GENERAL ASPECTS OF POISONING

Key points
Principles of assessment
and diagnosis of the A careful history and examination are essential in the risk
C

assessment of patients presenting with acute poisoning

poisoned patient C Online information on toxic effects of most common poisons is

freely available in the UK on TOXBASE (www.toxbase.org)
Ruben Thanacoody
C Poisoning must be considered as a potential cause of an
Abstract altered level of consciousness
Assessment of the patient with acute poisoning includes history-
taking, assessment of airway, breathing, circulation and conscious- C Recognition of toxidromes can assist with diagnosis and
ness level, physical examination to elicit relevant clinical signs and management
appropriate investigations. Diagnosis is usually based on history,
recognition of toxidromes (when present) and results of investigations.
Keywords Diagnosis; examination; history; toxicological analysis;
children can suffer severe toxicity from ingestion of even one or
toxidrome
two adult doses of a toxic drug, such as digoxin or a tricyclic
antidepressant.
Over 75% of adults presenting with overdose to hospital are
conscious on arrival and a quick history at triage establishes the
diagnosis. Patients presenting with deliberate self-harm can be
Introduction
emotionally and psychiatrically distressed and require sympa-
Acute poisoning is a common medical emergency, accounting for thetic assessment. To determine the risk of toxicity and likely
>100,000 presentations to emergency departments in the UK clinical course, it is important to establish the identity and
alone. Careful clinical assessment and diagnosis are essential to amount of the substance, the route of exposure (ingestion, in-
guide prompt management and improve the prognosis of jection, inhalation, dermal) the time of exposure and any clinical
poisoned patients. Clinical data can be difficult to collect, for features experienced to determine the risk of toxicity and likely
example where the patient is unconscious or a toddler. clinical course. However, the identity and amount taken is not
In most cases, the substance patients have been exposed to always accurate as patients often impulsively ingest what is
can be identified from the history. Assessment of the likely available to them and estimate the amount as ‘mouthfuls’ or
toxicity of that substance can then generally be predicted from ‘handfuls’, although they may be prompted to recall the number
the: of strips or packets of drugs ingested.
dose In patients who present with an altered level of conscious-
route of exposure ness, poisoning must always be considered as a potential cause.
substance’s physicochemical properties In unconscious patients, a history from relatives, friends or
substance’s pharmacological and/or toxicological actions paramedics can help. Circumstantial evidence such as empty
time since exposure. drug containers, tablets or capsules or presence of a ‘suicide
In most countries, information about likely toxicity can be note’ are reliable indicators of self-poisoning.
obtained from telephone-based poisons information services. In
the UK, healthcare professionals also have access to TOXBASE Examination
(www.toxbase.org), a web-based poisons database that provides
information about toxicity and management for >15,000 General observation can reveal useful information; for example,
products. the presence of track marks may reveal intravenous drug misuse,
and alcohol and solvents on the breath and stigmata of liver
History disease can suggest alcohol dependence. Presence of atypical
bruising or fractures may raise safeguarding concerns about
Children commonly present after accidental ingestion of products
possible domestic violence.
found in the environment and witness accounts may best identify
Physical signs are particularly helpful in unconscious patients.
the product, amount and route of exposure. Many household and
Head injury should be excluded as a contributing factor in
garden substances ingested accidentally by children are of low
comatose patients. Skin blisters also known as coma blisters can
toxicity and do not necessitate hospital admission. However,
be found in patients who have been unconscious, but they have
no relationship with specific poisons.
Neurological signs may provide important clues to the type of
Ruben Thanacoody MD FRCP FRCP(Edin) is a Consultant Physician poison involved:
and Clinical Toxicologist at Newcastle upon Tyne Hospitals NHS
Trust, Honorary Senior Clinical Lecturer at Newcastle University, Pupil size and reaction
and Director of the National Poisons Information Service (Newcastle
Widely dilated pupils (mydriasis) that react poorly to light may
Unit), UK. Competing interests: none declared.
be seen after poisoning with agents with anticholinergic activity

MEDICINE xxx:xxx 1 2019 Published by Elsevier Ltd.

