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Figure 10-99 Diabetic retinopathy with neovascularization of the disc, neovascularization elsewhere in the retina, preretinal hemorrhage, and fatty macular exudates.

Figure 10-99 Diabetic retinopathy with neovascularization of the disc, neovascularization elsewhere in the retina, preretinal hemorrhage, and fatty macular exudates.

Macular Hole ImageRoth Spot FundusRoth Spot Fundus
Figure 10-101 Proliferative diabetic retinopathy. Note the lesions of panretinal photocoagulation.
Retinal Heme Hypertension
Figure 10-102 Retinal changes in a patient with longstanding hypertension. Note the cotton-wool spots and flame-shaped hemorrhages. Part of a macular star is seen on the bottom right.

Figure 10-104 Macular exudates in a patient with hypertension.

Figure 10-104 Macular exudates in a patient with hypertension.

Figure 10-105 Macular star in hypertensive retinopathy.

vascular congestion. The most characteristic finding is blurring of the optic disc. This occurs in association with the loss of spontaneous retinal venous pulsation, hyperemia of the disc, hemorrhages and exudates of the disc, and dilated tortuous retinal veins. In spite of these changes, vision remains remarkably normal in the early or acute stages. Figure 10-107 is a photograph and a labeled schematic of the retinal changes in chronic papilledema. Figure 10-108 shows papilledema in another patient. Notice the blurring of the disc margins and the hyperemia of the disc. Figure 10-109 shows papilledema in yet another patient;notice the flame-shaped hemorrhages and the hyperemia of the disc. There are other causes of a blurred disc margin. Table 10-10 provides a differentiation of blurred disc margins due to different conditions.

Blood dyscrasias are frequently diagnosed from the examination of the retina. Figure 10-110 shows the retina of a patient with leukemia. Notice the multiple hemorrhages, perivascular infiltrates of the retinal arterioles, and Roth's spots. These spots have a clear white center and are surrounded by hemorrhage; they are believed to be areas of emboli and retinal infarcts. They are also seen in infective endocarditis and HIV retinitis.

Occlusive disorders of the retinal circulation are dramatic. A central retinal artery occlusion (CRAO) is usually caused by an embolus from the heart or large artery. It results in sudden, painless loss of vision in one eye. The pupillary direct light reflex is lost, and spontaneous venous pulsations are absent. Within minutes, the retina becomes pale and milky white with narrowed arteries, and a cherry-red spot appears at the macula. This cherry-red spot appears because in the foveal area, the retina is thin, allowing visibility of the underlying choroidal circulation that is obscured elsewhere by retinal edema. This is a true ocular emergency because if it is not treated within 45 minutes, the retina may not be saved. Figure 10-111 shows the left retina of a patient with a CRAO. Notice the pale retina with the cherry-red spot at the macula.

Figure 10-106 Macroaneurysms in hypertensive retinopathy. Note the hemorrhage lateral to the macula.

Fundus Photos That Show Hypertension

Figure 10-108 Papilledema. Note the hyperemia of the disc.

Figure 10-109 Papilledema. Note the hyperemia of the disc and the flame-shaped hemorrhages.

Figure 10-109 Papilledema. Note the hyperemia of the disc and the flame-shaped hemorrhages.

Roth Spots With Disc Edema

Figure 10-112 shows the retina of a patient with a CRAO with cilioretinal artery sparing. The cilioretinal arteries are present in 40% of normal individuals. They are derived from the posterior ciliary circulation and usually emerge from the temporal aspect of the disc to supply a small portion of the retina. Notice the area of retina that is spared as a result of perfusion by the cilioretinal artery. Figure 10-113 shows a CRAO in another patient. In this example, the retina is also pale (ischemic and edematous), but the area of the cherry-red spot at the macula is heavily pigmented. This is the finding in dark-skinned individuals with a CRAO.

