Primary Care of the Eye
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[edit] Primary Care of the Eye
Keith Doram
Yehia Mishriki
The eye is the most accessible and informative bi-directional "window" known to man. From the inside looking out, most of our daily wakeful activities significantly rely on visual input. From the outside looking in, the physical examination of the eye yields more useful information per unit area (or per unit weight) than any other organ in the body (Fig. 172-1). For example, direct inspection of the retina can often detect evidence for systemic disease—in some cases even before there are other obvious signs, symptoms, or laboratory abnormalities. Since the eye and the visual system are the most complex and developed sensory mechanisms of the body, primary care clinicians must be competent in the evaluation and management of the eye and eye-related disorders.
The Association of University Professors of Ophthalmology (AUPO) issued a policy statement regarding the areas of ophthalmology in which all physicians should be competent. These areas include visual acuity, red eye, traumatized eye, strabismus and abnormal eye movements, abnormal pupillary response, optic nerve and fundi abnormalities, initial management, and referral guidelines. Adequate competency helps ensure that many of the common mistakes made during the eye examination do not occur (Box 172-1).
| Box 172-1 - Common Mistakes Made During the Eye Examination |
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This chapter presents practical information that will better enable the primary care clinician to gain and maintain an acceptable level of competency in the evaluation and management of the eye and eye-related disorders. The main outline of information includes how to obtain an adequate directed ophthalmologic history and physical, as well as the recognition and implications of the four cardinal complaints related to the eye: change in vision, change in appearance, pain, and trauma (Box 172-2). The AUPO's core competencies, effective prevention measures, and treatment/referral guidelines are be incorporated. Additional information on the ocular manifestations of systemic disease, ophthalmologic procedures, and other special topics of interest to primary care clinicians are presented.
| Box 172-2 - The Four Cardinal Eye Complaints |
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[edit] OPHTHALMOLOGY ABBREVIATIONS
Often the primary care clinician can be confused by the cryptic abbreviations used in ophthalmology consultations. Box 172-3 includes some of the more commonly used abbreviations; these abbreviations are used throughout this chapter.
| Box 172-3 - Common Ophthalmologic Abbreviations |
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[edit] HISTORY
It is important to first determine the primary (cardinal) eye problem (see Box 172-2). The next step is to assess the eye complaints by time course, precipitating factor(s), palliative or exacerbating variables, and course history.
Adequate characterization of any discomfort is important. For example, is there any pain, a sensation of "something in the eye," itching, excessive tearing, or burning? Often a person can accurately localize the foreign body and help direct the focus of the ophthalmoscopic examination. Itching and excessive tearing can suggest an allergic cause.
If there were any changes in vision, it should be noted whether there was painless or painful loss of vision. It is also important to determine the extent of the visual change and whether it involves one or both eyes. Bilateral visual loss usually implies a primary neurologic etiology and not a primary ophthalmologic problem. The presence of multiple new flashes or floaters could represent a retinal tear or vitreous hemorrhage, whereas a single floater is probably a benign condition. The rate of onset of visual impairment may give a clue as to the etiology. In general, rapid deterioration of vision points to a vascular cause, whereas more gradual loss of vision suggests causes such as cataracts.
The tetanus immunization status is important in patients with a history of eye trauma. Also knowing the acidity or alkalinity of any fluid/chemical eye exposure is essential.
A detailed ocular history should also include information on any type of corrective lenses (i.e., glasses, contact lenses); any acute or chronic eye problems (e.g., glaucoma); any eye medications (e.g., antiglaucoma medications, topical antibiotics); any eye surgery history (e.g., cataract removal, refractive surgery); any associated systemic symptoms like headaches, nausea, or vomiting; and finally any relevant systemic diseases (e.g., diabetes, hypertension, and HIV disease).
[edit] PHYSICAL EXAMINATION
The eye examination should ideally proceed in a sequential fashion. The suggested order of the examination is shown in Box 172-4.
| Box 172-4 - Suggested Order of the Physical Examination |
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[edit] Vision Testing
Assessing VA should be the first step in essentially all ophthalmologic examinations. The severity of any eye disorder is greatly determined by its effect on VA. VA testing is the most fundamental component of evaluating a patient's visual function. In essence, VA testing is the "vital sign" of the eye. The examiner should measure vision using a standardized Snellen distance VA chart (Fig. 172-2A) or a near acuity card (Fig. 172-2, B). If these tools are unavailable, newsprint, the patient's chart, or other legibly printed materials can be used. In all physical eye examination procedures, each eye must be evaluated individually. This is especially important in cases of trauma, where the treating clinician often fails to recognize injury in the "uninjured" eye.
VA testing should always be done with the patient wearing his or her corrective lenses when possible. Patients may have preexisting myopia (nearsightedness), hyperopia (farsightedness), or astigmatism (unequal corneal or lenticular curvatures). The examiner should note whether corrective lenses were used during the visual testing, and each eye's VA should be documented separately. Patients over 40 years of age may require bifocals or reading glasses to compensate for the age-related stiffening of the crystalline lens (presbyopia) and the accompanying loss of focusing ability. If a patient's glasses or contact lenses are not available, pinhole testing of the visual acuity can correct any refractive error. (An 18-g needle or a sharp pencil can be used to punch holes in a 3×5-inch note card if a premade pinhole device is not available.) Pinhole testing generally corrects any uncorrected refractive errors. If correction is not seen, the examiner should look for other pathologic causes such as cataracts, optic nerve disease, or retinal diseases.
