Floaters
Characteristics: Moving objects in the visual field, such as bugs, threads, or dots.
Cause: Aggregation of vitreous collagen, formation of Weiss ring (prepapillary glial ring).
Course: Often subjectively diminishes within about 3 months.
Posterior Vitreous Detachment (PVD)
1. What is Posterior Vitreous Detachment (PVD)?
Section titled “1. What is Posterior Vitreous Detachment (PVD)?”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) of the retina, 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 chief complaints in ophthalmology outpatient clinics.
Epidemiology
Section titled “Epidemiology”Age-related PVD increases after age 40 and is frequently observed in older individuals. In myopic eyes, the incidence is even higher; in highly myopic eyes, partial PVD occurs earlier than in emmetropic eyes and may progress to complete PVD1,6).
In myopic eyes, PVD tends to occur earlier and may develop in the fellow eye within a certain period1,6). Some PVDs are found incidentally without symptoms6).
The annual incidence of rhegmatogenous retinal detachment (RRD) is 10–18 per 100,000 people6), with vitreous traction due to PVD being the most common mechanism.
When PVD is complete, a ring-shaped opacity of collagen (Weiss ring, prepapillary glial ring) formed when the vitreous detaches from the optic disc is perceived as floaters.
Q
Is posterior vitreous detachment a disease?
A
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.
2. Main symptoms and clinical findings
Section titled “2. Main symptoms and clinical findings”Subjective symptoms (floaters, photopsia, negative visual phenomena)
Section titled “Subjective symptoms (floaters, photopsia, negative visual phenomena)”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 PVD17).
- Floaters: Symptoms of seeing things like mosquitoes, soot, or rings moving with eye movements against bright backgrounds such as white walls or windows. They are caused by collagen aggregation or Weiss ring formed when the posterior vitreous cortex separates from the ILM1). They are strongly perceived immediately after PVD onset, but as vitreous liquefaction progresses and complete PVD with collapse occurs, the prepapillary glial ring moves away from the retina, reducing subjective symptoms. Differentiation from the blue field entoptic phenomenon (small bright dots moving randomly in the visual field when looking at a bright blue sky) is necessary. Floaters can also cause decreased contrast sensitivity12).
- Photopsia: Flashes of light in the peripheral visual field in dark environments or with eye movements. Light stimulation of the retina occurs due to vitreous traction on the ILM1). When floaters associated with PVD are accompanied by photopsia, it is judged that strong traction is acting on the retina, and a detailed fundus examination of every corner of the fundus is necessary.
- Negative dysphotopsia: A symptom perceived as black flashes rather than white light. It is thought to occur when vitreous traction on the optic disc and ILM impairs axonal transport4). It may appear before classic photopsia prior to PVD completion4).
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 diminish 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.
Photopsia
Characteristics: White flashes in the peripheral visual field. More likely to occur in dark environments or with eye movement.
Cause: Vitreous traction on the ILM stimulates the retina.
Importance: New photopsia is a sign of increased traction and risk of tear.
Negative dysphotopsia
Characteristics: Black flashes (different from photopsia).
Cause: Vitreous traction on the optic disc → impaired axonal transport.
Feature: May appear before classic photopsia.
Clinical Findings
Section titled “Clinical Findings”The following fundus and vitreous findings are observed.
- Weiss ring (prepapillary glial ring): A ring-shaped opacity of collagen floating in front of the optic disc. It is an indicator of complete PVD. It is often not a complete ring, and sometimes PVD occurs with the glial ring remaining on the optic disc.
- Shafer’s sign (tobacco dust): Tobacco dust-like pigment floating in the anterior vitreous is an important finding suggesting the presence of a retinal break. It originates from retinal pigment epithelial cells, and in approximately 80% of patients who develop a delayed retinal break, either vitreous pigment/hemorrhage at the initial visit or new symptoms prompting re-examination were observed 6).
