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Acute choroidal closure caused by hemodialysis accident in an amyloidosic patient

Authors
  • Lemaitre-Labilloy, Claire1
  • Bodaghi, Bahram1
  • Cassoux, Nathalie1
  • LeHoang, Phuc1, 2
  • 1 Pitie-Salpetriere Hospital, Department of Ophthalmology, Paris, France , Paris
  • 2 Hôpital Pitié-Salpétrière, Service d'Ophtalmologie, 43-87 bd de l'Hôpital, Paris, 75013, France , Paris
Type
Published Article
Journal
Graefe's Archive for Clinical and Experimental Ophthalmology
Publisher
Springer-Verlag
Publication Date
Oct 21, 2005
Volume
244
Issue
6
Pages
758–760
Identifiers
DOI: 10.1007/s00417-005-0090-8
Source
Springer Nature
Keywords
License
Yellow

Abstract

BackgroundWe report the case of a 43-year-old man haemodialysed for 20 years for systemic amyloidosis who underwent an acute choroidal occlusion after a haemodialysis accident.Case reportThe patient had cardiac, pulmonary, neurovegetative and renal localizations of amyloidosis. He complained during a haemodialysis session of uncomfort with abdominal pain, headache, bradycardia, vomiting, confusion and blurred vision. Acute haemolytic anemia was confirmed. In the following days, eyes were red and the vision was still altered.ResultsExamination showed decreased visual acuity (VA) to 20/80 OU, low intraocular pressure (IOP), major vitritis and pigmentary alterations of the fundus with yellow retinal deposits. Fluorescein and indocyanine green angiographies showed amyloid retinal deposits, pigmentary alterations, normal retinal perfusion and massive choroidal hypoperfusion persisting in the late sequence. Steroid therapy was tried unsuccessfully. The situation slowly improved within 3 months with complete clearing of the vitreous opacities and stabilisation of the pigmentary alterations. VA progressively recovered to 20/30, 1 year after the onset of the disease, but IOP remained low and choroidal perfusion did not improve 2 years after the accident.ConclusionChoroidal complications of amyloidosis have never been described so far. The acute occlusion observed here was the consequence of an intravascular haemolytic event that completed the preexisting amyloid vascular infiltration.

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