htm
3 Corey R, Armitage JO, Seifert SA. (2007) Venomous Snakebite. In: Cecil’s Textbook of Medicine, 23rd Edition. Russell L.

Cecil, D. A. Ausiello, and Lee Goldman Eds. W B Saunders Co. October, 2007.
4 http://www.who.int/bloodproducts/snake_antivenoms/en/

4
Table 1: Examples of venomous snakes
Snake family Species - some examples
Elapidae Cobra’s, including spitting cobra’s (Naja), coral
A large and diverse Family of exclusively snakes (Micrurus, Micruroides)
venomous snakes, covering all continents (except Kraits (Bungarus)
Antarctica) and several major oceans, these snakes Mamba’s (Dendroaspis) D.polylepsis
have well developed fangs towards the front of the Sea snakes
mouth, which can deliver often highly potent
venom, produced in paired venom glands.

Viperidae Subfamily Viperinae “Old World” and Subfamily

A large and diverse Family of exclusively Crotalinae (Pit Vipers)
venomous snakes, covering most continents
(except Australia and New Guinea, Antarctica), Russel’s Viper
with a highly evolved fang structure. The fangs are Puff viper, Gabon Viper, rhinoceros -horned viper
at the front of the mouth, attached to a mobile (Bitis)
maxilla, enabling the fang to fold away against the Bush Viper (Atheris)
roof of the mouth, thus permitting longer fangs Echis carinatus
compared to head size.
Colubridae Dispholidus typus (Boomslang) – sub-Saharan
This is the largest Family of snakes, generally Africa
considered non-venomous and distributed Thelotornis (Twig Snake)
globally. However, a few species have evolved
fangs towards the back of the mouth, which
deliver venom from venom glands.
Atractaspididae Atractaspis microlepidota (Burrowing Asp)
A small Family of exclusively venomous snakes,
found only in Africa and the Middle East,
characterised by their side-striking fangs and
unique venom components (sarafatoxins), only a
few species of which appear able to significantly
envenom humans.

It is important for MSF projects to have knowledge of the poisonous snakes that are common in
the areas where MSF is working. Information can be gathered through local and national
Governments of Health, universities and the local population.
Infomation should be listed and available for all in the mission – see Annex III

An excellent reference with country-specific lists can be found in Appendix 1 of the WHO
Guidelines for the Production and Control of Snake Antivenom Immunoglobulin found at:
http://www.who.int/bloodproducts/snake_antivenoms/snakeantivenomguideline.pdf

5
 2. Medical Effects of Venom

2.0 Venom
Snake venom differs between species and even within species depending on age, season, temperature, and
the snake’s diet. The most important components are toxins (mainly proteins, including enzymes and
polypeptide toxins) with cytotoxic, neurotoxic and coagulant effect. Venom is usually injected
subcutaneously or intramuscularly in humans. Another way of envenomation is through spitting in the
eyes (spitting cobras). Snake envenomation poisoning is a complex event. Not only can the local bite site
be severely affected, but there are also serious systemic consequences as it can affect multiple organs.

2.1 Neurotoxic effects

The neurotoxic mechanism can be pre or post synaptic. In practice the working mechanism is that the
nerve stimulation of muscles is inhibited, leading to paralysis.5 It presents with either moderate or no local
swelling sometimes accompanied by local lymph node enlargement. The paralysis is progressive and
descending starting with drooping of the eye lids and impairment of eye movements leading to double
vision. Vomiting can be present. Eventually problems with swallowing and respiration may develop.

2.2 Haemotoxic effects

Snake venom can interfere with blood coagulation in different ways (effects can occur rapidly, produce
bleeding and incoagulable blood within 30 - 60 minutes):
Activation of clotting cascade, leading to disseminated intravascular coagulation, resulting in
depletion of clotting factors (consumption coagulopathy)
Endothelium damage of blood vessels causing spontaneous systemic haemorrhage.

2.3 Cytotoxic effects

Other components of snake venom can cause increased permeability and damage to cell membranes of
endothelium, nerve cells, red blood cells, muscle cells. Clinically it presents with severe local reaction at
the bite wound, fluid leakage, bleeding and blistering and hypovolemic shock. Tissue necrosis and
gangrene may result.

2.4 Myotoxic effects

The bite may have minimal local swelling. There is generalized muscle pain and tenderness (myalgia)
associated with features of neurotoxic envenoming and progressive descending paralysis culminating
in paralysis of breathing.

Mixed types of envenoming may occur depending on the species of snake.

5 Pre-synaptic neurotoxins (Elapidae and some Viperidae) – toxic nerve damage that results in impaired acetylcholine release.

Post-synaptic neurotoxins (Elapidae) - polypeptides that compete with acetylcholine for receptors in the neuromuscular
junction (curare-like paralysis).

6
 3. Symptoms of Snake Bites

3.0 Signs and symptoms of venomous bites

Bites by poisonous snakes are not always dangerous: dry bites (without releasing any venom) occur in 50-
80% of bites. For unknown reasons venomous snakes may inject little or no venom and so it may be
impossible to differentiate a dry bite of a venomous snake from a bite of a non-venomous snake. The
important thing is to detect signs and symptoms of envenoming. Symptoms usually develop within
minutes or a few hours (e.g. persistent pain or bleeding at the bite site, local swelling, nausea and
vomiting, fainting) but, exceptionally, may develop slowly, but nearly always within 24 hr of the bite. This
is the basis for the rule that all cases of snake bite should be observed for at least 24 hr after the bite. In
most cases of viper and pit viper bites, the absence of local swelling after 2 hr makes it unlikely that there
has been significant envenoming. The interval between the bite and death can be wide, some examples
(mean and range):
Indian cobra (Naja naja): 8 hrs (15 mins - 60 hr)
Saw-scaled viper (Echis carinatus): 5 days (1 - 41 days)
Russell’s viper (Daboia russelii) : 40 hrs (15 mins - 9 days)

3.1 Non venomous

Not all symptoms of snake bites are due to envenomation as the bite can instead provoke anxiety and fear
reactions. Laboured breathing causing pins-and-needles and faintness, vomiting and fainting (vasovagal
collapse) can all be consequences of fear [timing is not helpful as some venoms cause collapse within
minutes from autacoids= oligopeptides].
Other symptoms (also not due to envenomation) may be caused by traditional or inappropriate treatment:
tourniquets, cutting of bite site, use of irritating juices, heating, use of scalding liquids. Bacterial infection
of the bite wound can occur, but is uncommon unless secondary to iatrogenic bite site interference.
Another longer term consequence can be tetanus infection (see chapter 7).

3.2 Venomous
3.2.1 Local signs and symptoms
Depending on species and amount of venom a variety of symptoms can occur.
• Fang marks can cause bleeding and swelling, tenderness, severe pain (a variable which may or
may not develop) lymphadenopathy and signs of lymphangitis. Some species are well known to
cause local necrosis: Viperidae, Asian cobras, African spitting cobras (e.g. Naja nigricollis, N pallida).
• Ecchymosis, blistering, necrosis, darkened or pale skin, loss of sensitivity, altered sense of smell
• Beware of bites on digits; often these require amputation if necrosis occurs.

