Intermediate Uveitis

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Background

Intermediate uveitis refers to inflammation localized to the vitreous and peripheral retina. Intermediate uveitis was first described in the literature as chronic cyclitis by Fuchs in 1908. According to the Standardization of Uveitis Nomenclature Working Group, the primary site of inflammation is the vitreous and such entities as pars planitis, posterior cyclitis, and hyalitis are encompassed. Intermediate uveitis may be initially associated with the development of a systemic disease, such as multiple sclerosis (MS) or sarcoidosis. As such, intermediate uveitis may be the first expression of autoimmunity in these patients.

Pars planitis is considered a subset of intermediate uveitis and is characterized by the presence of white exudates (snowbanks) over the pars plana and ora serrata or by aggregates of inflammatory cells in the vitreous (snowballs) in the absence of an infectious etiology (eg, Lyme disease) or a systemic disease (eg, sarcoidosis). Some authorities believe that patients with pars planitis have worse vitritis, more severe macular edema, and a guarded prognosis compared to other patients with intermediate uveitis. This primary form accounts for over 50% of patients with intermediate uveitis.

Pathophysiology

There may be an immunogenetic predisposition for the disorder in some cases (see Causes), accounting for family clustering that is seen on occasion, indicating environmental or hereditary associations. The available evidence would suggest an autoimmune mechanism; however, the antigenic stimulus remains elusive.

Epidemiology

Frequency

United States

Traditionally, the proportion of patients with intermediate uveitis is estimated to be 4-8% of uveitis cases in referral centers. The National Institutes of Health (NIH) reports a higher percentage (15%), which may indicate improved awareness or the nature of the uveitis referral clinic. In the pediatric population, intermediate uveitis can account for up to 25% of uveitis cases.

Mortality/Morbidity

Permanent loss of vision is most commonly seen in patients with chronic cystoid macular edema (CME). Every effort must be made to eradicate CME when present. Other less common causes of visual loss include rhegmatogenous retinal detachment, glaucoma, band keratopathy, cataracts, vitreous hemorrhage, epiretinal membrane, and choroidal neovascularization.

Race

No racial predilection exists for this disease.

Sex

The incidence of intermediate uveitis is equal in men and women.

Age

Although intermediate uveitis can develop at any age, it primarily afflicts children and young adults. There is a bimodal distribution with one peak in the second decade and another peak in the third or fourth decade.

In the pediatric age group, intermediate uveitis is associated with a worse presenting visual acuity. Poorer outcomes may be related to delayed presentation/diagnosis, the inherent difficulties of immunosuppression in children, or a more aggressive disease.

History

The most common symptoms of intermediate uveitis are blurry vision and floaters.

Pain and photophobia are the exception.

Bilateral involvement at initial presentation approaches 80%, although it is frequently asymmetric. Eventually, approximately one third of unilateral cases will become bilateral.

Later in the disease course, more severe visual loss may occur secondary to chronic CME (28-50%), uveitic glaucoma (15%), rhegmatogenous retinal detachment (3-22%), vitreous hemorrhage (6-28%), cataracts (15-20%), or cyclitic membrane development.

Physical

See the list below:

Causes

The cause of intermediate uveitis or pars planitis has not been elucidated. Intermediate uveitis is a category of uveitis based on an anatomical classification system that can include diseases of various etiology and clinical manifestations. Associations of the disease with such entities as MS, sarcoidosis, or inflammatory bowel disease suggest an autoimmune component in at least a subset of patients. The clustering of familial cases has led to the investigation of human leukocyte antigen (HLA) associations. The inciting event appears to be peripheral retinal perivasculitis and vascular occlusion, leading to ocular inflammation, vitritis, and snowbank formation. The etiology of the antigenic stimulus is not clear and may be either vitreal or perivascular in nature.

Laboratory Studies

See the list below:

Imaging Studies

Fluorescein angiography

Fluorescein angiography is useful in determining the presence and extent of CME.

Knowing if CME exists helps in choosing the appropriate treatment plan.

The angiogram provides information about the integrity of the retinal vasculature. Staining of the vessel walls and/or leakage indicates a perivasculitis.

