Clinicopathologic Correlations

There are many ophthalmoscopic conditions with which the examiner should be familiar. An image is normally focused directly on the retina. When the image is not focused on the retina, a refractive error is present. Lenses are used to correct refractive errors. The absence of a refractive error is called emmetropia. Refractive errors are extremely common. Listed here are the common refractive errors and their causes:

Hyperopia (farsightedness): Light is focused posterior to the retina.

Myopia (nearsightedness): Light is focused anterior to the retina.

Astigmatism: Light is not uniformly focused in all directions. Astigmatism is commonly a result of a cornea that is not perfectly spherical.

Presbyopia: Near vision decreases progressively as a result of a decrease in the eye's ability to accommodate. Presbyopia occurs after age 40 years.

Figure 10-85 illustrates normal (emmetropic), hyperopic, myopic, and astigmatic eyes.

Cataracts (see Figs. 10-68 and 10-69) are the most common cause of blindness. A cataract is a type of degenerative eye disease. One of the first symptoms that patients with cataracts experience is a ''mistiness'' of vision. Affected patients typically give a history in which vision has become ''like looking through a dirty window.'' As the lenticular opacity increases with time, there is a diminution of visual acuity in association with glare in bright light. This effect results from pupillary constriction limiting the light rays passing through the lens to the central portion of the lens, where the opacity is often most dense. These patients may wear dark glasses and hold their heads down to avoid excess light.

Figure 10-85 illustrates normal (emmetropic), hyperopic, myopic, and astigmatic eyes.

Cataracts (see Figs. 10-68 and 10-69) are the most common cause of blindness. A cataract is a type of degenerative eye disease. One of the first symptoms that patients with cataracts experience is a ''mistiness'' of vision. Affected patients typically give a history in which vision has become ''like looking through a dirty window.'' As the lenticular opacity increases with time, there is a diminution of visual acuity in association with glare in bright light. This effect results from pupillary constriction limiting the light rays passing through the lens to the central portion of the lens, where the opacity is often most dense. These patients may wear dark glasses and hold their heads down to avoid excess light.

Obstruction Aqueous HumorLenticular Opacity EyesAsymmetry Optic Cup

Figure 10-86 A and B, Optic cup asymmetry in glaucoma. The cup-disc ratio is approximately 30% in A (right eye) and 70% in B (left eye).

Figure 10-86 A and B, Optic cup asymmetry in glaucoma. The cup-disc ratio is approximately 30% in A (right eye) and 70% in B (left eye).

Narrow-angle glaucoma results from an obstruction to the drainage of aqueous humor at the canal of Schlemm. Patients with narrow-angle glaucoma have periodic attacks of acute elevation of intraocular pressure caused by intermittent obstruction. This is associated with pain, seeing halos, and poor vision. These attacks of glaucoma commonly occur in a darkened room, when pupillary dilatation occurs. When the pupil is fully dilated in a person with a narrow angle, the redundant iris folds at its base cause the increased obstruction and decreased drainage.

Primary open-angle, or chronic simple, glaucoma, in contrast, is associated with an open angle. There are many causes for simple glaucoma, which is a leading cause of slowly progressive blindness. The most important diagnostic difference from narrow-angle glaucoma is that in chronic simple glaucoma, pain is absent. Patients have reduced outflow of aqueous humor through the trabecular meshwork and into the canal of Schlemm, which results in elevated intraocular pressure. As a result, progressive cupping of the optic nerve (i.e., loss of nerve substance) occurs, accompanied by changes in the visual field. Although primary open-angle glaucoma is usually bilateral, its asymmetric onset results in a difference in optic cup size between the two eyes, one of the most characteristic early signs (Fig. 10-86). Peripheral field defects, especially in the nasal aspect, are common early in the disease. Vision is increasingly impaired as progressive atrophy of the optic nerve continues, owing to the increased intraocular pressure. Late in the disease, only a small area on the nasal aspect of the nerve head may remain. Figure 10-87 shows a close-up of the optic disc of a patient with 50% to 60% cupping of the optic nerve head. Table 10-9 lists the major characteristics of both types of glaucoma.

Glaucomatous Cupping
Figure 10-87 Glaucomatous cupping of the optic nerve head. The cup-to-disc ratio is approximately 50% to 60%.