- Vitreous hemorrhage: Occurs when retinal blood vessels are torn by vitreous traction. When vitreous hemorrhage is present, the probability of a retinal break increases to 50–70% 6).
- Retinal break: Complicates 5.4–8% of PVD cases 6). Horseshoe tears are the most common, and they frequently occur at lattice degeneration sites in the peripheral retina.
Floaters and photopsia associated with PVD require attention; in PVD accompanied by tobacco dust or hemorrhage within the vitreous gel, examination should proceed assuming a retinal break is present.
Changes in hyalocytes (resident macrophage-like cells at the posterior vitreous cortex interface) are also observed. In an en face OCT case report, hyperreflective dots thought to be hyalocytes increased and showed morphological changes within the posterior vitreous cortex of PVD eyes 2). In abnormal PVD, cellular reactions at the vitreoretinal interface may contribute to tractional membrane formation.
Q
What should be done if vitreous hemorrhage occurs?
A
Vitreous hemorrhage is highly likely to be a sign of a retinal break. Since the risk of a break reaches 50–70% in cases with vitreous hemorrhage, promptly see an ophthalmologist and undergo a detailed examination using indirect ophthalmoscopy or ultrasound B-scan. Once the hemorrhage is absorbed, the fundus can be observed, but until then, it is advisable to maintain rest.
PVD Classification
Section titled “PVD Classification”PVD is classified as follows based on slit-lamp microscopy findings.
| Classification | Description | Clinical Significance |
|---|---|---|
| Complete PVD (collapsed type) | No continuity of the posterior vitreous cortex to the retina. Vitreous is 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 the macula through the premacular ring | Important subtype that worsens ERM/DME prognosis |
In addition, OCT-based staging shows a gradual 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 and 60s. The AAO PPP 2024 also adopts a nearly identical 4-stage classification: Stage 1 = parafoveal separation with residual foveal adhesion, Stage 2 = complete macular separation, Stage 3 = extensive separation with residual optic disc adhesion, and Stage 4 = complete PVD6). These stages do not necessarily progress linearly6).
Shallow PVD is broadly divided into two types: with and without thickening/contraction of the posterior vitreous cortex. Shallow PVD with thickening/contraction is seen in vitreomacular traction syndrome (VMT) and diabetic retinopathy, and is often associated with ERM. The type without thickening/contraction is classified as either an early stage of age-related PVD or perifoveal shallow PVD associated with macular hole.
Association with disease prognosis
Section titled “Association with disease prognosis”The state of PVD (complete/partial/no PVD) greatly influences the prognosis of associated diseases.
- Rhegmatogenous retinal detachment: In no PVD, rapid progression of retinal detachment is less common. In flap tears associated with PVD, retinal detachment progresses rapidly.
- Epiretinal membrane (ERM): 80–95% of ERM cases are reported to occur after PVD7). Partial PVD without shrinkage (M) type worsens the prognosis of ERM and DME.
3. Causes and Risk Factors
Section titled “3. Causes and Risk Factors”Dual Mechanism of Vitreous Aging
Section titled “Dual Mechanism of Vitreous Aging”The development of PVD involves a dual mechanism of vitreous “liquefaction” and “weakening of adhesion between the posterior vitreous cortex and the ILM”1).
- Liquefaction (syneresis): The vitreous is a gel composed of type II collagen fibers and hyaluronic acid (HA), with water accounting for 98–99% of its content1). Hyaluronic acid retains a large amount of water, increasing viscosity and maintaining the gel structure of the vitreous. With aging, aggregation and rearrangement of collagen fibers progress, resulting in liquefied cavities occupying 25% at age 50 and 62% at age 801). Enlargement of liquefied cavities facilitates detachment of the posterior vitreous cortex from the ILM.
- Weakening of adhesion: Degeneration of adhesion molecules (e.g., fibronectin) between the posterior vitreous cortex and the ILM reduces adhesive strength1). PVD develops when both liquefaction and weakening of adhesion are present.
