Other / Other / MRI

Scleritis

Scleritis is inflammation of the sclera that typically presents in patients aged 30-50 years with a female predominance (2:1), often associated with systemic autoimmune conditions like rheumatoid arthritis, vasculitides, SLE, or IBD, or less commonly with infections such as herpes zoster.
Look For First
  • Focal or diffuse scleral thickening on CT or MRI
  • Scleral enhancement on contrast-enhanced imaging, particularly bright enhancement in the active phase
  • Periscleral soft tissue edema or cellulitis surrounding the inflamed sclera
  • Differentiation between anterior scleritis (visible anterior to rectus insertion) and posterior scleritis (posterior to rectus insertion)
Key Image Findings
  • Scleral thickening is the primary imaging hallmark on CT and MRI, appearing as abnormally increased thickness of the normally thin scleral layer; this finding is present in both anterior and posterior forms.
  • Scleral enhancement on contrast-enhanced CT or MRI is a key marker of active inflammation and inflammatory phase of disease, with the degree of enhancement correlating with disease activity.
  • Focal periscleral cellulitis or soft tissue edema surrounding the affected sclera is commonly visualized and indicates extension of inflammation beyond the sclera into surrounding tissues.
  • On ultrasound, B-mode imaging demonstrates scleral thickening particularly useful for evaluating posterior scleritis, where direct clinical visualization is limited.
  • The anatomic classification using CT/MRI helps distinguish anterior scleritis (involvement anterior to the rectus muscle insertion) from posterior scleritis (involvement posterior to the rectus insertion), which affects clinical management.
  • Necrotizing anterior scleritis may show areas of scleral thinning or defects on imaging, particularly in the severe form scleromalacia perforans where tissue necrosis occurs.
  • Imaging is most sensitive during the active phase of disease when inflammation and enhancement are maximal; imaging during quiescent phases may appear normal or show only mild residual thickening.
  • MRI may provide superior soft tissue characterization of periscleral inflammation and involvement of adjacent structures compared to CT.
Differential Diagnosis
  • Episcleritis: presents with superficial episcleral inflammation without true scleral thickening on imaging; shows more superficial enhancement and lacks deep scleral involvement.
  • Posterior uveal inflammation or choroiditis: can mimic posterior scleritis but lacks scleral thickening and shows more prominent choroidal involvement.
  • Orbital cellulitis or abscess: presents with diffuse orbital inflammation and may have focal collection; differentiated by absence of characteristic scleral thickening and different clinical presentation.
  • Acute arteritis or vasculitis of orbital vessels: may show enhancement of vessels but lacks the diffuse or nodular scleral thickening pattern seen in scleritis.
  • Sarcoidosis with ocular involvement: can present with scleral inflammation but usually shows additional systemic imaging findings and granulomatous features on biopsy.
Discussion

Scleritis is strongly associated with systemic autoimmune disease, with rheumatoid arthritis and granulomatosis with polyangiitis being the most common systemic associations; imaging of the eye should prompt investigation for underlying systemic conditions.

T-cell mediated inflammation is believed to be the primary pathogenic mechanism, though the exact immunopathology remains incompletely understood due to limited published pathogenesis data.

The Watson and Hayreh classification divides scleritis into anterior (diffuse, nodular, or necrotizing) and posterior forms, with important clinical implications for prognosis and treatment response.

Imaging is particularly useful for diagnosing posterior scleritis where clinical examination is limited and symptoms may be nonspecific such as posterior eye pain and visual symptoms.

Serial imaging can help assess response to therapy in active scleritis, with decreasing enhancement and normalization of scleral thickness indicating disease control.

Herpes zoster is the most common infectious cause of scleritis, whereas most cases are associated with non-infectious systemic conditions.

Reporting Pearls

Report scleritis by describing the type (anterior vs. posterior), the pattern (diffuse, nodular, or necrotizing), the degree of scleral thickening in millimeters, the presence and degree of enhancement post-contrast, and any associated periscleral edema or cellulitis; note that active phase disease shows prominent enhancement while quiescent disease may show thickening alone.

Pitfalls
  • Mistaking episcleritis for scleritis on imaging by misidentifying superficial episcleral inflammation as scleral thickening; true scleral involvement extends into the deeper scleral layer.
  • Underestimating the importance of periscleral findings as markers of disease activity; periscleral edema and cellulitis indicate active inflammation beyond the sclera alone.
  • Failing to differentiate anterior from posterior scleritis anatomically using the rectus muscle insertion as landmark; this distinction is critical for clinical management and prognosis.
  • Assuming negative imaging in quiescent scleritis indicates absence of disease; chronic scleritis may show only mild residual thickening without enhancement in inactive phases.