Drug Overdose (Paracetamol, Opiates, Benzos, TCAs & SSRIs) Flashcards

1
Q

What is the pathophysiology behind salicylate (aspirin) poisoning?

A
  • Pathophysiology
    • Usually aspirin.
    • Uncouples oxidative phosphorylation causing metabolic acidosis.
    • Also directly stimulates CNS respiratory centre causing ↑RR and respiratory alkalosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the common signs and symptoms of salicylate poisoning?

A
  • ASA-DOSE:
    • Agitation or delirium.
    • Sweating
    • Auditory symptoms: tinnitus or deafness.
    • Dizziness
    • Overbreathing: ↑RR due to CNS effect or response to metabolic acidosis.
    • Seizures and coma.
    • Emesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which investigations should be done in suspected salicylate poisoning?

A
  • Investigations
    • Plasma salicylate levels. Repeat every 2 hours until it peaks, which can take up to 6 hours.
    • U+E: ↓K+, AKI if severe.
    • ↓Glucose
    • ABG and HCO3-: initially alkalosis, later acidosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is salicylate poisoning managed?

A
  • ABCD:
    • Activated charcoal ± MDAC.
    • Sodium Bicarb for urine and serum alkalinisation: ionises salicylates so they can’t cross blood-brain barrier, and can’t escape renal tubules so are eliminated from circulation.
    • Correct glucose and K+ deficits.
    • Dialysis if: ↓pH, ↑↑salicylates, AKI.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the background of TCA poisoning?

A
  • TCA overdoses are rare – as the drug is not widely used now – but very dangerous.
    • In contrast, SSRI overdoses are commoner, but much less likely to be fatal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What signs and symptoms might be seen in TCA overdose? What effects are these symptoms due to?

A
  • Anticholinergic effects:
    • Hot dry skin.
    • Mydriasis: dilated pupils.
    • ↑HR
    • Urinary retention.
    • Agitation and delirium.
    • Neurological: seizures, coma, hypertonia, hyperreflexia.
  • Anti Na+ channel effects:
    • Arrhythmias, including VT and VF.
    • Cardiac arrest.
    • Heart block.
  • Anti α-adrenergic effects:
    • ↓BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which investigations should be performed in TCA overdose?

A
  • ECG: wide QRS, long QT, increased PR. Continue to monitor if large OD or initial abnormality found.
    • U+E
    • Glucose
    • ABG: metabolic acidosis secondary to seizures and/or tissue hypoxia from ↓cardiac output.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How can TCA overdose be managed?

A
  • Activated charcoal (± MDAC) if <2h since ingestion.
    • Sodium bicarbonate to reverse Na+ channel blockade if QRS >100 ms or there is ventricular arrhythmia.
    • DC cardioversion, lidocaine, or MgSO4 if bicarb fails. Most other anti-arrhythmic drugs are contraindicated.
    • Benzodiazepines if there are seizures.
    • Lipid emulsion if peri-arrest.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the signs and symptoms of benzodiazepine poisoning?

A
  • Drowsy. In severe cases, coma.
    • Neurological impairment, including motor impairment, diplopia, slurred speech, and ataxia.
    • Anterograde amnesia.
    • Rarely, paradoxical symptoms: anxiety, delirium.
    • ↓RR, which would suggest a combined OD.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is benzodiazepine poisoning managed?

A
  • Supportive treatment, especially airway.
    • Activated charcoal only if BZD taken in combo with something else.
    • Flumazenil is the antidote.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the indications for giving flumazenil? How does it work and how is it given?

A

Mechanism:
* BZD receptor antagonist, which mainly acts to reverse CNS depression.

  • Indications:
    • Severe OD – with marked impairment of consciousness or respiratory distress – in a first time or infrequent user.
    • In practice, it is most likely to be used for iatrogenic overdoses, when we can be sure that they are not long-term users and it is not a mixed overdose.
  • Contraindications due to seizure risk:
    • BZD-dependant patients.
    • Mixed TCA OD.
    • Epilepsy history.
  • Dose and administration:
    • Use the minimum effective dose.
    • Apply ECG monitoring when giving flumazenil as it may unmask an arrhythmia, especially if patient on TCA or carbamazepine.
  • Half life is less than BZD, so may wear off first.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the signs and symptoms of iron poisoning?

