Venomous bites and stings

SPECIAL SITUATIONS

Venomous bites and stingsDavid Lalloo

AbstractBites and stings are common in many tropical countries. Snakebite

predominantly affects the rural poor and causes both morbidity and

mortality. The clinical features of snake envenoming depend upon the

species: both local and systemic envenoming can occur. Spider bites

and scorpion, fish and jellyfish stings can all cause significant morbidity,

and occasional mortality.

Keywords antivenom; envenoming; snakebite

Epidemiology

Bites and stings from venomous animals occur throughout the

world, but are particularly important in tropical and subtropical

regions, where the large number of venomous species and the

rural activity of the population lead to significant morbidity and

mortality. In some countries, envenoming is one of the principal

causes of death in adults; annual mortality rates from snakebite

of 5e15/100,000 population have been reported in countries

such as Myanmar and Sri Lanka. Recent estimates suggest that

there are between 20,000 and 100,000 deaths and at least 420,000

envenomings annually worldwide. The sequelae of envenoming

can also be severe; disability from a severely damaged limb

following snakebite is particularly problematic in the tropics.

Furthermore, antivenom and the intensive treatment needed by

victims increase health costs in tropical countries with limited

health budgets.

Envenoming can be caused by a large variety of terrestrial and

marine animals. The most important are species of snake, scor-

pion, spider and jellyfish. Bee and wasp stings and marine

animals also cause problems in some parts of the world.

Snakebites

Venomous snakes are found throughout the world. Most patients

are bitten on the lower limb after disturbing snakes, often while

working in fields or hunting; snakes seldom attack humans

spontaneously. Some bites occur through handling of snakes,

and envenoming can occur even after a snake has been killed.

Venom is deposited subcutaneously by the hollow fangs of the

snake. Components of venom usually reach the circulation via

the lymphatics, although low-molecular-weight components may

be absorbed directly into capillaries.

Most venoms are complex mixtures of many different toxins:

� Proteinases act as cytotoxins, causing severe local swelling and

tissue damage in the region of the bite.

David Lalloo MD FRCP is a Professor of Tropical Medicine and Director of

the Wellcome Trust Tropical Centre at the Liverpool School of Tropical

Medicine, Liverpool, UK. Competing interests: none declared.

MEDICINE 38:1 52

� Neurotoxins interfere with neuromuscular transmission. Some

phospholipase A2 toxins also damage myocytes directly.

� Some venoms contain haemorrhagins (metalloproteinases that

damage vascular endothelium, causing bleeding).

� Components of venom can act at many different sites in the

coagulation pathway, causing anticoagulant or procoagulant effects

leading to a state resembling disseminated intravascular

coagulation. Components also act directly on platelets.

Clinical features of envenoming depend on the species;

accurate identification, ideally by examination of the dead snake,

is crucial. Careful clinical evaluation is necessary before treat-

ment is administered, because bites by a venomous species do

not always result in envenoming.

The bite of elapid snakes (kraits, cobras) most commonly

causes neurotoxicity, whereas viperine snakes (vipers, pit vipers,

rattlesnakes, British adder) cause local tissue damage, shock and

coagulopathies. However, this distinction is somewhat blurred;

for example, Australasian elapids can cause both neurotoxicity

and coagulopathies.

Envenoming causes both local and systemic effects. Symp-

toms of systemic envenoming (headache, lymph node pain and

collapse) often occur within several minutes of the bite. Most

signs of envenoming develop within the first few hours, though

neurotoxicity can occasionally take more than 12 hours.

� Fang marks are usually visible at the site of the bite.

� Following bites from some species, oedema (Figure 1) can

occur at the site of the bite and progress to involve the whole

limb. Some species cause tissue necrosis at the site of the bite.

� Painful regional lymph node enlargement is a common early

sign of envenoming.

Figure 1 Severe local oedema, blistering, bruising, bleeding and early

necrosis in a Thai boy bitten on the shin 3 days earlier by a Malayan pit

viper (Calloselasma rhodostoma). � 1997 Professor DA Warrell.

� 2009 Elsevier Ltd. All rights reserved.

Figure 2 Spontaneous bleeding from the gums in a patient bitten by

a Papuan taipan (Oxyuranus scutellatus canni). � 1997 Professor DA

Warrell.

SPECIAL SITUATIONS

� Venom haemorrhagins act on endothelium, causing bleeding

from the gums (Figure 2) and other sites (e.g. old sores).

Coagulopathies can exacerbate this effect, and occasionally lead to

life-threatening bleeding.

� Shock can occur as a result of loss of fluid into a limb or

haemorrhage.

� Neurological involvement classically causes progressive

paralysis. Ptosis occurs initially; this progresses to involvement of

the bulbar muscles (Figure 3) and, ultimately, paralysis of the

diaphragm.

� Destruction of skeletal muscle, following envenoming by species

such as sea snakes, leads to painful myopathy and paralysis.

� Renal failure complicates envenoming by several species.

