Harrison’s Manual of Medicine



Clinical Assessment
Specific Disorders

Clinical Assessment
The history and examination permit accurate diagnosis of most eye disorders, without resort to laboratory or imaging studies. The essential ocular exam includes assessment of the visual acuity, pupil reactions, eye movements, eye alignment, visual fields, and intraocular pressure. The lids, conjunctiva, cornea, anterior chamber, iris, and lens are examined with a slit lamp. The fundus is viewed with an ophthalmoscope.
Acute visual loss or double vision in a pt with quiet, uninflamed eyes often signifies a serious ocular or neurologic disorder and should be managed emergently (Chap. 10). Ironically, the occurrence of a red eye, even if painful, has less dire implications as long as the visual acuity is spared.
Specific Disorders
RED OR PAINFUL EYE   The most common causes of a red or painful eye are listed in Table 48-1. Minor trauma may result in corneal abrasion, subconjunctival hemorrhage, or foreign body. The integrity of the corneal epithelium is assessed by placing a drop of fluorescein in the eye and looking with a slit lamp or a blue penlight. The conjunctival fornices should be searched carefully for foreign bodies. Topical anesthesia with a drop of 0.5% proparacaine may be necessary to perform an adequate examination.

Table 48-1 Causes of a Red or Painful Eye

Chemical splashes and foreign bodies are treated by copious saline irrigation. Corneal abrasions may require application of a topical antibiotic, a mydriatic agent (1% cyclopentolate), and an eye patch for 24 h.

Infection of the eyelids and conjunctiva (blepharoconjunctivitis) produces redness and irritation but should not cause visual loss or pain. Adenovirus is the most common cause of “pink eye.” It produces a thin, watery discharge, whereas bacterial infection causes a more mucopurulent exudate. On slit-lamp exam one should confirm that the cornea is not affected, by observing that it remains clear and lustrous. Corneal infection (keratitis) is a more serious condition than blepharoconjunctivitis because it can cause scarring and permanent visual loss. A localized abscess or ulcer within the cornea produces visual loss, pain, anterior chamber inflammation, and hypopyon. A dendritic pattern of corneal fluorescein staining is characteristic of herpes keratitis.

Strict handwashing and broad-spectrum topical antibiotics for blepharoconjunctivitis (sulfacetamide 10%, polymixin-bacitracin-neomycin, or trimethoprim-polymixin). Trifluridine 1% 1 drop q2h, for herpetic keratitis.

Inflammation of the eye, without infection, can produce episcleritis, scleritis, or uveitis (iritis or iridocyclitis). Most cases are idiopathic, but some occur in conjunction with autoimmune disease. There is no discharge. A ciliary flush results from injection of deep conjunctival and episcleral vessels near the corneal limbus. The diagnosis of iritis hinges on the slit-lamp observation of inflammatory cells floating in the aqueous of the anterior chamber (cell and flare) or deposited on the corneal endothelium (keratic precipitates).

Mydriatic agents (1% cyclopentolate), NSAIDs, and topical steroids (note: prolonged treatment with ocular steroids causes cataract and glaucoma).

Acute angle-closure glaucoma is a rare but important cause of a red, painful eye. Because the anterior chamber is shallow, aqueous outflow via the canal of Schlemm becomes blocked by the peripheral iris. Intraocular pressure rises abruptly, causing ocular pain, injection, headache, nausea, and blurred vision. The key diagnostic step is measurement of the intraocular pressure during an attack.

The acute attack is broken by constricting the pupil with a drop of 4% pilocarpine and by lowering the intraocular pressure with topical 0.5% apraclonidine, 0.5% timolol, and a single oral dose of acetazolamide, 500 mg. Future attacks are prevented by performing an iridotomy with a laser.

CHRONIC VISUAL LOSS   The major causes of chronic visual loss are listed in Table 48-2. A cataract is a cloudy lens, due principally to aging. It is treated by surgical extraction and replacement with an artificial intraocular lens.

Table 48-2 Causes of Chronic, Progressive Visual Loss

Glaucoma is an optic neuropathy that leads to progressive visual loss from death of retinal ganglion cells. It is associated with elevated intraocular pressure, but many pts have normal pressure. Angle closure accounts for only a few cases; most pts have open angles and no identifiable cause for their pressure elevation. The diagnosis is made by documenting arcuate (nerve fiber bundle) scotomas on visual field exam and by observing “cupping” of the optic disc.

Topical adrenergic agonists (epinephrine, dipivefrin, apraclonidine, brimonidine), cholinergic agents (pilocarpine), beta blockers (betaxolol, carteolol, levobunolol, metipranolol, timolol), and prostaglandin analogues (latanaprost); oral carbonic anhydrase inhibitors (acetazolamide). Surgical filter to reduce pressure (trabeculectomy).

Macular degeneration occurs in both a “dry” and “wet” form. In the dry form, clumps of extracellular debris, called drusen, are deposited beneath the retinal pigment epithelium. As they accumulate, vision is slowly lost. In the wet form, neovascular vessels proliferate beneath the retinal pigment epithelium. Bleeding from these neovascular vessels can cause sudden, central visual loss in the elderly. Macular exam shows drusen and subretinal hemorrhage.

There is no treatment for dry macular degeneration. Wet macular degeneration can be treated with laser photocoagulation of the leaking vessels.

Diabetic retinopathy appears in most pts 10–15 years after onset of the disease. Background diabetic retinopathy consists of intraretinal hemorrhage, exudates, nerve fiber layer infarcts (cotton wool spots), and macular edema. Proliferative diabetic retinopathy is characterized by ingrowth of neovascular vessels on the retinal surface, causing blindness from vitreous hemorrhage and retinal detachment.

All diabetics should be examined regularly by an ophthalmologist for surveillance of diabetic retinopathy. Macular edema is treated by focal or grid laser application. Neovascularization is treated by panretinal laser photocoagulation.

Tumors of the optic nerve or chiasm are comparatively rare but often escape detection because they produce insidious visual loss and few physical findings, except for optic disc pallor. Pituitary tumor is the most common lesion. It causes bitemporal or monocular visual loss.

Large pituitary tumors producing chiasm compression are removed transphenoidally. In some cases, small tumors can be observed or controlled pharmacologically (e.g., bromocriptine for prolactinoma).


For a more detailed discussion, see Horton JC: Disorders of the Eye, Chap. 28, p 164, in HPIM-15.



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