Managing eye disease in primary care

Part 3. When to refer for ophthalmologic care

Steven R. Shields, MD

VOL 108 / NO 5 / OCTOBER 2000 / POSTGRADUATE MEDICINE

CME learning objectives

• To understand the levels of urgency for ophthalmologic referral for common eye symptoms
• To recognize which eye conditions require immediate treatment until an ophthalmologic consultant is available
• To learn appropriate initial management of ocular trauma, chemical eye injuries, and elevated intraocular pressure

The author discloses no financial interests in this article.

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Preview: In the final part of this three-part article, Dr Shields reviews ocular conditions that mandate referral to an ophthalmologist. He also gives recommendations about how to intervene with specific conditions, such as ocular trauma and chemical injuries, until an ophthalmology consultant is available to assume responsibility for patient care.
Shields SR. Managing eye disease in primary care: part 3. When to refer for ophthalmologic care. Postgrad Med 2000;108(5):99-106

Certain ocular signs and symptoms always warrant ophthalmologic referral. The urgency of referral depends on the nature of symptoms and signs present (table 1: not shown) or the extent of an eye injury (table 2: not shown). For five specific symptomatic eye conditions, initial management in the primary care setting is crucial to long-term visual outcome. Two of these conditions are injury-related: suspected high-velocity injuries and chemical injuries. The other three can produce acute, persistent vision loss: angle-closure glaucoma, arteritic anterior ischemic optic neuropathy, and central retinal artery occlusion.

Ocular injuries

Other than superficial corneal and conjunctival foreign bodies and abrasions (see part 2 of this three-part article), ocular injuries usually warrant ophthalmologic referral for evaluation of penetrating or perforating injuries of the globe. A penetrating injury enters only part of a tissue or organ, whereas a perforating injury passes completely through. For example, a carpentry nail that passes through the cornea into the anterior chamber of the eye perforates the cornea but only penetrates the globe.

Most eye traumas that warrant ophthalmologic management (table 2) are obvious on initial physical examination and require little or no intervention in the primary care setting. However, high-velocity injuries and chemical injuries deserve special comment because the seriousness of the injury is not always immediately apparent and, therefore, visual outcome is highly dependent on competent initial management.

High-velocity injuries
Eye injuries produced by high-velocity missiles (eg, those incurred during motor vehicle accidents or while hammering or lawn mowing) should be treated as penetrating globe injuries until proved otherwise. Small perforations of the cornea and sclera (figure 1: not shown) can look identical to superficial (ie, nonglobe-penetrating) corneal or conjunctival injuries. Inspection of the injury site with fluorescein sodium dye does not differentiate between superficial injuries and perforating injuries of the cornea and sclera. Therefore, accurate history taking is crucial in identifying patients at high-risk of occult penetration or perforation of the globe. Such patients should be referred immediately on the basis of the history alone, even if no physical signs are present (1).

A tragic case that I managed during my ophthalmology residency illustrates the potential seriousness of high-velocity injuries. A retired university professor who enjoyed sculpting miniature stone figures presented to his family physician with the complaint that "something flew into my eye" during a sculpting session. On history taking, he reported that he had not been wearing eye protection. An initial eye examination apparently revealed only evidence of mild superficial irritation of the eye. His symptoms worsened despite treatment with topical antibiotic drops. When the patient was referred to me several days later, his eye was severely inflamed and he had rapidly declining vision. Slit-lamp examination revealed a microscopic wound at the limbus and florid endophthalmitis. Despite immediate vitrectomy and administration of intraocular antibiotics, the patient lost his eye because of an almost invisible globe penetration.

Chemical injuries
"Treat first, examine later." A chemical injury to the eye is one of the rare instances in which treatment must be initiated immediately on the basis of patient history alone. By far the most serious chemical injuries are alkaline burns from such products as household cleaners, fertilizers, and pesticides (figure 2: not shown). Even a few seconds or minutes of exposure to undiluted strong alkali can result in irreversible vision loss. The appearance of a "white and quiet" eye soon after an alkaline injury is an ominous sign of chemical obliteration of the conjunctival and episcleral vessels.

