The chemical mediators involved in inflammation (see Chapter 1) result in vascular dilation (ciliary flush), increased vascular permeability (aqueous flare), and chemotaxis of inflammatory cells into the eye (aqueous and vitreous cellular reaction). Table 5-7 summarizes signs of uveitis.
Signs of uveitis in the anterior portion of the eye include
inflammatory cells (Fig 5-1)
flare (Fig 5-2)
fibrin in the anterior chamber
keratic precipitates (Figs 5-3, 5-4)
iris nodules (Fig 5-5)
iris atrophy or heterochromia
synechiae, anterior and posterior (Fig 5-6)
*Observed in long-standing uveitis
The major finding in anterior uveitis is the presence of inflammatory cells and flare in the anterior chamber, but there may be many additional sequalae. The SUN system grades the intensity of anterior chamber cells according to the number of inflammatory cells observed on slit-lamp examination in a field defined as a 1 × 1 mm high-power beam at full intensity at a 45°–60° angle in a dark room. Flare is defined by the visibility of the slit-lamp beam in the anterior chamber. The SUN system adopted the flare grading method described previously by Hogan and colleagues (Table 5-8).
Table 5-7 Signs of Uveitis
The anterior chamber reaction can be described as
serous (aqueous flare caused by protein influx)
purulent (polymorphonuclear leukocytes and necrotic debris causing hypopyon)
fibrinous (plasmoid, or intense fibrinous exudate)
sanguinoid (inflammatory cells with erythrocytes, as manifested by hypopyon mixed with hyphema)
Keratic precipitates (KPs) are collections of inflammatory cells on the corneal endothelium. Newly formed KPs tend to be white and smoothly rounded, later transitioning to crenated (shrunken), pigmented, or glassy in nature. Large, yellowish KPs are called mutton-fat KPs and are usually associated with granulomatous types of inflammation. Associated corneal edema may be present. Band keratopathy is seen in chronic uveitis (especially JIA associated).
Iris involvement may manifest as either anterior or posterior synechiae, iris nodules (Koeppe nodules at the pupillary border, Busacca nodules within the iris stroma [see Fig 5-5] and Berlin nodules in the angle, iris granulomas, heterochromia (eg, Fuchs uveitis syndrome), or stromal atrophy (eg, herpetic uveitis).
Figure 5-1 Inflammatory cells in the anterior chamber (grade 4+) of a patient with anterior uveitis.
(Courtesy of Emmett T. Cunningham Jr, MD, PhD, MPH.)
Figure 5-2 Aqueous flare (grade 4+) in a patient with acute anterior uveitis.
Figure 5-3 Keratic precipitates (medium and small).
(Courtesy of Debra Goldstein, MD.)
Figure 5-4 Large “mutton-fat” keratic precipitates in a patient with sarcoidosis. Large keratic precipitates such as these generally indicate a granulomatous disease process.
(Courtesy of Debra Goldstein, MD.)
Figure 5-5 Mid-iris nodules (Busacca nodules) in 2 patients (A, B) with sarcoidosis.
(Part A courtesy of Debra Goldstein, MD. Part B courtesy of Wendy Smith, MD.)
Figure 5-6 Multiple posterior synechiae preventing complete dilation of the pupil.
(Courtesy of David Forster, MD.)
Table 5-8 Grading Scheme for Anterior Chamber Cells and Based on Standardization of Uveitis Nomenclature (SUN) Criteria
With uveitic involvement of the ciliary body and trabecular meshwork, IOP is often low, secondary to decreased aqueous production or increased uveoscleral outflow, but IOP may increase precipitously if the meshwork becomes clogged by inflammatory cells or debris or if the trabecular meshwork itself is the site of inflammation (trabeculitis). Pupillary block with iris bombé and secondary angle closure may also lead to an acute rise in IOP.
Hogan MJ, Kimura SJ, Thygeson P. Signs and symptoms of uveitis. I. Anterior uveitis. Am J Ophthalmol. 1959;47(5, part 2):155–170.
Excerpted from BCSC 2020-2021 series: Section 9 - Uveitis and Ocular Inflammation. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.