Poisoning and Overdose

Poisoning and Overdose

Emergency management

Poisoning or overdose (OD) may be intentional or unintentional. It can occur via ingestion, injection, or inhalation, and rarely by transdermal or other routes. It may be obvious from the history and presentation, but a high index of suspicion may also be required.

The emergency management of poisoning involves:

  • Initial resuscitation.

  • Identification, where possible, of likely agent.

  • Specific treatments or antidotes.

  • General supportive measures.


Common poisoning agents include:

  • Pharmaceutical products including ‘over-the-counter medications’:

    • E.g. paracetamol (and paracetamol-containing products), aspirin (and other analgesics/NSAIDs), opiates/opioids, benzodiazepines and ‘Z-drugs’ (e.g. zopiclone), antidepressants (including SSRIs and tricyclics), and barbiturates

  • Recreational drugs (including alcohol, the most common drug to be co-ingested either with recreational drugs or as part of self-poisoning):

    • E.g. opiates/opioids, cocaine, amphetamines, ecstasy, gammahydroxybutyric acid (GHB), hallucinogenics (e.g. LSD), glues or volatile chemicals

  • Industrial chemicals, household chemicals, and environmental toxins including inhaled poisons (e.g. carbon monoxide and cyanide):

    • E.g. organophosphates, paraquat, methanol, ethylene glycol, household products (e.g. batteries, cleaning agents and detergents)

  • Animal, fish, and insect bites/stings.

Presentation and assessment

  • A history of attempted suicide, psychiatric illness, or substance abuse.

  • Airway or respiratory signs and symptoms:

    • Respiratory depression

    • Aspiration, pneumonitis, or bronchospasm

    • Oropharyngeal burns

  • Cardiovascular:

    • Hypotension, hypertension, cardiovascular collapse, cardiac arrest

    • ECG: tricyclics and antidepressants, amongst other drugs, cause conduction defects and arrhythmias, which may be resistant to treatment

  • Neurological:

    • Agitation, confusion, or hallucinations

    • Unexplained unconsciousness, especially if associated with compartment syndrome or prolonged contact burns

    • Convulsions

    • Profound weakness, or conversely muscle rigidity or dystonia

    • Ataxia or nystagmus

  • GI: vomiting or diarrhoea; liver failure.

  • Renal: renal failure, rhabdomyolysis.

Other features that may be associated with poisoning include:

  • Hypo- or hyperthermia.

  • Self-harm injuries.

  • Trauma, burns, drowning, and head injuries.

  • Electrolyte imbalance, especially sodium, potassium, or glucose.

  • Metabolic acidosis, especially with a raised osmolar or anion gap (see image p.205).

Individual signs and symptoms are associated with certain poisons (Tables 14.1, 14.2, 14.3, 14.4). Clusters of symptoms may occur together when poisoning with certain agents has occurred; these are commonly referred to as ‘toxidromes’ (Table 14.5).


The investigations required will be dictated by the patient’s severity of illness, and the most likely causative agent(s), but may include:

  • ABGs (hypoxia, hypercapnia, metabolic acidosis, raised anion gap).

  • FBC, coagulation studies (coagulation may be deranged).

  • Blood methaemaglobin concentration (see image p.453).

  • RBC cholinesterase activity (in organophosphate poisoning).

  • Serum calcium (in ethylene glycol poisoning) and phosphate.

  • Serum CK (raised in rhabdomyolysis).

  • Serum glucose.

  • Blood alcohol levels (or expired air levels if possible).

  • Paracetamol and salicylate levels (important to check timings).

  • Specific drug serum levels may be indicated for other substances (e.g. ethylene glycol, digoxin, valproic acid, phenytoin, theophylline, iron, lithium, carbamazepine).

  • Carboxyhaemoglobin (by co-oximetry).

  • Urine for myoglobin.

  • Consider taking blood, urine, and gastric aspirate samples for toxicology, or for storage in case later analysis is required.

  • 12-lead ECG (may show ischaemia, evidence of hyperkalaemia or QT prolongation).

