Diseases


Fig. 4.1

Structure of interface between lens and vitreous



During the development of vitreous (Fig. 4.2A), the primary vitreous is compressed by secondary vitreous to the center; it goes nasally and forward to the center of the cavity from the posterior lens, then it goes temporally and backward to the optic disc until it is surrounded by Cloquet’s canal and connected with Erggelet’s canal. Primary vitreous is only the condensation of the membranes, which separates the primary and secondary vitreous. Secondary vitreous occupies the largest part of the vitreous cavity. Tertiary vitreous derives from the nonpigmented ciliary epithelial cells, extends to the lens and fuses with capsule, which forms the zonular fibers (Fig. 4.2).

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Fig. 4.2

Schematic diagram of three grades of vitreous. A, B, and C represent primary, secondary and tertiary vitreous respectively


Lesions of the vitreous include congenital dysplasia, age-related opacities, liquefaction, posterior vitreous detachment, neovascularization, proliferation, etc. Most of the vitreous changes are complications of adjacent diseases [4]. For example, vitreous hemorrhage is the most common complication due to retinal tears, proliferative diabetic retinopathy, retinal vein occlusion, posterior vitreous detachment, etc. What’s more, the hemorrhage will show various manifestations. If it is confined to the inner limiting membrane, the border will be well-defined and like a boat. Sometimes, the different layers of the blood will be discriminated carefully. If the hemorrhage breaks into the vitreous cavity, the amount, the time, and the course of the primary disease will decide its appearance. If the hemorrhage is secondary to the retina tear, the retina tear, the traction of the vitreous on the apex of the retinal valve, the crossing blood between the two points of the break will be seen most temporarily and superiorly. Of course, the blood will precipitate on the lower half of the vitreous cavity with red or pale color according to its course. In some cases, the blood will become fibrous and make the retina contract, and tractional retinal detachment will be seen. When we observe the vitreous changes, the primary cause will be considered in mind. Due to the filamentous collagen of vitreous body, the various appearances of opacity, hemorrhage, and fibrous tissue can be detected (Fig. 4.3, 4.4, 4.5, 4.6, 4.7, 4.8, 4.9, 4.10, 4.11, 4.12, 4.13, 4.14, 4.15, 4.16, 4.17, 4.18, 4.19, 4.20, 4.21, 4.22, 4.23, 4.24, 4.25, 4.26, 4.27, 4.28 and 4.29).



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Fig. 4.3

Vitreous opacities


I. Location of occlusion of the inferior retinal vein branch, the diameter of the vein is increased sharply


II. Elevated and dilated retinal vessel, within it a grey column could be seen in the center and two blood streams on both sides. Suspected neovascularization is on it



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Fig. 4.4

Vitreous opacities


I. Ghost vessels of retinal vein


II. Dilated retinal veins (communicating branch)


III. Thinning and straight retinal artery


IV. Vitreous opacities of different layers



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Fig. 4.5

Vitreous opacities


I. Chronic vitreous hemorrhage


II. Subretinal hemorrhage


III. Deep retinal hemorrhage


IV. Chronic vitreous hemorrhage



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Fig. 4.6

Vitreous opacities


I. Neovascularization of the optic disc


II. Hemorrhage in the anterior vitreous


III. Hemorrhage in the middle vitreous


IV. Hemorrhage near the posterior hyaloids


V. Deep retinal exudates



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Fig. 4.7

Boat-like pre-retinal hemorrhage


I. The layer of serum


II. The layer of platelets


III. The layer of white blood cells


IV. The layer of deoxygenerated hemoglobin


V. The layer of oxygenated red blood cells


Mar 22, 2020 | Posted by in OPHTHALMOLOGY | Comments Off on Diseases

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