At a later stage: Bacterial infection (including tetanus) of the bite wound can occur. This is particularly
likely after necrosis.

3.2.2 Systemic signs and symptoms

The onset of systemic signs after envenomation may happen within minutes (e.g. shock and fainting after
some viper, pit viper and Australasian elapid bites) or, more exceptionally, after more than 9 hr (e.g. krait
bite neurotoxicity) and up to 24 hr (viperid and colubrid bleeding and clotting abnormalities). This
emphasises the need to observe snake bite patients for at least 24 hr before excluding the possibility of
systemic envenoming.

In the table below6 an overview of possible systemic symptoms is provided.

6 WHO/SEARO (2005) Guidelines for the Clinical Management of Snake Bite in the South-East Asia Region.

7
Table 2: Systemic symptoms of envenomation
Systemic Symptoms Snake Family
(not exhaustive)
General
Nausea, vomiting, malaise, abdominal pain, weakness, drowsiness,
prostration

Cardiovascular Viperidae
Visual disturbances, dizziness, faintness, collapse, shock, hypotension
(Serious: Blood pressure < 80 mmHG)
cardiac arrhythmias, pulmonary oedema, conjunctival oedema

Bleeding and clotting disorders Viperidae

- from recent wounds, fang marks, old partly-healed wounds Colubridae
- from gums, epistaxis, bleeding into the tears, haemoptysis, haematemesis, Australian Elapidae
rectal bleeding or melaena, haematuria, vaginal bleeding,
bleeding into the skin (petechiae, purpura, ecchymoses) and mucosae (eg
conjunctivae

Intracranial haemorrhage (meningism from subarachnoid haemorrhage,

lateralizing signs and/or coma from cerebral haemorrhage)

Neurological Elapidae including

Drowsiness, paraesthesiae, abnormalities of taste and smell, “heavy” Sea snakes
eyelids, ptosis, external ophthalmoplegia, paralysis of facial muscles and
other muscles Also: Russell’s Viper
innervated by the cranial nerves, aphonia, difficulty in swallowing
secretions, respiratory and generalised flaccid paralysis

Skeletal muscle breakdown Sea snakes

Generalised pain, stiffness and tenderness of muscles, trismus,
myoglobinuria, Russell’s viper
Hyperkalaemia, cardiac arrest, acute kidney injury

Renal Viperidae
Loin (lower back) pain, haematuria, haemoglobinuria, myoglobinuria,
oliguria/anuria Sea snakes
Symptoms and signs of uraemia: acidotic breathing, hiccups, nausea,
pleuritic chest pain

Endocrine (acute pituitary/adrenal insufficiency) Burmese Russell’s

Acute phase: shock, hypoglycaemia Viper

Chronic phase of pituitary/adrenal insufficiency (months to years after the

bite)

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 4. Principles of Snake Bite Management

4.0 Introduction
Initial response to a bite is to minimise the absorption of the toxin through immobilisation and
positioning of the limb. A number of initial treatments for snake bites have been studied and proven not
to be of benefit or dangerous. These methods include arterial tourniquets, incision, suction, venom
extraction devices, heat, cold, and electric shock, application of proteases and oxidizing agents In addition
to being ineffective these treatments can cause harm through additional trauma, increasing the risk of
infection and delaying more definitive treatment.

4.1 Pressure immobilisation (PI) and pressure pad

In many guidelines bandaging of the bitten limb with a long, wide elasticated pressure bandage has been
recommended. This is referred to as pressure immobilisation or PI. However, this method remains
controversial.

PI aims to delay the absorption of venom toxins from the bite through lymphatics and veins:
a broad (10 cm) and long elasticated bandage, is bound firmly around the bitten limb, starting distal to the
bite site, and extending up to the arm pit or groin. Excessive pressure (amounting to an arterial
tourniquet) is avoided by checking the peripheral arterial pulses and noting the patient’s complaint of
severe (ischaemic) pain in the bound limb.
PI is often applied ineffectively because:
It is difficult to teach people to apply it sufficiently tightly.
Necessary materials may not be available where they are needed.
It is effective only if it is applied immediately, before veins and lymphatic system are already filling with
venom components.

Alternatively (and also in cases of bites on the trunk and head) a firm pad of foam rubber of folded-up
bandage may be applied firmly over the site of the bite, using a tight bandage.

PI and pressure-pads remain controversial but they are the only effective and safe methods so far
developed to delay onset of life-threatening paralysis after Elapid bites. Recent studies have been
reassuring that PI does not increase the severity of local envenoming after rattlesnake bites.

4.2 Anti-venom
Anti-venoms are either intact or fragmented immunoglobulins (IgG) derived from animal serum (horse,
sheep). The production of the anti-venom includes purification of the IgG and processes to minimise
contamination with other proteins, protein fragments, endotoxins and pathogens. Although the safety
and effectiveness of anti-venoms has been improved, the large dose of foreign (horse or sheep) protein
administered intravenously creates a risk of anaphylactic and other reactions.

Monovalent anti-venoms are intended for use against the venom of a single species of snake or for other
closely related species whose venoms show cross reactivity to the serum. Their use requires specific
diagnosis of the snake responsible for envenoming.

Polyvalent anti-venoms cover the species of snakes of greatest medical importance in a particular
geographical area so that specific diagnosis of the biting species is less important. Their neutralising
capacity against a particular venom may be no less than for monovalent anti-venoms.7
In our settings, the recommendation is to use polyvalent anti-venoms as they are more practicable, having
wider therapeutic usefulness.

7 http://www.who.int/bloodproducts/snake_antivenoms/en/

9
4.2.1 Supply of anti-venom
Due to low demand (and hence profits) some pharmaceutical companies have stopped the production of
quality anti-venom. This results in a very risky market and there are many substandard and counterfeit
anti-venoms circulating in countries where MSF works. This issue has attracted worldwide attention8 and
WHO has now classified snake bites as a Neglected Disease.

Procurement of snake anti-venom is country specific and must take into account numerous factors
including (but not limited to):

- Is anti-venom really needed?

- Are there health facilities available with the capacity to manage patients and staff who are bitten by
snakes? If so, referral may be possible but this would need a full assessment of the capacity of the
facility including storage of anti-venom, availability of drugs and staff to manage anaphylactic
reactions etc.
- Which venomous snakes are present in the country?
- Which specific anti-venoms are needed?

An important issue is then how and where to procure the anti-venom.

It is very important to identify locally available polyvalent anti-venoms and their producers
Local purchase of anti-venom has to follow a strict procedure with the section pharmacist and should
always be in agreement with the Medical Director

4.2.2 Storage of anti-venom

Some anti-venom has to be kept at cool temperature (below 8° C) while others can be kept at any
temperature. The storage conditions on the vial from the manufacturers should be followed and the
expiration date respected.
Where to store the anti-venom needs consideration. The best location for storing anti-venom will differ
from project to project. The choice is dependent on storage conditions, proximity to the patients and
availability of qualified staff to handle the administration of the anti-venom, and respond to the possible
complications.

