Ординатура / Офтальмология / Английские материалы / Ophthalmology A Short Textbook_Lang_2000

11.5 The Role of the Vitreous Body in Various Ocular Changes 293

11.4.5 Vitreoretinal Dystrophies

11.4.5.1 Juvenile Retinoschisis

Juvenile retinoschisis is an inherited X-linked recessive disorder that affects only males. A retinal schisis at the macula sometimes referred to clinically as a “spoke phenomenon” usually develops between the ages of 20 and 30. This is associated with a significant loss of visual acuity. A peripheral retinal schisis is also present in about half of these cases. This splitting of the retina is presumably due to traction of the vitreous body. This splitting occurs in the nerve fiber layer in contrast to typical senile retinoschisis, in which splitting occurs in the outer plexiform layer.

11.4.5.2 Wagner’s Disease

This disorder is also inherited (autosomal dominant) and involves central liquefaction of the vitreous body. This “visual void” in the vitreous chamber and fibrillary condensation of the vitreous stroma associated with a cataract characterize vitreoretinal degeneration in Wagner’s disease.

11.5The Role of the Vitreous Body in Various Ocular Changes and Following Cataract Surgery

11.5.1Retinal Detachment

The close connection between the vitreous body and retina can result in retinal tears in vitreous detachment, which in turn can lead to rhegmatogenous retinal detachment (from the Greek word “rhegma,” breakage.

These retinal defects provide an opening for cells from the retinal pigment epithelium to enter the vitreous chamber. These pigment cells migrate along the surface of the retina. As they do so, they act similarly to myofibroblasts and lead to the formation of subretinal and epiretinal membranes and cause contraction of the surface of the retina. This clinical picture is referred to as proliferative vitreoretinopathy (PVR). The rigid retinal folds and vitreous membranes in proliferative vitreoretinopathy significantly complicate reattachmentoftheretina.Usuallythisrequiresmoderntechniquesofvitreoussurgery.

11.5.2Retinal Vascular Proliferation

Retinal vascular proliferation can occur in retinal ischemia in disorders such as diabetic retinopathy, retinopathy in preterm infants, central or branch retinal vein occlusion, and sickle-cell retinopathy. Growth of this retinal neovascularization into the vitreous chamber usually occurs only where vitreous detachment is absent or partial because these proliferations require a substrate to grow on. Preretinal proliferations often lead

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Fibrotic changes produce traction of the retina resulting in a tractional retinal detachment.

11.5.3Cataract Surgery

Increased postoperative inflammation in the anterior segment can progress through the hyaloid canal to the posterior pole of the eye and a cystoid macular edema can develop. This complication occurs particularly frequently following cataract surgery in which the posterior lens capsule was opened with partial loss of vitreous body. (Hruby-Irvine-Gass syndrome is the development of cystoid macular edema following intracapsular cataract extraction with incarceration of the vitreous body in the wound).

11.6Surgical Treatment: Vitrectomy

Definition

Surgical removal and replacement of the vitreous body with Ringer’s solution, gas, or silicone oil.

Indication: The primary indications include:

Unabsorbed vitreous hemorrhage.

Tractional retinal detachment.

Proliferative vitreoretinopathy.

Removal of intravitreal displaced lenses or foreign bodies.

Severe postoperative or post-traumatic inflammatory vitreous changes.

Procedure: The vitreous body cannot simply be aspirated from the eye as the vitreoretinal attachments would also cause retinal detachment. The procedure requires successive, piecemeal cutting and aspiration with a vitrectome

(a specialized cutting and aspirating instrument). Cutting and aspiration of the vitreous body is performed with the aid of simultaneous infusion to prevent the globe from collapsing. The surgical site is illuminated by a fiberoptic light source. The three instruments (infusion cannula, light source, and vitrectome), all 1 mm in diameter, are introduced into the globe through the pars plana, which is why the procedure is referred to as a pars plana vitrectomy (PPV). This site entails the least risk of iatrogenic retinal detachment (Fig. 11.7). The surgeon holds the vitrectome in one hand and the light source in the other. The procedure is performed under an operating microscope with special contact lenses placed on the corneal surface. Once the vitreous body and any vitreous membranes have been removed (Fig. 11.7), the retina can be treated intraoperatively with a laser (for example, to treat proliferative diabetic retinopathy or repair a retinal tear). In many cases, such as with an unabsorbed vitreous hemorrhage, it is sufficient to fill the eye with Ringer’s solution following vitrectomy.

Fig. 11.7 The illustration depicts the infusion cannula, light source, and vitrectome (cutting and aspirating instrument). A cerclage is usually placed around the equator to release residual traction and prevent retinal detachment. It is left in place after surgery.

Filling the eye with Ringer’s solution is not sufficient to treat a complicated retinal detachment with epiretinal or subretinal membranes and contraction of the surface of the retina (see proliferative vitreoretinopathy). In these cases, the detached retina must be flattened from anterior to posterior and held with a tamponade of fluid with a very high specific gravity such as a perfluorocarbon liquid (Fig. 11.8a). These “heavy” liquids can also be used to float artifical lenses that have become displaced in the vitreous body. The artificial lenses have a lower specific gravity than these liquids and will float on them (Fig. 11.8b). At the end of the operation, these heavy liquids must be replaced with gases, such as a mixture of air and sulfur hexafluoride, that are spontaneously absorbed within a few days or with silicone oil (which must be removed in a second operation). Postoperative patient positioning should reflect the fact that maximum gas pressure will be in the superior region (Fig. 11.9a) due to its buoyancy. Complicated retinal detachments will require a prolonged internal tamponade. Silicone oil has proven effective for this pur-

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Use of “heavy” liquids in vitreoretinal surgery.

