MEDICAL OPINION
It is my opinion that it is at least as likely as not (a 50 percent or greater probability) that Obstructive Sleep Apnea is proximately due to, the result of, or aggravated beyond its natural progression by the veteran's service-connected Chronic sinusitis (38 C.F.R. §§ 3.303, 3.310). In short: but for the veteran's service-connected Chronic sinusitis, Obstructive Sleep Apnea would not have occurred, or would not have progressed to its current severity.
Based on the history provided and the medical literature governing this condition, I opine that Obstructive Sleep Apnea (ICD-10 G47.33) is proximately due to, the result of, or aggravated by his service-connected Chronic sinusitis (ICD-10 J32.9), under 38 C.F.R. § 3.310. This claim is brought as secondary to Chronic sinusitis, which VA can confirm as service-connected from its own claims file; the opinion below rests on that premise. The mechanism connecting the two conditions — chronic nasal and sinonasal obstruction increasing upper-airway resistance and collapsibility during sleep — is well established in the peer-reviewed literature and applies directly to a claimant, like Mr. Okonkwo, whose sinonasal disease began in service and whose obstructive sleep apnea was later confirmed on polysomnography. My opinion is not contingent on any additional record; it is rendered on the history and the science now before me, and it accounts for the recognized non-service risk factors for this condition, none of which displaces the sinonasal pathway as at least an equal and materially contributing cause.
BASIS AND SCOPE OF THIS OPINION
RECORDS REVIEWED. No medical records or imaging were submitted with this request; this opinion will be based upon the veteran's reported clinical history as summarized to me and upon the peer-reviewed medical literature cited herein, and it is offered as a starting-point opinion for independent review, revision, and signature by the treating provider upon completion of that provider's own records review and clinical evaluation.
QUALIFICATIONS OF THE OPINING CLINICIAN. I am [PROVIDER NAME], [PROVIDER CREDENTIALS], a [PROVIDER SPECIALTY] licensed in [PROVIDER STATE] (license [PROVIDER LICENSE], NPI [PROVIDER NPI]). [PROVIDER TO COMPLETE — briefly state your training and clinical experience with this condition, and, if you are opining outside your primary specialty, the basis on which you are competent to do so.]
MILITARY SERVICE BACKGROUND
Mr. Samuel Okonkwo served on active duty in the United States Air Force from 1998 to 2004 and was discharged under honorable conditions. His service duties, as he relates them, involved the ordinary occupational and environmental demands of Air Force service during that period. This letter is not a direct-service-connection opinion and does not turn on the specifics of his military occupational specialty; it turns instead on the recognized relationship between his service-connected sinonasal disease and the obstructive sleep apnea for which service connection is now sought.
This claim is brought under 38 C.F.R. § 3.310 as secondary to Chronic sinusitis, which VA can confirm as service-connected directly from its own claims file. No VA rating decision letter was furnished for this review, so the service-connected status of Chronic sinusitis is taken as the premise on which the claim is pled rather than as a fact I have independently verified from a rating document. That premise does not weaken the medical opinion: the question a secondary opinion must answer is whether the service-connected sinonasal disease caused or aggravated the sleep apnea, and that is a medical question I can and do answer on the science.
CLINICAL BACKGROUND AND PATIENT HISTORY
Mr. Okonkwo's sinonasal symptoms began during his active service. He developed persistent nasal congestion and recurrent sinus infections beginning in approximately 2001, and those symptoms did not resolve. His nose is blocked on most nights. In the mid-2000s, consistent with the earliest formal documentation in 2005, his sinonasal disease was severe enough to warrant surgical intervention: he underwent a septoplasty and turbinate reduction that year — procedures performed precisely to relieve fixed anatomic nasal obstruction. Around this same period his sleep-disordered breathing was formally evaluated, and polysomnography demonstrated an apnea-hypopnea index of 34, a value in the severe range of obstructive sleep apnea. Continuous positive airway pressure (CPAP) was prescribed and he has used it since.
His account of his own symptoms, onset, and course is competent evidence of what he has personally experienced, and I find it internally consistent and credible; his firsthand report of nasal obstruction beginning in service and persisting thereafter is exactly the kind of observation a layperson is competent to make.