If you are notified by phone about a potentially serious chemical eye injury, instruct the caller to begin immediate irrigation of the eye with water (or any drinkable fluid if water is not readily available) and to arrange ambulance transport. Irrigation should be continued until the patient reaches the emergency department. Any patient who presents with a suspected chemical eye injury should be given immediate treatment (table 3) until an ophthalmologist is available to assume care of the patient.

Table 3. Management of chemical eye injuries

1. Whenever possible, identify the chemical. Ask patient to bring in the container or a sample of the product. 2. Briefly rule out globe perforations. Chemical explosions (eg, those involving a battery) may also produce an open globe injury or intraocular foreign bodies. 3. Use topical anesthetics liberally to facilitate irrigation and examination. A 1%-4% solution of lidocaine HCl (Xylocaine) can be used if proparicaine HCl or tetracaine HCl (Alcaine, Ophthaine, Ophthetic) is not readily available. 4. Irrigate the superior and inferior cul-de-sacs and remove any foreign bodies that may act as a depot for the chemical. Intravenous tubing connected to a container of normal saline or lactated Ringer's solution makes an ideal irrigation tool. A lid speculum greatly facilitates irrigation. 5. Continue irrigation with water or normal saline solution for at least 20 minutes. 6. After 20 to 30 minutes, perform a brief eye examination, including vision testing. 7. Five to 10 minutes after stopping irrigation, touch dry litmus paper to the inferior cul-de-sac to test pH. 8. Repeat irrigation in 20- to 30-minute intervals until pH is nearly neutral (pH 7) when checked 5 to 10 minutes after irrigation or until an ophthalmologic consultant assumes care of the patient.

Causes of acute, persistent vision loss

Many causes of acute, persistent vision loss (eg, retinal detachment, vitreous hemorrhage, optic neuritis) require little or no intervention in the primary care setting other than timely referral. However, for three relatively frequent causes--suspected acute angle-closure glaucoma, optic nerve infarction, and central retinal artery occlusion--appropriate management by an astute primary care physician can mean the difference between intact vision and blindness in affected patients. Therefore, in all patients who present with acute, persistent vision loss, careful history taking and eye examination are important to avoid preventable causes of permanent vision loss going undetected.

Acute angle-closure glaucoma
Pupillary block glaucoma is the most common form of acute angle-closure glaucoma seen in primary care. The classic presentation is severe aching in one eye, blurred vision, colored halos around point sources of light, circumlimbal hyperemia, dull corneal reflex, shallow anterior chamber, and mid-dilated, nonreactive pupil (figure 3a: not shown). Chief complaints can vary from a vague sense of discomfort of the eye to severe nausea and vomiting. Therefore, patients who present with acute eye pain--even though it is not their primary symptom--and any signs suggestive of acute glaucoma should have their intraocular pressure measured.

Intraocular pressure is measured in an anesthetized eye with a Schiøtz or Tono-Pen tonometer. The normal range is 6 to 22 mm Hg. A presumptive diagnosis of acute angle-closure glaucoma can be made when intraocular pressure is significantly asymmetrical (eg, 12 mm Hg in the asymptomatic eye and 24 mm Hg in the symptomatic eye) or when the pressure in the affected eye is above 30 mm Hg. However, intraocular pressure of less than 50 mm Hg is uncommon in patients presenting with acute vision loss and pain.

Delayed treatment of pupillary block glaucoma can cause chronic synechial angle-closure glaucoma, permanent corneal edema, retinal vascular occlusions, optic atrophy, and permanent blindness. Even several hours of highly elevated intraocular pressure that goes untreated can result in permanent vision impairment. Initial treatment involves use of aqueous suppressants, osmotic diuretics, and low- to medium-strength pilocarpine hydrochloride. Strong miotics and mydriatic-cycloplegic agents (eg, atropine sulfate, cyclopentalate hydrochloride [AK-Pentolate, Cyclogyl, Pentolair], phenylephrine hydrochloride) may exacerbate the attack and should be avoided. Table 4 outlines typical initial management of severely elevated intraocular pressure. An ophthalmologist should be consulted so that treatment can be individualized.

