Correspondence

Treatment of Retinal-Artery Embolism

N Engl J Med 1994; 331:1592-1593December 8, 1994

Article

To the Editor:

Dickens et al. (July 28 issue)1 describe a patient who underwent directional coronary atherectomy with an excimer laser. The procedure was complicated by chest pain and the acute onset of blurred vision. Funduscopic examination revealed a white plaque in the left eye, occluding the inferior hemiretinal artery. This was interpreted as a fibrin embolus. After therapy, the visual acuity improved from 20/80- to 20/40, but the visual-field defect remained. Unfortunately, there is no mention of the treatment given. Even in the concluding remarks, in which the authors stress the need for immediate therapy in retinal-artery occlusion, the treatment (anticoagulants, fibrinolytic agents, or acetazolamide?) is not specified.

In a review of retinal emboli, Younge2 proposed that the most common types are the cholesterol embolus (or Hollenhorst plaque) and the calcific embolus. In a series of 85 patients with retinal embolism, Howard and Russell3 found 69 patients with cholesterol emboli, 15 with calcific emboli, and only 1 with a platelet-fibrin embolus. Cholesterol-crystal embolization occurs through the dislodgement of crystalline cholesterol from atheromatous plaques. Intraarterial manipulation is considered to be the most frequent precipitating event. Both vascular surgery and procedures involving angiography and angioplasty have been implicated. Another risk factor for cholesterol embolism is treatment with anticoagulants or fibrinolytic agents. The disruption of platelet-fibrin thrombi exposes the atheromatous material to the bloodstream.4,5

Cholesterol embolism is an increasingly frequent but underdiagnosed disorder.4 After the embolization of cholesterol to the retinal vasculature, bright refractile plaques can be observed at funduscopy.2,4 They cannot always be clearly distinguished from platelet-fibrin emboli. Mixed forms also occur. The fundus photograph in the article on the patient described1 in no way excludes the possibility of a cholesterol embolus. The chest pain can also fit with cholesterol embolization. The administration of anticoagulants or fibrinolytic agents to such patients can make the situation worse by producing repeated showers of cholesterol crystals. The treatment of disseminated cholesterol embolism is mainly symptomatic and supportive.

Anton K.M. Bartelink, M.D.
Johan P. Kappelhof, M.D.
Eemland Hospital, 3816 CP Amersfoort, the Netherlands

5 References

1. 1

   Dickens MA, Greven CM, Slusher MM. Retinal-artery embolism after directional coronary atherectomy. N Engl J Med 1994;331:278-279
   Full Text | Web of Science | Medline

2. 2

   Younge BR. The significance of retinal emboli. J Clin Neuroophthalmol 1989;9:190-194
   Medline

3. 3

   Howard RS, Russell RW. Prognosis of patients with retinal embolism. J Neurol Neurosurg Psychiatry 1987;50:1142-1147
   CrossRef | Web of Science | Medline

4. 4

   Om A, Ellahham S, DiSciascio G. Cholesterol embolism: an underdiagnosed clinical entity. Am Heart J 1992;124:1321-1326
   CrossRef | Web of Science | Medline

5. 5

   Case Records of the Massachusetts General Hospital (Case 38-1993). N Engl J Med 1993;329:948-955
   Full Text | Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: Space restrictions prohibited our discussing the various treatments available in retinal arterial occlusive disease. The treatment depends on multiple factors, including the duration of symptoms, type of embolus, timing of referral, location of occlusion. In this case, because of the duration of the occlusion, we performed ocular digital massage, used ocular hypotensive medications in an attempt to allow the embolus to pass distally. Because the patient was already receiving oxygen therapy, this therapy was continued for an additional 24 hours. The improvement in visual acuity noted was not due to our therapy, but rather to the natural history of resolving edema in patients with branch-retinal-artery occlusions involving the fovea.

It is sometimes difficult to differentiate cholesterol, calcific, and platelet-fibrin emboli on ophthalmoscopy. Drs. Bartelink and Kappelhof suggest that our patient had a cholesterol embolus. However, our patient's embolus was not refractile, as are most cholesterol emboli. In addition, cholesterol emboli alone rarely cause retinal infarction, because they do not completely occlude the vessel. Clinically, this appeared to be a platelet-fibrin embolus.

We are intrigued with their comment that fibrinolytic agents and anticoagulants may cause repeated events. We do not use anticoagulants or fibrinolytic agents in patients with central-retinal-artery occlusion or branch-retinal-artery occlusion, because their efficacy has not been confirmed and these agents may have substantial nonocular side effects.

M. Alan Dickens, M.D.
Craig M. Greven, M.D.
M. Madison Slusher, M.D.
Wake Forest University Eye Center, Winston-Salem, NC 27157-1033

Citing Articles (2)

Citing Articles

1. 1

   Vctor R. Blanco, Csar Mors, Vicente Barriales, Carmen Gonzlez. (2000) Retinal cholesterol emboli during diagnostic cardiac catheterization. Catheterization and Cardiovascular Interventions 51:3, 323-325
   CrossRef

2. 2

   S. F. Egger, H. Domanovits, C. Scholda, V. P. Vecsei, V. Huber-Spitzy. (1999) Stellt eine Thrombolysetherapie bei akutem Myocardinfarkt ein Risiko für retinale Embolien dar?. Spektrum der Augenheilkunde 13:4, 148-150
   CrossRef