CASE OF THE MONTH

CASE #3

In this patient, the CNV was located both externally and internally to the RPE. The anatomical location of the CNV may affect visual outcome. If the CNV grows anteriorly to the RPE, excision may be accompanied by minimal removal of RPE–Bruch’s membrane, but if the CNV grows posteriorly to the RPE, excision will create a localized RPE defect and may be associated with damage to subjacent Bruch’s membrane. In AMD, the fibrovascular CNV may lie within Bruch’s membrane, and both anterior and posterior to the RPE. CNV removal usually is associated with excision of RPE and portions of Bruch’s membrane in such cases. In idiopathic and postinflammatory maculopathies, the CNV may grow anteriorly to the RPE into the subneurosensory subretinal space, but the CNV may grow on both sides of the RPE as well. In our patient, a large RPE defect was created by the CNV excision. This defect was evident clinically and was corroborated by the presence of RPE in the excised tissue. Several observations in vivo and in vitro demonstrate the ability of the RPE surrounding a localized defect to repopulate the denuded surface of Bruch’s membrane, although there is always some metaplasia and loss of pigmentation.

The presence of mottled choriocapillaris fluorescence 1 week after surgery, and the development of choriocapillaris nonperfusion and RPE atrophy over the next 6 months raises the possibility that native RPE did not repopulate adequately the dissection bed. In previous reports involving patients with patients, we and others have described the occurrence of areas of decreased choriocapillaris perfusion in the previous location of the excised CNV.

In general, the presence of choriocapillaris nonperfusion after CNV excision might be due to preexisting choriocapillaris atrophy, masked preoperatively by the hyperfluorescence of the CNV on angiography; choriocapillaris damage/removal at the time of surgery; and RPE removal at surgery with abnormal RPE repopulation of the dissection bed and subsequent choriocapillaris atrophy. On the basis of the work of Korte et al. in laboratory animals, the time course of the loss of choriocapillaris perfusion and the histology of the excised tissue suggest, but do not prove, that direct intraoperative trauma to the choroid was not the cause of these changes. Thus, we believe choriocapillaris nonperfusion in this case was secondary to abnormal/inadequate RPE repopulation of the dissection bed. Because of the patient’s young age and the presumed normality of Bruch’s membrane, we were surprised that choriocapillaris atrophy developed. However, the chronic exudative retinal detachment, which may have damaged the native RPE near the area of the dissection, and the size of the CNV and the corresponding RPE defect, may have played an important role in preventing adequate RPE resurfacing of the defect. The presence of RPE cells associated with basement membrane in the specimen may be important in this regard. The presence of Bruch’s membrane has been correlated with higher rate of postoperative choriocapillaris atrophy following CNV excision..