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Acute and Emergency > TCA overdose > Flashcards

TCA overdose Flashcards

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1
Q

What are TCA’s?

A

Tricyclic antidepressants

Developed initially for severe depression

Now used commonly for neuropathic pain and migraine propyhlaxis

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2
Q

What are examples of TCA’s?

A

amitriptyline, nortriptyline and dosulepin.

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3
Q

What is the MOA of TCA’s?

A

Act on multiple neurotransmitter pathways to enhance the effects of certain hormones while inhibiting others.

Two main MOA’s:

  1. Reuptake inhibition:
    - Prevents the neurotransmitter from being transported back into the pre-synaptic neurone once released into the synaptic cleft.
    - Subsequently, the neurotransmitter remains in the synaptic cleft and continues to activate the postsynaptic receptor, increasing its effect.
    - Pathways affected: Serotonin (5-HT receptors), Noradrenaline (NA receptors)
  2. Postsynaptic receptor antagonism:
    - Prevents the neurotransmitter from activating the postsynaptic receptor, overall reducing its effect.
    - Pathways affected: Histamine (H1 receptors), A-1 Adrenoreceptors, Acetylcholine receptors
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4
Q

Which TCA’s are especially dangerous?

A

Amitriptyline and dosulepin (dothiepin)

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5
Q

What is the key mechanism by which TCAs achieve their antidepressant effects?

A

Inhibiting the reuptake of serotonin and noradrenaline.

However, the lack of specificity and effects on other pathways results in an extensive side effect profile and contributes to their toxicity in overdose.

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6
Q

What are the clinical manifestations of the different pathways?

A

Serotonin: nausea, gastrointestinal upset, sexual dysfunction

Noradrenaline: tachycardia, tremors

Antihistamine: sedation, weight gain

Anticholinergic: dry mouth, blurred vision, confusion, constipation, tachycardia, urinary retention

Alpha-1 adrenergic: postural hypotension, drowsiness, dizziness

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7
Q

what is the relation between TCAs and sodium?

A

TCAs act on the fast sodium channels in myocardial cells, resulting in sodium channel blockade and risk of cardiac arrhythmias, convulsions, and coma in overdose.

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8
Q

What are RFs for a TCA overdose?

A

Intentional OD
- Suicide attempt
- Self harm

Unintentional or Accidental OD
- Less common
- Risk in elderly with cognitive impairment who take more than prescribed dose
- Risk with child who may ingest meds when unattended

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9
Q

Are TCA’s toxic and what are their more severe effects?

A

Highly toxic

Most severe effects: cardiovascular and neurological instability

Narrow therapeutic window - so toxicity can be seen at low levels

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10
Q

When do the sx of OD become apparent?

A

Within 6 hrs

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11
Q

What are the key clinical features of TCA toxicity?

A

Signs of anticholinergic activity and result of sodium channel blockade

Severe effects: arrhythmia, cardiovascular collapse, convulsions and coma.

Typical sx:
- Dry mouth
- Hot, dry skin
- Confusion and hallucinations
- Palpitations

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12
Q

What are features of severe poisoning?

A

arrhythmias
seizures
metabolic acidosis
coma

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13
Q

What should you cover in a hx for TCA OD?

A

History of ingestion:
- How much ingested
- Calculation of mg/kg ingestion helpful prognostically.
- Mixed OD taken? Manage each substance individually
- PMHx
- Past psychiatric history

Collateral Hx
- If pt has reduced level of consciousness
- From family or paramedics
- Paramedics often bring empty medication boxes

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14
Q

What are ABCDE clinical signs of TCA OD?

A

Airway
- Airway compromise (snoring, secretions, low RR)

Breathing
- Respiratory depression

Circulation
- Hypotension and arrhythmia (due to myocardial sedum channel blockade)
- Tachycardia and vasodilation (due to serotonergic activity)
- ECG findings

Disability
- AVPU or GCS
- Can have seizure or coma
- Pts may present actively seizing or in postictal state
- Check glucose!!

Exposure
- Hyperthermic - due to serotonergic effects
- Anticholinergic signs - dry skin, eyes and mouth, urinary retention and ileum

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15
Q

What increases the risk of serotonin syndrome?

