QTc Interval Prolongation Associated with Citalopram Overdose: A Case Report and Literature Review

Catalano, Glenn; Catalano, Maria C.; Epstein, Melissa A.; Tsambiras, Petros E.

doi:10.1097/00002826-200105000-00007

Cited by 73 publications

(29 citation statements)

References 12 publications

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“…The use of the Naranjo adverse drug reaction probability scale (10) indicated a probable relationship (score of 5) between the TdP observed and moxifloxacin therapy in this patient. Citalopram has also been reported to prolong the QTc interval, but this occurs only at toxic doses (11). Our patient used citalopram at a low dose for a long time before the event, and it did not cause any QTc prolongation itself; therefore; we think that citalopram was not responsible for the TdP, but it might have assisted in its development.…”

Section: Discussionmentioning

confidence: 60%

Torsade de pointes associated with moxifloxacin: A rare but potentially fatal adverse event

Altın

Özcan

Turhan

et al. 2007

Canadian Journal of Cardiology

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A long QT interval, which is the surface electrocardiogram (ECG) manifestation of a prolonged repolarization phase, is associated with an increased risk of torsade de pointes (TdP). If transient, it may present with syncope, and if is not transient, it may cause sudden death. A long QT interval may be congenital or acquired. The most common cause of an acquired long QT interval is drug administration (1). The drugs that interfere with potassium influx, commonly by blocking the human ether-a-go-go-related gene channel-dependent potassium current (as with fluoroquinolones) in myocyte membranes produce a prolongation of the corrected QT (QTc) interval and increase the risk of spontaneous arrhythmia generation (2). Fluoroquinolones have been reported to prolong the QTc interval and precipitate TdP in patients at high risk (1,3). We present a patient with bradycardia who developed TdP during oral moxifloxacin therapy for pneumonia. CASE PRESENTATIONAn 87-year-old woman with hypertension, chronic renal failure and dementia was admitted to the emergency department with presyncope. Junctional rhythm with a rate of 30/min was present on ECG, and the QT interval was 0.66 s; the QTc interval, according to Bazett's formula, was 0.47 s (Figure 1). There were no previous ECGs performed. Medications she was using at the time of admission included ginkgo glycosides (19.2 mg/day), valsartan 80 mg plus hydrochlorothiazide (12.5 mg/day), acetylsalicylic acid (100 mg/day) and citalopram (20 mg/day). Her serum creatinine level was 283 μmol/L and potassium level was 4.2 mmol/L at admission. Other biochemical tests were normal. A temporary transvenous cardiac pacemaker was implanted and set to a rate of 60 beats/min. The pacemaker was turned off 24 h after the implantation because sinus rhythm resumed, but it was left in place in case of bradycardia. On that day, 400 mg/day oral moxifloxacin was prescribed to the patient for aspiration pneumonia. At the beginning of moxifloxacin treatment, the rhythm was normal, with normal QT (0.40 s) and QTc (0.43 s) intervals at a heart rate of 68 beats/min. The patient was transferred to the intensive care unit for telemetric follow-up due to the possible recurrence of symptomatic bradycardia. Intermittant junctional rhythms were observed on the monitor, but sinus rhythm was dominant. On the fourth day of moxifloxacin therapy, TdP developed following a short-long-short sequence of junctional rhythm (Figure 2) and recovered spontaneously after 36 s. The QT interval on the ECG taken on the same Torsade de pointes occuring due to a long QT interval is a rare but potentially fatal arrhythmia. Acquired long QT develops most commonly because of drugs that prolong ventricular repolarization. It has been reported that fluoroquinolone antimicrobials prolong the corrected QT interval but rarely cause torsade de pointes. A patient with torsade de pointes risk factors (female sex, advanced age, extreme bradycardia and renal failure) who developed the condition on the fourth day of 400 mg/day of oral moxifloxa...

