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

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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-

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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. Symptomatic retinal flap tears ■ Trauma ■ are prophylactically treated, creating retinal scars Cataract surgery (chorioretinal adhesions) in order to seal down the detached retina. Operculated Retinal Hole Management of Retinal Breaks An operculated retinal hole represents a round, red The decision to refer for a treatment is anecdotal, full thickness retinal defect with an associated depending on variable factors, such as the type of avulsed piece of retinal tissue in the vitreous cortex. retinal break, risk factors, and accompanying symp- Operculated retinal holes are thought to be a sud- toms and signs.17 Various studies have confirmed den occurrence rather than a progressive change that symptoms are the single most likely predictor and most often occur at the same time as a PVD and that a retinal break will progress to a RRD.18,19 A reti- or associated with retinal tufts.16 Due to their close nal consult is typically considered for acute sympto- association with PVD, operculated retinal holes are matic retinal breaks. An acute symptomatic PVD found more commonly in older people.16 can co-exist with a longstanding retinal break. Operculated retinal holes are a result of increased Clinical trials have not aided in determining focal vitreoretinal adhesion in the periphery, whether these retinal breaks would benefit from pulling a plug of retinal tissue onto the cortex of the prophylactic treatment.18 The presence of a retinal vitreous. This avulsed retinal tissue (operculum) is or vitreal hemorrhage, along with Schaeffer’s sign often found directly overlying the retinal break, but can further help determine the acute nature of reti- can be found elsewhere depending on the direction nal break. of the force of the vitreous traction at the time of Retinal break with accompanying subclinical reti- the separation. The operculum is noted to be small- nal detachment (associated fluid cuff <2DD) should er than its associated retinal break due to degenera- also be referred for a retinal consult. While fluid tion that has occurred over time from vascular insuf- cuff surrounding a retinal break is an inauspicious ficiency previously supplied by the underlying reti- sign, retinal pigment epithelial changes are consid- nal layers. An operculum can be distinguished from ered a sign of chronicity and decrease the likeli- a vitreous floater due to its disc-shaped appearance hood that the retinal break will progress to a RRD. as compared to the spherical appearance of a vitre- Most retinal holes only require a yearly dilated ous floater.16 Operculated retinal holes may be fundus exam. Asymptomatic retinal holes are rou- symptomatic in the initial stages but symptoms sub- tinely monitored. On the other hand, a sympto- side once the traction is released and the opercu- matic operculated hole with persistent vitreoretinal lum is finally formed. Since they are not associated traction may benefit from a retinal consult, with continuous vitreoretinal traction, most are fol- although most have not been reported to progress lowed on an annual basis. to a RRD.10 Retinal flap tears carry the highest risk for pro- Retinal Flap Tear (Horseshoe tear) gression but there is some controversy as to weather A retinal flap tear, also known as a horseshoe tear, a non-symptomatic retinal flap tear should be treat- commonly occurs is association with an incomplete ed.18 Only 5% of asymptomatic retinal breaks