Note: only a minority of snake bites, even by venomous snakes, require anti-venom. Anti-venom should
not be used unless the medical staff are trained to give it intravenously and are able to recognise
anaphylactic reactions and treat them with epinephrine (adrenaline).
First aid and good patient management are always a crucial step in treatment.

8See WHO websites: http://www.who.int/neglected_diseases/diseases/en/ and

http://www.who.int/bloodproducts/snake_antivenoms/en/ and Warrell DA. ‘Unscrupulous marketing of snake bite
antivenoms in Africa and Papua New Guinea: choosing the right product – what’s in a name? Trans R Soc Trop Med Hyg. 2008
May;102(5):397-9.)

10
 5. First Aid and Transport

5.0 First aid after snake bite

First aid of a snake bitten patient is centred on two important aims:
1. Calming down the patient. An agitated patient is more likely to move which can increase absorption
of the venom.
2. Immobilisation of the whole patient and particularly the affected limb to reduce absorption of venom
from limb.

The bite wound should not be interfered with in any way, as this may increase absorption of the
venom. Local customs (e.g. application of snake stones) must be discouraged as they could lead to
delayed access to proper health care. No tourniquet!
Remove all rings and constrictive clothing.
Clear liquids may be administered but no alcohol or caffeine (stimulants) should be given to the
patient.

Pressure immobilisation (PI) or pressure-pad is recommended in the following settings:

In areas where neurotoxic bites occur.9 PI/pressure-pad should be recommended for all snake bites
unless an Elapid (e.g. cobra, mamba, krait, Australasian elapid) can be excluded with certainty.
Where the necessary materials (long, wide elasticated bandages, pads, splints) and skills are available.

A splint should be applied to the patient or added to the PI/pressure-pad in order to improve
immobilisation.

5.1 Transport of patients

Preferably transport the patient in the recovery position to minimise risk of aspirating vomit and in case
blood pressure falls. Transport patient to the best equipped health facility – often MSF, but hospitals are
also an option, depending on the setting. It is useful to know which medical facilities around have
capacity and experience for dealing with snake bites and which stock anti-venom.

Attempting to kill the snake responsible is dangerous and should never be encouraged. If the snake has
already been killed, take it for identification but beware, supposedly dead snakes should never be handled
with bare hands.

9 These snakes are found in all tropical and sub-tropical regions worldwide

11
 6. Clinical Management of Snake Bites10
6.0 Rapid assessment and resuscitation
When a patient arrives in the clinic severely envenomated or very late with serious symptoms
resuscitation may be needed. This is an emergency and the normal ABCs approach is applicable:

Airway free:
In case of vomiting: consider anti-emetic e.g.
Metoclopramide 10 mg. slow IV (adult dose), for children: see Essential Drugs guidelines
Breathing secured:
Exclude Respiratory paralysis from neurotoxic envenoming; endo-tracheal intubation mayt be
needed.
Circulation adequate:
Hypotension / shock treated: Insert large bore IV cannula (careful for bleeding risk)
IV Ringer solution or 0.9% Sodium Chloride
500 – 1000 ml over 2 hrs for adults
20 ml/kg for children as a bolus injection over 15-30 minutes
Anaphylaxis due to venom: Epinephrine (adrenaline) 0.5 ml 0.1 % intra-muscular11 (child: 0.01
mg/kg) – see part 6.4.3
The level of consciousness should be assessed
Even when resuscitation is not needed an IV line should be inserted for a patient after a snake
bite. However, aside from maintaining IV access, try to avoid any unnecessary veni-punctures

6.1 History
When airway, breathing and circulation have been established/secured, a rapid and precise history should
be taken. The history will guide the clinician in diagnosis and required treatment, expected outcome and
anticipate possible complications.

Which part of body is bitten?

Bitten once or multiple times? possibly higher dose of anti-venom needed
When did it occur? severity is measured in relation to time of bite and start of
symptoms
What are the complaints?
Urine changes? black/dark brown urine (myoglobinuria)
Pain? generalised pain, tenderness and stiffness of muscles,
trismus: suspect vipers or sea snakes
Was snake identified?
Past Medical History use of drugs (e.g. NSAIDs); renal-, or heart disease?
Pregnancy specific measures may be needed. See chapter 8
Tetanus vaccination (TV) if unvaccinated or partly vaccinated: TV is needed – see
‘Clinical Guidelines’.
Allergic reaction to equine serum (tetanus, rabies, previous anti-venom) and history of severe
atopic disease (asthma, eczema, etc)
History of previous snake bite, in particular anti-venom use
if yes, increased awareness for allergic reaction

6.2 Physical examination

The physical examination, guided by history, should focus on local signs and systemic signs. Particular
care should be paid to signs of haemostatic disturbances and neurological disturbances.

10http://www.searo.who.int/EN/Section10/Section17.htm
11Epinephrine (adrenaline) subcutaneously can be used as well, but intra-muscular is more rapidly bioavailable and is preferred.
Since epinephrine is vasoconstricting there is usually no problem with haemostasis

12
6.2.1 Local
Be aware and prepared for aggravation of situation when PI, pressure-pad or tourniquet is removed. If
possible try to exclude signs of envenomation before removing PI (History? Identification of snake?
Perhaps one can cut a hole in the PI first to observe bite site?).
A tourniquet has to be removed as it is a risk for severe ischaemia/gangrene. But be aware of sudden
development of systemic envenoming.
Inspection of bite site: bleeding fang marks suggest coagulopathy.
Record extent of swelling.
Examine regional lymph nodes, ecchymosis.
Early signs of necrosis: blistering, darkening, paleness skin, loss of sensibility.
Rare: compartment syndrome, see chapter 7.0

6.2.2 Systemic
Be complete and precise in examination, and look for possible signs of envenomation.
(Table 2, pg.8 can be used as a reference)

Circulation:
Blood pressure -standing up and lying down: a substantial difference suggest hypovolaemia.
Heart rate: arrhythmias, tachycardia?

Respiration:
Paradoxical respiration partly paralysed muscles
Signs of pulmonary oedema.

Skin and mucosa:

Bleeding? (Gingiva, nose)

Abdomen:
Tenderness? Be alert for internal bleeding.
Back (renal region) pain: kidney involvement?

Neurological examination:
Level of consciousness: be aware that paralysed, eyes closed people might still be able to move an
e.g. finger – communicate with them!
Intracranial haemorrhage is suspected by signs of lateralisation, asymmetrical pupils and
convulsions, and impaired consciousness.
Look for ptosis – patient looking upwards, upper eyelids should retract
Eye movements – signs of external ophthalmoplegia
Pupil size (mydriasis, miosis) and reactions
Opening mouth – signs of trismus
Protrusion of tongue possible?
Swallowing impaired?

