Primary open-angle glaucoma (POAG) is a progressive optic neuropathy characterized by specific optic disc changes and associated visual field defects. Estimated prevalence is 3.0%, making it the leading cause of irreversible blindness worldwide. Intraocular pressure (IOP) is the only proven modifiable risk factor for the development and progression of POAG, but even effective reduction of IOP by pharmacological or surgical means does not always change the course of the disease or prevent some people from developing glaucoma.
OSA is a sleep-related breathing disorder (SBD) caused by complete (apnoea) or partial (hypopnoea) narrowing of the upper airway, resulting in disturbed sleep and intermittent oxygen desaturations. These in turn have negative impact on cardiovascular system and potentially other organs. OSA is treated by continuous positive airway pressure (CPAP) applied by a nasal or a full face mask which maintains patency of the upper airway. CPAP is the first line treatment for moderately severe and severe OSA and, among currently used treatment modalities, it is also the most effective one. The prevalence of OSA continues to increase linked with the rising global incidence of obesity, though many remain undiagnosed. A recent study from the United States estimated that 35% of people between the ages of 50 and 70 years suffer from OSA, and approximately 12% may require treatment.
OSA and OAG are, therefore, two common conditions which may coexist in a significant proportion of patients. In fact, some studies indicate increased prevalence of OAG in patients with OSA, which is in line with a suspected causative role of OSA in glaucoma.
People with OAG and concomitant OSA associated with the relevant symptoms, particularly daytime sleepiness, currently receive standard treatment with CPAP. However, the impact of CPAP on their glaucoma is unknown. There are concerns that CPAP increases IOP, currently the only modifiable factor in glaucoma, though the evidence for this is limited. The exact mechanisms of the possible IOP-raising effect of CPAP are not clear. The favoured hypothesis is CPAP leads to increases in intrathoracic pressure, which in turn raises pressure in the venous circulation and a reduction in the aqueous humour outflow through the episcleral veins and ultimately IOP increase. A similar mechanism is believed to be responsible for IOP elevation in the transition from an upright to supine position in which venous drainage is reduced.
The relationship between the level of pressure used in CPAP treatment and IOP has not been studied. It is unknown if IOP increases in correlated way to CPAP or whether there is no straightforward correlation. If the first is true, application of CPAP only up to a certain pressure level would be safe and perhaps the threshold to use bi-level PAP should be lower in patients with glaucoma. If, however, IOP changes are a matter of individual response to CPAP, perhaps dependent on the severity of OSA or BMI, a routine measurement of the pressure should be performed once CPAP is started. This is currently not a part of standard clinical practice. It is also possible that CPAP set within the usual pressure range does not influence IOP or its effect is not mediated by simple mechanical pressure transmission.
Therefore understanding the influence of CPAP on IOP is important as it may inform the management of people with OSA and concomitant glaucoma. If CPAP is shown to raise IOP or alter ocular perfusion pressure (OPP) to levels that pose clinical risk it will be necessary to assess available alternative treatment options for OSA.
This is a prospective physiological controlled study which will assess IOP response to several different CPAP levels applied for short periods in wakefulness in three groups of people: POAG patients established on treatment (treated glaucoma group), newly diagnosed treatment naïve POAG patients (untreated glaucoma group) and control subjects without glaucoma (control subjects).
