Felis ISSN 2398-2950

Eye: chorioretinitis

Contributor(s): Dennis E Brooks, David Williams

Introduction

  • Inflammatory reaction of neurosensory retina (nsr) and vascular choroid.
  • Cause: all causes of uveitis.
  • Exogenous - penetrating trauma but anterior uveitis much more commonly seen.
  • Endogenous - infectious agents esp. FIP, FeLV, FIV, Toxoplasma gondii, fungi (cryptococcosis, histoplasmosis), Mycobacterium.
  • Also idiopathic (large group).
  • Signs: rarely causes objective signs unless associated with anterior uveitis.
  • Lens-induced inflammation is more commonly anterior.
  • Often even large lesions appear to have little effect on vision.
  • Diagnosis: ophthalmoscopic signs confirm clinical entity, underlying cause may be identified by full clinical examination, history, laboratory tests. Vitreocentesis may be helpful.
  • Treatment: attempt to diagnose and treat underlying cause.
  • Prognosis: depends on extent/distribution of lesions and underlying cause.

Pathogenesis

Etiology

Pathophysiology

  • Choroid usually focus of inflammation.
  • Retina and vitreous usually secondarily affected.
  • Vitreal haze may preclude visualization of fundus.
  • Acute inflammation followed by resolution and retinal scarring, usually seen as increased tapetal reflectivity with or without ectopic pigment deposition. Scars referred to as post inflammatory retinopathy/chorioretinitis.

Nomenclature

  • Reflects structure where inflammation commences:
    • Chorioretinitis:  choroid primarily involved, secondary spread to neurosensory retina (NSR) (most common).
    • Retinochoroiditis: NSR primarily involved, secondary spread to choroid.
    • Retinitis: NSR only involved.
    • Choroiditis: (or posterior uveitis): choroid only involved.
  • Distinctions difficult to make clinically, usually made on basis of histology.

Pathophysiology

  • Early in inflammatory process, exudates accumulate around retinal blood vessels   →   perivascular opacities/sheathing.
  • As exudates increase in quantity, retina becomes edematous, nsr may separate from retinal pigment epithelium (   →   retinal detachment ), exudate may extend into vitreous   →   vitreal opacification may preclude visualization of fundus.
  • Hemorrhage may accompany severe inflammation.
  • Shape of hemorrhage defines its location:
    • Subretinal: diffuse (between NSR and RPE).
    • Deep retinal: 'dot and blot' (confined by cell bodies and axons).
    • Superficial retinal: flame shaped (following distribution of fibers in nerve fiber layer).
    • Preretinal: keel shaped, following gravitational forces (between NSR and vitreal face).
  • Healing is mediated by tissue macrophages and RPE:
    • Connective tissue elements may proliferate   →   folding in retina.
    • NSR atrophies   →   hyper-reflectivity in tapetal region, pallor in nontapetal.
    • In atrophic area, there may be increased pigmentation.
    • Borders of lesion usually very distinct.
    • Blood vessels crossing lesion may be attenuated or tortuous.
  • FIP may lead to hyperviscosity   →   sludging in blood vessels   →   hypoxic damage   →   blood vessel incompetence.
  • FIP often associated with intense vasculitis.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

Other sources of information

  • Petersen-Jones S & Crispin S (2002) BSAVA Manual of Small Animal Ophthalmology. 2nd edn. British Small Animal Veterinary Association. ISBN 0 905214 54 4


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