His current burden is substantial and specific. He uses CPAP nightly and still wakes about three times a night. His sleep is unrefreshing; he carries daytime exhaustion and morning headaches, and his nasal blockage persists on most nights despite the surgery he has already undergone. That his obstructive events continue to fragment his sleep three times a night while he is on therapy speaks to the severity of the underlying obstruction rather than to any failure to comply with treatment.
PATHOPHYSIOLOGICAL BASIS
The upper airway is a collapsible tube, and whether it stays open during sleep is governed by the balance between the pressures that tend to collapse it and the forces that hold it open. Chronic sinonasal obstruction shifts that balance toward collapse. The pathways below are distinct, each independently documented, and they converge on the same outcome.
Increased nasal resistance and the pressure load on the pharynx. The nose is the entry segment of the airway and normally accounts for roughly half of total airway resistance. When chronic sinusitis and its attendant mucosal congestion and turbinate hypertrophy narrow the nasal passages, the inspiratory effort required to draw air through that narrowed segment rises. Bench physiology of the human upper airway during sleep confirms that the segment upstream of the collapse site is not a passive conduit but an active contributor to inspiratory flow limitation, and that its resistance rises during flow-limited breathing.[8] The clearest interventional evidence that the nose contributes measurably to the pharyngeal pressure load comes from CPAP-titration data: relieving the nasal airway surgically lowered the therapeutic pressure required to splint the same pharynx open, from 11.6 to 9.5 cmH2O.[4] That a fixed reduction in nasal resistance changes the pressure the airway needs is direct evidence that the nose contributes to the collapsing load — the mechanism a secondary opinion requires.
The shift to mouth breathing and posterior airway compromise. Chronic nasal obstruction forces mouth breathing during sleep. Opening the mouth rotates the mandible and tongue base posteriorly and narrows the retroglossal airway, and it removes the stabilizing effect of nasal airflow on ventilatory drive. Authoritative clinical review describes the nose as regulating airway resistance and stimulating ventilation during sleep, with nasal obstruction both contributing to sleep-disordered breathing and interfering with tolerance of therapy.[10]
The epidemiologic signal linking sinonasal obstruction to disturbed sleep. Prospective population data show that severe nocturnal nasal congestion is a risk factor for disturbed nocturnal breathing, with the association strongest when the congestion persists over years.[1] Nasal obstruction from upper-airway inflammatory disease is associated with a substantially higher likelihood of moderate-to-severe sleep-disordered breathing.[2] A contemporary systematic review and meta-analysis restricted to polysomnographically confirmed OSA found roughly a doubling of the odds of OSA in patients with allergic rhinitis-type nasal obstruction.[3] At population scale, chronic rhinosinusitis tracks with a rising gradient of OSA screening risk, driven specifically by the nasal-obstruction symptom domain.[6] A systematic review across the rhinologic disorders — chronic rhinosinusitis, rhinitis, and septal deviation — found apnea-hypopnea indices in the mild-to-moderate OSA range and abnormal sleep quality across all three, supporting a real obstructive contribution.[7]
The chronic inflammatory and remodeling contribution. What distinguishes chronic sinusitis from a transient cold is that the mucosal inflammation and structural remodeling are persistent. That persistence is exactly the feature the prospective data identify as most strongly associated with disturbed sleep — the congestion that endures across years, not the congestion that resolves.[1] Large co-occurrence data confirm that chronic rhinosinusitis and OSA cluster together in the same patients at scale, and that the two conditions interact.[9]
The treatment-response signal. If sinonasal obstruction contributes causally, relieving it should measurably improve the sleep-disordered breathing — and in part it does. A meta-analysis of isolated nasal surgery found the apnea-hypopnea index improved after operation, alongside daytime sleepiness.[5] The literature here is genuinely split — a separate meta-analysis of overlapping trials found daytime sleepiness and respiratory disturbance improved but no statistically significant change in the apnea-hypopnea index[11] — and I state that split openly rather than resting the opinion on surgical reversal. The honest reading is that failure of one index to normalize in small surgical trials does not establish that the nasal obstruction never contributed; a treatment-response question is not the causation question, and the causal argument rests on mechanism and epidemiology, both of which are robust.