The use of a Snellen chart at 20 feet is a time-honored method for determining VA. The patient stands 20 feet from the chart and covers one eye. (Or when using the pocket-sized near chart, it is held 14 inches from the patient's face.) The patient begins reading from the top line down. The examiner notes the acuity by the line where most (more than half) of the characters are read correctly. The first eye is then covered (with an eye cover or the palm) and the opposite eye is tested in the same manner. VA is reported as two numbers separated by a slash, followed by a minus sign and the number of characters missed on that line. The first number, usually "20," is the standard distance from the chart to the individual being tested. The second number is the distance, in feet, at which the letter subtends 5 minutes of an arc on the retina. For example, if a patient has 20/40 vision, he or she can see at 20 feet what a "normal" person can see at 40 feet. If the patient can read some but not all of the letters on a line, VA is recorded as the acuity for that line "minus" the number of letters missed (e.g., 20/40−2). For patients with less than 20/400 vision, the examiner can use the notations "CF," "hand motions," "LP," and "NLP" vision. Illiterate patients and small children can use other charts with "E" shapes or pictures (e.g., Allen chart).
[edit] Pupil Examination
Assessing the shape, size, and reactivity of the pupils is essential in determining the integrity of the anterior visual pathway. Pupillary dilation agents, of course, should not be used before pupil testing. Pupillary function testing is critical to evaluation of both the neurologic and the ophthalmologic status of the patient. Mistakenly, PERRLA is noted and substituted for an accurate assessment of pupil function. Both pupils should be round on examination. Irregularly shaped pupils are probably a result of prior ocular surgery, although it could be due to ocular rupture, laceration, or scarring from a previous inflammatory process of the iris or ciliary body. The pupils should be tested individually and in a dim light with the patient fixating on a distant object. Discrepancy in pupillary size is called anisocoria. A difference in pupillary size of ½ to 1 mm is common, and in the absence of any symptoms or other signs, does not necessarily indicate any pathology. The examiner directs a penlight at each pupil and notes the rapidity and amount of pupil constriction in each eye. As a general rule, a difference in pupil size greater than 1 mm or in the pupil that reacts poorly to direct light is abnormal. When confronted with a dilated pupil, the examiner must search for other signs of a third nerve palsy such as ptosis, diplopia, or ocular motor paresis. Even when these conditions are not present, a significantly dilated pupil is considered a medical emergency, particularly when accompanied by headache or other neurologic signs. The "swinging light" test helps determine if there is integrity of the visual pathways. A bright light is moved back and forth from one eye to the other eye quickly enough not to allow the pupil to dilate. If a pupil does dilate when the light is shined on it, a defect along that visual pathway is present. A RAPD or MG pupil is due to a defect anywhere in the visual pathway from the lens to and including the optic nerve. The pupil constricts consensually (due to the crossing neural fibers in the midbrain) when light is shined in the opposite eye but paradoxically dilates when the light is brought back and shined on the affected eye. This reaction must not be mistaken for a rhythmic wavering pupil (hippus), which is a normal finding. Also, if there is severe bilateral disease, both eyes may react equally. Therefore no RAPD exists. Cataracts and macular degeneration do not normally cause RAPD unless they are very advanced. In Horner's syndrome, sympathetic innervation of the pupil and levator palpebrae superioris muscle is interrupted. There is ptosis, miosis of the affected eye, and anhydrosis of the ipsilateral half of the face. The pupil is small but reacts to light. (Anhydrosis may be difficult to detect and is more easily assessed by looking for small droplets of sweat at the vermilion border of the upper lip using the ophthalmoscope set at +40 diopters.) A pupil that constricts very slowly and incompletely, or not at all, to direct light but is otherwise normal is called an Adie's tonic pupil. It may also constrict better to near light than to direct light. This is due to degeneration of the ciliary ganglia and the postganglionic parasympathetic fibers that constrict the pupil and effect accommodation. Adie's pupil is supersensitive to dilute solutions of pilocarpine and can be positively identified if 0.1% pilocarpine constricts the pupil. Patients with Adie's pupil may complain of difficulty reading because of accommodative paresis, but usually the dilated pupil is an incidental finding. Similar Adie's pupil findings can often be a manifestation of a mild dysautonomia and can also be associated with Shy-Drager syndrome, diabetes mellitus, and amyloidosis.
The much-taught Argyll Robertson pupil is uncommon. It was classically described in patients with tertiary syphilis, but today is more likely to be seen in diabetics. It has also been described in the meningoradiculitis of Lyme disease. The pupils are usually small, unequal, and irregular. They do not react to light but constrict on accommodation. Mydriatics cause an incomplete dilation.
[edit] External Examination
Examination of the eyelids, lid margins, periorbital position, and globe position is the next step in a comprehensive examination. In cases of trauma it is critical not to palpate the globe. Observe for proptosis or exophthalmos (protruding eye), which may indicate orbital disease (e.g., retrobulbar hemorrhage, orbital cellulitis, orbital tumor, Graves' disease). A sunken eye (enopththalmos) is often seen in fractures of the orbital floor (especially if associated with ecchymosis, point tenderness, and a palpable step-off around the orbital rim). These conditions can best be identified by observing the patient above the head and looking downward toward the eyes.
Examine the eyelids for any crusting, irregularity, lash loss, or lesions. A hordeolum (stye) is a painful localized infection of the lash follicle. A chalazion is a more chronic inflammatory painful lesion of the meibomian gland. The hordeolum is at the lid's edge, while the chalazion is not. Note any ectropion (out-turned lower lid margins)—commonly seen in elderly patients, entropion (in-turned lower lid margins), and trichiasis (posteriorly misdirected eye lashes).
