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Emergency Medicine Atlas > Part 1. Regional Anatomy > Chapter 3. Funduscopic Findings >

Normal Fundus (Disk, Macular Reflex, Background)

Associated Clinical Features

Disk

The disk is pale pink, approximately 1.5 mm in diameter, with sharp, flat margins (Fig. 3.1). The physiologic cup is located within the disk and usually measures less than six-tenths the disk diameter. The cups should be approximately equal in both eyes.

Figure 3.1

Normal Fundus The disk has sharp margins and is normal in color, with a small central cup. Arterioles and venules have normal color, sheen, and course. Background is in normal color. The macula is enclosed by arching temporal vessels. The fovea is located by a central pit. (Courtesy of Beverly C. Forcier, MD.)

Vessels

The central retinal artery and central retinal vein travel within the optic nerve, branching near the surface into the inferior and superior branches of arterioles and venules, respectively. Normally the walls of the vessels are not visible; the column of blood within the walls is visualized. The venules are seen as branching, dark red lines. The arterioles are seen as bright red branching lines, approximately two-thirds or three-fourths the diameter of the venules.

Macula

This is an area of the retina located temporal to the disk; it is void of capillaries. The fovea is an area of depression approximately 1.5 mm in diameter (similar to the optic disk) in the center of the macula. The foveola is a tiny pit located in the center of the fovea. These areas correspond to central vision.

Background

The background fundus is red; there is some variation in the color, depending on the amount of individual pigmentation and the visibility of the choroidal vessels beneath the retina.

Clinical Pearls

1. Fundal examination should be an integral part of any eye examination.

2. The cup/disk ratio is slightly larger in the African-American population.

3. The normal fundus should be void of any hemorrhages, exudates, or tortuous vasculature.

Age-Related Macular Degeneration

Associated Clinical Features

Age-related macular degeneration, the leading cause of blindness in the elderly, increases in incidence with each decade over 50. Degeneration of the macula may be evidenced by accumulation of either drusen (small, discrete, round, punctate nodules), or soft drusen (larger, pale yellow or gray, without discrete margins that may be confluent) (Fig. 3.2A and B). Most patients with drusen have good vision, although there may be decreased visual acuity and distortion of vision. There may be associated pigmentary changes and atrophy of the retina. Vision may slowly deteriorate if atrophy occurs.

Patients with early or late degenerative changes of the macula are at risk of developing subretinal neovascularization (SRNV), which is associated with distortion of vision, blind spots, and decreased visual acuity. Macular appearance may show dirty gray lesions, hemorrhage, retinal elevation, and exudation (Fig. 3.3).

Figure 3.2A

Age-Related Macular Degeneration, Drusen Typcial macular drusen and retinal pigment epithelial (RPE) atrophy (scalloped pigment loss) in age-related macular degeneration. (Courtesy of Richard E. Wyszynski, MD.)

Figure 3.2B

Age-Related Macular Degeneration, Drusen Drusen are clustered in the center of the macula. (Courtesy of Richard E. Wyszynski, MD.)

Figure 3.3

Age-Related Macular Degeneration Hemorrhage seen beneath the retina in association with subretinal neovascularization. (Courtesy of Richard E. Wyszynski, MD.)

Differential Diagnosis

Hereditary macular degenerations, other acquired macular disorders including toxicities, and retinal exudation may present similarly.

Hemorrhages and exudates can present from vascular disease, ocular disorders such as inflammations or infections, tumors, trauma, and hereditary disorders.

Emergency Department Treatment and Disposition

Patients with drusen need ophthalmologic evaluation every 6 to 12 months or sooner if visual distortion or decreasing visual acuity develops. If a patient complains of deterioration of visual acuity or image distortion, prompt ophthalmic evaluation is warranted, probably including fluorescein angiography. If SRNV is present, laser treatment may be indicated.

Clinical Pearls

1. Age-related macular degeneration is the leading cause of blindness in the United States in patients above 65 years of age.

