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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2853_Библиотеки_им_академика_М_И_Перельмана
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FIG. 7-39 Retinal Abnormalities I. A. Normal left retina: Th e background of t he retina is re d-orange; it c ontains a
variable amount of black pigments, depending on race and complexion. Diverging blood vessels emerge from the optic disk to
spread o ver the retin a, usually in pai rs of an arter y and a vein. The ve ins are solid an d dark red, and th ey may pulsat e normally.
The arteries are brighter red, contain central white stripes, and are pulseless. The width of an artery is usually approximately
four-fifths that of the adjacent vein. The optic disk is lighter red, with sharp borders, often outlined by a strip of black pigment
in the adjacent ret ina. The physiologic cup is white or pale yellow. The macula lies in the horizontal plane of the disk and from
2–3 disk diameters to the temporal side. The macular area is pale red with a central white or shining dot. B. Myelinated
nerve fibers: White brushes of myelinated nerves emerge from the disk, obscuring segments of vessels and disk margins.
C. Optic atrophy: The disk is chalk white with sharply defined borders. The blood vessels are normal. D. Papillitis: The
disk is hyperemic, and its borders are blurred.
frayed and the underlying vessels are partially or completely obscured. It is a
normal variation of no clinical signicance. Patches of myelinated nerves may
occur remote from the disc.
Disk pallor—optic atrophy. Optic nerve damage (compression, ischemia,
inammation, or increased intracranial pressure) leads to nerve ber atrophy and loss of normal vascularity (Figs. 7-39C and 7-40). The disk is pale
pink, yellow, or white; the margins may be less distinct and the physiologic cup and lamina cribrosa are variably seen. The emerging vessels may
be surrounded by perivascular glial sheathing, seen as white lines. DDX:
Pigmented high-water marks or residual exudate around the nerve suggest
previous disc edema and increased intracranial pressure producing the optic
atrophy. It is important to recognize that an atrophic nerve can no longer swell, so
it cannot be used to monitor increased intracranial pressure. Brain tumor is a common cause of incidentally found optic atrophy, thus all optic atrophy should be
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FIG. 7-40 Optic Atrophy. This left optic nerve demonstrates pallor of the rim, making the distinction of the cup difficult.
There is a small area of pink rim superonasally, but the remainder of the rim is atrophic. (Image used with permission from
Andrew Lee, MD.)
evaluated promptly by an ophthalmologist. In optic atrophy from chorioretinitis,
the disk may have a yellow cast, and the surrounding retina may contain
hemorrhages, areas of atrophy, and pigment. The distinction between optic
atrophy resulting from intrinsic optic nerve lesions versus increased intracranial pressure cannot be made reliably from the physical ndings. Disc pallor
does not occur in glaucoma until very late in its course.
CLINICAL OCCURRENCE: Intrinsic Optic Nerve Lesions: Multiple sclerosis,
syphilis; optic nerve compression without increased intracranial pressure.
Increased Intracranial Pressure: Idiopathic intracranial hypertension, brain
tumors.
Disk edema—papillitis, optic neuritis.
nerve within the globe, produces papillitis with loss of vision (Fig. 7-39D) and
disk edema indistinguishable from papilledema.
optic neuritis than with papilledema. The disk is hyperemic, and its margins
may be indistinct from edema in the peripapillary nerve ber layer. The disk
surface may be elevated above the surrounding retina (a + 1 or + 2 lens correction is required to focus on the disk).
CLINICAL OCCURRENCE: Ocular inammation (e.g., uveitis, retinitis, sym-
pathetic ophthalmia), intrinsic optic nerve inammation (e.g., demyelinating
optic neuritis in multiple sclerosis, neuromyelitis optica—Devic syndrome),
intracranial inammation (e.g., meningitis, venous sinus thrombosis), infections (e.g., syphilis, tuberculosis, inuenza, measles, malaria, mumps), and
intoxications (e.g., methyl alcohol).
Anterior ischemic optic neuropathy (AION). Infarction of the optic nerve
head results from inadequate perfusion of the posterior ciliary arteries. AION
occurs in two forms, the arteritic, related to giant cell arteritis, and the nonarteritic in patients with vasculopathies, e.g., hypertension or diabetes mellitus
and intercurrent hypotension. Onset is usually sudden and painless, with
profound visual loss, typically altitudinal, involving the upper and lower
Optic neuritis involving the optic
Visual loss occurs earlier in
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elds. The optic nerve is edematous with scant hemorrhage and more pallor
than typical for papilledema.
DDX: In patients aged >55 years, it is impera-
tive to search for giant cell arteritis. The nonarteritic form commonly follows
a period of systemic hypotension and is accompanied by a small to absent
optic cup in the uninvolved eye.