Table 4. Initial management of acute angle-closure glaucoma

1. Page ophthalmologist on-call. 2. Initiate pharmacologic lowering of intraocular pressure by first ruling out contraindications to drugs used:    a. Beta blockers: bronchial asthma, severe emphysema, overt cardiac failure, second- or third-degree heart block    b. Carbonic anhydrase inhibitors: sulfur allergy, marked kidney or liver disease, significant electrolyte or acid-base imbalance    c. Alpha2 agonists: use of monoamine oxidase inhibitors    d. Osmotic diuretics: anuria, severe dehydration, severe cardiac failure, pulmonary edema 3. Instill 1 drop each of 0.5% timolol maleate (Betimol, Timoptic), 1% apraclonidine HCl, and 2% pilocarpine HCl to affected eye, and give 500 mg oral acetazolamide (Dazamide, Diamox). 4. Wait at least 1 minute between each drop to allow absorption. 5. Reapply drops every 5 minutes for three repetitions. 6. Recheck intraocular pressure 30 to 60 minutes after last drop instilled. If pressure remains above 35 mm Hg, repeat topical drops as above, and give isosorbide (Ismotic), 1 to 1.5 g/kg by mouth. Or, if the patient is too nauseated to take oral osmotics, establish intravenous access and give 15% or 20% mannitol (Osmitrol), 0.5 to 2 g/kg over 20 minutes. 7. Recheck intraocular pressure 1 to 2 hours later, and continue medical intervention until ophthalmologic consultant is available.

The most common definitive therapy for pupillary block glaucoma is neodymium:yttrium-aluminum-garnet (Nd:YAG) laser iridotomy. When corneal edema precludes this procedure, surgical iridectomy is performed.

Arteritic anterior ischemic optic neuropathy
Anterior ischemic optic neuropathy (figure 3b: not shown) is caused by infarction of the anterior aspect of the optic nerve. It produces a pale swelling of part or all of the optic nerve head and sudden, painless loss of vision. The vision loss in the infarcted area of the optic nerve is irreversible. The majority of cases of anterior ischemic optic neuropathy are associated with systemic hypertension, diabetes, or arteriosclerosis and, therefore, are nonarteritic. Bilateral blindness from nonarteritic causes is uncommon. Although affected patients are at increased risk for cerebrovascular events and myocardial infarctions, overall life expectancy at 3 years is unchanged (2).

In contrast, anterior ischemic optic neuropathy caused by giant cell arteritis is associated with irreversible blindness in the contralateral eye in one third of cases within days or weeks of onset unless treated appropriately. Unfortunately, the fundus in both nonarteritic and arteritic anterior ischemic optic neuropathy may appear to be identical (3) (figure 3b: not shown). Therefore, the diagnosis must be suspected on the basis of nonocular findings.

Giant cell arteritis is a disease of the elderly. It rarely affects persons younger than 55 years, and the incidence increases with age (about 11 cases per 100,000 persons aged 50 and over, 27 cases per 100,000 persons over age 70) (4). Optic nerve infarction occurs in up to 50% of cases. Unilateral (or, rarely, bilateral) vision loss may be minimal, although it is often profound.

Review of systems may reveal a history of headache and jaw claudication, malaise, anorexia, fever, joint and muscle aches, and proximal weakness (polymyalgia rheumatica). However, some patients report no systemic symptoms. An elevated erythrocyte sedimentation rate (ESR), the only laboratory sign, is absent in up to 10% of cases.

Management of suspected arteritic anterior ischemic optic neuropathy consists of immediate high-dose corticosteroid therapy to prevent blindness in the contralateral eye and a temporal artery biopsy to confirm the diagnosis. For example, intravenous methylprednisolone sodium succinate (A-Methapred, Solu-Medrol), 250 mg every 6 hours, can be given for the first 24 to 48 hours, followed by a tapering dose of oral prednisone until biopsy results become available. Serial ESR measurements can guide therapy. Corticosteroids usually should not be administered for more than a year, because the disease typically resolves long before then.

