CENTRAL RETINAL ARTERY OCCLUSION Sudden, profound, painless, monocular loss of vision is characteristic of a central retinal artery occlusion (CRAO). The event is often preceded by episodes of amaurosis fugax. The first branch off the internal carotid artery is the ophthalmic artery, which supplies the central retinal artery, which, in turn, provides the blood supply to the inner retina. If the central retinal artery becomes occluded, the retina will infarct and become pale, less transparent, and edematous. The macula is the thinnest portion of the retina and the intact underlying choroidal circulation remains visible through this section of retina, creating the illusion of a "cherry-red spot." In fact, the macular area tends to maintain its normal color while the surrounding ischemic retina turns pale, thus causing this classic finding on funduscopy (Fig 230-17, Plate 17). An APD is a common finding associated with a CRAO. Causes include embolus (carotid and cardiac), thrombosis, giant-cell arteritis, vasculitis (lupus), sickle cell disease, and trauma. Often the patient will have atrial fibrillation. The retina will sustain irreversible damage within 90 min of total occlusion, so treatment should begin immediately. Unfortunately these patients rarely respond to therapy, but because the visual loss is usually so profound, every attempt should be made to reestablish circulation to the retina. Treatment in embolic cases (the majority) is aimed at trying to convert a CRAO into a branch retinal artery occlusion (BRAO). In the attempt to dislodge the embolus from the central artery and into one of its retinal branches, the other retinal branches may become reperfused, thereby reducing the size of the infarct. Maneuvers include digital massage, IOP-lowering drugs, and vasodilation techniques (breathing into a paper bag to increase Pa CO2). An ophthalmologist should be consulted immediately to evaluate the patient and decide whether performing an IOP-lowering anterior chamber paracentesis is indicated.
FIG. 230-17. (PJate_17). Central retinal artery occlusion. Note macular "cherry-red spot" and retinal pallor between macula and disk. The retinal veins appear normal size, but the arteries are barely visible and attenuated.
1. Consult ophthalmology the moment the diagnosis is made.
2. Administer ocular massage: Firm, steady digital pressure on the globe through closed lids for about 15 s, followed by sudden release of pressure. This may be repeated several times.
3. Administer topical b blocker (Timoptic 0.5%), one drop.
4. Give Diamox 500 mg IV or PO.
5. Consider having the patient breathe into a paper bag for 5 to 10 min if there are no respiratory contraindications.
CENTRAL RETINAL VEIN OCCLUSION Thrombosis of the central retinal vein causes retinal venous stasis, edema, and hemorrhage. Loss of vision is variable, painless, monocular, and rapid. Funduscopic examination typically reveals optic disk edema and diffuse retinal hemorrhages in all quadrants ("blood-and-thunder fundus," Fig 2.30-18, Plate 18). The contralateral optic nerve and fundus are generally normal, which helps distinguish central retinal vein occlusion (CRVO) from papilledema, and the diffuse retinal hemorrhages help distinguish it from optic neuritis (the peripheral retina is normal in optic neuritis). Typically these patients have a history of hypertension, although hypercoagulable disorders, vasculitis, and glaucoma may also be associated. No specific treatment is available, although the addition of aspirin 60 to 325 mg daily is reasonable. These patients should be referred to an ophthalmologist for confirmation of the diagnosis and monitoring of ischemia-induced neovascularization.
FIG. 230-18. (PlateJ8). Central retinal vein occlusion "blood and thunder fundus." Note diffuse retinal hemorrhages in all retina quadrants and blurred disk margins.
1. Ophthalmology referral.
2. Consider aspirin 60 to 325 mg/day PO.
GIANT-CELL ARTERITIS (TEMPORAL ARTERITIS) Giant-cell arteritis (GCA) is a systemic vasculitis involving medium-sized arteries in the carotid circulation and can include the aorta and its primary branches. GCA can cause a painless ischemic optic neuropathy with devastating visual consequences and rapid contralateral involvement if not diagnosed and treated promptly. Patients are generally over 50 years of age and frequently have a history of polymyalgia rheumatica. Women are more commonly affected than men. Symptoms may include headache, jaw claudication, myalgias, fatigue, fever, anorexia, and temporal artery tenderness. Up to 33 percent may have associated neurologic symptoms such as transient ischemic attacks or stroke. The patient can develop rapid and profound visual loss, with the contralateral eye becoming involved within days to weeks. The physical examination will frequently reveal an APD if the optic nerve circulation is involved. An elevated Westergren sedimentation rate is usually present, with the majority of biopsy-proven cases in the range of 70 to 110. The added presence of an elevated C-reactive protein also suggests the diagnosis. Treatment consists of several doses of intravenous steroids, followed by oral steroids. Steroids should not be delayed while waiting for a temporal artery biopsy to be performed. Biopsies will still be positive a week after initiation of steroid therapy.
1. Order sedimentation rate and C-reactive protein.
2. Consult patient's personal physician.
3. If highly suspicious or any visual loss: Admit for methylprednisolone 250 mg q 6 h IV for 3 days and temporal artery biopsy.
4. If not suspicious and no visual involvement: prednisone 80 to 100 mg PO per day and close outpatient monitoring.
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