Postprandial blindness.

Abstract

A 73-year-old man presented with a four-month history of blurred vision and diplopia while resting after meals. A quarter of an hour after a meal he developed blurring of vision and diplopia which worsened over the next 15 minutes. For the next half to two hours he was able to distinguish only light and dark. He complained of dizziness and slight nausea during this period, but had no loss of consciousness or sweating. The duration of the symptoms was proportional to the size of meal. Between meals his visual acuity was 6/9 bilaterally. For the two years before admission he had complained of dizziness, diplopia, and blurred vision after walking a decreasing distance (about 100 yards on admission) or on rising abruptly from a supine to standing position. These symptoms lasted for about 15 minutes on resting. In 1951 he had had a partial gastrectomy for duodenal ulcer from which he had noted no long-term problems. He smoked 20 cigarettes a day. The only palpable pulses in the limbs were the right femoral and popliteal with a femoral bruit. The right carotid pulse was very weak. The left carotid pulse was easily palpable with a bruit high in the neck. His blood pressure, measured with a large cuff on the right thigh, was 140/90 mm Hg (lying and standing) with a heart rate of 80/min in sinus rhythym. An electrocardiogram, chest radiograph, and 50-g glucose tolerance test (blood glucose and insulin) were within normal limits. After admission his symptoms occurred after eating a meal. His visual acuity was reduced to perception of finger movements. After a meal given under test conditions, however, his visual acuity, pulse, blood pressure (lying and standing), and electrocardiogram remained stable with blood glucose, insulin, pancreatic, and small intestinal enzyme profiles within normal limits. Arch aortography showed occlusions of the innominate artery and the proximal left subclavian artery. The right common carotid artery was patent but the right internal carotid was stenosed at its origin; both were filled only on late films via collaterals. Thus all the circulation to the brain passed through the patent left common carotid to the also stenosed left internal carotid, and through collaterals from the thorax to the vertebral and right internal carotid arteries. A left carotid endarterectomy was performed. The stump pressure in the intemal carotid artery was only 28 mm of blood. A Javid shunt was used for cerebral protection. Histology of the arterial wall showed atherosclerosis and calcification. His recovery was uncomplicated and he is now free of his postprandial symptoms. Selective left carotid angiography showed that the proximal segment of the internal carotid artery appeared normal.