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.