Horseshoe or flap tear
|Horseshoe or flap tear|
|Classification and external resources|
- 1 Disease Entity
- 2 Diagnosis
- 3 Management
- 4 References
International Classification of Diseases (ICD)
- H33.3: Horseshoe tear of retina without detachment
- 361.32: Horseshoe tear of retina without detachment
Horseshoe tears, also referred as flap or U-shaped tears, are full thickness breaks in the neurosensory retina that occur secondary to vitreous traction.
Tears usually occur suddenly as a result of vitreous traction to an area of preexisting vitreoretinal adhesion, with the retina frequently appearing completely normal before the acute event. Horseshoe tears are more common in middle age and appear most often near the equator of the eye. No statistical difference exists between men and women in the incidence of retinal breaks.
Risk factors are:
Age: the occurrence of retinal breaks is age dependent with increasing incidence accompanying increasing age.
Myopia: the prevalence of retinal breaks in myopic eyes is similar to that of eyes in the general population (11%). However, myopes account for 42% of all phakic RD and, therefore, myopia is considered a risk factor for retinal breaks that lead to RD.
Lattice Degeneration: is a condition in which peripheral retinal thinning is associated with liquefaction and separation of the overlying vitreous. It is often associated with round retinal holes but it can also be associated with flap tears. In fact, there can be a pronounced vitreoretinal adhesion located at the margin of lattice lesions, which can predispose to retinal tears after PVD. These tears typically occur at the posterior margin or posterior lateral margin of lattice degeneration. This condition occurs in 5% of eyes but is more prevalent in moderate myopia, and it is found in 30% of all eyes with rhegmatogenous retinal detachments. Long-term studies suggest that tractional tears are found in 2.9% of all eye at 10 years however, very few cases develop clinical significant retinal detachment (1).
Penetrating trauma: can increase the risk of retinal break either immediately after impact, due to direct retinal trauma or later on as a result of vitreous traction on the peripheral retina.
Blunt trauma: is more commonly associated with retinal dialysis but it can also cause other types of retinal breaks, such as horseshoe tears or macular holes.
Horseshoe tears also occur at sites of strong vitreoretinal adhesion, most commonly at the irregular posterior margin of the vitreous base during PVD. They are more common in the superior temporal quadrant followed by the superior nasal quadrant. U-tears consist of a flap in which its apex is pulled anteriorly by the vitreous while the base remains attached to the retina. The actual tear consists of two anterior extensions (horns) running forward from the apex.
These horseshoe tears occur at sites of strong vitreoretinal adhesion, most commonly at the vitreous base as a result of vitreous traction. Vitreous traction, resulting most frequently from spontaneous vitreous detachment, creates a tear, with the apex of the flap remaining adherent to the posterior vitreous surface. Because of the persistent associated vitreous traction, flap tears can frequently lead to detachment. When there is persistent traction, the base of the tear can be avulsed leaving a small round defect in the neural retina with an overlying operculum of retinal tissue, aptly named a round hole with operculum. They generally indicate complete relief of vitreoretinal traction in this area. So very rarely lead to retinal detachment unless vitreoretinal traction persists in the vicinity of the tear. These breaks are caused by isolated areas of vitreoretinal adhesion and are not contiguous to the vitreous base. They tend to be more posterior than horseshoe tears, and occasionally an operculated round hole is found posterior to a horseshoe tear in the same meridian.
There are no prophylactic measures against the development of retinal tears and PVD. The later is a common phenomenon of the aging eye and in most individuals it will develop without symptoms or pathological sequeale. Nonetheless, this process is also implicated in a large variety of vitreoretinal disorders, namely due to its role in retinal tear formation and subsequent development of most regmatogenous retinal detachments. Studies on prophylaxis of retinal detachment do not meet the standards of statistically significance, so there is uncertainty about the correct management of the majority of the retinal degenerations. In most circumstances, retinopexy of these lesions is not required.
The diagnosis is clinical, based on history and clinical exam.
Patients with acute retinal horseshoe tears may complain of floaters secondary to vitreous debris (thickened hyaloids membrane, a Weiss ring, hemorrhage, or retinal pigment epithelium cells) and flashes of light (photopsias), that result from persistent vitreous traction.
