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Retinal Detachment

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Retinal Detachment

The term "retinal detachment" denotes separation of the sensory retina, ie, the photoreceptors and
inner tissue layers, from the underlying retinal pigment epithelium. There are three main types:
rhegmatogenous detachment, traction detachment, and serous or hemorrhagic detachment.

Rhegmatogenous Retinal Detachment

The most common of the three major types of retinal detachments is rhegmatogenous retinal
detachment. The characteristics of a rhegmatogenous detachment are a full-thickness break (a
"rhegma") in the sensory retina, variable degrees of vitreous traction, and passage of liquefied
vitreous through the sensory retinal defect into the subretinal space. A spontaneous
rhegmatogenous retinal detachment is usually preceded or accompanied by a posterior vitreous
detachment. Myopia, aphakia, lattice degeneration, and ocular trauma are associated with this
type of retinal detachment. Binocular indirect ophthalmoscopy with scleral depression (Figures
2–16 and 2–18) reveals elevation of the translucent detached sensory retina. A careful search
usually reveals one or more full-thickness sensory retinal breaks such as a horseshoe tear, round
atrophic hole, or anterior circumferential tear (retinal dialysis). The location of retinal breaks
varies according to type; horseshoe tears are most common in the superotemporal quadrant,
atrophic holes in the temporal quadrants, and retinal dialysis in the inferotemporal quadrant.
When multiple retinal breaks are present, the defects are usually within 90 degrees of one
another.

Treatment

Scleral buckling or pneumatic retinopexy are the two most popular and effective surgical
techniques for the repair of rhegmatogenous retinal detachment. Each procedure requires careful
localization of the retinal break and treatment with cryotherapy or laser in order to create an
adhesion between the pigment epithelium and the sensory retina. With scleral buckling surgery,
the retinal break is mounted on sclera indented by an explant. The scleral indentation can be
achieved by a variety of techniques and materials, each of which has inherent advantages and
disadvantages. Pneumatic retinopexy, which may be performed with vitrectomy surgery,
involves the intraocular injection of air or an expandable gas in order to tamponade the retinal
break while the chorioretinal adhesion forms. An overall reattachment rate of 90% is reported;
however, the visual results are dependent on the preoperative status of the macula. If the macula
is involved in rhegmatogenous retinal detachment, the likelihood of complete visual recovery is
diminished.

Traction Retinal Detachment

Traction retinal detachment is the second most common type and is most commonly due to
proliferative diabetic retinopathy, proliferative vitreoretinopathy, retinopathy of prematurity, or
ocular trauma. In contrast to the convex appearance of rhegmatogenous retinal detachment, the
typical traction retinal detachment has a more concave surface and is likely to be more localized,
usually not extending to the ora serrata. The tractional forces that actively pull the sensory retina
away from the underlying pigment epithelium are caused by a clinically apparent vitreal,
epiretinal, or subretinal membrane consisting of fibroblasts and of glial and retinal pigment
epithelial cells. In diabetic traction retinal detachment, vitreous contraction draws the
fibrovascular tissue and underlying retina anteriorly toward the vitreous base. Initially the
detachment may be localized along the vascular arcades, but progression may spread to involve
the midperipheral retina and the macula. Proliferative vitreoretinopathy is a complication of
rhegmatogenous retinal detachment and is the most common cause of failure of surgical repair in
these eyes.

The basic pathologic process in eyes with proliferative vitreoretinopathy is growth and
contraction of cellular membranes on both sides of the retina and on the posterior vitreous
surface. Focal traction from cellular membranes can produce a retinal tear and lead to combined
tractional-rhegmatogenous retinal detachment.

Treatment

The primary treatment of traction retinal detachment is vitreoretinal surgery and may involve
vitrectomy, membrane removal, scleral buckling, and injection of intraocular gas or silicone oil.

Serous & Hemorrhagic Retinal Detachment

Serous and hemorrhagic retinal detachment can occur in the absence of either retinal break or
vitreoretinal traction. These detachments are the result of a collection of fluid beneath the
sensory retina and are caused primarily by diseases of the retinal pigment epithelium and
choroid. Degenerative, inflammatory, and infectious diseases limited to the macula, including the
multiple causes of subretinal neovascularization, may be associated with this third type of retinal
detachment and are described in an earlier section of this chapter. This type of detachment may
also be associated with systemic vascular and inflammatory disease as described in Chapter 7:
Uveal Tract & Sclera and Chapter 15: Ocular Disorders Associated with Systemic Diseases.