Papilledema.
Increased cerebrospinal uid (CSF) pressure within the optic
nerve sheath compresses the nerve resulting in axoplasmic ow stasis and
ischemia (Fig. 7-41A).
Early papilledema causes a C-shaped halo of nerve
ber layer edema that surrounds the disc with a gap temporally (Fig. 7-42).
With more advanced papilledema, the halo becomes circumferential. Next
there is obscuration of major vessels leaving the disc, and later there is obscuration of vessels on the optic disc. The emerging vessels bend sharply in
FIG. 7-41 Retinal Abnormalities II. A. Papilledema (choked disk): The disk surface is elevated, the nasal
borders blurred. The vessels curve downward over the borders. The veins are distended and pulseless. Both arteries and veins
in the di sk may be obscur ed by the swolle n structu re. B. Star figure of the macula: Edema t hrows the reti na into trac tion
folds that radiate from the macula as white lines.
FIG. 7-42 Disc Edema, Early. This left optic nerve head (disc) is hyperemic and the nerve fiber layer shows some
edema, obscuring the details of the disc margin. There is a hemorrhage inferiorly on the disc head, dilation of some smaller
disc vessels, and obscuration of some of the vessels as they cross within the edematous nerve fiber layer. (Image used with
permission from Andrew Lee, MD.)
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FIG. 7- 43 Disc Edema, Late. This r ight eye shows ma rked disc edem a with hypere mia, nerve fibe r layer edema o bscuring
the disc margins and disc vessels, and small flame hemorrhages. The disc is elevated, evidenced by the different focal plane
of the disc head and t he retina. The retinal veins are engorged and tortuous, and there is dilation of the smaller vessels on the
disc head. (Image used with permission from Andrew Lee, MD.)
passing over the elevated disk edge (Fig. 7-43). Macular retinal edema creates
traction folds (choroidal folds), seen as white lines radiating from the macula
(Fig. 7-41B). Patients with papilledema have an enlarged physiologic blind
spot documented by formal visual eld testing. The principal causes are brain
tumor and idiopathic intracranial hypertension. Less common causes are
hydrocephalus, malignant hypertension, subarachnoid hemorrhage, meningitis, and salicylate poisoning.
DDX: In contrast to papillitis, central vision is
unimpaired, but, like glaucoma, there is usually peripheral visual loss.
Pseudopapilledema—drusen bodies. These granular deposits in the optic
disk cause pseudopapilledema. Distinguishing early papilledema and from
drusen bodies is best done by an ophthalmologist.
Venous engorgement. Distented retinal veins suggest retinal vein occlusion, polycythemia vera, cyanotic congenital heart disease, leukemia, and
macroglobulinemia.
Retinal hemorrhage. Hemorrhage occurs in all layers of the retina. The
hemorrhage’s shape reects its depth. A large, deep hemorrhage in the choriocapillaris produces a dark, elevated area looking like a melanotic tumor
(Fig. 7-44A); suspect a subretinal vascular membrane seen in macular degeneration. Smaller, more supercial hemorrhage appears as a round red spot,
with blurred margins, called a blot hemorrhage (Fig. 7-44B). Microaneurysms are
also round red spots, but with sharp borders. Unlike hemorrhages, they are
not reabsorbed and may occur in clusters about vascular sprigs (Fig. 7-44C).
Striated red ame-shaped hemorrhages are in the nerve ber layer (Figs. 7-44D
and 7-45). In a subhyaloid or preretinal hemorrhage, blood pooling between the
retina and hyaloid membrane is seen as a turned-up half-moon; the straight
upper border is a uid level (Fig. 7-44E). A small hemorrhagic spot with
a central white area is a Roth spot, (Fig. 7-44F), classically seen in subacute
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FIG. 7-44 Hemorrhages and Similar Lesions in the Retina.
FIG. 7-45 Hypertensive Retinopathy: Flame Hemorrhages. The left eye of this poorly controlled, hypertensive
African American patient has a darkly pigmented choroid, a normal variant, which darkens the entire photograph. There are
multiple flame hemorrhages within the plane of the nerve fiber layer. There are several cotton wool spots (nerve fiber layer
infarctions). The nerve pallor is an artifact, but the enlarged cup-disc ratio of 0.6–0.7 suggests glaucoma.
bacterial endocarditis and leukemia. Many conditions produce retinal hemorrhages, examples are hypertension, diabetes mellitus, papilledema, retinal
vein occlusion, SBE, HIV, SLE, Takayasu arteritis, macroglobulinemia, thiamine deciency, leukemia, polycythemia, sickle cell disease, and sarcoidosis.
