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Case report illustrates wooden chest syndrome from fentanyl causing respiratory failure, highlighting urgent management needs.
Introduction Fentanyl, commonly used for ICU sedation, can rarely cause Wooden Chest Syndrome with ventilatory failure from muscle rigidity. We report a case that resolved after stopping the infusion, underscoring the need for early recognition and prompt management. Case Presentation A 41-year-old man with recently diagnosed hypertension presented with three weeks of worsening abdominal pain and decreased urine output. Labs in the ED revealed hemoglobin 4.4 g/dL, creatinine 23 mg/dL, BUN 144 mg/dL, and ABG with pH 7.30, pCO2 26 mmHg. Imaging showed anasarca and bilateral pleural effusions. He was started on a Bumetanide infusion and admitted to the ICU.On hospital day two, he developed altered mental status requiring intubation. Initial ventilator settings were PRVC mode, tidal volume 450 mL, PEEP 5 cmH2O, FiO2 80%, peak pressure 20 cmH2O, plateau 19 cmH2O. Hemodialysis was initiated the same day.On day three, a rapid response was called for acute hypoxemia despite ventilator adjustments. He was found to have a rigid chest wall and tense abdomen. Peak and plateau pressures had risen to > 50 cmH2O and >45 cmH2O respectively. At the time, he was receiving fentanyl at 200 mcg/hr and propofol at 50 mcg/kg/hr. Manual ventilation was started. CXR showed appropriate ET tube placement and no pneumothorax. Bronchoscopy ruled out obstruction. Bladder pressure was 8 mmHg. After receiving rocuronium 50 mg, the patient’s ventilation improved.A similar episode occurred later that evening, prompting discontinuation of fentanyl. Following this, the patient’s ventilatory status stabilized with no further events. This case illustrates Wooden Chest Syndrome as a rare complication of fentanyl requiring prompt recognition and intervention. Discussion Wooden Chest Syndrome (WCS) is a rare complication of fentanyl, caused by CNS μ-opioid receptor activation leading to muscle rigidity and impaired ventilation. Rapid administration or prolonged high-dose infusion may trigger it. Clinical signs include rigid chest/abdominal muscles, hypoxia, and poor ventilator compliance. Standard ventilation may be ineffective. Diagnosis requires excluding other causes of high airway pressures. Treatment includes IV naloxone, neuromuscular blockers, and discontinuation of fentanyl.
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Rizvi et al. (2026) studied this question.
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