Posterior vitreous detachment (PVD) is a condition in which the posterior vitreous cortex detaches from the retina due to age-related or pathological changes. It refers to the separation of the posterior vitreous cortex from the ILM (internal limiting membrane), and accurate diagnosis of PVD is important for determining the prognosis of vitreoretinal diseases and surgical indications.
It is widely recognized as a physiological phenomenon associated with aging and is the most common cause of “floaters,” one of the most frequent complaints in ophthalmology outpatient clinics.
Age-related PVD increases after age 40 and is frequently observed in the elderly. In myopic eyes, the incidence is even higher, and in highly myopic eyes, partial PVD may occur earlier than in emmetropic eyes and may progress to complete PVD 1,6).
In myopic eyes, PVD tends to occur earlier, and it may develop in the fellow eye within a certain period 1,6). Some PVDs are found incidentally without symptoms 6).
The annual incidence of rhegmatogenous retinal detachment (RRD) is 10 to 18 per 100,000 people 6), and vitreous traction due to PVD is the most common mechanism.
When PVD is complete, a ring-shaped opacity of collagen (Weiss ring, prepapillary glial ring) formed at the time of vitreous detachment from the optic disc is perceived as floaters.
Basically, it is a physiological change associated with aging and is not a disease itself. However, because serious complications such as retinal tears and retinal detachment can occur with the onset of PVD, appropriate ophthalmic examination and follow-up at the right time are essential.
The main subjective symptoms that occur at the onset of PVD are shown below. Floaters and photopsia are typical complaints of PVD, and the majority originate from PVD 17).
The greater the number of floaters, the higher the risk of complications. When there are 10 or more floaters, the risk of retinal tear is highest1)17). Floaters usually decrease subjectively within about 3 months1). The impact of floaters on quality of life has been reported to be comparable to the utility value before cataract surgery13), so it is important not to underestimate patients’ complaints.
Floaters
Appearance: Worm-like, thread-like, or dot-like floating objects move within the visual field.
Cause: Aggregation of vitreous collagen, formation of Weiss ring (prepapillary glial ring).
Course: Often subjectively improves within about 3 months.
Photopsia
Appearance: White flashes in the peripheral visual field. Often occur in dark environments or with eye movement.
Cause: The vitreous pulls on the internal limiting membrane (ILM), stimulating the retina.
Importance: New photopsia is a sign of increased traction and risk of tear.
Negative Photopsia
Appearance: Black flashes (different from photopsia).
Cause: Vitreous traction at the optic disc → disruption of axonal transport.
Feature: May appear before classic photopsia.
The following fundus and vitreous findings are observed.
Floaters and photopsia associated with PVD require attention; in PVD accompanied by tobacco dust or hemorrhage in the vitreous gel, a retinal tear should be suspected and examination should proceed accordingly.
Changes in hyalocytes (resident macrophage-like cells at the posterior vitreous cortex interface) are also observed. In en face OCT case reports, hyperreflective dots thought to be hyalocytes increase and show morphological changes in the posterior vitreous cortex of PVD eyes 2). In abnormal PVD, cellular reactions at the vitreoretinal interface may contribute to traction membrane formation.
Vitreous hemorrhage is likely a sign of a retinal tear. Since the risk of a tear reaches 50–70% in cases with vitreous hemorrhage, promptly see an ophthalmologist for examination with indirect ophthalmoscopy or B-scan ultrasound. Once the hemorrhage clears, the fundus can be examined; until then, it is advisable to maintain rest.
PVD is classified as follows based on slit-lamp microscopy findings.
| Classification | Description | Clinical Significance |
|---|---|---|
| Complete PVD (collapsed type) | No continuity of posterior vitreous cortex to retina. Vitreous collapsed. | Symptoms gradually diminish. |
| Complete PVD (non-collapsed type) | Posterior vitreous cortex detached but not collapsed | Observation |
| Partial PVD with shrinkage | No mobility (contracted type) | Strong traction → risk of tear |
| Partial PVD without shrinkage | Mobility present (non-contracted type) | Relatively weak traction |
| Partial PVD without shrinkage (M) | Vitreous gel adheres to macula through premacular ring | Important subtype worsening ERM/DME prognosis |
In addition, OCT-based stage classification shows a stepwise progression from Stage 1 (paramacular PVD) to Stage 4 (complete PVD). The progression from partial PVD (Stages 1–3) to complete PVD peaks in the 50s to 60s. The AAO PPP 2024 also adopts a nearly identical four-stage classification: Stage 1 = paramacular separation with foveal adhesion remaining, Stage 2 = complete macular separation, Stage 3 = extensive separation with optic disc adhesion remaining, and Stage 4 = complete PVD 6). These stages do not necessarily progress linearly 6).
