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10.18 Some poisonous plants and fungi, with their clinical effects
Species (common name) Toxins Important features of toxicity
Plants
Abrus precatorius (jequirity bean)
Ricinus communis (castor oil plant)
Aconitum napellus (aconite, wolf’s bane, monkshood)
Abrin
Ricin
Gastrointestinal effects, drowsiness, delirium, convulsions, multi-organ
failure
Aconite Gastrointestinal effects, paraesthesiae, convulsions, ventricular tachycardia
Aconitum ferox (Indian aconite, bikh)
Atropa belladonna (deadly nightshade)
Datura stramonium (Jimson weed, thorn apple)
Brugmansia spp. (angel’s trumpet)
Atropine,
scopolamine,
hyocyamine
Anticholinergic toxidrome (see Box 10.10)
Colchicum autumnale (autumn crocus) Colchicine Gastrointestinal effects, hypotension, cardiogenic shock
Conium maculatum (hemlock) Toxic nicotinic
Hypersalivation, gastrointestinal effects, followed by muscular paralysis
alkaloids
Digitalis purpurea (foxglove)
Nerium oleander (pink oleander)
Cardiac glycosides Nausea, vomiting, bradycardia and heart block, supraventricular and
ventricular tachyarrhythmias, visual disturbances, confusion (p. 224)
Thevetia peruviana (yellow oleander)
Laburnum anagyroides (laburnum) Cytosine Gastrointestinal effects; convulsions in severe cases
Taxus baccata (yew) Taxane alkaloids Hypotension, bradycardia, respiratory depression, convulsions, coma,
arrhythmias
Fungi
Amanita phalloides (death cap mushroom) Amatoxins Gastrointestinal effects, progressing to liver failure
Cortinarius spp. Orellanine Gastrointestinal effects, fever, progressing to renal failure
Psilocybe semilanceata (‘magic mushrooms’) Psilocybin, psilocin Hallucinations
10
Scombrotoxic sh poisoning
Under poor storage conditions, histidine in scombroid sh (e.g. tuna,
mackerel, bonito, skipjack and the dark meat of canned sardines) may
be converted by bacteria to histamine and other chemicals. Within min-
utes of consumption, ushing, burning, sweating, urticaria, pruritus,
headache, colic, nausea and vomiting, diarrhoea, bronchospasm and
hypotension may occur. Management is with nebulised salbutamol, intra-
venous antihistamines and, occasionally, intravenous uid replacement.
Tetrodotoxin poisoning
The highly toxic tetrodotoxin is found in the skin and viscera of Puffer
sh. Tetrodotoxin blocks voltage-gated sodium channels, inhibiting
action potential generation and propagation. Clinical features include
paraesthesiae, salivation, gastrointestinal disturbances, sweating, head-
ache, tachycardia, hypokalaemia, twitching or tremor, vertigo, dysphonia
and dysphagia. In severe cases ataxia, paralysis and xed dilated pupils
occur, mimicking brain death. Without appropriate ventilator support,
respiratory paralysis can be fatal. Otherwise there is no specic treatment
and management is supportive.
Plant poisoning
A substantial number of plants and fungi are potentially toxic if con-
sumed, with patterns of poisoning depending on their geographical dis-
tribution. Some toxic examples and the clinical features of toxicity are
shown in Box 10.18
Further information
Books and journal articles
Bateman DN, Jefferson R, Thomas SHL, eds. Oxford desk reference: toxicology.
Oxford: Oxford University Press; 2014.
Benson BE, Hoppu K, Troutman WG, etal. Position paper update: gastric lavage
for gastrointestinal decontamination. Clin Toxicol 2013;51:140–146.
Gosselin S, Hoegberg LCG, Hoffman RS, etal. Evidence-based
recommendations on the use of intravenous lipid emulsion therapy in
poisoning. Clin Toxicol 2016;54(10):899–923.
Thanacoody R. Position paper update: Whole bowel irrigation for gastrointestinal
decontamination of overdose patients. Clin Toxicol 2015;53:5–12.
Thompson JP, Watson ID, Thanacoody HK, etal. Guidelines for laboratory
analyses for poisoned patients in the United Kingdom. Ann Clin Biochem
2014;51:312–325.