Table 10-9 Characteristics of Glaucoma

Feature

Occurrence Cause

Age at onset Anterior chamber Chamber angle Symptoms

Cupping of disc Visual fields

Ocular pressure Other signs Treatment

Prognosis

Primary Open-Angle Glaucoma

85% of all glaucoma cases

Unclear*

Variable

Usually normal

Normal

Usually none Decreased vision, late

Progressive if not treated (see Figs. 10-86 and 10-87)

Peripheral fields are involved early

Central involvement is a very late sign

Progressively higher if not medically controlled

Late: high

Medical Laser surgery

Good if recognized early Very dependent on patient compliance

Narrow-Angle Glaucoma

15% of all glaucoma cases

Closed angle prevents aqueous drainage

50-85 years

Shallow

Narrow

Headache

Seeing halos around lights Sudden onset of severe eye pain Vomiting during attack

After one or more untreated attacks Involvement is a late sign

Early: detected with provocative tests only

Fixed, partially dilated pupil Conjunctival injection ''Steamy'' cornea{

Surgical

Good

•Thought to be a defect in the trabecular network ultrastructure. {Like looking through a steamy window.

Acute eye inflammations are common. They may be associated with local or systemic disease. The differential diagnosis of the red eye is important. The presence of pain, visual loss, and irregularities of the pupils are important signs signifying a serious, potentially blinding disorder. Figure 10-88 shows red eye. Table 10-2 provides an approach to the diagnosis of red eye.

Diabetic retinopathy is the leading cause of blindness in Americans aged 20 to 75 years. It is estimated that more than 12 million Americans have diabetes. Diabetic retinopathy is a highly specific vascular complication of type I and type II diabetes mellitus and is directly related to the duration of the disease. By 25 years after the onset of diabetes, nearly all patients with type I diabetes and 65% of patients with type II diabetes have some degree of retinopathy.

The retinal findings of diabetic retinopathy are the result of retinal microangiopathy, which causes increased vascular permeability that results in macular edema and decreased vision. In addition, vascular occlusive changes result in fibrovascular proliferation, hemorrhage, and scarring. The early changes of nonproliferative retinopathy are capillary microaneurysms, dilatation, tortuosity of vessels, and nonperfusion of areas of the retina. As the disease progresses to proliferative retinopathy, retinal neovascularization appears either at the optic disc (NVD) or elsewhere in the retina (NVE). Neovascularization may diminish vision still further by vitreous hemorrhage or traction detachment of the retina.

Nonproliferative, or background, retinopathy is the first stage of diabetic retinopathy. An early sign is the development of microaneurysms. These usually have smooth borders and sharp round shapes. In addition, intraretinal hemorrhages result from rupture of the micro-aneurysms, capillaries, and venules. The location of the hemorrhage within the retinal layers

Appearance Retinal Aneurysm

governs the shape of the hemorrhage: hemorrhages in the nerve fiber layer typically are flame-shaped with feathery borders, whereas hemorrhages in the deep areas of the retina have a fuzzy, blot-shaped appearance. Exudates may appear as clusters, streaks, or rings around the macula. These exudates result from leakage through the abnormally permeable capillary walls. Commonly, these microaneurysms, hemorrhages, and exudates occur near the macula. The retinal findings in a patient with nonproliferative diabetic retinopathy are shown in Figure 10-89. Note the hemorrhages and exudates. Figure 10-90 shows the marked tortuosity of the vessels in another patient with background retinopathy. Figure 10-91 shows the flame-shaped hemorrhages and exudates that are characteristic of nonproliferative diabetic retinopathy. Figure 10-92 shows circinate retinopathy in a diabetic patient.

Proliferative diabetic retinopathy is characterized by neovascularization, that is, new blood vessels that arise from the retinal and optic disc vessels. Neovascularization appears as a fine network (wisps or loops) of blood vessels that seem to bud off other vessels. Neovascularization of the disc (NVD) is shown in Figure 10-93; neovascularization elsewhere in the retina (NVE) is

Moderate Nonproliferative Retinopathy
Figure 10-89 Nonproliferative diabetic retinopathy.
Flame Hemorrhage Eye

Figure 10-90 Nonproliferative diabetic retinopathy. Note the Figure 10-91 Nonproliferative diabetic retinopathy. Note the markedly tortuous vessels. flame-shaped hemorrhages.