       

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The Optic Nerve

A wide variety of diseases affect the optic nerve (Table


14–1). Clinical features particularly suggestive of optic
nerve disease are an afferent pupillary defect, poor color
vision, and optic disk changes. It is important to
remember that the optic disk may be normal in the early
stages of disease affecting the retrobulbar optic nerve,
particularly compression by an intracranial lesion, even
when there has been severe loss of visual acuity and
field. Axons can be dysfunctional long before they
become atrophic.

Table 14–1. Etiologic Classification of Diseases


of the Optic Nerve.
Optic disk swelling occurs predominantly in diseases
directly affecting the anterior portion of the optic nerve
but also occurs with raised intracranial pressure and
compression of the intraorbital optic nerve. Optic disk
swelling can be a crucial clinical sign, such as in the
diagnosis of anterior ischemic optic neuropathy in
which optic disk swelling must be present in the acute
stage for the diagnosis to be made on clinical grounds.
Central retinal vein occlusion, ocular hypotony and
intraocular inflammation can produce optic disk
swelling and hence the misleading impression of optic
nerve disease.

Optic atrophy (Figure 14–6) is a nonspecific response to


optic nerve damage from any cause. Since the optic
nerve consists of retinal ganglion cell axons, optic
atrophy may be the consequence of primary retinal
disease, such as retinitis pigmentosa or central retinal
artery occlusion. Excavation of the optic nerve head
(optic disk cupping) is generally a sign of glaucomatous
optic neuropathy, but may occur with any cause of optic
atrophy. Segmental pallor and attenuated retinal blood
vessels are often the consequence of anterior ischemic
optic neuropathy. Hereditary optic neuropathies usually
produce bilateral temporal segmental disk pallor with
preferential loss of papillomacular axons. Peripapillary
exudates occur with optic disk swelling, due to
papillitis, ischemic optic neuropathy, or papilledema.
(The term "neuroretinitis" for the combination of optic
disk swelling and retinal exudates, including a macular
star, is a misnomer in that there is no inflammation of
the retina, the exudates being a response to the anterior
optic nerve disease. This may occur in demyelinative
and other types of optic neuritis, anterior ischemic optic
neuropathy, and papilledema. The term "neuroretinitis"
is more reasonably applied if there is true inflammation
of the retina and optic nerve [Figure 14–7].) Other
helpful signs of prior disk edema are peripapillary
gliosis and atrophy, chorioretinal folds, and internal
limiting membrane wrinkling.
Figure 14– Add to 'My Saved
6. Images'

  Examples of optic atrophy. Upper


left: Primary optic atrophy due to
View Large nutritional amblyopia. Upper right:
Secondary optic atrophy with
retinochoroidal collaterals (arrows) due
to optic nerve sheath meningioma.
Lower left: Optic atrophy with optic
disk drusen. Lower right: Pallor
(atrophy) of right optic disk due to
nerve compression by sphenoid
meningioma. The left disk is normal.

Figure 14– Add to 'My Saved


7. Images'

  Arcuate neuroretinitis due to acute


retinal necrosis syndrome.
View Large (Reproduced, with permission, from
Margolis T et al: Acute retinal necrosis
syndrome presenting with papillitis and
arcuate neuroretinitis. Ophthalmology
1988;95:937.)

In general, there is a correlation between degree of optic


disk pallor, and loss of acuity, visual field, color vision
and pupillary reactions, but the relationship varies
according to the underlying etiology. The major
exception to this rule is compressive optic neuropathy in
which optic disk pallor is generally a late manifestation.

Optic Neuritis

Inflammatory optic neuropathy (optic neuritis) may be


due to a variety of causes (Table 14–1) but the most
common is demyelinative disease, including multiple
sclerosis. Retrobulbar neuritis is an optic neuritis that
occurs far enough behind the optic disk that the disk
remains normal during the acute episode. Papillitis is
disk swelling caused by inflammation at the nerve head
(intraocular optic nerve) (Figure 14–8). Loss of vision is

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