Retinal tears can be associated systemic diseases specifically Marfan, Stickler, Wagner, and Ehlers–Danlos syndromes as well as homocystinuria.
Patients suspected of having a horseshoe tear require a 360º fundus examination by direct or/and indirect ophthalmoscopy, with special attention to the peripheral fundus. There can often by multiple retinal tears present at the same time; therefore, the examiner must thoroughly search the entire retina even after finding one tear. When there are multiple breaks, 75% of the time, they are found to be within 90 degrees of one another.
The signs commonly found during clinical examination are:
- Horseshoe-shaped tear with or without surrounding subretinal fluid
- Tears usually occur at the vitreous base but may occur near equator
- Giant retinal tears (three or more clock hours of extension)
- Posterior vitreous detachment
- Pigmented cells in the vitreous (tobacco dust)
- Vitreous hemorrhage
- Pigmentation surrounding tears
- Vitreous traction
- Localized abnormal vitreoretinal interface (ie, lattice degeneration)
A PVD can be diagnosed by a simple examination of the eye with a non contact lens. The presence of a Weiss ring indicates that a PVD has occurred. However it may not always be obvious and the PVD may only be partially detached. In the former cases it is important to search for the posterior hyaloid membrane, which, although difficult to find, can be recognized by the optically clear retrohyaloid space. The slit lamp diagnosis of a partial PVD can be extremely difficult because the signs of remaining vitreous attachments can be very subtle. Residual attachments are more frequently found at the optic disc, chorioretinal scars, epiretinal membranes, the macula, and the surrounding arcades.
PVD may induce optic disc hemorrhages (causing subtle visual field loss) or retinal hemorrhages in the periphery or in the macula.
In most patients with tears, retinal pigment epithelial cells, released through the tear, will be visible in the anterior vitreous (Shafer’s sign). This is highly predictive of a retinal tear (approximately 90%). The granules are relatively large, pigmented, and are seen in the anterior vitreous, especially inferiorly. Therefore, the patient should be examined during eye movements, allowing inferior vitreous to present itself through the pupil. Only one cell is required to make the diagnosis of Shafer’s sign and imply increased risk of a retinal tear. Although less suggestive than pigment cells, red blood cells may also be seen and should raise suspicion of a retinal tear. Red blood cells are smaller than pigment cells.
Patients often present with new onset floaters (from vitreous hemorrhage or vitreous detachment) and photopsia (from vitreoretinal traction).
Patients who experience symptoms during posterior vitreous separation have a 15% risk of developing a retinal tear, although characterization of the symptoms does not seem to help predict those eyes with tears.
Floaters are usually described by patients as cobwebs, veils, bugs, a ring, and single or multiple spots. These originate from thickened a posterior hyaloid membrane, a Weiss ring, and/or cells that have been dispersed into the vitreous. Floaters that occur before the age of 40 and are chronic in presentation can often be due to vitreous degeneration without PVD. However, it may take only a single floater of recent onset to indicate the development of a PVD. Floaters must be discriminated from paracentral scotomata.
Photopsias can also occur during a PVD. It is theorized that this phenomenon of flashing lights may be due to the depolarization of receptors when the retina is pulled by the vitreous.
It is critical that photopsias are differentiated from the flashes that occur with other disorders, such as the zigzag (often multi-colored) lights of an ocular migraine, flickering stars associated with occipital ischemia, and the coloured lights of the acute zonal outer occult retinopathy (AZOOR) syndromes.
The presence of new-onset floaters and photopsias, when accompanied by visual field loss are very premonitory of retinal detachment.
With clear media, the diagnosis of a retinal tear is straightforward. Indirect ophthalmoscopy with scleral depression and slit lamp biomicroscopy with a 60 to 90 diopter indirect lens or corneal contact lens are used to make the definitive diagnosis.
Slit lamp biomicroscopy with a Goldmann three mirror lens allows a broader view of the fundus from the posterior pole to the ora serrata and ciliary body.
An indirect ophthalmic examination with scleral depression may be required to identify retinal breaks adjacent to the ora serrata and allows for dynamic observation of potential changes that could indicate the presence of a retinal break.
