2.  The possibility of drug, or other substance
poisoning should be considered in any
patient with reduced consciousness, or
whose behaviour or physiology is aberrant
and/or unstable.
 Most commonly involving pre-school
children.
 2/3 accidental.
 Paracetamol, NSAIDs and antidepressants
are most common drugs.

3.  Managed as an medial emergency:
› O2, ABC, help.
› Except:
 organophosphates (protect yourself first).
 Cyanide (antidote asap)
 Foundation of all treatments is supportive.
› Then identify agent +/- specific therapy.
 Detailed history.
› Symptoms
› Physiology
› Witnesses
› Ambulance crew – empty packets
› GP
› Previous ODs
› ALWAYS do paracetamol level

4.  Atropine, hyoscine, scopolamine.
 Block action of acetylcholine at autonomic
receptors, can have mixed
parasympathetic and sympathetic
symptoms
 Altered cognition, mydriasis (and impaired
accomodation), urinary retention,
hyperthermia, dry mucous membranes.
› “red as a beet, dry as a bone, blind as a bat,
mad as a hatter, and hot as a hare”
› May also seize, dysrythmias, rhabdomyolysis.
 Support, consider anticholinesterases, cool.

5.  Organophosphates
 Salivate, lacrimate, sweat, nausea,
vomiting, urination, defecation, muscle
weakness, bronchorrhoea
 Bradycardia, pupillary changes, seizures,
paralyis.
 I+V, atropine, pralidoxime

6.  Aspirin
 Classically: respiratory alkalosis 
metabolic acidosis
 Altered mental state, tinnitus,
hyperpnoea, tachycardia, sweating.
 Fever, ketonuria, acute lung injury
 Multidose activated charcoal,
alkalinization of urine, K+ repletion,
haemolysis, hydration.

7.  Heroin, morphine etc.
 CNS respiratory depression, small pupils
 Hypothermia, bradycardia, respiratory
arrest
 I+V, naloxone

8.  Seretonin syndrome – similar to
anticholinergic
 Cognitive
› Confusion, hallucinations, agitation, coma
 Autonomic
› Shivering, sweating, hyperthermia, hypertension,
nausea, diaorrhea
 Somatic
› Myoclonus, hyperreflexia, tremor
 I+V, cooling, benzodiazepines.

9.  Cocaine, amphetamines
 Agitation, mydriasis, sweating,
tachycardia, hypertension, hyperthermia
 Seizures, rhabdomyolysis, myocardial
infarction, cardiac arrest, hyperthermia.
 I+V, cool, benzodiazepines, hydrate.

10.  FBC, U+E, lactate, LFTs, coags.
 Specific levels if suspected.
 CXR
 AXR
› Body packers.

11.  No benefit vs AC.
 Prolonged time in A+E, increased
aspiration

12.  Large bore OG tube, instilled and
reaspirated with litres of water, until no
pill fragments are seen.
 ? Post-pyloric transfer.
 Perforation and aspiration risk.

13.  Large surface area, binds drugs via van-der Waals forces.
 50g kg-1
 Ideally within 1hr of ingestion.
 In paracetamol may be efficacious within 2hrs.
 Patient must be intubated
 Not recommended with
› Alcohol
› Methanol
› Ethylene glycol
› Petrol
› Corrosives
› Acids
› Alkalis
 Multiple dosing may reduce enterohepatic recirculation.

14.  Polyethylene glycol 2litres/hour.
 Not routine.
 May be useful in body packers.
 Contraindicated in unprotected airways
bowel obstruction, perforation, ileus.

15.  Alkaline diuresis increases the elimation
of weak acids.
 NaHCO3 administered to maintain
urinary pH at 7.5-8.5.
› Careful about hypokalaemia.
› Careful in renal disease.

16.  Ethylene glycol, methanol, lithium,
theophylline, salicylate poisoning.
 Drug should have
› Low VD
› Low molecular weight
› Low protein binding
› Low water solubility

17.  Paracetamol metabolism produces the
toxic metabolite NAPQI which is then
neutralised by glutathione.
 N-Acetylcysteine should be given asap,
but may reduce liver damage up to
24hrs later.
 At risk groups
› Alcoholics, HIV, malignancy, antiepileptics.
› Should get NAC at lower levels.

18.  Rehydration, correction of acid-base
disturbance.
 Activated charcoal.
 Consider urinary alkalinisation when
patients are showing signs of toxicity or
plasma levels >300mg/l.
 Consider haemodialysis if levels
>700mg/l.

19.  Use flumazenil at your peril.
› VT
› Seizures esp with TCAs
› Raised ICP
› Withdrawal

20.  The usual.
 Convulsions, non-cardiogenic pulmonary
oedema, risk of compartment syndrome.
 Naloxone 100mcg  2mg.
› Precipitate acute confusional state
› Half-life 20mins.
› Rarely: hypertension, drowsiness.

21.  Cause 250 deaths per year.
 Cardiac depression by sodium channel
blockade.
 Tachycardia
 Mydriasis, coma, hyperreflexia, convulsions,
ECG changes, hypotension.
 Long QRS > 120ms indicates cardiac toxicity
and is predictive of ventricular arrhythmias and
seizures.
 Sodium bicarbonate should be administered
even in the absence of an acidosis.
 Phenytoin is the anti-arrhytmic of choice

22.  Citalopram, Fluoxetine, Sertraline
 Nausea, vomiting, nystagmus, dysrhytmias, mild
hypertension.
 If in combination with cocaine, TCAs or MAOis
may cause seretonin syndrome.
› Altered mental status
› Neuromuscular hyperactivity
› Autonomic Instability
 Supportive treatment
 Alkalinisation of the urine
 Haemodialysis

23.  Large anion gap acidosis.
 Metabolised via alcohol dehydrogenase
into toxic metabolites.
 Treat with oral or NG ethanol, as
preferentially metabolised by alcohol
dehydrogenase.

24.  O2, ABC
 Support
 Reduce absorption
 Antidotes
 Increase elimination
 PARACETAMOL LEVEL