Clevidipine infusion for 69 hours in a 55-year-old man with hypertensive emergency caused serum triglycerides to rise from 148 mg/dL to 1,037 mg/dL, resolving after discontinuation.
Case Report (n=1)
No
Prolonged clevidipine infusion can cause severe hypertriglyceridemia due to its lipid emulsion vehicle, highlighting the need for serum triglyceride monitoring in critical care settings.
Abstract Background Clevidipine is an intravenous short acting dihydropyridine calcium channel blocker indicated for the management of severe hypertension when rapid blood pressure reduction is required, particularly when intravenous bolus therapy is inadequate. While Clevidipine is widely used in hypertensive emergencies, secondary hypertriglyceridemia remains a rarely reported and under-recognized adverse effect. The incidence of clevidipine-associated hypertriglyceridemia has been estimated at approximately 12%, though the frequency of resultant complications is unknown. To date, only a few published cases have described this association, highlighting the need for greater clinical awareness of this potential complication. Case Presentation A 55-year-old man with a history of cerebrovascular accident, hypertension, diabetes, and hyperlipidemia (baseline triglycerides 123 mg/dL) presented with severe right-sided headache, dizziness, and dysarthria. CT angiography revealed a new right vertebral artery (V4 segment) occlusion with distal reconstitution. Patient was admitted to the ICU for management of hypertensive emergency with concern for recurrent stroke and potential development of intracerebral edema following TNK administration. After multiple intravenous labetalol boluses failed to control blood pressure, a clevidipine infusion was initiated. Baseline triglycerides on admission were 148 mg/dL, which rose to 1,037 mg/dL (∼600% increase) after approximately 69 hours of Clevidipine infusion titrated up to 21 mg/hr. Following discontinuation of Clevidipine and initiation of Nicardipine, daily labs were obtained to monitor triglycerides levels and triglycerides downtrended to 460 mg/dL and later normalized to 172 mg/dL. The patient did not receive propofol and was maintained on enteral nutrition with Glucerna formula. Discussion Clevidipine provides rapidly titratable blood pressure control through selective arteriolar vasodilation and is hydrolyzed by blood and tissue esterases independent of hepatic or renal metabolism. However, its lipid emulsion formulation contains approximately 0.2 g of fat per mL (2 kcal/mL). Hypertriglyceridemia during clevidipine infusion has been described in isolated reports, particularly when used concurrently with other lipid-based infusions such as propofol. Reports of isolated clevidipine-induced hypertriglyceridemia without concurrent lipid infusions are exceedingly rare. Our patient’s rapid triglyceride rise and resolution after discontinuation strongly implicate clevidipine’s lipid load as the cause. Conclusion This case highlights the importance of monitoring serum triglycerides during prolonged clevidipine infusions. Clevidipine is an effective antihypertensive agent in critical care, but clinicians should recognize its lipid emulsion vehicle as a potential contributor to hypertriglyceridemia. Monitoring serum triglycerides, minimizing infusion duration, and avoiding concurrent lipid infusions can prevent complications such as pancreatitis. This abstract is funded by: None
Al-Zawahreh et al. (Fri,) conducted a case report in Hypertensive emergency (n=1). Clevidipine was evaluated on Serum triglyceride levels. Clevidipine infusion for 69 hours in a 55-year-old man with hypertensive emergency caused serum triglycerides to rise from 148 mg/dL to 1,037 mg/dL, resolving after discontinuation.