Vitreous detachment

    Last updated date: 02-Mar-2023

    Originally Written in English

    Vitreous detachment

    Vitreous detachment


    A vitreous detachment is a disorder in which the vitreous, a component of the eye, shrinks and separates from the retina. The vitreous is a gel-like material that fills the inner chamber of the eyeball. The retina is a light-sensitive tissue located in the rear of the eye. 

    The vitreous fibers peel away from the retina as you age. Vitreous detachment is the medical term for this. When your vitreous detaches, you may not notice it or you may experience symptoms that impair your vision.


    Vitreous detachment definition

    Vitreous detachment definition

    Vitreous detachment (VD) is a frequent condition in the elderly. It is characterized as the separation of the cortical vitreous from the retina's neurosensory layer. Muller described the posterior vitreous detachment histopathologically in 1856 and clinically in 1875, although it was not properly investigated until 1914.

    When VD is worsened by a retinal rupture or vitreous hemorrhage, flashes and floaters become more visible. Floaters are little cobweb-shaped particles that emerge from the posterior vitreous cortex's dense collagen matrix. A sudden rise in the number of floaters combined with the commencement of photopsia (flashes) needs quick ophthalmic attention.

    This disease can progress to more serious consequences, such as retinal detachment or epiretinal membrane, which can result in irreversible visual loss. However, around 85 % of individuals with PVD do not develop problems, and the flashes and floaters usually go away within 3 months.



    There is little information on the prevalence of posterior vitreous detachment. Age appears to be a major determinant in the development of posterior vitreous detachment, according to data from hospital-based and post-mortem research.



    The most common cause of posterior vitreous detachment is elderly age. In a young, healthy person, the vitreous is normally adhering to the retina's internal limiting membrane. The vitreous adherence is greatest at the vitreous base. The optic disc borders, macula, and peripheral blood vessels are also affected by vitreoretinal adhesion.

    As a person ages, the gel-like quality of the vitreous degenerates, resulting in synchysis and syneresis. The stage of vitreous liquefaction known as synchysis precedes the stage of vitreous degeneration. Syneresis is the aggregation of collagen fibrils that causes the vitreous to collapse.

    This occurrence causes dense bundles of collagen fibrils to float in the vitreous, resulting in floaters (myodesopsia) in the eye. Vitreous degeneration also causes the vitreoretinal adhesion to weaken, which can lead to posterior vitreous separation.

    A posterior vitreous detachment occurs naturally, but it can be triggered by events like as cataract surgery, trauma, uveitis, panretinal photocoagulation, and laser capsulotomy. At the time of the initial examination, around 8% -22% of individuals with acute symptomatic PVD had retinal tears.

    Retinal tears are generally seen at or shortly after the beginning of symptoms in such situations. Tears or cracks in the retina are most commonly detected in the superotemporal region. A retinal break can have a variety of morphologies, including as U-tears (horseshoe), operculated tears, or retinal holes. On the follow-up appointment, retinal fractures (new or missing) are seen in around 2-5 percent of individuals diagnosed with acute PVD who did not have any on the first examination.

    PVD combined with vitreous hemorrhage has a higher risk of retinal tears than PVD without vitreous hemorrhage. It has been shown that around 50-70 percent of individuals with PVD accompanied by vitreous hemorrhage suffer retinal tears. In contrast, only 7–12% of individuals with PVD who do not have a vitreous hemorrhage manifest with a retinal rupture. Furthermore, individuals with acute PVD with retinal tears are seven times more likely to have vitreous pigments or granules than those without a retinal tear.

    The most important risk factors for PVD include:

    • Old age: After the age of 50, the frequency of posterior vitreous detachment is 53%, and it is 66% between the ages of 66 and 86. Postmortem examinations found that PVD was present in 27% of eyes by the seventh decade and 63% of eyes by the eighth decade of life.
    • Female gender: At the age of 60 or older, women move quicker than men in the evolution of a posterior vitreous detachment. This means that females have retinal diseases associated with posterior vitreous detachment at a younger age.
    • Myopia: The likelihood of posterior vitreous detachment is proportional to the axial length of the eyeball. Eyes with axial lengths higher than 30 mm are more likely to develop posterior vitreous separation than eyes with axial lengths less than 29 mm.
    • Underlying diseases like retinitis pigmentosa and sticklers syndrome. 
    • Menopause: Because of a lack of estrogen, postmenopausal female patients may be more prone to developing posterior vitreous detachment. In premenopausal women, estrogen may have a preventive effect against PVD.
    • Vitamin B6: Vitamin B6 contains anti-estrogen properties. In females, a larger consumption of vitamin B6 may raise the risk of posterior vitreous detachment.
    • Inflammation: Long-term inflammation is characterized by cellular proliferation and, eventually, fibrosis. Vitreous fibrosis causes tension on the retina, resulting in posterior vitreous detachments or retinal fractures.
    • Trauma: Posterior vitreous detachment happens as a result of a penetrating eye injury. In one investigation, it was identified as separation at the level of the internal limiting membrane or as cleavage inside the vitreous.
    • Ocular surgery: During eye procedures such as cataract extraction and intraocular lens insertion, LASIK (laser in situ keratomileusis), and others, various vitreous alterations occur. These changes might have a role in the development of postoperative posterior vitreous detachment. The vitreous modifications after cataract surgery include increased viscosity of vitreous near the retina compared to anterior hyaloid (opposite to normal), altered vitreous fluid proteome, destabilized vitreous body, anomalous PVD, and rheological changes of vitreous with no clear separation of vitreous and retina. Other risk factors include a posterior capsular tear, invasive surgical techniques, vitreous loss, laser capsulotomy, and myopia.
    • Retinal laser
    • The vitreous gel contains various angiogenic factors. Endothelial cell proliferation is responsible for neovascularization caused by these stimuli. The posterior hyaloid face serves as a scaffold for the formation of new vessels in the retina or optic disc. As a result, the presence of full PVD may inhibit neovascularization and protect the eye from the advancement of proliferative diabetic retinopathy.


    Clinical presentation 

    Clinical Presentation of Vitreous Detachment

    In most people, the early stages of posterior vitreous detachment are asymptomatic and are not recognized clinically until the vitreous separates from the optic disc borders causes discomfort.

    The patient usually complains of flashes of light (photopsia) and floaters (myodesopsia). Only 19% of individuals who report with flashes or floaters have posterior vitreous detachment. Light flashes are often brief and occur in the temporal quadrant. They are caused by head or eye movement and are particularly evident in low-light conditions.


    Floaters are tiny, movable vitreous particles that can be seen against a bright backdrop. 67 percent of individuals with posterior vitreous detachment report visual blurring. Blurring of vision may develop as a result of vitreous hemorrhage caused by retinal fractures or an abundance of floaters cluttering the visual field.

    Patients experiencing PVD symptoms must be carefully evaluated. A thorough retinal examination, including 360-degree viewing of the ora Serrata (through scleral indentation while utilizing indirect ophthalmoscopy) and slit-lamp biomicroscopy, should be conducted. A detached posterior hyaloid membrane is discovered during a thorough inspection. In mid vitreous, it appears as a folded transparent membrane. The presence of the Weiss ring is frequently used to make the diagnosis of full PVD.

    It is a ring of glial tissue seen anterior to the optic disc, linked to the posterior hyaloid. The diameter of a Weiss ring is around 1.5 mm. The presence of red cells and pigment granules in the anterior vitreous (Shafer sign or tobacco dust) indicates the existence of retinal tears as well as posterior vitreous separation. Such individuals require a thorough retinal examination and should be referred to a specialist. 



    Vitreous Detachment Diagnosis

    Binocular indirect ophthalmoscopy and three-mirror contact lens biomicroscopy are the primary diagnostic procedures used in the evaluation of acute posterior vitreous detachment. Traditionally, dynamic B-scan ultrasonography has been used to diagnose a PVD. In an effort to establish the diagnosis of posterior vitreous separation, optical coherence tomography (OCT) has recently been introduced.

    Slit-lamp Biomicroscopy

    Before undergoing slit lamp biomicroscopy, the patient's pupils are thoroughly dilated using mydriatic drugs. It facilitates in obtaining a broad light angle for diverse vitreous segments. Posterior vitreous detachment is classified as:

    • Complete (C-PVD) or
    • Partial (P-PVD)

    There is no connection of the divided posterior vitreous cortex at or beyond the globe equator in full Posterior vitreous detachment (PVD). It is simple to outline all the way to the vitreous base. C-PVD can be used to:

    • Collapsed or
    • Without a collapse

    The posterior hyaloid membrane is loose, severely detached, and plainly evident in full PVD with collapse. Slit-lamp biomicroscopy reveals a peripapillary glial band in this example. In the event of full PVD without collapse, however, the posterior hyaloid membrane is somewhat separated and may only be traced in front of the retina.

    Some vitreoretinal adhesion can be seen in partial PVD at or around the globe equator. The P-PVD is related to

    • The shrinkage of the posterior hyaloid membrane in some cases and
    • Without shrinkage of the posterior hyaloid membrane in others


    In a rare cases with partial PVD without shrinking, the vitreous gel is found adhering to the macula through a pre-macular hole in the posterior hyaloid membrane.