A
  • Signs and symptoms
    • Early (0-6 hours): GI symptoms including nausea, vomiting, diarrhoea, and abdo pain.
    • Delayed (2-72 hours): black stools, circulatory collapse, and CNS symptoms including drowsiness, seizures, and coma.
    • Late (2-4 days): liver and kidney failure.
    • Very late (2-5 weeks): gastric stricture.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which investigations should be done in suspected iron poisoning?

A
  • Establish amount of elemental iron from history.
    • Fe level, taken at least 4 hours after ingestion, then repeated 2-hourly.
    • ↑WBC
    • ↑Glucose
    • U+E and LFT.
    • Daily monitoring: clotting, HCO3-.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is iron poisoning managed?

A
  • Gastric lavage.
    • Desferrioxamine is the antidote.
  • Desferrioxamine (aka deferoxamine)
    • Chelates Fe, which is then excreted as red urine.
    • Indicated in severe OD, characterized by ↓consciousness, seizures, shock, metabolic acidosis, GI bleed.
    • Contraindicated in kidney failure.
    • Can cause ↓BP and pulmonary oedema.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the pathophysiology/background behind organophosphate poisoning?

A
  • Relatively common suicide method in developing world, taken in the form of fertilizer. Also used as chemical weapon (sarin, VX).
    • Percutaneous or oral entry → cholinesterase inhibition → ↑acetylcholine (ACh) levels → parasympathetic activation, NMJ depolarization, and CNS dysregulation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the signs/symptoms of organophosphate poisoning?

A
  • DUMBELLS:
    • Diarrhoea
    • Urination
    • Miosis
    • Bradycardia, Bronchospasm, Bronchorrhea. The ‘killer Bs’ most likely to cause death.
    • Emesis
    • Lacrimation
    • Lethargy
    • Salivation
  • Other symptoms:
    • Muscle: fasciculations and weakness.
    • Blurred vision.
17
Q

Which investigations may be done in organophosphate poisoning?

A
  • ↓Serum and RBC cholinesterase.

* Atropine therapeutic trial.

18
Q

How is organophosphate poisoning managed?

A
  • Decontaminate patient, while wearing personal protective equipment.
    • Atropine IV.
    • Contact public health authorities.
    • Pralidoxime – a cholinesterase reactivator – is the antidote. Use in severe poisoning.
19
Q

What is the pathophysiology of paracetamol overdose?

A
  • The usual paracetamol metabolism pathways – glucuronidation or sulfation – are rapidly saturated.
    • The other pathway – via the cytochrome P450 isoenzymes CYP2E1 and CYP3A4 – generates toxic NAPQI. The body can only detoxify a small amount with endogenous glutathione.
    • Risk is increased by malnutrition, concomitant enzyme inducer use (enzyme-inducing anti-epileptics, rifampicin), or chronic alcoholism (also causes enzyme induction). Reduces potentially toxic level from 12 g to 7.5 g.
20
Q

What are the signs and symptoms commonly seen in paracetamol overdose?

A
  • Symptoms takes up to 3 days to develop.
    • Early features: non-specific abdo pain, nausea and vomiting, altered clotting.
    • Later features: jaundice, RUQ pain, ALF, encephalopathy.
    • Presentation is often pre-symptomatic, among those who have regretted their OD (or been brought in by others).
21
Q

Which investigations can be done in paracetamol overdose?

A
  • Basic bloods: FBC, LFTs, U+E, coag, albumin, glucose.
    • Serum paracetamol levels should be measured ≥4 hours post-ingestion, as they take time to peak.
    • ABG: lactic acidosis if severe, due to NAPQI inhibition of aerobic respiration and ↓hepatic clearance of lactate.
22
Q

How is paracetamol managed?

A
  • N-acetylcysteine (NAC) IV is the antidote, and is most effective within 8 hours. Usually a 24 hour infusion.
    • Methionine PO is 2nd-line.
    • Activated charcoal if <1 hour from ingestion.
    • Transplantation indications (King’s College Criteria): pH <7.3 24h post ingestion, or all 3 of {INR >6.5 (PT >100 sec) and creatinine >300 μmol/l (3.4 mg/dL) and grade 3-4 encephalopathy}.
    • Correct any hypoglycaemia, but seek specialist advice before correcting INR.
23
Q

What are the complications of paracetamol overdose?

A
  • Acute liver failure.
    • AKI: develops at 3-7 days.
    • Death: usually occurs 3-6 days post-ingestion. Occurs in <1%, but in 50% of those who develop ALF.
    • Poor prognostic indicators: ↑ or rising PT, ↓pH, ↑lactate, ↑BR, grade 3/4 encephalopathy, ↑creatinine.