Paroxysmal supraventricular tachycardia associated with dexmedetomidine withdrawal in an adult liver transplant recipient: A case report

Abstract

BACKGROUND

Dexmedetomidine is a selective α₂-adrenergic receptor agonist widely used for sedation and anxiolysis in intensive care units (ICUs). Abrupt discontinuation after prolonged infusion may induce withdrawal symptoms because of sympathetic rebound. Although sinus tachycardia and hypertension are common manifestations, clinically significant tachyarrhythmias have rarely been reported in adults.

CASE SUMMARY

A woman in her 60 years was readmitted to the ICU for septic shock following liver transplantation. Prolonged high-dose dexmedetomidine infusion was required to manage sleep disturbance and anxiety. Two hours after abrupt discontinuation of dexmedetomidine, the patient developed paroxysmal supraventricular tachycardia that was refractory to adenosine triphosphate and landiolol. Reinitiation of dexmedetomidine promptly restored sinus rhythm, suggesting withdrawal-related sympathetic overactivity as the precipitating mechanism. Gradual tapering prevented recurrence.

CONCLUSION

Dexmedetomidine withdrawal should be considered in adult ICU patients presenting with unexplained tachyarrhythmia. Careful tapering and multimodal sedation strategies are essential when prolonged dexmedetomidine administration is anticipated.

Key Words: Paroxysmal supraventricular tachycardia; Dexmedetomidine withdrawal; Intensive care unit; Case report

Core Tip: Dexmedetomidine withdrawal in adults is often underrecognized owing to the absence of standardized diagnostic criteria. Although most reports have described hypertension and sinus tachycardia, this case demonstrates paroxysmal supraventricular tachycardia as a potentially severe manifestation. The arrhythmia was refractory to conventional antiarrhythmic therapy, including adenosine triphosphate and β-adrenergic antagonists, but resolved rapidly after dexmedetomidine reinitiation. Clinicians should carefully review medication timelines in unexplained intensive care unit arrhythmias and avoid abrupt discontinuation after prolonged high-dose dexmedetomidine infusion.

INTRODUCTION

Dexmedetomidine is a selective α₂-adrenergic receptor agonist that provides sedative, anxiolytic, analgesic-sparing, and sympatholytic effects[1]. Consequently, dexmedetomidine is widely used for sedation in intensive care units (ICUs). Compared with other sedatives, dexmedetomidine facilitates light sedation, improves patient-ventilator interaction, and is associated with a lower incidence of delirium, offering advantages during prolonged ICU management[2].

However, accumulating evidence suggests that abrupt reduction or discontinuation of dexmedetomidine after prolonged administration may result in withdrawal symptoms characterized by sympathetic hyperactivity. Reported manifestations include hypertension, tachycardia, hyperthermia, diaphoresis, nausea, vomiting, diarrhea, agitation, and altered mental status[3]. These phenomena are well described in pediatric ICU populations, for which validated assessment tools such as the Withdrawal Assessment Tool-1 (WAT-1) are available. In contrast, dexmedetomidine withdrawal in adults has been reported less frequently, and no standardized diagnostic criteria or assessment tools exist, making diagnosis challenging and largely dependent on the exclusion of alternative etiologies[4].

Cardiovascular manifestations of dexmedetomidine withdrawal in adults have predominantly been described as sinus tachycardia and hypertension. Clinically significant tachyarrhythmias have rarely been reported. In the ICU setting, where patients are exposed to multiple arrhythmogenic factors, including inflammation, electrolyte disturbances, autonomic instability, and polypharmacy, the contribution of dexmedetomidine withdrawal to supraventricular arrhythmias may be overlooked[5,6]. Here, we report a rare case of paroxysmal supraventricular tachycardia (PSVT) occurring after abrupt discontinuation of prolonged dexmedetomidine infusion in an adult patient following liver transplantation.

CASE PRESENTATION

Chief complaints

A woman in her 60 years (height 164 cm, weight 45 kg) with primary sclerosing cholangitis underwent living-donor liver transplantation. Sudden onset of persistent tachycardia during the ICU stay.

History of present illness

Her postoperative course was complicated by acute rejection and aspiration pneumonia. On postoperative day (POD) 54, she developed septic shock secondary to cholangitis and was readmitted to the ICU. Mechanical ventilation was initiated under sedation with propofol and dexmedetomidine. Hemodynamic stabilization was achieved using fluid resuscitation and vasopressors. On POD 57, the patient recovered from shock, allowing discontinuation of respiratory and vasopressor support.

Subsequently, the patient developed marked insomnia, anxiety, and depressive symptoms. Continuous infusions of dexmedetomidine and fentanyl were maintained to achieve a Richmond Agitation-Sedation Scale target between -1 and +1. Dexmedetomidine was gradually titrated upward, reaching a maximum infusion rate of 1.2 μg/kg/hour and a total daily dose of 16.7 μg/kg/day (Figure 1). No hypotension or bradycardia occurred, and repeated confusion assessment method for the ICU evaluations were negative for delirium.

Figure 1 Clinical course and dexmedetomidine administration during the intensive care unit stay. The upper panel shows hemodynamic parameters, including systolic and diastolic blood pressure (shaded area) and heart rate (solid line). The lower panel depicts dexmedetomidine dosing, showing the daily minimum and maximum infusion rates (μg/kg/hour). Paroxysmal supraventricular tachycardia developed immediately after abrupt discontinuation of dexmedetomidine on postoperative day 63, as indicated. Reinitiation of dexmedetomidine resulted in prompt rhythm conversion, followed by successful gradual tapering without recurrence. PSVT: Paroxysmal supraventricular tachycardia; POD: Postoperative day.

