Background: Visual impairment resulting from retinal, subhyaloid, or v
itreous hemorrhages in association with Tersons syndrome is often sign
ificant. The most common long-term sequelae that may result in permane
nt visual deficit is the formation of an epimacular membrane. Methods:
This report provides clinicopathologic documentation of epiretinal me
mbrane proliferation secondary to Tersons syndrome. Pars plana vitrect
omy was performed in 16 eyes of 11 patients with Tersons syndrome. Aft
er removal of vitreous hemorrhage, epimacular membranes were found in
10 eyes (62.5%). The posterior cortical vitreous and the epiretinal ti
ssue were examined histologically. Results: Immunostainings with glial
and retinal pigment epithelial cell markers showed that the majority
of cells derived form the glia. Perls staining, specific for iron, sho
wed that the high melanic-like component contained in the histopatholo
gic samples corresponded to degradation of blood products secondary to
chronic hemorrhage. Conclusion: The high risk of epiretinal membrane
formation and the toxicity of blood breakdown products over the inner
retina worsen the long-term visual prognosis in Tersons syndrome. Earl
y surgery is advocated in such cases.