The posterior wall of the posterior vitreous cortex pocket (Kishi pocket) gradually detaches from the perifoveal area with aging (Stage 1), eventually becoming 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).
Major Risk Factors
Section titled “Major Risk Factors”- Aging: The greatest risk factor. Prevalence increases sharply from 24% in those aged 50–59 to 87% in those aged 80–901).
- High myopia: Vitreous degeneration accelerates with axial elongation, and early changes may occur in the 20s. Onset is approximately 10 years earlier than in emmetropic eyes1). Even low myopia (1–3 D) increases the risk of rhegmatogenous retinal detachment (RRD) by 4-fold, and over −3 D by 10-fold15). More than half of nontraumatic RRD cases occur in myopic eyes15).
- Postmenopausal women: Estrogen deficiency promotes vitreous collagen degeneration1).
- After cataract surgery: The incidence of RRD within 1 year after cataract surgery is 0.21% (approximately 1 in 500) 20). 20–40% of all RRDs occur after cataract surgery 6). Nd:YAG laser posterior capsulotomy increases RRD risk by 4 times (especially in myopic eyes) 6).
- History of RRD in the fellow eye: The risk of RRD in the fellow eye after non-traumatic RRD is approximately 10% 6).
- History of intravitreal injection: Intravitreal anti-VEGF injections may induce PVD 6).
- Stickler syndrome: The most common hereditary vitreoretinal disease. Prophylactic 360° laser treatment is recommended 6).
- Trauma/inflammation: Rapid changes in vitreous structure can induce PVD.
4. Diagnosis and Examination Methods
Section titled “4. Diagnosis and Examination Methods”Diagnosis of PVD involves a combination of several examinations. In particular, a detailed fundus examination to check for the presence of tears is most important.
Slit-Lamp Microscopy
Section titled “Slit-Lamp Microscopy”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 light width narrow and the illumination intensity to maximum, and observe dynamically while being aware of vitreous movement.
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.
- After excluding tears and retinal detachment through peripheral retinal examination under mydriasis, if there is no obvious vitreous opacity other than the prepapillary glial ring besides PVD, physiological floaters are considered 6).
- If tobacco dust, hemorrhage, or flare is observed, the fundus should be thoroughly examined.
The prepapillary glial ring is often not a complete ring, and sometimes PVD occurs with the glial ring remaining on the optic disc.
Main Examination Methods
Section titled “Main Examination Methods”- Indirect ophthalmoscopy + scleral depression: Standard examination for direct observation of the peripheral fundus. Confirms the presence of retinal tears, lattice degeneration, and vitreous hemorrhage. The AAO PPP recommends peripheral examination with scleral depression in PVD cases6).
- Optical coherence tomography (OCT): Noninvasively visualizes the positional relationship between the posterior vitreous cortex and the ILM. The Kakehashi classification (Stages 0–4) can be used to evaluate the stage of PVD1). The clinical utility of PVD staging using circumpapillary OCT and macular volume OCT has also been reported6).
- Ultrasound B-scan: Useful for evaluating retinal detachment and PVD when fundus observation is difficult due to vitreous hemorrhage or other conditions.
- Wide-angle fundus photography: Can record and detect some peripheral tears, but does not replace careful peripheral fundus examination including scleral depression. May be useful as an adjunct in patients who cannot tolerate standard examination6).
- En face OCT: Enables en face evaluation of hyalocyte distribution at the posterior vitreous cortex interface. It has been reported that hyperreflective spots, thought to be hyalocytes, can be evaluated by en face OCT in PVD eyes2).
