Poisoning (tricyclic antidepressants, benzodiazepines, methanol, iron, lithium and digoxin) Flashcards
What two systems are most affected by TCA overdose?
CNS - delirium, seizure, lethargy, coma
CV - acidosis, decreased PVR, hypotension, impaired cardiac contractility, tachycardia
Name two TCAs commonly causing toxicity.
Amitriptyline and dosulepin
What are the clinical features of TCA overdose?
Anticholinergic symptoms, such as dry flushed skin, dilated pupils, absent bowel sounds, or urinary retention
Impaired consciousness level
Tachycardia
Hypotension
Arrhythmias
Seizures
Other variable clinical signs include divergent squint, INO and gaze paralysis, nystagmus, and myoclonic and choreoathetoid movements. Increased muscle tone, hyperreflexia, and extensor plantar responses may occur.
Why are TCA overdoses difficult to diagnose?
Presents with symptoms similar to:
- sepsis - tachycardia, hypotension
- antihistamine overdose
- ethanol
- PE
How is TCA overdose diagnosed?
ECG
-QRS >100ms -> 30% risk of seizures
-Prolonged QTc
-AV block
-Non-specific ST and T wave changes
-Downward sloping ST elevation in V1-3 with RBBB (Brugada wave)
NB: Serum or urine TCA levels can be obtained but ECG is more rapid for diagnosis.
What is the management of TCA toxicity?
Admit
ABCDE
Cardiac monitoring and IV access
If <2hrs repeated activated charcoal
Sodium bicarbonate IV (or sometimes NaCl 3%)
NB: if still asymptomatic 6hrs after overdose then can be managed as outpatient
What is the antidote to TCA overdose?
Sodium bicarbonate IV improves ECG parameters and reduces cardiotoxicity - ensure blood pH is <7.55 before giving
Why is haemofiltration/dialysis not as useful in TCA overdose?
TCAs have a large volume of distribution and high protein binding capacity
What is the problem with using flumazenil in benzodiazepine overdose?
Has very specific indications (pure benzo poisoning that will otherwise require mechanical ventilation) and in most patients presenting with benzodiazepine overdose it is contraindicated (e.g. TCA co-ingestion, benzo dependent)
Can only be given by specialists and may cause seizures.
Therefore the risks of using it usually outweigh the benefits
Which substances increase vs reduce absorption of benzodiazepines in an overdose?
Alcohol - increases absorption and toxicity
Antacids (containing Mg or Al) - reduce and delay absorption
What systems are mainly affected in benzodiazepine overdose?
CNS - depression (incl. resp), drowsiness, slurred speech, incoordination, unsteady git, impaired attention or memory
Unremarkable vital signs and no focal signs on neurological examination
What are the effects of benzodiazepines therapeutically?
sedation
hypnotic
anxiolytic
anticonvulsant
muscle relaxant
What is the management of benzodiazepine overdose?
ABCDE
Mechanical ventilation if respiratory arrest
Supportive care - observe for min. 4hrs
If <1hr since ingestion: activated charcoal
What is the management of methanol/ethylene glycol poisoning?
Fomepizole or ethanol - inhibit alcohol dehydrogenase
If acidotic <7.3 sodium bicarbonate IV
Haemodialysis if metabolic acidosis, high levels, end-organ damage
NB: activated charcoal and gastric lavage have no role in toxic alcohol exposures.
What systems are affected in methanol poisoning?
CNS - mild effects, sedation, but if metabolised into toxic byproducts then coma, seizures, hyperpnoea
What substances contain methanol?
-automotive coolant/antifreeze and -de-icing solutions
-windshield wiper fluid
-solvents
-cleaners
-fuels
What substance reduces the toxicity of methanol/ethylene glycol when co-ingested?
Ethanol
What are the clinical features of ethylene glycol/methanol poisoning?
3 stages of ethylene glycol toxicity:
Stage 1: symptoms similar to alcohol intoxication: confusion, slurred speech, dizziness
Stage 2: metabolic acidosis with high anion gap and high osmolar gap. Also tachycardia, hypertension
Stage 3: acute kidney injury
What is the end result of toxocity following methanol ingestion?
Toxicity following ingestion is produced by the ensuing metabolic acidosis and the formation of formic acid, which damages the eye, producing blindness.
What is the pathophysiology of ethylene glycol poisoning?
The substance itself is non-toxic, initially causing inebriation.
However, toxicity appears within 12 to 24 hours due to a metabolic acidosis and the formation of calcium oxalate from one of the metabolites.
Deposition of calcium oxalate in the lungs, myocardium, and kidney leads to respiratory and cardiac damage followed by acute kidney injury.
Hypocalcaemia can also occur due to the consumption of circulating calcium by crystal formation.
What are the phases of iron toxicity?
5 phases:
- Early gastrointestinal (GI) symptoms (persistent vomiting, hypovolemic shock, or altered mental status indicates moderate to severe poisoning)
- Latent (or relative stability)
- Shock and elevated anion gap metabolic acidosis
- Delayed hepatotoxicity/hepatic necrosis
- Remote gastric outlet obstruction
How is iron toxicity diagnosed?
What levels of iron are toxic?
Severe poisoning may result from the ingestion of more than 150 mg/kg. In small children, a dose of 20 mg/kg of elemental iron may cause illness and 600 mg may be fatal to a toddler weighing less than 10 kg
How do you diagnose iron toxicity?
Severe poisoning is indicated by serum iron levels above 5 mg/l in a child, or 8 mg/l in an adult. It may be fatal.
