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- Y6 Critical Care and Palliative Care > Poisoning (tricyclic antidepressants, benzodiazepines, methanol, iron, lithium and digoxin) > Flashcards

Poisoning (tricyclic antidepressants, benzodiazepines, methanol, iron, lithium and digoxin) Flashcards

1
Q

What two systems are most affected by TCA overdose?

A

CNS - delirium, seizure, lethargy, coma
CV - acidosis, decreased PVR, hypotension, impaired cardiac contractility, tachycardia

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2
Q

Name two TCAs commonly causing toxicity.

A

Amitriptyline and dosulepin

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3
Q

What are the clinical features of TCA overdose?

A

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.

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4
Q

Why are TCA overdoses difficult to diagnose?

A

Presents with symptoms similar to:
- sepsis - tachycardia, hypotension
- antihistamine overdose
- ethanol
- PE

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5
Q

How is TCA overdose diagnosed?

A

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.

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6
Q

What is the management of TCA toxicity?

A

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

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7
Q

What is the antidote to TCA overdose?

A

Sodium bicarbonate IV improves ECG parameters and reduces cardiotoxicity - ensure blood pH is <7.55 before giving

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8
Q

Why is haemofiltration/dialysis not as useful in TCA overdose?

A

TCAs have a large volume of distribution and high protein binding capacity

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9
Q

What is the problem with using flumazenil in benzodiazepine overdose?

A

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

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10
Q

Which substances increase vs reduce absorption of benzodiazepines in an overdose?

A

Alcohol - increases absorption and toxicity
Antacids (containing Mg or Al) - reduce and delay absorption

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11
Q

What systems are mainly affected in benzodiazepine overdose?

A

CNS - depression (incl. resp), drowsiness, slurred speech, incoordination, unsteady git, impaired attention or memory

Unremarkable vital signs and no focal signs on neurological examination

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12
Q

What are the effects of benzodiazepines therapeutically?

A

sedation
hypnotic
anxiolytic
anticonvulsant
muscle relaxant

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13
Q

What is the management of benzodiazepine overdose?

A

ABCDE
Mechanical ventilation if respiratory arrest
Supportive care - observe for min. 4hrs
If <1hr since ingestion: activated charcoal

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14
Q

What is the management of methanol/ethylene glycol poisoning?

A

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.

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15
Q

What systems are affected in methanol poisoning?

A

CNS - mild effects, sedation, but if metabolised into toxic byproducts then coma, seizures, hyperpnoea

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16
Q

What substances contain methanol?

A

-automotive coolant/antifreeze and -de-icing solutions
-windshield wiper fluid
-solvents
-cleaners
-fuels

17
Q

What substance reduces the toxicity of methanol/ethylene glycol when co-ingested?

A

Ethanol

18
Q

What are the clinical features of ethylene glycol/methanol poisoning?

A

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

19
Q

What is the end result of toxocity following methanol ingestion?

A

Toxicity following ingestion is produced by the ensuing metabolic acidosis and the formation of formic acid, which damages the eye, producing blindness.

20
Q

What is the pathophysiology of ethylene glycol poisoning?

A

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.

21
Q

What are the phases of iron toxicity?

A

5 phases:

  1. Early gastrointestinal (GI) symptoms (persistent vomiting, hypovolemic shock, or altered mental status indicates moderate to severe poisoning)
  2. Latent (or relative stability)
  3. Shock and elevated anion gap metabolic acidosis
  4. Delayed hepatotoxicity/hepatic necrosis
  5. Remote gastric outlet obstruction
22
Q

How is iron toxicity diagnosed?

A
23
Q

What levels of iron are toxic?

A

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

24
Q

How do you diagnose iron toxicity?

A

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.

25
Q

What is the pathophysiology of iron poisoning?

A

Corrosive effects on GI tract
Cellular toxicity due to excess iron uptake
Metabolic acidosis from systemic hypoperfusion and uncoupling oxidative phosphorylation

26
Q

What investigations should you do for iron toxicity?

A

AXR - can estimate ingested dose
BM
U&Es
VBG/ABG
Serum iron level at 4-8hrs

27
Q

What is the management of iron poisoning?

A

Desferrioxamine 15mg/kg/h IVI; max 80mg/kg/d.

NB: gastric lavage if iron ingestion in last hour; consider whole-bowel irrigation if pills present past pylorus on AXR.

28
Q

What are the clinical features of digoxin poisoning?

A

Reduced cognition
Yellow-green visual halos
Arrhythmias
Nausea
Anorexia
Gynaecomastia

29
Q

How do you diagnose digoxin toxicity?

A

Plasma concentration 1.5-3mcg/L - more likely for toxicity to occur

NB Plasma concentration alone does not determine whether a patient has developed digoxin toxicity. Toxicity may occur even when the concentration is within the therapeutic range. The BNF advises that the likelihood of toxicity increases progressively from 1.5 to 3 mcg/l.

30
Q

What is the management of digoxin toxicity?

A

ABCDE
If serious arrhythmias are present, correct hypokalaemia

Inactivate with digoxin-specific antibody fragments (DigiFab®).

If load or level is unknown, give 20 vials (800mg)—adult or child >20kg.

31
Q

What factors may precipitate digoxin toxicity?

A

HYPOKALAEMIA - digoxin binds to the same ATPase pump as potassium. Hypokalaemia means the digoxin binds more easily so there are more inhibitory effects
Increasing age
Renal failure
MI
Hypomagnasaemia, hypercalcaemia, hypernatraemia, acidosis
Hypoalbuminaemia
Hypothermia
Hypothyroidism
Drugs - amiodarone, verapamil, diltiazem, ciclosporin, thiazide and loop diuretics.

32
Q

How do you diagnose lithium toxicity?

A

Lithium levels >1.5mmol/L - it has a very narrow therapeutic range (0.4-1.0 mmol/L) and a long plasma half-life being (renal excretion)

33
Q

What may precipiatate lithium toxicity?

A

Dehydration
Renal failure
Drugs - diuretics (thiazide), ACEi/ARB, NSAIDs , metronidazole

34
Q

What are the features of lithium toxicity?

A

coarse tremor (a fine tremor is seen in therapeutic levels)
hyperreflexia
acute confusion
polyuria
seizure
coma

35
Q

What is the management of lithium toxicity?

A

Mild-mod toxicity = normal saline
Severe toxicity = haemodialysis

NB: sometimes sodium bicarb is used as it is meant to alkalinise the urine so promote lithium excretion.

- Y6 Critical Care and Palliative Care (25 decks)

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