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Heather Baid

, Fiona Creed

, and Jessica Hargreaves

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date: 05 May 2021

Assessment of poisoning

Poisoning caused by a harmful substance can be acute or chronic, and may be intentional or accidental. It can result from:

  • ingestion

  • injection

  • inhalation

  • exposure of body surfaces (skin, eyes, mucous membranes)

  • venomous stings or bites.

The National Poisons Information Service provides expert advice to healthcare professionals on chronic and acute poisoning:

  • TOXBASE® (Poisoning—a continually updated online database that provides guidance on individual poisons

  • a 24-hour telephone helpline to provide specific advice for healthcare professionals about complex poisoning situations.

The consequences of poisoning depend on:

  • the patient’s age, size, and general health

  • the medication(s) or other substance(s) taken

  • the route and quantity of these

  • onset or period of exposure

  • other substances taken at the same time (e.g. alcohol).

Focused health history

Subjective information about the patient’s symptoms and the known or suspected drug or substance can be obtained from:

  • evidence such as empty bottles, syringes, drugs, or suicide note

  • the patient, their relatives, ambulance personnel, friends, or GP

  • the patient’s medical history, including mental illness and previous overdose attempts

  • supervisors and co-workers from the same workplace order to ascertain the use of or exposure to any industrial chemicals or gases

Consider prescribed and illicit drugs, ‘legal highs’, complementary therapies, the use of herbs, plants, and mushrooms, and recent travel.

Focused physical assessment

Signs may be suggestive of particular substances. For example:

  • toxidromes—a collection of characteristic signs and symptoms that are elicited by a particular substance when it is taken in excess (see Poisoning p. [link])

  • breath odour:

    • cyanide—bitter almonds odour

    • phenol, salicylates, isopropyl alcohol—acetone odour

    • heavy metals, organophosphates—garlic odour

  • needle tracks or venepuncture marks from recreational drug use

  • colour of the skin and mucous membranes (jaundice, cherry red, cyanosed)

  • pupil size (e.g. opioids cause pinpoint pupils, anticholinergics cause dilated pupils)

  • presence of rashes, blisters, or other lesions.

In patients presenting with an altered conscious level, other causes of neurological dysfunction must be considered (e.g. meningoencephalitis, head injury, stroke, hypoglycaemia, hepatic encephalopathy).

Laboratory investigations

Guidance on investigations to be carried out should be obtained from the National Poisons Information Service’s TOXBASE®, and typically includes:

  • specific tests to confirm the presence of known or suspected poison(s) (e.g. in blood, urine, gastric aspirate, or vomitus)

  • blood glucose levels

  • urea, creatinine, and electrolytes

  • FBC

  • clotting screen

  • osmolality

  • LFTs

  • urinalysis

  • arterial blood gas (if carbon monoxide poisoning is suspected, use a co-oximeter to measure oxygen saturation, as it can identify the concentration of carboxyhaemoglobin)

  • 12-lead ECG

  • chest X-ray if indicated (aspiration is common, and pulmonary oedema may occur with salicylate and heroin poisoning).

Conditions that require admission to the critical care unit

  • Hypotension and hypertension.

  • Potential or actual cardiac arrhythmias and other ECG abnormalities (e.g. prolonged QT or QRS segments).

  • Heart failure.

  • Reduced conscious level (e.g. GCS score ≤ 8 or continuing to fall).

  • Repeated or prolonged seizures.

  • Need for endotracheal intubation with or without mechanical ventilation.

  • Need for specialist support (e.g. haemo(dia)filtration, haemoperfusion, temporary pacing).

  • Management of bleeding (e.g. from warfarin overdose).

Further reading

Boyle JS, Bechtel LK and Holstege CP. Management of the critically poisoned patient. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2009; 17: 29.Find this resource:

Ghannoum M and Gosselin S. Enhanced poison elimination in critical care. Advances in Chronic Kidney Disease 2013; 20: 94–101.Find this resource:

Patel SR. Toxicological emergencies in the intensive care unit: managing reversal agents and antidotes. Critical Care Nursing Quarterly 2013; 36: 335–44.Find this resource:

Pettie J and Dow M. Management of poisoning in adults. Nursing Standard 2013; 27: 43–9.Find this resource:

Management of poisoning

Initial management

  • Maintain a patent airway—if the patient is comatose, or there is no cough or gag reflex, endotracheal intubation and mechanical ventilation will be required.

  • Monitor heart rate, blood pressure, O2 saturation, and respiratory rate.