  • CXR (if aspiration suspected or prior to hyperbaric oxygen therapy).

  • AXR may be useful if ingestion of radiopaque substances is suspected (chloral hydrate, heavy metals, iron, enteric coated or sustained release preparations, ‘body packing’).

  • Consider head CT or LP to exclude other causes of unconsciousness.

Differential diagnoses

  • Conditions causing altered consciousness, altered behaviour, or respiratory depression (e.g. head injuries, meningitis/encephalitis, hypoglycaemia and post-ictal state).

  • Conditions causing cardiovascular collapse (e.g. anaphylaxis).

  • Conditions causing muscle weakness (e.g. Guillain-Barré and botulism)

  • Conditions causing non-specific symptoms such as vomiting or hypothermia (e.g. infections/sepsis, neurological injury/SAH).

Table 14.1 Cardiorespiratory changes and associated poisons

Signs and symptoms

Potential poisons

Respiratory depression; hypoventilation

Alcohols, barbiturates, benzodiazepines, botulinum toxin, neuromuscular blocking agents, opioids, sedatives, strychnine, tranquillizers, tricyclic antidepressants


Ethylene glycol, isoniazid, methanol, pentachlorophenol, salicylates

Pulmonary oedema

Cocaine, chlorophenoxy herbicides, ethylene glycol, hydrocarbons, irritant gases, organic solvents, opioids, paraquat, phosgene, salicylates




β-blockers, calcium-channel antagonists, carbamates, cholinergics, clonidine, digoxin, lithium, metoclopramide, opioids, organophosphates, phenylpropanolamine, physostigmine, propoxyphene, quinidine


Amphetamines, anticholinergics, antihistamines, caffeine, carbon monoxide, cocaine, cyanide, hydralazine, hydrogen sulphide, phencyclidine, phenothiazines, sympathomimetics, theophylline, thyroxine, tricyclic antidepressants


β-blockers, chloroquine, cyanide, digoxin, phenothiazines, quinidine, theophylline, tricyclic antidepressants


β-blockers, calcium channel antagonists, ethanol, opioids, sedatives, tranquillizers


Anticholinergics, sympathomimetics

Table 14.2 Temperature, skin, and oral changes

Signs and symptoms

Potential poisons


Anticholinergics, amphetamines, antihistamines, cocaine, dinitrophenols, hydroxybenzonitriles, LSD, MAOIs, phencyclidine, phenothiazines, pentochlorophenols, procainamide, quinidine, salicylates, tricyclic antidepressants


Barbiturates, carbon monoxide, colchicine, ethanol, lithium, opioids, phenothiazines, sedatives, tricyclic antidepressants

Excess salivation

Cholinesterase inhibitors, strychnine

Dry mouth

Anticholinergics, opioids, tricyclic antidepressants, phenothiazines


Cholinergics, hypoglycaemics, sympathomimetics

Dry skin


Hair loss



Bromide, organochlorine

Table 14.3 Neurological and eye changes

Signs and symptoms

Potential poisons

Coma, ↓consciousness

Alcohols, benzodiazepines, barbiturates, bethanechol, carbamates, clonidine, GHB, hypoglycaemic agents, lithium, nicotine, opioids, organophosphates, physostigmine, pilocarpine, salicylates, tranquillizers tricyclic antidepressants


Amphetamines, anticholinergics, antihistamines, antipsychotics, caffeine, camphor, carbamates, carbon monoxide, chlorinated hydrocarbons, cocaine, ethylene glycol, isoniazid, lead, lidocaine, lindane, lithium, methanol, nicotine, organophosphates, orphenadrine, phencyclidine, propranolol, salicylates, strychnine, theophylline, tricyclic antidepressants




Antihistamines, bromides, barbiturates, carbamazepine, carbon monoxide, diphenylhydantoin, ethanol, phenytoin, piperazine, sedatives, thallium


Barbiturates, carbamates, cholinergics, clonidine, ethanol, isopropyl alcohol, organophosphates, opioids, phencyclidine, phenothiazines, physostigmine, pilocarpine


