Retina Companion Note
Retinal Holes, Tears and Dialysis
Recognise the major peripheral retinal breaks, understand how they form, and relate their morphology to retinal-detachment risk and treatment.
Watch the lecture first, then use this companion note to compare how each retinal break forms, appears and influences the risk of retinal detachment.
What Is a Retinal Break?
A retinal break is a full-thickness discontinuity in the neurosensory retina.
Normally, the neurosensory retina lies against the underlying retinal pigment epithelium (RPE). When a full-thickness break develops, liquefied vitreous may enter the potential subretinal space and separate these layers.[1]
A partial-thickness retinal excavation does not provide a complete passage into the subretinal space and should not be classified as a retinal break.
How Retinal Breaks Form
Retinal breaks arise through three principal mechanisms.
| Mechanism | What happens? | Typical lesions |
|---|---|---|
| Degeneration and thinning | Focal retinal thinning produces a full-thickness defect without active vitreous traction. | Atrophic retinal hole |
| Vitreoretinal traction | Vitreous remains attached during separation and pulls or avulses retinal tissue. |
Horseshoe tear Operculated hole |
| Trauma | Rapid globe compression and equatorial expansion transmit force to the vitreous base and peripheral retina. |
Retinal dialysis Ragged equatorial tear Horseshoe tear Vitreous-base avulsion |
The next step is not simply to name the break, but to determine which mechanism produced it.
Why New Flashes and Floaters Matter
Photopsia means a perceived flash of light. During an acute posterior vitreous detachment (PVD), traction on the peripheral retina may mechanically stimulate the retina and produce brief flashes.
A sudden increase in floaters may accompany vitreous separation, pigment release or vitreous haemorrhage.
New flashes and floaters do not prove that a retinal tear is present. They indicate that a tear must be actively excluded.
had a retinal tear or retinal detachment at presentation
developed a delayed retinal tear within two months
These figures come from a contemporary prospective study of eyes presenting with symptomatic PVD.[2]
Migraine-related visual phenomena are often bilateral, evolve over several minutes and may have a scintillating or zigzag pattern. Retinal photopsias are commonly brief, peripheral and monocular. Symptoms alone, however, cannot safely exclude a retinal break.
Examining the Peripheral Retina
The peripheral retina should be examined through a dilated pupil using binocular indirect ophthalmoscopy, with scleral indentation where appropriate.[1][2]
Assess for a posterior vitreous detachment.
Look for vitreous pigment or vitreous haemorrhage.
Perform a 360° examination of the peripheral retina.
Carefully inspect the vitreous base and ora serrata.
Use scleral indentation to expose the far peripheral retina.
Continue examining after the first retinal break is found.
With the examination principles established, the individual lesions can now be compared using the same sequence: mechanism, appearance, clinical significance and management.
Atrophic Retinal Holes
Mechanism
An atrophic retinal hole develops when focal degeneration and thinning produce a round full-thickness defect in the neurosensory retina.
There is no active vitreoretinal traction pulling on its margins.[1]
Appearance
- Round or oval shape
- Smooth, well-defined margins
- No attached retinal flap
- No overlying operculum
- Frequently associated with lattice degeneration
- May occur as a solitary hole or as multiple holes
A small cuff of subretinal fluid may occasionally surround the hole.
Subretinal fluid extending at least one disc diameter from a retinal break, but no more than two disc diameters posterior to the equator, without a corresponding visual-field defect.[4]
Clinical significance
Most atrophic holes are asymptomatic and remain stable. Retinal detachment arising from an atrophic hole is uncommon and usually progresses slowly.[1][4]
When detachment occurs, the typical setting is a younger myopic patient, often with lattice degeneration and without an acute PVD. Because traction may be absent, flashes and a sudden shower of floaters may also be absent.
Management
Asymptomatic atrophic retinal holes rarely require prophylactic treatment.[1][3]
Observation is usual when there is no progressive subretinal fluid or associated retinal detachment. Treatment may be considered when subretinal fluid is progressing or when the complete clinical context suggests a meaningful detachment risk.
High myopia, lattice degeneration, pseudophakia or fellow-eye retinal detachment may influence the decision, but none automatically mandates laser treatment.[1][3]
Horseshoe Retinal Tears
Mechanism
A horseshoe tear, also called a flap tear, develops when the vitreous remains firmly attached to the retina during posterior vitreous separation.