Websites
toxbase.org Toxbase, the clinical toxicology database of the UK National
Poisons Information Service. Free for UK health professionals but registration
is required. Access for overseas users by special arrangement. Low-cost
smartphone app available.
wikitox.org/doku.php?id=wikitox:wikitox_home WikiTox, an open access
curriculum project to improve the treatment of people who are poisoned.
apps.who.int/poisoncentres World directory of poisons centres, as of 28 February
2019 (interactive map).
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Multiple Choice Questions
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10.1. Multiple doses of activated charcoal are useful in the treatment of
patients with poisoning involving which one of the following:
A. Ferrous sulphate
B. Yellow oleander (Thevetia peruviana)
C. Pesticides
D. Lithium carbonate
E. Dapsone
Answer: E.
Ferrous sulphate and lithium are not adsorbed by activated charcoal.
A clinical trial of multiple-dose activated charcoal for patients with yellow
oleander or pesticide poisoning showed no benet. The clearance of dapsone is enhanced by multiple-dose activated charcoal. This is also true for
carbamazepine, phenobarbital, quinine and theophylline (Box 10.7).
10.2. A 2-year-old child is assessed because the parents are
concerned he has swallowed some aspirin tablets. Which one of
the following clinical features is NOT consistent with a diagnosis
of salicylate poisoning in a child?
A. Respiratory alkalosis
B. Metabolic alkalosis
C. Hypoprothrombinaemia
D. Hypothermia
E. Hypotension
Answer: D.
Respiratory alkalosis is a common feature of salicylate poisoning, especially in children. Metabolic acidosis can also occur and is associated with
a worse prognosis. Hypoprothrombinaemia is typical of salicylate poisoning. Shock, including hypotension, and hyperpyrexia may also be seen in
severe poisoning. Hypothermia is not a feature of salicylate toxicity.
10.3. An adult male is found unconscious after a suspected drug
overdose. ECG ndings are as follows: heart rate 78/min, PR
interval 162 ms, QRS interval 162 ms and QT interval 363 ms.
The corrected QT interval (QTc, using Bazett’s formula) is 414 ms.
Which ONE of the following statements is correct?
A. Severe cardiac potassium channel blockade is present
B. Conduction velocity is increased in the bundles of His
C. First-degree heart block is present
D. Overdose with ecainide could account for the ECG ndings
E. Magnesium sulphate should be administered urgently
10.4. A homeless man aged 23 is found unconscious in the street after
smoking an unidentied illicit drug. No further history is available.
On examination his Glasgow Coma Scale (GCS) is 9, pupils are
mid-sized and equal, heart rate is 110/min, blood pressure is
116/84 mmHg, and temperature is 36.8°C. Arterial blood gases
show a mild respiratory acidosis. General physical examination
is otherwise normal. No needle marks are found. Which of the
following is the most likely substance causing this presentation?
A. Heroin
B. AMB-FUBINACA
C. Alprazolam
D. Ecstasy
E. Gamma hydroxybutyrate
Answer: B.
Ecstasy does not cause a reduction in level of consciousness, but
this can be caused by any of the other four drugs listed. Alprazolam (a
benzodiazepine) and gamma hydroxybutyrate (GHB) could both cause
this clinical presentation but are not used by smoking. Heroin can be
smoked (‘chasing the dragon’) but would usually cause small pupils.
AMB-FUBINACA is a synthetic cannabinoid receptor agonist. These
compounds, commonly referred to as ‘spice’, are usually smoked; they
can cause reduced level of consciousness and respiratory acidosis, without pupillary changes.
10.5. Which of the following antidotes does NOT act by binding to the
toxin it is used to treat?
A. Fomepizole
B. Digoxin-specic antibody fragments
C. Idarucizumab
D. Hydroxocobalamin
E. Desferrioxamine
Answer: A.
Fomepizole is an alcohol dehydrogenase inhibitor. It prevents the
metabolism of ethylene glycol and methanol to the toxic metabolites
responsible for the clinical features of poisoning. Digoxin-specic antibody fragments bind to digoxin (and other cardiac glycosides) and idarucizumab is a monoclonal antibody that binds to dabigatran etexilate.