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Section: Discussionmentioning

confidence: 60%

Torsade de pointes associated with moxifloxacin: A rare but potentially fatal adverse event

Altın

Özcan

Turhan

et al. 2007

Canadian Journal of Cardiology

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“…There were several level 4 or 6 articles with individual case information presented in detail. Specifically, there were 12 cases reported in 11 articles (42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52). Among them, the lowest dose of citalopram associated with any toxicity was 400 mg, which was reported to be associated with severe toxicity in at least two adults (42,47).…”

Section: Citaloprammentioning

confidence: 99%

Selective serotonin reuptake inhibitor poisoning: An evidence-based consensus guideline for out-of-hospital management

Nelson

Erdman

Booze

et al. 2007

Clinical Toxicology

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American Association of Poison Control Centers, Washington, District of Columbia, USAA review of US poison center data for 2004 showed over 48,000 exposures to selective serotonin reuptake inhibitors (SSRIs). A guideline that determines the conditions for emergency department referral and prehospital care could potentially optimize patient outcome, avoid unnecessary emergency department visits, reduce health care costs, and reduce life disruption for patients and caregivers. An evidencebased expert consensus process was used to create the guideline. Relevant articles were abstracted by a trained physician researcher. The first draft of the guideline was created by the lead author. The entire panel discussed and refined the guideline before distribution to secondary reviewers for comment. The panel then made changes based on the secondary review comments.The objective of this guideline is to assist poison center personnel in the appropriate out-of-hospital triage and initial management of patients with a suspected ingestion of an SSRI by 1) describing the process by which an ingestion of an SSRI might be managed, 2) identifying the key decision elements in managing cases of SSRI ingestion, 3) providing clear and practical recommendations that reflect the current state of knowledge, and 4) identifying needs for research. This guideline applies to ingestion of immediate-release forms of SSRIs alone. Co-ingestion of additional substances might require different referral and management recommendations depending on their combined toxicities.This guideline is based on an assessment of current scientific and clinical information. The expert consensus panel recognizes that specific patient care decisions may be at variance with this guideline and are the prerogative of the patient and the health professionals providing care, considering all of the circumstances involved. This guideline does not substitute for clinical judgment.Recommendations are in chronological order of likely clinical use. The grade of recommendation is in parentheses. 1) All patients with suicidal intent, intentional abuse, or in cases in which a malicious intent is suspected (e.g., child abuse or neglect) should be referred to an emergency department. This activity should be guided by local poison center procedures. In general, this should occur regardless of the dose reported (Grade D). 2) Any patient already experiencing any symptoms other than mild effects (mild effects include vomiting, somnolence [lightly sedated and arousable with speaking voice or light touch], mydriasis, or diaphoresis) should be transported to an emergency department. Transportation via ambulance should be considered based on the condition of the patient and the length of time it will take the patient to arrive at the emergency department (Grade D). 3) Asymptomatic patients or those with mild effects (defined above) following isolated unintentional acute SSRI ingestions of up to five times an initial adult therapeutic dose (i.e., citalopram 100 mg, escitalopram 50 mg, fluox...

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“…In contrast to the premarketing data, however, the postmarketing literature contains multiple case reports demonstrating that citalopram may produce significant cardiac toxicity in overdose [6][7][8][9][10]. It is postulated that a metabolite, didesmethylcitalopram, inhibits cardiac K + and Ca 2+ channels [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Citalopram overdose: Late presentation of torsades de pointes (TdP) with cardiac arrest

2008

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QTc Interval Prolongation Associated with Citalopram Overdose: A Case Report and Literature Review

Cited by 73 publications

References 12 publications

Torsade de pointes associated with moxifloxacin: A rare but potentially fatal adverse event

Torsade de pointes associated with moxifloxacin: A rare but potentially fatal adverse event

Selective serotonin reuptake inhibitor poisoning: An evidence-based consensus guideline for out-of-hospital management

Citalopram overdose: Late presentation of torsades de pointes (TdP) with cardiac arrest

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