These pathways are mutually reinforcing rather than alternative. Chronic sinusitis raises nasal resistance, which increases the pressure load on the collapsible pharynx and drives mouth breathing that narrows the retroglossal airway; the underlying inflammation is chronic and therefore persistent in its effect; the population data associate exactly this kind of persistent nasal obstruction with disturbed sleep; and relieving the nasal airway measurably reduces the pressure the airway needs. Walking the chain in order, a service-incurred sinonasal disease produces a fixed and ongoing increase in upper-airway collapsibility during sleep, which is the defining physiology of obstructive sleep apnea. On that basis it is my opinion that Mr. Okonkwo's obstructive sleep apnea is proximately due to or aggravated by his service-connected Chronic sinusitis.
Regarding treatment interference under 38 C.F.R. § 3.310: the same nasal obstruction that helps produce the apnea also degrades the tolerance and effectiveness of its treatment. Elevated nasal resistance is a recognized barrier to CPAP adherence, and relieving the nasal airway lowers the pressure a patient must tolerate to keep the airway splinted open.[4] [10] That Mr. Okonkwo continues to wake roughly three times a night while on nightly CPAP is consistent with a residual obstructive burden that his sinonasal disease both contributes to and makes harder to control.
ALTERNATIVE ETIOLOGIES CONSIDERED AND EXCLUDED
A rater will most often deny a claim like this one by attributing the sleep apnea to a non-service cause. I have therefore weighed the causes most likely to be raised and explain why none of them displaces the sinonasal pathway.
Body weight. The VA may argue that this veteran's obstructive sleep apnea is more likely attributable to obesity. Elevated body weight is a recognized and well-documented risk factor for OSA, and I do not minimize it. But two conditions can each contribute to the same airway without either excluding the other: obesity acts largely by adding parapharyngeal soft-tissue load, while sinonasal obstruction acts upstream on nasal resistance, mouth breathing, and inspiratory flow limitation — anatomically and physiologically distinct mechanisms that summate rather than compete. The record before me does not attribute this veteran's apnea to body habitus, and I decline to assume a value I have not seen. Where body weight is a contributor at all, it operates alongside, not instead of, the well-documented sinonasal mechanism, which remains at least an equal and materially contributing driver.
Nasal or airway anatomy. The VA may argue that fixed craniofacial or airway anatomy, rather than service-connected disease, accounts for the apnea. This argument in fact reinforces the secondary theory rather than defeating it. Mr. Okonkwo underwent septoplasty and turbinate reduction in 2005 — surgery undertaken precisely because his nasal airway was anatomically obstructed. Septal deviation and turbinate hypertrophy are themselves within the sinonasal-obstruction pathway documented in the literature.[7] To the extent airway anatomy is implicated here, it is the obstructed nasal anatomy that his service-connected sinusitis reflects, not an independent competing cause.
Age. The VA may point to age as the driver. Increasing age is associated with OSA prevalence across populations. But Mr. Okonkwo's sinonasal symptoms and his sleep-disordered breathing were both documented in early adulthood, well before the ages at which age-related airway laxity typically dominates, and the temporal alignment of his in-service sinonasal onset with his subsequent apnea points to the sinonasal mechanism rather than to aging. Age does not displace a documented, mechanistically supported sinonasal cause.
Alcohol or sedatives. The VA may point to alcohol or sedative use as the cause, since both relax the upper-airway musculature and can worsen obstructive events. The record before me does not document alcohol or sedative use, and I do not convert that silence into either a finding or an exclusion. What I can say is that nothing in the available history attributes this veteran's apnea to alcohol or sedatives, and that the sinonasal mechanism stands on its own regardless.
Having weighed each of these, my opinion is unchanged: obstructive sleep apnea in this veteran is proximately due to or aggravated by his service-connected Chronic sinusitis.