Hydroxocobalamin complexes with cyanide to form cyanocobalamin and
desferrioxamine complexes with iron to form ferrioxamine. In all four of
these examples, drug bound to the antidote no longer causes toxicity.
Answer: D.
The only abnormality identied is prolongation of the QRS interval,
which is a feature caused by severe sodium channel blockade. This
results in delayed phase 0 depolarisation and reduced conduction velocity in the bundles of His and in ventricular myocytes. Drugs that cause
sodium channel blockade in overdose include class 1a (e.g. quinidine)
and 1c (e.g. ecainide) anti-dysrhythmic drugs, tricyclic antidepressants, some β-blockers (e.g. propranolol), cocaine and diphenhydramine
(Box 10.8). Cardiac sodium channel blockade is associated with an
increased risk of monomorphic ventricular tachycardia and ventricular
brillation. Treatment is with intravenous sodium bicarbonate. Potassium
blockade is indicated by QTc prolongation and may culminate in torsades de pointes ventricular tachycardia, which is treated with magnesium sulphate; in this case, however, the QTc interval is normal, as is the
PR interval, so rst-degree heart block is also not present.
J White
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11
Envenomation
Comprehensive evaluation of the envenomed patient 240
Geographical distribution of venomous snakes 241
Bedside tests in the envenomed patient 241
Overview of envenomation 242
Venom 242
Venomous animals 242
Clinical effects 243
General approach to the envenomed patient 243
First aid 243
Assessment and management in hospital 246
Treatment 247
Follow-up 248
Prevention 248
Envenomation by specic animals 248
Venomous snakes 248
Scorpions 249
Spiders 249
Paralysis ticks 249
Venomous insects 249
Marine venomous and poisonous animals 250
240 E NVE N OM AT IO N
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Comprehensive evaluation of the envenomed patient
Airway, breathing, circulation
1 12
Blood pressure
Pulse
Respiration rate
Oxygen saturation
Dysrhythmias
2
Level of consciousness
Confusion
Agitation
Seizures
3
Mouth, gums
Evidence of bleeding
Increased salivation
Drooling
2
4
3
5
1
12
11
11
10
9
Cranial nerves
4
Drooling
Dysarthria
Dysphagia
Upper airway compromise
8
10
Bilateral mild ptosis
7
6
Eyes
Miosis or mydriasis
Increased lacrimation
neal injury (venom spit injury)
Cor
Chemosis – can indicate
capillary leak syndrome
Skin
In addition to (6):
Piloerection
Erythema
Blistering
Infection
Local increased sweating
Abdomen
Intra-abdominal, retroperitoneal
or renal pathology
Lymph nodes
9
Tender or enlarged nodes
draining bite/sting area
Ptosis and lateral
ophthalmoplegia
Fixed dilated pupils
Chest
5
Pulmonary oedema
Diminished respiration
Copyright © Julian White.
Bite/sting site
6
Pain
Swelling
Bruising
Discoloration
Necrosis
Local bleeding, blistering
Muscles
8
Weakness
Tenderness
Pain
7
Reflexes
Decreased or absent reflexes
Local bleeding
Geographical distribution of venomous snakes
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Be dsi de t est s i n th e e n ven ome d pa tie nt 241
Indian krait
Bungarus caeruleus
Puff adder
Bitis arietans
South American
rattlesnake
Crotalus durissus
European adder
Vipera aspis
Black-necked
spitting cobra
Naja nigricollis
Russell’s viper
Daboia russelii
Common Indian cobra
Naja naja
Green pit viper
Tr
Saw-scaled viper
Echis carinatus
Monacled cobra
Naja kaouthia
11
The geographical location of a snakebite determines the likely animal(s) involved and the nature and risks of the envenomation. Copyright ©
Julian White
Bedside tests in the envenomed patient
1 Obtain a clean glass container
(test tube or bottle) that is
either new, or has only been
washed with water (not
detergent/soap)
2 Place 2–3 mL venous blood
in the glass container
3 Allow to stand undisturbed
for 20 mins
4 Gently invert/tip the glass
container checking for
presence of a blood clot
4a Clot present = negative test
(no coagulopathy present)
4b Clot absent = positive test
(coagulopathy present)
Examination of urine. Haematuria may indicate
a coagulopathy. Dark urine is suggestive of
myoglobinuria, which is a sign of extensive
rhabdomyolysis. Copyright © Julian White.