The inferior aspects of the conjunctiva can be examined by pulling down the lower eyelid from the inferior orbital rim and have the patient look up. To see the inner aspect of the upper eyelid and the superior conjunctiva and cul-de-sac, a lid eversion procedure should be performed. The examiner should grasp the upper eyelash, pull the upper lid away from the globe, and use a small, slender object (e.g., applicator stick) to press the region of the superior tarsal plate inferiorly (Fig. 172-3). Never invert the lid if rupture of the globe is suspected. Look carefully in these areas for any suspected retained foreign body. Next examine the bulbar conjunctiva. Look for subconjunctival hemorrhage (spontaneous or due to trauma)—this is usually a harmless condition. However, globe rupture is more likely in cases of trauma and when the subconjunctival hemorrhage encircles the entire cornea. Conjunctival injection due to conjunctivitis is a common cause of "red eye." If the injection is just around the cornea, the inflammation could be the result of keratitis (corneal infection), iritis, or acute glaucoma. Ocular pain relieved by topical anesthetic is due to conjunctival or corneal disruption. Pain unrelieved by topical anesthetic is due to deeper eye structures.
[edit] Ocular Motility
Six eye muscles move the eyes in conjugate fashion (see Chapter 177 ). The six extraocular muscles are intact (EOMI) if they properly perform the cardinal movements as shown in Fig 172-4. Cranial nerve III innervates the medial rectus (adducts the eye), inferior rectus (depresses the eye), superior rectus (elevates the eye), and inferior oblique (abducts, elevates, and outwardly rotates the eye) muscles. Cranial nerve IV innervates the superior oblique (abducts, depresses, and inwardly rotates the eye) muscles. Cranial nerve VI innervates the lateral rectus (abducts the eye).
The extraocular movements involve complex coordination via neuropathways located in the frontomesencephalic and cerebellomesencephalic areas—the visual, vestibular, and ocular motor centers. Eye movements are responsible for capturing and locking onto a visual object of interest and for maintaining fixation on that object even during head and body movements. Any disturbance in intracranial processing, midbrain or cranial nerve function, or intraorbital muscle abnormalities may result in an ocular position imbalance. The examiner must carefully note the position of the eyes and their excursions relative to each other in patients with complaints of diplopia (double-vision), strabismus (misalignment), blurred vision, jumpy vision, those with more general complaints of unsteadiness, dizziness, or vertigo, and those with suspected neurologic or orbital disease. Abnormalities may be seen in the primary gaze (straight ahead) or congruity of gaze in the six cardinal positions (left, right, up and right, up and left, down and right, down and left).
A large degree of misalignment of the eyes is easily determined by inspection. In patients with subtle degrees of strabismus, the position of the corneal light reflexes can help determine if there is any squint or not, since these reflexes are normally located in identical positions on each eye (Hirchberg test). Fixation maintenance and smooth pursuit mechanisms are tested by asking the patient to fixate on a target, while slowly moving the target to extreme positions of gaze. During this process, it is important to observe the steadiness of eye position and fixation. The patient should be asked to look in each cardinal position and asked if diplopia develops and if so, in which direction of gaze. Inability to abduct the eye suggests a sixth cranial nerve (abducen's) palsy. This can be seen in patients with diabetes and is due to infarction of the nerve. It is also seen in patients with increased intracranial pressure, and in such a case, it is accompanied by papilledema. An abducen's palsy can also be seen with tumors, meningitis, or compression by an aneurysm. In a patient with a complete lateral gaze palsy, one should suspect a lesion of the abducen's nucleus since the nucleus contains interneruons that project via the medial longitudinal fasiculus (MLF) to the contralateral medial rectus. An eye that is "down and out" and is associated with ptosis is seen in patients with third cranial nerve (oculomotor) palsy. If the pupil is also dilated, one should suspect an aneurysm of the circle of Willis, especially if accompanied by pain. Sparing of the pupil suggests an infarction of the nerve. This is primarily seen in patients with diabetes. Patients with fourth cranial nerve (trochlear) palsy complain of vertical or oblique double vision, which worsens as they look downward. They may assume a characteristic head posture in which their head is turned and titled away from the affected side. Because of its close anatomic relationship to the tentorium, the fourth nerve is subject to physical injury during head trauma. For this reason, fourth nerve palsies are most frequently associated with trauma. However, microinfarctions along the nerve are also common. Complex eye movement deficits suggest myasthenia gravis or thyroid eye disease.
Nystagmus, which are involuntary rhythmic oscillations of the eyes, can be seen in a variety of disorders. Jerk nystagmus is characterized by a slow drift away from the visual target followed by a rapid correction. It can be downbeat, horizontal, or torsional. Acquired nystagmus is usually of the jerk form and can be divided into two major subcategories: nystagmus due to disorders of the peripheral vestibular apparatus and nystagmus due to disorders of the central nervous system (CNS). Peripheral nystagmus develops with vestibular dysfunction. It is usually purely horizontal, or horizontal and rotatory. It is often associated with severe vertigo. Symptoms can be recurrent, transient, and last days to weeks; but they usually resolve with time. Associated postural effects and hearing deficits are often noted. The common causes are infectious disease of the labyrinth (labyrinthitis) or the vestibular nerve (neuronitis), Ménière's disease, or trauma. Central nystagmus is much more variable and is not usually associated with severe vertigo. Symptoms may be transient or permanent. Central nystagmus often is a result of a brainstem or cerebellar lesion caused by demyelinating disease, vascular infarction, or tumor. Subtle nystagmus can sometimes be detected during funduscopic examination at which time one observes nystagmoid movements of the optic disc. End-gaze nystagmus is common even in patients without ocular or neurologic pathology and usually occurs for only a few beats. Exaggerated-gaze nystagmus can be caused by drugs (anticonvulsants, sedatives, alcohol), myasthenia gravis, demyelinating disease, and cerebellopontine angle, brainstem, and cerebellar lesions. Spontaneous nystagmus suggests labyrinthine vestibular disease or cerebellar disease. A torsional component is usually seen with labyrinthine disease. Vertical nystagmus implicates the pontomedullary or pontomesencephalic areas as the source. Vertical nystagmus of the upbeat type is seen in patients with demyelinating disease, brainstem vascular disease, tumors, or Wernicke's disease. Downbeat nystagmus may be seen in Wernicke's disease but is characteristic of syringobulbia. In pendular nystagmus, the to-and-fro oscillations are of nearly equal rate. It is usually observed in individuals in whom central vision has been compromised early in life (i.e., albinism, congenital diseases of the retina). This type of nystagmus is always bilateral and in one plane. Head oscillation may accompany the nystagmus and is felt to be compensatory.
