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Figure 10-49: (Plate 45) Background diabetic retinopathy. Retinal microaneurysms, dot-and-blot hemorrhages, and a few fine upper temporal hard exudates are diagnostic of early diabetic retinopathy. The patient had no visual symptoms, but retinopathy of this magnitude can often be seen in patients with insulin-requiring diabetes of 15 or more years' duration.

Neovascularization

In neovascularization the new vessels generally originate from capillaries from the venous side of the circulation and are associated with greater or lesser degrees of fibrosis. In all cases, however, the new vessels are incorporated in an associated fibrous membrane (Fig. 10-50, Plate 46; Fig. 1051).

Preretinal Neovascularization
Figure 10-50: (Plate 46) Proliferative diabetic retinopathy with preretinal hemorrhage. When neovascularization develops, preretinal and vitreous hemorrhages are much more likely to occur.

Easily visible neovascularization either in the periphery of the retina, as in this diabetic patient, or at the disk is an indication for immediate panretinal laser photocoagulation.

Preretinal Neovascularization

Figure 10-51: Proliferative diabetic retinopathy, left eye. There is extensive neovascularization of the disk with an associated small intravitreal hemorrhage that obscures the upper temporal vessels. Along the inferior temporal arcade is another area of neovascularization. These new vessels are incorporated in fibrous membranes that may tent up the vessels and cause traction detachments of the retina, as at the lower right edge of the photograph.

Figure 10-51: Proliferative diabetic retinopathy, left eye. There is extensive neovascularization of the disk with an associated small intravitreal hemorrhage that obscures the upper temporal vessels. Along the inferior temporal arcade is another area of neovascularization. These new vessels are incorporated in fibrous membranes that may tent up the vessels and cause traction detachments of the retina, as at the lower right edge of the photograph.

Retinal Hemorrhage

Hemorrhage into the retina indicates further breakdown in the integrity of the vascular wall. When the hemorrhage occurs in the inner retina, as in hypertension, it assumes a feathery flame shape as it is molded and dispersed by the nerve fibers coursing toward the disk. In obstruction of the central retinal vein, the fundus may be splattered with blood (Fig. 10-52, Plate 47).

Figure 10-52: (Plate 47) Branch retinal vein obstruction. Thickening of the retinal arterial wall in diabetes and hypertension may compromise the lumen of the vein, where they share a common adventitial sheath at an arteriovenous crossing. The resulting obstruction produces hemorrhage retinopathy in the drainage area of the affected vein. Note here how the flame-shaped pattern of blood outlines the arcuate pattern of the nerve fibers as they run toward the optic disk.

Vascular Occlusion

When the central artery or one of its branches is occluded, the nonperfused retinal area becomes cloudy in a matter of minutes. At the fovea, where the retina is one cell layer thick and nourished by the choroid, the normal color and transparency persist. By contrast with the surrounding pallor, the fovea then has a cherry-red appearance Fig. 10-53, Plate 48). Occlusions of branches of the central vein produce edema and hemorrhage in the drained area. As collateral drainage channels develop (see Fig 10-52 and Plate 47), the edema and hemorrhagic retinopathy subside, leaving white-walled veins, neovascularization, and microaneurysms in the affected area (Fig. 1054, Plate 49).

Retinal New Vessels Collaterals

Figure 10-54: (Plate 49) Neovascularization after branch retinal vein obstruction. New vessels may develop late after obstruction of a branch of the central retinal vein. These most often serve to shunt flow around the obstructed vessel site and are thus not as exuberantly proliferative as those seen in diabetic retinopathy.

Figure 10-54: (Plate 49) Neovascularization after branch retinal vein obstruction. New vessels may develop late after obstruction of a branch of the central retinal vein. These most often serve to shunt flow around the obstructed vessel site and are thus not as exuberantly proliferative as those seen in diabetic retinopathy.

Optic Disk Edema

The term papilledema is reserved for the form of disk edema that is the result of increased intracranial pressure. It therefore has an etiologic connotation and is not used generally to mean optic disk edema. Papillitis is the term applied to inflammatory disk edema. Patients with anterior ischemic optic neuropathy commonly have a pale, edematous disk with an altitudinal field effect.