1 3
2
4a
4b
Twenty-minute whole-blood clotting test (20WBCT). The presence of coagulopathy is a
key indicator of major envenoming for some species. While full laboratory coagulation
studies may be the ideal, the 20WBCT has emerged as a simple standardised bedside
test of coagulopathy, applicable even in areas with limited health facilities.
Copyright © Julian White
242 E NVE N OM AT IO N
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Overview of envenomation
Envenomation occurs when a venomous animal injects sufcient venom
by a bite or a sting into a prey item or perceived predator to cause deleterious local and/or systemic effects. This is dened as a venom-induced disease (VID). Venomous animals generally use their venom to
acquire and, in some cases, pre-digest prey, with defensive use a secondary function for many species. Where defensive use of venom is an
important evolutionary driver, immediate and severe local pain is a common feature, though the toxin mechanisms causing pain are diverse.
Accidental encounters between venomous animals and humans are
frequent, particularly in the rural tropics, where millions of cases of venomous bites and stings occur annually. Globally, an increasing number
of exotic venomous animals are kept privately, so cases of envenoming
may present to hospitals where doctors have insufcient knowledge to
manage potentially complex presentations. Doctors everywhere should
thus be aware of the basic principles of management of envenomation
and how to seek expert support. It is important for doctors to know what
types of venomous animal are likely to occur in their geographical area
(hospital hinterland; see p. 241) and the types of envenoming they may
cause.
Venom
Venom is a complex mixture of diverse components, often with several
separate toxins that can cause adverse effects in humans, with each
potentially capable of multiple effects (Box 11.1). Venom is produced
at considerable metabolic cost, so is used sparingly; only some bites/
stings by venomous animals result in signicant envenoming, the remainder are ‘dry bites’. The concept of dry bites is important in understanding
approaches to rst aid and medical management.
Venomous animals
There are many animal groups that contain venomous species (Box 11.2).
The epidemiological estimates of envenomation episodes reect
the importance of snakes and scorpions as causes of severe or
lethal envenomation, but also the fragmentary nature of the data. For
snakebites, recent studies have proposed widely varying estimates,
but even the higher estimates may be too low. In India, studies indicate
there are at least 45 000 snakebite-related deaths annually, far above
both government gures and previous estimates. In many areas of the
rural tropics, health resources are limited and few envenoming cases
are either seen or recorded within the ofcial hospital system, compared
to the actual community burden of disease. While fatal cases may gain
most attention, long-term disability from envenomation affects significantly more people and has a major social and economic cost. The
World Health Organization (WHO) has recently recognised snakebite as
a ‘Neglected Tropical Disease’ and this may improve access to funding.
11.2 Venomous animals and human envenoming
Principal
Phyla
venomous
animal groups
Chordata Snakes
Spiny sh
Stingrays
Arthropoda Scorpions
Spiders
Paralysis ticks
Insects
Mollusca Cone snails
Blue-ringed
Estimated
number of
human cases/
year
> 2.5 million > 100 000
? > 100 000
? > 100 000 ? < 10
> 1 million ? < 5000
? > 100 000 ? < 100
? > 1000 ? < 10
? > 1 million ? > 1000*
? < 1000 ? < 10
? < 100 ? < 10
Estimated
number of
human deaths/
year
Close to zero
octopus
Coelenterata Jellysh
*Social insect stings cause death by anaphylaxis rather than primary venom toxicity, except for
massive multiple sting attacks.