Diabetic retinopathy. Diabetic retinopathy leads to blindness by damaging
the macula. Microaneurysms occurring around the macula need to be distinguished from blot hemorrhages. With advanced diabetic retinopathy there
are white or yellow waxy exudates having distinct, often serrated, borders
(Fig. 7-46). The exudates gradually coalesce forming a broken circle around
the macula. Neovascularization of the disk or elsewhere in the retina is an indication for laser phototherapy (Figs. 7-47 and 7-48). Signs of atherosclerosis and
hypertension are sometimes superimposed. DDX: Although microaneurysms
around the macula are characteristic of diabetes, retinal microvasculopathy
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FIG. 7-46 Diabetic Retinopathy: Non-Proliferative Retinopathy. This right eye shows diffuse, scattered dot
and blot hemorrhages and microaneurysms. There is a small flame hemorrhage in the inferior macula. There is evidence of
old superior macular focal photocoagulation for diabetic macular edema, as well as peripheral panretinal photocoagulation
(PRP) for proliferative diabetic retinopathy (small, dull grey spots). There is recurrent neovascularization of the disc superotemporally. The central macula is dull and the landmarks indistinct suggesting persistent macular edema. The arterial caliber
is narrow and the reflex increased, and there are several areas of arteriovenous nicking along the superior temporal arcade
suggesting coexisting hypertension.
FIG. 7-47 Diabetic Retinopathy: Neovascularization of the Disc (NVD). This left eye shows a superior area
of NVD, as well as scattered and inferior macular exudate around background microaneurysms and dot-blot hemorrhages. The
disc pallor is an artifact due to manipulating this photo to better demonstrate the diabetic findings.
with cotton–wool spots, intraretinal hemorrhages, and microaneurysms also
occur in radiation retinopathy and HIV-AIDS.
Retinal artery occlusion. Sudden loss of vision occurs when the central reti-
nal artery is occluded, usually from thrombosis or embolism. Initially, the
retina is pale from ischemic edema, the arteries are narrowed, the smaller
arteries being invisible (Figs. 7-49A and 7-50). The veins are full but pulseless.
The absence of circulation is demonstrated by failure to induce pulsation in
arties or veins with pressure on the eyeball. Retinal edema and pallor are less
dense over the fovea because it lacks a nerve ber layer. The fovea becomes
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FIG. 7- 48 Diabetic Retinopathy: Proliferative Neovascularization. Th is left eye show s multifoca l areas of proli fer-
ative fibrovascular diabetic neovascularization elsewhere (NVE), with traction between the superior and inferior vascular arcades.
There are multiple omega loops in the veins, with venous beading and irregularity. There are several vessels on the disc head
suspicious for neovascularization of the disc (NVD), and evidence peripherally of old incomplete pan retinal photocoagulation.
There are multiple areas of dot blot hemorrhages and microaneurysms.
FIG. 7-49 Retinal Vascular Occlusions. A. Retinal artery occlusion: The retinal background is white, and the
arteries are much narrowed. The veins are pulseless. B. Retinal vein occlusion: The affected veins are engorged and
tortuous. Hemorrhages occur near the veins.
a cherry red spot due to visualizing choroidal blood ow within the macular
edema. It disappears as the edema resolves over weeks. Branch artery occlusion causes ndings limited to its distribution area. Common causes of retinal
artery occlusion are vascular disease, cardiac valve disease or vegetations,
rheumatic fever, and vasculitis, most commonly temporal arteritis. Rarely, it
complicates SLE, sickle cell disease, cryoglobulinemia, syphilis, or thromboangiitis obliterans.
Retinal vein occlusion. Central retinal vein thrombosis produces engorge-
ment and tortuosity of all retinal veins (Fig. 7-49B). Nerve ber layer and
blot hemorrhages appear throughout the retina. Macular and disk edema
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FIG. 7-50 Central Retinal Artery Occlusion (CRAO). This right eye shows a CRAO from cholesterol emboli, frag-
ments of which are lodged in the superior and inferior temporal arteries (Hollenhorst plaques). There is diffuse macular edema,
a central cherry red spot, and thready residual arterial flow.
TABLE 7-2 Grades of Retinal Arteriolar Sclerosis
Grade 1 Thickening of vessels with slight depression of veins at
Grade 2 Definitive AV crossing changes and moderate local sclerosis
Grade 3 Venule beneath the arteriole is invisible; severe local
Grade 4 To the preceding signs are added venous obstruction and
Kirkendall WM, Armstrong ML. Vascular changes in the eye of the treated and
untreated patient with hypertension. Am J Cardiol. 1962;9:663.
arteriolar–venular (AV) crossings
sclerosis and segmentation
arteriolar obliteration
are commonly present. Findings of branch vein occlusion are limited to its
drainage area. Vein occlusion is associated with hypertension, the stiffened
arterioles compressing the more compliant retinal veins as they cross in their
common sheath. Hypercoagulable states also cause venous occlusion from
sluggish blood ow as in polycythemia, multiple myeloma, macroglobulinemia, and leukemia. In sickle cell disease, neovascularization accompanies
multiple retinal vein thromboses.
