Changes in continuous positive airway pressure (CPAP) therapy may have contributed to choroidal detachment in a patient with obstructive sleep apnea (OSA), although the relationship remains unproven.
The case involved a 76-year-old male patientwhoreceived CPAP therapy for OSA for 8 years. Twenty weeks prior to presentation, his therapeutic pressure was increased from 4 to 5.5 cm H₂O, and he received a new oronasal mask. The changes reduced mask leakage. About 13 weeks prior to presentation, he developed red-tinted tunnel vision, floaters, photopsias, and redness in the left eye.
At presentation, best-corrected visual acuity (BCVA) was 1.0 in both eyes, and intraocular pressure (IOP) was within normal limits. Examination of the left eye revealed dilated, tortuous episcleral vessels and massive choroidal effusion. Ocular ultrasonography showed anterior rotation of the ciliary body and forward displacement of the iris diaphragm, with subsequent shallowing of the anterior chamber and narrowing of the angle. Laboratory findings were unremarkable, and contrast-enhanced computed tomography (CT) excluded intracranial hemorrhage and pathologic masses. The patient began topical dexamethasone 0.1% and cyclopentolate.
Choroidal detachment progressed over the following 3 weeks to a kissing configuration involving the macular visual axis. BCVA in the affected eye declinedto hand movements, while IOP increased to 27 mmHg. Dorzolamide plus timolol was added. Pulmonology consultation determined that the CPAP parameters met treatment standards and recommended continuing therapy. Rheumatologic evaluation found no evidence of an underlying systemic inflammatory or rheumatologic disease associated with choroidal detachment.
The ocular findings improved while CPAP therapy continued. At week 7, BCVA improved to 0.2, IOP decreased to 17 mmHg, and the episcleral vessel dilation and choroidal effusion had partially resolved. Complete anatomical resolution of the choroidal detachment was documented by week 16. At week 18, BCVA had improved to 0.4 and IOP was 16 mmHg, with the ciliary body and iris returning to their normal positions. Progressive lens opacification was noted, and the patient was qualified for cataract surgery.
Researchers highlighted the temporal relationship between the CPAP adjustments and symptom onset. The new mask reduced leakage, which they proposed resulted in greater effective pressure exposure. The researchers hypothesized that positive airway pressure could reduce venous return and impair choroidal venous drainage, potentially leading to venous congestion, increased choroidal hydrostatic pressure, fluid accumulation in the suprachoroidal space, and choroidal detachment. Available evidence did not directly link CPAP therapy with episcleral venous pressure, and the mechanism remained uncertain.
A single case could not establish that CPAP therapy caused the choroidal detachment, particularly because CPAP was continued as the ocular findings resolved during corticosteroid, cycloplegic, and IOP-lowering treatment. Thyroid-associated orbitopathy could not be formally excluded because thyroid function testing was not performed. In addition, magnetic resonance imaging, magnetic resonance angiography, and digital subtraction angiography were not performed,modalities that are more sensitive than CT in detecting low-flow carotid-cavernous fistulas, dural arteriovenous fistulas, and subtle cavernous abnormalities.
The findings suggested that CPAP therapy may warrant consideration as a possible contributor when patients receiving treatment develop otherwise unexplained choroidal detachment.
“We hope that this report will contribute to raising awareness of the choroidal detachment as the potential complication of the treatment,” wrote lead study author Emilia Żurowska, of the Department of Ophthalmology at the Poznań University of Medical Sciences in Poland, and colleagues.
The study authors reported no conflicts of interest.