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progress to RRD.20,21 At the site of a retinal flap tear, of a PVD. Scleral depression should also be con- the retina is incompletely pulled away and vitreo- sidered, in order to rule out the presences of a reti- retinal traction exerts tractional forces upon the nal break or retinal detachment. The vitreous edge of the tear. Since retinal tears have a predispo- should be carefully scrutinized for the presences of sition to evolve to a RRD, one may consider that all hemorrhages or pigment. flap tears, at the very least, deserve a retinal consult. In the absence of any complications, patients This is especially true in the presence of other risk should be followed-up on a one–two week basis factors such as aphakia, myopia, or history of RD in (depending on risk factors and associated signs or the fellow eye. symptoms), until complete detachment of the pos- terior vitreous is noted. This commonly occurs What Happens in the Macula? within six weeks and is typically associated with res- Vitreomacular Tractional Syndrome (VMT) olution of photopsias. Any changes or progression Vitreomacular traction is described an incomplete in signs or symptoms, warrants prompt re-exami- posterior vitreous detachment with continuous nation. Accompany risk factors, signs and symp- adherence as the macula.22-24 (Figure 5) This con- toms, in addition to a complete clinical evaluation tinuous vitreomacular adherence induces traction- can aid in the appropriate management of a al forces upon the macula. VMT is commonly patient presenting with a PVD. described as a taut posterior hyaloid in a “dumb- bell“ configu- REFERENCES ration. The 1. Foos RY. PVD. Trans Am Acad Ophthalmol Otolaryngoal 1972; 76: 480-97. clinical pic- 2. Farve M, Goldmann H: Zur Genese der hinteren Glaskorperabhebung. Ophthalmologica 1956; 132: ture is vari- 87-97. 3. Uchino E, Uemura A, Ohba N. Initial Stages of PVD in healthy eyes of older person evaluated by able with OCT. Arch ophthalmol 2001; 119: 1475-79. symptoms 4. Hikichi T,Trempe CL. Relationship between floaters, light flashes, or both and complications of PVD. ranging from AJO 1994; 117: 593-8. mild blurred 5. Hayreh SS. Jonas JB. PVD: Clinical correlations. Ophthalmologica 2004; 218: 333-343. 6. Berdahl JP,Mruthyunjaya P.Vitreous Hemmorhage: Diagnosis and Treatment. American Academy Figure 5. vision and metamor- of Ophthalmology. http://www.aao.org/publications/eyenet/200703/pearls.cfm. Last accessed April 10th, 2008 phopsia to severe decrease in visual acuity and 7. Seabag J. Anomalous posterior vitreous detachment: a unifying concept in vitreo-retinal disease. accompanying photopsias. The typical patient is Graef Arch Clin Exp Ophthalmol 2004; 242: 690-8. older with no history of cataract surgery. The 8. Coffee R, Westfall A, Davis G, et al, Symptomatic Posterior Vitreous Detachment and the nature of the vitreomacular attachment has been Incidence of Delayed Retinal Breaks: Case Series and Meta-analysis. AJO 2007; 144: 409-413. associated with a number of maculopathies, includ- 9. Tasman WS. PVD and peripheral breaks. Tran Am Acad Ophthalmol & Otol 1967; 72: 217-223. ing cystoid macular edema, macular hole forma- 10. American Academy of Ophthalmology, Preferred Practice Pattern. Posterior Vitreous 24-26 Detachment, Retinal Breaks, and Lattice Degeneration. Preferred Practice Pattern Guideline 2003. tion and epiretinal membranes. The dynamic http://www.aao.org/education/guidelines/ppp/pvd_new.cfm. Last accesses April 10th, 2008 nature of the traction, strength of remaining 11. Novak MA. Welch RB. Complications of acute symptomatic PVD. AJO 1984; 97: 308-314. attachment and extent of vitreoretinal separation 12. Brodley WW. Risk of retinal tears in patients with vitreous floaters. AJO 1983: 96: 783-7. may all contribute to the distinct type of associated 13. Jaffe NS. Complications of acute PVD. Arch Ophthal 1968; 79: 568-571. maculopathy.27 The clinical course is unpredictable 14. Austin KL. Palmer JR. Seddon JM, et al. Case-control study of idiopathic RD. Int J Epi 1990; with a few cases remaining stable for years or asso- 19: 1045-50. 15. National guidelines clearinghouse. RD and related peripheral vitreoretinal diseases. ciated with spontaneous posterior vitreous detach- http://www.guideline.gov/summary/ summary.aspx?ss=15&doc_id=1996&string=. Last accessed ment. A spontaneous PVD is typically associated April 14th, 2008. with alleviation of both the associated symptoms 16. Jones W. Reidy RW. Atlas of peripheral ocular fundus. MA: Butterworth Publ 1985. and maculopathies, but the occurrence is low.28 17. Colyear BH. Pischel D. Preventive treatment of RD by means of light coagulation. Trans Pac The classic course is one of progression associated Coast Oto-Ophthalmol Soc 1060; 41: 1934-217. with further deterioration. Thus, in many cases, 18. Wilkinson CP. Evidence-based analysis of phrophylactic treatment of asymptomatic RD and LD. 28 Ophthalmol 2000; 107: 12-18. pars plana vitrectomy is a necessity. 19. Tanner V. Harle D, Tan J. Acute PVD: the predictive value of vitreous pigment & symptomology. BJO 2000;84: 1264-68. Conclusion 20. Neumann E, Hyams S. Conservative management of RB. BIO 1972; 56: 482-6. Many PVD result in a complete detachment from 21. Byer NE. What happens to untreated asymptomatic RD, and are they affected by PVD? the retina without any further complication. Yet, Ophthalmol 1008; 105: 1045-50. depending on the site of firm vitreoretinal attach- 22. Reese AB, Jones IR, Cooper WC. VMT syndrome confirmed histologically. AJO 1970; 69:975-977. 23. Jaffe. NS. Vitreous traction at the posterior pole of the fundus due to alterations in the vitreous ment, the PVD process may lead to the develop- posterior. Trans Am Acad Ophthalmol Otolaryngol 1967; 71: 642-52. ment of vitreoretinal traction resulting in a vitre- 24. Smiddy WE, Michels RG, Green WR. Morphology, pathology, and surgery of idiopathic vitreo- ous hemorrhage, retinal break, which may be asso- retinal macular disorders. Retina 1990; 10:288-296. ciated with a retinal detachment, or vitreomacular 25. Hotta K, Hotta J. Retinoschisis with macular retinal detachment associated with VMTS. Retina traction syndrome (VMT). The vitreoretinal con- 2004; 24: 307-309. dition reaffirms the importance of further evalua- 26. Gass JDM. Idiopathic senile macular hole: its early stages and pathogenesis. Arch Ophthalmol 1988; 106: 629-39. tion of every patient presenting with an acute PVD. 27. Johnson MW. Tractional CME: variant of VMT syndrome. AJO 2005; 140: 184-192. A dilated fundus exam should be performed in all 28. Smiddy WE, Michels RG, Glaser BM, et al. Vitrectomy for macular traction caused by incomplete patients who present with signs and/or symptoms vitreous separation. Arch Ophthalmol 1988; 106: 624-628.