  • Give O2 therapy to maintain O2 saturations at ≥ 94%.

    • The exception to this is carbon monoxide poisoning, in which case give 100% O2 because O2 saturation monitoring is unreliable (see Poisoning p. [link]).

  • Continuous ECG monitoring and regular rechecking of 12-lead ECG.

  • Haemodynamic monitoring.

  • Establish IV access, correct hypovolaemia, and treat excessively high or low blood pressures.

  • Recognize and promptly manage seizures.

  • Monitor core temperature and treat hyper- or hypothermia.

  • Monitor blood glucose levels and treat hypo- or hyperglycaemia.

  • Monitor renal function and electrolytes and treat accordingly.

  • Perform a thorough neurological assessment and institute regular neuromonitoring with GCS scoring.

  • Monitor liver function.

  • Check the limbs, buttocks, and back for evidence of compartment syndrome, and the blood and urine for rhabdomyolysis.

  • Examine the skin for signs of injury, blisters, or venepuncture marks.

  • Regularly reassess the patient.

  • Review the TOXBASE® guidelines if the poison is known or a particular poison is suspected.

  • Educate the patient and their family as appropriate.

Minimizing further absorption of poison

Gastric lavage and emesis are rarely used, due to doubts about their efficacy and also the risk of serious complications.

Activated charcoal

  • This prevents absorption from the stomach.

  • Give 1 g/kg charcoal orally or via nasogastric tube.

  • Ideally give it as early as possible after ingestion of the substance, although it can be effective up to 24 h after ingestion.

  • It is effective for benzodiazepines, anticonvulsants, antihistamines, phenothiazines, tricyclics, and theophylline, but not for heavy metals (e.g. iron).

  • The airway must be protected, as there is a risk of aspiration.

  • Do not give charcoal to patients with an ileus.

Whole bowel irrigation

  • A solution of polyethylene glycol is given orally or via nasogastric tube at a rate of 2 L/h until the rectal effluent runs clear.

  • This procedure is used for substances such as enteric-coated preparations, those for which activated charcoal is ineffective, and for intact elimination of packets of cocaine or heroin.

  • Do not use in patients with an unprotected airway, ileus, bowel obstruction, or perforation.

Increasing excretion of poison

Forced diuresis

Large volumes of IV fluid are infused with diuretics to promote urinary excretion. Forced diuresis is contraindicated in patients with renal dysfunction or heart failure.

  • Maintain urine output at > 200 mL/h.

  • Avoid excess positive fluid balance.

  • Monitor blood electrolytes and magnesium levels.

  • For forced alkaline diuresis (used for acid poisons such as aspirin), infuse aliquots of 8.4% sodium bicarbonate to maintain urinary pH at > 7. If the pH is > 7.5, alternate with 0.9% saline or 5% glucose.

  • For forced acid diuresis (used for soluble alkaline drugs), use 5% glucose with added ammonium chloride to maintain urinary pH close to 6.5.

Extracorporeal elimination

  • This involves the use of haemodialysis, haemofiltration/diafiltration, or haemoperfusion.

  • It is effective for removal of small-molecule poisons with limited protein binding (e.g. methanol, ethylene glycol, lithium, theophylline).

Antidotes and alteration of drug metabolism

Specific antidotes can be given for certain poisons (e.g. naloxone for opiates, flumazenil for benzodiazepines, ethanol for methanol, acetylcysteine for paracetamol).

Mental health assessment

An assessment of the patient’s mental health should be undertaken if clinically appropriate (i.e. if the patient is able to speak or communicate well using aids). This is particularly important if the poisoning was an intentional overdose. For a systematic approach to assessment of mental health, see Poisoning p. [link]. Consideration should be given to whether there is a need for referral to mental health services both while the patient remains in the critical care setting and upon discharge.

Further reading

Brooks DE et al. Toxicology in the ICU: Part 2: specific toxins. Chest 2011; 140: 1172–85.Find this resource:

Levine M et al. Toxicology in the ICU: Part 1: general overview and approach to treatment. Chest 2011; 140: 795–806.Find this resource:

Levine M et al. Toxicology in the ICU: Part 3: natural toxins. Chest 2011; 140: 1357–70.Find this resource:


A toxidrome is a collection of characteristic signs and symptoms elicited by a particular substance when taken in excess, and based on the pharmacology and physiological effects of the substance. Recognizing a toxidrome helps to guide treatment without specific knowledge of the substance. Table 17.1 provides a list of common toxidromes and their corresponding signs and symptoms.

