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| REVIEW ARTICLE |
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| Year : 2021 | Volume
: 3
| Issue : 1 | Page : 13 |
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Clinical approach to a case of anterior uveitis - A non-systematic review
Barkha Mehta1, Mithun Thulasidas2
1 Centre for Sight, New Delhi, India
2 Glaucoma and Anterior Segment Services, Sankara Eye Hospital, Coimbatore, Tamil Nadu, India
| Date of Submission | 07-Feb-2021 |
| Date of Acceptance | 20-Feb-2021 |
| Date of Web Publication | 07-Apr-2021 |
Correspondence Address:
Dr. Mithun Thulasidas
Sankara Eye Hospital, Sathy Road, Sivanandapuram, Coimbatore - 641 035, Tamil Nadu
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/pajo.pajo_81_21
Anterior uveitis is the most common form of uveitis, with varying incidences reported in the literature. Anterior uveitis can be benign at the time of presentation; however, it often can lead to severe morbidity if not managed appropriately. The present article assists ophthalmologists in correctly diagnosing anterior uveitis and improving the quality of patient care. It is essential to go into the detailed history of the patient complaints. A thorough and detailed extraocular and ocular examination should be done. Ophthalmologists need to work up each case in a systematic manner.
Keywords: Anterior uveitis, history-taking, ocular examination, uveitis
How to cite this article:
Mehta B, Thulasidas M. Clinical approach to a case of anterior uveitis - A non-systematic review. Pan Am J Ophthalmol 2021;3:13 |
| Introduction | |  |
The term “uveitis” refers to an inflammation of various components of the uveal tract, including the primary inflammation of the retina and vitreous. Anterior uveitis consists of 30%-“73% of all uveitis cases and causes 0.6%-“11% of blindness, as reported in various studies.[1] Hence, a proper workup and management are required to reduce visual morbidity caused by this disease.
Uveitis is a multifactorial disease. In 2005, the Standardization of Uveitis Nomenclature Working Group classified it based on anatomy and various descriptors such as mode of onset, duration, and course [Table 1] and [Table 2].[2] It can be divided into granulomatous and nongranulomatous uveitis based on the pathological features [Table 3]. It is associated with systemic disease in approximately 30% of cases. Another 30% is caused by an infectious agent, whereas the condition remains idiopathic in the remaining 40% of cases.[3] Therefore, it is important to have an appropriate clinical approach to rule out various probable etiologies, with minimal investigations for better compliance and cost-effectiveness for the patients. | Table 1: The Standardization of Uveitis Nomenclature Working Group anatomic classification of uveitis
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 | Table 2: The Standardization of Uveitis Nomenclature Working Group descriptors of uveitis based on mode of onset, duration, and course
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| Workup of a Case of Anterior Uveitis | | |
A detailed history is a key to diagnosis of uveitis. Parameters that play a crucial role in the final diagnosis and management include age, gender, race, initial or recurrent episode, duration of symptoms, unilateral or bilateral, and acute or chronic presentation. Specific questions need to be asked to a patient suspecting for anterior uveitis.
Age
Although uveitis can occur in any age group, adults aged 20-“50 years are most commonly affected, with reports ranging from 60% to 80% of the total number of uveitis cases occurring in this age group.[4],[5] Specific types of uveitis may affect particular age groups [Table 4].[1],[6],[7]
Gender
Diseases with male preponderance are human leukocyte antigen-B27-associated anterior uveitis and syphilitic uveitis (mainly due to the incidence of human immunodeficiency virus disease in men).[8] On the other hand, diseases with female preponderance include chronic anterior uveitis of juvenile idiopathic arthritis (JIA), multiple sclerosis, sarcoidosis, and Vogt-Koyanagi-Harada disease (VKH). Overall, noninfectious uveitis tends to be more prevalent in women. Variation exists between different infectious uveitis due to the influence of occupational exposures, sexual behaviors, and other environmental factors that differ between the sexes.[9]
Race
Individual races can predispose to uveitic conditions such as ankylosing spondylitis, Reiter's in Caucasians, VKH syndrome, and Behcet's syndrome in Orientals.[7]
| History-Taking | | |
Patient complaints should be noted in the chronological order. Usually, a patient of uveitis presents with pain, redness, photophobia, watering, and blurred vision developing over hours to days.[10] Presence of floaters indicates intermediate or posterior uveitis. Pain is generally dull aching, throbbing type, usually worse at night, referred along the branches of trigeminal nerve, especially forehead and scalp. Blurred vision may be due to ciliary spasm, corneal edema, keratic precipitates (KPs), aqueous turbidity, complicated cataract, vitreous haze, cyclitic membrane, associated macular edema, papillitis, or secondary glaucoma. It is essential to note down the onset, duration, laterality of the disease, and specific medical history to rule out certain diseases [Table 5]. Treatment history and previous history of any ocular surgery must be enquired.