Amphetamines, anticholinergics, antihistamines, cocaine, dopamine, glutethimide, LSD, MAOIs, phencyclidine, tricyclic antidepressants


Quinine, methanol

Table 14.4 Gastrointestinal and renal changes

Signs and symptoms

Potential poisons


Aspirin, iron, fluoride, theophylline

GI bleed

Anticoagulants, corrosive compounds, NSAIDs, salicylates

Liver failure

Carbon tetrachloride, paracetamol


Arsenic, cholinesterase inhibitors


Lead, opioids, thallium

Urinary retention

Atropine, opioids, tricyclic antidepressants


Carbamates, organophosphates

Crystals in urine

Ethylene glycol, primidone

Renal failure

Amanita toxin, aminoglycosides, cadmium, carbon tetrachloride, ethylene glycol, oxalates, paracetamol, polymyxin, mercury, methanol.

Table 14.5 Toxidromes and combinations of symptoms and the likely associated poisons


Constellation of signs and symptoms

Possible toxins

Anticholinergic activity

Agitation, delirium, diminished consciousness, mydriasis hyperthermia, dry skin and mucosal membranes, flushing, tachycardia, bowel stasis, urinary retention

Anticholinergic alkaloids (e.g. in plants such as belladonna), antihistamines, antiparkinsonian drugs, atropine, baclofen, cyclopentolate, phenothiazines, propantheline, scopolamine, tricyclic antidepressants

Cholinergic activity (muscarinic and/or nicotinic effects)

Miosis or mydriasis, blurred vision, sweating, excess salivation, lacrimation or bronchial secretions, wheezing or dyspnoea, tachycardia or bradycardia, hypertension, vomiting and diarrhoea, abdominal cramps, urinary and faecal incontinence, muscle weakness, fasciculations, paralysis

Acetylcholinesterase inhibitors: carbamates, neostigmine, organophosphates (pesticides or agents such as sarin), physostigmine, pyridostigmine

Acetylcholine agonists: carbachol, choline, metacholine, pilocarpine

Sympathetic hyperactivity α and β-adrenergic activity

Agitation, mydriasis, sweating, flushing, pyrexia, tachycardia, hypertension

Amphetamines, cocaine, ecstasy, ephedrine, PCP, phencyclidine, pseudoephedrine

If predominantly β-adrenergic

Tremor, tachycardia, hypotension

Caffeine, salbutamol, terbutaline, theophylline

If predominantly α-adrenergic

Bradycardia, hypertension

Phenylephrine, phenylpropanolamine


Cog-wheel rigidity, tremor, trismus, hyper-reflexia, dyskinesia, dystonia, posturing, opisthotonos, choreoathetosis

Haloperidol, olanzapine, phenothiazines, risperidone


Agitation, psychosis, hallucinations, mydriasis, hyperthermia

Amphetamines, cannabinoids, cocaine, LSD


Decreased consciousness, miosis, bradypnoea, bradycardia, hypotension, hypothermia, bowel stasis

Clonidine, dextromethorphan, opiates, pentazocine, propoxyphene


Confusion, slurred speech, ↓consciousness, normal or reduced respiratory rate, normotension, normocardia

Anticonvulsants, antipsychotics, barbiturates, benzodiazepines, ethanol, GHB, meprobamate

Volatile inhalation

Euphoria, confusion, slurred speech, headache, restlessness, ataxia, seizures, respiratory depression, arrhythmias

Acetone, chlorinated hydrocarbons, fluorocarbons, hydrocarbons (petrol, butane, propane), nitrites (isobutyl, amyl, butyl), toluene


Agitation, confusion, mydriasis, flushing, sweating, tremor, hyperreflexia, clonus, myoclonus, trismus, hyperthermia, tachypnoea, tachycardia, hypertension

Amphetamine, ecstasy, MAOIs, serotonin re-uptake inhibitors

Chemical pneumonitis

Cough, dyspnoea, wheeze, respiratory distress, cyanosis, fever Can occur without aspiration or loss of consciousness

Essential oils, petroleum distillates, turpentine, white spirit


Headache, diminished consciousness, dyspnoea, tachypnoea, severe hypoxia, tachycardia, chocolate coloured blood

Alanine dyes, benzocaine, chlorates, chloroquine, dapsone, nitrates and nitrites, nitrobenzene, nitrophenol, phenacetin, phenazopyridine, primaquine, sodium nitroprusside

Further management

Specific information on how to manage poisonings can be obtained from databases (e.g. Toxbase). Complex cases can be discussed with staff from a specialist poisons unit.


