Discussion
This study investigated the effect of UPPP surgery for OSA on laryngeal
reflux symptoms based on patient responses to the RSI and RFS
questionnaire. We found (1) a close correlation between OSA and LPR: LPR
are more prevalent in OSA patients than the general population and the
degree of AHI and CT90 were positively and L-SpO2 negatively related
with LPR symptoms. (2) UPPP surgery,
especially
successful surgery significantly lowered not only in terms of the mean
RSI and mean RFS scores but also individual variables of RSI.
The coexistence of OSA with LPR has been reported to have a prevalence
of 20%–67%.11, 12 Although previous studies were
unable to demonstrate a direct relationship between OSA and LPR, they
did suggest a possible causative relationship between
them.13 Our study indicated OSA patients had higher
RSI and RFS than non-OSA patients. RSI and RFS of severe OSA patients
were higher than mild to moderate OSA. The degree of AHI and CT90 were
positively and L-SpO2 negatively related with LPR symptoms. All these
means the degree of OSA is associated with the severity of LPR and there
is a close correlation between OSA and LPR.
Interreaction
of OSA and LPR can explain our results. OSA causes inflammatory injury,
low intrathoracic pressure and leakage of lower esophageal sphincter; in
turn, LPR (Acid reflux) results in esophagus,
larynx, and pharynx mucosal injury and laryngopharyngeal symptoms.
Some studies report that anti-reflux therapy on OSA patients improve the
symptoms and PSG parameters of OSA.14 At the same
time, other studies report that CPAP can reduce GER events and improve
nocturnal GER symptoms in OSA patients.10, 11 But few
studies have reported the effect of OSA surgery on
LPR.15 UPPP is not the first choice of treatment in
most OSA patients
compared
to CPAP. If CPAP is refused or obstructive plane is definite, surgery
can be considered for OSA,
especially
multilevel surgery. UPPP can achieve favorable result when airway
obstruction
only at the level behind palate, and our study included participants
whose block plane in the oropharynx. The present study demonstrated
post-operative AHI, nighttime SpO2 (CT90 and L-SpO2), RSI and RFS got a
great improvement. Interestingly, the mean postoperative RSI and RFS in
successful surgery group showed significant decrease, but there just one
significant difference (mean RFS) occurred in unsuccessful group. We
proposed successful UPPP surgery lowered RSI and RFS scores;
unsuccessful surgery just improved RFS.
In the study, we supposed that effective UPPP could improve LPR symptoms
and signs via three ways. Firstly, UPPP solves the problem of
OSA-induced inflammatory injury via reducing airflow obstruction and
increasing nocturnal blood oxygen saturation. Published studies have
proposed that mouth breathing and snoring aggravates pharyngeal
inflammation and LPR, and chronic intermittent hypoxia can lead to
systemic inflammation of
the whole body
and respiratory in OSA.16-18 Secondly, successful UPPP
lowers OSA-induced esophageal change. It has been postulated that OSA
causing lowering intrathoracic pressure and leakage of lower esophageal
sphincter19: (1) when either apneas or
hypopnea
occur, OSA patient overcome the hypoxia by sleep breathing effort, which
produce high transdiaphragmatic pressure and low intrathoracic pressure,
exacerbating the lower esophageal sphincter(LES) pressure gradient and
favoring acid reflux into esophagus, resulting in laryngeal mucosal
injury.20-22 (2) the inflammation that goes with OSA
may make the patient prone to dysphagia by hypoxia-reoxygenation,
promoting narrow the upper airway.17 Additionally,
some studies have found that hypoxia inducible factor(HIF)-2α may play
an important role in reflux esophagitis, indicating that nocturnal low
oxygen saturation may aggravate LPR symptoms.23 (3)
the OSA-induced
airway resistance
cause reflux events coexisting transient LES pressure
relaxation.24, 25 Thirdly, LPR-induced inflammation
cannot be ignored in the cycle between OSA and LPR. Previous studies
have proposed that LPR results in esophagus, larynx, and pharynx mucosal
injury and laryngopharyngeal symptoms, which promote: (1) tissue
thickening and hypertrophy caused by chronic inflammation can directly
cause narrow upper airway and (2) increased sensitivity of the
laryngopharyngeal mucosa, inflammation-mediated tissue damage and
sensory impairment contribute to upper respiratory
collapse.13 UPPP improves LPR in two aspects mentioned
above, which break the cycle between OSA and LPR.
Patients often have postoperative complaints after UPPP surgery,
including pharyngeal pain, swallowing difficulty and lump sensation.
Most symptoms are the same as listed on the RSI questionnaire and might
result from scarification of surgical wound. But our study found most
symptoms improved after UPPP. This unexpected finding
likely benefited from UPPP which removes the upper airway obstruction.
Our study has limitations. Firstly, a more objective and easy measure to
evaluate the effects of UPPP to LPR is needed to clarify our results and
evaluate obstruction level. There are several reasons we chose RSI and
RFS instead of 24-hour pH monitoring to diagnose LPR and
evaluate
the effect of UPPP. First of all, RSI and RFS are not only easy to
operate for both patients and doctors, but also convenient for
follow-up.
Secondly, 24-hour pH monitoring is difficult for patients to accept
leading to poor adherence. In addition, further discussion was focused
on subjective sensation of upper respiratory tract after UPPP surgery.
Secondly, OSA patients often complain similar symptoms (lump sensation,
throat-clearing, difficulty swallowing) listed in the RSI questionnaire
after surgery treatment, which are difficult to tell apart. Further
study need compare every OSA patient pre-operative and post-operative
changes of each items in RSI and RFS questionnaires. Thirdly, UPPP can
solve IH or upper airway resistance of OSA. Future study with more cases
is needed to explore whether IH or upper airway resistance improve LPR.