S3552 Navigating the Risks of Rescue Therapy: A Case of High-Dose Tigecycline (TGC)-Induced Pancreatitis

Introduction: Tigecycline (TGC) is a broad-spectrum antibiotic used for multidrug-resistant infections, including carbapenem-resistant Acinetobacter baumannii (CRAB). While gastrointestinal side effects are common, acute pancreatitis is a rare adverse reaction. We report a case of TGC-induced pancreatitis in a critically ill patient. Case Description/Methods: A 55-year-old woman with a complex medical history—including hemorrhagic stroke with craniotomy, chronic respiratory failure requiring tracheostomy and mechanical ventilation, primary adrenal insufficiency on hydrocortisone, and multiple thromboembolic events—presented from a skilled nursing facility with fever and vomiting. Initial evaluation revealed leukocytosis (WBC 13.9 × 10⁹/L), elevated procalcitonin (0.48 ng/mL), and bilateral interstitial infiltrates on chest imaging. Blood and urine cultures were negative, but sputum culture grew CRAB. Empiric broad-spectrum antibiotics were escalated to high-dose TGC (200 mg loading dose followed by 100 mg every 12 hours) and cefiderocol. The patient subsequently developed worsening leukocytosis (WBC 45 × 10⁹/L), hypotension requiring intensive care unit transfer, and acute kidney injury. Six days after TGC initiation, she developed nausea, vomiting, and a marked elevation in serum lipase (2132 U/L). Computed tomography imaging confirmed acute pancreatitis with diffuse peripancreatic inflammation but no necrosis or fluid collections, compared to a normal pancreas on computed tomography abdomen 8 days earlier. Alternative etiologies—including gallstones, alcohol use, hypertriglyceridemia, trauma, and other medications—were ruled out. TGC was identified as the most likely cause and was promptly discontinued. Discussion: TGC-associated pancreatitis is a rare but potentially life-threatening adverse effect. While the mechanism remains unclear, proposed theories include direct cytotoxicity and biliary excretion-related pancreatic injury. High-dose regimens may increase this risk, particularly in patients with multiple comorbidities or organ dysfunction. In this case, the temporal correlation between high-dose TGC initiation and symptom onset, the exclusion of other causes, and clinical improvement following drug discontinuation support a diagnosis of TGC-induced pancreatitis. Clinicians should remain vigilant for this adverse event, especially in critically ill patients receiving high-dose or prolonged TGC therapy. Early recognition and prompt withdrawal are essential to mitigate morbidity.