[edit] Visual Field Testing
The usual techniques used in VF testing by confrontation are crude, and if there is any suspicion that the patient may have a VF defect, formal testing should be sought. The usual technique is as follows:
- Sit 2 feet from the patient.
- Ask the patient to cover one eye and fixate on your eye that is directly in front of him or her (i.e., if the patient were to fixate with his or her right eye, he or she would look at your left eye, and vice versa).
- Begin by first checking to see if there is a central field defect. Ask the patient if he or she sees your entire face with his or her uncovered eye. If the patient can only see your hair and chin but not your eye or nose, he or she has a central defect.
- Stretch your arms out in a plane that is equidistant from the patient and at the outermost periphery of your vision.
- Wiggle the index and middle fingers on one hand and ask the patient if he or she sees movement, and if so, on which side.
- Move your hands to different positions, checking the patient's superior, inferior, nasal, and temporal fields. Randomly change fingers that are wiggled.
Some ophthalmologists recommend that patients identify the number of fingers being held outstretched rather than whether or not the examiner's finger is being wiggled. Since red vision is affected earliest, using a red object to test VFs increases the sensitivity of the test. A lesion affecting the visual pathway anterior to the optic chiasm will produce a monocular VF defect. A central scotoma (blind spot) usually represents optic nerve or macular pathology. The visual system and VF defects resulting from lesions at various points in the visual pathway are shown in Fig. 172-5.
[edit] Slit-Lamp Examination
An ophthalmologist (or optometrist) usually is the examiner who has the slit lamp along with the necessary expertise and training to use it. The SLE is essential in any condition requiring an accurate and highly magnified view of the anterior and posterior segments of the eye.
[edit] Intraocular Pressure
The IOP of the eye is analogous to the systemic blood pressure of the cardiovascular system in that both pressures should be periodically assessed and maintained in the optimal range (see Chapter 173 ). As in systemic hypertension, the risk for IOP elevation increases with age—especially 35 years and older. Normal IOP is 8 to 21 mm Hg, but in pathologic states can range from 0 (in cases of ruptured globe, after glaucoma surgery, and severe intraocular inflammation) to 70 or 80 (in cases of angle-closure glaucoma). However, most primary care examiners do not have the necessary equipment to safely and accurately directly measure the IOP. The primary care examiner must rely on the recommended glaucoma screening guidelines, crude manual techniques, and other observational methods (e.g., optic nerve cupping, unexplained blurred monocular vision) to determine if more formal testing for IOP should be performed.
The IOP can be measured in a variety of ways. The applanation tonometer (found on most slit lamps, although there is a Perkins handheld version) and the pneumotonometer are not available for most primary care examiner usage. The Schiøtz tonometer (see Fig. 173-3 ), although easily available, is not the preferred method because of its disadvantages (increased risk in spreading infection, cumbersome, can cause injury). The tonometer pen (see Fig. 173-4 ) is the preferred device for the primary care examiner. It is easy to use and is fairly accurate. Table 172-1 compares the advantages and disadvantages of each IOP testing modality.
Table 172-1 Intraocular Pressure Testing Modalities
| Modality | Advantages | Disadvantages |
|---|---|---|
| Applanation tonometer | Very accurate, easy to use | Expensive, requires direct contact to cornea and globe, ineffective on abnormal corneal surfaces and irregular tear films |
| Tonometer pen (Tono-pen) | Relatively accurate, easy to use, has disposable covers to prevent infection | Accuracy diminishes outside the normal IOP range; pens are fragile and expensive |
| Pneumotonometer (Air-puff tonometer) | Accurate, easy to use, effective on abnormal corneal surfaces and irregular tear films | Expensive to maintain, not portable, must be calibrated often |
| Schiøtz (indentation) tonometer | Inexpensive, accurate to ±3 mm Hg | Cumbersome, can spread infection, prone to false-positive elevations of IOP, more likely to cause corneal injury |
| Manual assessment | Does not require instrumentation | Extremely inaccurate if performed by persons who are not ophthamologists, only rough approximations can be made |
[edit] FUNDUSCOPIC EVALUATION
The final part of the comprehensive eye examination is direct ophthalmoscopy—it is invaluable diagnostic tool for the primary care clinician. Ideally, after vision and pupillary testing, dilation of the pupils should be done, especially if an abnormality in the posterior eye is suspected. Funduscopic evaluation is best accomplished after the pupils are dilated with a weak mydriatic agent such as tropicamide 0.5% to 1% or phenylephrine 2.5% (both reverse effects in 4 to 6 hours). Always document the time of dilation and the agents used for dilation. Atropine drops should not be used because they produce dilation for up to 1 to 2 weeks. The pupils should not be dilated if serial neurologic examinations are required, in elderly patients who have had cataract surgery (can cause artificial lens displacement), or if acute angle-closure glaucoma is suspected. One can do a simple screen for angle-closure glaucoma by shining a handlight obliquely across the anterior chamber. If a shadow on the iris is noted on the opposite side of the illuminator, there may be narrowing of the anterior chamber and the presence of angle-closure glaucoma (see Fig. 173-6 ). Although trying to view the fundi without pupillary dilation has been likened to trying to view the contents of a room while looking through a keyhole, for practical and logistic reasons primary care clinicians do not dilate the pupils in the vast majority of their patients. Therefore it is important to refer all patients to an ophthalmologist if a more sensitive and complete funduscopic evaluation is deemed necessary.
