Abstract
<title>Abstract</title> <p>Rationale Octogenarian patients with multiple cardiovascular comorbidities undergoing transurethral prostatectomy under neuraxial anesthesia are susceptible to perioperative consciousness disturbances, which are frequently misdiagnosed as acute cerebrovascular events. Delayed severe lethargy induced by routine low-dose oxycodone remains rarely documented and poses great challenges to perioperative anesthetic management. This report systematically analyzes cumulative pharmacokinetic risks of oxycodone in a frail elderly patient with multimorbidity, and highlights the dual diagnostic and therapeutic significance of low-dose naloxone rescue. Patient Concerns An 84-year-old underweight male patient (50 kg, BMI 17.3 kg/m²) presented with progressive dysuria secondary to benign prostatic hyperplasia. His medical history included long-term poorly controlled hypertension, prior silent cerebral infarction, and ischemic cardiomyopathy with a left ventricular ejection fraction of 48% complicated by arrhythmia. Preoperative anxiety caused severe sleep deprivation, and fluid restriction was applied preoperatively due to cardiac insufficiency. After spinal anesthesia with ropivacaine and intraoperative intravenous oxycodone 3 mg, the patient developed intractable severe somnolence 2 hours postoperatively, with no verbal response but preserved pain reflexes. Diagnosis Relative oxycodone overdose caused by altered drug pharmacokinetics; mild postoperative hyponatremia (serum sodium 130 mmol/L); concurrent benign prostatic hyperplasia, grade 2 hypertension, ischemic cardiomyopathy, arrhythmia, and remote cerebral infarction. Acute cerebral infarction, intracranial hemorrhage, postoperative delirium, severe TURP syndrome, hypoglycemia and hypercapnia were fully excluded by cranial magnetic resonance imaging, blood gas analysis and clinical evaluation. Bilateral miosis confirmed opioid-mediated central nervous system suppression. Interventions A single low-dose intravenous naloxone (0.2 mg) was administered for diagnostic confirmation and reversal of opioid intoxication. Continuous monitoring of vital signs, neurological status, pupillary changes and serum electrolytes was maintained throughout observation. Fluid intake was strictly limited to prevent cardiac overload, and comprehensive supportive care was provided. Outcomes One hour after naloxone administration, the patient regained weak verbal response, with complete consciousness recovery and normalized pupillary size within 3 hours. No recurrent somnolence was observed on postoperative day 1; the patient recovered normal oral intake and ambulation, and was discharged on postoperative day 5. One-month telephone follow-up revealed intact self-care ability without permanent neurological sequelae. Lessons Advanced age, low body mass, and cardiac dysfunction-induced hepatic and hypoperfusion jointly slow oxycodone metabolism and excretion, triggering drug accumulation and relative overdose even at standard low doses. Preoperative sleep loss and mild hyponatremia synergistically potentiate central opioid inhibition, while intrathecal ropivacaine acts only as a mild auxiliary central depressant. For patients over 80 years old complicated with cardiac insufficiency and multiple comorbidities, intraoperative opioids should be initiated at minimal doses and titrated cautiously. Low-dose naloxone achieves balanced reversal without severe pain and sympathetic overexcitation, serving as an optimal diagnostic and therapeutic intervention for unexplained delayed postoperative somnolence.</p>