• Summary
• Background
• Clinical features
• Diagnosis
• Differential diagnoses
• Management
• Normal tension glaucoma
• Summary
• Background
• Clinical features
• Diagnosis
• Management
• References
• Author(s)

Summary

Ocular hypertension refers to an IOP > 21 mmHg without apparent glaucomatous damage, (no optic nerve damage or visual field loss).

Background

The mean IOP is 16 mmHg, with the normal range being 11-21 mmHg (two standard deviations either side.) However, 4-10% of the population above the age of 40 is likely to have an IOP > 21 mmHg, without any glaucomatous damage. In these cases, if there is no angle closure or any other cause of secondary glaucoma, we have ocular hypertension (OHT).

The exact cause has not been determined, however the Ocular Hypertension Treatment Study (OHTS) through a longitudinal trial, suggested various risk factors at play.

These include:

• Raised IOP
• Older age
• Central corneal thickness: Eyes with a low CCT are at greater risk to higher - possibly in part due to under and over estimation of the IOP respectively
• Cup/disc ratio: The greater the C/D ratio, the higher the risk (optic nerve heads with a large cup may be structurally more vulnerable)
• Pattern standard deviation: Visual field loss in glaucoma is highly irregular, and therefore a measure which quantifies irregularities is required. Pattern standard deviation is a way of measuring irregularities in perimetry, and a larger value may represent a greater risk for developing OHT.

Clinical features

• Raised IOP, generally defined as > 21 on 2+ visits.
• Open anterior chamber angle, with normal appearance, and normal anatomy on gonioscopy
• Apparently normal optic nerve, retinal nerve fibre layer, and visual field

Diagnosis

Ocular hypertension should be investigated in the same way as POAG. However, extra consideration may be given to whether any systemic medication is being taken that could reduce (beta blockers) or increase (steroids) IOP.

Differential diagnoses

• POAG
• Secondary open angle glaucoma
• Chronic angle closure glaucoma

Management

Treatment has greatly reduced progression from ocular hypertension to POAG. However, the number needed to treat to prevent the development of glaucoma in individuals with ocular hypertension is high. Therefore, current guidelines suggest only those at high risk be treated. In general, an IOP over 30 mmHg warrants treatment, however factors such as age, life expectancy, patient preference, family history, initial IOP and optic nerve appearance play a role.

Treatment options are typically the same as for POAG, however a less aggressive pressure lowering approach is usually adopted. E.g. alternate day prostaglandin dosing and low intensity selective laser trabeculoplasty. Often a therapeutic trial in one eye is started.

Normal tension glaucoma

Summary

Also known as normal-pressure glaucoma, normal tension glaucoma is a variant of primary open angle glaucoma in which there is no measured elevation of the intraocular pressure. There is however, chronic progressive glaucomatous damage as in POAG.

Background

The pathogenesis of NTG is debated, and a variety of IOP independent factors such as vascular dysregulation, hypotension, and lamina cribrosa abnormalities have been thought to play a role in the disease process. Therefore, investigation of these factors must be taken into account in the history when making a diagnosis. Additionally, interventions such as modification of blood pressure and optic nerve perfusion may slow down disease progression. Drance et al in 1973 identified two main types: 1) a non-progressive form associated with transient vascular compromise, and 2) a progression form resulting from chronic venous insufficiency at the optic nerve.

It has been observed that overall corneal central thickness is on average much lower in normal tension glaucoma patients than in POAG. Additionally, many patients have been seen to experience nocturnal IOP spikes, detected on testing in the supine position.

Comparison of NTG with POAG

Clinical features

History and examination are the same as for POAG, but there are some specific points which may warrant attention in order to highlight any risk factors or to even uncover other underlying neurological conditions. It is a diagnosis of exclusion and therefore other causes of optic neuropathy must be ruled out first.

• History: Migraine and Raynaud phenomenon, shock, head injury, localising neurology
• Optic nerve head: May be larger on average in NTG than POAG, similar pattern of cupping but acquired optic disc pits + focal nerve fibre layer. Peripapillary atrophic changes may be more prevalent. Disc haemorrhages may be more frequent than in POAG, and are associated with greater likelihood of progression. Pallor disproportionate to cupping should prompt a suspicion of an alternative diagnosis.
• Visual field defects tend to be closer to fixation, deeper, steeper and more localized. In 50%+ patients, field changes are non progressive over a period of 5 years or more without treatment. However, perhaps because of delayed diagnosis, patients tend to present with more advanced damage than in POAG.
• Gonioscopic confirmation of open anterior chamber angle with no other secondary cause of glaucoma

Diagnosis

As for POAG, but in some patients some extra investigations can be considered, such as assessment of systemic vascular risk factors, blood perfusion pressure, 24 hour ambulatory monitoring to exclude nocturnal systemic hypotension, blood tests for other non glaucomatous optic neuropathy (vitamin B12 etc), cranial MRI, carotid duplex imaging.

Management

Despite the lack of IOP elevation, lowering of IOP is effective in reducing progression in most patients. This constitutes the medical and surgical treatment given in other forms of glaucoma. However, as a large proportion of untreated patients will not deteriorate, progression needs to be demonstrated before commencing treatment. Exceptions include advanced glaucomatous damage, particularly if threatening central vision, and young age. Regular assessment including perimetry should be performed should be performed at 4-6 monthly intervals.

Liaising with primary care may be beneficial in order to control cardiovascular problems (arrythmias, anaemia, hypotension) which could further compromise optic nerve head perfusions.

References

1. Salmon, John F., and Jack J. Kanski. Kanski’s Clinical Ophthalmology: A Systematic Approach. Ninth Edition, Elsevier, 2020.
2. Gordon, Mae O., et al. ‘The Ocular Hypertension Treatment Study: Baseline Factors That Predict the Onset of Primary Open-Angle Glaucoma’. Archives of Ophthalmology, vol. 120, no. 6, June 2002, pp. 714–20. Silverchair, https://doi.org/10.1001/archopht.120.6.714.
3. Anderson, Douglas R. and Normal Tension Glaucoma Study. ‘Collaborative Normal Tension Glaucoma Study’. Current Opinion in Ophthalmology, vol. 14, no. 2, Apr. 2003, pp. 86–90. PubMed, https://doi.org/10.1097/00055735-200304000-00006.
4. ‘Open Angle Glaucoma’. Wills Eye Hospital, https://www.willseye.org/open-angle-glaucomas/. Accessed 9 Apr. 2023.
5. ‘Normal Tension Glaucoma’. Wills Eye Hospital, https://www.willseye.org/disease_condition/average-intraocular-pressure-glaucoma-also-known-low-tension-glaucoma-normal-tension-glaucoma/. Accessed 9 Apr. 2023.

Author(s)

Dr Sara Memon

Sara is the Co-Founder of Ophtnotes. She is a doctor who graduated from UCL Medical School in London. She won the Allen Goldsmith Prize in Ophthalmology. Sara is also the co-founder of PAMSA: an organisation linking doctors and medical students of Pakistani origin. She’s especially passionate about teaching and education, having presented a workshop she designed herself at the 2019 Annual GMC Conference.