The vitreous pulls a flap of retina forward, creating a full-thickness U-shaped tear.[1]
Appearance
The tear may occur beside lattice degeneration or another area of strong vitreoretinal adhesion.
Directed posteriorly
Directed anteriorly
Remains attached to the vitreous
Clinical significance
The attached flap shows that vitreoretinal traction has not been released. Continued pulling may enlarge the tear, while liquefied vitreous may pass through the break into the subretinal space.
Acute horseshoe tears commonly present with:
- New flashes
- A sudden increase in floaters
- Vitreous pigment
- Vitreous or retinal haemorrhage
Pigmentation around a break may suggest chronicity. It does not prove that the tear is safe or that a sufficiently protective adhesion has developed.
Management
An acute symptomatic horseshoe tear usually requires prompt retinopexy because persistent traction creates a substantial risk of progression to rhegmatogenous retinal detachment.[1]
An asymptomatic horseshoe tear requires individual assessment based on the presence of:
- Persistent traction
- Subretinal fluid
- Haemorrhage
- The wider retinal-detachment risk context
Operculated Retinal Holes
Mechanism
An operculated retinal hole develops when focal vitreoretinal traction avulses a small plug of neurosensory retina.
The separated retinal tissue is called the operculum.
Appearance
- A round full-thickness retinal defect
- A small overlying plug of retinal tissue
- An operculum that may remain partly attached or become free-floating
Operculated holes may arise at focal areas of strong vitreoretinal adhesion, including retinal tufts.
Clinical significance
Symptoms may occur while traction is actively pulling on the retina.
Focal traction pulls on the retina.
A small plug of retina is avulsed.
Once the operculum separates completely, focal traction is usually released.
The subsequent risk of retinal detachment is therefore generally lower than with a horseshoe tear, in which the retinal flap remains attached to the vitreous.[1]
Management
Asymptomatic operculated holes rarely require treatment.[1]
Even an acutely symptomatic operculated hole may be observed when examination confirms that:
- Traction has been released
- There is no progressive subretinal fluid
- No associated higher-risk retinal tear is present
Do Not Confuse These Lesions
The practical distinction is whether vitreoretinal traction is absent, released or still active.
Swipe across the table to see all columns →
| Feature | Atrophic hole | Operculated hole | Horseshoe tear |
|---|---|---|---|
| Mechanism | Retinal thinning | Focal traction with tissue avulsion | Persistent vitreoretinal traction |
| Shape | Round or oval | Round defect with an operculum | U-shaped retinal flap |
| Vitreous attachment | None | Operculum attached to the vitreous | Retinal flap attached to the vitreous |
| Persistent traction | No | Usually released after separation | Yes |
| Detachment risk | Low | Usually low | Higher |
| Usual approach | Observe | Usually observe | Prompt treatment if acute and symptomatic |
Giant Retinal Tears
A giant retinal tear is a full-thickness circumferential retinal break extending through at least 3 clock hours or 90°, in association with posterior vitreous separation.[5]
Mechanism
The tear commonly develops near the posterior border of the vitreous base.
Appearance
The unsupported posterior flap becomes highly mobile and may fold or invert.
When the flap inverts, the undersurface of the retina may become visible.
Clinical significance
A giant retinal tear may lead to:
- Rapidly progressive retinal detachment
- Extensive retinal mobility
- Flap inversion
- Proliferative vitreoretinopathy
- Technically complex retinal surgery
Prognosis
The prognosis is not uniformly poor. Modern anatomical outcomes are substantially better than historical teaching suggested.
Visual outcome still depends on macular status, the extent of retinal detachment and the presence of proliferative vitreoretinopathy.
Retinal Dialysis
A retinal dialysis is a circumferential disinsertion of the retina at or close to the ora serrata.[6][7][8]
It is commonly associated with blunt ocular trauma, although the history of trauma may be remote or initially overlooked.
Mechanism
Unlike a giant retinal tear, posterior vitreous detachment is not the primary mechanism.
Appearance
- The vitreous base commonly remains attached to the posterior retinal edge.
- The posterior margin retains vitreous support and therefore does not usually invert.
- A subtle dialysis may appear as a slit at the ora serrata and may open during scleral indentation.
Clinical significance
Retinal detachment associated with dialysis may progress slowly. Patients may remain asymptomatic until the detachment becomes extensive or reaches the macula.[6][7][8]
A remote history of blunt trauma does not exclude traumatic retinal dialysis.
In a historical series, only 15.8% presented within one month of injury, while 41% were diagnosed more than one year later.[6]
Management
Retinal dialysis requires specialist retinal assessment.
