Published review articles describe Wooden Chest Syndrome (WCS), a combination of chest wall and diaphragm rigidity, often with laryngospasm, as essentially unique to fentanyl and fentanyl analogs. It can occur after intravenous, transdermal, or inhalational administration, with incidence and severity closely related to dose and speed of delivery. Human studies report WCS as a rare but clinically significant complication in perioperative or critical care settings, where it can reduce chest wall compliance, impair spontaneous ventilation, and complicate weaning from mechanical ventilation. Upper airway obstruction due to glottic or supraglottic closure may further contribute to respiratory compromise, highlighting the need for prompt recognition and management. Conversely, traditional opioids such as morphine may produce abdominal wall muscle rigidity at high doses but have not been shown to cause upper airway compromise in humans unless combined with anesthetic gases, and reports of morphine-induced laryngospasm are extremely rare. This supports that WCS is a fentanyl-specific phenomenon. Mechanistic studies in humans and animals indicate that rigidity is centrally mediated, involving noradrenergic, glutamatergic, dopaminergic, and serotonergic pathways, and is independent of classic opioid-induced respiratory depression. Rapid administration and higher doses increase the risk, underscoring the importance of careful dosing and monitoring in clinical practice. [1], [2]
In a 2022 multicenter phase IV study of 2,438 adults undergoing elective surgery under general anesthesia, patients received either intravenous remifentanil (0.5 mcg/kg/min for induction, followed by 0.25 mcg/kg/min infusion) or fentanyl per routine anesthesiologist practice, with transition analgesia using either morphine or fentanyl as appropriate. Muscle rigidity occurred only in the remifentanil group, with 4 outpatient cases (0.3% of all remifentanil-treated patients; 0.5% of outpatients), while no cases were observed with fentanyl. Other adverse event. including hypertension, bradycardia, respiratory depression, and apnea, were similar between groups. The authors noted that the low incidence of rigidity (0.3%) compared with previous reports (6-17%) likely reflected careful anesthetic technique, including avoidance of bolus dosing, lower infusion rates, and judicious use of anesthetic agents and muscle relaxants, particularly in outpatients. Overall, it was suggested that rigidity occurred exclusively in outpatients due to lighter anesthesia and reduced muscle relaxant use, highlighting the importance of dosing strategy and vigilance during induction. [3]