Copyright © Julian White
? > 1 million ? < 10
11.1 Key venom effects*
Venom component Clinical effects Type of venomous animal
Neurotoxin
Paralytic Flaccid paralysis (may develop in a descending pattern,
commencing rst in cranial nerves, or in an ascending
pattern, with early ataxia)
Some snakes (descending)
Paralysis ticks (ascending)
Cone snails (descending)
Blue-ringed octopus (descending)
Excitatory Neuroexcitation: autonomic storm, cardiotoxicity,
Some scorpions, spiders, jellysh (irukandji)
pulmonary oedema
Myotoxins Systemic or local myolysis Some snakes
Cardiotoxins Direct or indirect cardiotoxicity; cardiac collapse, shock Some snakes, scorpions, spiders and jellysh (box jellysh)
Haemostasis system toxins Variation from rapid coagulopathy and bleeding to
thrombosis, deep venous thrombosis and pulmonary
Many snakes and a few scorpions (Hemiscorpius)
Brazilian caterpillars (Lonomia)
emboli
Haemorrhagic toxins Local vessel damage, uid extravasation, blistering,
Mainly some snakes
ecchymosis, shock
Nephrotoxins (direct or indirect) Renal damage Some snakes, massed bee and wasp stings
Necrotoxins Local tissue injury/necrosis, shock Some snakes, a few scorpions (Hemiscorpius), spiders
(recluse spiders), jellysh and stingrays
Allergic toxins Induction of acute allergic response (direct and indirect) Almost all venoms but particularly those of social insects
(i.e. bees, wasps, ants)
*All venom components have lethal potential.
Copyright © Julian White
Gene ra l app ro ach t o the enve no med p atien t 243
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Snakebite occurs frequently in low resource areas of the rural tropics
and so is an important poverty trap; it is also a predominantly occupational disease, with farmers and other agricultural workers at particularly
high risk. Although snakebite is undoubtedly the most impactful form of
envenoming globally, there are some areas where scorpion stings have a
higher impact on health systems than snakebite.
Stings by social insects such as bees and wasps may also cause lethal
anaphylaxis and mass stings may cause severe, even lethal, envenomation. Other venomous animals may commonly envenom humans, but
cause mostly non-lethal effects. A few animals only rarely envenom
humans, but have a high potential for severe or lethal envenoming. These
include box jellysh, cone snails, blue-ringed octopus, paralysis ticks and
Australian funnel web spiders. Within any given group, particularly snakes,
there may be a wide range of clinical presentations. Some are described
here, but for a more detailed discussion of the types of venomous animal,
their venoms and their effects on humans, see toxinology.com.
Clinical effects
With the exception of dry bites, where no signicant toxin effects occur,
venomous bites/stings can result in three broad classes of effect.
Local effects
These vary from trivial to severe (Box 11.3). There may be minimal or no
local effects with some snakebites (not even pain), yet lethal systemic
envenoming may still be present (e.g. kraits in Asia). For other species,
local effects predominate over systemic, and for some, (e.g. certain
snakes) both are important (p. 240). Some species commonly cause
local necrosis, notably some snakes, brown recluse spiders, an Iranian
scorpion (Hemiscorpius lepturus) and some stingrays. Globally, amputations secondary to snakebite are an important cause of long-term morbidity and social disadvantage.
General systemic effects
By denition, these are non-specic (see Box 11.3). Shock is an important complication of major local envenoming by some snake species and
if inadequately treated can prove lethal, especially in children.
11.3 Local and systemic effects of envenomation
Local effects
Pain
Sweating
Erythema
Major direct tissue trauma
(e.g. stingray injuries)
Non-specic systemic effects
Headache
Nausea
Vomiting and diarrhoea
Abdominal pain
Tachycardia or bradycardia
Hypertension or hypotension
Specic systemic effects
Neurotoxic accid paralysis (descending or ascending)
Excitatory neurotoxicity (catecholamine storm-like and similar)
Rhabdomyolysis (systemic or local)
Coagulopathy (procoagulants, anticoagulants, brinolytics and platelet-active
toxins)
Cardiotoxicity (decreased/abnormal cardiac function or arrhythmia or arrest)
Acute kidney injury (polyuria or oliguria or anuria or isolated elevated
creatinine/urea)
Copyright © Julian White.
Blistering
Necrosis
Swelling
Bleeding and bruising
Pulmonary oedema
Dizziness
Collapse
Convulsions
Shock
Cardiac arrest
Specic systemic effects
These are important in both diagnosis and treatment.