Key Points in History Taking
Section titled “Key Points in History Taking”For patients with floaters and photopsia, systematically inquire about the following6):
- Onset and course of PVD symptoms (floaters, photopsia)
- Family history of RRD and hereditary diseases (e.g., Stickler syndrome)
- History of ocular trauma
- Presence and degree of myopia
- History of intraocular surgery (cataract surgery, Nd:YAG posterior capsulotomy)
- History of intravitreal injection
PVD Stage Classification (Kakehashi Classification)
Section titled “PVD Stage Classification (Kakehashi Classification)”The staging classification of PVD based on OCT findings is shown.
| Stage | Condition |
|---|---|
| Stage 0 | No separation of the posterior vitreous face |
| Stage 1 | Perifoveal separation with persistent adhesion to the fovea |
| Stage 2 | Separation from the macula with persistent adhesion to the optic disc |
| Stage 3 | Extensive separation with persistent adhesion to the optic disc |
| Stage 4 | Complete PVD with separation from the optic disc (physiological attachment at the vitreous base remains) |
In this 4-stage classification, Stage 4 is not defined as a state of detachment down to the vitreous base6).
5. Differential Diagnosis
Section titled “5. Differential Diagnosis”In patients presenting with floaters and photopsia, the most important step is to differentiate between physiological changes and pathological conditions.
Physiological Floaters vs. Pathological Floaters
Section titled “Physiological Floaters vs. Pathological Floaters”Slight 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, the possibility of strong traction on the retina should be considered, and a detailed fundus examination should be conducted. In PVD accompanied by tobacco dust or hemorrhage within the vitreous gel, the examination should proceed with the assumption 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 sky, is different from floaters. It is caused by leukocytes flowing through retinal capillaries and does not require treatment.
Main Differential Diagnoses
Section titled “Main Differential Diagnoses”| Differential Diagnosis | Features / Key Points |
|---|---|
| Retinal tear / Retinal detachment | Shafer’s sign positive, visual field defect, vitreous hemorrhage. Confirmed by indirect ophthalmoscopy. |
| Vitreous hemorrhage | Sudden vision loss, worsening of floaters. B-scan to rule out retinal detachment. |
| Uveitis | Vitreous opacity, flare. Often accompanied by anterior chamber inflammatory findings. |
| Epiretinal membrane (ERM) | Metamorphopsia, decreased vision. OCT confirms macular membrane formation. |
| Vitreomacular traction syndrome (VMT) | OCT shows macular traction findings. 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. |
6. Standard Treatment
Section titled “6. Standard Treatment”Basic Observation Policy
Section titled “Basic Observation Policy”Floaters associated with age-related PVD generally do not require active treatment; observation is the mainstay1)18). Physiological floaters do not require treatment. In many cases, floaters subjectively decrease 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 method to prevent vitreous liquefaction, PVD, or RRD6).
Management Recommendations by Lesion Type
Section titled “Management Recommendations by Lesion Type”Management strategies by lesion type based on AAO PPP 2024 are shown6).
| 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 break | 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 |
Follow-up Schedule
Section titled “Follow-up Schedule”The following table shows recommended follow-up intervals by condition based on the AAO PPP 20246).
| Condition | Follow-up Interval |
|---|---|
| Asymptomatic PVD | Routine examination only unless symptoms develop |
| Symptomatic PVD (no tear, no high-risk findings) | 4–6 weeks later; thereafter if symptoms change |
| Symptomatic PVD (no tear, with vitreous/retinal hemorrhage) | 1–2 weeks depending on severity of retinal hemorrhage; weekly until vitreous hemorrhage resolves; B-scan as needed |
| Acute symptomatic horseshoe tear (post-treatment) | 1–2 weeks → 4–6 weeks → 3–6 months → then annually |
| Acute symptomatic operculated round 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 round hole | Every 1–2 years |
| Lattice degeneration (no tear) | Annually |
| Atrophic round hole or lattice degeneration with history of RRD in fellow eye | Every 6–12 months |
Treatment of Cases with Retinal Tear
Section titled “Treatment of Cases with Retinal Tear”When a tear is confirmed, prompt closure of the tear is necessary. Retinal vitreous diseases associated with PVD are indications for surgical treatment such as retinal photocoagulation, buckling surgery, and vitrectomy.