Table 17.1 Common toxidromes


Signs and symptoms

Examples of drugs


  • Hypertension

  • Tachycardia

  • Dilated pupils

  • Hyperthermia

  • Delirium

  • Dry, flushed skin

  • Urinary retention

  • Seizures

  • Coma

  • Psychosis

  • Atropine

  • Antihistamines

  • Psychoactive drugs


  • Bradycardia

  • Hypotension

  • Tachypnoea

  • Confusion

  • Seizures

  • Sweating

  • Vomiting

  • Lacrimation

  • Defaecation

  • Fasciculations

  • Dilated pupils

  • Organophosphates

  • Nerve agents (e.g. sarin)

  • Common pesticides


  • Respiratory depression

  • Slurred speech

  • Depressed mental state

  • Ataxia

  • Barbiturates

  • Ethanol

  • Anticonvulsants

  • Benzodiazepines

  • Some antidepressants


  • Respiratory depression

  • Depressed mental state

  • Bradycardia

  • Hypotension

  • Pinpoint pupils

  • Morphine

  • Heroin

  • Fentanyl

  • Codeine

Paracetamol poisoning


Hepatic glucuronide and sulphate are depleted following a paracetamol overdose, with a consequent increase in P450-catalysed oxidation. This leads to increased production of a reactive arylating metabolite, N-acetyl-p-benzoquinone imine (NAPQI). NAPQI is usually rendered non-toxic by conjugation with glutathione, but this is reduced following overdose. NAPQI causes cellular damage and hepatic necrosis.

Toxic effects are serious or fatal at 150 mg/kg in adults, or around 75 mg/kg in those with impaired hepatic metabolism. For example:

  • malnutrition—decreases glutathione stores

  • alcoholism—decreases glutathione stores

  • HIV infection—decreases glutathione stores

  • chronic disease—decreases glutathione stores

  • enzyme-inducing drugs (e.g. rifampicin, barbiturates, carbamazepine, ethanol, phenytoin)—increase P450 activity.

Assessment findings

Patients are often asymptomatic for the first 24 h, or experience non-specific abdominal pain, nausea, and vomiting. After 24 h, hepatic necrosis develops, causing elevated transaminase activity, jaundice, and right upper quadrant pain. This can progress to:

  • encephalopathy

  • oliguria

  • hypoglycaemia

  • hypotension

  • lactic acidosis

  • coagulopathy

  • acute liver failure (on day 2–7)

  • acute kidney injury (on about day 3).


  • Serum paracetamol levels—take the first sample as soon as possible after 4 h post ingestion.

  • Urea, creatinine, and electrolytes—if needed, repeat 12-hourly.

  • LFTs—if needed, repeat 12-hourly (ALT > 1000 IU/L indicates severe liver damage).

  • Clotting screen—monitor INR (perform 12-hourly if needed).

  • FBC.

  • Arterial blood gas.

  • Regular monitoring of blood glucose levels.


  • Consider activated charcoal (50 mg) if more than 150 mg/kg paracetamol or 12 g, whichever is the smaller, has been ingested, and if it can be given within 1 h of the overdose.

  • Monitor urine output.

  • Take hourly blood glucose measurements—treat hypoglycaemia.

  • Provide renal support for acute kidney injury.

  • Acetylcysteine:

    • acts as a precursor for glutathione, promoting normal conjugation of the remaining paracetamol

    • its protective effect is greatest within 12 h of ingestion, but can decrease mortality in late-presenting patients up to 36 h

    • protection is most effective if given within 8 h of ingestion.

  • Start acetylcysteine infusion if:

    • the paracetamol level exceeds the treatment line on the paracetamol treatment graph (see Figure 17.1)

    • > 150 mg/kg paracetamol has been ingested within the past 8–24 h

    • the overdose was staggered or the time of ingestion is uncertain

    • the patient is a late presenter (> 24 h) with detectable paracetamol levels or elevated transaminase levels

    • there is evidence of severe toxicity regardless of time of overdose

    • consider its use for high-risk patients with depleted glutathione levels or on enzyme-depleting drugs.

  • Liver transplantation—contact the Regional Liver Centre. Consider liver transplantation if:

    • arterial pH is < 7.3 or arterial lactate level is > 3.0 mmol/L after fluid resuscitation

    • creatinine concentration is > 300 µmol/L

    • prothrombin time is > 100 s

    • INR is > 6.5

    • there is grade III/IV encephalopathy in a 24-h period.