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Questions Examination Answer Sheet Valid for credit through November 30, 2009 1. Which of the following is not a common complaint of a patient with an acute PVD? Posterior Vitreous Detachment: A Common Process a. diplopia with Potential for Ocular Morbidity b. flashes c. floaters Directions: Select one answer for each question in the exam and completely darken the appropriate circle. A minimum score of 70% is required to earn credit. d. patient may be asymptomatic and have no complaints Mail to: Optometric CE, PO Box 488, Canal Street Station, New York, NY 10013 2. Common peripheral pathological conditions associated COPE approved for 1 hour of CE Credit. Cope ID 21798-GO with onset of acute PVD include all the following except ______. There is an eight-to-ten week processing time for this exam. a. retinal detachment 1. ABCD 11. The goal statement was achieved: b. retinal flap tears Very Well Adequately Poorly c. operculated holes 2. ABCD d. subchoroidal neovascular membrane 12. The information presented was: 3. ABCD Very Useful Useful Not Very Useful 3. Which of the following is not a complication of an incomplete posterior vitreous detachment? 4. ABCD 13. The difficulty of the course was: a. vitreomacular traction syndrome Complex Appropriate Basic b. macular degeneration 5. ABCD c. vitreous hemorrhage 14. Your knowledge of the subject was increased: d. retinal detachment 6. ABCD Greatly Somewhat Hardly

4. Most retinal breaks are located in the: 7. ABCD 15. The quality of the course was: a. superior retina Excellent Fair Poor b. inferior retina 8. ABCD How long did it take to complete this course? c. nasal retina d. temporal retina 9. ABCD Comments on this course: 5. An incomplete PVD associated with continuous adherence 10. ABCD to the macula is known as ______. Topics you would like in the future CE articles: a. vitreomacular traction syndrome b. a macular hole c. juxta foveal retinal telangiectasia Please retain a copy for your records. Please print clearly. d. neovascularization You must choose and complete one of the following three identifier types:

6. What is the main component of the vitreous? 1 SS # - -

a. water Last 4 digits of your SS # and date of birth State Code and License #: (Example: NY12345678) b. hyaluronic acid - c. collagen 2 3 d. glial tissue First Name

7. What is the strongest vitreoretinal attachment? Last Name a. along the retinal vessel b. ora serrata E-Mail c. optic nerve The following is your: Home Address Business Address d. macula Business Name ______8. A is the characteristic pattern of the Address PVD located in front of the optic nerve. a. idioptahic City State b. Weiss’ ring ZIP c. tractional detachment d. disciform Telephone # - - Fax # - - 9. All of the following are main causes of vitreal hemorrhages except: By submitting this answer sheet, I certify that I have read the lesson in its entirety and completed the a. superficial retinal neovascularization self-assessment exam personally based on the material presented. I have not obtained the answers to this exam by any fraudulent or improper means. b. non-exudative macular degeneration c. trauma d. complicated PVD Signature Date 10. Where is the apex of a flap tear orientated towards? a. anterior retina b. temporal arcade c. posterior pole d. ora serrata Lesson 105727 RO-UAB2-0408

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