Purtscher's retinopathy associated with acute pancreatitis.

PURPOSE: Purtscher's retinopathy is a rare condition that is associated with complement-activating systemic diseases such as acute pancreatitis. After pancreatic injury or inflammation, proteases such as trypsin activate the complement system and can potentially cause coagulation and leukoembolization of retinal precapillary arterioles. Specifically, intermediate-sized emboli are sufficiently small enough to pass through larger arteries yet large enough to remain lodged in precapillary arterioles and cause the clinical appearance of Purtscher's retinopathy. This pathology may present with optic nerve edema, impaired visual acuity, visual field loss, as well as retinal findings such as cotton-wool spots, retinal hemorrhage, artery attenuation, venous dilation, and Purtscher flecken. CASE REPORT: A 57-year-old white man presented with an acute onset of visual field scotomas and decreased visual acuity 1 week after being hospitalized for acute pancreatitis. The retinal examination revealed multiple regions of discrete retinal whitening surrounding the disk, extending through the macula bilaterally, as well as bilateral optic nerve hemorrhages. The patient identified paracentral bilateral visual field defects on Amsler Grid testing, which was confirmed with subsequent Humphrey visual field analysis. Although the patient presented with an atypical underlying etiology, he exhibited classic retinal findings for Purtscher's retinopathy. After 2 months, best corrected visual acuity improved and the retinal whitening was nearly resolved; however, bilateral paracentral visual field defects remained. CONCLUSIONS: Purtscher's retinopathy has a distinctive clinical presentation and is typically associated with thoracic trauma but may be a sequela of nontraumatic systemic disease such as acute pancreatitis. Patients diagnosed with acute pancreatitis should have an eye examination to rule out Purtscher's retinopathy. Although visual improvement is possible, patients should be educated that there may be permanent ocular sequelae.

Nonclassic retinitis pigmentosa: A challenging clinical diagnosis solved by pedigree analysis and electrodiagnostic testing.

PURPOSE: The aim of this study was to describe a case of nonclassic retinitis pigmentosa, to highlight ancillary testing tools for proper diagnosis, and to differentiate between common hereditary fundus dystrophies. METHODS: Methods used in this study included complete ophthalmologic evaluation, optical coherence tomography, visual field testing, pedigree analysis, and electrodiagnostic testing. RESULTS: Reduced vision and photopsia were the initial complaints of a patient who had an overall normal ocular appearance. However, a strong family history of retinitis pigmentosa and depressed scotopic and photopic electroretinograms confirmed the diagnosis of autosomal dominant retinitis pigmentosa. CONCLUSION: In cases of atypical-appearing retinitis pigmentosa, both pedigree analysis and electrodiagnostic testing are fundamental in correct diagnosis of this multifaceted hereditary fundus disorder.

Advanced visual field loss secondary to optic nerve head drusen: case report and literature review.

BACKGROUND: Optic nerve head drusen (ONHD) is a relatively uncommon condition that results from calcific degeneration of axons within the optic nerve. The abnormal drusen bodies can enlarge, compressing normal nerve structures, and ultimately may result in vision loss. Drusen often are discovered through clinical evaluation with a dilated funduscopic examination. Ancillary testing, including computed tomographic (CT) imaging, B-scan ultrasonography, autofluorescence imaging, nerve fiber layer imaging, and threshold visual field evaluation are helpful to confirm the existence of ONHD and to evaluate for progression of this condition. CASE REPORT: This case report discusses the clinical presentation of a patient with advanced visual field loss from ONHD and the ancillary testing used to confirm the diagnosis. A complete review of literature on ONHD is discussed. CONCLUSIONS: Currently, there is no cure or direct treatment for progressive vision loss or complications that may develop from ONHD. Useful diagnostic tools include serial automated threshold visual fields, nerve fiber layer analysis, and fundus photography. It is suggested that ocular hypotensive agents be used to lower intraocular pressure prophylactically to prevent further nerve fiber layer and optic nerve damage.