Pregnancy: see chapter 8

6.3 Laboratory testing

If possible additional testing should be done.
An easy to perform laboratory test to detect coagulation disorders (Vipers and Australian elapids) is the
20 minute whole blood clotting test (20WBCT)12:
1) Place a few ml. of freshly sampled venous blood in a small normal glass vessel e.g. plain blood
tube give code from catalogue
2) Leave undisturbed for 20 minutes at ambient temperature

12 WHO/SEARO (2010) Guidelines for the Clinical Management of Snake Bite in the South-East Asia Region. 2nd Ed

http://www.searo.who.int/EN/Section10/Section17.htm

13
 3) Tip the vessel once

If the blood is still liquid (unclotted), the patient has hypofibrinogenaemi ("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
A complete SOP (standard operating procedure) for performing the test can be found in Annex
IV

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 the test will be invalid

If there is any doubt, repeat the test in duplicate, including a control blood from a healthy person

Arterial punctures are contra-indicated when coagulation disorders are suspected.

6.4 Therapy decision: anti-venom or not?

One needs to be aware of what anti-venom is, when is it indicated and what the risks are before asking
the most important question: does this particular patient who has been bitten by a snake need anti-venom
or not?

As the use of anti-venom is not without risk, medical decisions need to be based on clinical
manifestations of envenomation only.
A clear balance needs to be made between the benefits of administration versus the risks
(mortality of anti-venom administration is 1/1000).
Anti-venom is also costly, and at the moment supplies are limited. Unnecessary use should be
avoided at all times.
Even though vomiting can be an early sign of systemic envenomation, vomiting alone is never an
indication to start treatment with anti-venom.
When no anti-venom is available, supportive medical treatment can in many occasions save the
life of a patient.

6.4.1 Indications for anti-venom

Indications differ from country to country. WHO recommends anti-venom also for serious local
envenoming13 in contrast to Australian guidelines14.

Indications:

a) Signs of Systemic envenoming present (see table 2, pg.8)

• Coagulation disorders – 20WBCT (see above)
• Neurotoxic signs
• Cardiovascular abnormalities
• Acute renal failure
• Signs of haemolysis or rhabdomyolysis (dark urine)
• Impaired consciousness

b) Signs of Serious local envenoming present

• Local swelling with more than half bitten limb involved within 48 hr of the bite
• Rapid spread (beyond wrist after bite to hand, beyond ankle after bite to foot within approx.4
hrs)

13 WHO/SEARO (2010) Guidelines for the Clinical Management of Snake Bite in the South-East Asia Region. 2nd Ed

http://www.searo.who.int/EN/Section10/Section17.htm
14 NSW Health (2007) Snakebite & Spider bite Clinical Management Guidelines 2007

14
In order to anticipate as early as possible the need for administration of anti-venom one can approach the
symptoms in a clinical syndrome approach: the table below is not exhaustive, but gives an overview of
typical danger signs – next to the obvious ones such as shock and other symptoms given in table 2.

6.4.2 Timing of administration

When the indication is present anti-venom should be administered as soon as possible. Half-life of anti-
venom can be 1 to 4 days; snake venom can have a longer half time. In case of serious intoxication anti-
venom can be given up to 3-4 days or longer after a bite.
In case of neurotoxic envenoming with bulbar and respiratory paralysis one cannot rely upon anti-
venom alone. Artificial ventilation remains imperative.

Table 3: Clinical syndromes of envenomation

Painful progressive Progressive weakness Bleeding
swelling ‘Elapid syndrome’ ‘Viperid
syndrome’

Severe Rapid extension of Paraesthesia, excessive Bleeding from fang

envenomation swelling > 15 cm per hour sweating, hyper- punctures/wounds,
anticipated salivation, strange taste severe headache,
dizzy, convulsion
Swelling to knee or elbow Bilateral ptosis, - myosis
at 4 hrs

Severe / life Swelling of whole limb Trismus, shortness of Positive clotting

threatening breath respiratory test
envenomation paralysis
present
Swelling threatening airway Spontaneous
bleeding
Shock

A simple overview of treatment decisions is given in Annex II

6.4.3 Side effects - general and managing

As anti-snake venom is produced from animal serum it contains animal proteins that can lead to
dangerous side effects. Depending on the quality of the product this can occur in between 5% - 85% of
patients.15 The types of reaction can be divided into anaphylaxis, pyrogenic reactions and serum sickness
(late). These side effects are mentioned here first as they are extremely important to recognise. The next
subchapter (6.4.4) will deal with actual anti-venom administration.
There is an increased risk for atopic patients and those who had severe reactions to anti-venom before to
develop a serious reaction. Anti-venom should therefore ONLY be given for severe/life threatening
envenomation in this group of patients. Pre-medication with antihistamine and corticosteroids may be
helpful. All patients should be closely monitored for at least an hour after administration of anti-venom.

Anaphylactic reaction
Anaphylactic reaction usually develops within first hours after anti-venom administration.
The early signs of itching, urticaria, fever, tachycardia, dry cough, vomiting can progress towards a severe
anaphylactic reaction: hypotension, bronchospasm, angio-oedoema.

Treatment:
- Epinephrine (adrenaline) intramuscular

15 Warrell DA (1995). ‘Clinical toxicology of snakebite in Africa and the Middle East/Arabian peninsula, Asia’. In: Meier J, White

J eds. Handbook of Clinical Toxicology of Animal Venoms and Poisons. Florida, CRC Press, pp. 433-594

15
Table 4: Dosage of epinephrine
Dosage for epinephrine intramuscular injection for anaphylactic shock - 1 : 1000 (1 mg/ml)
Age Dose Volume of epinephrine
Child < 6 years 120 micrograms(µg) 0.12 ml
Child 6 – 12 yrs 250 µg 0.25 ml
Adult and child 12 – 18 yrs 500 µg 0.5 ml
Use a 1 ml syringe graduated in 0.1 ml
Dosages might be repeated several times with 5 minutes interval according to blood pressure, pulse, and
respiratory function.
If circulatory collapse or deterioration after i.m., give by intravenous route diluting dosage as per
instructions in Essential Drugs.

Adjunctive treatment:
- Promethazine (25 mg/ml) adult and child > 10 years: 25 to 50 mg i.m.
child (5-10 yrs) 12.5 mg i.m.

- Hydrocortisone (sodium succinate) adult: 200 mg

child: 2 mg/kg bodyweight
Dissolve 100 mg in 2 ml water for injection and administer by i.m injection or slow i.v. push

- In case of persistent bronchospasm: Salbutamol 100mcg / metered inhalation – 2-4 puffs

(1-2 puffs for young children) every 10 – 30 minutes depending on severity. Consider use of
spacer device.

Pyrogenic reaction
Other early reactions (usually 1 – 2 hours after treatment) are the pyrogenic reactions: high fever, rigors,
febrile convulsions (children), lowering of blood pressure after 1-2 hrs after administration of anti-venom,
caused by contamination products in the anti-venom. Paracetamol should be administered, combined
with cooling of the patient.