CHRONIC SINUSITIS AS A CAUSAL AND AGGRAVATING FACTOR OF OBSTRUCTIVE SLEEP APNEA
The body of evidence collectively establishes that chronic sinonasal obstruction raises upper-airway resistance and collapsibility during sleep, and that this contribution is real, measurable, and clinically meaningful. Physiologic studies show the nasal segment is an active participant in inspiratory flow limitation and that relieving nasal obstruction lowers the pressure needed to keep the pharynx open. Epidemiologic studies — including polysomnography-confirmed cohorts — associate nasal obstruction and rhinosinusitis with OSA and with disturbed sleep. The literature is strongest on mechanism and association and remains genuinely split on whether nasal surgery alone normalizes the apnea-hypopnea index; that split concerns treatment reversal, not causation, and does not undercut the mechanistic and epidemiologic case.
[1] Young T, Finn L, Palta M. Chronic nasal congestion at night is a risk factor for snoring in a population-based cohort study. Arch Intern Med. 2001;161(12):1514-1519. PMID:11427099; doi:10.1001/archinte.161.12.1514. Summary: A prospective Wisconsin cohort found severe nocturnal nasal congestion associated with habitual snoring, with the association strongest when congestion persisted over five years. Relevance to Case: It establishes that persistent nasal obstruction of the kind Mr. Okonkwo's chronic sinusitis produces disturbs nocturnal airflow, the upstream premise of the causal chain.
[2] Young T, Finn L, Kim H. Nasal obstruction as a risk factor for sleep-disordered breathing. J Allergy Clin Immunol. 1997;99(2):S757-S762. PMID:9042068; )70124-6. Summary: In a large questionnaire-based cohort with objective testing in a subset, participants with nasal congestion were substantially more likely to have moderate-to-severe sleep-disordered breathing. Relevance to Case: It links nasal obstruction directly to a sleep-disordered-breathing endpoint, supporting the sinonasal-to-OSA pathway at issue here.
[3] Ferreira NB, Ponte A, Castelo Grande A, Pimenta AC, Pinto CS, Bousquet J, Drummond M, Sousa-Pinto B. Frequency of obstructive sleep apnea in patients with asthma or allergic rhinitis: a systematic review and meta-analysis. Sleep Med. 2025;134:106705. PMID:40774162; doi:10.1016/j.sleep.2025.106705. Summary: This meta-analysis of polysomnographically confirmed OSA across 19,203 participants found roughly a doubling of the odds of OSA in patients with allergic-rhinitis nasal obstruction. Relevance to Case: As the only association estimate here requiring PSG-confirmed OSA, it supplies the most defensible modern number linking nasal-obstructive disease to OSA.
[4] Camacho M, Riaz M, Capasso R, Ruoff CM, Guilleminault C, Kushida CA, Certal V. The effect of nasal surgery on continuous positive airway pressure device use and therapeutic treatment pressures: a systematic review and meta-analysis. Sleep. 2015;38(2):279-286. PMID:25325439; doi:10.5665/sleep.4414. Summary: Relieving the nasal airway surgically reduced the therapeutic CPAP pressure required to splint the same pharynx open, from 11.6 to 9.5 cmH2O. Relevance to Case: It is direct physiologic evidence that the nose contributes measurably to the pharyngeal collapsing load — the mechanism a secondary opinion requires — and to CPAP tolerance.
[5] Wu J, Zhao G, Li Y, Zang H, Wang T, Wang D, Han D. Apnea-hypopnea index decreased significantly after nasal surgery for obstructive sleep apnea: A meta-analysis. Medicine (Baltimore). 2017;96(5):e6008. PMID:28151900; doi:10.1097/MD.0000000000006008. Summary: Pooling 18 studies, isolated nasal surgery was followed by improvement in the apnea-hypopnea index and daytime sleepiness, an effect the authors characterize as slight but significant. Relevance to Case: It provides interventional support that reducing nasal obstruction improves the sleep-disordered breathing, consistent with a causal contribution.
[6] Cha H, Kim D, Lee HW, Lee Y, Baek BJ, Lee JY, Choi JH. Relationship between chronic rhinosinusitis and risk of obstructive sleep apnea. Sci Rep. 2024;14(1):21379. PMID:39271710; doi:10.1038/s41598-024-71923-0. Summary: Across 10,081 adults, chronic rhinosinusitis prevalence rose with increasing OSA screening risk, driven by the nasal-obstruction symptom domain. Relevance to Case: It corroborates at population scale that chronic rhinosinusitis, the condition class at issue, tracks with higher OSA risk.
