C49-42 Fentanyl-Induced Chest Wall Rigidity (“Wooden Chest Syndrome”) Following Brainstem Surgery: A Rare ICU Complication

Abstract Introduction Fentanyl is a widely used ICU sedative and analgesic. A rare but life-threatening complication is chest wall rigidity, or “wooden chest syndrome” (WCS), which can cause ventilatory failure. Most reports describe rapid bolus administration; prolonged high-dose infusion-related cases, particularly after neurosurgery, remain underrecognized. Case Report A 49-year-old man with hypertension, obstructive sleep apnea, and diabetes presented with progressive dysphagia. MRI revealed a cystic medullary hemangioblastoma. He developed aspiration-related respiratory failure and was intubated with etomidate and rocuronium, then sedated with fentanyl (25 mcg/hr) and propofol (30 mcg/kg/min). Initial ventilation was stable with satisfactory arterial blood gases. Following suboccipital craniotomy and C1 laminectomy, sedation was escalated for agitation: fentanyl 175 mcg/hr and propofol 35 mcg/kg/min. Approximately 10 hours later, the patient developed acute ventilator dyssynchrony, decreased tidal volumes, and markedly reduced chest wall compliance. ABG showed severe hypercapnia (pH 7.20, PaCO2 68 mmHg, PaO2 232 mmHg). Despite increasing inspiratory time and pressure, compliance did not improve. Physical exam revealed board-like thoracoabdominal rigidity without wheezing or bronchospasm. Suspecting fentanyl-induced rigidity, the infusion was discontinued, and midazolam (1 mg/hr) initiated. Rocuronium (100 mg) was administered, producing immediate improvement in ventilator synchrony and chest wall compliance. Over the next 18 hours, ventilatory parameters normalized and repeat ABG showed full correction (pH 7.42, PaCO2 41 mmHg, PaO2 109 mmHg). No other sedatives or metabolic factors explained the acute rigidity. Discussion This case underscores an unusual presentation of WCS triggered not by bolus dosing but by sustained high-dose fentanyl infusion in the setting of recent brainstem surgery. The mechanism is believed to involve μ-opioid-mediated inhibition of brainstem GABAergic pathways, leading to unopposed excitatory outflow and skeletal muscle rigidity. Recognized risk factors include high cumulative opioid dose, concurrent sedatives, and neurologic disease—all present here. The neurologic substrate (brainstem mass and surgery) may have further lowered the threshold for WCS. Conclusion Fentanyl-induced WCS should be suspected in ICU patients with unexplained ventilator dyssynchrony and decreased chest wall compliance—even in the absence of rapid bolus dosing. Our case highlights the unique vulnerability of neurosurgical patients, in whom subtle ventilatory changes may be misattributed to neurologic status rather than opioid effect. Heightened awareness, immediate fentanyl discontinuation, and neuromuscular blockade are lifesaving. This abstract is funded by: none