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Retinal Detachment

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Title: Retinal Detachment

Author: Brian Besch, 4th Year Medical Student, University of Utah School of Medicine

Introduction: Retinal detachment (RD) is the separation of the neurosensory retina from the underlying retinal pigment epithelium (RPE) and choroid.  Retinal photoreceptors are transducers which convert photons into electoral impulses, subsequently delivered by optic neural tracts to the visual cortex.  The retina is one of the most metabolically active tissues in the body, and heavily reliant on support of the underlying RPE and choroid to provide oxygen, nutrients, and metabolic waste removal to maintain function.  Physical separation of these layers results in retinal ischemia; when sustained, photoreceptor atrophy leads to decreased vision.

Pathophysiology: Broadly, RD is categorized into three major etiologies: rhegmatogenous, traction, and exudative.  Rhegmatogenous RD, the most common type, develops from a full-thickness retinal tear; the defect allows adjacent vitreous fluid to leak under the tear, dissecting the layers.  This typically stems from posterior vitreous detachment (PVD), a physiological normal part of aging in which the gel-like vitreous degrades to a more liquid consistency.  Pockets of developing fluid within the vitreous alter its shape, causing an overall inward collapse, placing tension on the vitreoretinal interface that may lead to tears.  PVD generally manifests between age 50-75, and increased risk of tears are observed in myopic patients, or those with a history of ocular trauma or inflammation.  In the latter two cases, excessive fibrosis and tissue remodeling strengthens vitreoretinal adhesions, increasing propensity for tears during detachment.  Traction RD is similar to rhegmatogenous RD, as mechanical traction forces create undue tension; however, no overt retinal tears or holes trigger detachment.  Traction RD is most commonly associated with retinal pathology involving neovascularization – a few examples include proliferative diabetic retinopathy, retinopathy of prematurity, or vitreomacular adhesions.  Ischemia induces new blood vessel growth, but the vasculature is disorganized, weak, and prone to leakage and fibrosis.  Exudative RD results when fluid accumulates between the retina and RPE in the absence of a tear or hole.  Fluid collection can be associated with central serous chorioretinopathy, macular edema, neoplasms, or other inflammatory conditions which increase vascular permeability.  Additionally, RD may occur as a combination of these pathologies.

Signs & Symptoms: Patients with RD present with variable complaints of vision change depending on the underlying etiology and anatomical location of the tear.  The most common associated scenario, PVD, typically presents with the sudden onset of new floaters – translucent rope-like or cobweb-type structures which slowly move across the visual field, often more prominent with eye movement.  Flashes of light (photopsias) lasting a couple seconds may occur in the peripheral vision; these result from mechanical traction on photoreceptors causing depolarization and neural firing.  Larger, superior RDs may draw the retina anterior/inferior giving the patient the perception of a veil or curtain descending from the upper visual fields.  Release of pigment from underlying RPE can present as a shower or dark specks.  Tears may be accompanied by damage to small vessels, causing vitreous hemorrhage; depending on severity, this may present suddenly as small regions of blurring or distortion, to severe vision compromise with acuity reduced to finger-counting or light perception.  Less acute etiologies may present more insidiously, with slowly progressive changes preceding detachment – difficulty reading fine print, or field distortions or cuts.

Diagnosis & Management: Patients exhibiting aforementioned symptoms should be referred to an ophthalmologist for further evaluation within 24 hours, including slit-lamp biomicroscopy to examine the fundus, indirect ophthalmoscopy to assess the peripheral retina, and possibly optical coherence tomography (OCT) scanning.  The latter is non-invasive, high-resolution imaging of the retinal fundus in cross-sections to assess for macular involvement.  Patients with cornea or lens pathology obscuring adequate retina visualization can be assessed using ultrasound B-scan.  While these techniques are highly specialized to ophthalmology, the primary care practitioner can perform simple, brief, and inexpensive screening tests to guide referral.  These include assessing visual acuity and confrontation fields, and direct ophthalmoscopy.  Having the patient view an Amsler grid to identify blind spots, linear distortions, or other abnormalities is a quick test for retinal pathology.  Detailed discussion of RD treatment is beyond the scope of this article.  However, patients with PVD but no RD require careful monitoring and should be educated about alarm symptoms which may warrant reevaluation.  Those with retinal holes or tears are at elevated risk of developing RD, and may be treated with laser retinopexy or cryoretinopexy.  RDs themselves may be managed with scleral buckling, vitrectomy, retinal tamponade with gas bubble or silicone oil, or some combination of therapies depending on the specific scenario.  RDs associated with neovascularization or subretinal exudates due to inflammation will additionally benefit from interventions targeting the respective underlying pathology.


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Hollands H, Johnson D, Brox AC, et al. Acute-onset floaters and flashes: is this patient at risk for retinal detachment? JAMA 2009; 302:2243.

Identifier: Moran_CORE_23968