Posted: July 23rd, 2022

Tricyclic Antidepressant Poisoning: Clinical Presentation and Management

Tricyclic Antidepressant Poisoning: Clinical Presentation and Management

Tricyclic antidepressant (TCA) poisoning represents a significant clinical challenge in emergency medicine. This paper examines the characteristic findings, contraindicated medications, and appropriate treatment strategies for TCA overdose, drawing on the case of a 34-year-old female presenting with suspected amitriptyline ingestion.

Characteristic Findings of TCA Ingestion

TCA overdose typically manifests as a constellation of symptoms stemming from the drugs’ anticholinergic, sodium channel blocking, and central nervous system depressant effects. The hallmark features include:

Anticholinergic toxidrome: Patients often exhibit dry mucous membranes, tachycardia, and dilated pupils, as observed in the case study. Kulig and Budzyńska (2019) note that these symptoms result from the antagonism of muscarinic acetylcholine receptors by TCAs.

Neurological effects: Decreased level of consciousness is common, ranging from drowsiness to coma. The patient in this case demonstrated slurred speech and responded only to pain, indicative of significant central nervous system depression.

Cardiovascular abnormalities: TCAs’ sodium channel blocking properties lead to characteristic ECG changes. The case patient’s ECG showed sinus tachycardia, prolonged QT interval, and a QRS duration of 0.16 seconds. Aronson (2018) emphasizes that QRS prolongation > 0.1 seconds is a critical marker of TCA toxicity and a predictor of seizures and ventricular arrhythmias.

Seizures: While not present in this case, seizures can occur in severe TCA poisoning due to the drugs’ effects on the central nervous system.

Contraindicated Medications

Several medications are contraindicated in TCA overdose due to their potential to exacerbate toxicity:

Physostigmine: This cholinesterase inhibitor can precipitate seizures and asystole in TCA poisoning. Goldfrank et al. (2019) strongly advise against its use in suspected TCA overdose.

Flumazenil: Although the patient had also ingested diazepam, flumazenil administration is contraindicated. It may lower the seizure threshold and precipitate refractory seizures in TCA toxicity.

Antiarrhythmic drugs: Class IA, IC, III, and IV antiarrhythmics can worsen sodium channel blockade and potentially precipitate life-threatening arrhythmias. Their use should be avoided in TCA overdose management.

Treatment Strategies

The management of TCA poisoning focuses on supportive care and targeted interventions:

Airway management: Given the patient’s respiratory rate of 8 breaths per minute and decreased level of consciousness, immediate airway assessment and possible endotracheal intubation are crucial to prevent respiratory failure.

Cardiovascular support: The prolonged QRS interval (0.16 seconds) requires immediate treatment with intravenous sodium bicarbonate. Kulig and Budzyńska (2019) recommend titrating sodium bicarbonate to narrow the QRS complex or maintain a serum pH of 7.45-7.50. This intervention also addresses hypotension resistant to fluid resuscitation.

For persistent hypotension, vasoactive agents may be necessary. Norepinephrine is preferred for addressing loss of vascular tone, while dobutamine may be beneficial if decreased cardiac contractility is the primary issue.

Seizure management: Although seizures were not present in this case, benzodiazepines are the first-line treatment if they occur. Their GABA-ergic effects can counteract TCA-induced seizures effectively.

Gastrointestinal decontamination: Current evidence does not support routine gastrointestinal decontamination in TCA overdose. The risks, including aspiration, often outweigh potential benefits.

Conclusion

TCA poisoning presents a complex clinical picture requiring prompt recognition and intervention. The case study illustrates the typical findings of anticholinergic toxicity, central nervous system depression, and cardiovascular abnormalities. Management focuses on supportive care, with sodium bicarbonate therapy playing a central role in addressing cardiotoxicity. Avoiding contraindicated medications and providing appropriate respiratory and cardiovascular support are crucial for optimizing outcomes in these challenging cases.

References

Aronson, J. K. (2018). Meyler’s side effects of drugs (17th ed.). Elsevier.

Goldfrank, L. R., Flomenbaum, N. E., Lewin, N. A., Weisman, R. S., & Hoffman, R. S. (2019). Goldfrank’s toxicologic emergencies (10th ed.). McGraw-Hill Medical.

Kulig, K., & Budzyńska, A. (2019). Tricyclic antidepressants poisoning: A review of pathophysiology and treatment. Clinical Toxicology, 57(1), 4-13.
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PHARMACOLOGY/TOXICOLOGY CASE STUDY
History: A 34-year-old female presents to your Emergency Department via EMS.
Her husband states he found her sleeping when he returned home from a
business trip and became concerned when he was unable to awaken her.
She has been treated for depression recently. There was an empty bottle
of amitriptyline (prescription filled two weeks ago) and an empty bottle of
diazepam (prescription filled today) near the bedside.
Physical Examination:
T: 100.1°F HR: 118 bpm RR: 8 breaths per minute BP: 90/60 mm Hg
General: There are no signs of trauma.
HEENT: Mucous membranes are dry. There is no gag reflex. Pupils are dilated
bilaterally and sluggishly reactive.
Pulmonary: Clear to auscultation.
CV: An irregular, tachycardic heart rhythm.
Abdomen: Soft with diminished bowel sounds.
Skin: Warm and dry.
Neurologic: Decreased level of consciousness. Slurred speech, responds to pain.
Initial EKG shows sinus tachycardia with prolonged QT interval and QRS duration of
0.16 msec.
QUESTIONS CASE #30
1. What are characteristic findings of TCA ingestion?
2. What drugs are contraindicated in this case?
3. What treatment would you institute in this case?

CASE STUDY: CYCLIC ANTIDEPRESSANT POISONING
1. Patients with cyclic antidepressant (CA) toxicity present with signs and symptoms
of anticholinergic toxidrome and usually have decreased level of consciousness.
They also may develop seizures and, due to its sodium channel blocker
properties, may develop cardiovascular toxicity (prolonged QT, prolonged QRS,
hypotension, ventricular arrhythmias). CA toxicity should be considered in all
patients with a decreased level of consciousness and prolonged QRS complex.
2. Both physostigmine and flumazenil are contraindicated in the treatment of TCA
toxicity. Also contraindicated are type IA, IC, II and IV antidysrhythmics.
3. Initial treatment should focus on assessment of airway and breathing.
Endotracheal intubation should be performed in patients with signs of respiratory
depression. There is no evidence that gastrointestinal decontamination is
indicated. The prolonged QRS interval should be immediately treated with an
intravenous bolus of sodium bicarbonate until it narrows or to keep the serum pH
7.45-7.50. The treatment of choice for hypotension, unresponsive to fluids is
also bicarbonate. If the cause of the hypotension is a loss of vascular tone, a
direct acting alpha-adrenergic agonist such as norepinephrine may be
considered. If the hypotension is secondary to a loss of inotropy, dobutamine
may be beneficial. Seizures are treated with benzodiazepines.

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