A

Co-ingestion with other medications which up-regulate serotonin

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16
Q

What is serotonin syndrome?

A
  • Potentially life-threatening presentation
  • Due to over activation of central and peripheral serotonin receptors
  • Causes by serotonergic drugs
17
Q

What are features of serotonin syndrome?

A
  • Altered mental state
  • Neuomuscular hyperactivity
  • Autonomic hyperactivity
  • HTN
  • Tachycardia
  • Diaphoresis
  • Myoclonus
  • Hyperreflexia
  • Severe: Hyperthermia, muscle rigidity
18
Q

How is serotonin syndrome managed?

A

Supportive

Benzodiazepines are often used for sedation

19
Q

What investigations are done in TCA OD? Why may they be done? What may they show?

A
  • Obs - tachycardia, hypotension, hyperthermia
  • ECG
  • Glucose - exclude hypoglycemia
  • Blood gas - mixed acidosis (requires bicarbonate as tx)
  • FBC - to establish baseline
  • U & E - hypokalaemia
  • Mg and bone profile - electrolyte disturbances can worsen arrhythmia
  • LFTs - if concerned re co-ingestion of other meds, esp paracetamol
  • Paracetamol and salicylate levels: typically checked in all patients
  • CXR - airway compromise, risk of aspiration pneumonia
  • CT head - pt has significantly reduced GCS, or seizures.
20
Q

What ECG changes may be seen?
What may they be a/w?

A

sinus tachycardia
widening of QRS
prolongation of QT interval

Widening of QRS > 100ms a/w increased risk of seizures

QRS > 160ms a/w ventricular arrhythmias

These rhythms predispose to VTach and VFib

21
Q

How may TCA OD be diagnosed?

A

Hx of ingestion and collateral hx

22
Q

How Is TCA OD managed?

A
  • No specific antidote
  • Activated charcoal if conscious and presenting within 1 hr of ingestion
  • Sodium bicarbonate in arrhythmia and acidosis to prevent ventricular arrhythmias
  • Resus and ABCDE

1st line : IV Bicarbonate

  1. Other drugs for arrhythmias
  2. IV lipid emulsion increasing used to bind free drug and reduce toxicity
23
Q

IV bicarbonate as a tx?

A

1st line for hypotension or arrhythmias

Indications:
- Widening of the QRS interval >100 msec
- Ventricular arrhythmia

24
Q

What drugs are contraindicated in tx and why?

A
  • Class 1a (e.g. quinidine) and class Ic antiarrhythmics (e.g. Flecainide)
  • They prolong depolarisation
  • Class III drugs such as amiodarone should also be avoided as they prolong the QT interval
  • Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in the management of tricyclic-induced arrhythmias
25
Q

What is the first line management of tricyclic induced arrhythmias?

A

Correction of acidosis

26
Q

Is dialysis effective?

A

No

dialysis is ineffective in removing tricyclics

27
Q

What are complications of TCA OD?

A

Untreated - can result in death secondary to cardiac or neurological effects.

Prolonged seizure activity can –> brain injury and coma.

Those with reduced consciousness are at risk of aspiration pneumonia if their airway is not managed effectively.

28
Q

What are the main toxic effects of TCAs?

A
  • Cardiovascular system (quinidine-like effect): TCAs competitively inhibit the myocardial fast sodium channels resulting in slowed cardiac conduction (e.g. increased QRS duration, prolonged QTc, increased PR interval, AV block) and ventricular dysrhythmias.
  • TCAs also inhibit peripheral alpha -adrenergic receptors, resulting in vasodilation and orthostatic hypotension.
  • Neurologic toxicity (seizures and anticholinergic stigmata) results from CNS receptor blockade
29
Q

Is gastric lavage useful in TCA OD?

A

Tricyclics delay gastric emptying so that lavage, or emesis in a child, followed by activated charcoal may be useful up to 12 hours after ingestion. Charcoal by itself may reduce absorption in patients presenting 12 to 24 hours after ingestion.

Acute and Emergency (17 decks)

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