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Glaucoma: a Brief Update for 2017

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Glaucoma: a Brief Update for 2017 South African Family Practice 2017; 59(6):5-10 S Afr Fam Pract Open Access article distributed under the terms of the ISSN 2078-6190 EISSN 2078-6204 Creative Commons License [CC BY-NC-ND 4.0] © 2017 The Author(s) http://creativecommons.org/licenses/by-nc-nd/4.0 REVIEW Glaucoma: a brief update for 2017 Natalie Schellack,1 Gustav Schellack,2 Selente Bezuidenhout,1 Lucille Malan,1 Hanneke de Klerk1 1 School of Pharmacy, Sefako Makgatho Health Sciences University 2 Clinical research professional in the private sector Corresponding author, email: [email protected] Abstract Glaucoma is a complex condition of the eye and the second leading cause of blindness around the globe. It is an ophthalmic neurodegenerative condition and is characterised by a raised intra-ocular pressure (IOP). The latter also constitutes the only modifiable risk factor in glaucoma management. When left untreated patients may gradually experience a visual field loss, and even lose their sight completely. This article provides a brief overview of this condition, the pharmacological treatment options that are available in South Africa, as well as the rational use thereof. Keywords: glaucoma, intra-ocular pressure, IOP, ocular hypertension, visual field loss, carbonic anhydrase Introduction Table I: Major types of glaucoma7 Glaucoma is progressive optic neuropathy that affects the Open-angle glaucoma (OAG) Angle-closure glaucoma (ACG)* eye and is associated with an increased intra-ocular pressure Accounts for at least 90% of all Less common form of glaucoma glaucoma cases (IOP), which also constitutes the only modifiable risk factor in glaucoma management. When left untreated patients may Caused by the slow clogging of Develops very quickly the drainage canals, resulting in gradually experience a visual field loss, and even lose their sight increased intraocular pressure completely. It is the number one cause of irreversible vision loss Has a wide and open angle Has a closed or narrow angle and the second leading cause of blindness around the globe.1,2 between the iris and cornea between the iris and cornea Has symptoms and damage that Has symptoms and damage that Glaucoma may be defined as a condition that causes progressive are not readily noticed are usually very noticeable neuropathy in the optic field that is characterised by structural *Also known as closed-angle or narrow-angle glaucoma changes in the optic nerve head (or optic disk). This may lead to functional changes in the patients’ visual field, when no other normal physiological balance between the secretion of aqueous ocular diseases or congenital abnormalities could be found.3 humour and the drainage thereof is affected by this condition. Aqueous humour is secreted by the ciliary body and drainage Around 66.8 million people worldwide are afflicted with of the humour takes place via two independent pathways, glaucoma. Predictions are that glaucoma will affect almost namely the trabecular meshwork and the uveoscleral outflow 4 80 million people by 2020 and 111.8 million people by pathway.9,10 2040, affecting more people residing in Asia and Africa.5 The estimated prevalence of glaucoma is around 5 to 7% in the black The filtration is dependent on pressure gradients, blood population and 3 to 5% in the white population of South Africa. pressure and increased IOP. Osmotic gradients produced A total of approximately 200 000 people are currently affected by the active secretion of sodium and bicarbonate ions and by glaucoma in South Africa.6 There are different variations of other solutes, produce a pressure gradient that allows for the glaucoma but the two major types are listed in Table I. movement of the humour from the pool of ciliary stromal ultra- filtrate into the posterior chamber, thereby forming aqueous Pathophysiology and classification humour. Various receptors and transmitters are found in the The pathophysiology of glaucoma is not completely ciliary epithelium and the smooth muscle structures of the understood, but is related to retinal ganglion cell death. A better eye. Carbonic anhydrase (primarily of the type II isozyme), α- understanding of the pathophysiological mechanisms involved and β-adrenergic receptors, sodium and potassium-activated in the onset and progression of glaucomatous optic neuropathy triphosphates, prostaglandins and muscarinic receptors all is crucial in the development of better therapeutic options.8 The play a role in the normal functioning of the eye. Glaucoma can www.tandfonline.com/oemd 5 The page number in the footer is not for bibliographic referencing Glaucoma: a brief update for 2017 6 Table II: Classification of glaucoma9-10 Vasodilators (low risk) For example, nitro-glycerine