2. Patient may have normal peripheral vision.

3. Untreated SRNV can lead to visual loss within a few days.

4. Patients frequently complain of distortion with SRNV.

Exudate

Associated Clinical Features

Hard exudates (Figure 3.4A) are refractile, yellowish deposits with sharp margins composed of fat-laden macrophages and serum lipids. Occasionally the lipid deposits form a partial or complete ring (called a circinate ring) around the leaking area of pathology. If the lipid leakage is located near the fovea, a spoke, or star-type distribution of the hard exudates is seen.

Cotton wool spots, or soft "exudates," are actually microinfarctions of the retinal nerve-fiber layer, and appear white with soft or fuzzy edges (Fig. 3.4B).

Inflammatory exudates are secondary to retinal or chorioretinal inflammation.

Figure 3.4A

Hard Exudates Linear collection of yellow lipid deposits with sharp margins in macula. (Courtesy of Beverly C. Forcier, MD.)

Figure 3.4B

Cotton Wool Spots White lesions with fuzzy margins, seen here approximately one-fifth to one-fourth disk diameter in size. Orientation of cotton wool spots generally follows the curvilinear arrangement of the nerve fiber layer. Intraretinal hemorrhages and intraretinal vascular abnormalities are also present. (Courtesy of Richard E. Wyszynski, MD.)

Differential Diagnosis

Hard exudation and cotton wool spots are associated with vascular diseases such as diabetes mellitus, hypertension, and collagen vascular diseases but can be seen with papilledema and other ocular conditions. Inflammatory exudates are seen in patients with such diseases as sarcoidosis and toxoplasmosis.

Emergency Department Treatment and Disposition

Routine referral for ophthalmologic and medical workup is appropriate.

Clinical Pearl

1. Hard exudates that are intraretinal may easily be confused with drusen occurring near Bruch's membrane, which separates the retina from the choroid.

Roth's Spot

Associated Clinical Features

Roth's spots are retinal hemorrhages with a white or yellow center (Fig. 3.5). They are seen in patients with a host of diseases such as anemia, leukemia, multiple myeloma, diabetes mellitus, collagen vascular disease, other vascular disease, intracranial hemorrhage in infants, septic retinitis, and lung carcinoma.

Figure 3.5

Roth's Spot Retinal hemorrhage with pale center. (Courtesy of William E. Cappaert, MD.)

Differential Diagnosis

Flamed-shaped or splinter hemorrhages or dot-blot hemorrhages may resemble Roth's spots.

Emergency Department Treatment and Disposition

Routine referral for general medical evaluation is appropriate.

Clinical Pearls

1. Roth's spots are not pathognomonic for any particular disease process and can represent a variety of clinical conditions.

2. These lesions represent red blood cells surrounding inflammatory cells.

Emboli

Associated Clinical Features

Plaques, if present, are often found at arteriolar bifurcations (Fig. 3.6). Patients may have signs and symptoms of vascular disease including a "source" of emboli such as carotid bruits or stenosis, aortic stenosis, aneurysms, or atrial fibrillation. Amaurosis fugax, a transient loss of vision often described as a curtain of darkness obscuring vision with sight restoration within a few minutes, may be present in the history.

Figure 3.6

Emboli Refractile cholesterol plaques usually lodge at vessel bifurcations. (Courtesy of William E. Cappaert, MD.)

Differential Diagnosis

Cholesterol emboli (Hollenhorst plaques), associated with generalized atherosclerosis often from carotid atheroma, are bright, highly refractile plaques; platelet emboli (carotid artery or cardiac thrombus) are white and very difficult to visualize; and calcific emboli (cardiac valvular disease) are irregular and white or dull gray and much less refractile.

Emergency Department Treatment and Disposition

Referral for routine general medical evaluation is appropriate unless the patient presents with signs or symptoms consistent with showering of emboli, transient ischemic attack, or cerebrovascular accident, in which case referral for admission is indicated.

Clinical Pearls

1. Retinal emboli may produce a loss of vision, either transient or permanent in nature.

2. Arteriolar occlusion may occur either in a central or peripheral branch location.

Central Retinal Artery Occlusion (CRAO)

Associated Clinical Features

The typical patient experiences a sudden, painless monocular loss of vision, either segmental or complete. Visual acuity may range from finger counting or light perception to complete blindness. Fundal findings include: fundal paleness due to retinal edema; the fovea does not have the edema and thus appears as a cherry-red spot; the retinal arterioles are narrow and irregular; and the retinal venules have a "boxcar" appearance (Fig. 3.7).

