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Review
. 2016 Apr-Jun;6(2):58-68.
doi: 10.1016/j.tjo.2015.09.002. Epub 2015 Dec 2.

Impact of swept source optical coherence tomography on ophthalmology

Affiliations
Review

Impact of swept source optical coherence tomography on ophthalmology

Shoji Kishi. Taiwan J Ophthalmol. 2016 Apr-Jun.

Abstract

Swept source optical coherence tomography (SS-OCT) was introduced in clinical practice in 2012. Because of its deeper penetration and faster acquisition time, SS-OCT has the ability to visualize choroid, vitreous, and retinal structures behind dense preretinal hemorrhages. Swept source optical coherence tomography has positively influenced and hugely contributed to the research of the vitreous body. It is the first ophthalmic diagnostic technology to demonstrate the entire structure of the posterior precortical vitreous pocket (PPVP) in vivo. The roles of the PPVP in physiological posterior vitreous detachment and vitreoretinal interface disorders have now been elucidated. The presence of a connecting channel between the PPVP and Cloquet's canal suggests that the aqueous humor drains into the premacular space. Deeper penetration of SS-OCT has made it possible to view the choroid. It also has an important role in central serous chorioretinopathy and uveitis. We have also been able to treat Harada disease by monitoring the choroidal thickness by SS-OCT.

Keywords: Harada disease; macular hole; posterior precortical vitreous pocket; swept source optical coherence tomography; vitreoretinal interface disease.

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Conflict of interest statement