Late serum sickness

Late serum sickness can start more than 7 to 21 days after treatment; this reaction is related to the dose of
anti-venom. The clinical symptoms vary widely: fever, rash, arthralgias, lymphadenopathy.
Treatment:
- Antihistamine: chlorpheniramine 4mg tablets
Adult 4mg every 4-6 hours Max 24mg/day
Child: See Essential Drugs for dosages
- In severe cases or therapy resistant: prednisolone 50mg/day for 5 days (adults), 0.5-1.0
mg/kg/day children for 5 days

6.4.4 Administration of snake anti-venom and dealing with side effects

When administering snake anti-venom, always be prepared to treat an anaphylactic reaction.
Prepare 1) anti-venom and 2) drugs and material for anaphylactic reaction.

1) Anti-venom should be given by the intravenous16 route.

The prescription on the anti-venom package should be followed; for adults and children.
Anti-venom (10 ml) can be given direct IV (reconstituted, but undiluted) over 10 - 15
minutes, or
by intra-venous infusion over 30 minutes after diluting in sodium chloride 0.9 % or another
isotonic IV fluid (use 5 ml diluent/kg bodyweight)

16Only in VERY exceptional and life saving circumstances can anti-venom be given intramuscularly; it should then be given in
anterior thighs, NOT gluteal region. IM injection should be followed by massage to increase absorption.

16
 The advantage of direct IV is that the health care worker is present at the moment of
administering and taking care of side reactions.
The diluted method is often recommended, especially in case of expected risk of poor
purification of the anti-venom.
It is advised to have two IV lines when administering anti-venom: one for the anti-venom
and one (large bore) for emergency resuscitation.

2) Prepare epinephrine (adrenaline) 0.5 ml 0.1% (1mg/ml) or 0.01 mg/kg for children (see table
above).
Have means ready for respiratory support: ambu-bag, airway guedell, if possible (and if
experienced operator available) equipment for endo-tracheal intubation.

- Infusion should be started slowly while reaction in patient is observed: rash, tachycardia,
drop in blood pressure, coughing, bronchospasm, pruritus (nasal, eyes), and sweating,
abdominal pain, faecal or urinary urgency.
- Mild reactions might resolve by a short stop of administration.
- Management of severe reactions (bronchospasm, sudden hypotension): suspend anti-venom
infusion, lay patient horizontally, if available support with oxygen, rapid infusion of 1 litre
0.9% sodium chloride or Ringers over 5 minutes (20 ml/kg children)
- Inject epinephrine (adrenaline)
- If patient does not improve: repeat sodium chloride bolus infusion, repeat epinephrine
(adrenaline)

6.4.5 Dosages
Dosages for treatment with anti-venom are not standardised: dosages therefore differ depending on the
producer. Treatment protocols have to be adapted to the locally available anti-venom.
Children require the same dosage as adults, as the amount of venom injected by the snake is the same as
in adults.17

In general: minimum dose is at least one vial of appropriate anti-venom, however for some anti-venoms
the starting dose is higher; it can be higher when severe envenomation is suspected (multiple bites, rapid
onset).
The dosage can be repeated after 1-2 hours if symptoms of systemic envenomation persist.
Observe not only clinical signs and symptoms, but clotting status as well (repeat clotting test after 6
hours). In case of severe continuation of bleeding one should not wait 6 hours, but an extra dose of anti-
venom should be given (at 1-2 hours).

6.4.6 Additional treatment

For pain management Paracetamol is preferred or small doses of morphine (be careful in neurotoxic
envenomation). NSAIDs or ASA are contra-indicated.
Infection rate is low unless the wound has been tampered with or there is already tissue necrosis: there is
no place for routine systematic prophylactic antibiotics. If the wound is necrotic, Clostridium tetani
should be eliminated with a large dose of benzyl penicillin or metronidazole and an aminoglycoside such
as gentamicin should be given for 48 h. If a local abscess develops, it should be drained and penicillin,
chloramphenicol, or erythromycin given.

A booster dose of tetanus toxoid should be given.

Neostigmine can reduce the activity of the venom of several neurotoxic snakes (probably not for pre-
synaptic venom, see footnote 5). Based on this principle an anti-cholinesterase test can be done for all
patients with neurotoxic symptoms with the exception of those bitten by a mamba. The venom of

17 WHO/SEARO (2010) Guidelines for the Clinical Management of Snake Bite in the South-East Asia Region 2nd Ed

http://www.searo.who.int/EN/Section10/Section17.htm

17
mamba contains an anti-cholinesterase so the test should not be administered.18 This test (especially in
our settings) might spare the need for intubation and mechanical ventilation, or even save lives. Literature
(1988, 1989)19 supports this test, especially for Asian/African neurotoxic cobra bites.
1) Record patient (neurological) status
2) Atropine 0.6 mg IV (children 50 µg/kg bodyweight) 20
3) Neostigmine 2.5 mg slow IV21 (paediatrics use 50mcg/kg, max 2.5 mg)
4) Observe patient 1 hour for improvements (e.g. reduction of ptosis or improvement in
ventilatory capacity).

If positive:
• Neostigmine per infusion 25-100 µg/kg/hr up to maximum 10mg/24 hours.
• Alternately, neostigmine may be administered by subcutaneous injection, 0.5 mg -2.5 mg q 1-
3h, again to maximum 10mg/24 hours.
• Children can receive 0.01-0.04 mg/kg q2-4 hours.
• Plus Atropine 0.6 mg IV 4-6 hourly

6.4.7 Conservative treatment without anti-venom

Due to the current, worldwide shortage of anti-venoms (in quantity and in quality), safe supplies of anti-
venom in many areas might not be available.
It probably depends on the capacity of the health facility (and – workers) regarding what treatments are
possible.

- In case of respiratory paralysis:

As (respiratory) paralysis is reversible in time, prolonged mechanically ventilation (including
manually) can save someone’s life, even in the absence of anti-venom. Endotracheal intubation is
needed.
If neostigmine and atropine are available always try anti-cholinesterase test in case of neurotoxic
envenomation.

- In case of coagulation disorders:

Avoid all trauma, bed rest indicated. Fresh whole blood or fresh frozen plasma to control active
bleeding.

- In case of circulatory disorders:

Hypovolemia should be corrected with colloid/crystalloid. Hypotension derived from
bradycardia should be treated with atropine.

6.5 Admission and follow up/monitoring

Patients should be observed at least 24 hours after a snake bite. Monitoring depends on initial pathology:
- When anti-venom is given close monitoring for at least an hour is needed
- For local symptoms: measure circumference of bitten body parts, lymph nodes, developing
necrosis, intra-compartmental syndrome
- Systemic: follow up on central venous pressure, blood pressure, heart rate, respiratory system,
temperature, abdominal pain, vomiting
- Paralytic signs
- Urine production
- Muscle myolysis: pain, strength, myoglobinuria
- Blood coagulation – oozing, haematuria, active bleeding
- Clotting test, other laboratory tests

18World Health Organization Regional Office for Africa (2010) Guidelines for the Prevention and Clinical Management of
Snakebite in Africa
19 Watt et al., Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja naja philippinensis). A

placebo-controlled study. N Engl J Med. 1986; 315: 1444-8.