  • Provide psychosocial support for the patient and their family, and refer the patient to mental health services as appropriate.

Figure 17.1 Paracetamol treatment graph.

Figure 17.1 Paracetamol treatment graph.

(Reproduced from Singer and Webb (2005) with permission from Oxford University Press.)

Further reading

Singer M and Webb AR. Oxford Handbook of Critical Care, 3rd edn. Oxford University Press: Oxford, 2009.Find this resource:

Salicylate poisoning


The most common cause of salicylate poisoning is ingestion of aspirin, and it is less commonly caused by ingestion of oil of wintergreen (used in liniments) or methyl salicylate. The toxic blood level is > 150 mg/kg.

Salicylates impair cellular respiration by uncoupling oxidative phosphorylation, stimulating the respiratory centre in the medulla, and interfering with lipid, amino acid, and carbohydrate metabolism. They may also cause gastrointestinal erosions, bleeding, ulceration, and (rarely) perforation, as well as renal or liver failure.

Assessment findings

Mild to moderate poisoning (150–300 mg/kg)

  • Vertigo.

  • Tinnitus.

  • Diarrhoea.

  • Vomiting.

  • Headache.

  • Confusion.

  • Tachycardia.

  • Hyperventilation.

Severe poisoning (300–500 mg/kg)

  • Altered mental state (delirium, hallucinations, coma).

  • Acid–base disturbances (respiratory alkalosis due to central stimulation, followed by metabolic acidosis due to the acidic nature of the drug and increased metabolic rate).

  • Pulmonary oedema.

  • Seizures.

  • Gastrointestinal bleeding.

  • Liver failure.

  • Acute kidney injury.

  • Respiratory failure.

  • Rhabdomyolysis.

  • Hypoglycaemia.

  • Hyperthermia.

  • Dehydration and electrolyte imbalance (renal Na+, K+, and water loss is increased).


  • Serum salicylate levels (serial levels are needed to determine whether absorption is continuing).

  • Arterial blood gases.

  • Blood glucose levels.

  • Coagulation studies (including INR).

  • Urea, creatinine, and electrolytes.

  • LFTs.

  • Serum creatine kinase and urinary myoglobin if rhabdomyolysis is suspected.


  • Give activated charcoal to prevent absorption (give as soon as possible after acute ingestion).

  • Urinary alkalinization increases elimination—aim for a urinary pH in the range 7.5–8.0.

  • Forced diuresis—aim for a urine output of 2–3 mL/kg/h, although the evidence for any benefit over urinary alkalinization is weak.

  • Correct dehydration.

  • Avoid fluid overload, particularly in the elderly or those with cardiac or renal disease.

  • Monitor electrolytes—give K+ supplements as required.

  • Monitor blood glucose levels—treat hypoglycaemia.

  • Observe for seizures—treat with benzodiazepines.

  • Monitor core temperature—active cooling is needed if the patient is hyperthermic.

  • Haemodialysis is required for significant acute kidney injury, refractory acidosis, coma, seizures, pulmonary oedema, or serum salicylate level > 6.2 mmol/L.

Carbon monoxide poisoning


Carbon monoxide (CO) is a colourless, odourless gas produced by the incomplete burning of organic compounds. Haemoglobin has a greater affinity for CO than for O2, forming carboxyhaemoglobin, which then prevents the uptake of O2 on to the Hb. The oxyhaemoglobin (OxyHb) dissociation curve is shifted to the left, decreasing release of O2 at the tissues. CO also binds to myoglobin, which has an even greater affinity for it than does Hb, further exacerbating tissue hypoxia.

The elimination half-life of CO from blood is:

  • 4.5 h in room air

  • 1.5 h in 100% O2

  • 15–23 min in 2.5 atm hyperbaric O2.

CO also competes with O2 for binding to the haem moiety within cytochrome oxidase, the last part of the mitochondrial electron transport chain responsible for generating most of the body’s ATP. As mitochondrial pO2 levels are much lower than arterial levels, the CO is harder to displace—hence the rationale for hyperbaric treatment.

Assessment findings

  • Headache.

  • Nausea.

  • Vomiting.

  • Tiredness and weakness.

  • Confusion, memory disturbance, and amnesia.

  • Abdominal pain.

  • Coordination problems.

  • Angina (if there is pre-existing heart disease).

  • Dyspnoea.

  • Loss of consciousness.

  • Coma.

  • Seizures.

