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Figure 1. Color fundus photograph showing multiple areas of superficial ischemic retinal whitening and retinal hemorrhages adjacent to the optic discs in each eye.
Figure 2. Color fundus photograph taken eight weeks after the photographs seen in Figure 1 . Compared to the initial presentation, nearly complete resolution of the lesions is noted.
A 33-year-old alcoholic man was admitted for acute pancreatitis. Amylase and liver function tests were moderately elevated. The patient denied any recent history of trauma. During his hospitalization, he noted bilateral onset of blurred vision. Visual acuity was correctable to 20/40 OU. The anterior segment examination was unremarkable OU. Both fundi showed multiple areas of superficial ischemic retinal whitening in the posterior poles and retinal hemorrhages adjacent to the optic discs (Figures 1A & B).
Photographs taken eight weeks after initial presentation show nearly complete resolution of the lesions (Figures 2A & B). Visual acuity was 20/20 OU with no signs or symptoms at one-year follow-up.
Purtscher's retinopathy typically presents with visual loss following compression injury to the head or thorax. A similar fundus appearance has also been described following pregnancy, retrobulbar injection, long bone fractures, or after involuntary Valsalva maneuver. Also, patients with acute pancreatitis, renal failure, central retinal artery occlusion, or collagen vascular disorders may have similar ocular manifestations.1 Purtscher's retinopathy can be unilateral or bilateral. Characteristic findings include multiple areas of superficial retinal whitening, soft exudates, and retinal hemorrhages adjacent to the optic disc. Fluorescein angiography may reveal leakage of dye from small retinal vessels near the white lesions, and in more severe cases, arteriolar obstruction and leakage.1 Late perivenous staining, optic disc edema, and capillary nonperfusion have been described as well.2
The pathogenesis of Purtscher's retinopathy is not clear and multiple theories have been proposed. Complement-induced granulocyte aggregation and leukoembolization have been suggested in some reports.3,4 Primary endothelial damage to the peripapillary retinal vessels may be involved as well. Other proposed mechanisms include air, or fat emboli, or intravascular transmission of a hydrostatic pressure wave through the venous system of the head and neck into the retinal circulation.2 The suàen increase in venous pressure may cause direct endothelial damage or may result in a disturbance of autoregulation of die retinal vessels leading to subsequent loss of vascular integrity.
The lesions in Purtscher's retinopathy typically resolve and vision usually improves, altliough some patients have residual loss of visual acuity, central or paracentral scotomata, and occasionally an afferent pupillary defect or optic atrophy. There is no proven treatment, although some have proposed that highdose intravenous corticosteroids may result in more rapid visual recovery.5
1. Gass JDM. Purtscher's Retinopathy. In: Gass JDM, ed. Stereoscopic Atlas of Macuhr Diseases: Diagnosis and Treatment. St. Louis, Mo: Mosby; 1996:746-747.
2. Beckingsale AB, Rosenthal AR. Early fundus fluorescein angiographic findings and sequelae in traumatic retinopathy: case report. Br J Ophthalmol. 1983;67:119-123.
3. Jacob HS, Goldstein IM, Shapiro I, et al. Sudden blindness in acute pancreatitis. Arch Intern Med. 1981;141:134-136.
4. Kincaid MC, Green WR, Knox DL, Mohler C. A clinicopadiologic case report of retinopathy of pancreatitis. Br J Ophthalmol. 1982;66:219-226.
5. Atabay C, Kansu T, Nurlu G. Late visual recovery after intravenous methylprednisolone treatment of Purtscher's retinopathy. Ann Ophthalmol. 1993;25:330-333.