Myopic maculopathy and presumed ocular histoplasmosis
Key Takeaways
Pathologic myopia is defined by structural posterior disease rather than prescription alone.
Myopic CNV may have little fluid; haemorrhage at a lacquer crack still requires confirmation of activity.
Foveoschisis is a tractional problem and does not automatically benefit from anti-VEGF.
Classic POHS has scars, peripapillary atrophy and possible CNV without active vitritis; treat the active vascular complication.
Structural stretching and neovascular activity differ
Pathologic myopia involves posterior structural changes such as a posterior staphyloma and myopic maculopathy; a large negative spectacle prescription alone does not define every aspect of the disease. Myopic eyes can lose vision from atrophy, traction, a macular hole, retinal detachment or choroidal neovascularization (CNV). Distinguishing these mechanisms prevents an inappropriate injection for a purely mechanical problem or delayed treatment of active neovascular disease.
Measure corrected acuity and refraction, examine the peripheral retina and document the posterior contour. Optical coherence tomography (OCT) should be interpreted with awareness of curved anatomy, segmentation artifacts and thin choroid. A staphyloma is a localized outpouching with a change in curvature, not simply a synonym for any long eye. Prior photographs and OCT help separate stable atrophic change from newly active lesions.
Atrophic and neovascular myopic lesions
A tessellated fundus, diffuse or patchy chorioretinal atrophy and lacquer cracks may coexist. Lacquer cracks are breaks in the RPE–Bruch membrane–choriocapillaris complex and can be associated with haemorrhage. A haemorrhage near a lacquer crack is not automatically CNV; examine and image for an active vascular lesion. A Fuchs spot describes a pigmented scar associated with previous myopic neovascularization, not a current treatment indication by itself.
Myopic CNV often appears as a small lesion with comparatively little fluid. New metamorphopsia, central blur and a small subretinal haemorrhage warrant timely assessment. OCT may show a hyperreflective lesion, while fluorescein angiography can establish leakage when the diagnosis or activity is uncertain. OCT angiography can demonstrate a vascular network but cannot independently measure leakage or prove every detected network needs treatment.
Anti-vascular endothelial growth factor (anti-VEGF) therapy is an established treatment for active myopic CNV. Primary trials such as RADIANCE support ranibizumab-based treatment, with retreatment according to the specified protocol and activity. Do not impose the chronic AMD injection schedule on every myopic lesion. Counsel about recurrence, the need to return for new distortion and visual limits imposed by underlying atrophy even when the CNV becomes inactive.
Myopic traction maculopathy
A stretched posterior wall with persistent vitreoretinal and epiretinal traction may produce macular retinoschisis, foveal detachment or a macular hole. OCT distinguishes splitting of retinal layers from exudative cysts. Look for residual posterior hyaloid, epiretinal membrane and the relationship to staphyloma. The apparent increase in retinal thickness does not imply diabetic oedema.
Observe selected stable cases with useful vision and reliable monitoring. Progressive symptomatic traction, foveal detachment or a hole may require specialist surgery. Vitrectomy with careful management of traction and selected internal limiting membrane techniques, or a macular buckle in selected anatomy, has a different purpose from anti-VEGF. These procedures carry risks including hole formation, cataract and retinal detachment; the surgical approach should fit the pattern rather than simply the axial length.
| Myopic finding | Principal mechanism | Treatment direction |
|---|---|---|
| Stable patchy atrophy | Tissue loss | Rehabilitation and surveillance |
| Active CNV | Neovascular growth | Anti-VEGF after confirmation |
| Foveoschisis | Traction and posterior geometry | Monitor or selected surgery |
| Macular hole with detachment | Break plus complex traction | Vitreoretinal surgical planning |
Presumed ocular histoplasmosis syndrome
Presumed ocular histoplasmosis syndrome (POHS) classically combines punched-out chorioretinal scars, peripapillary atrophy and CNV, with absence of active vitreous inflammation. The syndrome has geographic associations with Histoplasma exposure, but an ocular photograph does not prove active systemic fungal infection. Not every person with peripheral scars has POHS; consider toxoplasmosis, multifocal choroiditis and other inflammatory or infectious lesions.
The clinically important complication is active CNV near the macula. Treat confirmed active neovascularization with an appropriate anti-VEGF strategy and monitor activity. Old scars alone do not require injection. Routine systemic antifungal therapy is not the treatment for the classic inactive-scar syndrome, and corticosteroids are not a universal substitute for treating the vascular lesion. Active inflammation or systemic infection changes the differential and requires its own work-up.
Applying the differential
A highly myopic patient develops new distortion and a tiny macular haemorrhage. Check for a small active CNV even if there is little OCT fluid. Another has slowly worsening vision with multilayer foveal splitting and no leakage: traction is the likely driver. A patient from an endemic region has peripheral punched-out scars, peripapillary atrophy and an active macular vascular lesion without vitritis: POHS is plausible, but the treatment targets CNV rather than assuming active fungal invasion.
Explain the mechanism to the patient, give clear instructions for new visual change and check the fellow eye. In a viva, naming myopia or POHS earns less than linking the observed lesion to the required investigation and treatment.
Sources: Primary anti-VEGF versus PDT study and EBO curriculum.
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