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HomemieyecareLTG & Sleep Apnoea: Experience of an Optometrist

LTG & Sleep Apnoea: Experience of an Optometrist

The case of a myopic optometrist with presumed low tension glaucoma associated with obstructive sleep apnoea, and concomitant retinal pathology, highlights the need for ongoing vigilant, collaborative care.

Low tension glaucoma (LTG) is a diagnosis of exclusion that is difficult to make and especially difficult in myopic patients with ‘myopic discs’, or those who have ocular co-morbidity. Being aware of specific systemic risk factors may allow for earlier diagnosis.

most studies suggest an additional correlation between LTG and an increasing severity of sleep apnoea

Figure 1. Significant RNFL thinning, greater in the right eye than the left

In 2016, 49 year old optometrist George Ploumidis elected to have an ophthalmic exam and ocular coherence tomography to assess his ocular health in view of his complex ophthalmic history:

  • Moderate myopia (R -4.00/-025×175, L -4.25/-0.25×40)
  • No family history of glaucoma


  • A right inferonasal branch retinal vein occlusion (BRVO) from undiagnosed hypertension,
  • Retinal ischemia secondary to the occlusive event, which required laser photocoagulation of the right inferonasal retina, and
  • Subsequent retinal neovascularisation with four episodes of persistent vitreous haemorrhages

Figure 2. Significant thinning of the macular GCL, again greater in the right eye than the left


  • Diagnosis of severe obstructive sleep apnoea


  • Diagnosis of paroxysmal atrial fibrillation.

Previous examinations conducted in 2005, using two different retinal imaging technologies pre-dating optical coherence tomography (OCT) and frequency doubling technology (FDT) perimetry, were normal with no optic nerve pathology or significant field changes detected.

On this occasion, OCT demonstrated significant retinal nerve fibre layer (RNFL) loss (Figure 1):

  • Average RNFL: R 59μ, L 64μ,
  • Global thinning of the right retinal nerve fibre layer,
  • Thinning of the left retinal nerve fibre layer superiorly, and
  • Inferiorly ganglion cell inner plexiform layer (GCiPL) thinning (Figure 2).

Swedish Interactive Testing Algorithm (SITA) fast perimetry (Figure 4) demonstrated field loss, which was greater in the right eye than the left, correlating with the above ganglion cell layer (GCL) findings. The field loss was close to fixation in the right eye. This defect may also be due to previous laser, however the laser had been performed more peripherally. These fields highlight the difficulty in making a definite diagnosis of glaucoma in a myopic eye with previous laser in a patient with significant known risk factors for LTG.

Best corrected vision was 6/12+2 and 6/9 in the right and left eyes respectively, with no improvement with pinhole in either eye. Anterior segments were normal and gonioscopy showed open angles. Cup to disc ratios were measured by OCT as right 0.66 and left 0.52. Intraocular pressure (IOP) was 14mmHg in the right eye and 13mmHg in the left, and central corneal thickness 536 microns in the right eye and 520 microns in the left. An MRI scan of the orbit and brain was normal.

Weighing Up the Findings 

Various findings had to be weighed in order to determine whether a diagnosis of normal tension glaucoma could be entertained or not.

Figure 3a. Disc photos

These findings were:

  • Previous right retinal laser, which could contribute to the right field defect,
  • Increased cup disc ratio,
  • Progressive visual field defects,
  • History of sleep apnoea for at least eight years,
  • Vasculopathic history, and
  • Possible tilted myopic discs with resultant increased blind spots (tilted discs can give superior field defects but these are usually a little more peripheral. Tilted myopic discs can co-exist in patients with glaucoma).

The visual field defects anticipated in LTG are thought by some, to be deeper and closer to fixation than those otherwise found in glaucoma. If there is a visual field defect in one eye, then there may also be a 40 per cent chance of a defect developing in the other eye in five years.

Diagnosis and Treatment 

A diagnosis of LTG was tentatively made and treatment with a prostaglandin analogue was commenced, lowering intraocular pressures (IOPs) to 11mmHg in both eyes. An alternative approach may have been to monitor the fields for progression as 40 per cent of patients with LTG do not deteriorate after five years with follow up.

A management plan with documented goals must be communicated to the patient’s general practitioner

Figure 3b. Disc photos

The decision to treat was made after a discussion weighing the perceived benefits and risks associated with ongoing medical treatment, especially taking into account both the obstructive sleep apnoea and ocular vascular disease.

Both blood pressure and cholesterol were assessed as being within normal limits and a further sleep study confirmed that the current treatment setting of the constant positive airway pressure (CPAP) was well within therapeutic targets. Pulmonary vein isolation, a surgical form of ablative surgery, was undertaken in June 2018, which effectively treated the existing atrial fibrillation.


Low tension glaucoma (LTG) is a condition comprising the classical glaucomatous features of disc and field changes in the presence of open angles and IOPs within the statistically normal range.1 In the absence of elevated IOPs as the recognised modifiable risk factor, vascular and pathogenic mechanisms other than IOP effects have been postulated, but the exact cause remains unknown.