  • The classic cherry-red appearance of the skin and mucosa rarely occurs—usually there is pallor.

  • Tachycardia.

  • Hypotension or hypertension.

  • Hyperglycaemia.

  • Hypokalaemia.

  • Hyperthermia.

  • Bright red retinal veins.

  • Papilloedema.

  • Retinal haemorrhages.

  • Non-cardiogenic pulmonary oedema.


  • Myocardial depression, ischaemia, or infarction.

  • Cardiac arrhythmias secondary to hypoxia or myocardial injury.

  • Non-traumatic rhabdomyolysis.

  • Renal failure (secondary to myoglobinuria from rhabdomyolysis).

  • Cerebral oedema.

  • White matter demyelination.

  • Permanent brain damage or long-term neuropsychiatric sequelae.


Do not rely on O 2 saturation monitoring by pulse oximetry (PaO 2 ) or from the arterial blood gas analysis (SaO 2 ). Machines are unable to tell the difference between carboxyhaemoglobin (COHb) and oxyhaemoglobin (OxyHb), and may give falsely high and inaccurate O2 saturation results.

  • COHb levels—measure on a co-oximeter.

  • Arterial blood gases—metabolic acidosis may be present secondary to lactic acidosis.

  • Troponin.

  • Creatinine kinase and urine myoglobin.

  • FBC, U&Es, LFTs, and glucose.

  • 12-lead ECG.

  • Urinalysis—this is positive for albumin and glucose in chronic intoxication.

  • Chest X-ray.

  • CT of the head if the patient is comatose or has unresolving CNS symptoms.


  • Give 100% O2 (do not rely on pulse oximetry to guide O2 therapy).

  • Continue 100% oxygen until COHb levels are < 10%.

  • Give ventilatory support as required.

  • Give hyperbaric oxygen (if feasible) if COHb levels are > 25%. Benefits have been shown for long-term cognition.

  • Continuous haemodynamic monitoring.

  • Serial neurological assessments.

  • Monitoring of electrolytes—correct hypokalaemia.

  • Monitoring of blood glucose levels.

Tricyclic antidepressant poisoning


Tricyclic antidepressants are rapidly absorbed and then metabolized in the liver. Conjugates are subsequently excreted renally, and impaired renal function may prolong toxicity. They have long elimination half-lives (often > 24 h).

Assessment findings

Toxic effects are related to the following:

  • Anticholinergic effects:

    • dry mouth and blurred vision

    • urinary retention

    • agitation and hallucinations

    • depressed mental state

    • pyrexia

    • delayed gastric emptying.

  • Direct alpha blockade—vasodilation causing profound hypotension.

  • Inhibition of noradrenaline (norepinephrine) and serotonin reuptake—hypokalaemia.

  • Blockade of fast sodium channels in myocardial cells, causing depression of myocardial contractility and arrhythmias.

Cardiovascular effects

  • Prolonged PR and QT interval, and widened QRS.

  • Unstable ventricular arrhythmias or asystole.

  • Atrioventricular block.

  • Sinus tachycardia.

  • Hypotension.

Neurological effects

  • Drowsiness or coma.

  • Rigidity.

  • Extrapyramidal signs.

  • Ophthalmoplegia.

  • Respiratory depression (causing hypoxia).

  • Delirium.

  • Seizures.


  • U&Es.

  • LFTs.

  • Arterial blood gases.

  • Toxicology screen is not particularly helpful, as serum tricylic antidepressant levels do not correlate with toxic effects. The high degree of protein binding and their lipophilic nature mean that tissue levels are often much higher than serum levels of free drug.

  • 12-lead ECG.

  • Chest X-ray.


  • Give activated charcoal to reduce absorption.

  • Provide respiratory support:

    • monitor respiratory rate

    • give O2 therapy

    • intubate to protect the airway if the patient is obtunded or comatose

    • use mechanical ventilation for severe respiratory depression.

  • Continuous haemodynamic monitoring—treat hypotension with fluid with or without inotropes (use agents with α‎-adrenergic effects).

  • Continuous ECG monitoring—observe for arrhythmias. Correct hypotension, hypoxia, and acidosis, and consider magnesium therapy before using anti-arrhythmic drugs, as these may potentially worsen myocardial depression (e.g. beta blockers) and/or further prolong the QT interval (e.g. amiodarone), increasing the risk of serious ventricular arrhythmias. Monitoring should continue for 24 h after the patient is symptom-free.

