Case Report

Open Access

Volume 1 | Issue 1

Terlipressin Induced Cardiac Arrest: A Case Report

Mads J Niemann and Abbas A Qayyum

Received: May 03, 2019

Accepted: May 22, 2019

Published: May 24, 2019

Introduction

Increased portal venous pressure causes esophagus varices, mostly due to liver cirrhosis. Esophagus varices have a potential risk of bleeding and an acute esophageal bleeding is associated with a 20-50% mortality [1]. The guideline of World Gastroenterology Organization for treatment of bleeding esophagus varices has terlipressin-infusion as first-line of pharmacological therapy followed by gastroscopic banding of the bleeding site during the first 12 hours of hospitalization [2]. Terlipressin has been showed to reduce mortality, rebleeding and failure of hemostasis [3]. However, only a few case reports have been published about the serious side effect of terlipressin infusion resulting in cardiac arrhythmia (Table 1).

Terlipressin

The prodrug terlipressin used to treat esophagus varices is cleaved enzymatic to lysinvasopressin, a synthetic antidiuretic hormone. Approximately, 30 min after intravenous injection of terlipressin, lysinvasopressin can be detected in plasma and maximum concentration occurs after 1-2 hours. Terlipressin has a plasma half-life of 40 min and is 99% metabolized by peptidases. The effect of terlipressin is primarily vasoconstrictive on vascular smooth muscles in the portal and splanchnic circulation, which is mediated by V_1a receptors. This causes a decrease in esophageal venous blood pressure and thus the clinically required effect - hemostasis. However, terlipressin can increase systemic mean arterial pressure, which is also mediated by V_1a receptors. The increased pressure can trigger a decrease in heart rate mediated by glomus caroticum. This bradycardic effect can further be amplified by all drugs known to cause bradycardia [4-8].

Case Presentation

A 34-years-old unmedicated female known with anorexia, chronic alcoholism, liver cirrhosis and esophagus varices grade 1-2 was admitted to the emergency department due to upper gastrointestinal bleeding. Initially 2 mg terlipressin was administrated intravenously every 4 hours. Terlipressin infusion had no hemodynamic effect on the patient. On the second day gastroscopy confirmed bleeding esophagus varix, which was banded. After 36 hours of hemostasis, terlipressin was reduced to 1 mg every 4 hours. On the third day of hospitalization, the patient was found with unwitnessed cardiac arrest. 30 min previously, she had received 1 mg of terlipressin intravenously. Cardiopulmonary resuscitation according to European resuscitation guidelines was immediately started. Initial rhythm was ventricular fibrillation. All seven assessments of rhythm showed ventricular fibrillation. Return of spontaneous circulation (ROSC) occurred after 25 min of resuscitation. Bedside transthoracic echocardiography showed left ventricle ejection fraction on 50%, general myocardial hypokinesia but no sign of cardiac tamponade or dilated right ventricle. ECG post-ROSC showed global ST-depressions (Figure 1A) but normalized quickly in serial ECG taken 15 min and 25 hours after ROSC (Figure 1B and Figure 1C). Prolonged QT interval (QTc 580 ms) was seen 25 hours after ROSC (Figure 1C). Troponin I was measured to 170 ng/L (reference 24 ng/L) 2 hours after ROSC, reached a maximum on 515 ng/L, 7 hours after ROSC and decreased afterwards. Clinically, there was no suspicion of an acute myocardial infarction, and ECG and troponin changes were considered related to cardiopulmonary resuscitation. Chest x-ray was without any pathology. Terlipressin was discontinued.

At the time of admission, the patient was slightly hypokalemic with a potassium on 3.3 mmol/L (reference 3.5-4.6 mmol/L). Supplements were administered. On the day of cardiac arrest, potassium had decreased to 2.1 mmol/L. Post-ROSC, the patient had hypomagnesemia on 0.64 mmol/L (reference 0.70-1.10 mmol/L) and supplements were given. Terlipressin was discontinued. The patient was transferred to intensive care unit without any new arrhythmias but died two weeks later due to hepatic encephalopathy.

Discussion

Terlipressin is known to induce QT prolongation. This may be enhanced by electrolyte abnormalities and by medication known to prolong QT interval. This case report illustrates the importance of measurement of electrolytes at the time of admission along with observation of patient during and after administration of terlipressin. The administration of terlipressin, the hypokalemia and hypomagnesemia might all be either cause or a contributor to ventricular fibrillation. In high-risk patients, cardiac monitoring should be considered.

Conflicts of Interest

None declared.

Source of Funding

None declared.

References

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