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Posterior Vitreous Detachment: a Common Process with Potential for Ocular Morbidity Diana L

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Posterior Vitreous Detachment: a Common Process with Potential for Ocular Morbidity Diana L CE Posterior Vitreous Detachment: A Common Process with Potential for Ocular Morbidity Diana L. Shechtman, OD, F.A.A.O. and Diane E. Calderon, OD, F.A.A.O. POSTERIOR VITREOUS DETACHMENT PVD. Flashes do not always specify (PVD) is a frequent consequence of the presence of a retinal break or OF OPTO EW ME VI T aging. With age the vitreous retinal detachment. Flashes indi- E R R Y degenerates, leading to a PVD. A cate traction upon the retina, posterior vitreous detachment is resulting in stimulating of the pho- described as a separation of the toreceptors. posterior cortex of the vitreous Although we have recognized from the internal limiting mem- the vitreous as an important ocular brane of the retina. Vitreopapil- structure for over a century5,weare lary separation is the most com- only recently beginning to under- mon location. (Figure 1) This is stand its pathogenic role in various Release Date vitreoretinal diseases. PVD is typi- November 2008 cally described as a benign process; however, the location of firm vitreo- Expiration Date retinal adhesions plays a critical November 30, 2009 role in various pathological vitreo- Goal Statement retinal conditions. The process is Posterior vitreous detachment (PVD) described as local, partial or total. There are a number of firm pos- is a frequent consequence of aging. terior vitreoretinal attachments, Understanding the anatomical Figure 1. which include areas along retinal makeup and biochemical properties vessels, the vitreous base, macula of the vitreous are critical in the described as an annular ring, and optic nerve. Depending on the diagnosis of PVD as well as associ- known as a Weiss’ ring, attached to site of firm vitreoretinal attach- ated vitreoretinal conditions. the posterior hyaloid and located ment, an incomplete PVD may lead anterior to the optic nerve. (Figure to the development of a vitreous Faculty/Editorial Board 2) This process is readily observed hemorrhage, retinal break (RB), Dr. Diana L. Shechtman and in the elderly population, affecting rhegmatogenous retinal detach- Dr. Diane E. Calderon. 65% of patients over the age of ment (RRD), or vitreomacular trac- 1,2 Credit Statement 65. Even though a PVD is usually tion syndrome (VMT). Understand- detected in an older female both ing the anatomical makeup and This course is COPE approved for 1 genders may be affected and it is biochemical properties of the vitre- hour of CE credit. COPE ID is XXX. believed that the process starts ous are critical in the diagnosis of Please check your state licensing much earlier.3 Conditions, such as PVD as well as associated vitreoreti- board to see if this approval counts myopia, trauma, nal conditions. towards your CE requirement for inherited vitreoreti- relicensure. nal disease, surgery, Vitreous Anatomy & and inflammation Biochemistry Joint Sponsorship Statement may accelerate the The vitreous is con- This continuing education course is process.4 Floaters are sidered to be a trans- joint-sponsored by the University of the most common parent gel, primarily Alabama School of Optometry. symptoms, described composed of water. A as “cobwebs, flies or small but vital compo- Disclosure Statement hair like-structures.“ nent of the vitreous Dr. Shechtman is on the speakers’ Flashes, or photop- consists of collagen bureau of VSP, MSS and Alcon. sias, may also be asso- and hyaluronic acid, ciated with an acute Figure 2. COURTESY OF DR. J. SOWKA which contributes to NOVEMBER 2008 REVIEW OF OPTOMETRY 11 CE the “gel-like“ consistency of the vitreous.6,7 Collagen localized hemorrhage without characteristic bor- is a structural protein, which is connected to ders or as a single streak of blood. Vitreous hemor- hyaluronic acid.1 As we age, there is alteration rhages tend to clot quickly while resolving slowly. between the hyaluronic-collagen complex, causing Patients may present with a history of multiple vitreous liquefaction and shrinkage. In addition, floaters or smoky vision, typically described as a with age, the internal limiting membrane becomes “red“ haze. Decrease in visual acuity is dependent thickened causing a decrease in vitreoretinal adhe- upon the density and location of the VH. Since the sion throughout the fundus.7 This weakening fur- VH is situated in a gel within a cavity, it will shift with ther facilitates the migration of the liquid vitreous head movements. Thus, patients may experience into the subhyaloid space. The vit- intermittent visual obstruction reous volume displacement causes a with head movement. forward collapsing of the vitreous PVD without retinal breaks, and a complete separation of the vit- account for of less than 10% of reous cortex from the retina, a PVD. VH cases.9,10 Although PVD may This entire process commonly runs be associated with a VH in the a complete and benign course with absence of a retinal break, the