Primary glaucoma Secondary glaucoma used to treat acute angina may cause visual blurring, increases • Open-angle • Open-angle intra-ocular pressure, vasodilation • Angle-closure ◦ Pre-trabecular and a coloured halo, albeit in rare ◦ With pupillary block ◦ Trabecular instances. ◦ Without pupillary block ◦ Post-trabecular • Angle-closure Cimetidine and ranitidine (low These medicines have weak ◦ With pupillary block risk) anticholinergic side-effects, thus ◦ Without pupillary block raising the intraocular pressure. Closed-angle glaucoma Mechanism be classified as either a primary inherited disorder, secondary Topical anticholinergics Medicines that stimulate the sympathomimetic system or inhibit to a disease, trauma or drugs, or as being congenital in nature Topical sympathomimetics the parasympathomimetic system 9,10 (Table II). Systemic anticholinergics cause pupillary dilatation, thus precipitating acute angle-closures Systemic sympathomimetics Open-angle glaucoma may result from optic nerve damage at in patients with occlusive anterior (low risk) any range of intra-ocular pressure. The rate of progression can chamber angles. be either fast or slow, with patients who may have had increased Heterocyclic antidepressants Cause acute angle closures, either due to the indirect anticholinergic Selective serotonin reuptake intra-ocular pressures and then only present with changes in the effects or increased levels of inhibitors (SSRIs) optic disk or visual fields at a much later stage. This increases the serotonin causing mydriasis. Imipramine challenge to diagnose and treat open-angle glaucoma, because Venlafaxine the early disease is often asymptomatic.9-12 Low-potency phenothiazines Due to the inhibition of the Closed-angle glaucoma may be due to a physical blockage of parasympathomimetic system the trabecular meshwork. This can be more acute in onset. When Antihistamines Due to the weak anticholinergic effects the IOP is > 40 mmHg optic nerve damage and even permanent Ipratropium bromide Anticholinergic effects causing nerve damage (> 60 mmHg) can occur. However, since the dilatation of the pupil and leading trabecular meshwork is intrinsically normal, it is possible to to closure of the anterior chamber drainage angles. restore the trabecular function by early removal of the synechiae Benzodiazepines (low risk) Induces relaxation of the sphincter 9-11,13 before irreversible ultra-structural changes have occurred. muscle of the iris and have a mild anticholinergic effect Medicine-induced glaucoma may be due to an increased Methylxanthines (e.g. The methylxanthines may intraocular pressure brought about by various medicines. theophylline and caffeine (low precipitate an attack of Medicines may worsen pre-existing glaucoma or induce risk)) angle-closure glaucoma, by accentuating the anti-cholinergic glaucoma based on their mechanisms of action, and patients’ action on the eye. predisposition. Table III provides an overview of medicines that Sulpha-containing medications May involve different mechanisms, may induce or potentiate an increased intraocular pressure:9-11,14-17 including anterior rotation of the ciliary body with or without choroidal effusions, which result Table III: Drugs that may potentiate or induce raised intraocular in a shallow anterior chamber pressure in 9-11,14-18 and blockage of the trabecular IOP Mechanism meshwork by the iris. Ophthalmic corticosteroids Glucocorticosteroids reduce the The exact reason for ciliary (high risk) facilitation of aqueous humour body swelling is unknown but it occurs in susceptible individuals. Systemic corticosteroids outflow through the trabecular meshwork. Accumulation of the Topiramate is a sulpha-containing Nasal/inhaled corticosteroids extracellular material blocks the anticonvulsant. Some cases have trabecular channels and thus the been reported with topiramate outflow. having induced an acute angle-closure. Fenoldopam Through dopamine-1 receptor- mediated effects, an increase in Tetracyclines (low risk) The mechanism may involve intraocular pressure is observed anterior rotation of the ciliary in both healthy volunteers and body with choroidal expansion, patients with accelerated systemic secondary to the accumulation of hypertension. serous fluid in the extravascular choroidal space, causing closed- Ophthalmic anticholinergic Produce a rise in intraocular angle glaucoma. agents pressure Monoamine oxidase inhibitors Cause a pupillary dilatation with Succinylcholine Via an unknown mechanism (low risk) subsequent obstruction of the succinylcholine increases the trabecular meshwork, and a intraocular pressure by 5-10 mmHg possible increase in inflow during for 5-10 minutes, with an onset of the papillary dilatation. 2-4 minutes after administration. www.tandfonline.com/oemd 6 The page number in the footer is not for
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