We read with interest Mantel and associates’ recent description of the features of peripheral exudative hemorrhagic chorioretinopathy (PEHCR). The authors correctly state that PEHCR “can be vision threatening because of hemorrhage and exudation” and we would like to share our experience with respect to treatment of this peripheral retinal disorder.
As the lesions associated with PEHCR typically regress, we frequently observe such eyes of patients. However, we have found that there are instances in which intervention should be undertaken. Recently, 2 unrelated Hispanic women had abrupt visual decline related to dense vitreous hemorrhages. B-scan ultrasonography in 1 patient (80 years old) showed a dense vitreous hemorrhage and flat retina. In this case, the patient was monocular and the vitreous hemorrhage in her only seeing eye warranted diagnostic vitrectomy. After hemorrhage removal, internal retinal examination revealed subretinal pigmentary and subneurosensory hemorrhages from 7 to 2 o’clock, consistent with PEHCR. One week later, persistent subneurosensory retinal hemorrhages extending towards the superior macular area were seen. In light of her monocular status with only the right eye providing functional vision, intravitreal bevacizumab (2.5 mg in 0.1 mL; Genentech/Roche, San Francisco, California, USA) was offered off-label to the patient to prevent extension of hemorrhage into the macula. Three injections were performed at monthly intervals. Three months later, vision improved to 20/40 and the lesions remained stable with some regression of the subretinal hemorrhage. In the other patient (83 years old), a large macula-off inferotemporal hemorrhagic retinal detachment warranted drainage of the subretinal hemorrhage in a manner previously described. In addition, intravitreal bevacizumab (2.5 mg in 0.1 mL) was administered to prevent new subretinal hemorrhages. There were no further subretinal hemorrhages noted during postoperative convalescence and the retina remained flat and attached.
PEHCR can resemble melanomas, and these lesions typically remain stable or regress. Presumably, the lesions represent neovascular membranes, which extravasate blood leading to subretinal hematomas. Such neovascular origins have been supported by fluorescein and indocyanine green angiography, but recent histologic examination of an eye with PEHCR did not reveal choroidal neovascular membranes. Further histopathology will prove useful in elucidating the pathophysiology involved in the development of the subretinal hematomas.
We agree with Mantel and associates that PEHCR typically has a benign outcome. Observation of PEHCR plays a role when subretinal hematomas involve few clock hours far from the macula in binocular patients. However, PEHCR can menace sight. In patients with extensive retinal involvement, lesions that threaten the macula, or progressive lesions in monocular patients, more aggressive therapy may be warranted. Surgical intervention can treat the vitreous and subretinal hemorrhages while intravitreal anti-VEGF therapy may aid in regression of vision-threatening lesions. Further studies are indicated to prove anti-VEGF efficacy in PEHCR.