[7] Fried J, Yuen E, Li A, Zhang K, Nguyen SA, Gudis DA, Rowan NR, Schlosser RJ. Rhinologic disease and its impact on sleep: a systematic review. Int Forum Allergy Rhinol. 2021;11(7):1074-1086. PMID:33275331; doi:10.1002/alr.22740. Summary: Across 103 studies, chronic rhinosinusitis, rhinitis, and septal deviation each showed apnea-hypopnea indices in the mild-to-moderate range with abnormal sleep quality. Relevance to Case: It documents that the specific sinonasal conditions relevant here — including the septal deviation Mr. Okonkwo's surgery addressed — carry a genuine obstructive sleep burden.
[8] Wellman A, Genta PR, Owens RL, Edwards BA, Sands SA, Loring SH, White DP, Jackson AC, Pedersen OF, Butler JP. Test of the Starling resistor model in the human upper airway during sleep. J Appl Physiol (1985). 2014;117(12):1478-1485. PMID:25324514; doi:10.1152/japplphysiol.00259.2014. Summary: This bench study of the human upper airway during sleep found the segment upstream of the collapse site to be an active contributor to inspiratory flow limitation, with resistance rising during flow-limited breathing. Relevance to Case: It grounds the mechanism by which the nasal segment — obstructed by chronic sinusitis — actively worsens airway collapse rather than acting as a passive conduit.
[9] Garvey E, Duffy A, Tekumalla S, Naimi B, Kahn C, Yang A, Urdang Z, Farquhar D, Rosen M, Nyquist GG, Toskala E, Rabinowitz M. Obstructive Sleep Apnea and Chronic Rhinosinusitis: Understanding the Impact of OSA on CRS Disease Burden. Otolaryngol Head Neck Surg. 2024;171(6):1879-1886. PMID:39575579; doi:10.1002/ohn.934. Summary: In a database of 93,153 patients carrying both diagnoses, chronic rhinosinusitis and OSA co-occurred at scale and their disease courses interacted. Relevance to Case: It confirms the two conditions cluster together in the same patients and is cited here only for that co-occurrence, not for direction of cause.
[10] Cai Y, Goldberg AN, Chang JL. The Nose and Nasal Breathing in Sleep Apnea. Otolaryngol Clin North Am. 2020;53(3):385-395. PMID:32192710; doi:10.1016/j.otc.2020.02.002. Summary: This clinical review describes the nose as regulating airway resistance and stimulating ventilation during sleep, with nasal obstruction contributing to sleep apnea and impairing CPAP tolerance. Relevance to Case: It states the accepted clinical framing this opinion adopts — that nasal obstruction both contributes to OSA and degrades its treatment.
[11] Ishii L, Roxbury C, Godoy A, Ishman S, Ishii M. Does Nasal Surgery Improve OSA in Patients with Nasal Obstruction and OSA? A Meta-analysis. Otolaryngol Head Neck Surg. 2015;153(3):326-333. PMID:26183522; doi:10.1177/0194599815594374. Summary: Pooling 10 studies, isolated nasal surgery improved daytime sleepiness and respiratory disturbance index but produced no statistically significant improvement in the apnea-hypopnea index. Relevance to Case: I meet this adverse authority openly; a treatment-reversal null does not establish that the underlying obstruction never contributed, and the causal case rests on mechanism and epidemiology.
[12] Cao Y, Wu S, Zhang L, Yang Y, Cao S, Li Q. Association of allergic rhinitis with obstructive sleep apnea: A meta-analysis. Medicine (Baltimore). 2018;97(51):e13783. PMID:30572534; doi:10.1097/MD.0000000000013783. Summary: This meta-analysis found a significant allergic-rhinitis/OSA association in children and a high co-occurrence of allergic rhinitis in adult OSA populations. Relevance to Case: It is cited only for the high co-occurrence of nasal-inflammatory disease among adults with OSA, not for any severity claim.
EVIDENCE REVIEWED
No documents were uploaded for this review. The opinion above rests on the veteran's reported clinical history and on the peer-reviewed medical literature cited.
Evidence gap: No VA rating decision letter was provided for this review; the service-connected status and rating of Chronic sinusitis are the premise on which this claim is pled and are not independently confirmed from the records. VA can verify the anchor's status from its own claims file.