Shallow PVD is broadly divided into two types: those without thickening and contraction of the posterior vitreous cortex and those with it. Shallow PVD with thickening and contraction is seen in vitreomacular traction syndrome (VMT) and diabetic retinopathy, and often coexists with ERM. Those without thickening and contraction are classified as either an early stage of age-related PVD or perifoveal shallow PVD associated with macular hole.
The state of PVD (complete/partial/no PVD) greatly influences the prognosis of related diseases.
The development of PVD involves a dual mechanism of vitreous “liquefaction” and “weakening of adhesion between the posterior vitreous cortex and the ILM” 1).
The posterior wall of the posterior vitreous cortex pocket (Kishi pocket) gradually detaches from the perifoveal area with aging (Stage 1), then becomes parafoveal PVD (Stage 2). Subsequently, the pocket detaches from the fovea (Stage 3), and finally detaches from the optic disc, leading to complete PVD (Stage 4).
The diagnosis of PVD involves a combination of several examinations. In particular, a detailed fundus examination to check for the presence of retinal tears is most important.
This is the first step in diagnosing whether floaters are physiological or pathological. The vitreous is observed using a slit-lamp microscope and a non-contact biconvex lens. Set the slit beam width narrow and the illumination intensity to maximum, and observe dynamically while paying attention to the movement of the vitreous.
The presence of a prepapillary glial ring (Weiss ring) is used as an indicator to confirm the presence of PVD, and the type of PVD (complete/partial) is classified based on the continuity of the posterior vitreous cortex with the retina.
The prepapillary glial ring is often not a complete ring, and sometimes PVD occurs leaving the glial ring on the optic disc.
For patients with floaters and photopsia, systematically inquire about the following 6):
The staging classification of PVD based on OCT findings is shown.
| Stage | Condition |
|---|---|
| Stage 0 | No separation of the posterior vitreous cortex |
| Stage 1 | Partial detachment at the macula |
| Stage 2 | Detachment of the posterior pole including the optic disc |
| Stage 3 | Complete detachment except for the vitreous base |
| Stage 4 | Complete detachment including the vitreous base |
In patients presenting with floaters and photopsia, the most important step is to differentiate between physiological changes and pathological conditions.
Minor fibrous vitreous opacities or floaters associated with age-related PVD are called physiological floaters and do not require treatment. In contrast, floaters associated with retinal tears, retinal detachment, vitreous hemorrhage, or uveitis are pathological floaters and require active treatment.
If tobacco dust, hemorrhage, or flare is observed, it should be considered pathological, and a thorough fundus examination should be performed. In cases of PVD combined with photopsia, consider the possibility of strong traction on the retina and perform a detailed fundus examination. In PVD accompanied by tobacco dust or hemorrhage within the vitreous gel, proceed with examination assuming that “there is a retinal tear somewhere.”
Note that the blue field entoptic phenomenon, in which small bright dots move randomly within the visual field when looking at a bright blue light such as the sky, is different from floaters. It is caused by leukocytes flowing through retinal capillaries and does not require treatment.
| Differential Diagnosis | Features / Key Points |
|---|---|
| Retinal Tear / Retinal Detachment | Positive Shafer’s sign, visual field defect, vitreous hemorrhage. Confirm with indirect ophthalmoscopy. |
| Vitreous Hemorrhage | Sudden vision loss, worsening floaters. Exclude retinal detachment with B-scan. |
| Uveitis | Vitreous opacity, flare. Often accompanied by anterior chamber inflammation. |
| Epiretinal membrane (ERM) | Metamorphopsia, decreased vision. OCT confirms macular membrane formation. |
| Vitreomacular traction syndrome (VMT) | OCT shows macular traction. Associated with incomplete PVD (Stage 1–3). |
| Macular hole | Central scotoma, metamorphopsia. OCT confirms full-thickness defect. |
| Scintillating scotoma (migraine aura) | Binocular zigzag lights. Resolves within 15–30 minutes. |
| Branch retinal artery occlusion | Acute visual field defect. Retinal whitening on fundus exam. |
Floaters associated with age-related PVD generally do not require active treatment; observation is the standard approach1)18). Physiological floaters do not require treatment. In many cases, floaters subjectively improve within 3 months as patients adapt.