Embolism

Table 10-6 lists the characteristics of retinal emboli of cardiovascular significance. Of these, platelet emboli are at once the most common and the most evanescent. Hollenhorst cholesterol plaques may be identified at the same bifurcations for months to years after the embolic shower. Platelet emboli, Hollenhorst plaques (seeB*;B; Fig. 10-53, Plate 48; Fig. 10-55, Plate 49), and calcium emboli (Fig. 10-56, Plate 50) are usually seen along the course of a retinal artery. Roth spots (Fig. 10-57, Plate 51) and fat emboli may not appear to be intravascular and may not be associated with a vessel that is ophthalmoscopically visible (see Table 10-6).201

Carotis Atheroscleros

Figure 10-55: Retinal emboli often lodge at bifurcations, as in this patient with carotid atherosclerosis. Note that the embolic material often seems larger than the containing vessel, as in the embolus at the lower left edge of the photograph. Emboli may damage the vessel wall and cause leakage, as can be seen by the exudate deposited about the inferior embolus. Hollenhorst cholesterol plaques rarely obstruct arterial flow completely, and this patient maintained vision.

Figure 10-55: Retinal emboli often lodge at bifurcations, as in this patient with carotid atherosclerosis. Note that the embolic material often seems larger than the containing vessel, as in the embolus at the lower left edge of the photograph. Emboli may damage the vessel wall and cause leakage, as can be seen by the exudate deposited about the inferior embolus. Hollenhorst cholesterol plaques rarely obstruct arterial flow completely, and this patient maintained vision.

Figure 10-56: (Plate 50) Calcific retinal embolus associated with aortic valvular disease. Calcific aortic valvular disease and valve replacement surgery may result in retinal emboli. Like cholesterol emboli, these calcific flecks lodge at arterial bifurcations but seldom obstruct flow completely. They are white and glitter in the ophthalmoscope beam. Somewhat similar emboli may be seen after the intravenous injection of illicit drugs expanded with talc.

Figure 10-57: (Plate 51) Retinal hemorrhages after cardiac catheterization. Following cardiac catheterization, symptomatic and asymptomatic retinal hemorrhages may occur. The latter are more common. Presumably, these are the result of embolic events. Note, in this recently catheterized patient, the two oval hemorrhages and a small area of cloudy swelling just inferior and temporal to the fovea.

Table 10-6: Emboli of Cardiovascular Significance

Type

Appearance

Significance

Platelet

Dull pink to gray often with associated fibrin

Downstream vegetations, mural thrombi

Hollenhorst plaque Glistening yellow-orange plaques at bifurcations

Downstream atheroma (containing cholesterol)

Calcium plaque

Glistening white plaques

Calcific aortic stenosis

Roth spot

Hemorrhage with gray-white center (see Plate 51 Fig. 10-57)

Blood dyscrasia or septic embolus as in subacute bacterial endocarditis

Fat embolus

Fuzzy-bordered gray-white spot without hemorrhage

Severe trauma with long bone fractures

Myxoma

Disk edema, retinal edema in arterial Life-threatening atrial myxoma supply zone

Diabetes Mellitus

In diabetes mellitus, focal loss of a portion of the capillary bed is followed by microaneurysm formation and vascular dilatation around the borders of the area of capillary dropout (see Fig. 1049 and Plate 45). Vascular leakage occurs with dot and blot hemorrhages and deposits of hard exudate (Fig 10-58). New blood vessels develop along the vascular arcades and at the optic nerve head (see Figs. 10-50 and 10-51 and Plate 50).

Diabetic Macular Oedema Exudative

Figure 10-58: Exudative diabetic retinopathy, right eye, illustrating microaneurysms, dot-and-blot hemorrhages, and venous engorgement with extensive deposits of hard, yellow exudate.

Vasoconstriction of the arterial tree and thickening of the arterial vessel walls with consequent reduction in lumen diameter are homeostatic responses to hypertension. Arteriosclerotic narrowing of the vessels acts to insulate the capillary bed from the elevated pressure of the arterial supply. These arteriosclerotic changes are visible as narrowing, increases in central light reflexes, and copper and silver "wiring" of the arteries Fig. 10-59, Plate 52). Radial arrangement of such exudate deposits in the macula produces a "star" (see Fig 10-48 and Plate 48). Hemorrhage may occur in the retinal layers in a characteristic flame pattern, and focal ischemia in the nerve fiber may result in cotton-wool microinfarcts. In severe hypertensive decompensation, the optic nerve head becomes swollen and edematous (see Fig. 10-48 and Plate 48).

Hypertensive patients should be classified as to whether or not their retinal circulation is compensated or has decompensated with observable edema, cotton-wool spots, flame hemorrhages, or swelling of the optic disk.201

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