Hollenhorst plaques are cholesterol emboli found at the bifurcation of the retinal arteries. The source of these emboli is usually the heart or the carotid arteries. They are usually unilateral and occur in elderly individuals with advanced atherosclerosis. Symptoms of fleeting alterations of vision may accompany these emboli. Figure 10-114 shows a classic example of a Hollenhorst plaque. Figure 10-115 shows a branch retinal artery occlusion (BRAO). Note the area of the ischemic retina and the cotton-wool spots and adjacent flame-shaped hemorrhage. Figure 10-116 shows a BRAO in another patient that involves the superior portion of the left retina. Note the superior pallor representing the ischemic retina.

Venous occlusion is one of the most common retinal vascular disorders. A central retinal vein occlusion (CRVO) occurs at the lamina cribrosa. The patient experiences painless loss of

Table 10-10 Differentiation of Blurred Disc Margins

Feature Papilledema* Papillitis'

Drusen'

Myelinated Nerve Fibers8

Central Retinal Vein Occlusion}

Visual acuity Normal

Venous pulsations Absent Pain Headache

Decreased

Variable

Normal Present No

Normal Present No

Decreased Usually absent No

Visual acuity Normal

Venous pulsations Absent Pain Headache

Light reaction

Hemorrhage Visual fields

Present

Present

Enlarged blind spot

Decreased

Variable

Eye movement pain

Marcus Gunn (see text)

Present

Central scotoma

Normal Present No

Present

Uncommon

Enlarged blind spot

Normal Present No

Present

Scotomata correspond to areas of myelination

Decreased Usually absent No

Present

Marked Variable

Laterality

Bilateral

Unilateral

Bilateral

Seldom bilateral

Unilateral

*Edema of the optic disc resulting from increased intracranial pressure. See Figures 10-107 to 10-109.

inflammation of the optic disc.

{See Figure 10-119.

§Myelination of the optic nerve ends at the optic disc. When it continues into the retina, white, flame-shaped areas obscure the disc margins. See Figures 10-76 to 10-78. }See Figure 10-117.

Eye Retina Sun Damage Photo
Figure 10-110 Leukemia-related retinitis. Note the multiple hemorrhages, perivascular infiltrates, and Roth's spots.
Retinal Artery Occlusion Quadrant
Figure 10-111 Central retinal artery occlusion.
Cilioretinal Artery Anatomy
Figure 10-112 Central retinal artery occlusion with cilioretinal artery sparing.
Hollenhorst Plaque Images
Figure 10-114 Hollenhorst plaque.

Figure 10-113 Pigmented central retinal artery occlusion in a person of color.

vision in one eye. The fundus exhibits venous dilatation and tortuosity, disc edema, flame-shaped hemorrhages in all quadrants, blurred optic disc, cotton-wool spots, and often a large hemorrhage at the macula. The disc is usually edematous with blurred margins. The fundus in a CRVO has been described as a ''pizza thrown against a wall.'' The patients are usually from 70 to 80 years of age. The causes of CRVO are many: hypertension, glaucoma, atherosclerosis, diabetes, and hyperviscosity syndromes. Figure 10-117 shows the retina of a patient with a CRVO. Notice the dark, engorged, tortuous, dusky-colored retinal veins. A branch retinal vein occlusion (BRVO) occurs at a site of retinal arteriovenous crossing. BRVO is commonly

Fundus Photos That Show Hypertension
Figure 10-115 Branch retinal artery occlusion.
Figure 10-116 Branch retinal artery occlusion. Note the pallor of the superior left retina, resulting from occlusion of the artery supplying this area.

associated with systemic hypertension, although any systemic disease associated with hypercoagulability may predispose to BRVO. Distal to the site of occlusion, the retinal vein becomes engorged and tortuous with associated capillary dysfunction that leads to intraretinal edema and hemorrhage. Figure 10-118 shows two examples of the retinas of patients with a BRVO.

