Possible central anticholinergic syndrome following transdermal scopolamine in an ambulatory surgery patient

To the Editor, We share an interesting case wherein use of a scopolamine transdermal patch for postoperative nausea and vomiting (PONV) prophylaxis may have contributed to the delayed emergence of an ambulatory surgery patient. The patient gave written consent for publication of this article. A 28-yr-old female (height 1.65 m, weight 90 kg) with a history of obsessive-compulsive disorder treated with citalopram presented for elective outpatient ankle arthroscopy. On a previous occasion, she had experienced severe PONV following a similar procedure performed under general anesthesia. A decision was made to administer a regional technique (sciatic and saphenous nerve blocks) combined with an intravenous general anesthestic using propofol. In the preoperative holding area, a transdermal scopolamine patch 1.5 mg was placed behind the patient’s left ear for additional PONV prophylaxis. Following application of routine monitors and block placement, the patient was administered propofol 200 lg kg min iv which was titrated down to 150 lg kg min during the procedure. Oxygen was administered via nasal cannula at 2 L min while ventilation was monitored via capnography. For additional PONV prophylaxis, dexamethasone 8 mg iv and later ondansetron 4 mg iv were administered intraoperatively. After approximately 45 min of surgery, the patient’s heart rate began to increase (from 80 beats min baseline to 110 beats min), and fentanyl 100 lg iv was administered slowly for suspected pneumatic tourniquet pain. Following completion of the one-hour procedure and deflation of the tourniquet, the patient’s heart rate remained elevated. Administration of propofol was discontinued approximately 15 min prior to room departure, and she was moved to the recovery area with continued monitoring while breathing spontaneously—though unresponsive to either verbal or tactile stimulation. Ten minutes after her arrival in the postanesthesia recovery unit, the patient remained unresponsive with an elevated heart rate of 140 beats min and blood pressure of 120/70 mmHg. The patient’s oxygen saturation was 100% with nasal cannula oxygen, and on examination, her pupils revealed bilateral mydriasis, nearly unresponsive to light, and a disconjugate gaze. A gag reflex was also present. Over the next 30 min, blood gas, electrolyte, and blood glucose readings were ordered, with normal results, while her electrocardiogram showed sinus tachycardia. Consideration was given to the possibility of central anticholinergic syndrome, and the scopolamine patch was removed after being in place for approximately two hours. Our hospital’s internal medicine colleagues, who had been notified relatively early in the case, had begun preparations for further neurological evaluation, workup, and intensive care unit admission. A decision was made to administer physostigmine for possible diagnostic and therapeutic intervention. Over the next 30 min, physostigmine 1.5 mg iv was administered in 0.5 mg increments. Within minutes of administering the last 0.5 mg dose, the patient became responsive and followed commands. Her blood pressure remained stable while her heart rate decreased to her baseline. The patient was admitted to hospital overnight for observation, and she was discharged the next morning with complete resolution of the suspected anticholinergic signs and without further sequelae. J. A. Norton, DO (&) B. Khabiri, DO F. L. Arbona, MD A. J. Kover, MD The Ohio State University, Columbus, OH, USA e-mail: john.norton@osumc.edu