TFCC Avulsion at Fovea: Treatment Approach
I need to clarify that the question appears to contain a terminology mismatch. "TFCC" typically refers to the triangular fibrocartilage complex in the wrist, which is unrelated to the fovea (an ocular structure). Based on the expanded context provided and the evidence supplied, I will address traumatic foveal choroidal neovascularization (CNV) secondary to choroidal rupture, which appears to be the intended clinical scenario.
Primary Treatment Recommendation
Intravitreal anti-VEGF therapy is the treatment of choice for choroidal neovascularization secondary to traumatic choroidal rupture affecting the fovea. 1, 2
Evidence-Based Treatment Algorithm
Initial Management
Confirm diagnosis with multimodal imaging including OCT, OCT-A, fluorescein angiography (FA), and indocyanine green angiography (ICGA) to document active CNV and rule out other macular pathology 1
Initiate intravitreal anti-VEGF injections (bevacizumab, ranibizumab, or aflibercept) for active, exudative CNV affecting the fovea 1, 3, 2
Treatment Expectations
Fewer injections are typically required compared to age-related macular degeneration—the largest case series showed a mean of 4.2 injections (range 1-8) over 5 years for traumatic CNV 2
Visual improvement is achievable in most treated eyes, with regression of CNV noted in all cases in the largest published series 2
Treatment should be initiated promptly when active CNV is documented, as delayed treatment is associated with worse visual outcomes 4
Prognostic Factors
Poor Visual Outcome Predictors
Subfoveal location of the original choroidal rupture is the strongest predictor of poor visual outcome 4
Baseline visual acuity <20/40 independently predicts failure to recover driving vision 4
CNV formation itself significantly reduces the likelihood of achieving 20/40 or better vision (only 8% of eyes with CNV vs. 38% without CNV) 4
Older age at time of trauma is positively associated with CNV formation (p=0.04) 4
Important Clinical Caveat
The presence of CNV secondary to traumatic choroidal rupture carries a guarded prognosis—only 1 of 12 eyes (8%) with CNV achieved driving vision in the largest natural history study, compared to 38% without CNV 4. However, this data predates modern anti-VEGF therapy, and more recent evidence shows better outcomes with prompt anti-VEGF treatment 2.
Alternative Considerations
If Anti-VEGF Alone is Insufficient
Consider combination therapy with photodynamic therapy (PDT) if there is evidence of pachychoroid features or polypoidal components, though this is more commonly applied to non-traumatic CNV 1, 5
Re-evaluate diagnosis if inadequate response to anti-VEGF therapy, as other conditions may mimic traumatic CNV 1
Observation Strategy
- Inactive CNV without exudation may be observed without treatment, as demonstrated in 4 patients in the largest traumatic CNV series who underwent watchful waiting 2
Treatment Monitoring
Follow-up imaging with OCT should be performed regularly to assess for persistent or recurrent subretinal fluid requiring additional injections 2
Long-term surveillance is necessary as CNV can develop months after the initial trauma (mean interval 5.7 months, range 2-12 months) 2
Key Clinical Pitfall
Do not delay treatment waiting for spontaneous resolution—unlike acute central serous chorioretinopathy where observation may be appropriate, traumatic CNV requires prompt intervention to optimize visual outcomes 2, 4. The window for visual recovery narrows with delayed treatment, particularly when the fovea is involved 4.