- Extent of the dialysis
- Associated subretinal fluid
- Presence and extent of retinal detachment
- Chronicity
- Macular status
Traumatic retinal breaks usually require treatment, but the intervention depends on the individual lesion and whether retinal detachment is already present.[1]
Giant Retinal Tear or Retinal Dialysis?
These lesions differ in their site, mechanism and relationship to the vitreous. The behaviour of the posterior retinal edge is an especially useful distinction.[5][6][7][8]
Swipe across the table to see all columns →
| Feature | Giant retinal tear | Retinal dialysis |
|---|---|---|
| Definition | A circumferential full-thickness retinal tear extending through at least 3 clock hours or 90°. | A circumferential disinsertion of the retina at or close to the ora serrata. |
| Typical site | Near the posterior border of the vitreous base. | At or close to the ora serrata. |
| Main mechanism | Develops in association with posterior vitreous separation. | Usually results from peripheral retinal disinsertion, commonly following blunt ocular trauma. |
| Vitreous relationship | The anterior retinal edge remains related to the vitreous base, while the posterior flap loses vitreous support. | The vitreous base usually remains attached to the posterior retinal edge. |
| Posterior flap and inversion | The unsupported posterior flap becomes highly mobile and may fold or invert. When inverted, the undersurface of the retina may be visible. | The posterior edge retains vitreous support and therefore does not usually invert. |
| Role of posterior vitreous detachment | Posterior vitreous separation is an important part of the mechanism. | Posterior vitreous detachment is not the primary mechanism. |
| Typical course | May produce a rapidly progressive retinal detachment. | Associated retinal detachment may progress slowly. |
| Presentation | Usually an acute, sight-threatening vitreoretinal presentation. | May present months or years after trauma, and the original injury may be overlooked. |
Traumatic Retinal Breaks
Blunt ocular trauma can produce several patterns of peripheral retinal injury. The breaks may be multiple, so identifying one lesion does not complete the examination.[1]
Mechanism
Blunt ocular trauma
Rapid anteroposterior compression
Equatorial expansion of the globe
Traction at the vitreous base
Break patterns
- Retinal dialysis at or close to the ora serrata
- One or more ragged equatorial retinal breaks
- Vitreous-base avulsion
- Horseshoe retinal tears
Examination
Ask specifically about previous blunt trauma, including trauma that occurred months or years earlier.
Examine the entire peripheral retina using indirect ophthalmoscopy with scleral indentation. A subtle dialysis may appear only as a narrow slit at the ora serrata and may become visible during indentation.[7]
Clinical approach
Traumatic retinal breaks require specialist retinal assessment. Management depends on the type and extent of the break, associated subretinal fluid, established retinal detachment and macular status.
Traumatic breaks usually require treatment, although the precise intervention must be tailored to the individual lesion.[1]
Which Breaks Need Treatment?
Treatment is guided by acute symptoms, persistent vitreoretinal traction, associated subretinal fluid and the patient’s overall detachment risk—not simply by the presence of a retinal break.[1]
Swipe across the table to see all columns →
| Clinical situation | Usual approach | Reasoning |
|---|---|---|
| Acute symptomatic horseshoe tear | Treat promptly | The retinal flap remains attached to the vitreous, so traction is still active and the risk of rhegmatogenous retinal detachment is higher.[1] |
| Asymptomatic horseshoe tear | Individualise | Consider the lesion’s appearance, surrounding subretinal fluid and additional patient-specific risk factors. |
| Atrophic retinal hole | Usually observe | The usual detachment risk is low because vitreoretinal traction is absent. Treatment may be considered when subretinal fluid progresses or the wider clinical context substantially increases risk.[1][4] |
| Operculated retinal hole | Usually observe | Once the operculum has separated, traction is usually released. Acute symptoms or other concerning features may justify individual consideration. |
| Giant retinal tear | Urgent retinal management | This is a sight-threatening lesion that may progress rapidly and generally requires urgent vitreoretinal assessment rather than routine prophylactic laser alone. |
| Retinal dialysis or another traumatic break | Specialist assessment | Traumatic breaks usually require treatment. The intervention depends on the extent of the break, subretinal fluid, established detachment, chronicity and macular status.[1] |
| Progressive subretinal fluid or established detachment | Prompt retinal management | The decision is no longer based on the break alone; progression of fluid indicates an evolving or established retinal detachment. |
Factors that may shift the decision towards treatment
- High myopia
- Retinal detachment in the fellow eye
- Strong family history
- Hereditary vitreoretinal disorder
- Aphakia or pseudophakia
- Unreliable access to urgent review or follow-up
What Retinopexy Achieves
Retinopexy creates a chorioretinal adhesion around the retinal break. This forms a barrier that limits the passage of liquefied vitreous into the subretinal space.[1]
Fluid can pass towards the subretinal space
Chorioretinal adhesion develops around the break
The break is walled off from the surrounding retina
What it does
- Produces a firm adhesion between the retina, retinal pigment epithelium and choroid around the break
- Reduces the opportunity for vitreous fluid to spread beyond the treated boundary
- Lowers the risk that a treated retinal break will progress to a rhegmatogenous retinal detachment
What it does not do
- It does not physically close or replace the missing retinal tissue
- It does not remove the vitreoretinal traction that produced the tear
- It does not prevent a patient from developing additional retinal breaks elsewhere
- It is not a substitute for retinal-detachment surgery when an established detachment requires operative management
After treatment
Fresh laser marks later develop visible pigmentation as the chorioretinal adhesion matures.