The Beaver Dam Eye Study previously identified the prevalence of LTG within a population as approximately 0.2 per cent of patients age 43 to 54 years, rising to 1.6 per cent in patients over 75 years of age.3 Vascular risk factors such as migraine, nocturnal hypotension, and disc haemorrhage are also associated with LTG.

Figure 4. Bilateral reduction of sensitivity with SITA fast threshold perimetry; and a dense paracentral visual field defect (R) encroaching central vision (green arrow). The right superotemporal arcuate defect (red arrow) is
attributable to previous laser photocoagulation post ischaemic inferonasal branch retinal vein occlusion.

Obstructive Sleep Apnoea 

Obstructive sleep apnoea (OSA) is characterised by multiple episodes of upper respiratory obstruction during sleep combined with daytime sleepiness, along with difficulty concentrating, memory problems, and daytime headaches. OSA negatively effects pulmonary, cardiovascular, and cerebrovascular physiology function. The pathophysiology of sleep apnoea is summarised in Figure 5.

The association between OSA and ocular disease is well documented including; glaucoma, non-arteritic ischaemic optic neuropathy (NAION), bilateral disc oedema, floppy lid syndrome, blepharitis, ptosis, papillary conjunctivitis, filamentary keratitis, retinal tortuosity, and central serous retinopathy.4 The presence and severity of OSA is commonly measured by the number of respiratory events per hour – respiratory disturbance index (RDI) or apnoea-hypopnea index (AHI). During sleep, blood flow autoregulation is designed to maintain routine perfusion requirements of tissues as changes in sympathetic activity occur. OSA disrupts this autonomic regulation resulting in pathological changes that are independent of IOP.5

LTG and OSA 

With respect to the incidence of LTG within the OSA literature, the presence of OSA appears to represent a significant risk factor with incidence rates between 5.7 per cent and 15.4 per cent across multiple studies.6-8 Furthermore, most studies suggest an additional correlation between LTG and an increasing severity of sleep apnoea. Against this however, in a large review of a medical records database, Stein and co-authors found no correlation between OSA and glaucoma. In that study there were confounding factors which may have underrepresented any connection.

The ocular changes linked to OSA that lead to the development of glaucomatous disease include:

  • Lowered ocular perfusion pressure10 (defined as blood pressure – IOP),
  • Ischaemia,5
  • Inflammation and oxidative stress affect the vascular endothelium, altering blood flow in and around the optic nerve, lowering ocular perfusion and increasing the risk of glaucoma,4
  • Compromised mitochondrial function occurs due to low blood flow to the optic nerve, leaving the nerve more vulnerable to threats of raised IOP, photopic damage or inflammatory substances,11 and
  • Hypercapnia (elevated carbon dioxide levels in the blood) causes metabolic stress and acidosis, potentially compromising optic nerve head circulation.12 

The clinical significance of these changes are multifactorial and hence differ between individuals. Measures such as retinal nerve fibre layer (RNFL) thickness and mean deviations in perimetry have been shown to correlate directly with OSA and AHI/RD. The literature also suggests a link between RDI and untreated IOP, field loss and the eventual diagnosis of glaucoma.13 There is a statistically higher mean deviation and pattern standard deviation in perimetry in moderate to severe OSA patients when compared to age matched patients.14


New knowledge about the effects of sleep apnoea on a patient’s ocular health should guide the clinician to suspect and look for a current or past history of OSA.

Figure 5. Cycle summarising the pathophysiology of obstructive sleep apnoea (OSA)

A positive history should initiate OCT and perimetry testing to document the presence of physical nerve changes and field loss.

A management plan with documented goals must be communicated to the patient’s general practitioner to allow for collaborative care.

In our case report, other systemic vasculopathic health issues may have predisposed the right eye in particular to glaucomatous changes. Indeed, the medical retina specialist who treated the BRVO in the right eye suggested increased vigilance for ocular comorbidity at the time of diagnosis.

Similarly, patients exhibiting RNFL and field loss akin to the above case should be referred to the patient’s general practitioner for investigation for OSA. Ongoing treatment with a prostaglandin analogue, regular ophthalmological reviews, and managing cardiovascular risk factors are at the core of successful management in this case.

George Ploumidis is a locum optometrist and an optometry committee member of Glaucoma Australia. He completed his Bachelor of Optometry and Certificate 1 and 2 in low vision at University of Melbourne, and a Masters of Health Administration at Monash University. 

Dr Lewis Levitz practices from the Vision Eye institute in Camberwell, Blackburn South and Coburg, Melbourne. He has reviewed articles on cataract surgery for the Journal of Cataract and Refractive Surgery, Clinical and Experimental Ophthalmology and the Asia Pacific Journal of Ophthalmology. He also presents annual papers and audits at the Australian Society of Cataract and Refractive surgical meetings. He has an interest in oculoplastic surgery having completed a Fellowship in Cardiff, Wales. 


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