Corticosteroid ocular effects

Intranasal corticosteroids are effective in reducing ocular symptoms as well as nasal symptoms. The mechanism of action is unclear it may partly be due to a systemic effect resulting from local absorption, although system-ically related adverse effects are uncommon. These are used once or twice daily depending on choice and should be used regularly during the hay fever season. 

If mast cell stabilizers or multiple-action agents are not successful, a trial of a topical NSAID is appropriate. Ketorolac is the only approved topical agent for ocular itching. NSAIDs do not mask ocular infections, affect wound healing, increase intraocular pressure, or contribute to cataract formation like the topical corticosteroids. However, for allergic conjunctivitis, topical ketorolac is not as effective as olopatadine or emedas-tine in trials.15 Full efficacy of ketorolac takes up to 2 weeks.17... 

Corticosteroids administered intravitreally bypass the blood-ocular barrier to achieve therapeutic levels in the eye while minimizing systemic side effects. Initial studies of intravitreal corticosteroids combined dexamethasone and gentamicin in the treatment of inflammation associated with experimentally reduced endophthalmitis.As of late, interest has shifted to triamcinolone acetonide because of the longer half-life in the vitreous and its use in treatment of proliferative vitreoretinopathies. 

The success of intravitreal implants, such as achieved with ganciclovir, has renewed interest in developing an intravitreal corticosteroid implant to further enhance the intravitreal route of administration, thus reducing the need for multiple injections. Bausch and Lomb and Control Delivery Systems have developed an intravitreal implant that can deliver the corticosteroid fluocinolone acetonide (Retrisert) to posterior eye tissue for up to 3 years. The implant, which was approved in 2005 by the U.S. Food and DrugAdministration (FDA), delivers 0.59 or 2.1 mg of fluocinolone acetonide. The long-term ocular side effects of this device are unknown at this time. 

Both systemic and topical ocular steroid therapy can retard corneal healing. Persistent punctate staining of the cornea can indicate epithelial damage by the corticosteroid if the original disease has been eliminated. Effects on collagen synthesis and fibroblast activity have been proposed as a possible mechanism. 

Because side effects can complicate the use of corticosteroids, a careful history and certain tests may be advisable, particularly if a patient may require prolonged ocular therapy. Steroids should be used with great caution in patients with diabetes mellitus, infectious disease, chronic renal feilure, congestive heart feilure, and systemic hypertension. Systemic administration is generally contraindicated in patients with peptic ulcer, osteoporosis, or psychoses. Topical steroids should be used with caution and only when necessary in patients with glaucoma. 

Most patients show improvement with corticosteroids. Steroids may be of optimum benefit when added to another therapeutic regimen such as anticholinesterase therapy or immunosuppressants such as azathioprine. Moderate-dose daily prednisone for 4 to 6 weeks, followed by low-dose alternate-day therapy as needed, has been foimd to improve ocular motility and decrease the development of generalized myasthenia. Steroid therapy must be used cautiously in these patients because of the worrisome character and incidence of unwanted effects of these drugs. It is possible for patients to develop immunosuppression such that tapering of... 

The ocular side effects of corticosteroids are many and are related to the route of administration. The most common concerns are increased intraocular pressure (lOP) and cataracts, but delayed epithelial woimd healing and increased risk of infection due to immime modulation and decreased tear lysozyme levels are issues for the cornea. Changes to other ocular tissues have been noted (subconjunctival hemorrhages, blue sclera, eyelid hyperemia and edema, retinal emboUc events, central serous choroidopathy) and neurologic compUcations reported (diplopia, nerve palsies, intracranial hypertension) (see Appendix 35-1). 

Until recently, very few systemic drug therapies were implicated in ocular adverse effects in the episclera, sclera, and uvea. Topical ocular medications such as beta-blockers, latanoprost, and corticosteroids as well as other topical ocnlar medications have been associated with uveitis. 