  • Look for and treat causes of agitation, e.g. hypoxia or full bladder.

  • Sedation may be required in profoundly agitated patients, but may provoke a drop in consciousness requiring endotracheal intubation; sedation may also worsen any hypotension.

  • Antipsychotics are sometimes used to treat agitation, but may lower the seizure threshold.


  • If opioids or benzodiazepines are suspected of contributing to ↓level of consciousness naloxone (0.6-1.2 mg IV) or flumazenil (0.5 mg IV) may be administered as a diagnostic challenge:

    • Flumazenil may lower the seizure threshold, and can provoke arrhythmias (avoid in suspected tricyclic overdose)


  • Hypothermia is common following prolonged unconsciousness; or it can occur as a result of certain drugs (classically barbiturates).

  • Hypothermia may be profound and require rewarming (image p.250); there may be an associated bradycardia (image p.132).


  • Hyperthermia is associated with stimulants, neuroleptic and antimuscarinic drugs; cooling and specific antihyperthermic therapy may be required (image p.248).


  • Catheterization and urine output measurements may be required.

  • Regular blood sugar measurements may be required in order to monitor/treat any hypoglycaemia.

  • Invasive monitoring and continuous ECG monitoring are required for many poisonings and overdoses.

Active removal of drugs and poisons

  • Haemodialysis or haemoperfusion may be useful in the removal of certain toxins (see image p.457).

  • Urinary alkalinization (often known as forced alkaline diuresis) using sodium bicarbonate can be used to encourage the renal excretion of specific acidic drugs (moderately severe aspirin/salicylate overdoses not requiring haemodialysis; 2,4-dichlorophenoxyacetic acid and chlorphenoxy herbicides; mecoprop):

    • Different regimens exist for achieving urinary alkalinization, an example is the infusion of 1000 ml 1.4% sodium bicarbonate in
      water solution over 2.5 hours; urine should be tested to ensure a pH of 7.8-8.5

    • Urinary alkalinization may also be of benefit in methotrexate, fluoride, or diflunisal poisoning, although the evidence for this is not clear

    • It is not recommended for phenobarbital (multiple-dose activated charcoal is superior), or chlorpropamide (supportive care with glucose infusion mostly adequate)

    • It is associated with hypokalaemia and alkalotic tetany (electrolytes should be monitored and replaced)

    • It is relatively contraindicated in patients with incipient renal failure or significant pre-existing heart disease

  • Urinary acidification has previously been considered for drugs such as amphetamines, quinine, and phencyclidine, but is generally not recommended because of associated complications.

  • Whole bowel irrigation using balanced polyethylene glycol electrolyte solution (1500-2000 ml/hour NG) to promote bowel transit and liquefy stool has only limited evidence of effectiveness, but has been used in the following circumstances:

    • For sustained release drug preparations, and drugs not absorbed by charcoal (e.g. iron and lithium)

    • For ‘body-packers’ (drug couriers who have ingested packages/condoms filled with drugs)

    • Contraindications include: unprotected airway; bowel perforation, obstruction, or haemorrhage; haemodynamic instability

Table 14.6 Specific antidotes and treatments

Drug or chemical








Calcium channel antagonists1

Calcium chloride/gluconate


Sodium-nitrate with sodium-thiosulphate

Dicobalt edetate



Fab fragments

Ethylene glycol/methanol

Ethanol or fomepizole

Heavy metal poisoning

Sodium calcium edetate





Glucose, glucagon






Methylene blue



Organophosphates/nerve agents

Atropine or pralidoxime


Acetylcysteine or methionine



Snake bites

Antivenom (antivenin/antivenene)


Prothrombin complex

Vitamin K

1 β-blocker and calcium channel antagonist toxicity have also been successfully treated with high-dose insulin therapy. This therapy should only be used where there is an established protocol for its use.