20 Atropine is given to prevent side effects such as diarrhea, , hyper secretions, sweating
21 A short acting anti-cholinesterase (edrophonium) is preferred, but not available in our settings

18
 7. Complications

7.0 Local complications

Compartment syndrome:
Compartment syndrome is a relatively rare complication of pit viper envenomation. It can be confused
with muscle damage due to direct effects of the venom. Signs of compartmental syndrome include
tightness of the compartment, pain, paralysis/paresis of the muscles, and altered sensation. Pain is out of
proportion to the injury and is exacerbated by passive movement of the muscles involved in the affected
compartment. Confirmation requires measurement of intra-compartmental pressure which is not often
available in MSF settings. Where compartment syndrome is suspected, a surgeon should be consulted
urgently to determine if fasciotomy is indicated. Surgical decompression can only be done when
coagulation disorders are corrected. Referral is almost always required.

Early treatment with anti-venom is best way to prevent compartment syndrome.

7.1 Systemic complications

Tetanus
As people in rural areas are more at risk for snake bites and are less likely to be (fully) immunised against
tetanus, developing tetanus after a snake bite is a real risk. Be careful not to mistake the trismus of a sea
snake for the beginning of tetanus (also trismus). History and timeframe will help making right diagnosis.
Treatment of tetanus infection is described in the Clinical Guidelines.

Acute kidney injury:

Renal failure can be multi-factorial: hypotension/shock, diffuse intra-vasal coagulation, myo - and
haemoglobinuria. Anti-venom can cause immunocomplex nephritis.
Symptoms:
Decreased or no urine output (< 400 ml/day)
“Uraemic syndrome”: nausea, vomiting, hiccups, foetor, signs of fluid overload, drowsiness etc.

Endocrine (pituitary/adrenal insufficiency)

Chronic phase (months to years after the bite): weakness, loss of secondary sexual hair, amenorrhoea,
testicular atrophy, hypothyroidism etc.

19
 8. Special cases

8.0 Pregnant (and lactating) women

Envenomed pregnant women are at risk of fetal distress, premature labour, ante and post-partum
bleeding and stillbirth. Observe for bleeding disorders and fetal distress. Fetal bradycardia may indicate
fetal envenomation due to cross placental transmission. Anti-venom treatment is indicated as it outweighs
the risk of anaphylaxis. If severe anaphylaxis does occur in response to anti-venom, epinephrine should
be used in this situation.

Lactating women may continue breast feeding after a snake bite.

8.1 Spitting cobra22

Eye lesions can occur due to spitting venom (spitting cobra). Pain, oedema, eyelid spasms may also occur.
In more than 50 % of cases cornea lesions occur (detection with fluorescein staining, blue light), and
occasionally loss of sight.
First Aid: fluid irrigation in eyes (use plenty of water!)
Pain relief: tropicamide 0.5% eye drops – mydriatic, cycloplegic
Treatment: topical antimicrobials (Tetracycline 1% eye ointment or Chloramphenicol 0.5% eye drops) to
prevent ophthalmitis.
A dressing pad can be applied.
Anti-venom is not required.

9. Prevention
Snake bites cannot be avoided completely, but risk can be reduced through knowledge and appropriate
behaviour.
All MSF staff should be made aware of risk reduction, including environmental measures. These
measures can also be part of health education messages for target population:
• Vigilance during night, after rain/flooding
• Proper shoes/boots when in field
• Use of light at night
• Avoid sleeping on ground
• Avoid rubbish on compound, termite mounds, domestic animals (e.g. chickens) as all this attracts
snakes
• Grass should be cut short on compound (house and clinics)
• Avoid types of house construction that are ‘snake prone’ (straw walls, cracks etc)
• No barehanded touching of apparently dead snakes (bite reflex can remain until one hour after
death) – be careful in removal
• Careful with swimming in certain areas (water snakes)

22Chu et al., Venom ophthalmia caused by venoms of spitting elapid and other snakes: Report of ten cases with review of
epidemiology, clinical features, pathophysiology and management. Toxicon. 2010 Mar 21.

20
References
• Chu et al. ‘Venom ophthalmia caused by venoms of spitting elapid and other snakes:
Report of ten cases with review of epidemiology, clinical features, pathophysiology and
management.’ Toxicon. 2010 Mar 21 (electronic publication ahead of print).
• Corey R, Armitage JO, Seifert SA. (2007) ‘Venomous Snakebite’. In: Cecil’s Textbook of
Medicine, 23rd Edition. Russell L. Cecil, D. A. Ausiello, and Lee Goldman Eds. W B
Saunders Co. October, 2007
• Kasturiratne et al. ‘The global burden of snakebite: a literature analysis and modeling
based on regional estimates of envenoming and deaths’. PLoS Medicine Nov 2008
Volume 5 Issue 11 e 218
• NSW Health. Snakebite & Spiderbite Clinical Management Guidelines 2007.
• Smalligan et al. ‘Crotaline snake bite in the Ecuadorian Amazon: randomised double
blind comparative trial of three South American polyspecific antivenoms’. BMJ 2004
;329:1129
• Warrell DA.‘Clinical toxicology of snakebite in Africa and the Middle East/Arabian
peninsula, Asia’. In: Meier J, White J eds. Handbook of Clinical Toxicology of Animal Venoms
and Poisons. Florida, CRC Press, pp. 433-594
• Warrell DA. Unscrupulous marketing of snake bite anti-venoms in Africa and Papua
New Guinea: choosing the right product – what’s in a name?’ Trans R Soc Trop Med
Hyg. 2008;102: 397–399.
• Warrell DA. Snakebite. Lancet 2010; 375:77-88.
• Warrell DA. Commissioned article: management of exotic snakebites. Q J Med 2009;
102: 593-601.
• Warrell DA. Treatment of bites by adders and exotic venomous snakes. BMJ 2005;
331:1244-1247.
• Watt et al. (1986) Positive response to edrophonium in patients with neurotoxic
envenoming by cobras (Naja naja philippinensis). A placebo-controlled study. N Engl J
Med. 1986; 315: 1444-8.
• WHO Website: http://www.who.int/bloodproducts/snake_antivenoms/en/
• WHO Website:
http://www.who.int/neglected_diseases/diseases/snakebites/en/index.html
• WHO/SEARO (2010) Guidelines for the Clinical Management of Snake Bite in the
South-East Asia Region 2nd Ed
http://www.searo.who.int/EN/Section10/Section17.htm
• Williams, DJ and Jensen SD. (2009) Snake bite management in Cambodia: Supplementary
Report: 2009 Snake bite treatment training courses. Papua New Guinea: WHO, Western Pacific
Office for the Cambodian Ministry of Health.
• Williams, DJ, Jensen SD., and O’Shea, M. (2009) Snake bite management in Cambodia: towards
improved prevention, clinical treatment and rehabilitation. Papua New Guinea: WHO, Western
Pacific Regional Office for the Cambodian Ministry of Health.
• World Health Organization Regional Office for Africa (2010) Guidelines for the
Prevention and Clinical Management of Snakebite in Africa.
http://www.afro.who.int/en/clusters-a-programmes/hss/essential-
medicines/highlights/2358-whoafro-issues-guidelines-for-the-prevention-and-clinical-
management-of-snakebite-in-africa.html
• www.toxinology.com

21
Annex I: Snake families and species

Source: www.who.int/bloodproducts/snake_antivenoms/en/ and www.toxinology.com

As different names may appear on anti-venoms (in Ministries etc) it might be helpful to have the
following list at hand.