Retinal neovascularization and optic nerve edema can be recognized easily.

B-scan ultrasonography

When media are obscured by vitreous hemorrhage, inflammatory debris, cyclitic membrane, or cataract, B-scan ultrasonography can be useful.

Obtain B-scan ultrasonography to document the extent of vitreous debris, retinal detachment, and cyclitic membranes.

Ultrasound biomicroscopy may show features that are not clinically obvious, such as uveal thickening, the exact nature of inflammatory condensations in the vitreous, and vitreoretinal adhesions with traction.

Both 50 MHz and 20 MHz ultrasound imaging in patients with intermediate uveitis readily demonstrated inferior pars plana exudates and cyclitic bands, which are of extreme value in preoperative planning in patients with dense media and/or a secluded pupil due to posterior synechiae.

Optical coherence tomography (OCT)

OCT has replaced traditional fluorescein angiography as the imaging modality of choice in establishing a diagnosis of CME.

OCT can help demonstrate the presence of cysts in the fovea and measure macular thickness. OCT is a highly sensitive, noninvasive method to help diagnose CME and provides the best method to monitor the therapeutic response of patients to treatment as macular thickness appears to correlate with visual acuity to some degree.

OCT can also help demonstrate the presence of epiretinal membranes, a known late complication of ocular inflammation.

The presence of neurologic symptoms or a history of optic neuritis should prompt the clinician to obtain an MRI of the brain and subsequent consultation with a neurologist to rule out MS.

If there is a high clinical suspicion of sarcoidosis as the cause of intermediate uveitis, a chest X-ray or a Gallium scan should be obtained as indicated. Older women with a negative chest X-ray and ACE may have hilar adenopathy identified on chest CT.

Histologic Findings

Histologic examination of the pars plana snowbank shows that it is not a true protein exudate. The snowbanks are predominantly a combination of collapsed vitreous, blood vessels, inflammatory cells (mainly lymphocytes), fibroblasts, and glial elements. Histologic studies also failed to identify cells positive for GFAP, an important glial cell marker, within the snowbanks. Peripheral veins may manifest lymphocytic infiltration and cuffing. The vascular component of the snowbanks has been shown to be continuous with retinal vessels. Vitreous snowballs are composed of epithelioid cells and multinucleated giant cells.

Medical Care

See the list below:

Surgical Care

See the list below:

Consultations

A cost-effective, directed, patient-specific laboratory diagnostic evaluation is best directed by the informed ophthalmologist. This approach incorporates the demographics, history, and examination findings into a comprehensive, practical diagnostic approach to the patient with uveitis.

For any patient with uveitis, seek an internist for a general medical evaluation.

Input from a gastroenterologist, neurologist, or infectious disease specialist may be necessary, depending on physical findings or pertinent elements of the review of systems.

Consultation with an experienced chemotherapist is mandatory when using alkylating and cytotoxic agents.

Medication Summary

The goal is to suppress intraocular inflammation, which usually is accomplished with systemic corticosteroids. In some cases, this treatment is inadequate, and immunosuppressive or immune-modulating agents are required to control the disease. These agents can be used adjunctively with steroids or alone.

Prednisone (Deltasone, Meticorten, Orasone)

Clinical Context:  Readily absorbed through the GI tract and inhibits phospholipase A2 (an enzyme that liberates arachidonic acid from phospholipids in the production of inflammatory mediators).

Triamcinolone (Amcort)

Clinical Context:  A long-acting depo-steroid. For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Observe for ptosis or anterior dissection. Generic preparations appear to be equally efficacious compared to proprietary Kenalog.

Prednisolone 1% (Pred Forte)

Clinical Context:  Has 3-5 times the anti-inflammatory action as hydrocortisone. Glucocorticoids inhibit the edema, fibrin deposition, capillary dilation and phagocytic migration of the acute inflammatory response. Steroids are also potent inhibitors of the inflammatory enzyme cascade, angiogenesis, and mast-cell degranulation. Steroids stabilize cell membranes.

