Description, Causes and Risk Factors:
Glaucoma: A disease of the eye characterized by increased intraocular pressure (IOP), excavation, and atrophy of the optic nerve; produces defects in the field of vision.
Corticosteroid-induced glaucoma is defined as glaucoma caused by a hereditary predisposition in which local instillation of eye drops containing corticosteroid causes increased intraocular pressure (IOP).
A rise in intraocular pressure (IOP) can occur as an adverse effect of corticosteroid therapy. If the ocular hypertensive effect is of sufficient magnitude, for an adequate duration, damage to the optic nerve (steroid-induced glaucoma) may ensue.
It has long been known that IOP fluctuates diurnally and it has been postulated that this may be linked to cortisol levels. The peak in diurnal IOP occurs at around 0700 hours and the trough during the early evening, the daily fluctuation in IOP correlating closely with plasma cortisol levels. Furthermore, cases have been described of raised IOP secondary to adrenal gland hyperplasia, and although direct cause and effect has not been proven, it is known that there is no diurnal IOP variation in patients who have had their adrenals removed.
A corticosteroid-induced IOP rise has been shown to occur with various methods of steroid administration, but is most commonly identified as a complication of topical corticosteroid application. In responsive patients, the IOP typically rises after several weeks of continual corticosteroid therapy and returns to normal following cessation of such therapy.
Several genes have been shown to be up-regulated in TM (trabecular meshwork) cells, including genes representing a serine protease inhibitor (Alpha-1-antichymotrypsin), a neuroprotective factor (pigment epithelium-derived factor), an anti-angiogenesis factor (cornea-derived transcript factor 6) and a prostaglandin synthase (prostaglandin D2 synthase) enzyme. However, the most extensively studied gene is that representing the protein myocilin (initially referred to as TM-inducible glucocorticoid response or TIGR, gene product), the gene being identical to GCL1A and now referred to as the myocilin gene. The myocilin gene, which is a 55 kDa protein, has been shown to be induced in human cultured TM cells after exposure to dexamethasone for 2-3 weeks. The role of myocilin in corticosteroid-induced ocular hypertension has been proposed because: (1) it is highly expressed in trabecular cells exposed to glucocorticoids, (2) the delay in its expression is similar to the delay in the pressure rise in glucocorticoid-treated eyes and (3) the dose required to cause the protein expression is similar to that required to raise IOP. Linkage analysis of a large single family with juvenile onset POAG has shown that mutations in a gene on chromosome 1q are responsible for most cases of autosomal dominant juvenile onset POAG. This gene, previously called the TIGR gene, produces the protein myocilin. Different mutations within myocilin lead to widely variable glaucoma phenotypes involved in both juvenile and adult onset POAG. The role of myocilin remains poorly understood and experiments altering its expression have provided conflicting results. In perfused human anterior segment cultures, recombinant myocilin increased outflow resistance, while viral-mediated transfer of myocilin in TM cells caused an overexpression of myocilin and lead to reduction in outflow resistance.
There are certain conditions which are associated with increased risk of steroid-induced glaucoma such as:
First degree relatives of POAG.
Connective tissue disorder.
Eyes with traumatic angle recession and their fellow eyes.
Pigment dispersion syndrome.
Patient with primary open-angle glaucoma (POAG).
Although there has been marked progress in the last few years in understanding the mechanisms behind corticosteroid-induced glaucoma, further research needs to be undertaken. The genetics are not fully understood, and it appears that a number of gene loci interact in controlling the corticosteroid-induced glaucoma response rather than it following simple Mendelian inheritance. Better identification of patients at risk of corticosteroid-induced IOP rises would allow them to be more closely monitored than others. It is important to identify those patients who have a corticosteroid-induced pressure rise early enough to prevent them from developing permanent visual loss. In most cases, corticosteroid-induced glaucoma can be treated successfully by topical anti-glaucoma therapy, although cessation of corticosteroid therapy is the ideal course of action.
The prognosis of corticosteroid-induced glaucoma depends on the duration of the IOP elevation and the control of IOP after diagnosis. Uncontrolled increase in IOP can lead to permanent optic nerve damage and hence permanent blindness. In patients with controlled IOP, the prognosis can be favorable depending on the severity of disease on presentation. Drug-induced IOP rise can be asymptomatic initially especially in open-angle type. General practitioners should be aware of the risk factors for glaucoma before prescribing a drug that has the potential to cause, precipitate or exacerbate glaucoma. Topical steroids can cause IOP rise in susceptible individuals in a fairly short period of time and therefore it is advised that topical steroids should be prescribed by doctors capable of measuring IOP. Whenever in doubt, an Ophthalmologist should be consulted.
It is possible that further development of nonsteroidal anti-inflammatory therapies will provide effective alternatives to corticosteroids. It is also hoped that a full understanding of the steroid-induced response may result in the development of novel therapies for the treatment of other types of glaucoma, including primary open-angle glaucoma (POAG).
