S5721 Acute Hypoxemic Respiratory Failure Following Dose Escalation of Terlipressin in a Patient With HRS-AKI

Introduction: Hepatorenal syndrome–acute kidney injury (HRS-AKI) is a life-threatening complication of cirrhosis. Terlipressin is favored as the first line treatment for HRS-AKI, but respiratory failure is a feared complication. While guidelines suggest dose escalation in partial responders, it is unclear if higher doses of terlipressin increase the risk of adverse events. We present a case of terlipressin-associated acute hypoxemic respiratory failure after dose escalation. Case Description/Methods: A 52-year-old woman with alcohol-associated liver disease and Roux-en-Y gastric bypass presented with hepatic encephalopathy. Labs were notable for creatinine 1.4 mg/dL (baseline 0.7 mg/dL), international normalized ratio (1.9), aspartate aminotransferase 142 U/L, alanine aminotransferase 42 U/L, and total bilirubin 2.5 mg/dL. Computed tomography imaging revealed hepatic steatosis, large volume ascites, and multifocal pneumonia. HRS-AKI was suspected, and she was treated with midodrine, octreotide, and albumin. Therapy was stopped after HRS-AKI resolution, but her creatinine subsequently worsened to 2.28 mg/dL, prompting re-initiation of the initial regimen. Her creatinine continued to worsen to 3.66 mg/dL, and with pneumonia resolved and the patient on room air, terlipressin 0.85 mg every 6 hours with albumin 12.5 g every 8 hours was initiated. On day 4 of therapy, with partial renal improvement, the terlipressin dose was escalated to 1.7 mg every 6 hours. Though the creatinine continued to improve, the patient developed acute hypoxemic respiratory failure with pulmonary edema the following day. Terlipressin was discontinued, the patient was intubated, and hemodialysis was initiated. Over the following week she was extubated, no longer required dialysis, and was later discharged. Discussion: Terlipressin is contraindicated in patients with hypoxia or respiratory distress and relatively contraindicated in those with creatinine >5 mg/dL. While our patient did not meet guideline criteria for withholding terlipressin, her recent pneumonia and relatively high creatinine may have placed her at increased risk for respiratory failure following dose escalation. The mechanism remains unclear but may be due to terlipressin-induced pulmonary venoconstriction or volume overload from concomitant albumin administration. This case highlights a potential dose-dependent relationship between terlipressin and acute hypoxemic respiratory failure and underscores the need for caution when escalating doses in patients with risk factors.