An International Publisher for Academic and Scientific Journals
Author Login
Scholars Journal of Medical Case Reports | Volume-14 | Issue-09
Catecholamine-Refractory Vasoplegic Shock and Severe Abdominal Pain During Remimazolam Sedation in a Patient Receiving Capecitabine Chemotherapy: A Case Report and Literature Review
Se Rom Song, Sein Kwak, Hyun Joo Heo, Ji Hye Lee
Published: Sept. 9, 2026 |
10
9
Pages: 1973-1976
Downloads
Abstract
Refractory vasoplegic shock during procedural sedation poses a life-threatening challenge in perioperative medicine [1, 8]. Capecitabine, an oral prodrug of 5-fluorouracil (5-FU), is widely prescribed for gastrointestinal malignancies [2]. While fluoropyrimidine-induced coronary vasospasm is well recognized, its contribution to catecholamine-refractory vasoplegic shock remains poorly understood [2, 3]. A 73-year-old female with underlying diabetes mellitus, hypertension, and gallbladder cancer receiving adjuvant oral capecitabine underwent right foot extensor tendon repair under peripheral nerve block (PNB) and remimazolam sedation. Ten minutes following remimazolam administration, she developed sudden, profound hypotension (blood pressure < 50/30 mmHg). The hypotension was completely refractory to repeated boluses and continuous infusions of ephedrine, epinephrine, and norepinephrine, as well as 20% lipid emulsion (administered for suspected local anesthetic systemic toxicity [LAST]) and intravenous volume expansion. High-dose intravenous corticosteroids (methylprednisolone) were administered for suspected anaphylactic shock or acute relative adrenal insufficiency [5, 6]. The patient continuously complained of severe abdominal pain. Focused abdominal ultrasound, electrocardiography, and arterial blood gas analyses ruled out intra-abdominal hemorrhage, acute myocardial infarction, and severe metabolic acidosis. Hemodynamics spontaneously normalized in the intensive care unit (ICU) approximately 10 hours postoperatively. Capecitabine was held, and she was discharged without end-organ sequelae. Concurrent capecitabine therapy may induce subclinical vascular smooth muscle dysfunction and α_1-adrenoceptor desensitization [3]. When unmasked by remimazolam sedation [4], this state can trigger severe vasoplegic shock refractory to conventional catecholamines [1]. Early administration of stress-dose corticosteroids [6] and consideration of non-adrenergic vasopressors (e.g.,


