|Year : 2021 | Volume
| Issue : 4 | Page : 665-666
Commentary: Bacillary layer detachment in retinochoroidal pathologies: The concept of retinal acute fluid accumulation
Eye Institute, Cleveland Clinic Abu Dhabi, Al Maryah Island, Abu Dhabi, UAE
|Date of Web Publication||09-Oct-2021|
Dr. Aniruddha Agarwal
Department of Ophthalmology, Cleveland Clinic Abu Dhabi, Al Maryah Island, Abu Dhabi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Agarwal A. Commentary: Bacillary layer detachment in retinochoroidal pathologies: The concept of retinal acute fluid accumulation. Indian J Ophthalmol Case Rep 2021;1:665-6
|How to cite this URL:|
Agarwal A. Commentary: Bacillary layer detachment in retinochoroidal pathologies: The concept of retinal acute fluid accumulation. Indian J Ophthalmol Case Rep [serial online] 2021 [cited 2021 Oct 26];1:665-6. Available from: https://www.ijoreports.in/text.asp?2021/1/4/665/327713
The outer retinal changes particularly in Vogt-Koyanagi-Harada (VKH) disease have led to several studies each proposing a different hypothesis for the pathological alterations. Optical coherence tomography (OCT) in patients with acute VKH characteristically shows multifocal “compartments” of fluid with a number of “septae” dividing it into intra- and outer-retinal zones. This finding is not restricted to VKH disease alone and can occur in sympathetic ophthalmia (as demonstrated in this case)—acute posterior multifocal placoid pigment epitheliopathy (APMPPE) and toxoplasmosis, to name a few.
Mehta et al. proposed the term “bacillary layer detachment” (BLD) after analyzing one of their patients with toxoplasma retinochoroiditis who had “septae” and “compartments” of fluid on OCT. Essentially, BLD is reminiscent of a commonly encountered post-mortem artifact in the eyes with age-related macular degeneration (AMD) and a split occurring in the photoreceptor myoid. Subsequently, BLD has been observed in a variety of acute inflammatory conditions such as APMPPE,, tubercular choroidal granuloma, VKH disease, and acute idiopathic maculopathy, among others. Therefore, it is generally believed that BLD occurs in inflammatory retinochoroidal pathologies. However, Cicinelli et al. in their series of eight patients (nine eyes) with BLD described a single case of central serous chorioretinopathy (CSC) with underlying lupus presenting with BLD. This case, however, cannot be strictly regarded as non-inflammatory, since there was evidence of ongoing systemic inflammation (lupus erythematosus). Thereafter, many entities regarded as non-inflammatory have been shown to develop BLD including macular neovascularization and macular telangiectasia. Therefore, the occurrence of BLD may not be always restricted to inflammatory pathologies alone.
So, what is the ground truth of BLD? Published literature suggests that BLD occurs in the eyes which have a sudden influx of intra- and subretinal fluid, i.e., retinal acute fluid accumulation (RAFA). It commonly occurs in conditions such as VKH disease, sympathetic ophthalmia, toxoplasmosis, tuberculosis, and hyper-acute stage of APMPPE—all of which have been shown to develop BLD.,,,, The report by Jung et al. also concluded that RAFA in the eyes with AMD led to the formation of BLD in their series. Zatreanu et al. also showed that sudden RAFA with pre-eclampsia in a young pregnant female led to the development of BLD. Finally, the most recent report by Ramtohul et al. showed the presence of BLD due to acute, intense leakage and hemorrhage in a patient with macular telangiectasia type 2. Therefore, more than the underlying inflammation, the rapidity, and speed of fluid accumulation in the outer retina may be responsible for the development of BLD. RAFA may result in a sudden distortion of the outer retinal structures (”photoreceptor fracture”) leading to the split in the inner myoid zone at various places in the retina, thereby, resulting in the OCT appearance of BLD.
While RAFA seems to be a plausible underlying explanation for BLD formation, other possible mechanisms cannot be rejected, since there is no animal model that shows such an occurrence. It is likely that BLD could represent either a split within the photoreceptor inner myoid zone, or the junction between the myoid and ellipsoid zone, or within the ellipsoid zone. Until we have a direct histopathological correlation between the observations on OCT and tissue specimens, the ultrastructure of BLD is speculative. For reasons unknown, the incidence of BLD in CSC seems to be rare with less than a handful of cases reported in the literature.
It is important to identify BLD because visual recovery closely follows the resolution of BLD on OCT. In the series of 112 eyes with BLD secondary to VKH, the resolution of BLD occurred after a mean of 3.4 ± 1.3 days. The timeline of visual recovery closely matched with the resolution of BLD; the best-corrected visual acuity improved from 20/184 to 20/50 Snellen's equivalent after a mean of 3.4 days. Therefore, the resolution of BLD may result in a rapid recovery of the photoreceptors if the disease is treated in a timely manner.
In summary, BLD seems to be an interesting explanation for a finding that was recognized since the early days of spectral-domain OCT. RAFA, which commonly occurs in the inflammatory pathologies and occasionally in other retinochoroidal pathologies, may lead to splitting at the level of photoreceptors and accumulation of fluid in the intra- and subretinal compartments. Until a direct histopathological correlation is available, the exact pathogenesis of BLD will remain enigmatic.
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