SIGNS AND SYMPTOMS
The patient typically is elderly and often has concurrent history of hypertension, diabetes, carotid artery disease, peripheral vascular disease, hypercholesterolemia, hyperlipidemia, and/or atherosclerosis. The patient may be totally asymptomatic and the plaque(s) may be found on routine eye exam.
However, the patient may have previously experienced transient episodes of monocular blindness (amaurosis fugax). Rarely, the patient has experienced a transient ischemic attack with hemiparesis, paraesthesia, and/or aphasia. These episodic bouts of amaurosis fugax may be quite frequent, and may last from several seconds to several minutes. Rarely does the patient have any lasting visual deficits.
Frequently, the patient previously experiencing amaurosis fugax will not exhibit retinal emboli, but may have arteriolar narrowing and sheathing. A Hollenhorst plaque appears as a bright, glistening, refractile plaque, usually at the bifurcation of a retinal arteriole. These have the propensity to break up and move, and may not be present at subsequent visits.
The Hollenhorst plaque is an embolus composed of cholesterol that forms from an ulcerated ipsilateral carotid artery plaque. The patient frequently has concurrent hypertension and elevated cholesterol levels. The stress on the arteries induced by hypertension leads to reduced elasticity of the vessels.
Cholesterol is deposited within the vessel walls and forms an atheroma, narrowing the artery. Turbulent blood flow over the atheroma can lead this plaque to ulcerate, which allows small particles to break off and flow within the blood stream. Eventually, the embolus enters a vessel whose caliber is too small to allow it to flow any further, and it lodges. Ischemia to the tissue occurs if blood flow is significantly impaired distal to the blockage. If the emboli lodges within a retinal vessel, then retinal ischemia with corresponding loss of vision occurs. The result may be a retinal artery occlusion.
In the case of cholesterol emboli, however, the blockage often quickly dislodges without permanent visual impairment. Instead, the patient experiences a brief interruption of vision and/or visual field (amaurosis fugax). Multiple bouts of amaurosis fugax may indicate multiple emboli. In cases where the patient is asymptomatic, yet a Hollenhorst plaque is visible, there is rarely permanent ischemia. This is because the cholesterol emboli are malleable and blood flow may be able to get past the emboli.
There is no direct treatment of the visible emboli. In fact, because blood often can flow through an apparently complete blockage, direct removal is not necessary. In any case of retinal embolization, the concern must be further embolization with ensuing retinal infarct or cerebrovascular accident with permanent sequela of stroke. Survival rate decreases with the appearance of a retinal embolus. The primary cause of mortality in patients with retinal emboli is coronary artery disease and myocardial infarction.
A retinal embolus indicates significant systemic vascular disease. Refer the patient to an internist, vascular surgeon, or cardiologist for hypertension, coronary artery disease, diabetes, and carotid artery disease. A complete physical, carotid ultrasound, stress echocardiogram, fasting glucose and lipid levels, and blood chemistry with cardiac enzymes are indicated. Treatment of carotid stenosis, TIAs, and retinal emboli may include carotid endarterectomy, carotid angioplasty, or aspirin therapy, depending upon the risks of future ischemic events.
Patients with cholesterol emboli have a 15 percent mortality rate in the first year, 29 percent by the third year, and 54 percent by the seventh year. The main cause of mortality is cardiac death.
The patient, though in no apparent distress, must be referred to the proper medical specialist in order to appropriately manage the underlying systemic diseases and reduce morbidity and mortality.