Loteprednol etabonate binds to anti-inflammatory receptors 4.3 times more avidly than dexamethasone. Possible reduced risk of glaucoma due to ester substitution for ketone moiety at the 20 position on the steroid cholesterol ring. Shake well for susp (acetate).

Class Summary

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Cyclosporine (Sandimmune, Neoral)

Clinical Context:  A cyclic polypeptide produced as a fungus metabolite, capable of reversibly arresting the T-lymphocyte cell cycle in the G0 and G1 phases. Potent down-regulator of interleukin 2 production and receptor expression. Newer Neoral preparation is better absorbed and may require marked dosage reductions.

Azathioprine (Imuran)

Clinical Context:  Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.

Methotrexate (Folex PFS, Rheumatrex)

Clinical Context:  Antimetabolite that inhibits dihydrofolate reductase, thereby inhibiting DNA synthesis in rapidly replicating cells. Immunosuppressive actions may be related to reduction in cytokines. Available as 2.5-mg pills.

Class Summary

Inhibit cell-mediated and (to a lesser degree) humoral immunity by arresting T-lymphocyte activity. The ultimate goal is to suppress inflammation.

Cimetidine (Tagamet)

Clinical Context:  Used as prophylaxis against corticosteroid induced gastric and duodenal ulcer.

Consult with internist if patient has preexisting symptoms of GERD or peptic ulcer disease prior to beginning corticosteroid therapy.

Ranitidine (Zantac)

Clinical Context:  Used as prophylaxis against corticosteroid-induced gastric and duodenal ulcer.

Class Summary

Reduces postprandial daytime and nighttime gastric acid secretion by about 50-80%. May increase gastromucosal defense and healing in acid-related disorders (ie, stress-induced ulcers) by increasing production of gastric mucus, increasing mucosal secretion of bicarbonate and gastric mucosal blood flow as well as increasing endogenous mucosal synthesis of prostaglandins. Histamine H2-receptor antagonists can be used prophylactically to prevent gastritis and ulcer disease in patients taking oral or intravenous corticosteroids.

Omeprazole (Prilosec)

Clinical Context:  Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump.

Lansoprazole (Prevacid)

Clinical Context:  Inhibits gastric acid secretion.

Esomeprazole magnesium (Nexium)

Clinical Context:  S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+ -ATPase enzyme system at secretory surface of gastric parietal cells.

Class Summary

Thought to be a gastric pump inhibitor in that it blocks the final step of acid production by inhibiting the H+/K+ -ATPase system at the secretory surface of the gastric parietal cell. Both basal and stimulated acid secretions are inhibited. Short-term (4-8 wk) treatment of active duodenal ulcer, active benign gastric ulcer, erosive esophagitis (all grades), and heartburn and other symptoms associated with GERD.

Adalimumab (Adalimumab-atto, Amjevita, Humira)

Clinical Context:  A fully humanized anti-TNF alpha antibody FDA-approved for the treatment of intermediate uveitis, posterior uveitis, and panuveitis.

Fluocinolone intravitreal implant (Retisert, Yutiq)

Clinical Context:  The implants are surgically inserted by the ophthalmologist and indicated for chronic, noninfectious uveitis of posterior segment of eye. Retisert releases 0.6 mcg/day initially; amount released decreases after the first month to 0.3-0.4 mcg/day over ~30 months. Yutiq releases at a rate of 0.25 mcg/day over ~36 months.

Dexamethasone intravitreal implant (Ozurdex)

Clinical Context:  The implant is surgically inserted by the ophthalmologist and indicated for chronic, noninfectious uveitis of posterior segment of eye.

Further Outpatient Care

Observe patients every 1-4 weeks during the active phase of the disease, more frequently if CME or severe inflammation is present.

Since corticosteroids can cause glaucoma at anytime, it is imperative that patients return for intraocular pressure monitoring at 4-week intervals while using corticosteroids or after periocular injections. Periocular triamcinolone can cause steroid responsive glaucoma many months after an injection.

Consider fluorescein angiography and/or OCT whenever CME is suspected.