Arteriolar sclerosis. Table 7-2 presents the Kirkendall and Armstrong modication of the Scheie classication for scoring retinal artery sclerosis. The
retinal changes do not necessarily parallel atherosclerotic disease elsewhere
in the body.
Artery stripe. Normal retinal arteries have a bright central stripe caused by
light reecting off the curved vessel. Increased wall thickness produces a
wider and brighter stripe. In moderate disease, the walls look like burnished
copper (copper wire reex); in advanced disease, the entire width of the artery
reects as a white stripe (silver wire reex).
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Vessel sheaths. Normal vessel walls are invisible. Lipid inltration thickens
the walls producing a milky white streak on either side of the blood column
called pipestem sheathing.
Arteriovenous crossings. As the arterial and arteriolar walls become less compliant, arteriovenous crossing signs are produced (Fig. 7-51A). Arteriovenous
nicking (Fig. 7-51B) occurs when the thickened arterial sheath obscures a short
segment of the more compliant vein, seen as a notch on either side of the
artery at their crossing. The vein deviates when the stiffened artery causes
it to make a 90-degree crossing angle (Fig. 7-51C); the normal angle is acute.
Elevation of a vein by a thickened artery is called humping (Fig. 7-51D). When
the artery compresses the vein, tapering is seen (Fig. 7-51E). Partial obstruction of venous ow dilates the vein upstream from the artery. This is banking
(Fig. 7-51F), and may lead to retinal vein occlusion.
Hypertensive retinopathy. Arterial hypertension produces distinctive retinal
signs that often coexist with the signs of arteriolar sclerosis (Figs. 7-45 and
7-52). For example, the retina may be classied as “grade 3 arteriolosclerosis, grade 4 hypertension.” The signs attributed to hypertension may also be
graded by using the Kirkendall and Armstrong classication (Table 7-3). Most
ophthalmologists describe the retinal and vascular nding without the use of
these scales.
Retina spots. Many diseases and processes leave scars, deposits, pigmentation, etc., in the retina. Active retinal disease and systemic diseases with
retinal manifestations cause unifocal or multifocal spots against the normal
retina. Carefully examining the retina in patients with confusing systemic disease presentations may assist diagnosis. A challenge is to distinguish active
disease from residuae of past events.
Cholesterol emboli.
carotid artery shed cholesterol crystals that lodge at the retinal artery bifurcations.
FIG. 7-51 Retinal Signs of Arteriolar Sclerosis.
Ulcerated atherosclerotic plaques in the ascending aorta or
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FIG. 7-52 Hypertensive Retinopathy: Cotton Wool Spots and Arteriolar Changes. The superior aspect
of this right eye and has multiple cotton wool spots (nerve fiber layer infarctions). There is increased arteriolar light reflex,
arteriolar narrowing, and arteriovenous crossing changes consistent with hypertensive retinopathy.
TABLE 7-3 Grades of Retinal Hypertension
Signs
Grade 1 Narrowing in terminal branches of vessels
Grade 2 General narrowing of vessels with severe local constriction
Grade 3 To the preceding signs are added striate hemorrhages and
Grade 4 Papilledema is added to the preceding signs
soft exudates
Patients may be asymptomatic or present with transient monocular visual
loss, amaurosis fugax, or transient ischemic neurologic attacks (TIA) in the carotid distribution. Finding cholesterol emboli proves plaque rupture with embolization. It is difcult, if not impossible, to differentiate cholesterol emboli
from calcic emboli from diseased heart valves.
Cotton-wool patches.
Infarcts produce thickening and swelling of the terminal retinal nerve bers. Gray to white areas with ill-dened uffy borders in
the posterior pole of the retina (Fig. 7-52) are often accompanied by microaneurysms which can rupture producing small striate ame hemorrhages.
Cotton-wool patches are found with hypertension, diabetes, SLE, HIV, central
retinal vein occlusion, and papilledema.
Hard exudates. Lipids deposited by leaking capillaries are left behind after
the retinal pigment epithelium resorbs the associated serous uid. These are
small white spots with sharply dened edges. They are deeper than the retinal vessels and cotton wool patches.
Pigmented spots. Old inammation or scarring produces a pigmented region
in the retina.
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