Cerclage

(encircling band)

Perfluorocarbon

liquid

Fig. 11.8 a Repairing the retina in a complicated retinal detachment using

Use of gas and silicone oil in vitreoretinal surgery.

b Completely filling the globe with silicone oil fixes the retina to its underlying tissue at practically every location (arrows).

Silicone oil

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pose as it completely fills the vitreous chamber and exerts permanent pressure on the entire retina (Fig. 11.9b). However, silicone oil inevitably causes cataract formation and occasionally corneal changes and glaucoma. Therefore, it must be removed in a second operation.

Complications: Vitrectomy nearly always leads to subsequent lens opacification, and rarely to retinal tears, bleeding, or endophthalmitis.

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12 Retina

Gabriele K. Lang and Gerhard K. Lang

12.1Basic Knowledge

The retina is the innermost of three successive layers of the globe. It comprises two parts:

A photoreceptive part (pars optica retinae), comprising the first nine of the 10 layers listed below.

A nonreceptive part (pars caeca retinae) forming the epithelium of the ciliary body and iris.

The pars optica retinae merges with the pars ceca retinae at the ora serrata.

Embryology: The retina develops from a diverticulum of the forebrain (proencephalon). Optic vesicles develop which then invaginate to form a doublewalled bowl, the optic cup. The outer wall becomes the pigment epithelium, and the inner wall later differentiates into the nine layers of the retina. The retina remains linked to the forebrain throughout life through a structure known as the retinohypothalamic tract.

Thickness of the retina (Fig. 12.1)

Layers of the retina: Moving inward along the path of incident light, the individual layers of the retina are as follows (Fig. 12.2):

1.Inner limiting membrane (glial cell fibers separating the retina from the vitreous body).

2.Layer of optic nerve fibers (axons of the third neuron).

3.Layer of ganglion cells (cell nuclei of the multipolar ganglion cells of the third neuron; “data acquisition system”).

4.Inner plexiform layer (synapses between the axons of the second neuron and dendrites of the third neuron).

5.Inner nuclear layer (cell nuclei of the bipolar nerve cells of the second neuron, horizontal cells, and amacrine cells).

6.Outer plexiform layer (synapses between the axons of the first neuron and dendrites of the second neuron).

7.Outer nuclear layer (cell nuclei of the rods and cones = first neuron).

8.Outer limiting membrane (sieve-like plate of processes of glial cells through which rods and cones project).

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Thickness of the retina.

Around the fovea: 0.23 mm

Fovea centralis: 0.10 mm

At the optical disk: 0.56 mm

Fig. 12.1 Retinal tears most often occur close to the ora serrata.

9.Layer of rods and cones (the actual photoreceptors).

10.Retinal pigment epithelium (a single cubic layer of heavily pigmented epithelial cells).

11.Bruch’s membrane (basal membrane of the choroid separating the retina from the choroid).

Macula lutea: The macula lutea is a flattened oval area in the center of the retina approximately 3–4 mm (15 degrees) temporal to and slightly below the optic disk. Its diameter is roughly equal to that of the optic disk (1.7–2 mm). The macula appears yellow when examined under green light, hence the name macula lutea (yellow spot). Located in its center is the avascular fovea

Fig. 12.2 a Layers of the retina and examination methods used to diagnose abnormal ! processes in the respective layers (EOG = electro-oculogram; ERG = electroretinogram; VEP = visual evoked potential). b Histologic image of the 10 layers of the retina.

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centralis, the point at which visual perception is sharpest. The fovea centralis contains only cones (no rods) each with its own neural supply, which explains why this region has such distinct vision. Light stimuli in this region can directly act on the sensory cells (first neuron) because the bipolar cells (second neuron) and ganglion cells (third neuron) are displaced peripherally.

Vascular supply to the retina: The inner layers of the retina (the inner limiting membrane through the inner nuclear layer) are supplied by the central artery of the retina. This originates at the ophthalmic artery, enters the eye with the optic nerve, and branches on the inner surface of the retina. The central artery is a genuine artery with a diameter of 0.1 mm. It is a terminal artery without anastomoses and divides into four main branches (see Fig. 12.8).

Because the central artery is a terminal artery, occlusion will lead to retinal infarction.

The outer layers (outer plexiform layer through the pigment epithelium) contain no capillaries. They are nourished by diffusion primarily from the richly supplied capillary layer of the choroid. The retinal arteries are normally bright red, have bright red reflex strips (see Fig. 12.8) that become paler with advancing age, and do not show a pulse. The retinal veins are dark red with a narrow reflex strip, and may show spontaneous pulsation on the optic disk.

Pulsation in the retinal veins is normal; pulsation in the retinal arteries is abnormal.

The walls of the vessels are transparent so that only the blood will be visible on ophthalmoscopy. In terms of their structure and size, the retinal vessels are arterioles and venules, although they are referred to as arteries and veins. Venous diameter is normally 1.5 times greater than arterial diameter. Capillaries are not visible.

Nerve supply to the retina: The neurosensory retina has no sensory supply.

Disorders of the retina are painless because of the absence of sensory supply.

Light path through the retinal layers: When electromagnetic radiation in the visible light spectrum (wavelengths of 380–760 nm) strikes the retina, it is absorbed by the photopigments of the outer layer. Electric signals are created in a multi-step photochemical reaction. They reach the photoreceptor synapses as action potentials where they are relayed to the second neuron. The signals are relayed to the third and fourth neurons and finally reach the visual cortex.

Light must pass through three layers of cell nuclei before it reaches the photosensitive rods and cones. This inverted position of the photoreceptors is due to the manner in which the retina develops from a diverticulum of the forebrain.