However, even in undilated eyes, examination with the direct ophthalmoscope can give useful information on both the anterior and posterior aspects of the eye. The examination should be done in dim light. The examiner's right eye should be used to examine the patient's right eye, and visa versa. Begin at a distance of 1 to 2 feet from the patient's eye, standing slightly to the side of the patient. The patient should be asked to focus on a distant object. Usually setting the ophthalmoscope diopter lens to −2 to −3 (the red 2 or 3) will generate a comfortable view of the fundus. Black numbers focus anteriorly and red numbers focus posteriorly (toward the reddish retina). Focus anteriorly on the lids, cornea, conjunctiva, and iris. A diminished red reflex or irregularities in the red reflex may result from cloudy media (e.g., corneal or lens opacities, vitreous blood) and unusual refractive errors (Fig. 172-6). Next focus posteriorly toward the vitreous humor. With the red reflex in view, aim the ophthalmoscope toward the opposite mastoid process and then move as close to the eye as possible to bring the optic disc into view. (The small aperture setting allows for an easier fundus view through an undilated pupil.) If you do not visualize the disc, just follow the vessels in the right direction until you see the disc. The green (or red-free) light aids in viewing vessels and hemorrhages, which appear almost black (the veins appear bluer). Follow the outlines of the vessels in each quadrant.
The optic disc should have sharp margins and the vessels should appear crisp as they cross the edge of the disc. If the margins are indistinct or seem elevated above the rest of the fundus, the patient may have papilledema. The examiner notes any hemorrhages or infarctions of the nerve fiber layer (cotton-wool spots) near the nerve head. Pale optic discs may indicate atrophy and should be evaluated by an ophthalmologist. Marked or asymmetric cupping of the nerve is a possible sign of glaucoma.
The macula is very sensitive to light, so it should be examined last. The best view of the macula occurs when the patient looks directly at the examining light (Fig. 172-7). The presence of the foveal light reflex is one indicator of normal foveal anatomy. Systemic diseases, such as diabetes mellitus and hypertension, can often result in funduscopic microvascular abnormalities (e.g., exudates, arteriovenous nicking, hemorrhage, microaneurysms, and edema). In significant carotid atherosclerosis, cholesterol emboli (Hollenhorst plaques) may lodge in the retinal arterioles at their bifurcations. If a patient has experienced a significant change in vision, the examiner should look specifically for a central retinal artery occlusion (pale fundus with cherry-red spot at macula), a retinal vein occlusion (diffuse venous dilation and retinal hemorrhages), or a retinal detachment (a "billowing sail" retinal appearance) or tear (Fig. 172-8).
[edit] Documentation of the Eye Examination
The many abbreviations that are used in ophthalmology have been considered by many primary care physicians to be rather cryptic. However, there are many aspects to the eye examination, and abbreviations are necessary to aid in succinct documentation. Some of the more common abbreviations used in documenting the eye examination findings are included in Box 172-3.
[edit] Assessment and Management Stratification
Since it is often the primary care physician who initially evaluates patients with any of the four cardinal eye complaints, it is very important that the examiner knows what is emergent (requiring immediate ophthalmologic consultation); urgent (needing ophthalmologic follow-up in 1 day or less; and nonurgent (follow-up with ophthalmology within 2 days or as needed) (Box 172-5).
| Box 172-5 - Categories of Eye Complaint Severity |
Emergent
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[edit] CHANGE IN VISION
There is often a discrepancy between the patient's perceived degree of visual loss and the examiner's objective determination of vision, thus formal testing of visual acuity is essential. In addition, because a field defect may be perceived as visual loss, testing of VFs by confrontation is imperative. Finally, testing of color vision is also indicated as impairment of color discrimination suggests disease of the optic nerve or central retina. The rapidity with which the patient has had impairment of vision determines the urgency of the need for evaluation. Impairment of vision in one eye implicates the eye itself or disease of the optic nerve anterior to the optic chiasm. Bilateral, symmetric visual field defects suggest a central etiology.
Visual loss can be separated into categories based on anatomic location. Refractory problems can usually be corrected with a pinhole device to 20/25 or 20/30. Opacities in the media (cornea, aqueous humor, lens, vitreous humor) can result in an abnormal red reflex that does not correct with a pinhole device. Examples include cataracts, corneal ulceration, and vitreous hemorrhage. Retinal diseases, such as central retinal artery occlusion, retinal detachment, macular degeneration or hemorrhage, diabetic retinopathy, cytomegalovirus (CMV), central retinal vein occlusion, and "ocular migraine," can be seen on ophthalmoscopic examination. Optic nerve diseases can result in anterior ischemic optic neuropathy (e.g., temporal arteritis, glaucoma, papilledema, neuroretinitis, optic neuritis). Chiasmal diseases can be inferred from abnormal findings during the pupil, optic disc, and VF tests. Advanced disease is associated with bilateral enlarged, sluggish pupils and pale optic discs. VF deficits ultimately define the chiasmal disease. Pituitary adenomas can result in bitemporal field defects. Cortical blindness is the result of bilateral lesions in the occipital cortex that produce bilateral homonymous hemianopia. A unilateral cortical lesion produces a VF loss on one side only and the visual acuity is not affected. Functional visual loss is a diagnosis of exclusion after comprehensive ocular and neurologic examinations are found to be normal. Various techniques are used that can help determine if a patient is feigning blindness. For example, it is possible to bring one's outstretched hands together or legibly and neatly sign one's name—even if totally blind. Patients with functional total or near-total blindness often show an inability to do these tasks. Fig. 172-9 depicts serious causes of acute vision loss that every primary care physician should be able to recognize.