NB Local anaesthetic agent toxicity has been successfully treated with IV lipid therapy (see image p.493). This treatment is also being investigated for use with for other lipid-soluble drugs.

Pitfalls/difficult situations

  • If a deliberate release of toxic agents, or a mass poisoning event, is suspected follow the guidelines on image p.496.

  • Accidental or deliberate self-poisoning is commonly associated with other injuries, including trauma.

  • The use of multiple agents is common in self-poisoning, and signs and symptoms are often a mixture of those caused by various drugs.

  • The combination of stimulant and sedatives (particularly GHB) taken together can result in profound fluctuations in consciousness.

  • Where there is any doubt as to the aetiology of ↓consciousness or seizures a CT scan is indicated:

    • Alcohol is associated with head trauma and intracranial bleeding

  • Paracetamol and salicylate are extremely common ingredients in overdose ‘cocktails’, check plasma levels for these agents in cases of self-poisoning, even if there is no evidence of ingestion.

  • Prior to blood levels being available, or where no blood tests exist, treatment can be based upon the calculated maximum dose (e.g. if all the available pill bottles were full at the time of ingestion).

  • Blood levels of toxins taken soon after ingestion may be falsely low.

  • Identification of tablets, plants, or snakes brought in to hospital is often wrong, expert advice may be required either via direct contact or via programs such as TICTAC.

  • Activated charcoal may sometimes be of use in cases where ingestion took place >1 hour prior to admission, or where the timing of ingestion is unknown; where there is doubt discuss the case with a poisons expert.

  • ‘Body-packers’ (drug couriers who have ingested packages filled with drugs), require a surgical referral, treatment will depend upon the risks posed by the drug(s) involved and their position within the GI tract.

  • Self-poisoning requires appropriate evaluation of any future suicide risk; ideally this should be arranged prior to ICU discharge.

Legal pitfalls

  • Deaths from poisoning should be reported to the coroner.

  • Most patients will cooperate with treatment though some, particularly those who have attempted suicide, may refuse it:

    • Patients who are mentally competent have the right to refuse any, and all, treatment, even if they risk death in doing so

    • Mental competency requires the ability to understand, retain, believe and evaluate information

  • Life-saving treatments may be administered to patients against their will only if they are not mentally competent and have no legally binding advance directive.

  • When in doubt ask for senior advice or psychiatric advice early.

  • Carefully document any refusal of treatment, or any treatment against a patient’s wishes.

1The elimination of many more drugs can be enhanced by extracorporeal techniques, but in many cases the clinical benefit is unknown, or there are more effective treatments (e.g. digoxin and fab fragments)

2CVVH is unlikely to be of benefit.

3Haemodialysis can also be used but is considered to be less effective.

Further reading

Brooks DE, et al. Toxicology in the ICU. Part 2: Specific toxins. Chest 2011; 140(4): 1072-85.

Joint Formulary Committee. Emergency treatment of poisoning In British national formulary. London: BMJ Group and Pharmaceutical Press, latest edn September 2012.

Position paper on urine alkalinization. Clin Toxicol 2004; 42(1): 1-26.

Position paper: gastric lavage. Clin Toxicol 2004; 42(7): 933-43.

Position paper: whole bowel irrigation. Clin Toxicol 2004; 42(6): 843-54.

Position paper: single-dose activated charcoal. Clinical Toxicol 2005; 43: 61-87.

Position statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning. Clin Toxicol 1999; 37(6): 731-51.

Mental Capacity Act 2005. London: HMSO, 2005.

Levine M, et al. Toxicology in the ICU. Part 1: general overview and approach to treatment. Chest 2011; 140(3): 795-80.

Levine M, et al. Toxicology in the ICU. Part 3: natural toxins. Chest 2011; 140(5): 1357-70.

