Hemolytic Uremic Syndrome Associated With Purtscher-like Retinopathy | JAMA Ophthalmology | JAMA Network
[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Case Reports and Small Case Series
August 1998

Hemolytic Uremic Syndrome Associated With Purtscher-like Retinopathy

Arch Ophthalmol. 1998;116(8):1119-1120. doi:

Purtscher reported the findings of cotton-wool spots, hemorrhages, and edema in the posterior fundus of 2 patients who experienced severe head trauma. Later, angiopathica retinae traumatica,1 or Purtscher retinopathy, was described following long-bone fractures, rapid deceleration injuries, and compressive injuries to the trunk. Subsequently, Purtscher-like retinopathy was observed in atraumatic cases such as pancreatitis, collagen vascular disease, amniotic fluid embolism, retrobulbar anesthesia, chronic renal failure, and thrombotic thrombocytopenia purpura.2 We report a case of Purtscher-like retinopathy in a patient with hemolytic uremic syndrome (HUS).

A 31-month-old boy was admitted to a hospital with a history of pallor, lethargy, and oliguria preceded by gastroenteritis. After experiencing 2 brief tonic-clonic seizures, he was transferred to the pediatric intensive care unit where examination revealed a lethargic child with scattered petechiae and periorbital and peripheral edema. The child was anuric. Computed tomography of his brain was normal on admission. Laboratory findings revealed microcytic hemolytic anemia (hemoglobin, 68 g/L; mean corpuscular volume, 72.5 mm3), thrombocytopenia (platelets, 33×109/L), and acute renal failure (creatinine, 407 µmol/L [4.6 mg/dL]). Stool culture yielded Escherichia coli (0157:H7). Diagnosed as having HUS, the patient underwent plasmapheresis and hemodialysis. Three days after admission to the pediatric intensive care unit, a repeated computed tomographic scan revealed bilateral infarctions of the basal ganglia (Figure 1). The patient had not experienced any trauma, cardiopulmonary resuscitation, assisted ventilation, or further seizures. On the fourth day of his intensive care admission, an ophthalmic evaluation disclosed sluggishly reacting pupils without relative afferent pupillary defect and moderate conjunctival chemosis. Funduscopic examination revealed ischemic retinal whitening in both posterior poles, most prominently in the peripapillary area. Retinal arteriolar attenuation and scattered intraretinal hemorrhages were also present bilaterally. Additionally, a preretinal hemorrhage and peripapillary nerve fiber layer hemorrhage were noted in the left eye (Figure 2).