Clinical examination alone is usually sufficient. An ultrasound is needed to identify possible retinal tears and/or detachment when vitreous hemorrhage prevents direct visualization of the retina. In some cases, experienced ultrasonographers are able to detect the presence of larger retinal breaks in attached retina when cloudy media prevents direct observation, and ultrasound-guided cryotherapy can be utilized in these cases.
There are many conditions in the peripheral fundus that can simulate retinal tears. Obstacles to an accurate diagnosis include inadequate pupillary dilatation, media opacities, and patient compliance. Binocular indirect ophthalmoscopy with scleral depression to see the peripheral retina, complemented by Goldmann three-mirror examination, remains the gold standard method to differentiate these lesions.
Differential diagnosis of retinal breaks include:
- Pars Plana cysts
- Enclosed oral bays
- Meridional folds/complexes
- Ora Serrata pearls
- Granular tags
- Paving-stone degeneration
- Chorioretinal scars
- Peripheral cystoid degeneration
- White with/without pressure
- Retinal erosions
The decision to treat a retinal tear is based on several factors, which include: symptomatology, patient age and systemic health, refractive error, location, age, type, size of the break; status of the fellow eye, lens status, and family history of retinal break and/or retinal detachment.
Patients with symptomatic retinal horseshoe tears and persistent vitreoretinal traction can progress to a retinal detachment in 33 to 55 % of cases, and these patients should always be immediately treated. The goal of treatment is to create a chorioretinal adhesion around the tear to prevent vitreous fluid from entering the subretinal space and creating a retinal detachment. New onset floaters and flashes are the typical symptoms of an acute retinal break, and studies have shown that their presence is the most important prognostic criterion for progression to retinal detachment.
Treating asymptomatic retinal horseshoe tears is less straight forward. In phakic patients that develop asymptomatic horseshoe tears without previous history of retinal disease or of high myopia, prophylactic treatment is controversial, but often performed. Patients who have greater than 6D of myopia have an increased incidence of retinal detachment; the treatment of asymptomatic retinal tears is still controversial in this group, but is usually performed. It is theorzied that extensive prophylactic therapy has the potential to stimulate changes in the vitreous, which can result in increased subsequent vitreoretinal traction and rsultantt retinal tear and/or detachment.
Long-standing tears often have retinal pigment epithelial changes adjacent to them, and this indicates a decreased likelihood of retinal detachment. Superotemporal breaks have a greater likelihood of a macula-off retinal detachment, and larger breaks are more likely to cause a retinal detachment.
The management of asymptomatic horseshoe tears remains controversial in patients who need cataract surgery, in aphakic or pseudophakic patients, and in patients who have retinal detachments in their fellow eye. In general, because of the increased incidence of detachment in these scenarios, strong consideration should be given to prophylactic treatment.
Finally, in patients with a family history of retinal detachment, prophylatic therapy maybe of value, especially in eyes with retinal breaks or visible retinal percusors of retinal tears. However, there are no studies that properly stratify the several high risk factors associated with retinal detachment and evaluate the natural course and the effect of prophylactic therapy in patients with a familial predisposition to retinal detachment.
Although some authors consider that asymptomatic horseshoe tears may not be treated, others stress that all tears require treatment by retinopexy, either laser photocoagulation or cryotherapy. Any retinopexy performed must cover both the posterior aspect of the tear and its anterior corners. This should be performed immediately after the diagnosis, and subsequent reviews are merely to determine that the retinopexy is adequately encompassing the defect.
Cryotherapy is delivered transconjunctivally. It induces adhesive chorioretinitis around the tear, preventing liquid vitreous access from traveling through the hole into the subretinal space. Partial adhesion occurs after 1 week and full adhesion after 3 weeks. This technique has the advantage of not requiring a clear media, as opposed to laser photocoagulation.
Laser photocoagulation treatment of retinal breaks utilizes argon, or an equivalent, laser. Two main delivery systems are used, the slit lamp and the indirect ophthalmoscope. In contrast to cryotherapy, chorioretinal adhesion seems to occurs sooner, but maximal adhesion occurs roughly 7–10 days later. The retinal tear should be surrounded with a minimum of three concentric rows of laser. Although the spots need not be confluent, there should be no more than half a spot size of untreated retina between burns. Typically, the settings are 200–500 mm spot size and 0.1–0.2 seconds application at the power necessary to generate a gray-white burn. In general, indirect ophthalmoscopic laser photocoagulation and retinal cryopexy and are preferred for anterior retinal breaks because of difficulty in treatment of the anterior margin at the slit lamp. Posterior breaks can be managed more easily with the slit lamp or an indirect laser delivery system.