Socioeconomic history should not be missed as plumbers and sewer workers are at an increased risk of leptospirosis, transmitted by a spirochete in sewage water and urine of rats, cattle, or other animals.[7] Patients involved in recreational activities such as swimming in open water reservoirs have a risk of water-borne diseases that may cause uveitis. Cats' and dogs' handlers are at greater risk of infection to the intestinal parasite.
| Clinical Examination | | |
After a detailed history, clinical examination is required to correlate patient's data into subjective clinical findings, which then help in making a differential diagnosis, and to plan out investigations and modality for treatment.
Visual acuity
Visual acuity has to be checked, which is generally reduced.[11]
Intraocular pressure
Intraocular pressure (IOP) due to uveitis may be increased or decreased. In acute anterior uveitis, IOP is usually reduced due to an inflammation-induced reduction in aqueous production. Hypotony is usually measured in severe uveitis involving the ciliary body such as in childhood-onset uveitis.[12] Raised IOP is usually associated with Fuchs heterochromic uveitis, Posner-“Schlossman syndrome, herpetic uveitis, cytomegalovirus-associated anterior uveitis, and JIA.[13],[14]
Ocular movements
Extraocular muscles should be checked; although its involvement is rare in uveitis, it can rule out any neurological involvement.[15]
Pupil
A pupillary examination is a must before dilatation. The size, shape, and reaction of the pupil should be examined carefully. The pupil is usually miotic due to sphincter irritation by toxins and irregular in shape due to synechiae formation. Pupillary reactions may be sluggish due to edema and hyperemia of the iris.
Conjunctiva
Conjunctival hyperemia is a common sign in acute cases but may be absent in chronic cases. Conjunctival injection predominantly involves perilimbal area because of the involvement of ciliary vessels. Conjunctival nodules may be present which is suggestive of sarcoidosis.[16]
Cornea
Corneal edema should be looked for, including any scar of viral keratitis or active lesion. KPs should not be missed. KPs are corneal endothelial deposits that are frequently observed in association with anterior-segment inflammation.[17] These precipitates are formed by the aggregation of polymorphonuclear cells, lymphocytes, and epithelioid cells.[18] KPs are of two types: granulomatous and nongranulomatous. Usually, nongranulomatous KPs are small, white, and irregular, while large, yellowish (mutton-fat) KPs indicate granulomatous inflammation.[17] The presence of KPs can indicate whether the disease is active or not. Fresh KPs are round, elevated with smooth margins and with hydrated appearance. However, old KPs are pigmented, dehydrated, and flat with crenated margins. Location of KPs is also important to rule out various etiologies. In most cases, KPs are located inferiorly in base-down triangular configuration known as “Arlt triangle.” This specific pattern of deposition is due to convection currents of aqueous humor, which is due to gravity and temperature difference between cornea endothelium and iris. The diffuse pattern is a hallmark of Fuchs heterochromic iridocyclitis.[19] The central pattern is present in viral uveitis and Posner-“Schlossman syndrome.[20] Ehrlich turk line refers to the vertical deposition of KPs on the corneal endothelium. Calcium deposition on the cornea in the form of band-shaped keratopathy can occur in chronic cases.[21]
Anterior chamber
Anterior-chamber depth should be examined centrally and peripherally as it can be affected by iris bombe or synechiae formation. Signs of inflammation should be carefully checked. Aqueous cells and flare to be looked at and grading should be done to denote severity and improvement in treatment [Table 6] and [Table 7].[2] Aqueous cells are inflammatory cells, mainly lymphocytes in most cases of acute anterior uveitis and neutrophils in a few cases. Presence of cells in the anterior chamber is an indicator of active disease. Aqueous flare is seen because of the Tyndall effect, due to exudation of protein and disruption of blood-“aqueous barrier. Hypopyon may be present in severe cases, whereas shifting hypopyon is a feature of Behcet's disease due to less fibrin.[22] Gonioscopy evaluation of anterior-chamber angle should be done as glaucoma is a common complication of acute anterior uveitis. Neovascularization, synechiae, or any nodules at the angle should be looked for. | Table 6: The Standardization of Uveitis Nomenclature Working Group grading scheme for anterior-chamber cells
