I strongly appreciate the interest shown by Dr. Rabiolo in my recent publication “Overview of the Complications of High Myopia.”1 I would also like to thank Dr. Rabiolo for pointing out the important role played by myopic subretinal hemorrhage (mSH) without myopic choroidal neovascularization (mCNV) in pathologic myopia. As emphasized in Dr. Rabiolo's letter, mSH is believed to occur after a rupture of retinal pigment epithelium/Bruch's membrane and/or of the choriocapillaris, proportional in magnitude to the elongation of the axial length. Myopic subretinal hemorrhage occasionally precedes new lacquer crack formations and is regarded as an important symptom for the differential diagnosis of mCNV. Fluorescein angiography typically shows a hyperfluorescein leak from CNV, whereas mSH results in a hypofluorescence because of blocking. Because of the manuscript space limitations in the published article, I was unable to go into further detail regarding this condition. However, I believe this exchange to be a fortunate one because it allows me the opportunity to describe in greater detail the clinical features of mSH.
Recent imaging advances have provided the tools to obtain a more detailed pathology of mSH, in addition to important information regarding its relationship with mCNV. For instance, a scanning laser ophthalmoscope provides clearer images of the retina in highly myopic eyes that allow for a precise visualization of the lacquer crack, even in atrophic cases. We documented a high rate of accompanying lacquer crack in mCNV cases (35 of 37 eyes; 95%) in the late phase of scanning laser ophthalmoscope–indocyanine green angiography.2 This finding supports the hypothesis that mSH can be believed of as an early stage mCNV that later evolves through lacquer crack formations. Optical coherence tomography angiography showed low-density choriocapillaris in all eyes and further revealed medium and large choroidal vessels in seven of the nine eyes (78%) with diffuse atrophy examined, indicating that lacquer crack formations may be, at least in part, related to the choriocapillaris damage observed in these eyes.3
Dr. Rabiolo also cited an article by Dr. Hayasaka in 1990 that documented the visual time course of both mSH and mCNV. However, at the time of its publication, it was not clear, which condition had a better prognosis. Furthermore, the prognosis of mCNV has probably improved because of the introduction of anti-VEGF antibodies. We recently compared the 1-year visual results for both conditions and found that mSH had a significantly more favorable outcome. Furthermore, this study showed that the preservation of the ellipsoid line observed with optical coherence tomography to be a significant prognostic factor.4
Finally, it is worth mentioning that we recently documented using conventional optical coherence tomography that the hemorrhaging invaded the space between the retinal synapses. The magnitude of the invasion was found to be significantly associated with the final visual outcome. Although any evidence of hemorrhaging disappeared after several months, hyperintensities could still be observed with optical coherence tomography between the retinal synapses.5
As Dr. Rabiolo pointed out, mSH is an important symptom for not only differential diagnoses, but it is also potentially related to other critical conditions such as choriocapillary loss or mCNV.