The peripheral retina must still be examined carefully because the original tractional process may produce another tear outside the treated area.
Mechanism in One View
When examining a peripheral retinal break, ask whether traction is absent, released or still active—and whether the normal vitreous support of the retinal edge has been altered.
Swipe across the table to see all columns →
| Lesion | How it forms | Key distinction |
|---|---|---|
| Atrophic retinal hole | A round or oval full-thickness defect develops through retinal thinning. | Traction is absent. The usual detachment risk is low.[1] |
| Operculated retinal hole | Focal vitreoretinal traction avulses a small piece of retinal tissue, producing an operculum. | Traction is usually released after the operculum separates.[1] |
| Horseshoe retinal tear | Persistent vitreoretinal traction pulls a U-shaped retinal flap away from the underlying tissue. | Traction remains active. The flap remains attached to the vitreous, creating a higher detachment risk.[1] |
| Giant retinal tear | A circumferential full-thickness tear of at least 90° develops in association with posterior vitreous separation. | The posterior flap loses vitreous support and may become highly mobile, fold or invert.[5] |
| Retinal dialysis | The retina becomes circumferentially disinserted at or close to the ora serrata, often after blunt trauma. | The vitreous base usually remains attached to the posterior retinal edge. Posterior vitreous detachment is not the primary mechanism.[6][7][8] |
References
Clinical statements in this note were checked against the following ophthalmology guidelines, reviews and primary studies.
-
American Academy of Ophthalmology Preferred Practice Pattern Retina/Vitreous Committee. Posterior vitreous detachment, retinal breaks, and lattice degeneration Preferred Practice Pattern. Ophthalmology. 2025;132(4):P163–P196.
DOI: 10.1016/j.ophtha.2024.12.023 -
Nixon TRW, Davie RL, Snead MP. Posterior vitreous detachment and retinal tear—a prospective study of community referrals. Eye. 2024;38(4):786–791.
DOI: 10.1038/s41433-023-02779-3 -
Wilkinson CP. Interventions for asymptomatic retinal breaks and lattice degeneration for preventing retinal detachment. Cochrane Database of Systematic Reviews. 2014;(9):CD003170.
DOI: 10.1002/14651858.CD003170.pub4 -
Byer NE. Subclinical retinal detachment resulting from asymptomatic retinal breaks: prognosis for progression and regression. Ophthalmology. 2001;108(8):1499–1503.
DOI: 10.1016/S0161-6420(01)00652-2 -
Shunmugam M, Ang GS, Lois N. Giant retinal tears. Survey of Ophthalmology. 2014;59(2):192–216.
DOI: 10.1016/j.survophthal.2013.03.006 -
Zion VM, Burton TC. Retinal dialysis. Archives of Ophthalmology. 1980;98(11):1971–1974.
DOI: 10.1001/archopht.1980.01020040823005 -
Vote BJ, Casswell AG. Retinal dialysis: are we missing diagnostic opportunities? Eye. 2004;18(7):709–713.
DOI: 10.1038/sj.eye.6701310 -
Rohowetz LJ, et al. Retinal detachment associated with retinal dialysis: clinical features and outcomes of surgery in a 10-year study. Ophthalmology Retina. 2023;7(10):857–861.
DOI: 10.1016/j.oret.2023.06.013