Although far less common than arteritic anterior ischemic optic neuropathy, giant cell arteritis also has been associated with ocular motility disturbances (eg, third nerve palsy), ptosis, and central retinal artery occlusion.

Central retinal artery occlusion
Like anterior ischemic optic neuropathy, central retinal artery occlusion causes sudden, painless loss of vision. The only way to differentiate the two conditions is to know the typical fundus appearance of each (figures 3b through 3d: not shown).

Retinal artery occlusions usually result from thrombosis or embolism. Systemic arteriosclerosis is the most common underlying condition. Less common causes include cardiogenic emboli, vasculitis (including giant cell arteritis), and hypercoagulable states.

Experimentally, total occlusion of the central retinal artery causes irreversible, complete infarction of the retina within 100 minutes. However, clinical cases of the disorder are often incomplete; therefore, intervention begun several hours after onset still may restore some vision. Unfortunately, a reliable treatment is lacking at present (5). Nonetheless, it is reasonable to attempt to dislodge the thrombus or clot from the vessel in patients presenting within 24 hours of onset of decreased vision.

Treatment consists of immediate lowering of intraocular pressure or vasodilation, or both. This approach theoretically reduces resistance to a thrombus or embolus moving distally, thereby limiting the extent of retinal infarction. The simplest method of mechanically lowering intraocular pressure and producing transient vasodilation is alternate compression and rapid decompression of the eye. Firm digital pressure sufficient to produce mild discomfort is applied to the globe for 10 to 15 seconds. Sudden release of pressure produces an immediate decrease in intraocular pressure and vasodilation. This procedure can be repeated multiple times. Inspection of the fundus between repetitions of digital pressure can reveal whether blood flow has returned to the retinal circulation.

Other treatments that have been tried for central retinal artery occlusion include topical beta blockers, intravenous acetazolamide, oral nitrates, inhalation of carbogen (a mixture of 95% oxygen and 5% carbon dioxide), and anterior chamber paracentesis. No one treatment has proved more effective than another. Consequently, overall prognosis for vision recovery remains poor.

Patients with retinal artery occlusions or unexplained amaurosis fugax (transient monocular blindness) should undergo evaluation for arteriosclerotic risk factors, and noninvasive studies of the heart and carotid arteries should be performed to detect sources of emboli. Patients with visible emboli at the time of retinal infarction have a strikingly lower life expectancy owing to subsequent stroke and cardiovascular disease (6). Also, an ESR measurement should be obtained, because up to 2% of cases of central retinal artery occlusion are associated with giant cell arteritis.

Summary

Most severe eye diseases and injuries ultimately require intervention by an ophthalmologist. The urgency of referral depends on various factors, including level of vision loss, duration of symptoms, and presence of comorbid diseases. Of special importance are five acute eye problems in which emergency management by primary care physicians can be critical to visual outcome: high-velocity injuries, chemical injuries, acute angle-closure glaucoma, arteritic ischemic optic neuropathy, and central retinal artery occlusion.

References

1. Trobe JD. The physician's guide to eye care. San Francisco: American Academy of Ophthalmology, 1993:65-76
2. Guyer DR, Miller NR, Auer CL, et al. The risk of cerebrovascular and cardiovascular disease in patients with anterior ischemic optic neuropathy. Arch Ophthalmol 1985;103(8):1136-42
3. Hayreh SS. Anterior ischaemic optic neuropathy: differentiation of arteritic from non-arteritic type and its management. Eye 1990;4(Pt 1):25-41
4. Trobe (1), p 142
5. Brown GC. Retinal arterial obstructive disease. In: Ryan SJ, ed. Retina. 2d ed. St Louis: Mosby, 1994:1361-8
6. Savino PJ, Glaser JS, Cassady J. Retinal stroke: is the patient at risk? Arch Ophthalmol 1977;95(7):1185-9

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