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 | Table 7: The Standardization of Uveitis Nomenclature Working Group grading scheme for anterior chamber flare
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Iris
Iris-specific findings include color, pattern, synechiae formation, nodules, and atrophy. Iris is usually muddy in color, may show pigmented and depigmented areas, or may become edematous due to waterlogging. Synechiae is defined as adhesion between pupillary margin and lens capsule (posterior synechiae) or adhesion between the cornea and peripheral part of the iris (peripheral anterior synechiae) [Figure 1]. Synechiae are formed due to firm adhesion due to fibrous band between them. In severe cases or recurrent attacks, whole 360° ring synechiae can be formed, known as annular ring or seclusion pupillae, which can lead to iris bombe formation and secondary angle closure glaucoma. The anterior chamber may look like funnel-shaped (deep at center and shallow in the periphery). In severe cases, the exudates fill the pupillary area, which is known as occlusion pupillae [Figure 2]. Exudates may also organize in posterior chamber, which tie lens to iris and is known as total posterior synechiae. In severe cases, cyclitic membrane can also be formed behind the lens, which can lead to phthisis bulbi. | Figure 1: Slit-lamp photograph showing a case of chronic anterior uveitis with posterior synechiae formation at 9 o'clock position
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 | Figure 2: Slit-lamp photograph showing a case of chronic anterior uveitis with fibrous tissue covering whole pupillary area (occlusio pupillae)
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Iris nodules are the accumulation of inflammatory cells on the surface of iris. They are suggestive of specific etiologies such as sarcoidosis, VKH, Fuchs heterochromic iridocyclitis, multiple sclerosis, and infectious uveitis.[23],[24],[25],[26] Koeppe's nodules are present at pupillary margin which are usually small and white in color while Busacca nodules are larger, seen along collarette and greenish-white in color. Atrophic patches in iris may occur due to recurrent attacks. Sectoral atrophy of iris is seen in herpes zoster infection, patchy atrophy is seen in herpes simplex, and diffuse atrophy is seen in Fuchs uveitis.[14]
Lens
Pigments and opacities on the anterior lens capsule should be seen carefully. Cataract formation is a common complication in long-standing cases of uveitis and in long-term corticosteroid therapy.[27]
Vitreous
Vitreous involvement indicates intermediate, posterior, or panuveitis. Indirect ophthalmoscopy is a must in a case of uveitis. Vitreous is examined for cells, haze for which grading can be done accordingly. Vitreous cells appear as black dots and may be confused with vitreous debris. Debris is often pigmented and forms clumps that are larger than individual cells. Vitreous strands, membranes, areas of vitreoretinal traction, and vitreous hemorrhage can be seen. Retinal detachment may occur in rare cases. In sarcoidosis and pars planitis, vitreous cells tend to aggregate into clumps called snowballs can be seen in anterior vitreous. Peripheral retina and pars plana should be examined for snow banking.[28],[29]
Optic disc
Optic disc involvement includes disc edema, hyperemia, neovascularization, infiltration, and cupping. Granulomas may present on the optic nerve and optic disc in diseases such as sarcoidosis.[29],[30]
Macula
Chronic inflammation can lead to cystoid macular edema.