The use of intravitreal corticosteroids was first popularized by Machemer in 1979 (33) in an effort to halt cellular proliferation after retinal detachment surgery, and Graham (34), McCuen (35), Tano (36), and others have studied its use in both animal models and humans. In contrast to other corticosteroids with short half-lives following intravitreal injection, triamcinolone acetonide is an effective and well-tolerated (35,37) agent for intravitreal injection in conditions such as uveitis (38,39), macular edema secondary to ocular trauma or retinal vascular disease (40), proliferative diabetic retinopathy (41), intraocular proliferation such as proliferative vitreoretinopathy (42), and choroidal neovascularization from AMD (43,44). 

Inclusion criteria for patients enrolled in the study included severe uveitis with posterior segment involvement with or without iridocyclitis, previous favorable response to oral or periocular corticosteroids, treatment-limiting side effects associated with systemic or periocular corticosteroids or systemic nonsteroidal immunosuppressive agents, intraocular pressure controlled at <21 mmHg with no more than one anti-ocular hypertensive drop and ability to attend follow-up visits. In total, seven eyes of five patients were included and the patients had a diagnosis of Bechet s syndrome or idiopathic panuveitis. The mean uveitis duration before device implantation was six years and the mean visual acuity was 20/207. 

Corticosteroids have been investigated as a potential treatment for PVR. It has been hypothesized that they might directly inhibit cellular proliferation and suppress inflammation, and thereby prevent epiretinal and subretinal membrane formation (30). The safety and efficacy of corticosteroids to treat PVR have been demonstrated in animal studies (30-33). Systemic corticosteroids have been used to treat a variety of ocular and nonocular conditions in humans. Systemic side effects of corticosteroids are well-documented and include, among others, Cushingoid changes, osteoporosis, elevated serum glucose, hypertension, peptic ulcer disease, and psychiatric disturbance. 

Corticosteroids have been used to treat a variety of ocular diseases. Traditionally, delivery of corticosteroids for posterior-segment eye diseases has been achieved through oral systemic therapy and periocular injections. Oral corticosteroids have not been widely used to treat DME, but when used for posterior inflammatory uveitis, they require high concentrations to reach therapeutic levels in the posterior segment. These high doses often result in systemic side effects (24). Periocular corticosteroid administration often must be repeated and may be associated with complications such as ptosis and inadvertent needle penetration of the globe. 

Editor s notes In this chapter adverse effects and reactions that arise from the oral or parenteral administration of corticosteroids (glucocorticoids and mineralocorti-coids) are covered in the section on systemic administration. Other routes of administration are dealt with in the sections after that inhalation and nasal administration are dealt with in Chapter 16, topical administration to the skin in Chapter 14, and ocular administration in Chapter 47. 

Inflammatory bowel disease (Crohn s disease and ulcerative colitis) occurs among all age groups but has peaks of incidence in the second and fourth decade of life. Currently, corticosteroid therapy is the most effective treatment for moderate to severe cases of IBD. Ocular pathology in the setting of IBD may be related to inflammation of the gastrointestinal tract or secondary to corticosteroid treatment. The two major ocular side effects of systemic corticosteroid therapy are posterior subcapsular cataract (PSC) and raised intraocular pressure (lOP). Recently, we reported that PSC was detected in 12 of 58 (20.7%) corticosteroid-treated pediatric IBD patients and that 21 patients of the same population (36.2%) had raised lOP. Because pediatric IBD patients continue corticosteroid therapy into adulthood, we analyzed the prevalence of PSC and raised lOP in a series of adult IBD patients. 

The incidence of PSC in the general adult population ranges from 0.2% to 6.0% and that of raised lOP in subjects of 40 years old is approximately 1.5%. The high incidence of PSC and raised lOP (50% and 8%, respectively) in our population of adult patients with IBD at a mean age of 38.5 years, implicates corticosteroids as the causative factor for the development of these ocular abnormalities. Association of IBD with certain inflammatory eye lesions such as uveitis, episcleritis, and keratoconjunctivitis has been reported. However, cataracts (PSC) and raised lOP, have not been ascribed as direct ocular side effects of IBD. Likewise, the supplementary medications which the IBD patients received have not been incriminated in inducing PSC or raised lOP. ... 

Since corticosteroids reduce the immunological defences of the body to most types of infection, their use in the eye should be monitored carefully. The specific type of ocular disease and its response to steroid therapy may determine whether to use topical, systemic and/or local injections. Systemic side effects do not generally occur with limited topical administration. 

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