Figure 3.7

Central Retinal Artery Occlusion The retinal pallor due to retinal edema is well demonstrated, contrasting with the "cherry red spot" of the nonedematous fovea. Note the vascular narrowing and the "boxcar" appearance of the venules. (Courtesy of Richard E. Wyszynski, MD.)

Differential Diagnosis

Arteriosclerosis, arterial hypertension, carotid artery disease, diabetes mellitus, and valvular heart disease are the most common systemic disorders associated with central retinal artery occlusion (CRAO). Other associated disorders include vascular disorders, trauma, and coagulopathies. Temporal arteritis may present with similar visual complaints.

Emergency Department Treatment and Disposition

Attempts to restore retinal blood flow may be beneficial if performed in a very narrow time window after the acute event. This may be accomplished by (1) decreasing intraocular pressure with topical beta-blocker eye drops or intravenous acetazolamide; (2) ocular massage, applied with cyclic pressure on the globe for 10 s, followed by release and then repeated. Urgent consultation with an ophthalmologist if the CRAO is less than a few hours old is indicated to determine if more aggressive acute therapy (paracentesis) is warranted. However, such aggressive treatment rarely alters the poor prognosis. Medical evaluation and treatment of associated findings may be warranted.

Clinical Pearls

1. History should focus on how long ago the episode occurred. If the loss of vision occurred recently, then the patient should be triaged and examined quickly so as to consult an ophthalmologist within the treatment window.

2. Sudden, painless monocular vision loss is typical.

3. CRAO may be associated with temporal arteritis. This diagnosis should be strongly considered in all patients presenting with signs and symptoms of CRAO who are older than 55 years.

Central Retinal Vein Occlusion (CRVO)

Associated Clinical Features

Patients are usually older individuals and complain of sudden, painless visual loss in one eye. The vision loss is usually not as severe as CRAO and may vary from normal to hand motion. Funduscopy in a classic, ischemic central retinal vein occlusion (CRVO) shows a "blood and thunder" fundus: hemorrhages (including flame, dot or blot, preretinal, and vitreous) and dilation and tortuosity of the venous system. The arterial system often shows narrowing. The disk margin may be blurred. Cotton wool spots and edema may be seen (Fig. 3.8).

Figure 3.8

Central Retinal Vein Occlusion The amount of hemorrhage is the most striking feature in this photograph. Also note the blurred disk margin, the dilation and tortuosity of the venules, and the cotton wool spots. Retinal edema is suggested by blurring of the retinal details. (Courtesy of Department of Ophthalmology, Naval Medical Center, Portsmouth, VA.)

Differential Diagnosis

Retinal detachment, papilledema, and central retinal artery occlusion can have a similar appearance.

Emergency Department Treatment and Disposition

Treatment is rarely effective in preventing or reversing the damage done by the occlusion and is directed toward systemic evaluation to identify and treat contributing factors, hopefully decreasing the chance of contralateral CRVO. Ophthalmologic evaluation is necessary to confirm the diagnosis, estimate the amount of ischemia, and follow the patient so as to minimize sequelae of possible complications such as neovascularization and neovascular glaucoma.

Clinical Pearls

1. Sudden, painless visual loss in one eye should be evaluated promptly to determine its etiology.

2. Look for the classic "blood and thunder" funduscopic findings.

3. Consider the differential diagnosis of acute painful (glaucoma, retrobulbar neuritis) versus painless vision loss (CRAO, anterior ischemic optic neuropathy, retinal detachment, subretinal neovascularization, and vitreous hemorrhage).

Hypertensive Retinopathy

Associated Clinical Features

Fundus changes that may be seen with hypertension include generalized and focal narrowing of arterioles, generalized arteriolar sclerosis (resembling copper or silver wiring), arteriovenous crossing changes, hemorrhages (usually flame-shaped), retinal edema and exudation, cotton wool spots, microaneurysms, and disk edema (Fig. 3.9).

