Intraocular inflammation

Eye Infections Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness, [nih]... 

Another example of a biomaterial is the intraocular lens, which have been commonly used to treat cataracts. They were traditionally made of inflexible materials, but more recently consist of poly(methyl methacrylate) and soft flexible materials such as silicone and acrylic. The first person to successfully implant an intraocular lens was Sir Harold Riley at the St Thomas Hospital in London in 1949. The first lenses were made of glass, were heavy, and carried several risks including infection, inflammation, loosening of the lens, lens rotation, and night time halos (Thompson, 2007). These problems, now less frequent, still occur today in a small fraction of more than one million intraocular lenses that are implanted annually in the USA. 

Active intraocular inflammation Use bimatoprost and latanoprost with caution in patients with active intraocular inflammation (eg, uveitis). 

Absorption - Intraocular penetration occurs after topical instillation. Decreased corneal integrity or stromal or uveal inflammation may enhance the penetration into the aqueous humor. Systemic absorption following therapeutic dosing appears negligible. 

Uses Neovascular wet macular degenoation Action Vascular endothelial growth factor inhibitor Dose 0.5 mg intravitreal inj qmo Caution [C ] Hx thromboembohsm Contra Periocular Infxn Disp Inj SE Endophthalmitis, retinal detachment/hemorrhage, cataract, intraocular inflammation, conjunctival hemorrhage, eye pain, floaters EMS None OD Unlikely, but immediate effect would be vision loss and pain d/t t ocular pressure... 

Iritis, which affects up to 25% of patients undergoing fomivirsen therapy, can be managed with topical corticosteroids. Vitreitis and increased intraocular pressure may also result from fomivirsen administration. Fomivirsen is contraindicated in patients who have been treated with cidofovtr within the previous 2 to 4 weeks because cidofovir increases the risk of ocular inflammation. 

Intraocular inflammation (iritis), hypotension, depression, dizziness, dry mouth, nausea, vomiting, tearing... 

Mechanism of Action An NSAID that inhibits prostaglandin synthesis and reduces prostaglandin levels in the aqueous humor. TiicrapcuticEffect Relieves pain stimulus and reduces intraocular inflammation. 

A 0.1% ophthalmic preparation is recommended for prevention of postoperative ophthalmic inflammation and can be used after intraocular lens implantation and strabismus surgery. A topical gel containing 3% diclofenac is effective for solar keratoses. Diclofenac in rectal suppository form can be considered for preemptive analgesia and postoperative nausea. In Europe, diclofenac is also available as an oral mouthwash and for intramuscular administration. 

A Tyndall effect in the anterior chamber. The presence of an intraocular inflammation is a bad prognosis... 

Band-shaped keratopathy is caused by the deposition of calcium salts in the basement membrane of the corneal epithelium and superficial stroma. It is typically a chronic process that develops over a period of months and years, and is associated with chronic corneal or intraocular inflammation. 

The ocular adverse effects of latanoprost include conjunctival hyperemia, iris pigmentation, periocular skin color changes, anterior uveitis, and cystoid macular edema in pseudophakic patients (77,78). H. simplex dendritic keratitis has been reported after treatment with latanoprost (79). In patients with uveitic glaucoma, latanoprost can cause increased intraocular pressure and recurrence of inflammation (80). 

The drug is slowly cleared from vitreous with a half-life of approximately 55 hours in humans and is subsequently cleared from the retina. Measurable concentrations of drug are not detected in the systemic circulation following intravitreal administration. Immediate therapy of CMV retinitis with fomivirsen was more effective in delaying progression than deferred treatment in a recent clinical trial. Concurrent systemic anti-CMV therapy is recommended to protect against extraocular and contralateral retinal CMV disease. Potential side effects include iritis and vitreitis as well as increased intraocular pressure and changes in vision. An interval of at least 2-4 weeks is recommended between cidofovir administration and use of fomivirsen because of the risk of ocular inflammation. 

J. F. Howes, H. Baru, M. Vered, and R. Neumann, Loteprednol etabonate comparison with other steroids in two models of intraocular inflammation, J. Ocul. Pharmacol. 10 289 (1994). 

Gonjunctival hyperemia is the most frequent side effect associated with bimatoprost therapy and generally occurs more often than in patients treated with travoprost or latanoprost. Most occurrences, however, are mild. For most patients the hyperemia occurs within 6 weeks of initiating treatment. However, hyperemia can be seen as early as within 24 hours for some patients. The severity of hyperemia often diminishes over time and is not associated with ocular surface or intraocular inflammation. The only other frequent side effect (reported in more than 10% of patients) is eye pruritus. 

Like fluorometholone, medrysone is a synthetic derivative of progesterone. As compared with prednisolone, dexamethasone, and fluorometholone, medrysone exhibits limited corneal penetration and a lower affinity for glucocorticoid receptors. In clinical use it appears to be the weakest of the available ophthalmic steroids. Medrysone can be useful for superficial ocular inflammations, including allergic and atopic conjunctivitis, but intraocular inflammatory conditions generally do not respond. Clinical experience with medrysone has also indicated that it is less likely to cause a significant rise in lOP. However, caution needs to be exercised in patients known to respond to steroids with a rise in lOP (so-called steroid responders), because pressure increases can lead to ocular damage. 

Damage to the iris sphincter muscle by high intraocular pressure, trauma, or inflammation may impair pilocarpine s ability to constrict the pupil. Clinically, these conditions can usually be excluded by a careful history taking and biomicroscopic examination. Mechanical foctors associated with malpositioned intraocular lenses or posterior synechiae may also limit movement of the iris. Depending on the extent of iris damage, the pupil may demonstrate complete to nonexistent constriction. 

Conservative treatment of zoster-associated conjunctivitis, including cold compresses, lubricants, and decongestants, carries the lowest risk of treatment-related complications. Treatment of the acute conjunctivitis with topical broad-spectrum antibiotics may help to prevent secondary bacterial infection. Increased patient comfort by reduction of conjunctival inflammation may be affected by the use of topical steroids. Often, a combination antibiotic-steroid is used to accomplish both of these goals. In contrast to herpes simplex infection in which steroids are specifically contraindicated, topical steroids do not exacerbate herpes zoster infection. If steroids are used, the patient should be carefully monitored for intraocular pressure elevation. 

A thorough examination should be performed to determine the cause of bullous keratopathy. The specific treatment plan depends on both the cause and severity. Examination of the endothelium, internal structures, and fundus can be enhanced by the use of topical hyperos-motics to decrease epithelial edema. Internal examination is essential to determine if there is corneal touch by the intraocular lens or vitreous face and to rule out cystoid macular edema or intraocular inflammation. 

Epithelial bullae can be found in some cases of disciform keratitis, as can a Wessley ring, which is composed of immune cells surrounding the discoid edema.A mild to moderate uveitis with keratic precipitates is usually present, although it may not be visible due to corneal edema. Secondary glaucoma can also develop, primarily the result of intraocular inflammation (trabeculitis). 

---