Posterior Vitreous Detachment
Title: Posterior Vitreous Detachment
Author: James Ellis, 4th year medical student , University of Utah School of Medicine
Photographer: Becky Weeks CRA, COA
Keywords: Posterior vitreous detachment, macula, retina
Disease: Posterior vitreous detachment (PVD) is the term used to describe the separation of the vitreous cortex and its’ enveloping posterior hyaloid membrane from the internal limiting membrane (ILM) of the retina. PVD is the result of age-related changes of the vitreous gel and vitreoretinal adhesions that result in pathological alterations at the vitreoretinal interface.
Pathophysiology: The vitreous is the largest anatomic structure in the eye. It occupies greater than 75% of the total volume of the eye. Age related degeneration of the vitreous leads to gel liquefaction and the development of fluid filled pockets, or lacunae, that typically begin to develop in the central vitreous cavity and at the area in front of the macula.1 This liquefaction occurs throughout life and can be seen in patients as young as four years old. As we age, the liquefied lacunae begin to increase in both size and number and by the age of 70, it is estimated that approximately 50% of the vitreous is liquefied in the general population.1 Additionally, during the aging process, there is progressive degeneration of the adhesions found between the ILM and the posterior vitreous cortex.2 Liquefaction of the vitreous gel begins to increase traction force on the retina. A posterior vitreous detachment does not occur until there has been sufficient weakening of the vitreoretinal adhesions.3
PVD is presumed to be an acute event that is precipitated by the sudden development of a break in the posterior cortical vitreous layer that overlays the macular region.4 As the adhesions are weakened, a rupture can develop in the posterior hyaloid membrane that allows liquefied vitreous to flow into the retrovitreous space, resulting in a rapid separation of the vitreous cortex and overlaying posterior hyaloid membrane from the ILM.2 This separation is believed to begin posteriorly and progress peripherally until it reaches the vitreous base. PVD is classically divided into four stages. In stage 1, there is perifoveal separation with adhesion of the vitreous to the fovea. In stage 2, there is complete separation of the vitreous from the macula. In stage 3, more extensive separation is appreciated with remaining adhesion at the optic disc. Finally, in stage 4 there is complete PVD. When a PVD occurs, there is most often complete separation of the complete vitreous with its hyaloid membrane from the retina.3 However, in some eyes, the posterior vitreous cortex can split which leads to areas of cortical vitreous remnants in areas of firm adhesions. Vitreoretinal adhesions appear to be strongest in areas that the ILM is thinnest like the vitreous base, main retinal vessels, the optic disc margin and the macula.1 Vitreous traction at firm adhesion sites can result in complications of PVD that are discussed below.
Risk Factors for early PVD: Although PVD will develop in almost all aging eyes, high myopia, hereditary vitreoretinal syndromes involving collage type II metabolism like Marfan syndrome, retinal vascular disease, trauma, aphakia, and vitreous hemorrhage may be associated with earlier PVD. Patients with high myopia, retinal vascular disease, trauma, and vitreous hemorrhage are at increased risk of developing complications from the PVD.
Signs and Symptoms: In most individuals, the early stages of PVD are asymptomatic until separation of the vitreous cortex from the optic disc margin, where there is separation of the peripapillary glial tissue from the optic nerve head. Once symptomatic, patients typically experience temporal photopsias or floaters, or both. Floaters are the most common complaint and are a result of vitreous opacities casting a shadow on the retina. On slit lamp examination, a Weiss ring may be seen. A Weiss ring is epipapillary glial tissue torn from the optic nerve head.
Differential Diagnosis: A differential for a patient presenting with a symptomatic PVD, temporal photopsia and floaters, should include the following:
- Retinal detachment
- Retinal Tear
- Vitreous hemorrhage
- Vitreous inflammation (uveitis and endophthalmitis)
- Vitreous amyloidosis
- Vitreous syneresis
Complications: Complications of PVD are caused by the dynamic vitreous traction due to firm focal vitreous adhesions and can include retinal tears, vitreous hemorrhage, rhegmatogenous retinal detachment, and retinal or optic disc hemorrhage.5,6 Complications are more likely to occur in eyes where the accelerated liquefaction of the vitreous outpaces the progressive weakening of the vitreoretinal adhesions. A late complication that can occur following a PVD is an epiretinal membranes (ERM). The exact role of PVD in the development of epiretinal membranes is unknown. However, PVD is thought to play a role in the development of epiretinal membranes through dehiscences of the ILM during development of the PVD, leading to migration of glial cells and proliferation on the retinal surface. Alternatively, it is believed that ERMs are a result of proliferation and transdiferrentiation of hyalocytes found in vitreous cortical remnants.1 Other late complications of PVD include lamellar macular holes and full thickness macular holes.3
Management/Treatment: Evaluation of a PVD should be done using both indirect ophthalmoscopy with scleral indentation and slit lamp biomicroscopy. These techniques allow a provider to effectively identify a PVD and rule out retinal tears, retinal detachment, or other vitreous complications. B-scan ultrasonic microscopy and OCT have also demonstrated sufficient resolution to detect PVD.2
Patients with an acute PVD should be observed by following strict retinal detachment precautions, subsequent follow up exams should be scheduled in order to rule out retinal breaks. In the case of patients with a vitreous hemorrhage that has not cleared out, a vitrectomy can be considered. An uncomplicated PVD is not an indication for surgery. If an incomplete PVD begins to cause vitreomacular traction syndrome, then a vitrectomy with membrane peeling could be considered for treatment.7
The prognosis of a PVD is generally very good.
- Johnson MW. Posterior Vitreous Detachment: Evolution and Complications of Its Early Stages. Am J Ophthalmol. 2010;149(3). doi:10.1016/j.ajo.2009.11.022
- Fincham GS, James S, Spickett C, et al. Posterior Vitreous Detachment and the Posterior Hyaloid Membrane. In: Ophthalmology. Vol 125. Elsevier Inc.; 2018:227-236. doi:10.1016/j.ophtha.2017.08.001
- Hayashi K, Manabe SI, Hirata A, Yoshimura K. Posterior vitreous detachment in highly myopic patients. Investig Ophthalmol Vis Sci. 2020;61(4). doi:10.1167/iovs.61.4.33
- Hayashi K, Sato T, Manabe S ichi, Hirata A, Yoshimura K. Posterior vitreous detachment in patients with diabetes mellitus. Jpn J Ophthalmol. 2020;64(2):187-195. doi:10.1007/s10384-020-00720-9
- Gishti O, van den Nieuwenhof R, Verhoekx J, van Overdam K. Symptoms related to posterior vitreous detachment and the risk of developing retinal tears: a systematic review. Acta Ophthalmol. 2019;97(4):347-352. doi:10.1111/aos.14012
- Petrash JM. Aging and age-related diseases of the ocular lens and vitreous body. Investig Ophthalmol Vis Sci. 2013;54(14):ORSF54. doi:10.1167/iovs.13-12940
- Toyama T, Kawai H, Shiraya T, et al. Posterior vitreous detachment and macular microvasculature in the elderly. PLoS One. 2020;15(4). doi:10.1371/journal.pone.0231351
Faculty Approval by: Griffin Jardine MD
Copyright statement: James Ellis, ©2021. For further information regarding the rights to this collection, please visit: URL to copyright information page on Moran CORE