Retina and choroid
Vascular sheathing, perivascular exudate, infiltration of inflammatory cells into the choroid, retinitis, and retinal detachment may be seen.[28]
| Systemic Examination | | |
Approximately 26% of anterior uveitis is associated with a systemic disease.[31] Therefore, a thorough systemic evaluation is necessary.
| Investigations | | |
Investigation of the anterior uveitis is needed in cases of bilateral inflammation, recurrent, moderate, or severe inflammation with granulomatous features, and systemic symptoms or signs, suggesting an underlying medical diagnosis [Table 8]. Investigations are not required if it is the first episode of nongranulomatous anterior uveitis, herpes zoster ophthalmicus-associated uveitis, and Fuchs heterochromic iridocyclitis.[31],[32],[33] After proper evaluation, treatment should be planned accordingly.
Acknowledgments
The authors thank Maj Gen Dr JKS Parihar (Senior consultant, Centre for Sight, New Delhi) for providing the clinical images.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Bajoria SK, Biswas J. Recent approach in diagnosis and management of anterior uveitis. J Clin Ophthalmol Res 2018;6:36-41.  [Full text] |
| 2. | Jabs DA, Nussenblatt RB, Rosenbaum JT. Standardization of Uveitis Nomenclature (SUN) Working Group. Standardization of uveitis nomenclature for reporting clinical data. Results of the First International Workshop. Am J Ophthalmol 2005;140:509-16. |
| 3. | van Laar JA, Rothova A, Missotten T, Kuijpers RW, van Hagen PM, van Velthoven ME. Diagnosis and treatment of uveitis; not restricted to the ophthalmologist. J Clin Transl Res 2015;1:94-9. |
| 4. | Tsirouki T, Dastiridou A, Symeonidis C, Tounakaki O, Brazitikou I, Kalogeropoulos C, et al. A focus on the epidemiology of uveitis. Ocul Immunol Inflamm 2018;26:2-16. |
| 5. | Rothova A, Buitenhuis HJ, Meenken C, Brinkman CJ, Linssen A, Alberts C, et al. Uveitis and systemic disease. Br J Ophthalmol 1992;76:137-41. |
| 6. | Heiligenhaus A, Minden K, Föll D, Pleyer U. Uveitis in juvenile idiopathic arthritis. Dtsch Arztebl Int 2015;112:92-100. |
| 7. | Rathinam SR, Babu M. Algorithmic approach in the diagnosis of uveitis. Indian J Ophthalmol 2013;61:255-62. [ PUBMED] [Full text] |
| 8. | Smith JR. HLA-B27--associated uveitis. Ophthalmol Clin North Am 2002;15:297-307. |
| 9. | Yeung IY, Popp NA, Chan CC. The role of sex in uveitis and ocular inflammation. Int Ophthalmol Clin 2015;55:111-31. |
| 10. | Hogan MJ, Kimura SJ, Thygeson P. Signs and symptoms of uveitis. Am J Ophthalmol 1959;47:155-70. |
| 11. | Durrani OM, Tehrani NN, Marr JE, Moradi P, Stavrou P, Murray PI. Degree, duration, and causes of visual loss in uveitis. Br J Ophthalmol 2004;88:1159-62. |
| 12. | Sen HN, Drye LT, Goldstein DA, Larson TA, Merrill PT, Pavan PR, et al. Hypotony in patients with uveitis: The Multicenter Uveitis Steroid Treatment (MUST) Trial. Ocul Immunol Inflamm 2012;20:104-12. |
| 13. | Siddique SS, Suelves AM, Baheti U, Foster CS. Glaucoma and uveitis. Surv Ophthalmol 2013;58:1-0. |
| 14. | Herbort CP. Appraisal, work-up and diagnosis of anterior uveitis: A practical approach. Middle East Afr J Ophthalmol 2009;16:159-67. [ PUBMED] [Full text] |
