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CLINICAL: CHRONIC ILLNESS Lynn Ring


RN MSc BSc(hons) RNT IP Advanced Clinical Nurse Specialist, Epsom & St. Helier


University Hospitals NHS Trust


Glaucoma: why do we need


to know? Encouraging patients to take prescribed medication is vital to prevent irreversible sight loss in chronic glaucoma


G


laucoma is not a single disease but the name given to a wide spectrum of disorders that are characterised by optic neuropathy and permanent visual field loss. These conditions are broadly linked to either open or closed drainage angles. It is important to demystify the group of conditions that all fall


under the ‘glaucoma’ umbrella. This first part of two articles focusing on glaucoma will concentrate on open angle conditions. Chronic or primary open-angle glaucoma (COAG) is a term given


to conditions with open drainage angles and variation in intraocular pressure (IOP) eventually leading to optic nerve head (optic disc) damage and irreversible sight loss. The main risk factor for optic disc damage is variation in the individual’s IOP. IOP is dependent on a continuous process of aqueous formation


and drainage within the eye. Aqueous is the clear fluid that provides nutrients to the clear structures of the eye such as the lens, and is constantly produced by the ciliary body through a metabolic process of active secretion. It exits the eye via two pathways; trabecular and uveoscleral. Trabecular meshwork cells act as a pressure sensitive system allowing 90% of the aqueous into the canal of Schlemm, draining through the episcleral veins. The remaining aqueous constantly seeps across the ciliary body into the space between the choroid and sclera and drains via the venous circulation. Normal IOP readings range from 10-21mmHg and raised IOP is caused by a disruption of this balance between formation and drainage.1


SIGNS AND SYMPTOMS COAG is often called ‘the thief of sight’ as the patient is asympto- matic in the early stages with insidious creeping visual field loss. Typically an arc-shaped blind spot in the upper nasal field of one eye develops, gradually increasing in size.2


This is invisible at first


because the visual fields of both eyes overlap, and the fellow eye offsets the blind spot temporarily. The signs for COAG are often


detected at routine optician visits and NICE guidance3


requires any


abnormal finding such as IOP above 21mmHg to be referred for further assessment.


RISK FACTORS The greatest risk factor for developing COAG is IOP measured outside of the normal range. Prevalence increases with age; approximately 2% of people over 40, and 10% over 75 years old will suffer from glaucoma. Family history of COAG increases the risk by 4-10% for first degree relatives. Afro-Caribbean patients often present with advanced disease at likely due to a tendency for thinner central corneal


an earlier age4


thickness (CCT). Goldman applanation tonometry (GAT) exerts pressure on the central cornea to flatten a small area and assumes CCT equals 555µm. The OHTS5 study identified variations in CCT measurements creating IOP under or over estimation. NICE3 identifies that GAT is the gold standard for measuring IOP but should be considered alongside CCT readings. A possible relationship between diabetes and glaucoma may exist although the evidence is inconclusive.6


However, systemic


hypotension with poor diastolic perfusion is one of the major causative factors for developing optic neuropathy, with IOP in the normal range, migraine headaches and peripheral vascular spasms also implicated.7


BOX 1. DIAGNOSTIC TESTS


1. Anterior segment examination of cornea, anterior chamber depth, trabecular meshwork, iris, pupil and lens.


2. IOP using Goldmann applanation tonometry. 3. Pachymetry – measurement of central corneal thickness. 4. Dilated posterior segment examination of optic nerve head (optic disc), macula and peripheral retina.


32 Nursing in Practice March/April 2012


www.nursinginpractice.com


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