Drusen of the optic disc are acellular, calcified hyaline deposits in the substance of the optic nerve that occur secondary to axonal degeneration. The disc margins are irregular or blurred. Drusen are found to be bilateral in 70% of affected patients, and the condition is transmitted as an irregular dominant trait with incomplete penetrance. Drusen occur almost exclusively in white individuals. Figure 10-119 shows optic disc drusen. Notice the scalloped appearance of the optic nerve border. Because of the irregular disc border, optic disc drusen sometimes can be confused with papilledema. The absence of optic disc hyperemia, exudates, and venous congestion differentiates drusen from papilledema.

Optic disc drusen should not be confused with retinal drusen. Diffuse retinal drusen, as shown in Figure 10-120, are not age-related phenomena and are benign. On the other hand, hard and soft retinal drusen at the level of the RPE located near the macula are part of the disorder known as age-related macular degeneration (AMD). AMD is the most common cause of blindness in patients older than 60 years in the United States. It is usually bilateral but may be asymmetric. Retinal drusen are yellowish-white, round lesions that may vary in size and are frequently concentrated at the posterior pole. Figure 10-121 shows the retina of a patient with AMD and subfoveal choroidal neovascularization. The neovascularization appears as the gray pigmentation around the drusen at the macula. This gray area represents new blood vessels grown in from the choroid between it and the RPE. Figure 10-122 is a close-up photograph of the macular drusen in another patient. The growing vessels leak blood, lipids, and serum under

Figure 10-117 Central retinal vein occlusion.

Figure 10-118 A and B, Two examples of branch retinal vein occlusions.

Amd Fibrous Scar

Figure 10-119 Optic disc drusen.

Figure 10-120 Diffuse retinal drusen, which are not age related.

Macula

Drusen

Macula

Drusen

Figure 10-121 Age-related macular degeneration and subfoveal choroidal occularization.

the sensory retinal layer that stimulate the formation of a fibrous scar, further damaging the sensory retinal layers. Studies have implicated vascular endothelial growth factor (VEGF) in the pathogenesis of AMD. This growth factor is naturally expressed in the retina, with high levels concentrated in the RPE. In the normal eye, VEGF may play a protective role in maintaining adequate blood flow to RPE and photoreceptors. Studies have indicated that a reduction of choroidal blood flow and oxidative stress may stimulate the initial overexpression of VEGF in the RPE and retina. This stimulates proliferation and permeability, promoting angiogenesis, increased vascular permeability, and the breakdown of the blood-retinal barrier, which are hallmarks of choroidal neovascularization and AMD. Figure 10-123 shows the retina of a patient with long-standing AMD; note that the macula has been destroyed and only a scar exists.

Figure 10-122 Close-up photograph of macular drusen.

Figure 10-122 Close-up photograph of macular drusen.

Picture Scarred Optic Nerve

Optic atrophy is a reduction in size and substance of the optic nerve, caused by loss of axons and myelin sheaths. Optic atrophy may result from a lesion anywhere in the anterior visual pathway between the retina and the lateral geniculate body. The ophthalmoscopic hallmark of optic atrophy is optic disc pallor. The patient may have a loss of visual acuity, narrowed visual fields, deficit in color vision, or an afferent defect. The pallor of the disc is caused by the loss of its capillary network and by glial tissue formation. There are two basic types of optic atrophy: ''primary,'' in which disc pallor is accompanied by a clearly defined margin as a result of retrobulbar or intracranial disease;and ''secondary,'' in which disc pallor is accompanied by a blurred disc margin as a result of optic neuritis or chronic papilledema. Figure 10-124 shows the right retina of a patient with optic atrophy. Note the pallor of the temporal aspect of the disc.