Consider reordering any relevant laboratory tests if the clinical situation changes. For example, a patient who initially presents with routine intermediate uveitis and negative findings on workup is found to have multiple choroidal granulomata 14 months later. In this case, unless proven otherwise, consider sarcoidosis (or other granulomatous disease).

Further Inpatient Care

Patients generally are treated on an outpatient basis.

Inpatient & Outpatient Medications

Topical steroids (prednisolone acetate 1%, loteprednol etabonate 0.5%) are used for anterior segment inflammation. Frequency of use depends on severity of inflammation. Possible discrepancy in potency between proprietary Pred Forte 1%, and generic prednisolone acetate 1%, wherein the generic preparation is less potent due to markedly higher suspension particle diameter and resultantly decreased surface exposure and intraocular absorption.

Triamcinolone is given as a periocular injection in the office setting to suppress intraocular inflammation and CME. The most commonly used dose of triamcinolone acetonide is 20 mg. If no response occurs, it can be repeated as soon as 2 weeks after the initial injection. If no improvement occurs after 3 consecutive injections, a different treatment modality must be considered.

Use oral prednisone (0.5-1 mg/kg) in the presence of moderate-to-severe inflammation, especially when it is bilateral. Tapering can be initiated as soon as 2 weeks after treatment was started, according to the clinical response of the patient, and the minimum effective dose controlling the inflammation should be maintained for at least 4 months.

Immunosuppressive agents (ie, methotrexate, cyclosporine, tacrolimus, azathioprine) generally are used as steroid-sparing agents or for severe inflammation that is unresponsive to steroids. Immune-modulating agents (ie, infliximab) can be considered to treat persistent macular edema or to decrease the steroid requirements of selective patients. Consult with a specialist who is familiar with these drugs.

Deterrence/Prevention

Smoking cessation should be strongly encouraged. Thorne et al found a 4-fold increased risk of uveitic CME in smokers with intermediate uveitis.[19]

Complications

See the list below:

Prognosis

See the list below:

Patient Education

Since this disease is long term and recurrent, patients must recognize symptoms of a flare-up (ie, floaters, blurred vision, redness, discomfort) early and seek medical attention appropriately.

Author

Robert H Janigian, Jr, MD, Clinical Associate Professor, Department of Surgery (Ophthalmology), The Warren Alpert Medical School of Brown University

Disclosure: Nothing to disclose.

Coauthor(s)

Brian A Welcome, MD, Staff Physician, Department of Ophthalmology, Rhode Island Hospital

Disclosure: Nothing to disclose.

Theodoros Filippopoulos, MD, Head of Glaucoma Clinic, Athens Vision Eye Institute; Clinical Lecturer, Department of Ophthalmology, Second Ophthalmology Clinic, University of Athens Medical School, Greece

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

R Christopher Walton, MD, Adjunct Professor, Department of Ophthalmology, University of Texas Health Science Center at San Antonio

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Additional Contributors

John D Sheppard, Jr, MD, MMSc, Professor of Ophthalmology, Microbiology and Molecular Biology, Clinical Director, Thomas R Lee Center for Ocular Pharmacology, Ophthalmology Residency Research Program Director, Eastern Virginia Medical School; President, Virginia Eye Consultants

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: 1-800-DOCTORS; AbbVie; Alcon; Aldeyra; Allergan; Alphaeon; ArcScan; Baush+Lomb; Bio-Tissue; Clearside; EyeGate; Hovione; Mededicus; NovaBay; Omeros; Pentavision; Portage; Santen; Science Based Health; Senju; Shire; Sun Pharma; TearLab;TearScience;Topivert<br/>Serve(d) as a speaker or a member of a speakers bureau for: AbbVie; Alcon; Allergan; Bausch+Lomb; Bio-tissue; EyeGate;Hovione;LayerBio; NovaBay;Omeros;Portage; Santen; Shire; Stemnion; Sun Pharma;TearLab;TearScience; Topivert <br/>Received research grant from: Alcon; Aldeyra; allergan; Baush+ Lomb; EyeGate; Hovione; Kala; Ocular Therapeutix;Pfizer; RPS; Santen;Senju;Shire;Topcon; Xoma.

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