Please cite this article as: Thanacoody R, Principles of assessment and diagnosis of the poisoned patient, Medicine, https://doi.org/10.1016/
j.mpmed.2019.12.002
(e.g tricyclic antidepressants) or sympathomimetic activity (e.g
Commonly recognized clusters of symptoms and signs in
amphetamines, ecstasy).
acutely poisoned patients
Pinpoint pupils (miosis) occur after exposure to opioids or
agents with cholinergic activity (e.g organophosphorus and Toxidrome Clinical features Likely poison
carbamate pesticides, nerve agents). Unequal pupils and poor
Anticholinergic Agitation/delirium, Tricyclic
reactivity to light are common in poisoning but are of little
mydriasis, dry skin, antidepressants,
diagnostic value.
ileus, urinary retention, antihistamines, Datura
Eye movements
tachycardia species
Strabismus, internuclear ophthalmoplegia, dysconjugate roving
Cholinergic Miosis, hypersalivation, Organophosphorus and
eye movements and total external ophthalmoplegia may be seen
lacrimation, carbamate insecticides,
in poisoning with tricyclic antidepressants, barbiturates, pheno-
bronchorrhoea, nerve agents
thiazines and anticonvulsants such as phenytoin and
diarrhoea, urination,
carbamazepine.
fasciculations and
Dysconjugate eye movements may only become apparent
when muscle weakness
performing brainstem testing in comatose patients using caloric Opioid Coma, miosis, reduced Opioid drugs, e.g
stimuli. The normal response to instillation of ice-cold water respiratory rate morphine and heroin
in one ear is deviation of both eyes to the irrigated side. Failure of Sedative- Coma, hypotonia, Barbiturates,
one eye to deviate suggests an internuclear ophthalmoplegia. hypnotic hyporeflexia, benzodiazepines,
Loss of oculocephalic and oculo-vestibular reflexes can occur hypotension ethanol, zopiclone
in comatose patients poisoned with tricyclic antidepressants and Serotonin Agitation, confusion, Serotoninergic drugs,
anticonvulsants, and should not be regarded as a sign of brain- myoclonus, e.g citalopram, tramadol
stem death. hyperreflexia, sweating, and ecstasy
tremor, diarrhoea,
Visual acuity and visual fields incoordination/ataxia,
Blurring, loss of vision and tunnel vision (from loss of peripheral fever
vision) can occur with methanol and quinine poisoning. Sympathomimetic Agitation, convulsions, Amphetamines, cocaine,
mydriasis, sweating, theophylline, caffeine
Abnormal movements tremor, tachycardia
Acute dystonic movements (torticollis, orolingual dyskinesia,
oculogyric crisis) can occur after exposure to antidopaminergic Table 1
drugs such as metoclopramide and antipsychotic drugs. Chor-
can develop. Laboratory abnormalities can include metabolic
eoathetosis is a rare feature of organophosphorus pesticide
acidosis, elevated serum creatine kinase and transaminases,
poisoning. 1
Hypertonia, hyperreflexia and extensor plantar responses can and renal impairment.
occur in tricyclic antidepressant poisoning. Decerebrate and Several diagnostic criteria have been developed to aid diag-
decorticate posturing can occur in comatose poisoned patients nosis of this protean symptom complex. Sternbach’s classifica-
but does not indicate irreversible brain injury. tion was described in psychiatric patients given therapeutic doses
of a serotonergic agent; it consists of at least three of mental
Toxidromes status changes (confusion/hypomania), agitation, myoclonus,
hyperreflexia, sweating, tremor, diarrhoea, incoordination/
A single physical sign is rarely diagnostic in acute poisoning. A ataxia and fever.
cluster of physical signs, also known as toxidrome, can point to a 2
Hunter’s classification was derived in patients with overdose
specific or class of poison (Table 1). of serotonergic agents and consists of any of:
Serotonin syndrome is a potentially life-threatening spontaneous clonus
reaction
inducible or ocular clonus and agitation or diaphoresis
resulting from drugs acting on central and peripheral serotonergic
tremor and hyperreflexia
receptors. It classically consists of a triad of features e alteration
hypertonia and hyperpyrexia (temperature exceeding
of mental status, neuromuscular hyperactivity and autonomic
38 C) and ocular/inducible clonus.
insta- bility e but all three are not always present. Around 40%
In routine clinical practice, clonus and hyperreflexia in pa-
of pa- tients have mental status changes ranging from agitation,
tients taking serotonergic agents should raise suspicion of sero-
confusion, delirium and hallucinations to drowsiness and
tonin syndrome.
coma. Around 50% of patients have evidence of neuromuscular
hyper- activity including profound shivering, tremor, tooth-
Investigations
grinding, myoclonus, ocular clonus, inducible or spontaneous
clonus and hyperreflexia. Autonomic instability occurs in Toxicological analysis
around 40% of in- dividuals and includes features such as When the poisonous agent is known, it may be possible to
dilated pupils, diarrhoea, profuse sweating, flushing, measure the concentration in blood or urine. The concentration
tachycardia and hypertension or hy- potension. In severe cases, is usually measured in serum or plasma except for lead,
seizures, hyperthermia, rhabdomyol- ysis, renal failure and
disseminated intravascular coagulopathy
 Common blood test abnormalities in acutely poisoned patients
Investigation Decreased Increased