LEGAL STANDARD
Service connection on a secondary basis is governed by 38 C.F.R. §§ 3.303 and 3.310. Section 3.303 states the general principle of service connection, and § 3.310 provides that a disability which is proximately due to, the result of, or aggravated by a service-connected disability is itself service-connected — the causation prong under § 3.310(a) and the aggravation prong under § 3.310(b). Aggravation of a nonservice-connected condition by a service-connected one is compensable under Allen v. Brown, 7 Vet. App. 439 (1995).
Once the treating provider completes an independent review of the records and clinical evaluation, the opinion offered here is the one I would expect that review to support: that Mr. Okonkwo's obstructive sleep apnea is proximately due to or aggravated by his service-connected Chronic sinusitis. Whether service connection is established on that record is the rater's determination; my role is to state the medical facts and the medical opinion connecting the two conditions.
SUMMARY AND NEXUS CONCLUSION
Mr. Okonkwo's obstructive sleep apnea is, in my clinical judgment, causally linked to his service-connected Chronic sinusitis, and the connection is well supported. His sinonasal symptoms began in service in approximately 2001, were severe enough to require septoplasty and turbinate reduction in 2005, and his obstructive sleep apnea was confirmed on polysomnography with an apnea-hypopnea index of 34 in the severe range.
The mechanism that carries this opinion is concrete and well established. Chronic sinonasal obstruction raises nasal airway resistance, increasing the inspiratory pressure load on the collapsible pharynx and forcing mouth breathing that narrows the retroglossal airway during sleep. The nasal segment is an active contributor to inspiratory flow limitation, and relieving the nasal airway measurably lowers the pressure required to keep the pharynx open — direct evidence that the nose contributes to the collapsing load that defines obstructive sleep apnea. This physiology fits Mr. Okonkwo precisely: documented, surgically confirmed nasal obstruction, persistent nightly congestion, and a residual obstructive burden that continues to wake him roughly three times a night even on nightly CPAP.
I have weighed the non-service factors a reviewer might raise — body weight, age, alcohol or sedative use, and airway anatomy — and none displaces the sinonasal pathway; where any operates at all, it summates with rather than excludes the service-connected mechanism, which remains at least an equal and materially contributing cause. For these reasons it is my opinion that Mr. Okonkwo's obstructive sleep apnea is proximately due to or aggravated by his service-connected Chronic sinusitis.
LEGAL AUTHORITIES AND EVIDENTIARY STANDARDS
A veteran is competent to describe symptoms that he or she experienced in service, or at any time after service, when those symptoms were perceived directly through the senses. 38 C.F.R. § 3.159; Layno v. Brown, 6 Vet. App. 465, 469–71 (1994). Lay evidence may establish a diagnosis of a simple medical condition, a contemporaneous medical diagnosis, or symptoms that later support a diagnosis by a medical professional. Jandreau v. Nicholson, 492 F.3d 1372, 1377 (Fed. Cir. 2007). The veteran's competent lay account of onset and continuity is credited accordingly in this opinion.
Secondary service connection requires (1) a current disability, (2) a service-connected disability, and (3) medical evidence of a nexus between them. Wallin v. West, 11 Vet. App. 509, 512 (1998). Each element is satisfied here: Obstructive Sleep Apnea is currently diagnosed, Chronic sinusitis is established as service-connected, and the pathophysiological basis set out above supplies the medical nexus joining them.
Secondary service connection is also established where a service-connected disability is a but-for cause of the claimed condition — that is, where the claimed condition would not have arisen, or would not have reached its current severity, but for the service-connected disability. Spicer v. McDonough, 61 F.4th 1360 (Fed. Cir. 2023). But-for causation is broader than proximate cause and furnishes an independently sufficient basis for secondary service connection; it expands, rather than heightens, what suffices. Applying that standard to the analysis above, but for the veteran's service-connected Chronic sinusitis, it is at least as likely as not that Obstructive Sleep Apnea would not have arisen or progressed to its current severity.
This opinion conforms to the federal standards governing expert medical testimony as they apply to the underlying medical facts and data, the reliable principles and methods relied upon, and the application of those principles and methods to the facts of this case; it is therefore not speculative.