Figure 3.9

Hypertension Chronic, severe systemic hypertensive changes are demonstrated by hard exudates, increased vessel light reflexes, and sausage-shaped veins. (Courtesy of Richard E. Wyszynski, MD.)

Differential Diagnosis

Diabetic retinopathy, many hemopoietic and vascular diseases, traumas, localized ocular pathology, and papilledema should all be considered.

Emergency Department Treatment and Disposition

Medical treatment of hypertension.

Clinical Pearls

1. Hypertensive arteriolar findings may be reversible if organic changes have not occurred in the vessel walls.

2. Always consider hypertensive retinopathy in the differential diagnosis of papilledema.

Diabetic Retinopathy

Associated Clinical Features

The early ocular manifestations of diabetes mellitus are referred to as background diabetic retinopathy (BDR). Fundus findings include flame or splinter hemorrhages (located in the superficial nerve fiber layer) or dot and blot hemorrhages (located deeper in the retina), hard exudates, retinal edema, and microaneurysms (Fig. 3.10A and B). If these signs are located in the macula, the patient's visual acuity may be decreased or at risk of becoming compromised, requiring laser treatment. Preproliferative diabetic retinopathy can show BDR changes plus cotton wool spots, intraretinal microvascular abnormalities, and venous beading. Proliferative diabetic retinopathy is demonstrated by neovascularization at the disk (NVD) or elsewhere (NVE) (Fig. 3.10C). These require laser therapy owing to risk of severe visual loss from sequelae: vitreous hemorrhage, tractional retinal detachment, severe glaucoma.

Figure 3.10A

Background Diabetic Retinopathy Hard exudates, dot hemorrhages, blot hemorrhages, flame hemorrhages, and microaneurysms are present. Because these changes are located within the macula, this is classified as diabetic maculopathy. (Courtesy of Richard E. Wyszynski, MD.)

Figure 3.10B

Background Diabetic Retinopathy An example of diabetic maculopathy with a typical circinate lipid ring. (Courtesy of Richard E. Wyszynski, MD.)

Figure 3.10C

Proliferative Diabetic Retinopathy In addition to the signs seen in background and preproliferative diabetic retinopathy, neovascularization is seen here coming off the disk. (Courtesy of Richard E. Wyszynski, MD.)

Differential Diagnosis

Many vascular and hemopoietic diseases—such as collagen vascular disease, sickle cell trait, hypertension, hypotension, anemia, leukemia, inflammatory and infectious states—and ocular conditions can be associated with some of or all the above signs.

Emergency Department Treatment and Disposition

Routine ophthalmologic referral for laser or surgical treatment is indicated.

Clinical Pearls

1. Periodic ophthalmologic evaluations are recommended.

2. Microaneurysms typically appear 10 years after the initial onset of diabetes, although they may appear earlier in patients with juvenile diabetes.

3. Control of blood sugar alone does not prevent the development of vasculopathy.

4. Blurred vision can also occur from acute increases in serum glucose, causing lens swelling and a refractive shift even in the absence of retinopathy.

Vitreous Hemorrhage

Associated Clinical Features

Patients may complain of sudden loss or deterioration of vision in the affected eye, although bilateral hemorrhage can occur. The red reflex is diminished or absent, and the retina is obscured because of the bleeding. Large sheets or three-dimensional collections of red to red-black blood may be detected (Fig. 3.11A and B).

Figure 3.11A

Vitreous Hemorrhage Large amount of vitreous hemorrhages associated with metallic intraocular foreign body. The large quantity of blood obscures visualization of retinal details. (Courtesy of Richard E. Wyszynski, MD.)

Figure 3.11B

Vitreous Hemorrhage A smaller amount of vitreous hemorrhage is more easily photographed. Gravitational effect on the vitreous blood creates the appearance of a flat meniscus (keel-shaped blood) in this patient with vitreous hemorrhage associated with proliferative diabetic retinopathy. (Courtesy of Richard E. Wyszynski, MD.)

Differential Diagnosis

Multiple underlying etiologies include proliferative diabetic retinopathy, retinal or vitreous detachments, hematologic diseases, trauma (ocular or shaken impact syndrome), subarachnoid hemorrhage, collagen vascular disease, infections, macular degeneration, and tumors.