Neurotoxic accid paralysis can develop very rapidly, progressing
from mild weakness to full respiratory paralysis in less than 30 minutes (blue-ringed octopus bite, cone snail sting), or may develop far
more slowly, over hours (e.g. kraits, some cobras) to days (paralysis
tick). For neurotoxic snakes, the cranial nerves are usually involved
rst, with bilateral ptosis a common initial sign, often progressing
to partial and later complete ophthalmoplegia, xed dilated pupils,
drooling and loss of upper airway protection (p. 240). From this,
paralysis may extend to the limbs, with weakness and loss of deep
tendon reexes, the neck (‘broken neck’ sign), then nally respiratory
paralysis affecting the diaphragm.
Excitatory neurotoxins cause an ‘autonomic storm’, often with pro-
fuse sweating (p. 240), variable cardiac effects and cardiac failure,
sometimes with pulmonary oedema (notably, Australian funnel web
spider bite, some scorpions such as Indian red scorpion). This type
of envenomation can be rapidly fatal (many scorpions, funnel web
spiders), or may cause distressing symptoms with a lesser risk of
death (widow spiders, banana spiders).
Myotoxicity can be localised in the bitten limb, or systemic, affecting
mostly skeletal muscles. It can initially be silent, then present with
generalised muscle pain, tenderness, myoglobinuria (p. 241) and
substantial rises in serum creatine kinase (CK). Secondary renal
failure can precipitate potentially lethal hyperkalaemic cardiotoxicity.
Cardiotoxicity is often secondary, but symptoms and signs are
non-specic in most cases. For some scorpions, envenomation can
cause direct cardiac effects, including decreased cardiac output,
arrhythmias and pulmonary oedema.
Haemostasis system toxins cause a variety of effects, depending on
the type of toxin (Fig. 11.1). Coagulopathy may present as bruising
and bleeding from the bite site (p. 240), gums and intravenous sites.
Surgical interventions are high risk in such cases. Other venoms
cause thrombosis, usually presenting as deep venous thrombosis (DVT), pulmonary embolus or stroke (particularly Caribbean/
Martinique vipers).
Haemorrhagic toxins (associated with some snakebites) cause vas-
cular damage, especially in the bitten limb, with extravasation of uid
and sometimes hypotensive shock. They may also cause internal
bleeding such as retroperitoneal haemorrhage. The role of these
toxins in causing late-developing capillary leak syndrome (p. 240) is
uncertain (seen notably with Russell’s viper),
Renal damage in envenoming is mostly secondary, although some
species (such as Russell’s vipers) can cause primary renal damage.
The presentation is similar in both scenarios, with changes in urine
output (polyuria, oliguria or anuria), proteinuria, or rises in creatinine
and urea. In cases with intravascular haemolysis, secondary renal
damage is likely. The clinical effects of specic animals in different
regions of the world are shown in Boxes 11.4–11.6.
General approach to the envenomed patient
First aid
First aid can be crucial in determining the outcome for envenomed
patients, yet throughout much of the world inappropriate and dangerous
rst aid is often administered.
A signicant proportion of venom is transported from the bite/sting
site via the lymphatic system, particularly for venoms with larger molecular weight toxins, such as many snake venoms. It is recommended
that for most forms of envenoming, the patient should be kept still, the
bitten limb immobilised with a splint and vital systems supported, where
required. A patent upper airway should be ensured and respiratory
11
244 E NVE N OM AT IO N
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Haemorrhagic metalloproteinases and disintegrins