[edit] Acute, Painless Loss of Vision
The inner, posterior, nonconjunctival aspects of the eye are usually involved in acute, painless loss of vision. The following information gives key history and physical examination characteristics of each entity.
[edit] Vitreous Hemorrhage
[edit] History.
There is often a sensation of seeing through a "spider web" or of having had floaters. Associated diseases include diabetes mellitus, retinal tears and detachments, sickle cell anemia, and blood dyscrasias.
[edit] Examination.
The red reflex may be decreased or nonhomogeneous, and there may be difficulty focusing on the retina. Smaller, vitreous hemorrhages may not be visible with direct ophthalmoscopy.
[edit] Treatment.
The head must be elevated, as well as immediate referral to an ophthalmologist. Delayed vitrectomy may be required for blood that does not clear with time.
[edit] Retinal Detachment
[edit] History.
The patient may experience flashes and floaters before the detachment. There may be a sense of loss of part of the VF or of looking through a sheer curtain. Trauma, severe myopia, and eye surgery are all predisposing conditions. Elderly males are predisposed to retinal detachment.
[edit] Examination.
Visual field testing discloses a unilateral defect that may be sectoral, quadrantal, hemifield, or total. On funduscopic examination, one may see retinal hydration lines, or rugae, which have the appearance of a "ripple on a pond" or a "billowing sail." A relative afferent pupillary defect may be present. Unfortunately, visualization of a peripheral detachment may not be possible with direct ophthalmoscopy (Fig. 172-10).
[edit] Treatment.
Immediate referral to an ophthalmologist is a priority. Treatment includes various surgical options including photocoagulation, cryotherapy, diathermy, scleral buckling, or air/silicon oil injections.
[edit] Retinal Artery Occlusion
[edit] History.
Loss of vision is quite abrupt and nearly complete if the central retinal artery is involved. There may be an antecedent history of transient loss of vision sometimes described as a curtain coming down over the VF, which resolves completely within a short time (amaurosis fugax). Giant cell arteritis should be considered in an elderly patient, especially if they have had headaches, jaw or lingual claudication, or proximal musculoskeletal pain. In addition, patients with migraine headaches, particularly if they have had focal neurologic signs or symptoms associated with their headaches, are at risk for retinal artery occlusion. Young women taking oral contraceptives, elderly males, and patients with cardiac valve abnormalities (i.e., emboli prone) also have an increased risk.
[edit] Examination.
There is severe impairment of visual acuity often limited to hand motion or light perception. Visual field may be restricted to a small island in the temporal field. On ophthalmoscopy, a refractile object within one of the arterioles may be visualized (Hollenhorst plaque). With central retinal artery occlusion, the retina is diffusely pale and attenuated. A "cherry-red spot" may be seen in the fovea (an area of thin retina overlying the "reddish" choroidal layer) (Fig. 172-11).
[edit] Treatment.
Patients should be immediately referred to an ophthalmologist. In the interim, the patient should be made to lie down and the globe should be gently massaged intermittently (few seconds on and off) in an attempt to dislodge the embolus. Permanent damage can often ensue if the visual loss persists for 2 or more hours. Other interim measures include having the patient breathe into a paper bag every 10 to 15 minutes per hour (increases Pco2 and artery dilation) or alternatively, inhalation of 95% oxygen and 5% CO2 (also increases vasodilation). If available, a 250-mg dose of acetazolamide (Diamox) should be given intravenously.
[edit] Retinal Vein Occlusion
[edit] History.
The patient complains of prolonged visual obscurations. Although most often idiopathic, hypertension, diabetes, hyperviscosity syndromes, and glaucoma are risk factors.
[edit] Examination.
The retinal veins are distended and appear "phlebitic." Multiple retinal hemorrhages are often present and one may see cotton-wool spots. If the thrombosis does not resolve spontaneously, extensive retinal bleeding may occur ("blood and thunder" appearance). Despite the striking retinal picture, the visual loss is often slight and limited to a mild decrease in central visual acuity due to macular hemorrhage and edema (Figs. 172-12 and 172-13).
[edit] Treatment.
There is no proven effective therapy. Naturally, any underlying hypercoaguable/hyperviscous state should be corrected (e.g., polycythemia, thrombocytosis).
[edit] Anterior Ischemic Optic Neuropathy
[edit] History.
Anterior ischemic optic neuropathy (AION) is caused by decreased blood flow through the posterior ciliary arteries that supply the optic disc. Two forms are (1) arteritic—most commonly due to giant cell (temporal) arteritis and (2) nonarteritic (the more common form)—the specific cause is unknown but hypertension and diabetes are risk factors. The vision loss is sudden, although patients may on occasion describe premonitory obscurations. If associated with giant cell arteritis, patients may have myalgias, headaches, low grade fever, jaw claudication, weight loss, and anemia.
[edit] Examination.
An afferent pupil defect (MG pupil) is present. The optic disc is swollen and surrounded by nerve fiber layer splinter hemorrhages.
[edit] Treatment.
No treatment is available. However, if giant cell arteritis is suspected, glucocorticoid therapy should be started pending determination of a sedimentation rate and temporal artery biopsy to prevent loss of vision in the contralateral eye.
[edit] Optic Neuritis
[edit] History.
Optic neuritis most often occurs in young women and in patients with multiple sclerosis. Vision loss is gradual, occurring over several days. There may be ocular pain, especially with eye movement.
[edit] Examination.