Figure 3 Severe ptosis and bulbar palsy requiring intubation in a patient

bitten by a Papuan taipan.

MEDICINE 38:1 53

Investigations e the white blood cell count is commonly

elevated and thrombocytopenia often occurs, particularly in

patients with coagulopathy. Renal function should be checked.

Creatine kinase elevation occurs in myotoxicity.

The whole-blood clotting test is an important bedside indi-

cator of envenoming by species that cause coagulopathy. Blood

left in a clean, dry glass tube is examined after 20 minutes to see

whether clotting has occurred. In some cases, the test can also be

used to follow the response to antivenom. If available, standard

clotting assays. (prothrombin time (PT), activated partial

thromboplastin time (APTT), fibrinogen) are sensitive indicators

of a coagulopathy.

Management e most traditional first aid procedures (e.g.

incision, suction) are more harmful than beneficial. Immobili-

zation of the bitten limb and compression bandaging, when

properly applied, appear to be helpful in slowing lymphatic

spread of venom. It should be used for bites by species that do

not cause local tissue necrosis, to allow time for transport of the

victim to hospital. Intramuscular injections and aspirin should be

avoided in patients with coagulopathy.

Antivenom is indicated for the treatment of systemic or severe

local envenoming. A delay in administration reduces the efficacy,

but antivenom can remain useful as long as signs of systemic

envenoming persist. The antivenom used depends on the biting

species; in many parts of the world, polyspecific antivenoms

covering the commonly occurring species are available.

Antivenom should be given by slow intravenous infusion. The

appropriate dose is dictated by local experience. Children require

the same dose as adults. Test doses have no role in predicting

antivenom reactions. In some countries, antihistamine or

adrenaline (epinephrine) is given as routine prophylaxis against

reactions. Most evidence suggests that there is no role for routine

prophylaxis but adrenaline (epinephrine) should always be

available for treatment of reactions.

Effective antivenom treatment should halt local oedema and

reverse coagulopathy within 6e12 hours. The whole-blood

clotting test 6 hours after administration of antivenom, or

measurement of PT or APTT after 6 hours can help to determine

whether further doses are necessary.

Most toxins acting postsynaptically are reversed by anti-

venom, but presynaptic neurotoxicity is less responsive;

supportive therapy may be needed until spontaneous recovery

occurs.

Delayed absorption of venom from a depot at the bite site can

occur. Repeated doses of antivenom may be needed after initial

therapy if coagulopathy redevelops, neurological deterioration

occurs or limb oedema progresses.

Care of the airway is critical in severe neurotoxicity. Bulbar

involvement (demonstrated by inability to swallow secretions) is

an indication for early intubation and mechanical ventilation if

facilities are available; patients have been ventilated successfully

by hand for several days. Hypotension requires appropriate

management with fluids. Peritoneal dialysis can be instituted in

many tropical regions and can be life-saving.

Fasciotomy is seldom, if ever, necessary, even in severe

oedema. The only indication is raised intracompartmental pres-

sure. Surgery should not be performed until coagulopathy has

been corrected.


SPECIAL SITUATIONS

Anticholinesterases are effective in some patients with

neurotoxic envenoming; the therapeutic response may be

dramatic. A trial of a short-acting anticholinesterase such as

neostigmine or edrophonium should be performed in such cases;

in the absence of antivenom, it can be life-saving.

Plasma or clotting factors are seldom needed unless life-

threatening haemorrhage occurs, and should not be given until

adequate doses of antivenom have been administered.

Scorpion stings

Venomous scorpion stings are a major problem in the Americas,

North Africa, the Middle East and South Asia. Scorpion venoms

are usually less complex than snake venoms; most components

are peptides that affect sodium and potassium channels. The

severity of envenoming varies between species.

Clinical features e severe pain in the region of the sting is

common. A small proportion of patients, particularly children,

develop signs and symptoms caused by the action of scorpion

venom on the autonomic nervous system. Hyperexcitability,

sweating, lacrimation, excessive salivation and tachypnoea may

occur. In severe envenoming, catecholamine release causes hyper-

tension, cardiac arrhythmias, myocardial failure and pulmonary

oedema. Skeletal muscle stimulation can lead to muscular spasms.

Management e antivenom therapy is the mainstay of therapy,

with supportive medical treatment. Atropine may be required in

patients with severe bradyarrhythmia, but has no other proven

value. Vasodilator therapy (particularly prazosin) can be useful

in the treatment of cardiovascular manifestations of envenoming.

Figure 4 Box jellyfish, Chironex fleckeri.

Spider bites

Species of venomous spiders are found throughout the world, in

temperate and tropical regions.

Clinical features e the most common venomous spiders are

the widow spiders (Latrodectus spp.): their venom stimulates

transmitter release from neurones throughout the nervous system,

causing severe local and generalized pain, muscle cramps and

spasms, sweating, and occasionally severe hypertension.