no further complications. presence of a vitreous hemorrhag- During the PVD process, if vitre- es is considered a risk factor for ous liquefaction surpasses the the presence of a coexisting reti- extent of weakening of vitreoreti- nal break.11 Vitreous hemorrhages nal adherence, tractional forces are indicative of vitreoretinal trac- will ensue upon areas of firm tion and potential impending reti- attachments.7 Depending on the nal break. Since many VHs settle site of the firm vitreoretinal attach- Figure 3. inferiorly due to gravity, location ment, a number of pathological of VH does not aid in detecting events can occur during the PVD process, invariably the possible site of an accompany RB. In the pres- attributing to retinal disturbances, such as a vitreous ence of a VH, it is imperative to scrutinize the reti- hemorrhage, VMT or retinal break which potential- na for any evidence of retinal breaks. In cases of ly can lead to a rhegmatogenous retinal detachment dense VH, ultrasonography (B-scan) may aid in (RRD).4,7,8 (Table 1) ascertaining the presence of retinal detachment, retinal tear, or any other associated etiologies. In What Happens in the Vitreous? the absence of a retinal break, VH should be fol- Vitreous Hemorrhage (VH) lowed until complete resolution has occurred. A VH is characterized by the presence of blood posterior to the crystalline lens and anterior to the What Happens in the Periphery? internal limiting membrane. (Figure 3) Since the Retinal Break (RB) vitreous is an avascular structure, blood found Retinal breaks commonly result from the vitreous within the vitreous must come from the superfi- pulling on the retina, causing a full thickness retinal cial retinal vasculature. The main causes of a vit- defect. This is common following the evolution of a reous hemorrhage include superficial retinal neo- partial PVD with associated continuous localized vascularization, trauma and a PVD (with or with- traction onto the retina. Up to 15% of all patients out associated retinal breaks). A firm vitreoretinal who present with acute symptomatic PVD have at attachment is maintained along the retinal vessels. least one retinal break.9,10,12 Since the strongest vit- During the PVD process sufficient traction along a reoretinal attachment is at the vitreous base, most vessel can lead to a vessel tear, resulting in a vitre- retinal breaks are located between the equator and ous hemorrhage. the ora.12,13 There is a downward gravitational force A VH can present as a large dense diffusely dis- exerted on the remaining attached vitreous base, perse hemorrhage within the vitreous cavity or a causing a greater prevalence for superior retinal breaks. Vitreoretinal traction induced by a PVD increases the risk for a RRD. Ominous accompany signs include symptomatic breaks, as well as the Table 1. Complications Associated with PVD presence of vitreoretinal traction, a vitreal or pre- retinal hemorrhage, pigmented vitreal cells VR traction site Retinal condition (Schaffer’s sign) and large retinal cuff of fluid. It is Retinal vasculature Retinal hemorrhage or VH not uncommon for patients to present with an Avulse retinal vessel asymptomatic retinal break, which is only discov- Macula VMT ered during a routine eye exam The most common types of retinal breaks Periphery Retinal breaks include; atrophic retinal holes, operculated retinal Retinal detachment holes and flap tears. Pathogenesis of each is associ- ated with distinct mechanisms, contributing to vari- 12 REVIEW OF OPTOMETRY NOVEMBER 2008 AD CE able propensity towards the progression to a RRD. PVD. During the Since atrophic retinal holes are not typically associ- PVD process, trac- ated with vitreoretinal traction, this entity will not be tion at this site may discussed in this article. A retinal break provides a lead to the devel- passage for the vitreous into the retina, thus the opment of a flap potential for a RRD. Management depends on the tear. The cardinal type of RB, associated findings, and risk factors feature of a retinal (Table 2). For example, myopia (>6D) and aphakia flap tear is a “U” or are considered risk factors for retinal breaks14,15 to “Horseshoe” shape, progress to RRD. representing an Categorizing the type of retinal break, in addition incomplete full thick- to identifying associated signs and symptoms, is ness retinal tear imperative. Not all retinal breaks progress to a RRD. Figure 4. associated with par- Proper management relies on determining which RB tial vitreoretinal ad- may progress to RRD. In other words, which retinal herence. As the vitreous is displaced forward, the breaks would benefit from prophylactic treatment. flap assumes a triangular shape, with the apex ori- ented towards the posterior pole and the attached base parallel with the peripheral retina. (Figure 4) Horseshoe tears are the leading cause of rheg- Table 2. Predisposing Risk Factors matogenous retinal detachments (RRD). Even an asymptomatic horseshoe tear can result in RRD; ■ High myope ■ making the timely diagnosis of this condition History of previous RD extremely important.
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