An afferent pupillary defect is present. Since the demyelinating process is retrobulbar most of the time, the optic disc appears normal at presentation. One third of patients have optic disc pallor and edema at presentation. Many but not all patients, later develop multiple sclerosis.
[edit] Treatment.
Nearly all patients gradually or spontaneously recover most of their vision after a single episode of optic neuritis. If not, the initial diagnosis should be reconsidered. Administration of glucocorticoids in patients with monocular optic neuritis is controversial, and consultation with a neurologist or neuroophthalmologist is strongly recommended. In patients with bilateral disease, the case for systemic glucocorticoids is much stronger.
[edit] Exudative, Age-related Macular Degeneration
[edit] History.
Exudative, age-related macular degeneration occurs in elderly patients greater than 60 years. Visual blurring is gradual but may suddenly worsen over several days. Patients have diminished central vision, as well as distortion of images (metamorphopsia). Often both eyes are affected, although one eye may be more severely affected than the other.
[edit] Examination.
Testing with an Amsler grid detects the distortion of images in the central VF. Retinal hemorrhage can sometimes be seen in the macula, although the neovascular membrane (associated with "wet" macular degeneration) may be difficult to see because of its subretinal location. Fluorescein angiography is often needed for its detection (Figs. 172-14 and 172-15).
[edit] Treatment.
Supplementation with various vitamins and minerals has not been shown to be beneficial. Laser ablation of the choroidal neovascular membrane can arrest the exudative process.
[edit] "Ocular Migraine"
[edit] History.
The patient may or may not have a headache. However, he or she often has a personal or family history of migraine. The loss of vision is fairly rapid but is not sudden.
[edit] Examination.
On occasion, the retinal arterioles may be attenuated. In some patients, disc edema and peripapillary hemorrhages may be seen. Vision may only partially recover over the course of several months.
[edit] Treatment.
Vasoconstrictive medications should be avoided. There is anecdotal support for use of rapid-acting calcium channel blockers (e.g., sublingual nifedipine).
[edit] Cerebral Infarction
[edit] History.
Vision loss is sudden and usually bilateral. The nature of the VF deficit depends on the location of the infarction as it relates to the optic radiations. Patients often have a history of or risk factors for arteriosclerotic disease.
[edit] Examination
- Homonymous hemianopia: Interruption of the optic radiations after the chiasm.
- Superior quadrantanopia: Involvement of Myerson's loop as the postchiasmal fibers dip into the temporal lobe.
- Inferior quadrantanopia: Involvement of the more cephalad fibers of the postchiasmal within the parietal lobe.
- Homonymous hemianopia with macular sparing: Infarction within one of the visual cortices.
[edit] Treatment.
Aside from rehabilitation, there is no treatment for the completed stroke. Rapid response to acute stroke syndromes and controlling the risk factors for stroke are important prevention strategies.
[edit] Functional Visual Loss
[edit] History.
The history may be atypical and there is inconsistency of responses on repeated questioning. Secondary gain may be appreciable.
[edit] Examination.
Pupillary reflexes and funduscopic findings are normal. Optokinetic nystagmus is also present. Normal visual-evoked responses confirm the intactness of the retinooccipital pathways. The patients may not perform doable tasks that even totally blind patients should be able to perform (e.g., writing their name legibly).
[edit] Treatment.
Psychiatric consultation is indicated.
[edit] Acute Painful Loss of Vision
In contradistinction to conditions causing painless loss of vision, patients with pain accompanying their vision loss often have conjunctival injection due to ocular inflammation.
[edit] Corneal Ulcer
[edit] History.
There is often a history of eye trauma or of wearing contact lenses. Patients unable to completely close one or both eyes are also at risk (i.e., severe nerve VII palsy, proptosis, severe ectropion). A painful, vesicular rash in the distribution of the first division of the fifth cranial nerve may be present. In addition, strangely, herpes simplex corneal ulcers are not very painful.
[edit] Examination.
Observing the cornea with the ophthalmoscope set at +40 diopters (in effect fixing a 10× magnifying lens) may reveal the corneal ulcer. However, staining the cornea with fluorescein is more sensitive in identifying early ulcers. With more advanced infections, a layering of white cells in the anterior chamber (hypopyon) may be seen. This is best appreciated by SLE. With herpes zoster, involvement of the cornea (herpes zoster ophthalmicus) is more likely if the rash involves the tip of the nose (Hutchinson's) as both areas are supplied by the nasociliary branch of the first division of the trigeminal nerve.
[edit] Treatment.
If the corneal ulcer is small and due to trauma, antibiotic drops and patching the eye for a few days may be all that is needed. In patients with corneal ulcers due to impaired closure of the eye, patching and frequent application of a lubricating ointment allows the ulcer to heal and prevent recurrence. The patient should then be referred to an ophthalmologist for possible definitive treatment of the predisposing condition. If the corneal ulcer is due to herpes zoster, the patient should be prescribed any of the available oral herpes zoster antivirals, have his or her eye patched, and be referred immediately to an ophthalmologist.
[edit] Uveitis.
In general, inflammation of the iris or ciliary body is termed anterior uveitis, whereas involvement of the vitreous, retina, or choroid is termed posterior uveitis. Iritis describes involvement of the iris only and iridiocyclitis describes involvement of the iris-ciliary complex. Endophthalmitis describes inflammation predominantly of the vitreous body. Although inflammation of the unveal tract (iris, ciliary body, and choroid) is often idiopathic, it may be associated with many systemic disorders including sarcoidosis, tuberculosis, syphilis, Lyme disease, Behçet's disease, and various seronegative spondyloarthropathies—the HLA-B27–associated disorders (e.g., Reiter's syndrome, ankylosing spondylitis, inflammatory bowel disease, psoriasis). Distinguishing which segment of the uveal tract is involved is often beyond the skill of most primary care physicians, but is important as it determines the differential diagnosis, work-up, and treatment.