On POD 60, trazodone (12.5 mg) was introduced for sleep disturbance, while restricting further dexmedetomidine escalation.

History of past illness

No history of arrhythmia.

Personal and family history

The patient had no known history of arrhythmia or cardiovascular disease, and there was no relevant family history.

Physical examination

On POD 63, dexmedetomidine was abruptly discontinued from an infusion rate of 0.80 μg/kg/hour. Approximately two hours later, PSVT developed with a sustained heart rate of approximately 170 beats/minute, as confirmed by two intensivists. No hypotension was observed, and the patient remained alert throughout the episode.

Laboratory examinations

No significant electrolyte abnormalities were observed (Na 144 mEq/L, K 3.9 mEq/L, Cl 105 mEq/L, and Mg 1.9 mg/dL). Tacrolimus, used for immunosuppression, had been dose-reduced after septic shock, with a trough concentration of 3.2 ng/mL on the day of the event. The fentanyl infusion rate remained stable at 25 μg/hour.

Imaging examinations

Transthoracic echocardiography performed after the PSVT episode demonstrated normal left ventricular function, no significant valvular abnormalities, and no evidence of left atrial enlargement.

FINAL DIAGNOSIS

Paroxysmal supraventricular tachycardia associated with dexmedetomidine withdrawal.

TREATMENT

Intravenous adenosine triphosphate disodium hydrate (20 mg) was administered as a rapid bolus according to institutional practice in Japan. Transient asystole lasting several seconds was observed following the injection, with subsequent return to the PSVT rhythm. An intravenous bolus of landiolol (12 mg) was then administered; however, no rhythm conversion was achieved. Considering the temporal relationship with drug discontinuation, dexmedetomidine withdrawal was suspected. Continuous dexmedetomidine infusion was restarted at 0.4 μg/kg/hour, and sinus rhythm was restored approximately 20 minutes later. Thereafter, dexmedetomidine and landiolol (6.2 μg/kg/minute) were continued. Gradual tapering was initiated by reducing the dexmedetomidine dose by 0.04 μg/kg/hour every 24 hours. To manage persistent nocturnal wakefulness, trazodone (25 mg) and quetiapine (25 mg) were administered at bedtime, with lorazepam (0.5 mg) used as needed.

OUTCOME AND FOLLOW-UP

No arrhythmia requiring medical intervention recurred during tapering or after complete discontinuation. The patient was discharged from the ICU three months postoperatively.

DISCUSSION

Dexmedetomidine withdrawal in adults may present with clinically significant supraventricular tachyarrhythmias. In this case, the arrhythmia was resistant to standard antiarrhythmic therapy but resolved rapidly after dexmedetomidine reinitiation, strongly suggesting sympathetic rebound as the underlying mechanism.

In adults, the diagnosis of dexmedetomidine withdrawal is challenging because no validated assessment tool comparable to WAT-1 used in pediatric patients is available[4]. Consequently, diagnosis relies largely on excluding alternative etiologies such as infection, delirium, pain, electrolyte disturbances, or withdrawal from other sedatives or opioids. Although tacrolimus is not commonly recognized as a primary cause of supraventricular tachyarrhythmias, case reports have suggested an association between tacrolimus therapy and various arrhythmias, potentially mediated by electrolyte disturbances, QT prolongation, or autonomic effects[7]. In this case, sepsis had resolved, electrolyte levels were normal, opioid tapering was gradual, and tacrolimus trough concentrations were low, making these factors less likely contributors.

Importantly, supraventricular tachyarrhythmias generally require a triggering sympathetic surge and an underlying electrophysiological substrate, which may develop during critical illness through inflammation, volume overload, or prolonged ICU stay[5,6,8,9]. Abrupt dexmedetomidine withdrawal-associated sympathetic overactivity may therefore act as the final trigger for PSVT.

Previous studies have reported withdrawal symptoms in 30%-64% of ICU patients receiving prolonged dexmedetomidine infusion[10,11]. Higher maximum infusion rates (> 0.8 μg/kg/hour) and larger daily doses (> 12.9 μg/kg/day) have been suggested as potential risk factors[11]. In our patient, dexmedetomidine had been administered for eight days at doses exceeding these thresholds and was abruptly discontinued from a relatively high infusion rate, which may have contributed to withdrawal onset.

Prompt recognition of dexmedetomidine withdrawal is crucial because the condition is potentially reversible. In this case, conventional antiarrhythmic therapies were ineffective, whereas dexmedetomidine reinitiation rapidly restored sinus rhythm. Considering the lack of adult-specific treatment guidelines, management strategies are often extrapolated from pediatric practice, in which dexmedetomidine reinitiation followed by gradual tapering is effective[12]. A conservative tapering strategy for more than 10 days resulted in no recurrent arrhythmias requiring therapeutic intervention in our patient, underscoring the importance of avoiding abrupt discontinuation and incorporating multimodal sedation strategies when prolonged dexmedetomidine use is anticipated.

CONCLUSION

Dexmedetomidine withdrawal in adults may present with clinically significant tachyarrhythmia. In the absence of validated adult assessment tools, careful evaluation of medication timelines and the systematic exclusion of alternative etiologies are essential. In adult ICU patients receiving prolonged high-dose dexmedetomidine, abrupt discontinuation should be avoided. When unexplained tachyarrhythmia occurs, medication timelines should be carefully reviewed before escalating antiarrhythmic therapy.