1
Damage blood vessel wall, cause leakage of blood,
degrade platelet plug response
Procoagulants
Clotting
factor pathways
2
Activate specific coagulation factors to activate clotting
cascade and promote formation of fibrin clots. Can also
activate fibrinolytic system, resulting in defibrination and
reduced ability to form protective clots
Factor II Factor IIa
3
Direct fibrinolytics
Split fibrinogen, often abnormally, resulting in poor clot
Fibrinogen Fibrin
formation and a bleeding tendency
4
Other haemostasis system toxins
Target various parts of haemostasis, either as activators
(e.g. plasminogen activators), or as inhibitors of coagulation
(e.g. serpin inactivators, platelet aggregation inhibitors)
Fig. 11.1 Sites of action of venoms on the haemostasis system. Copyright © Julian White
11.4 Selected important venomous animals in Asia
Scientic name
South Asia
Bungarus spp. (E) Kraits Flaccid paralysis
1
Common name Clinical effects Antivenom/antidote/treatment
2 3
, myolysis4, hyponatraemia
5
Indian PV or specic
Naja spp. (E) Cobras Flaccid paralysis3, local necrosis/blistering, shock Indian PV or specic
Ophiophagus hannah (E) King cobra Flaccid paralysis
Echis spp. (Vv) Saw-scaled vipers Procoagulant coagulopathy, local necrosis/
3
, local necrosis, shock Indian PV or specic
Indian PV or specic
blistering, renal failure
Daboia russelii (Vv) Russell’s viper Procoagulant coagulopathy, local necrosis/
blistering, myolysis, renal failure, shock, accid
2
paralysis
Indian PV or specic
Hypnale spp. (Vc) Hump-nosed vipers Procoagulant coagulopathy, shock, renal failure No available AV; Indian PV unlikely to be effective
Trimeresurus
6
spp. (Vc) Green pit vipers Procoagulant coagulopathy, local necrosis, shock Indian PV unlikely to be effective; consider specic
AV from Thailand
Hottentotta spp. (Sc) Indian scorpions Neuroexcitation, cardiotoxicity Indian specic AV
Prazosin
East Asia
Bungarus spp. (E) Kraits Flaccid paralysis
2 3
Specic AV from country
Naja spp. (E) Cobras (some spitters) Flaccid paralysis3, local necrosis/blistering, shock Specic AV from country
Ophiophagus hannah (E) King cobra Flaccid paralysis3, local necrosis, shock King cobra AV
Calloselasma rhodostoma (Vc) Malayan pit viper Procoagulant coagulopathy, local necrosis/
Specic AV from country
blistering, renal failure, shock
Daboia siamensis (Vv) Russell’s viper Procoagulant coagulopathy, local necrosis/
Specic AV from country
blistering, renal failure, capillary leak syndrome,
shock, anterior pituitary haemorrhage and failure
Gloydius spp. (Vc) Mamushis, pit vipers Procoagulant coagulopathy, local necrosis/
blistering, shock, renal failure, accid paralysis
Trimeresurus
6
spp. (Vc) Green pit vipers, habus Procoagulant coagulopathy, local necrosis/
Specic AV from country
2
Specic AV from country
blistering, shock
Hydrophis schistosus + other
species
1
Family names: C = ‘Colubridae’ (mostly ‘non-venomous’; family subject to major taxonomic revisions); E = Elapidae (all venomous); Sc = Scorpionoidea; Vc = Viperidae Crotalinae (New World and
Asian vipers); Vv = Viperidae viperinae (Old World vipers).
candidus6Genus is subject to major taxonomic change (split into at least eight genera).
(AV = antivenom; PV = polyvalent)
More information is available from the World Health Organization, Regional Ofce for South-East Asia and from toxinology.com. See ‘Further Information’.
Copyright © Julian White
Sea snakes (all species
globally)
2
Pre-synaptic.
Flaccid paralysis and/or myolysis Seqirus sea snake AV
3
Post-synaptic.
4
Only reported so far for B. candidus, B. niger and B. caeruleus
5
Only reported so far for B. multicinctus and B.