[edit] Anterior Uveitis (Iritis)
[edit] History.
The onset is usually subacute or insidious. Pain as well as photophobia, is present. Vision may be normal or blurred. Extraocular symptoms are present, if the uveitis is part of a systemic disorder.
[edit] Examination.
One or both eyes may be involved. The conjunctiva is injected, especially at the limbus (ciliary flush). The pupil may be constricted and, if adhesions (synechiae) have developed between the iris and the lens, the pupil may be irregular. On funduscopic examination, deposits may be seen on the posterior surface of the cornea (keratic precipitates). Floating inflammatory cells and protein are not usually seen with the direct ophthalmoscope but if the inflammation is severe enough, these cells may layer out in the lower portion of the anterior chamber (hypopyon).
[edit] Treatment.
No work-up is necessary for the patient with a first attack of unilateral, nongranulomatous anterior uveitis and an unremarkable comprehensive history and physical, but the patient should be referred to an ophthalmologist within 24 hours. A topical cycloplegic agent (homatropine hydrobromide 5%, atropine sulfate 1%) should be administered 2 to 3 times a day. If the patient has bilateral disease, recurrent disease, or granulomatous inflammation, a search for a systemic disorder is warranted.
[edit] Posterior Uveitis
[edit] History.
Either one or both eyes can be involved. Vision is decreased or blurred. Floaters are common. Onset may be acute or insidious. Again, if the eye is involved as part of a systemic disease, other symptoms referable to that disease may be present. As toxoplasmosis is the most common cause, a history of cat exposure or of AIDS (a significant risk factor) may be elicited.
[edit] Examination.
The conjunctivae and sclerae are clear. On ophthalmoscopy, the fundus may appear hazy due to inflammation of the vitreous. The optic disc appears swollen and indistinct. There may be retinal and choroidal hemorrhages, exudates, and vascular "sheathing," although these may be difficult to see with direct ophthalmoscopy.
[edit] Treatment.
A complete history and physical are mandatory with attention being paid to identify any of the disorders associated with posterior uveitis. If there is associated anterior segment inflammation, topical cycloplegic/mydriatic agents (e.g., 1% cyclopentolate, 2% homatropine) should be prescribed. The patient should be referred to an ophthalmologist within 24 hours. If a systemic disorder is present, work-up and treatment of that disease should occur concurrently.
[edit] Acute Angle-closure Glaucoma.
The ciliary body (located at the inner base of the iris next to the lens—the PC) produces the clear liquid aqueous humor that fills the AC and PC of the eye. The aqueous humor flows from the PC (just behind the iris and in front of the lens) through the pupil into the AC and into the trabecular meshwork. The meshwork functions as a one-way valve and filter. The ciliary muscle inserts on this meshwork and helps pump the aqueous humor through and increase the rate of drainage. The aqueous humor primarily drains into Schlemm's canal (located at the AC angle) and drains into episcleral veins. Any process that significantly disrupts this flow/drainage process may result in a significant increase in IOP. Predisposing risk factors for angle-closure glaucoma (see Chapter 173 ) usually involve any condition that reduces (narrows) the flow/drainage channels, e.g., hypermetropia (because of corneal shape), aging (lens thicken and push iris forward), or pupillary dilation (increases contact of the iris and the lens).
[edit] History.
Acute angle-closure glaucoma occurs most often in older individuals, particularly those who have hyperopia. Women are affected 3 to 4 times more often than men. Patients usually present with sudden onset of blurred vision and eye pain. There may be antecedent blurring of vision, halos about lights, and eye pain brought on by being in the dark or in dimmed ambient lighting. During an attack, the patient will have a headache and be nauseated and diaphoretic due to increased IOP. These symptoms may predominate and focus attention away from the eyes as their cause.
[edit] Examination.
The patient is obviously in pain and is photophobic. During an acute attack, only one eye is affected. Vision is decreased. There may be edema of the eyelids and the conjunctiva is injected. The pupil is midpoint and not reactive to light. There is corneal edema, which blurs the red reflex, and the IOP is elevated, often to a shallow AC.
[edit] Treatment.
Immediate referral to an ophthalmologist is indicated. The initial IOP-lowering therapies include decreasing aqueous humor production (using topical β-adrenergic antagonists and acetazolamide), reducing vitreous humor volume (using systemic hyperosmotic agents like intravenous mannitol), and facilitating aqueous humor outflow (using miotic agents like pilocarpine that pull the iris from the iridocorneal angle). In most cases, laser iridectomy (creating an alternative pathway for the egress of aqueous humor) reopens a portion of the angle with marked lowering of the IOP.
[edit] Endophthalmitis
[edit] History.
Endophthalmitis is most often related to recent eye surgery and can occur as a complication of a full-thickness wound to the globe. Infrequently, this condition is due to metastatic infection from a distant source (i.e., endogenous endophthalmitis). Pain is not always present. Vision is diminished, and the patient experiences floaters. Intravenous drug users, immunocompromised individuals, and patients with chronic indwelling intravenous lines are a risk for endogenous endophthalmitis. These patients are often very ill and septic.
[edit] Examination.
Conjunctival injection is present. The red reflex may be diminished and there may be a hypopyon. The vitreous may be hazy or the posterior pole of the fundus may be obscured due to inflammation of the vitreous. Patients with candidal endophthalmitis may have small focal areas of localized retinitis that enlarge into large vitreous opacities.
[edit] Treatment.
Immediate consultation with an ophthalmologist is indicated. In patients with endogenous endophthalmitis, treatment of the primary source of infection is necessary.