Figure 10-90 Nonproliferative diabetic retinopathy. Note the Figure 10-91 Nonproliferative diabetic retinopathy. Note the markedly tortuous vessels. flame-shaped hemorrhages.

shown in Figure 10-94. These vessels proliferate along the retinal surface and into the vitreous humor, often with fibrous band components. The vessels are often adherent to the posterior vitreous, and preretinal hemorrhages occur as a result of vitreoretinal separation pulling on the friable vessels. The blood resulting from a preretinal hemorrhage is trapped in the potential space between the retina and the vitreous humor (under the inner limiting membrane), forming a classic boat-shaped hemorrhage (Fig. 10-95). Further pulling on the retina can progress to retinal tears and tractional retinal detachments. Figures 10-96 to 10-98 show vitreous strands in patients with proliferative diabetic retinopathy. Figure 10-98 shows vitreous traction and a macular hole. Note the light-colored area surrounding the macula.

Figure 10-99 shows a patient with proliferative diabetic retinopathy with NVE, NVD, pre-retinal hemorrhage, and a fatty exudative maculopathy.

The therapy for proliferative retinopathy is panretinal photocoagulation (PRP) to cause regression of the neovascularization. Figures 10-100 and 10-101 show proliferative retinopathy and the laser burns of PRP. Note the PRP-treated areas that appear as round, punched-out spots with pigmentation in the center or at the margins. The treated areas first appear white or yellow, but within several weeks, pigmentation occurs. The laser burns are brought up to the vascular arcades and up to one disc diameter from the optic disc. Vitrectomy is also indicated for tractional detachments. The final stages of diabetic retinopathy, known as involutional or burned-out retinopathy, show a tangle of new vessels, hemorrhages, traction, and fibrosis.

Figure 10-92 Nonproliferative retinopathy, circinate retinopathy. Note the ring of exudates around or near the macula, as well as the hemorrhages at the macula.

Neovascularization Disk
Figure 10-93 Proliferative diabetic retinopathy. Note the neovascularization of the disc (NVD).

Hypertension also produces significant characteristic retinal features. Systemic hypertension may be reflected in the retina in terms of irregularities in arteriolar size, tortuosity of the retinal arteries, retinal edema, and changes in the arteriovenous crossings. Progressive changes of hypertension include arteriolar narrowing with increasing areas of retinal ischemia, which is evident by the development of cotton-wool exudates, hemorrhages, retinal edema, and papilledema. Figure 10-102 shows the retinal changes in a patient with hypertension. Notice in Figure 10-103 the tortuosity of the retinal vessels in another patient with hypertension;a red-free (green) contrast filter is used to enhance the visualization of the vessels. Cotton-wool spots and flame-shaped retinal hemorrhages in another patient with hypertension are shown in Figure 10-83. As the arteriole walls thicken as a result of sustained hypertension, the arter-ioles lose their transparency, and noticeable changes are seen at the crossings of the arteries and veins. Veins appear to disappear abruptly on either side of an artery. Some of the arteries develop a burnishing of the red reflex.

Macular exudates are also common in hypertension (Fig. 10-104). These are well-defined, whitish-yellow intraretinal collections of lipids secondary to vascular leakage. A macular star is

Preretinal hemorrhage

Figure 10-95 A and B, Proliferative diabetic retinopathy. Note the preretinal hemorrhage.

Diabetic Papillitis
Figure 10-96 Proliferative diabetic retinopathy. Note the vitreoretinal fibrous bands.

an accumulation of edema residues arranged in a stellate pattern around the macula. Macular stars are commonly seen in patients with hypertension, papilledema, papillitis, and central retinal venous occlusion (CRVO). A macular star is shown in Figure 10-105. Arteriolar dilations may also develop. These are known as arteriolar macroaneurysms and are prone to leak blood and serous fluid. A hemorrhage from a macroaneurysm is shown in Figure 10-106.

Increased intracranial pressure, frequently secondary to a space-occupying intracranial lesion, produces a classic picture of papilledema. Papilledema is a swelling of the optic disc. It is believed that the increased pressure is transmitted to the optic nerve sheath, causing axoplasmic flow stasis in the disc. This in turn causes axonal swelling and secondary

Central Fibrous Body
Figure 10-97 Proliferative diabetic retinopathy. Note the vitreoretinal fibrous bands.

Figure 10-98 Proliferative diabetic retinopathy. Note the vitreoretinal fibrous bands and macular hole.

Figure 10-98 Proliferative diabetic retinopathy. Note the vitreoretinal fibrous bands and macular hole.

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