The clinical features of corticosteroid-induced glaucoma are similar to those of POAG (primary open-angle glaucoma) with the exception that patients with corticosteroid-responsive glaucoma have a history of significant corticosteroid use. The elevated IOP, induced as part of the corticosteroid response, increases the risk of optic nerve fiber damage, leading to characteristic visual field and optic nerve changes indistinguishable from those associated with POAG.
With corticosteroid-induced glaucoma, the pressure elevation is gradual. Therefore, there are very few symptoms during the early stage of disease. At a later stage, patients may complain of loss of the peripheral visual field. At the more advanced stage, when the central vision is also affected, patients may complain of blurring of vision, headaches, and halos around bright objects.
Infants may presentwith features of congenital glaucoma having tearing,photophobia, blepharospasm, cloudy corneas,buphthalmos, elevated IOP and optic disc cupping.
Diagnosis may include a complete ophthalmic examination including the followings:
Pupil reflex: Acute angle-closure presents with a fixed, mid-dilated pupil while an afferent pupillary defect indicates unilateral optic nerve damage.
Intraocular pressure: Acute angle-closure usually presents with a much higher IOP than steroid-induced glaucoma which presents with a gradual IOP elevation.
Slit lamp examination: Examination of the anterior chamber is essential to look for signs of other secondary glaucomas such as uveitic, pigment dispersion and pseudoexfoliation glaucoma. It can also assess the depth of the anterior chamber and to exclude pupillary block.Cataract is also associated with chronic steroid use.
Gonioscopic examination: Gonioscopy can evaluate the angle anatomy (i.e. openor narrow) and to determine whether the angle is occludable during pupil dilation.
Optic disc evaluation: Stereoscopic examination of the optic disc is necessary to exclude glaucomatous damage. The signs of glaucoma optic nerve damage include increased cup-to-disc ratio in horizontal and vertical meridians; progressive enlargement of the cup; evidence of nerve fiber layer damage with red-free filter; notching or thinning of disc rim; pallor; presence of hemorrhage; asymmetry between discs; and peripapillary atrophy.
Perimetry. Visual field testing such as Humphrey or Goldman is used to evaluate the severity of optic neuropathy.
Optical Coherence Tomography (OCT): OCT is an optical signal acquisition and processing method. It captures micrometer-resolution, three-dimensional images from within the optical scattering media (e.g., biological tissue). OCT is an interferometric technique, typically employing near-infrared light. It is used to evaluate the retinal nerve fiber thickness around the optic disc in glaucoma patients. Serial scans can be used to demonstrate any progression of disease.
Ultrasound Biomicroscopy (UBM): UBM is an imaging technique that uses high frequencyultrasound to produce images of the eye at near microscopic resolution. This technique is used to evaluate the anterior chamber angle configuration (i.e. open or closed) and the position of the ciliary body (any anterior rotation).
Visual acuity and refraction: Patients with acute angle-closures have significant drops in visual acuity. Patients with hyperopia are at higher risks for narrow anterior chamber angles.
A baseline measurement of IOP should be taken prior to commencement of corticosteroid therapy. Patients on topical therapy should then have their IOP measured again 2 weeks after initiation of treatment, then every 4 weeks for 2-3 months, then 6-monthly if therapy is to continue.
Patients undergoing intravitreal triamcinolone should be monitored for several months following the steroid injection. Ophthalmologists found that 40.4% of patients receiving triamcinolone show a pressure rise to greater than 24 mmHg over at an average of 100 days after treatment.
Ideally, patients requiring long-term systemic corticosteroid therapy should have glaucoma screening and those receiving 10 mg or more of prednisolone daily should have their IOP checked at 1, 3, and 6 months and 6 monthly thereafter. Glaucoma screening can be performed by optometrists in the community, or in local ophthalmic departments should there be a suspicion of established glaucoma.
The most effective management is discontinuation of the drug and administering anti-glaucoma medications till the IOP is reduced. If the patient's underlying medical condition can tolerate discontinuation of corticosteroids, then cessation of the medication usually will result in normalization of IOP. In the case of topical corticosteroid drops, a lower potency steroid medication such as the phosphate forms of prednisolone and dexamethasone, rimexolone, loteprednol etabonate, fluorometholone, or medrysone may be substituted. These lower potency drugs have a lesser propensity to raise the IOP, but they usually are not as effective as anti-inflammatory drugs. Topical nonsteroidal anti-inflammatory medications are other alternatives that have no potential to elevate IOP, but they may not have enough anti-inflammatory activity to treat the patient's underlying condition. If sub-Tenon depot steroids are causing an elevation of IOP, they should be excised and removed. It is important to remember that steroid may also cause a rise in the IOP after a filtering surgery and in such patients low potency steroids should be substituted and rapidly tapered.
When medical therapy is ineffective laser or surgery can be tried. In patients with an open angle and the absence of ocular inflammation laser trabeculoplasty can be attempted to lower the IOP. In patients whom both medical and laser therapy have failed to lower the IOP then surgical therapy is warranted. Usually, trabeculectomy with or without intraoperative antimetabolites is the primary procedure. In cases of eyes with active neovascularization or inflammation, a glaucoma drainage implant may be used as the primary procedure.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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