Gene ra l app ro ach t o the enve no med p atien t 245
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11.5 Selected important venomous animals in the Americas and Australia
Scientic name
North America
Crotalus spp. (Vc) Rattlesnakes Procoagulant coagulopathy, local necrosis/blistering
1
Common name Clinical effects Antivenom/antidote/treatment
CroFab (Fab’) AV or Anavip (F(ab’)
(accid paralysis2 rare), shock
Sistrurus spp. (Vc) Massasaugas Procoagulant coagulopathy, local necrosis/blistering, shock CroFab (Fab’) AV or Anavip (F(ab’)
Agkistrodon spp. (Vc) Copperheads and moccasins Procoagulant coagulopathy, local necrosis/blistering, shock CroFab (Fab’) AV or Anavip (F(ab’)
Micrurus spp. (E) Coral snakes Flaccid paralysis
3
Bioclon Coralmyn AV
Latrodectus mactans Widow spider Neuroexcitation MSD Widow spider AV
Centruroides sculpturatus Arizona bark scorpion Neuroexcitation Bioclon Anascorp AV
Central and South America
Crotalus spp. (Vc) Rattlesnakes Flaccid paralysis
2
, myolysis, procoagulant coagulopathy,
Specic AV from country
shock, renal failure
Bothrops spp. (Vc) Lancehead vipers Procoagulant coagulopathy, local necrosis/blistering,
Specic AV from country
shock, renal failure
Bothriechis spp. (Vc) Eyelash pit vipers Shock, pain and swelling Specic AV from country
Lachesis spp. (Vc) Bushmasters Procoagulant coagulopathy, shock, renal failure, local
Specic AV from country
necrosis/blistering
Micrurus spp. (E) Coral snakes Flaccid paralysis
2 3
, myolysis, renal failure Specic AV from country
Tityus serrulatus Brazilian scorpion Neuroexcitation, shock Instituto Butantan scorpion AV
Loxosceles spp. Recluse spiders Local necrosis Instituto Butantan spider AV
Phoneutria nigriventer Banana spider Neuroexcitation, shock Instituto Butantan spider AV
Potamotrygon, Dasyatis spp. Freshwater stingrays Necrosis of bite area, shock, severe pain and oedema No available AV; good wound care
Australia
Pseudonaja spp. (E) Brown snakes Procoagulant coagulopathy, renal failure, accid
paralysis
2
(rare)
Notechis spp. (E) Tiger snakes Procoagulant coagulopathy, myolysis, accid paralysis
Seqirus brown snake AV or PVAV
2 3
,
Seqirus tiger snake AV or PVAV
renal failure
Oxyuranus spp. (E) Taipans Procoagulant coagulopathy, accid paralysis
2 3
, myolysis,
Seqirus taipan or PVAV
renal failure
Acanthophis spp. (E) Death adders Flaccid paralysis
3
Seqirus death adder or PVAV
Pseudechis spp. Black and mulga snakes Anticoagulant coagulopathy, myolysis, renal failure Seqirus black snake AV or PVAV
Hydrophis schistosus +
other species
Sea snakes (all species
globally)
Flaccid paralysis and/or myolysis Seqirus sea snake AV
Atrax, Hadronyche spp. Funnel web spiders Neuroexcitation, shock Seqirus funnel web spider AV
Latrodectus hasseltii Red back spider Neuroexcitation, pain and sweating Seqirus red back spider AV
Chironex eckeri Box jellysh Neuroexcitation, cardiotoxicity, local necrosis Seqirus box jellysh AV
Synanceia spp. Stonesh Severe local pain Seqirus stonesh AV
1
For family name, see Box 11.4
(AV = antivenom; MSD = Merck, Sharpe & Dohme; PV = polyvalent)
Copyright © Julian White
2
Pre-synaptic.
3
Post-synaptic.
) AV
2
) AV
2
) AV
2
11
support provided, if required. For some animals, notably snakes in certain regions, the use of a local pressure pad bandage over the bite site
(Myanmar) or a pressure immobilisation bandage (Australia, New Guinea)
is recommended.
Ineffective or dangerous rst aid, such as suction devices, ‘cut and
suck’, local chemicals, snake stones (stones of some sort placed over
the snakebite), electric shock devices and tourniquets, should not be
used. Tourniquets, in particular, have the potential to cause catastrophic
ischaemic distal limb injuries in snakebite when applied too narrowly or
too tightly, or left on too long. Caution is required when removing tourniquets or other constricting rst aid, as there may be a sudden rush of
venom into the circulation causing rapid effects and cardiorespiratory
collapse.
Transporting patients
Where possible, transport should be brought to the patient. It is vital to
obtain medical assessment and intervention at the earliest opportunity, so
any delay in transporting the patient to a medical facility should be avoided.
Severely envenomed patients may develop life-threatening problems during transport, such as shock or respiratory failure, so ideally the transport
method should allow for management of these problems en route.
In resource-poor environments, simple solutions for rapid transport have
been successfully employed, such as motorbikes or similar with the patient
supported between the driver in front and another person behind the
patient. However, this method cannot cope with a patient developing airway
compromise or respiratory failure, such as from developing neurotoxicity.
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