Observation without treatment is indicated when:
- The tear is chronic
- The tear is demarcated by pigmentation
- There is absence of vitreous
- Found in selected asymptomatic patients
Medical follow up
The eye should be re-examined after approximately 7 days. Vigorous physical activity is often discouraged initially, although there are no clinical studies supporting that diminished activity improves treatment results. A firm chorioretinal adhesion is present 3 weeks after either technique.
Any subretinal fluid around the tear indicates that a retinal detachment is present and a surgical retinal detachment procedure is usually required. If the subretinal fluid is minimal, cryotherapy can sometimes be successful on its own, however this should be done rarely and the eye should be closely monitory.
Epiretinal membrane and macular pucker are the most frequent visually significant complications associated with prophylactic treatment of a retinal break, with an incidence of 1-5%. Other complications that can rarely occur include Adie’s pupil, subretinal and vitreous hemorrhage, and breaks in Bruch’s membrane. An extremely rare complication in patients that have staphylomatous sclera treated with cryotherapy is scleral rupture.
At least one-half of untreated symptomatic retinal breaks with persistent vitreoretinal traction will cause a clinical retinal detachment unless treatment is applied. Prompt creation of a chorioretinal adhesion around these symptomatic tears reduces the chances of retinal detachment to less than 5%. Failure rates for prophylactically treated retinal breaks depend on type of retinal break, indications for treatment, length of follow-up, and definition of failure. Reported failure rates are in the range 0–22%. (6) In eyes that fail prophylactic therapy, retinal detachment repair by pneumatic retinopexy, scleral buckling, or vitrectomy is usually successful in the anatomic reattachment of the retina.
1. Byer NE., Long-term natural history of lattice degeneration of the retina. Ophthalmology 1989;96:1396–401.
2. Kun E., Gross and microscopic pathology in autopsy eyes. Part III. Retinal breaks without detachment. Am J Ophthalmol 1961; 51:369-391.
3. Haiman M.H., Burton T.C., Brown C.K., Epidemiology of retinal detachment. Arch Ophthalmol 1982; 100:289-292.
4. Byer N.E., What happens to untreated asymptomatic retinal breaks, and are they affected by posterior vitreous detachment?. Ophthalmology 1998; 105:1045-1050
5. Davis M.D.: Natural history of retinal breaks without detachment. Arch Ophthalmol 1974; 92:183-194.
6. Smiddy W.E., Flynn H.W., Nicholson D.H., et al, Results and complications in treated retinal breaks. Am J Ophthalmol 1991; 112:623-631.
7. Preferred Practice Patterns: Posterior Vitreous Detachment, Retinal Breaks, and Lattice Degeneration. AAO 2008.
8. Daniel A. Brinton, MD, and C. P. Wilkinson, MD, Retinal Detachment, Principles and Practice, Third Edition, Oxford University Press, 2009.
9. Thomas H. Williamson , Vitreoretinal Surgery, Springer-Verlag Berlin Heidelberg 2008, Chapter 3, 41-46.
10. Kanski, Jack. Clinical Ophthalmology, a Systematic approach, 7th edition. Butterworth-Heinemann Elsevier; 2011.
11. Nerad J., Carter K., Alford, Rapid Diagnosis in Ophthalmology, Mosby 2008, 139-159.
12. AAO, Basic and Clinical Science Course, Section 12: Retina and Vitreous, 2010-11.
13. Yanoff and Duker: Ophthalmology, 3rd edition, Chapter 6.73 - Retinal Breaks, Craig M. Geven.
14. Wilkinson C., Rice T., Michels Retinal Detachment, Second Edition, Mosby.
15. Wilkinson, CP. Prevention of Retinal Detachment. In: Ryan, Stephen J. Retina. 4th Edition. Mosby, an affiliate of Elsevier; 2006:2107-2119