| 15. | Allegri P, Rissotto R, Herbort CP, Murialdo U. CNS diseases and uveitis. J Ophthalmic Vis Res 2011;6:284-308. [Full text] |
| 16. | Obenauf CD, Shaw HE, Sydnor CF, Klintworth GK. Sarcoidosis and its ophthalmic manifestations. Am J Ophthalmol 1978;86:648-55. |
| 17. | Mocan MC, Kadayifcilar S, Irkec M. Keratic precipitate morphology in uveitic syndromes including Behçet's disease as evaluated with in vivo confocal microscopy. Eye (Lond) 2009;23:1221-7. |
| 18. | Wertheim MS, Mathers WD, Planck SJ, Martin TM, Suhler EB, Smith JR, et al. In vivo confocal microscopy of keratic precipitates. Arch Ophthalmol 2004;122:1773-81. |
| 19. | Nalçacıoğlu P, Çakar Özdal P, Şimşek M. Clinical characteristics of fuchs' uveitis syndrome. Turk J Ophthalmol 2016;46:52-7. |
| 20. | Babu K, Konana VK, Ganesh SK, Patnaik G, Chan NS, Chee SP, et al. Viral anterior uveitis. Indian J Ophthalmol 2020;68:1764-73. [ PUBMED] [Full text] |
| 21. | Galor A, Leder HA, Thorne JE, Dunn JP. Transient band keratopathy associated with ocular inflammation and systemic hypercalcemia. Clin Ophthalmol 2008;2:645-7. |
| 22. | Tugal-Tutkun I. Behçet's uveitis. Middle East Afr J Ophthalmol 2009;16:219-24. [ PUBMED] [Full text] |
| 23. | Moorthy RS, Inomata H, Rao NA. Vogt-Koyanagi-Harada syndrome. Surv Ophthalmol 1995;39:265-92. |
| 24. | Rothova A, La Hey E, Baarsma GS, Breebaart AC. Iris nodules in Fuchs' heterochromic uveitis. Am J Ophthalmol 1994;118:338-42. |
| 25. | Bachman DM, Rosenthal AR, Beckingsale AB. Granulomatous uveitis in neurological disease. Br J Ophthalmol 1985;69:192-6. |
| 26. | Myers TD, Smith JR, Lauer AK, Rosenbaum JT. Iris nodules associated with infectious uveitis. Br J Ophthalmol 2002;86:969-74. |
| 27. | Chan NS, Ti SE, Chee SP. Decision-making and management of uveitic cataract. Indian J Ophthalmol 2017;65:1329-39. [ PUBMED] [Full text] |
| 28. | Ozdal PC, Berker N, Tugal-Tutkun I. Pars planitis: Epidemiology, clinical characteristics, management and visual prognosis. J Ophthalmic Vis Res 2015;10:469-80. [ PUBMED] [Full text] |
| 29. | Mochizuki M, Smith JR, Takase H, Kaburaki T, Acharya NR, Rao NA, et al. Revised criteria of International Workshop on Ocular Sarcoidosis (IWOS) for the diagnosis of ocular sarcoidosis. Br J Ophthalmol 2019;103:1418-22. |
| 30. | Arellanes-García L, Navarro-López P, Concha-Del Río LE, Unzueta-Medina JA. Idiopathic intermediate uveitis in childhood. Int Ophthalmol Clin 2008;48:61-74. |
| 31. | Sinha R, Naithani P, Garg S. Newer investigations and management guidelines in uveitis. Indian J Ophthalmol 2010;58:88-91. [Full text] |
| 32. | Forooghian F, Gupta R, Wong DT, Derzko-Dzulynsky L. Anterior uveitis investigation by Canadian ophthalmologists: Insights from the Canadian National Uveitis Survey. Can J Ophthalmol 2006;41:576-83. |
| 33. | Agrawal RV, Murthy S, Sangwan V, Biswas J. Current approach in diagnosis and management of anterior uveitis. Indian J Ophthalmol 2010;58:11-9. [ PUBMED] [Full text] |
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]
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