Overdose and Poisoning
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Naloxone will reverse the effect of opiate overdose, typically in the presence of CNS and respiratory depression.
  • It competitively binds opioid receptors, causing a blockade
  • Usually given IV for fastest action (<1 min)
  • Opioid overdose typically seen in heroin users who have been incarcerated / ‘gone cold turkey’ who subsequently return to heroin abuse. Upon returning to opioid use they often take the same dose they were taking before cessation, which, in the absence of tolerance, can be fatal.
  • CAUTION – the half-life of naloxone is shorter than that of opiates, thus the naloxone can wear off, and the patient can go back into a state of opiate overdose.


symptoms: agitation, euphoria, blurred vision, slurred speech, ataxia, slate-grey cyanosis
Flumazenil – can reverse the effect of benzodiazepines, however, is not always recommended. It is mainly used to reduce the sedative / drowsiness effects of benzodiazepines
  • In long-term benzo abusers, it can induce withdrawal (including seizures), thus use is not recommended
  • It competitively binds benzodiazepines
  • Its half-life is shorter than benzodiazepines, so multiple doses may need to be administered


Paracetamol overdose is considered separately in its own article.


Aspirin (salicylic acid)

Note that Pepto-Bismol(R) is very high in salicylate!
<125mg/Kg is not toxic
250mg/Kg is mildly toxic. Signs and symptoms include:
  • Tinnitus
  • Lethargy
  • Dizziness
  • Nausea / vomiting

500mg/Kg is severe. Signs and symptoms include (as well as the above)

  • Dehydration
  • Sweating  / warm extremities
  • Bounding pulse
  • Deafness
  • Breathlessness
  • Glucose disturbance (hypo or hyper)
  • Confusion / disorientation, rarely coma

Other features indicating a life-threatening attack include:

  • pulmonary oedema
  • metabolic acidosis
  • salicylate conc >700mg/L


Salicylate concentration should be measured, but unlike paracetomal is not an indication of the severity of poisoning

  • It is most accurate >4 hours after ingestion. Repeat after a further 2 hours to asses for rising levels

Renal function (U+E’s)
Plasma Potassium – hypokalaemia likely, correct with IV KCl
Urine pH + ABG – Check hourly – severity of poisoning can be asses using blood pH and urine pH:

  • Stage I – blood >7.4, urine >6.0
  • Stage II – blood >7.4, urine <6.0
  • Stage III – blood < 7.4, urine <6.0


Activated charcoal – if >125mg/Kg ingested <1hr ago
Gastric lavage – if >500mg/Kg ingested <1hr ago
Aggressive rehydration
Consider glucose – intracellular glucose is often depleted even if blood glucose remains normal
Increase alkalinity of urine – can increase excretion of salicylate

  • Give sodium bicarbonate if >500mg/Kg ingested. Optimum urine pH is 7.5 – 8.5
  • Hypokalaemia reduces the effectiveness of urine alkalisation

CAUTION – forced dieresis is not effective at increasing salicylate excretion and may cause pulmonary oedema.
HAEMODIALYSIS is the treatment of choice for severe cases (also continue alkalisation or urine providing no oliguria). Consider in:

  • Plasma salicylate >700mg/Kg
    • Lower if patient <10 or >70 years
  • Renal failure
  • Heart failure
  • Coma
  • Convulsions
  • Non-resolution of CNS symptoms, despite correction of acidosis
  • Severe metabolic acidosis (pH <7.2)

β – blockers

Positively inotropic agents (e.g. dobutamine, or catecholamines, e.g. dopamine, noradrenaline, adrenaline) are often not effective in β-blockade. Glucagon is usually the treatment of choice.
Hypocalcaemia may also be present, and should be corrected with calcium.


Dry cough, increased appetite, social withdrawal and paranoia, altered perception of time

Sympathomimetics e.g. cocaine, amphetamines

Tachycardia, mydriasis, euphoria, formication- insects crawling, agitation, tremor, dilated pupils, tachycardia, arrhythmias, convulsions.
  • Treatment: Benzodiazepine e.g. diazepam

Carbon Monoxide

Inebriation, coma, reduced reflexes, tachycardia, pulmonary oedema, shock, met acidosis, flushed cherry pink skin. headache.
  • Treatment –  hyperbaric oxygen


  • Anti-freeze (ethylene glycol) poisoningEthanol
  • Cyanide poisoning Dicobalt edetate
  • Lead poisoning Sodium calcium edetate
  • Organophosphate poisoning Atropine
  • Heparin overdose Protamine sulphate

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

This Post Has 2 Comments

  1. Ellie

    Why is prothrombin time a good indicator of AKI?

    1. tom

      Errr… it isn’t! It’s a mistake. Meant to be acute liver failure!
      I’ve fixed it up now

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