    B-Scan Ultrasonography

    Ultrasonography (US) has long been used to assess the condition of the vitreous gel. It also aids in determining the existence and amount of posterior vitreous separation. The B-scan US premise is that powerful echoes are created by acoustic interfaces located at media junctions. These echoes have varying sound velocities and densities. The larger the density difference between the two mediums, the more obvious the echo.


    Optical Coherence Tomography (OCT)

    In 1991, optical coherence tomography (OCT), a non-invasive ocular imaging method, was introduced. Based on the intensity of the reflected light, it generates a false-color representation of the tissue architecture. OCT analyzes the form and thickness of the tissue under examination. OCT demonstrates the separation of the posterior vitreous face and retina in the event of posterior vitreous detachment. OCT offers an advantage over slit-lamp biomicroscopy and B scan US because it can detect superficial PVD. Slit-lamp biomicroscopy and B scan US, on the other hand, fail to detect superficial PVD. PVD often begins as a vitreous retinal detachment near the fovea, according to OCT.


    OCT categorizes PVD into five stages: 

    • Stage 0: is characterized by the nonexistence of PVD.
    • Stage 1: is characterized by focal perifoveal PVD in three or less than three quadrants. In this stage, there is a persistent attachment of the vitreous cortex at the fovea, optic nerve head, and mid-peripheral retina.
    • Stage 2: is the same as stage 1 but with perifoveal PVD in all four quadrants of the retina.
    • Stage 3: in this stage, the vitreous cortex is not attached to the level of the fovea. However, adherence to the optic nerve head and mid-peripheral retina persist.
    • Stage 4: is characterized by complete PVD along with a prominent Weiss ring on slit-lamp biomicroscopy.


    OCT demonstrating an oblique foveal vitreoretinal attachment with no abnormalities in the foveal contour is referred to as a stage 0 macular hole (vitreomacular adhesion). These findings, which have a normal biomicroscopic appearance, are seen on OCT prior to the emergence of clinical alterations.



    Vitreous Detachment Management

    Acute symptomatic posterior vitreous detachment without vitreous hemorrhage and peripheral retinal fractures should be followed up with a scleral indentation at 2-4 weeks. A patient who complains of floaters is treated cautiously. Patients are encouraged that adaptation to the visual symptoms will occur with time, or that the floaters will go away.

    Floaters, on the other hand, can last anywhere from six months to a year in many circumstances. Acute PVD-related vitreous hemorrhage is often modest, with a glob of bleeding directly in front of the posterior pole.

    There might be intraretinal bleeding around the optic disc. Around the equator, a circular circumferential attachment of the vitreous to the retina is usually seen, with some preretinal bleed deposited inferiorly just beyond the posterior vitreous face. The majority of related fractures are seen in the superior retina. In the event that a vitreous hemorrhage prevents a comprehensive inspection, the patient is recommended to take a propped-up position, rest, and bilateral eye patching is an alternative.

    Ultrasonography should be used to rule out the existence of retinal fractures and other retinal disorders if there is a vitreous hemorrhage obstructing the fundal vision.

    The interventional alternatives in situations with severely symptomatic floaters that are clinically substantial and persistent and have an impact on quality of life are as follows. 



    Floaters can have serious psychological consequences, with some patients experiencing suicidal thoughts as a result of them. Pars plana vitrectomy is an effective therapeutic option for the control of vitreous floaters caused by PVD. The pars plana vitrectomy significantly reduces the symptoms of floaters, resulting in a clean visual field. However, it is fraught with complications.

    Cataract development, postoperative retinal detachment, and cystoid macular edema are all serious consequences that can result in irreversible vision loss. Before deciding for vitrectomy, the postoperative visual prognosis must be balanced against the preoperative symptoms of floaters.


    YAG Laser Vitreolysis

    The YAG laser emits short, powerful pulses that generate enough energy to melt the vitreous opacities to plasma. This is accomplished by raising the regional temperature over 1000 Kelvin (726.85°C) in a limited area. The huge floaters are therefore split down into smaller and less conspicuous ones.


    Vitreolysis by Drugs

    Enzymatic and non-enzymatic vitreolytic agents are the two types of vitreolytic agents. Enzymatic agents are the most often utilized. Tissue plasminogen activator (tPA), plasmin, microplasmin, nattokinase, chondroitinase, and hyaluronidase are among them. Non-enzymatic agents include urea and the arginine-glycine-aspartate peptide.