The predominant feature of envenoming by recluse spiders

(Loxosceles spp.) is severe, slowly-evolving local necrosis. The

Australian funnel web spider (Atrax robustus) releases a presyn-

aptic neurotoxin that can stimulate the autonomic and peripheral

nervous system and can cause cardiovascular instability and

severe pulmonary oedema.

Management e pressure immobilization is recommended for

funnel web spider bites, but is not used for other species. The

availability of antivenom depends on the species and the

geographical location. Antivenom should be used for significant

systemic envenoming.

Venomous fish

Many different venomous fish sting if they are stood on or

touched. Systemic envenoming is rare. Excruciating pain at the

site of the sting is the major effect. Regional nerve blocks and

MEDICINE 38:1 54

local infiltration of lidocaine can be effective, but most marine

venoms are heat labile. Immersing the stung part in hot water is

extremely effective in relieving pain. Care should be taken to

avoid scalding; the envenomed limb may have abnormal

sensation.

Coelenterate stings

Venomous jellyfish occur throughout the world, but are partic-

ularly common in the tropical waters of the Indo-Pacific region. A

mechanical stimulus causes nematocysts on the tentacles to

discharge, injecting venom subcutaneously.

Clinical features depend on the species. Most cause imme-

diate pain at the site of contact and an acute local inflammatory

response. The box jellyfish, Chironex fleckeri (Figure 4), can

cause full-thickness skin damage and systemic involvement;

death can occur rapidly from myocardial toxicity. Some tiny

carybdeid jellyfish stings cause Irukandji syndrome, often in the

absence of skin lesions. Pain, hypertension and cardiopulmonary

decompensation can occur 30e40 minutes after the sting.

Management e undischarged nematocysts adherent to the

skin should be prevented from firing; vinegar is effective on

stings from the box jellyfish found in Pacific and Australasian

regions. Stings from hydroids (e.g. Portuguese man-of-war),

should be washed with fresh sea-water and adherent tentacles

picked off.

In patients with box jellyfish stings, compression bandaging

can reduce systemic absorption of venom. In severe envenoming,

collapse may occur on the beach. Cardiopulmonary resuscitation

may be life-saving.

Antivenom is not available for hydroid stings or Irukandji

syndrome. Pain relief can be achieved by the use of ice and


SPECIAL SITUATIONS

opioids: immersion in hot water is also effective for some

species. Supportive therapy is necessary for the management of

cardiovascular manifestations. A

Vipera berus (adder)

The adder inflicts about 50e100 bites each year in the UK. Most

patients present with minimal symptoms and signs; serious

envenoming is rare and death extremely uncommon.

In most cases, symptoms develop within 6 hours of the bite.

The most common local features are pain and swelling that may

spread to involve the whole limb. Gastrointestinal disturbances,

abdominal pain, vomiting and diarrhoea may be prominent if

systemic absorption of venom occurs. Severe systemic enve-

noming causes circulatory disturbances with tachycardia, hypo-

tension and shock; these can occur within minutes of the bite or

be delayed for hours. Bleeding and coagulopathy are rare. Leu-

cocytosis, metabolic acidosis or raised creatine phosphokinase

may indicate systemic envenoming.

Antivenom should be given to patients with severe local

envenoming or evidence of systemic envenoming, particularly

shock, or protracted gastrointestinal symptoms.

Indication for antivenom

C Severe local envenoming (oedema extending over more than

half the bitten limb or necrosis)

C Coagulopathy

C Bleeding

C Shock

C Neurotoxicity

C Myotoxicity

C Renal failure

MEDICINE 38:1 55

FURTHER READING

Kasturiratne A, Wickremasinghe AR, de Silva N, et al. The global

burden of snakebite: a literature analysis and modelling based on

regional estimates of envenoming and deaths. PLoS Med 2008; 5:

e218. doi:10.1371/journal.pmed.0050218.

Sano-Martins IS, Fan HW, Castro SC, et al. Reliability of the simple 20

minute whole blood clotting test (WBCT20) as an indicator of low

plasma fibrinogen concentration in patients envenomed by Bothrops

snakes. Toxicon 1994; 32: 1045e50.

Theakston RDG, Lalloo DG. Venomous bites and stings. In: Zuckerman J,

ed. Principles and practice of travel medicine. Chichester: John Wiley

and Sons, 2001.

Warrell DA. Treatment of bites by adders and exotic venomous snakes.

BMJ 2005 Nov 26; 331: 1244e7.

Practice points

C Not all patients bitten by a venomous snake are envenomed

C The 20-minute whole-blood clotting test is a rapid, easy test

for envenoming following bites by some species

C Antivenom should be given only when there are clear signs of

envenoming

C Doses of antivenom are the same for children and adults

C Observe patients carefully after administration of antivenom,

to detect reactions and to monitor the need for further

treatment

Acknowledgement

We are grateful to Professor DA Warrell for granting permission to

use his photographs for Figures 1 and 2.


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Venomous bites and stings