I. Family Colubridae

Several of these species have caused human fatalities or major envenoming.

TABLE: Colubrid snakes reported to have caused major or lethal envenoming.

Scientific name Common name Effect
Dispholidus typus Boomslang Coagulopathy & haemorrhage
Thelotornis spp. Vine snakes Coagulopathy & haemorrhage
Yamakagashi, red
Rhabdophis spp. Coagulopathy & haemorrhage
necked keelback
Malpolon monspessulanus Montpelier snake Mild neurotoxicity (poorly defined)
Philodryas olfersii Coagulopathy & haemorrhage
Local swelling, plus respiratory distress & possible
Boiga irregularis Brown tree snake
mild paralysis in infants only

A further group of Colubrid snakes have evolved toxic oral secretions, inoculated during the biting
process though not using fangs. There is increasing evidence that at least some of these species can cause
significant injury to humans. Some other Colubrids reported to cause effects in humans are listed below.
This list is not exhaustive and most Colubrids should be considered as having some potential to cause at
least local envenoming, whether via back-fangs or inoculation of toxic oral secretions.

TABLE: Some Colubrid snakes reported capable of causing mild envenoming (list not exhaustive).
Scientific name Common name Effect
Asian green
Ahaetulla nasuta Local swelling, ± discolouration, lymphangitis.
whipsnake
African many
Amplorhinus multimaculatus Local swelling, ±, headache, nausea.
spotted snake
Local swelling, ± discolouration, bleeding,
Balanophis ceylonensis Sri Lankan keelback
lymphangitis.
Boiga spp. (eg. blandingii, Tree snakes from Local swelling, ± discolouration, bleeding,
ceylonensis, dendrophila, forsteni) Africa & Asia lymphangitis; headache, nausea.
Indian dog faced
Cerberus rhynchops Local swelling, ± discolouration, lymphangitis.
water snake
Coluber spp. (eg ravergieri, Local swelling, ± discolouration, bleeding,
African racer
rhodorachis) lymphangitis.
African herald
Crotaphopeltis hotamboeia Local swelling.
snake
Asian rainbow
Enhydris enhydris Local swelling, ± discolouration, lymphangitis.
water snake
Local swelling, ± discolouration, bleeding,
Madagascarophis meridionalis Madagascan snake blistering, necrosis, lymphangitis, headache,
nausea.
Malpolon moilensis African hooded Local swelling, ± discolouration, lymphangitis.

22
 malpolon

Local swelling, ± discolouration, bleeding,

Psammophis sibilans African racer
lymphangitis, headache, nausea.

African Local swelling, ± discolouration, bleeding,

Psammophylax spp. (selected)
Telescopus semiannulatus
skaapstekers lymphangitis, headache, nausea.
Local swelling, ± discolouration, bleeding,
African tiger snake
lymphangitis, headache, nausea.

II. Family Elapidae

The archtypical Elapid snake is the Indian cobra, but the typical cobra hood is only present in a few
Elapids. Some smaller species are unable or unlikely to successfully envenom humans, but essentially all
the larger species are capable of causing envenoming and many are potentially lethal. Elapids are a major
cause of snakebite morbidity and mortality globally.

TABLE: Major groups of Elapid snakes and their principal clinical effects.
Scientific name Common name Effect
Australian death
Acanthophis spp. Neurotoxic paralysis
adders
Australian
Austrelaps spp. Neurotoxic paralysis
copperheads
Aspidelaps spp. African coral snakes Neurotoxic paralysis
Bungarus spp. Asian kraits Neurotoxic paralysis
Boulengeria spp. African water cobras Neurotoxic paralysis
Calliophis spp. Asian coral snakes Neurotoxic paralysis
Dendroaspis spp. African mambas Neurotoxic paralysis & fasciculation
Elapsoidea spp. African garter snakes Local effects only
African rinkhals
Hemachatus haemachatus Local tissue injury, paralysis
spitting cobra
Australian broad
Hoplocephalus spp. Coagulopathy & haemorrhage
headed snakes
Maticora spp. Asian coral snakes Neurotoxic paralysis
New Guinea small
Micropechis ikaheka
eyed snake Paralysis, coagulopathy, myolysis
American coral
Micrurus spp. Depending on species, paralysis and/or myolysis
snakes
Micruroides euryxanthus Arizona coral snake Neurotoxic paralysis (rarely severe)
African & Asian Depending on species severe local tissue injury
Naja spp.
cobras and/or paralysis
Australian tiger
Notechis spp. Paralysis, coagulopathy, myolysis, renal damage
snakes
Ophiophagus hannah Asian king cobra Paralysis, local tissue injury
Oxyuranus spp. Australian taipans Paralysis, coagulopathy, myolysis, renal damage
African burrowing
Paranaja multifasciata Local effects only
cobra
Australian mulga & Depending on species, myolysis, coagulopathy
Pseudechis spp.
black snakes (anticoagulant), renal damage

23
Pseudohaje spp. African tree cobras Local effects only
Australian brown
Pseudonaja spp. Coagulopathy, renal damage, rarely paralysis
snakes
Australian rough
Tropidechis carinatus Paralysis, coagulopathy, myolysis, renal damage
scaled snake
Middle East desert
Walterinnesia aegyptii Neurotoxic paralysis
black snake
Various Sea snakes Paralysis and/or myolysis

III Family Atractaspididae

TABLE: Atractaspid snakes and their principal clinical effects.