Chorioretinitis is an inflammatory process that originates in the choroidal tissues and subsequently spreads to involve the retina. Most inflammatory changes in the choroid are of endogenous origin, including tuberculosis, syphilis, Q fever, HIV, herpes zoster, cytomegalovirus (CMV), measles, sarcoidosis, histoplasmosis, Aspergillus infection, Candida infection, crypto-coccosis, coccidioidomycosis, toxoplasmosis, Toxocara infection, onchocerciasis, and retinoblastoma. In acute chorioretinitis, there is cloudy vision resulting from vitreous haze, and the patient sees light flashes and multiple floating spots. Loss of vision may occur if the macula is involved. In chronic chorioretinitis, there is clumping of pigment around the lesions, which are whitish owing to the presence of scar tissue and the underlying sclera that is visible because the retina and choroid have been destroyed.

Toxoplasmosis, caused by the organism Toxoplasma gondii, is most frequently a congenital condition, transmitted to the fetus from the mother during the first trimester of pregnancy. The early lesions heal once the organisms become encysted; only retinochoroidal scarring is

Figure 10-124 Right retina with optic atrophy. Note the marked pallor of the temporal aspect of the disc.

Retinal Haemorrhage With White Lesion

seen on routine ophthalmoscopy. The condition may recur with the liberation of the encysted organisms and further retinal damage. The visual prognosis depends on the location of the lesion. Figure 10-125 shows the retina of the right eye of a patient with AIDS and acute toxoplasmosis chorioretinitis. The acute lesions are round with an overlying yellow-white haze as a result of a vitreitis;these acute lesions have been described as looking like a ''headlight in fog.'' Notice the multifocal areas of retinal involvement. This patient had similar multifocal lesions in the left eye. The multifocal areas and bilaterality are typical of acute toxoplasmosis retinitis in patients with AIDS. Figure 10-126 shows another patient with acute toxoplasmosis; notice the dense ''fog'' caused by the active vitreitis. Figure 10-127 shows a retina of another patient with a healed, inactive lesion of toxoplasmosis chorioretinitis at the macula. Figure 10128 shows another patient with diffuse retinal scars secondary to inactive toxoplasmosis.

The presumed ocular histoplasmosis syndrome (POHS) has a distinct retinal appearance characterized by small atrophic areas in the retina. Histoplasmosis is caused by a dimorphic yeast, Histoplasma capsulatum. It exists in humans in the yeast form and in the soil as the mold form. It is endemic in the soil along the Ohio and Mississippi River valleys and in Maryland, Florida, and Texas. Histoplasmosis enters the body through inhalation of the spores. Infection may be asymptomatic, or it may cause a mild flulike syndrome. Dissemination throughout the body may occur. Histoplasmosis infections in immuno-compromised patients may cause a fulminating, life-threatening systemic infection. In POHS, there is a ring of pigmented atrophic scarring surrounding the optic nerve. The macula may [

Figure 10-127 Chronic (inactive) toxoplasmosis chorioretinitis scar.

Roth Spots Causes

also be affected. POHS is so-named because the organism has never been isolated from the choroid of individuals who have been ill with histoplasmosis and have developed retinal lesions. Figure 10-129 shows the classic lesion of POHS.

CMV chorioretinitis is the most common ocular opportunistic infection in patients with AIDS. Autopsy studies have shown that more than 95% of viral chorioretinitis in patients with AIDS is a result of CMV infection. CMV chorioretinitis is progressive and often preterminal. It appears that the patient with AIDS is at greatest risk for CMV retinitis when the CD4+ T cell count is less than 40/mm3. Figure 10-130 depicts retinal necrosis and vasculitis in a patient with AIDS and CMV chorioretinitis. Figure 10-131 shows the retina of the left eye of a patient with CMV chorioretinitis. Notice the marked retinal necrosis extending from the optic nerve superiorly and temporally. Figure 10-132 shows the retina of the right eye of another patient with CMV retinitis. There is extensive necrotizing optic neuritis with retinal necrosis and retinal vasculitis. Notice the white sheathing of the retinal vessels (especially superiorly off the disc), which is typical of vasculitis. Figure 10-133 shows the left eye of another patient with active CMV retinitis;notice the retinal vessel sheathing and extensive necrotizing optic neuritis. Figure 10-134 shows the retina of a patient with burned-out CMV retinitis. Notice the sclerosed retinal arteries and the paucity of vessels. The patient was blind as a result of the CMV infection.