Emergency Department Treatment and Disposition

Refer to an ophthalmologist and an appropriate physician for associated conditions. Ophthalmic observation, photocoagulation, and surgery are all therapeutic options. Bed rest may help to increase visualization of the fundus.

Clinical Pearl

1. The patient's vision may improve somewhat after a period of sitting or standing as the blood layers out.

Retinal Detachment

Associated Clinical Features

Patients often complain of monocular decreased visual function and may describe a shadow or curtain descending over the eye. Other complaints include cloudy or smoky vision, floaters, or flashes of light. Central visual acuity is diminished with macular involvement. Fundal examination may reveal a billowing or tentlike elevation of retina compared with adjacent areas. The elevated retina often appears gray. Retinal holes and tears may be seen, but often the holes, tears, and retinal detachment cannot be seen without indirect ophthalmoscopy (Fig. 3.12).

Figure 3.12

Retinal Detachment A red, flat, well-focused macula is contrasted with the pale, undulating, out-of-focus, elevated retina surrounding the macula. (Courtesy of Richard E. Wyszynski, MD.)

Differential Diagnosis

Retinal detachments due to retinal tears or holes can be associated with trauma, previous ocular surgery, nearsightedness, family history of retinal detachment, and Marfan's disease. Retinal detachments due to traction on the retina by an intraocular process can be due to systemic influences in the eye, such as diabetes mellitus or sickle cell trait. Occasionally retinal detachments are due to tumors or exudative processes that elevate the retina. Symptoms of "light flashes" may occur with vitreous changes in the absence of retinal pathology. Patients may note flashes of light occurring only in a darkened environment because of the mechanical stimulation of the retina from the extraocular muscles, usually in a nearsighted individual.

Emergency Department Treatment and Disposition

Urgent ophthalmologic evaluation and treatment are warranted.

Clinical Pearls

1. Often patients have had sensation of flashes of light that occur in a certain area of a visual field in one eye, corresponding to the pathologic pulling on the corresponding retina.

2. Visual loss may be gradual or sudden.

Cytomegalovirus (CMV) Retinitis

Associated Clinical Features

Patients may complain of the gradual onset of the following visual sensations: floaters, scintillating scotomas (quivering blind spots), decreased peripheral visual field, and metamorphopsia (wavy distortion of vision). Cytomegalovirus (CMV) infiltrates appear as focal, small white lesions in the retina that look like cotton wool spots. CMV is a necrotizing virus that is spread hematogenously, so that damage is concentrated in the retina adjacent to the major vessels and the optic disk. Often hemorrhage is involved with significant retinal necrosis (dirty white with a granular appearance), giving the "pizza pie" or "cheese and ketchup" appearance (Fig. 3.13). Optic nerve involvement and retinal detachments can be present.

Figure 3.13

CMV Retinitis "Pizza pie" or "cheese and ketchup" appearance is demonstrated by hemorrhages and the dirty, white, granular-appearing retinal necrosis adjacent to major vessels. (Courtesy of Richard E. Wyszynski, MD.)

Differential Diagnosis

The differential includes other infections such as toxoplasmosis, other herpesviruses, syphilis, and occasionally other opportunistic infections.

Emergency Department Treatment and Disposition

Reversal, if possible, of immunosuppression. Ganciclovir and foscarnet have been used with some effectiveness.

Clinical Pearls

1. HIV retinopathy consists of scattered retinal hemorrhages and scattered, multiple cotton wool spots that resolve over time, whereas CMV lesions will typically progress.

2. Although exposure to the CMV virus is widespread, the virus rarely produces a clinically recognized disease in nonimmunosuppressed individuals.

Papilledema

Associated Clinical Features

Papilledema involves swelling of the optic nerve head, usually in association with elevated intracranial pressure. The optic disks are hyperemic with blurred disk margins; the venules are dilated and tortuous. The optic cup may be obscured by the swollen disk. There may be flame hemorrhages and infarctions (white, indistinct cotton wool spots) in the nerve fiber layer and edema in the surrounding retina (Fig. 3.14).