Serum sodium Ecstasy Sodium salts

Serum potassium Theophylline, Digoxin, potassium salts
salbutamol
Plasma creatinine Ethylene glycol
Blood glucose Insulin, sulfonylureas,
salicylate
Serum calcium Ethylene glycol, Calcium salts
hydrogen fluoride
Serum phosphate Paracetamol
Serum alanine Paracetamol, iron,
aminotransferase hepatotoxic mushrooms
Serum creatine Amphetamines, heroin,
kinase ecstasy, citalopram,
olanzapine
Prothrombin time Anticoagulants,
paracetamol
Whole blood Nitrites
methaemoglobin
Red blood cell Organophosphorus
cholinesterase insecticides,
activity nerve agents

Table 2

carboxyhaemoglobin and methaemoglobin, which are measured Routinely available haematological and biochemical in-
in blood. Some toxicological assays may not be readily available, vestigations, including arterial blood gas analysis, can be very
especially in smaller hospitals. To guide appropriate clinical helpful in making a diagnosis and guiding management. Exam-
management after overdose, it is recommended that hospital ples of abnormalities encountered are shown in Table 2.
laboratories have the capability to measure concentration of Routine ECGs should be recorded and continuous ECG
carbamazepine, digoxin, ethylene glycol, iron, lithium, meth- monitoring should be considered in patients who have ingested
anol, methotrexate, paracetamol, phenytoin, salicylate, theoph- potentially cardiotoxic drugs. Characteristic ECG changes include
3
ylline or valproate. QRS prolongation and right axis deviation (tricyclic antidepres-
In unconscious patients or where the agent is not known, sants), bradycardia and atrioventricular block (cardiac glyco-
toxicological analysis should be used judiciously taking into ac- sides, b-adrenoceptor blockers, calcium channel blockers) and
count the clinical picture and likely exposures and whether QT prolongation (antipsychotics, citalopram).
toxicology will affect clinical management. Routine screening for Routine radiology has limited value diagnostically. It can be
toxins is labour-intensive, time-consuming and expensive. used to show whether metal objects (e.g. coins, button batteries)
Plasma paracetamol concentration should be routinely measured have been ingested. It may also identify the ingestion of some
in such cases as it is common and the timely administration of enteric-coated or sustained-release drug formulations, but ordi-
antidote is critical to prevent liver injury. Salicylate concentration nary formulations, apart from iron tablets, are seldom seen on
should not be measured routinely in the absence of symptoms plain abdominal X-ray. Ingested packets of illicit substances in
and signs suggestive of salicylate poisoning. body-packers may be discernible on plain X-ray but are more
reliably detected by computed tomography (CT) or magnetic
Non-toxicological investigations resonance imaging (MRI).
Chocolate-coloured blood is the hallmark of meth- Radiology has more use for revealing complications of
aemoglobinaemia which may be caused by recreational use poisoning, especially in the lung: acute respiratory distress
(inhalation, ingestion) of organic nitrites such as amyl or isobutyl syn- drome, aspiration pneumonia, non-cardiogenic pulmonary
nitrite, and therapeutic use of drugs such as dapsone. Chemicals oedema (salicylates), pulmonary fibrosis (paraquat) or
causing intravascular haemolysis (e.g sodium chlorate) typically bronchio- litis obliterans (nitrogen oxides). CT or MRI can also
cause pink plasma. Circulating myoglobin due to rhabdomyol- be useful in confirming the extent of corrosive damage to the
ysis can lead to brown-looking plasma and urine. Oxalate crys- oesophagus as endoscopy may not delineate the depth of injury
tals may be seen in the urine after ingestion of ethylene glycol. clearly. A
KEY REFERENCES 3 Thompson J, Watson I, Thanacoody H, et al. Guidelines for labo-
1 Boyer EW, Shannon M. Current concepts: the serotonin syndrome. ratory analyses for poisoned patients in the United Kingdom. Ann
N Engl J Med 2005; 352: 1112e20. Clin Biochem 2014; 51: 312e25.
2 Dunkley EJ, Isbister GK, Sibbritt D, et al. The Hunter serotonin
toxicity criteria: simple and accurate diagnostic decision rules for
serotonin toxicity. QJM 2003; 96: 635e42.

TEST YOURSELF
To test your knowledge based on the article you have just read, please complete the questions below. The answers can be found at the
end of the issue or online here.
Question 1 Question 2
A 30-year-old woman presented in an unconscious state. On A 28-year-old woman presented in an unconscious state after an
clinical examination, she had dilated pupils, a divergent squint, overdose of amitriptyline, codeine, lansoprazole, theophylline
dry skin, tachycardia, absent bowel sounds, hypertonia and and zopiclone.
hyperreflexia.
Toxicological analysis of which drug is most likely to help
Which type of drug action is most likely to have caused this with clinical management?
toxidrome (collection of symptoms and signs)? A. Amitriptyline
A. Anticholinergic B. Codeine
B. Cholinergic C. Lansoprazole
C. Opioid D. Theophylline
D. Serotonin E. Zopiclone
E. Sympathomimetic