Discussion
Although UAO can develop as a manifestation of PD,1 it seemed necessary to rule out other causes of UAO in this patient. First, anesthesia- or opioid-related respiratory depression or UAO was unlikely because the patient showed adequate respiration, alertness, and responsiveness before extubation. Second, UAO due to alterations in the upper airway anatomy caused by cervical spine surgery3 was unlikely because of no finding of upper airway stenosis on cervical spine X-rays taken before extuabation. Therefore, it was likely that UAO developed as a manifestation of PD.1
The patient had taken the last antiparkinson drugs 13 hours before anesthesia. The withdrawal of drugs might be long enough to diminish their effects, thereby causing UAO. Reportedly, duration of action of levodopa-carbidopa to reduce motor disability lasts as short as 3 to 6 hours.4, 5 After a 12-hour withdrawal of antiparkinson drugs, a significant change in the spirometry indicative of UAO occurs in a substantial number of PD patients,6, 7 which is reversed by levodopa.6 Especially, PD patients exhibiting laryngopharyngeal motor dysfunction, indicated mainly by hypophonia, after a 12-hour drug withdrawal have a threefold greater chance of presenting with obstructive sleep apnea (OSA) unrelated to obesity, neck circumference, or the Mallampati score, compared with those without such dysfunction.7 Episodes of severe UAO that were successfully reversed by antiparkinson drugs, including levodopa, have been reported.8-10 These data suggest that in our patient, daily antiparkinson drugs should have been continued perioperatively or replaced by intravenous levodopa to minimize the risk of developing UAO and subsequent NPPE.
In our patient, UAO and NPPE improved with HFNC without a resumption of antiparkinson drugs. HFNC is able to deliver a consistent oxygen supply to the alveoli by constantly applying positive pressure, enabling the patient to maintain a high level of oxygen supply.11Further, generation of PEEP helps in reduction of anatomical dead space, carbon dioxide washout, recruitment of collapsed alveoli, and ultimate improvement in oxygenation.11 Through such effects, HFNC improves pulmonary edema.11 In addition, HFNC improves UAO in patients with OSA.12 Therefore, our experience also suggests that HFNC is effective in improving UAO and subsequent NPPE in patients with PD.