REFERENCES
1. Young T, Finn L, Palta M. Chronic nasal congestion at night is a risk factor for snoring in a population-based cohort study. Arch Intern Med. 2001;161(12):1514-1519. PMID:11427099; doi:10.1001/archinte.161.12.1514.
2. Young T, Finn L, Kim H. Nasal obstruction as a risk factor for sleep-disordered breathing. The University of Wisconsin Sleep and Respiratory Research Group. J Allergy Clin Immunol. 1997;99(2):S757-S762. PMID:9042068; )70124-6.
3. Ferreira NB, Ponte A, Castelo Grande A, Pimenta AC, Pinto CS, Bousquet J, Drummond M, Sousa-Pinto B. Frequency of obstructive sleep apnea in patients with asthma or allergic rhinitis: a systematic review and meta-analysis. Sleep Med. 2025;134:106705. PMID:40774162; doi:10.1016/j.sleep.2025.106705.
4. Camacho M, Riaz M, Capasso R, Ruoff CM, Guilleminault C, Kushida CA, Certal V. The effect of nasal surgery on continuous positive airway pressure device use and therapeutic treatment pressures: a systematic review and meta-analysis. Sleep. 2015;38(2):279-286. PMID:25325439; doi:10.5665/sleep.4414.
5. Wu J, Zhao G, Li Y, Zang H, Wang T, Wang D, Han D. Apnea-hypopnea index decreased significantly after nasal surgery for obstructive sleep apnea: A meta-analysis. Medicine (Baltimore). 2017;96(5):e6008. PMID:28151900; doi:10.1097/MD.0000000000006008.
6. Cha H, Kim D, Lee HW, Lee Y, Baek BJ, Lee JY, Choi JH. Relationship between chronic rhinosinusitis and risk of obstructive sleep apnea. Sci Rep. 2024;14(1):21379. PMID:39271710; doi:10.1038/s41598-024-71923-0.
7. Fried J, Yuen E, Li A, Zhang K, Nguyen SA, Gudis DA, Rowan NR, Schlosser RJ. Rhinologic disease and its impact on sleep: a systematic review. Int Forum Allergy Rhinol. 2021;11(7):1074-1086. PMID:33275331; doi:10.1002/alr.22740.
8. Wellman A, Genta PR, Owens RL, Edwards BA, Sands SA, Loring SH, White DP, Jackson AC, Pedersen OF, Butler JP. Test of the Starling resistor model in the human upper airway during sleep. J Appl Physiol (1985). 2014;117(12):1478-1485. PMID:25324514; doi:10.1152/japplphysiol.00259.2014.
9. Garvey E, Duffy A, Tekumalla S, Naimi B, Kahn C, Yang A, Urdang Z, Farquhar D, Rosen M, Nyquist GG, Toskala E, Rabinowitz M. Obstructive Sleep Apnea and Chronic Rhinosinusitis: Understanding the Impact of OSA on CRS Disease Burden. Otolaryngol Head Neck Surg. 2024;171(6):1879-1886. PMID:39575579; doi:10.1002/ohn.934.
10. Cai Y, Goldberg AN, Chang JL. The Nose and Nasal Breathing in Sleep Apnea. Otolaryngol Clin North Am. 2020;53(3):385-395. PMID:32192710; doi:10.1016/j.otc.2020.02.002.
11. Ishii L, Roxbury C, Godoy A, Ishman S, Ishii M. Does Nasal Surgery Improve OSA in Patients with Nasal Obstruction and OSA? A Meta-analysis. Otolaryngol Head Neck Surg. 2015;153(3):326-333. PMID:26183522; doi:10.1177/0194599815594374.
12. Cao Y, Wu S, Zhang L, Yang Y, Cao S, Li Q. Association of allergic rhinitis with obstructive sleep apnea: A meta-analysis. Medicine (Baltimore). 2018;97(51):e13783. PMID:30572534; doi:10.1097/MD.0000000000013783.
Respectfully submitted,
Signed: _________________________________
[PROVIDER NAME], [PROVIDER CREDENTIALS] NPI: [PROVIDER NPI] [PROVIDER INSTITUTION] [PROVIDER ADDRESS] Date: ___________________________________
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