Conflicts of interest: The author has no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Schematic drawing of the swept source optical coherence tomography device. The light source is a tunable laser.
Figure 2
Figure 2
A comparison of the B scan images between spectral-domain optical coherence tomography (SD-OCT) and swept source optical coherence tomography (SSOCT) in a patient with uveitis. OD = oculus dextrus; SD-OCT = spectral-domain optical coherence tomography; SS-OCT = swept source optical coherence tomography.
Figure 3
Figure 3
Posterior precortical vitreous pocket (PPVP) in a postmortem eye in which the vitreous is stained with fluorescein. The posterior wall of the PPVP is a thin layer of the vitreous cortex (arrows). P = posterior precortical vitreous pocket.
Figure 4
Figure 4
The swept source optical coherence tomography image of the posterior precortical vitreous pocket (PPVP) in the normal right eye of a 24-year-old female. (A) The horizontal section. The mean height (h) is 0.7 mm and the mean width (w) is 6.4 mm. There is connecting channel (yellow arrow) between the PPVP (P) and Cloquet's canal (C). (B) The vertical section. The anterior wall of the PPVP (arrows) approaches the superior portion of the PPVP. C = Cloquet's canal; h = height; P = posterior precortical vitreous pocket; w = width.
Figure 5
Figure 5
Evolution of the posterior precortical vitreous pocket (PPVP) during childhood. (A) In a 3-year-old child, the posterior precortical vitreous pocket (P) is the narrow space in front of the fovea. (B) In a 6-year-old child, the PPVP (P) is enlarged but smaller than in the adult. The PPVP and Cloquet's canal (denoted “C”) appears to be independent. (C) In an 8- year-old, the PPVP is similar to the adult PPVP in size and shape. The connecting channel (arrow) is collapsed in the image. (D) The connecting channel (arrow) is opened. C = Cloquet's canal; P = posterior precortical vitreous pocket.
Figure 6
Figure 6
A 40-year-old male with a foveal cyst and midperipheral retinoschisis. (A) Horizontal section by spectral-domain OCT. Foveal cyst and retinoschisis (arrow) are visible. The vitreous structure is not visible. (B, C) Horizontal section by swept source OCT. (B) The posterior precortical vitreous pocket (P) with central depression is visible. Retinoschisis is clearly evident (red arrow). (C) The fibrous structure of the vitreous is visible. Tractus preretinalis (i.e., vitreous veil) is visible (yellow arrows). C = Cloquet's canal; OCT = optical coherence tomography.
Figure 7
Figure 7
Evolution of physiological posterior vitreous detachment (PVD). Stage 0 is a posterior precortical vitreous pocket with no detached cortex. Stage 1 is focal PVD around the macula. Stage 2 is perifoveal PVD. Stage 3a is macular PVD with intact posterior precortical vitreous pocket (PPVP). Stage 3b is macular PVD with a break in the posterior wall of the PPVP.
Figure 8
Figure 8
The incidence of partial and complete posterior vitreous detachment (PVD) in each decade of life.
Figure 9
Figure 9
Stage 1 macular hole in a 56-year-old male. (A) At the initial visit, swept source optical coherence tomography shows perifoveal posterior vitreous detachment (PVD) and a foveal cyst. (B) One month later, the perifoveal PVD persists but the foveal cyst has collapsed. (C) Four months later, the vitreous cortex has detached from the macula and the foveal cyst is resolved. P = posterior precortical vitreous pocket. Values 0.7, 1.0 and 1.2 denotes decimal visual acuity.
Figure 10
Figure 10
Stage 3 macular hole in a 69-year-old man. The operculum is attached on the posterior wall of the posterior precortical vitreous pocket (P). P = posterior precortical vitreous pocket.
Figure 11
Figure 11
The possible mechanism of idiopathic epiretinal membrane (ERM). The posterior wall of the posterior precortical vitreous pocket (P) is a collagen sheet that serves as a structure of the ERM. When posterior vitreous detachment occurs, the posterior wall of the posterior precortical vitreous pocket may remain on the macula. Cellular proliferation on the collagen sheet may modify the nature of ERM. P = posterior precortical vitreous pocket.
Figure 12
Figure 12
The epiretinal membrane (ERM) in a 52-year-old female. She has no posterior vitreous detachment. (A) Her left eye shows the ERM (arrows) in the macula. (B) Swept source optical coherence tomography shows that the thickened posterior wall (arrows) of the posterior precortical vitreous pocket (P) is itself the ERM. P = posterior precortical vitreous pocket.
Figure 13
Figure 13
Diabetic retinopathy in a 45-year-old female. (A) In her right eye, posterior vitreous detachment has occurred in the macular area. Small cystoid macular edema (CME) is evident at the fovea. (B) In her left eye, crescent subhyaloid hemorrhage exists around the inferior vascular arcade. Swept source optical coherence tomography shows perifoveal posterior vitreous detachment with large CME and subhyaloid hemorrhage (yellow arrow). CME = cystoid macular edema; PVD = posterior vitreous detachment. Values 0.5 and 0.3 denotes decimal visual acuity.
Figure 14
Figure 14
(A) Ruptured retinal macroaneurysm in a 79-year-old female. (B) In spectral-domain optical coherence tomography, the inner structure of the hematoma is not visible. (C) In swept source optical coherence tomography, the internal structure of the hematoma is visible.
Figure 15
Figure 15
(A) Polypoid choroidal vasculopathy associated with subretinal hemorrhage in a 66-year-old man. (B) Fluorescein angiography image. (C) Indocyanine angiography image. (D) Horizontal section of swept source optical coherence tomography. FA = fluorescein angiography; ICG-A = indocyanine angiography; SS-OCT = swept source optical coherence tomography.
Figure 16
Figure 16
A 36-year-old male with acute central serous chorioretinopathy. (A) Serous retinal detachment with subretinal precipitates. (B) The precipitates emit autofluorescence. (C) Swept source optical coherence tomography shows marked swelling of the outer choroidal vessels (yellow arrowheads). In serous retinal detachment, photoreceptor outer segments are elongated (white arrow). Subretinal fibrin is visible (green arrow). FAF = fundus autofluorescence.
Figure 17
Figure 17
Acute central serous chorioretinopathy in a 56-year-old male. (A) One week after photodynamic therapy, choroidal swelling has decreased by approximately 10%. The outer choroidal vessels remain swollen. (B) One month later, the choroidal thickness has decreased to 276 μm and dilatation of outer choroidal vessels is diminished. CCT = central choroidal thickness; PDT = photodynamic therapy.
Figure 18
Figure 18
Harada disease in a 40-year-old woman. (A) The color fundus photograph shows serous retinal detachment in lobular pattern. Swept source optical coherence tomography reveals subretinal fluid (a), intraretinal fluid (b) and layer of the outer segment (c). The choroid is extensively swollen and the chorioscleral border is not visible. CT = central choroidal thickness.
Figure 19
Figure 19
Harada disease in a 51-year-old female. (A)At the initial visit, both eyes have serous retinal detachment. The choroid is so swollen that the chorioscleral border cannot be determined. (B) Three days after steroid pulse therapy, the subretinal fluid is remarkably absorbed. The choroid has reduced to normal thickness (yellow arrow). (C) Three weeks after steroid pulse therapy exudative retinal detachment recurred in the left eye. Fluid with fibrin has accumulated in the outer retinal space between the retina and detached outer segment. (D) The right eye shows no apparent recurrence; however, the choroid is remarkably thickened, which suggests an early relapse. OD = oculus dextrus; OS = oculus sinister.

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