Figure 3.14

Papilledema Disk is hyperemic and swollen with loss of sharp margins. The venules are dilated and tortuous. The cup is obscured. A small flame hemorrhage is seen at 12 to 1 o'clock on the disk margin. (Courtesy of Department of Ophthalmology, Naval Medical Center, Portsmouth, VA.)

Differential Diagnosis

Ocular inflammation (e.g., papillitis), tumors or trauma, central retinal artery or vein occlusion, optic nerve drusen, and marked hyperopia may present with similar findings.

Emergency Department Treatment and Disposition

Expeditious ophthalmologic and medical evaluation is warranted.

Clinical Pearls

1. The top of a swollen disk and the surrounding unaffected retina will not both be in focus on the same setting on direct ophthalmoscopy.

2. Papilledema is a bilateral process, though it may be slightly asymmetric. A unilateral swollen disk suggests a localized ocular or orbital process.

3. Vision is usually normal acutely, though the patient may complain of transient visual changes. The blind spot is usually enlarged.

4. Diplopia from a sixth cranial nerve palsy can be associated with increased intracranial pressure and papilledema.

Optic Neuritis

Associated Clinical Features

Most cases of optic neuritis are retrobulbar and involve no changes in the fundus, or optic disk, during the acute episode. With time, variable optic disk pallor may develop (Fig. 3.15). Typical retrobulbar optic neuritis presents with sudden or rapidly progressing monocular vision loss in patients younger than 50 years. There is a central visual field defect that may extend to the blind spot. There is pain on movement of the globe. The pupillary light response is diminished in the affected eye. Over time the vision improves partially or completely; minimal or severe optic atrophy may develop. Papillitis, inflammation of the intraocular portion of the optic nerve, will accompany disk swelling, with a few flame hemorrhages and possible cells in the vitreous.

Figure 3.15

Optic Nerve Pallor Optic nerve pallor, either segmental (top) or generalized (bottom), is a nonspecific change that may be associated with a previous episode of optic neuritis or other insults to the optic nerve. (Courtesy of Richard E. Wyszynski, MD.)

Differential Diagnosis

Optic neuritis must be differentiated from papilledema (bilateral disk swelling, typically with no acute visual loss with the exception of transient visual changes), ischemic neuropathy (pale, swollen disk in an older individual with sudden monocular vision loss), tumors, metabolic or endocrine disorders. Most cases of optic neuritis are of unknown etiology. Some known causes of optic neuritis include demyelinating disease, infections (including viral, syphilis, tuberculosis, sarcoidosis), or inflammations from contiguous structures (sinuses, meninges, orbit).

Emergency Department Treatment and Disposition

Treatment is controversial; often none is recommended. Oral steroids may worsen prognosis in certain cases. Intravenous steroids may be considered after consultation with an ophthalmologist.

Clinical Pearls

1. Monocular vision loss with pain on palpation of the globe or with eye movement are clinical clues to the diagnosis.

2. Sudden or rapidly progressing central vision loss is characteristic.

3. Most cases of acute optic neuritis are retrobulbar. Thus ophthalmoscopy shows a normal fundus.

Anterior Ischemic Optic Neuropathy (AION)

Associated Clinical Features

Anterior ischemic optic neuropathy (AION) presents with a sudden loss of visual field (often altitudinal), usually involving fixation, in an older individual. The loss is usually stable after onset, with no improvement, and only occasionally, progressive over several days to weeks. Pale disk swelling is present involving a sector or the full disk, with accompanying flame hemorrhages (Fig. 3.16).

Figure 3.16

Anterior Ischemic Optic Neuropathy Pale disk swelling and flame hemorrhages are present. This patient also has an unrelated retinal scar due to toxoplasmosis. (Courtesy of William E. Cappaert, MD.)

Differential Diagnosis

The common, nonarteritic causes of AION (probably arteriosclerosis) need to be differentiated from arteritic ones, such as giant cell arteritis. If untreated, the latter will involve the other eye in 75% of cases, often in a few days to weeks. These elderly individuals often have weight loss, masseter claudication, weakness, myalgias, elevated sedimentation rate, and painful scalp, temples, or forehead.

Emergency Department Treatment and Disposition

Routine ophthalmologic and medical evaluation is appropriate.