Scientific name Common name Effect
African burrowing
asps, stiletto snakes Depends on species; may cause local effects,
Actractaspis
or mole or side necrosis, cardiotoxicity
fanged vipers

IV Family Viperidae

TABLE: Major groups of viperid snakes and their principal clinical effects.
Scientific name Common name Effect
Atheris spp. African bush vipers Coagulopathy & haemorrhage
Depends on species, but some cause severe local
African puff adders,
Bitis spp. tissue injury, coagulopathy & haemorrhage, shock,
Gaboon vipers etc
cardiotoxicity
Causus spp. African night adders Local pain and swelling only
African horned
Cerastes spp. Local effects, coagulopathy, haemorrhage, shock
adders
Local effects, coagulopathy, haemorrhage, acute
Daboia russelii Russell’s viper kidney injury,
Paralysis & myolysis (Sri Lanka/S India only)
African & West
Echis spp. Asian saw scaled Local effects, coagulopathy, haemorrhage, shock
vipers
Macrovipera spp. Eurasian vipers Local effects, coagulopathy, haemorrhage, shock
Middle East horned
Pseudocerastes spp. Local pain and swelling
vipers
Local effects, necrosis, shock, coagulopathy &
Vipera spp. European vipers
haemorrhage, paralysis (rare)

TABLE: Major groups of crotalid snakes and their principal clinical effects.
Scientific name Common name Effect
Nth American Local effects, necrosis, coagulopathy,
Agkistrodon spp.
copperhead, haemorrhage, shock

24
 cottonmouth, cantil
Central American
Atropoides spp. Local effects, necrosis
jumping pit vipers
Central American
Bothriechis spp. Local effects, necrosis, shock
palm pit vipers
Depends on species, but may include local
Sth & Central
Bothrops spp. effects, necrosis, coagulopathy, haemorrhage,
American pit vipers
acute kidney injury, myolysis, shock
Local effects, necrosis, coagulopathy,
Calloselasma rhodostoma Malayan pit viper
haemorrhage, shock
Central American
Cerriphidion spp. Local effects, necrosis
montane pit vipers
Depends on species; in Nth America, local
effects, necrosis, coagulopathy; shock; in Sth
Crotalus spp. Rattlesnakes
America, local effects, paralysis, coagulopathy,
myolysis, acute kidney injury
Chinese hundred Local effects, necrosis, coagulopathy,
Deinagkistrodon acutus
pace viper haemorrhage, shock
Asian terrestrial pit Local effects, necrosis, coagulopathy,
Gloydius spp.
vipers haemorrhage, shock, paralysis
Sri Lankan hump Local effects, coagulopathy & haemorrhage,
Hypnale spp.
nosed vipers acute kidney injury
Central & Sth
Local effects, necrosis, coagulopathy, shock,
Lachesis spp. American
diarrhoea
bushmasters
Central American
Ophryacus spp. Local effects, necrosis, shock
horned pit vipers
Asian montane pit
Ovophis spp. Local effects, coagulopathy, haemorrhage
vipers
Central American
Porthidium spp. Local effects, necrosis, shock
montane pit vipers
North American
Sistrurus spp. pygmy rattlesnakes Local effects, necrosis, rarely haemorrhage
& massasauga
Trimeresurus (now re-named
Asian green pit Depends on species; local effects, rarely
Cryptelytrops, Protobothrops etc
vipers necrosis, coagulopathy, haemorrhage
etc.) spp.
Local effects, rarely necrosis, coagulopathy,
Tropidolaemus spp. Asian tree vipers
haemorrhage

25
Annex II: A simple anti-venom administration algorithm

Bitten by snake

Resuscitation needed

Yes No

Resuscitate

Signs of envenoming present: No signs of envenomation

Systemic: Bleeding
Progressive weakness
Severe Local
Admit: TV, IV maintenance
24 hours observation

Signs of envenoming present

Administration of anti-venom
+ No signs of envenoming
Supportive therapy
TV

No signs of envenoming Signs of envenoming still present

after 2 hours

Monitor 24 hours
Repeat anti-venom

Discharge with advice

Follow up OPD
Complete TV according to schedule

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Annex III: Mission Snake Bite inventory list

Date:

Filled in by: Function:

Medically important (venomous) snakes in country and Clinical presentation (neurotoxic, haematoxic):
If no: questionnaire not applicable

Specified for each project:

Hospitals in country with adequate snake bite treatment:

Contact persons/ experts in country:

Antivenom used in country:

Address of purchase of anti-venom:

Anti-venom present in mission: Y / N

If Y:

Expiry date:…………………………………………..
Where is anti-venom located?.....................…………….
Amount of anti-venom in stock………….…………….
Which anti-venom(s) present: ………………………….
Drugs for side effects on country standard drug list:
Epinephrine (adrenaline) Y/N
Hydrocortisone Y/N
Promethazine Y/N
etc

Mission made protocol anti-venom (type and amount) present: Y/N

Explanation of First Aid for snake bites given to all relevant staff: Y/N

Prevention measures included in staff health policy: Y/N

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Annex IV: Clotting Test for Snake venom
Standard Operating Procedure
Staff able to perform the test: Laboratory technician junior or higher.

Purpose:
Detect coagulation disorders following a snake bite and subsequent envonomisation of blood.
Appropriate setting: basic health laboratory

Principle:
Clinical significance of the test:
Testing for coagulopathy in envenomed patients.
Laboratory: Snake venom causes a reduction in the blood fibrin levels impairing coagulation.
Thus, lack of coagulation can be used to demonstrate venom presence in suspected snake bite
patients.

Safety:
All blood samples are potentially infectious. Follow standard safety precautions.

Specimen:
Special conditions for patient preparation: none
Type of sample: whole blood.
Volume of sample: At least 2ml of venous blood.
Optimal times between collection and testing: immediately after collection.
Rejection Criteria: incorrectly or not labelled samples. Haemolysed samples. Fingerstick sample.
Anticoagulated blood.

Reagents and Equipment:

Sterile glass 10ml bottle such as McCartney bottle. A clean 15ml glass test tube is appropriate.
Tourniquet

Procedure:
Place the 2ml blood in the bottle and replace the lid (if using a test tube, use a cotton plug).
Place the bottle in an upright position, in a safe room-temperature location free from human
traffic and vibrations.
Wait for twenty minutes for the blood to clot. Do not shake or disturb the bottle or its contents
in any way during this time. If disturbance happens, collect a fresh sample and start the test again.
After twenty minutes, gently invert the bottle.
If the blood is still liquid (un-clotted), the patient has hypofibrinogenaemia as a result of venom-
induced consumption coagulopathy.

Quality Control:
Ensure only glass containers are used and that they are clean and
Check samples for haemolysis before running the test.
Timers must be used.

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Reporting results:
Report as negative for clotted blood and positive for un-clotted blood.

Positive Negative

Cause of error:
Misidentification of blood samples
Use of containers with clot activator (like red topped vacutainers)
Placing the bottle with the test blood on the same bench with the centrifuge or other sources of
vibration.
If the container used for the blood is not glass.
If the container used has been used before.

Invalid results
If the container used for the test has been used before and cleaned with detergent, it may not stimulate
clotting in the same way and the test will be invalid.

Limitations and Procedure Notes:

Although in-coagulable blood is associated with viper envonomation, not all vipers have the
ability to cause it. Therefore a negative test does not automatically exclude viper bite.
While it is possible to use plastic containers for this test, glass containers are the best option.

References:
• Guidelines for the Clinical Management of Snake bites in the South-East Asia Region.
WHO/SEARO 2nd ed 2010 http://www.searo.who.int/EN/Section10/Section17.htm
Australian Venom Research Unit www.avru.org
District Laboratory Practice in Tropical Countries. Part 2 Monica Cheesebrough
Stone, R. et al (2006) "Plastic containers and the whole-blood clotting test: glass remains the best
option" Transactions of the Royal Society of Tropical Medicine and Hygiene Volume 100, Issue
12, December 2006, Pages 1168-1172

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