Figure 10-135A shows the left retina of a patient with HIV chorioretinitis. Notice the cottonwool spots and the extremely large flame-shaped hemorrhage. Figure 10-135B shows another patient with HIV chorioretinitis infection. Notice the many cotton-wool spots. Roth's spots are commonly seen in patients with HIV chorioretinitis Figure 10-110 shows examples of Roth spots in a patient with leukemia.

There are several important tumors of the ocular fundus. Retinoblastoma is the most common malignant tumor of the sensory retina. It has been estimated to occur in 1 per

Figure 10-128 Inactive toxoplasmosis chorioretinitis. Note the diffuse retinal scars.

Figure 10-128 Inactive toxoplasmosis chorioretinitis. Note the diffuse retinal scars.

Ocular Histoplasmosis ToxoplasmosisOcular Histoplasmosis Syndrome
Figure 10-129 Presumed ocular histoplasmosis syndrome.
Roth Spot Fundus

Figure 10-131 Cytomegalovirus chorioretinitis, left retina.

White Retinal Sheathing
Figure 10-133 Active cytomegalovirus retinitis. Note the retinal sheathing, retinal vasculitis, and the necrotizing optic neuritis.

18,000 live births. It can be sporadic or familial with an autosomal dominant mode of inheritance. The abnormal gene has been localized to the long arm of chromosome 13. Persons who inherit the gene are more likely to have bilateral retinoblastomas than are those without the gene. Children with retinoblastomas present with leukokoria, or a white pupil. Look at Figure 10-136. Leukokoria is present because most of the globe contains the large white endophytic or exophytic tumor. Figure 10-137 shows the right and left retinas of a child with bilateral retinoblastomas. Note the large tumor mass in the left retina.

The two most important tumors of the choroid are the choroidal nevus and the choroidal melanoma. The choroidal nevus is the most common fundus tumor. It is commonly a flat, slate-gray lesion with a slightly ill-defined border. Figure 10-138 shows a choroidal nevus. A nevus must be differentiated from a choroidal melanoma. A choroidal melanoma is the most common primary intraocular malignancy. It occurs in about 6 per 1 million people per year. It has no sex predisposition and is usually nonfamilial. It is rare in African Americans and is most common in white persons. Unlike the choroidal nevus, the choroidal melanoma has depth and is frequently dome-shaped or mushroom-shaped. Figure 10-139 shows the retina of a patient with a choroidal melanoma.

Figure 10-134 Burned-out cytomegalovirus retinitis.

White Marks Choroid
Figure 10-135 A, Human immunodeficiency virus (HIV) chorioretinitis. Note the large flame-shaped hemorrhage and the cotton-wool spots. B, Another patient with HIV chorioretinitis. Note the many cotton-wool spots.

Colobomas of the retina and choroid are congenital defects in these tissues caused by failure of the embryonic fissure to fuse properly. Colobomas appear as large white areas in which the retina or choroid is absent, and thus the white sclera is seen. Retinal vessels may cross into the lesion. Typically, colobomas are seen in the inferior aspect of the fundus because the embryonic fissure is inferonasal in the developing eye. Figure 10-140 shows the classic features of a coloboma. See also Figure 10-62, which shows an iris coloboma.

Leukokoria
Figure 10-136 Leukokoria.

Figure 10-137 Retinoblastoma. A, Right retina. B, Left retina.

Figure 10-141 shows a giant retinal tear. A large area of bare choroid is visible through the break.

Retinitis pigmentosa is a very rare, genetically determined degenerative disease of the retina with an onset from the ages of 6 and 12 years. It is more common in boys than in girls and is almost always bilateral. Night blindness is the first symptom, followed by a gradually

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  • Esther Gallagher
    What can a retinal hemoragembe thr result ofRoth Spot?
    7 days ago

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