Clinical Pearls

1. Consider AION in an elderly patient with sudden, usually painless visual field loss.

2. Rule out giant cell arteritis. These patients tend to be older (age > 55) and may have associated CRAO or cranial nerve palsies (III, IV, or VI) with diplopia.

Glaucoma

Associated Clinical Features

Narrow or closed-angle glaucoma results from a physical appositional impedance of aqueous humor outflow. Symptoms range from complaints of colored halos around lights and blurred vision to severe pain (may be described as a headache or brow ache) associated with nausea and vomiting. Intraocular pressures are markedly elevated. Perilimbal vessels are injected, the pupil is middilated and poorly reactive to light, and the cornea may be hazy and edematous (see also Chap. 2 for external ocular images).

Two-thirds of glaucoma patients have open-angle glaucoma due to an abnormality of primary tissues responsible for the outflow of fluid out of the eye. Often they are asymptomatic. They may have a family history of glaucoma. Funduscopy may show asymmetric cupping of the optic nerves (Fig. 3.17). The optic nerve may show notching, local thinning of tissue, or disk hemorrhage. Optic cups enlarge, especially vertically, with progressive damage. Tissue loss is associated with visual field abnormalities, usually in arcuate patterns. The intraocular pressure is often but not always greater than 21 mmHg.

Figure 3.17

Glaucomatous Cupping The cup is not central; it is elongated toward the rim superotemporally. (Courtesy of Department of Ophthalmology, Naval Medical Center, Portsmouth, VA.)

Differential Diagnosis

Acute Glaucoma

Painful visual loss (retrobulbar optic neuritis, iritis, endophthalmitis), referred pain from nonophthalmic source.

Chronic Glaucoma

Normal variants, ocular conditions like disk drusen or optic neuropathy.

Emergency Department Treatment and Disposition

Acute Narrow-Angle Glaucoma

Emergent ophthalmologic consultation and administration of medications to decrease intraocular pressure. Beta-blocker drops (timolol), carbonic anhydrase inhibitors (acetazolamide), cholinergic stimulating drops (pilocarpine), hyperosmotic agents (osmoglyn), and alpha-adrenergic agonists (apraclonidine) may be employed prior to laser or surgical iridotomy (see also Chap. 2).

Open-Angle Glaucoma

Long-term ophthalmic evaluation and treatment with medications and laser or surgery.

Clinical Pearls

1. A high index of suspicion must be maintained, since associated complaints such as nausea, vomiting, and headache may obscure the diagnosis.

2. Open-angle glaucoma usually causes no symptoms other than gradual loss of vision.

3. Congenital glaucoma is rare. However, because of prognosis if diagnosis is delayed, consider congenital glaucoma in infants and children with any of the following: tearing, photophobia, enlarged eyes, cloudy corneas.

4. Asymmetric cupping, enlarged cups, and elevated intraocular pressure are hallmarks of open-angle glaucoma.

Subhyaloid Hemorrhage in Subarachnoid Hemorrhage (SAH)

Associated Clinical Features

Subhyaloid hemorrhage appears as extravasated blood beneath the retinal layer (Fig. 3.18). These are often described as "boat-shaped" hemorrhages to distinguish them from the "flame-shaped" hemorrhages on the superficial retina. They may occur as a result of blunt trauma but are perhaps best known as a marker for subarachnoid hemorrhage (SAH). In SAH, the hemorrhages appear as a "puff" of blood emanating from the central disk.

Figure 3.18

Subhyaloid Hemorrhage Subhyaloid hemorrhage seen on funduscopic examination in a patient with subarachnoid hemorrhage. (From Edlow and Caplan: Primary care: Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med 2000; 342:29–36, with permission.)

Differential Diagnosis

SAH, shaken impact syndrome, hypertensive retinopathy, and retinal hemorrhage should all be considered and aggressively evaluated.

Emergency Department Treatment and Disposition

No specific treatment is required for subhyaloid hemorrhage. Treatment is dependent on the underlying etiology. Appropriate specialty referral should be made in all cases.

Clinical Pearl

1. A funduscopic examination looking for subhyaloid hemorrhage should be included in all patients with severe headache, unresponsive pediatric patients, or those with altered mental status.