  • Serum alkalinization is required, using sodium bicarbonate to achieve a blood pH in the range 7.45–7.55. This increases protein binding, decreases QRS width, stabilizes arrhythmias, and can raise blood pressure. Administer sodium bicarbonate as an initial slow bolus of 1–2 mEq/kg body weight (70–140 mL of 8.4% solution for a 70 kg adult) through a central venous catheter, followed by an infusion.

  • Observe for seizures—treat with benzodiazepines if necessary.

  • Use a urinary catheter to relieve retention and monitor output.

Illicit drug overdose

Street drugs are often ‘cut’ with various contaminants. Purity, and hence dosage, is therefore difficult to determine. Allergic reactions to the cutting agents (e.g. quinine) can also occur.

Assessment and management

  • Respiratory—monitor respiratory rate. Endotracheal intubation may be required for airway protection with or without mechanical ventilation.

  • Neurological—assess conscious level, and observe for and treat seizures.

  • Cardiovascular—provide continuous cardiac monitoring, and treat hypertension and hypotension.

  • Renal—monitor urine output, and provide renal support if necessary.

  • Active cooling if patient is hyperthermic—dantrolene may be considered if the core temperature exceeds 40°C.

  • Specific antidotes—these are available for some of these agents (e.g. naloxone for opiates, flumazenil for benzodiazepines). Short-term reversal may be useful for diagnostic purposes or in life-threatening situations where respiratory support is not immediately available. The half-lives of these drugs are short, so the patient may deteriorate within minutes. Longer-term infusions are very expensive, and in general such patients are intubated and may also be ventilated until the airway, respiratory, and neurological depressant effects of the overdose have worn off. Sudden reversal of the neurological depression with flumazenil or naloxone may precipitate seizures, so these drugs should generally be avoided if the patient has a history of epilepsy or presents with seizure activity.

Illicit drugs


This is a potent CNS stimulant. Crack cocaine is made from cocaine ‘cooked’ with ammonia or sodium bicarbonate to create ‘rocks’ that can be smoked.


  • Hyperthermia, hypertension, cerebral haemorrhage.

  • Myocardial infarction or cardiomyopathy, leading to heart failure.

  • Seizures, tremors, delirium.

  • Acute kidney injury.

Ecstasy (methylenedioxymethamphetamine, or MDMA)

This is a stimulant and hallucinogenic drug. Adverse effects are more likely to occur with exercise in hot environments (e.g. dancing in nightclubs). Encouragement to drink large volumes of water has led to cases of death from severe hyponatraemia.


  • Tachycardia, hypertension, heart failure.

  • Hyperthermia and dehydration (sometimes severe).

  • Loss of consciousness, seizures, stroke, DIC.

  • Muscle cramps.

  • Rhabdomyolysis leading to compartment syndrome and acute kidney failure.

  • Permanent neurological damage (e.g. impaired thinking and memory).

Heroin (diamorphine)

This is an opiate synthesized from morphine.


  • Slow, shallow, and laboured breathing, respiratory arrest.

  • Hypotension.

  • Disorientation, delirium, drowsiness, coma.

  • Pinpoint pupils, and cold, clammy skin.

  • Muscle cramps, gastrointestinal spasms.

Specific treatment

  • Naloxone.


These include short-acting (e.g. midazolam), medium-acting (e.g. lorazepam), and long-acting (e.g. diazepam) agents.


  • Respiratory depression.

  • Confusion, drowsiness, coma.

  • Blurred vision, slurred speech.

Specific treatment

  • Flumazenil.

Gamma-hydroxybutyrate (GHB)

This is a synthetic depressant, which can be snorted, smoked, or mixed into drinks.


  • Nausea, dizziness, amnesia.

  • Drowsiness, visual disturbances.

  • Respiratory distress.

  • Seizures, coma.


These potent psychostimulants cause release of the neurotransmitters dopamine and noradrenaline (norepinephrine).


  • Tachypnoea, tachycardia.

  • Confusion, hallucinations, psychosis.

  • Arrhythmias, hypertension.

  • Hyperthermia.

  • Stroke, seizures, coma.

Specific treatment

  • Acidification of the urine can increase excretion.

  • IV phentolamine for severe hypertension.


These depress the activity of the CNS, respiratory, and cardiovascular systems.


  • Severe weakness.

  • Confusion, extreme drowsiness.

  • Shortness of breath.

  • Bradycardia.

  • Hypotension.

Specific management

Alkalinization of the urine increases the elimination of phenobarbital.