- Laser retinal photocoagulation: Create 2–3 rows of coagulation spots around the horseshoe tear to seal it. It is considered superior to retinal cryocoagulation1). If the tear cannot be surrounded by laser or cryocoagulation, extend treatment to the ora serrata6). The most common cause of treatment failure is inadequate treatment, especially insufficient treatment of the anterior edge6). At least half of untreated symptomatic horseshoe tears progress to RRD, but treatment can reduce the risk of RRD from symptomatic tears to less than 5%6).
- Retinal cryopexy: Selected for cases where laser is difficult (e.g., peripheral tears).
- Scleral buckling surgery: Surgical treatment for retinal detachment associated with PVD. Cochrane SR comparing PPV vs SB found no significant difference in anatomical or visual outcomes (low to very low evidence)6). Over 95% of uncomplicated RRD can be repaired (may require multiple surgeries)6).
- Vitrectomy: Surgical treatment for vitreoretinal diseases associated with PVD. For symptomatic floaters, it is an option when quality of life is significantly impaired, but there is no sufficient consensus on management6).
Treatment of Floaters
Section titled “Treatment of Floaters”Vitreous surgery (PPV): Selected when symptoms significantly impair QOL. It can remove Weiss rings and vitreous opacities1). Sebag et al. (2014) prospectively analyzed efficacy and retrospectively assessed safety11). Nguyen et al. (2022) reported that PPV improves contrast sensitivity in multifocal pseudophakic eyes with floaters19). However, attention should be paid to risks of complications such as infection, retinal detachment, and cataract progression.
YAG laser vitreolysis: In the RCT by Shah et al. (2017) (JAMA Ophthalmol), the YAG vitreolysis group had significantly higher symptom improvement rates compared to the sham group10). However, for floaters treatment in general, it is stated that “no consensus on management, insufficient evidence” (AAO PPP 2024)6), and the Cochrane SR (Kokavec et al. 2017) also concluded that comparative evidence is insufficient14).
QOL impact: Wagle et al. (2011) reported that the utility value of floaters is comparable to that before cataract surgery13). Garcia et al. (2016) reported decreased contrast sensitivity after PVD12).
Q
Can floaters be treated with surgery?
A
When symptoms significantly impair quality of life, vitrectomy (PPV) or YAG laser vitreolysis are options. Prospective efficacy analyses and retrospective safety evaluations have been reported for PPV11). For YAG vitreolysis, a randomized controlled trial (Shah 2017) showed significant improvement compared to sham10), but both treatments are still being established as standard care, and indications should be carefully considered. The impact of floaters on quality of life has been reported to be comparable to that before cataract surgery13), and it is important not to underestimate patients’ complaints.
7. Pathophysiology and Detailed Mechanisms
Section titled “7. Pathophysiology and Detailed Mechanisms”Structure of the Vitreous
Section titled “Structure of the Vitreous”The vitreous is a gel-like transparent tissue that occupies approximately 80% of the ocular volume, composed of 98–99% water1). 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 a large amount of water, increasing viscosity and maintaining the vitreous gel structure. The posterior vitreous cortex adheres to the internal limiting membrane (ILM), with an adhesion layer of fibronectin and other fibronectin-binding proteins between them.
The retina and vitreous are particularly strongly adherent at the following sites:
- Vitreous base: The strongest adhesion site. Vitreous fibers run perpendicularly into the basement membrane of the ciliary body.
- Wieger ligament: Adhesion between the posterior lens capsule and the anterior vitreous.
- Optic disc margin
- Macula
- Major retinal vessels
Mechanism of Abnormal PVD
Section titled “Mechanism of Abnormal PVD”Normal PVD occurs through a process where “liquefaction precedes and adhesion weakens uniformly.” In contrast, in abnormal PVD (vitreoretinal traction), even if liquefaction progresses, adhesion weakening is uneven, causing the vitreous to continue locally strong traction on the ILM1).