Pathological floaters (caused by retinal tear, retinal detachment, vitreous hemorrhage, uveitis, etc.) require treatment of the underlying condition. No preventive measures for PVD have been established. There is no effective way to prevent vitreous liquefaction, PVD, or RRD6).
Management strategies by lesion type based on AAO PPP 2024 are shown 6).
| Lesion type | Management strategy |
|---|---|
| Acute symptomatic horseshoe tear | Treat promptly |
| Acute symptomatic operculated round hole | Treatment may not be necessary |
| Acute symptomatic retinal dialysis | Treat promptly |
| Traumatic retinal tear | Usually treat |
| Asymptomatic horseshoe tear (no subclinical RRD) | Consider treatment if no signs of chronicity |
| Asymptomatic operculated round hole | Treatment is rarely recommended |
| Asymptomatic atrophic hole | Treatment rarely recommended |
| Asymptomatic lattice degeneration (no tear) | No treatment unless PVD causes a horseshoe tear |
| Floaters | No consensus on management; insufficient evidence |
The following shows recommended follow-up intervals by condition based on AAO PPP 20246).
| Condition | Follow-up Interval |
|---|---|
| Asymptomatic PVD | Routine exams only unless symptoms develop |
| Symptomatic PVD (no tear, no high-risk findings) | 4–6 weeks later; then as needed if symptoms change |
| Symptomatic PVD (no tear, with vitreous/retinal hemorrhage) | 1–2 weeks depending on retinal hemorrhage severity; weekly until vitreous hemorrhage resolves; B-scan if needed |
| Acute symptomatic horseshoe tear (post-treatment) | 1–2 weeks → 4–6 weeks → 3–6 months → then annually |
| Acute symptomatic operculated hole | 1–4 weeks → 1–3 months → 6–12 months → annually |
| Asymptomatic horseshoe tear | 1–4 weeks → 2–4 months → 6–12 months → annually |
| Asymptomatic atrophic hole | Every 1–2 years |
| Lattice degeneration (no tear) | Annually |
| Atrophic hole or lattice degeneration with history of RRD in fellow eye | Every 6–12 months |
When a tear is confirmed, prompt closure is necessary. Retinal vitreous diseases associated with PVD are indications for surgical treatments such as laser photocoagulation, buckling surgery, and vitrectomy.
Vitreous surgery (PPV): Selected when symptoms significantly impair QOL. It can remove Weiss rings and vitreous opacities 1). A prospective study by Sebag et al. (2014) confirmed its safety and efficacy 11). Nguyen et al. (2022) reported that PPV improves contrast sensitivity in multifocal pseudophakic eyes with floaters 19). However, attention should be paid to complications such as infection, retinal detachment, and cataract progression.
YAG laser vitreolysis: In a RCT by Shah et al. (2017) (JAMA Ophthalmol), the YAG vitreolysis group had significantly higher symptom improvement rates compared to the sham group 10). However, for the overall treatment of floaters, it is stated that “there is no consensus on management and insufficient evidence” (AAO PPP 2024) 6), and the Cochrane SR (Kokavec et al. 2017) also concluded that comparative evidence is insufficient 14).
QOL impact: Wagle et al. (2011) reported that the utility value of floaters is comparable to that before cataract surgery 13). Garcia et al. (2016) reported decreased contrast sensitivity after PVD 12).
When symptoms significantly impair quality of life, vitrectomy (PPV) or YAG laser vitreolysis are options. PPV can remove Weiss rings and vitreous opacities, and its safety and efficacy have been confirmed in prospective studies 11). Regarding YAG vitreolysis, an RCT (Shah 2017) showed significant improvement compared to sham 10), but both treatments are still being established as standard therapy, and indications should be carefully considered. Reports indicate that the impact of floaters on QOL is comparable to that before cataract surgery 13), so it is important not to underestimate patients’ complaints.
The vitreous is a gel-like transparent tissue that occupies about 80% of the eye’s volume, composed of 98-99% water 1). The remaining 1-2% consists mainly of hyaluronic acid (HA) and type II collagen fibers, which form a network structure maintaining the gel state. Hyaluronic acid retains large amounts of water, increasing viscosity and maintaining the vitreous gel structure. The posterior vitreous cortex adheres to the ILM, with an adhesion layer of fibronectin and other proteins between them.