    In clinical practice, ocriplasmin has a success rate of 78%. Ocriplasmin is a protease inhibitor. It dissolves the protein component of the vitreous (collagen, laminin, fibronectin) that is responsible for vitreomacular adhesion.

    Ocriplasmin's effective dosage is 125 mcg intravitreal injection. The goal of using these drugs is to elicit vitreous gel liquefaction and total vitreous dehiscence from the retina.

    The kind of tear determines the management guidelines for posterior vitreous detachment associated with retinal tears. Operculated tears, whether symptomatic or asymptomatic, may not necessitate therapy. Whereas at least 50% of acute symptomatic U-tears with prolonged vitreoretinal tension result in clinical retinal detachment if not addressed and require immediate therapy.

    Other abnormalities that require treatment, according to the American Academy of Ophthalmology (AAO), include acute symptomatic retinal dialysis and traumatic retinal fractures. In this scenario, the therapy choices are as follows:

    • Laser Retinopexy: This technique is done using topical anesthetic. Around the lesion, two to three rows of confluent burns are administered.
    • Cryo-retinopexy: Regional or subconjunctival anaesthetic is used for this surgery. If the lesion is located beyond the equator, a subconjunctival incision may be used to get unobstructed access. The lesion is meticulously incised with a binocular indirect ophthalmoscope, and the cryoprobe is triggered until the retina whitens. The probe should not be withdrawn from the operated location until it has thawed (2-3 seconds), since this might result in subretinal bleeding. A single confluent row of applications surrounds the lesion.

    To guarantee adequate adhesion of the tear after laser or cryo-retinopexy, the patient should be encouraged to rest and avoid excessive exertion. Laser retinopexy is more accurate than cryo-retinopexy and generates less collateral retinal damage. Laser retinopexy has a lower risk of epiretinal membrane development than cryo-retinopexy. Cryotherapy, on the other hand, is preferable in eyes with cloudy corneas and tiny pupils.


    Differential Diagnosis

    Causes of Photopsia other than posterior vitreous detachment include the following:

    • A retinal tear or retinal detachment
    • Migraine with aura (classic)
    • Migraine headache without aura
    • Both early and the late stage of retinitis pigmentosa 


    Causes of floaters other than posterior vitreous detachment include the following:

    • Vitreous hemorrhage due to any cause including retinal tear or retinal detachment, proliferative diabetic retinopathy
    • Vitreous exudates in posterior uveitis, endophthalmitis
    • Vitreous pigments
    • Vitreous amyloidosis
    • Intravitreal injection of drugs


    Can vitreous detachment lead to retinal detachment? 

    Sometimes. When any part of the retina, the eye's light-sensitive tissue, is raised or removed from its natural location at the back wall of the eye, this is referred to as retinal detachment. This can occur immediately following a vitreous detachment.

    The vitreous detaches from the retina in the same way as an address label peels off an envelope. Sometimes the label peels completely off, while other times it shreds portions of the underlying envelope. When the vitreous detaches and rips the retina, the injury can worsen into a retinal detachment.

    It usually takes three months after a person's first floater for the vitreous to separate fully. If you experience a floater for the first time, you should see your eye doctor often over the next several months to ensure you don't have a retinal detachment.

    If a retinal detachment is detected early, it may typically be corrected in the eye doctor's office using laser therapy. If the retinal detachment is left untreated for too long (even just a few days), a far more dangerous procedure, such as vitrectomy or scleral buckle, may be necessary.

    If you recently had a vitreous detachment, keep an eye out for signs of retinal detachment, such as flashes of light, a shower of dots, and a pitch-black curtain entering and moving across your vision in any direction. If you experience any of these symptoms, especially if you have more than one, contact your eye doctor or go to the local emergency department very away.



    PVD (posterior vitreous detachment) is an eye disorder in which the vitreous membrane separates from the retina. It is characterized by the detachment of the posterior hyaloid membrane from the retina anyplace posterior to the vitreous base 

    The illness is frequent in older persons; it affects more than 75% of those over the age of 65. Although it is less frequent among persons in their 40s and 50s, the disorder is not uncommon in those age groups. According to some study, the illness is more frequent among women.

    PVD is not life-threatening, and the great majority of patients' symptoms resolve. After three months, most patients no longer feel flashes, and floaters tend to improve. PVD does not require any special therapy. However, while PVD consequences are uncommon, they can be significant and need immediate treatment, such as laser therapy for a retinal rupture or surgery for a retinal detachment.

    As a result, one or more checks are advised within three months following the commencement of PVD. In rare situations, floaters caused by PVD remain, and vitrectomy surgery to remove them is helpful; you and your doctor may consider this after reviewing the risks and advantages of surgery.