- Vitreoschisis: A condition where the posterior vitreous cortex splits into inner and outer layers, with the outer layer remaining on the ILM. It contributes to vitreoretinal interface diseases (macular hole, epiretinal membrane, vitreomacular traction)2).
- Role of hyalocytes: Resident macrophage-like cells present at the posterior vitreous cortex interface. They may become activated during anomalous PVD and contribute to the formation of tractional membranes (epiretinal membranes)2).
Mechanism of negative dysphotopsia
Section titled “Mechanism of negative dysphotopsia”Alsahaf et al. (2025) reported three cases of negative dysphotopsia4). It was hypothesized that vitreous papillary traction pulls on Elschnig’s membrane and the ILM, impairing axonal transport in ganglion cells, leading to neuropathic scotoma (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.
8. Prognosis and course
Section titled “8. Prognosis and course”Prognosis of physiological PVD
Section titled “Prognosis of physiological PVD”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 diminish. Floaters usually subjectively decrease within about 3 months1). Long-term prospective observation also shows that early management at the stage when PVD is recognized serves as the first line of defense against RRD18).
Risk of delayed-onset retinal tears
Section titled “Risk of delayed-onset retinal tears”- Acute PVD without initial tear: approximately 2% develop a delayed tear within a few weeks6)
- Symptomatic PVD with a tear at initial visit: 5–14% develop additional tears during long-term follow-up6)
- Approximately 80% of patients who develop a delayed tear had either vitreous pigment, hemorrhage at the initial visit, or new symptoms prompting re-examination6)
- Coffee et al. (2007) meta-analysis clarified the incidence and clinical characteristics of delayed tears after symptomatic PVD8)
- Seider et al. (2022) conducted a retrospective cohort using 8,305 medical records to examine risk factors for retinal tears and detachment associated with acute symptomatic PVD9)
- Jindachomthong et al. (2023) reported the incidence and risk factors of delayed tears after acute symptomatic PVD16)
- Vangipuram et al. (2023) analyzed the timing of delayed retinal lesions in patients presenting with acute PVD using the IRIS® Registry21)
Q
If diagnosed with PVD, are regular checkups necessary?
A
Even without an initial tear, about 2% develop a delayed tear within a few weeks, so a follow-up visit after 4–6 weeks is recommended6). Especially when vitreous hemorrhage or pigment cells (tobacco dust) are observed, follow-up every 1–2 weeks is necessary. Thereafter, the basic approach is to visit as needed when symptoms change. If new floaters increase, photopsia intensifies, visual field defects appear, or a curtain-like shadow occurs, please seek immediate medical attention.
Risk of progression from tear to RRD
Section titled “Risk of progression from tear to RRD”- Untreated symptomatic horseshoe tear: at least half progress to RRD6)
- Treatment (chorioretinal adhesion around the tear by photocoagulation) can reduce this to less than 5%6)
- Asymptomatic horseshoe tear: about 5% progress to RRD6)
- Asymptomatic round hole with operculum or atrophic hole: progression to RRD is rare6)
Prognosis of PVD status and related diseases
Section titled “Prognosis of PVD status and related diseases”- Rhegmatogenous retinal detachment: With PVD and flap tear, it progresses rapidly. With no PVD, rapid progression is less common.
- Epiretinal membrane (ERM): 80–95% of ERM occurs after PVD7). Partial PVD without shrinkage (M) type worsens the prognosis of ERM and DME.
9. Latest research and future perspectives (reports under investigation)
Section titled “9. Latest research and future perspectives (reports under investigation)”Association between vitreoretinal interface diseases and PVD
Section titled “Association between vitreoretinal interface diseases and PVD”After completion of PVD, residual vitreous cortex components and activated hyalocytes on the ILM serve as a foundation for epiretinal membrane (ERM) formation. It has been reported that 80–95% of epiretinal membranes occur after PVD7), and OCT evaluation of the macula during PVD follow-up contributes to early detection of the disease.