The retina and vitreous are particularly strongly adherent at the following sites:
Normal PVD occurs through a process where “liquefaction precedes and adhesion weakens evenly.” In contrast, in anomalous PVD (vitreoretinal traction), even though liquefaction progresses, adhesion weakening is uneven, causing the vitreous to continue exerting strong local traction on the ILM 1).
Alsahaf et al. (2025) reported three cases of negative dysphotopsia 4). It was hypothesized that vitreous traction on the optic disc pulls on Elschnig’s membrane and the ILM, impairing axonal transport in ganglion cells and leading to negative dysphotopsia (ND). In Case 1, after 6 months of ND, a complete PVD and retinal tear were found, and laser treatment was performed. In Case 2, after 5 months of ND, the condition progressed to rhegmatogenous retinal detachment, requiring vitrectomy.
Physiological PVD and physiological floaters do not require treatment. Symptoms are strongly perceived immediately after PVD onset, but after complete PVD, the Weiss ring moves away from the retina, and subjective symptoms decrease. Floaters usually diminish subjectively within about 3 months 1). Long-term prospective observation also shows that early management at the time PVD is recognized serves as the first line of defense against RRD 18).
Even without an initial tear, about 2% develop a delayed tear within a few weeks, so a follow-up visit at 4–6 weeks is recommended 6). Especially if vitreous hemorrhage or pigment cells (tobacco dust) are present, follow-up every 1–2 weeks is necessary. Thereafter, it is generally recommended to visit as needed when symptoms change. Please seek prompt evaluation if new floaters increase, photopsia intensifies, visual field defects appear, or a curtain-like shadow is perceived.
Vitreous cortex components and activated hyalocytes remaining on the ILM after completion of PVD serve as a basis for epiretinal membrane (ERM) formation. It has been reported that 80–95% of ERM occur after PVD7), and OCT evaluation of the macula during PVD follow-up contributes to early detection of the disease.
Quantitative evaluation of hyalocytes using en face OCT may help predict the risk of vitreoretinal interface diseases (epiretinal membrane, VMT, macular hole). It has been reported that cells considered to be hyalocytes can be visualized and quantified by en face OCT in eyes with PVD 2), and cellular reactions at the vitreoretinal interface are attracting attention as a new research target.
Matsui et al. (2025) reported a 53-year-old woman with spontaneous separation of Stage 3 epiretinal membrane associated with an eye without PVD 5). The spontaneous separation rate of epiretinal membrane is usually 1-3%, but in eyes without PVD it is as high as 13.4%, far exceeding the 0.47-1.5% in eyes with existing PVD. OCT findings showed a decrease in epiretinal membrane thickness from 408 μm to 267 μm. It was suggested that vitreoschisis occurs at the adhesion site between the epiretinal membrane and the ILM in eyes without PVD, possibly involved in the mechanism of spontaneous separation.
Negative photopsia (dark flashes) is not distinguished from classic photopsia, and diagnosis may be delayed 4). In a case report by Alsahaf et al. (2025), a patient experienced negative photopsia before PVD progression, which later progressed to a tear and rhegmatogenous retinal detachment 4). The clinical importance of recognizing negative photopsia as a specific complaint has been pointed out.
Chen et al. (2023) reported a case of spontaneous closure of a myopic macular hole without PVD 3). The spontaneous closure rate of myopic macular holes is reported to be 6.2% (3.5% in some reports), and elucidating the mechanism by which spontaneous closure occurs despite persistent vitreous traction in cases without PVD is a future challenge.
Attempts are underway to pharmacologically cleave the adhesion between the vitreous and ILM by injecting enzyme preparations such as ocriplasmin into the vitreous cavity 1). It has been approved in some countries for vitreomacular traction syndrome (VMT), but its position as a standard treatment has not been established.
An RCT by Shah et al. (2017) (JAMA Ophthalmol) showed that the YAG vitreolysis group had a significantly higher symptom improvement rate than the sham group 10). On the other hand, a Cochrane SR (Kokavec et al. 2017) concluded that the comparative evidence for YAG vitreolysis vs PPV is insufficient 14), and consensus formation on floaters treatment remains a future challenge.
Garcia et al. (2016) reported that high-frequency contrast sensitivity significantly decreases after PVD 12). Nguyen et al. (2022) showed that contrast sensitivity improves after PPV in patients with floaters in multifocal pseudophakic eyes 19), and quantitative assessment of the functional impact of floaters is gaining attention.
