2. Johnson RN, Gass JDM. Idiopathic macular holes: observa-tions, stages of formation, and implications for surgical inter-vention. Ophthalmology 1988;95:917-24.

3. de Bustros S, The Vitrectomy for Prevention of Macular Hole Study Group. Vitrectomy for prevention of macular holes: results of a randomized multicenter clinical trial. Ophthalmol-ogy 1994;101:1055-9.

4. Williams GA. Vitrectomy for prevention of macular holes: results of a randomized multicentered clinical trial: discussion. Ophthalmology 1994; 101:1060.

5. Wendel RT, Patel AC, Kelly NE, Salzano TC, Wells JW, Novack GD. Vitreous surgery for macular holes. Ophthalmol-ogy 1993;100:1671-6.

Vitreous Hemorrhage and Retinal Vein Rupture Eddie F. Kadrmas, M.D., and John M. Pach, M.D.

PURPOSE/METHODS: We examined a 23-year-old woman who had a sudden onset of floaters after self-induced emesis. RESULTS/CONCLUSIONS: Examination showed a dense vitreous hemorrhage originating from a rupture site in the wall of the superotemporal branch vein. We postulate a preexisting weakness in the retinal vein wall as a predisposing factor to rupture. This mechanism may explain some cases of vitreous hemorrhage associated with a Valsalva maneuver.

A 23-YEAR-OLD WOMAN HAD A SUDDEN ONSET OF floaters in her left eye immediately after self-

induced emesis. Her medical history was remarkable only for mild acne for which she was taking tetracy-cline, 250 mg orally twice a day. Ocular history and family history were unremarkable.

Examination approximately 90 minutes after the event disclosed a visual acuity without correction of R.E.: 20/20 and LE.: 20/80. Pupils were equal and reactive to light and were without an afferent pupil-lary defect. Tensions by applanation tonometry were 18 mm Hg in both eyes. Confrontational visual fields

Department of Ophthalmology, Mayo Clinic and Mayo Foundation. Supported in part by an unrestricted grant from Research to Prevent Blindness, Inc., New York, New York, and the Mayo Foundation, Rochester, Minnesota.

Inquiries to John M. Pach, M.D., Department of Ophthalmology, Mayo Clinic, 200 First St. S.W., Rochester, MN 55905.

Fig. 1 (Kadrmas and Pach). Fundus photograph shows a large area of layered preretinal hemorrhage superotem-poral to the fovea. Enlargement, magnified view of the superotemporal branch vein demonstrates a rupture site in the vessel wall (arrow).

and extraocular eye movements were intact in both eyes. The anterior segments were normal. Fundus examination of the left eye showed a large area of layered preretinal hemorrhage superotemporal to the fovea as well as a smaller preretinal hemorrhage inferior to the disk (Fig. 1). We observed a more diffuse area of vitreous hemorrhage over the inferior half of the macular region that was funneling into a pocket in the formed vitreous and creating a large collection of intravitreal blood inferiorly. An area of discontinuity in the wall of the superotemporal branch vein with surrounding intraretinal hemor-rhage was seen above the large layered preretinal hemorrhage (Fig. 1). A small stream of preretinal blood, connected with the layered preretinal hemor-rhage below, originated from a rupture site in the vessel wall, which was occluded by a small white plug, presumably fibrin. Results of fundus examination of the right eye were unremarkable. A pinpoint hyper-fluorescence in the wall of the superotemporal branch vein corresponded to the rupture site on fluorescein angiography (Fig. 2).

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Fig. 2 (Kadrmas and Pach). Late-phase fluorescein angiogram demonstrates pinpoint hyperfluorescence (ar-row) in the wall of the superotemporal branch vein.

The next day her visual acuity returned to 20/20 in the left eye, with clearing of the overlying vitreous hemorrhage in the macula. Three weeks later the vessel appeared to be normal except for a trace amount of intraretinal hemorrhage and retinal thick-ening surrounding the rupture site. A partial posterior vitreous detachment had developed.

Valsalva hemorrhagic retinopathy was first coined by Duane1 in 1972 to describe retinal and vitreous hemorrhage in association with emesis, coughing, straining at stool, or heavy lifting. Patients often note a sudden decrease in vision in association with a Valsalva maneuver. Hemorrhages typically are located in or near the fovea and are often immediately beneath the internal limiting membrane and are intraretinal in location. The hemorrhages may break through into the vitreous cavity or may also occasion-ally extend into the subretinal space. The visual prognosis is excellent, with most patients returning to their previous level of visual acuity, as occurred with our patient.

The presumed mechanism of retinal hemorrhage in Valsalva retinopathy is thought to be a rupture of superficial retinal capillaries caused by a sudden increase in retinal venous pressure after a rapid increase in intrathoracic or intra-abdominal pres-sure.2 In our patient's case, this sudden increase in venous pressure apparently caused a direct rupture of

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the wall of a relatively large-caliber vein. We postulate a preexisting weakness, either congenital or acquired, in the retinal vein wall as a predisposing factor for rupture. This mechanism may explain some cases of vitreous hemorrhage associated with a Valsalva ma-neuver.

REFERENCES

1. Duane TD. Valsalva hemorrhagic retinopathy. Trans Am Ophthalmol Soc 1972;70:298-313.

2. Balles MW. Traumatic retinopathy. In: Albert DM, Jakobiec FA, editors. Principles and practice of ophthalmology. Phila-delphia: WB Saunders, 1994:1030.

Delayed Fellow Eye Involvement in Acute Retinal Necrosis Syndrome Eric Ezra, F.R.C.S., Russell V. Pearson, F.R.C.S., David E. Etchells, F.R.C.S., and Zdenek J. Gregor, F.R.C.S.

PURPOSE/METHOD: We studied a case of acute retinal necrosis in which a 30-year delay occurred between involvement of the first and fellow eyes. After systemic treatment with acyclovir and pred-nisolone, the fellow eye developed a retinal detach-ment requiring vitrectomy and silicone oil tam-ponade.

RESULTS/CONCLUSION: The fellow eye retained a useful Snellen acuity of 20/120. In a patient who has had acute retinal necrosis, any symptoms or signs in the fellow eye, even several decades later, should alert the examining physician to the possi-bility of delayed involvement of the fellow eye.

THE ACUTE RETINAL NECROSIS SYNDROME IS A VISU-

ally devastating condition, characterized by an acute panuveitis, retinal vasculitis, and midperipheral retinal necrosis.1 The development of multiple atrophie retinal breaks followed by retinal detach-ment is common,1 and early diagnosis and treatment with systemic acyclovir is associated with an improved

Vitreo-retinal Service, Moorfields Eye Hospital (E.E., R.V.P., Z.J.G.); and Department of Ophthalmology, Royal Victoria Hospital (D.E.E.).

Inquiries to Eric Ezra, F.R.C.S., Vitreo-retinal Service, Moorfields Eye Hospital, City Road, London EC1V 2PD, United Kingdom; fax: (44) 71-2534696.

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