TICTAC tablet identification system: image <http://tictac.vhn.net/home/>.

TOXBASE—web-based database of the National Poisons Information Service available to registered users (i.e. A&E departments): image <http://www.spib.axl.co.uk/>.


! Paracetamol poisoning

Paracetamol (acetaminophen) is a common hepatotoxic agent in deliberate overdose. It is found in many over-the-counter medications.


  • Paracetamol poisoning occurs when healthy individuals take moderate to large overdoses (10 g/20 tablets or 150 mg/kg within 24 hours).

  • Certain patients have depleted stores of glutathione and are susceptible to hepatotoxicity at much lower doses, including:

    • Malnourished: anorexia, alcoholism, HIV

    • Taking enzyme inducing drugs: carbamazepine, phenobarbital, phenytoin, primidone, rifampicin, St John’s wort

  • In rare cases in high-risk individuals, poisoning may occur at normal doses administered over a prolonged time.

Presentation and assessment

  • Initial presentation is mostly asymptomatic unless other agents are also involved, although nausea and vomiting may occur.

  • In exceptionally high overdoses (>5000 µmol/L or 800 mg/L) acute deterioration in GCS may occur accompanied by lactic acidosis.

  • Delayed presentation (12 hours-4 days) can be accompanied by RUQ pain with liver and/or renal failure.

  • Liver damage is maximal at 4 days after the overdose, and may result in encephalopathy, cerebral oedema, haemorrhage, and hypoglycaemia.


(See also image p.449.)

  • ABGs, if compromised (acidaemia).

  • FBC and coagulation studies (deranged INR).

  • U&Es, LFTs (raised transaminases).

  • Serum glucose (hypoglycaemia may occur).

  • Serum paracetamol levels (at 4 hours post ingestion if possible).

Fig. 14.1 Paracetamol poisoning nomogram. Patients whose plasma-paracetamol concentrations are above the normal treatment line should be treated with acetylcysteine by IV infusion (or, if acetylcysteine cannot be used, with methionine by mouth, provided the overdose has been taken within 10-12 hours and the patient is not vomiting).

Patients at high-risk of liver damage, and who should be treated if their plasma concentration is above the high-risk treatment line, include:

  • Those taking liver-enzyme-inducing drugs (e.g. carbamazepine, phenobarbital, phenytoin, primidone, rifampicin, efavirenz, nevirapine, alcohol, St John’s wort).

  • Those who are malnourished (e.g. anorexia or bulimia, cystic fibrosis, hepatitis C, in alcoholism, or those who are HIV positive); or who have not eaten for a few days.

The prognostic accuracy after 15 hours is uncertain but a plasmaparacetamol concentration above the relevant treatment line should be regarded as carrying a serious risk of liver damage. Graph reproduced with permission from Professor PA Routledge, All Wales Therapeutics and Toxicology Centre, Cardiff and Vale University Health Board. Text adapted from the British National Formulary.

Further management

(See also image p.456.)

  • Monitor for hepatotoxicity using serial PT/INR and bilirubin measurements; LFT changes often occur late; renal failure may also occur.

  • Discuss impending hepatic failure with a specialist liver centre: INR >3, oliguria, raised creatinine, hypoglycaemia, acidosis and encephalopathy.

Pitfalls/difficult situations

  • Medications may contain co-drugs needing treatment, in particular co-proxamol (available but no longer licensed).

Aspirin/salicylate and NSAID poisoning

Most NSAIDs are benign in overdose, but salicylate overdoses can produce life-threatening, difficult-to-manage, complex clinical pictures.


NSAIDs are available as prescription and over-the-counter medicines and are commonly involved in multiple-drug overdoses. Salicylates overdoses have become less common than other NSAIDs but are far more toxic Salicylate (mild to moderate toxicity 150-200 mg/kg) is found in:

  • Aspirin ingestion.

  • Salicylic acid ingestion.

  • Oil of wintergreen.

Jun 13, 2016 | Posted by in CRITICAL CARE | Comments Off on Poisoning and Overdose

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