Biomarker application of hyalocytes
Section titled “Biomarker application of hyalocytes”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 PVD2), and cellular reactions at the vitreoretinal interface are attracting attention as a new research target.
Relationship between spontaneous epiretinal membrane peeling and PVD
Section titled “Relationship between spontaneous epiretinal membrane peeling and PVD”Matsui et al. (2025) reported a case of spontaneous peeling of a Stage 3 idiopathic epiretinal membrane associated with progression of PVD5). This is a single case report and does not indicate the general spontaneous peeling rate or prognosis of epiretinal membranes.
Increased awareness of negative photopsia
Section titled “Increased awareness of negative photopsia”Negative photopsia (dark flashes) is often not distinguished from classic photopsia, leading to delayed diagnosis4). A case report by Alsahaf et al. (2025) described a patient who experienced negative photopsia before PVD progression, which subsequently developed into a tear and rhegmatogenous retinal detachment4). The clinical importance of recognizing negative photopsia as a specific complaint has been highlighted.
PVD and spontaneous closure of myopic macular hole
Section titled “PVD and spontaneous closure of myopic macular hole”Chen et al. (2023) reported a case of a myopic macular hole without PVD that spontaneously closed twice3). Spontaneous closure of myopic macular holes is limited to a few case reports, and the spontaneous closure rate has not been established.
Pharmacologic vitreolysis
Section titled “Pharmacologic vitreolysis”Ocriplasmin is a drug that has been investigated for pharmacologic release of vitreoretinal adhesion in vitreomacular traction (VMT)7). Its availability and role vary by country and region, and it is not a treatment for uncomplicated PVD.
Accumulating evidence for YAG laser vitreolysis
Section titled “Accumulating evidence for YAG laser vitreolysis”An RCT by Shah et al. (2017) (JAMA Ophthalmol) showed that the YAG vitreolysis group had a significantly higher rate of symptom improvement than the sham group10). On the other hand, a Cochrane SR (Kokavec et al. 2017) concluded that the comparative evidence for YAG vitreolysis vs. PPV was insufficient14), and consensus formation regarding treatment for floaters remains a future challenge.
Floaters and contrast sensitivity
Section titled “Floaters and contrast sensitivity”Garcia et al. (2016) reported that high-frequency contrast sensitivity significantly decreases after PVD12). Nguyen et al. (2022) showed that contrast sensitivity improves after PPV in patients with floaters in multifocal pseudophakic eyes19), and quantitative assessment of the functional impact of floaters is attracting attention.
10. References
Section titled “10. References”- Johnson MW. Posterior vitreous detachment: evolution and complications of its early stages. Am J Ophthalmol. 2010;149(3):371-382.e1. doi:10.1016/j.ajo.2009.11.022.
- Ahsanuddin S, Rahimy E, Chai R, et al. 3-D OCT imaging of hyalocytes in partial posterior vitreous detachment and vaso-occlusive retinal disease. Am J Ophthalmol Case Rep. 2023;30:101836. doi:10.1016/j.ajoc.2023.101836. PMCID: PMC10139967.
- Chen FT. Spontaneous Closure of Myopic Macular Hole Twice Without Posterior Vitreous Detachment. Retin Cases Brief Rep. 2023;17(5):554-556. doi:10.1097/ICB.0000000000001235. PMID:37643041; PMCID:PMC10448797.
- Alsahaf M, Brookes M, Shanmuganathan V, Williamson TJ. Black Flashes (Dysphotopsia) As A Symptom of Vitreo-Papillary Traction in Evolving Posterior Vitreous Detachment - An Optical Coherence Tomography Case Series. Am J Ophthalmol Case Rep. 2025;39:102362. doi:10.1016/j.ajoc.2025.102362.
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