Signs and Symptoms

Lattice degeneration of the retina is named for its resemblance to a fine, white, linear criss-cross lattice pattern seen in the peripheral neurosensory retina.1-15 The condition is common to 7% to 10% of adult eyes, with affected patients usually diagnosed over the age of 20.1-5,12-15 The condition is predominantly seen in the superior quadrants, with less frequency in the horizontal meridans.1 Axially myopic patients seem to have a higher incidence of lattice degeneration.1,6-11 There appears to be no racial predilection, although there is some controversy in the literature.1-11,12

Lattice degeneration classically runs circumferentially between the equator and the ora serrata, parallel to the vitreous base.1-10,13 The individual lesions usually measure from 0.5 disc diameter (DD) to 6 DD and can run 360° around the eye. Most of the time, the lesions are observed in discontinuous patterns, with the majority of lesions in the vertical meridians.1,13 Lattice degeneration is typically bilateral.12,13

Sometimes, retinal pigment epithelial hyperplasia associated with significant retinal thinning or the physiology of healing (secondary to micro-injury) conceals the lattice lines.1,12-15 This is often termed pigmented lattice degeneration. The retinal thinning causes overlying vitreous degeneration with subsequent accumulation of small pockets of liquid vitreous, known as lacunae, residing over top of the lesions.12-17

When atrophic holes develop, liquid vitreous can seep under the neurosensory retina to produce a shallow retinal detachment. The majority of shallow lattice-related detachments are asymptomatic. However, when a prominently lifted edge of a hole or linear tear along a lesion edge interacts with adherent vitreous, mechanical forces are translated into electrical retinal stimuli that are perceived by the patient as flashing lights (photopsia).1 These forces can also create larger holes or tears that may be symptomatic.1,6-8 Tractional retinal tears along the edge of lattice degeneration have the highest association with the development of retinal detachment arising from lattice retinal degeneration.1,6-8


The etiology of lattice degeneration remains unclear. Recent research has hypothesized that the condition may occur secondary to genetic variants in the COL4A4 gene.5 Pathophysiologically, lattice degeneration occurs as the result of dropout of peripheral retinal capillaries, with resulting ischemia and subsequent thinning affecting all layers of the retina.15-17 The acellular thickening and sclerosis of the lumens of these peripheral retinal arterioles is what creates the characteristic linear appearance.17

Profound retinal thinning has several effects: first, the overlying vitreous becomes disturbed, resulting in a pocket of liquefaction overlying the lattice lesion, known as a lacuna; second, the vitreous along the edges of the lattice lesion maintains its adhesions, creating forces on the retina. Finally, the ischemia and retinal thinning may disturb the retinal pigment epithelium, resulting in RPE hyperplasia and a pigmented appearance.16,17 Fluorescein angiography of lattice lesions demonstrates zones of avascularity.17

In one study, using optical coherence tomography, four characteristic changes of the retina and vitreous were seen in 13 eyes with lattice degeneration: (1) anterior/posterior U-shaped vitreous traction around the lesion, (2) retinal breaks, (3) the presence of focal retinal thinning and (4) vitreous membrane with evidence of traction, thought to be fibrosis from extracellular products of cell breakdown.15 The morphologic appearance of vitreous traction and retinal breaks imaged in cases were concluded to be consistent with known histologic reports.15

The process becomes more significant when the thinning becomes profound, to the point of development of full-thickness atrophic holes in lattice lesions.15-17 There exists the potential for overlying liquefied vitreous to pass through a hole into the subretinal space and possibly lead to rhegmatogenous retinal detachment. While the published data from larger studies demonstrate a wide range of prevalence, all generally agree that this is uncommon (0.5% to 3% over a five- to 11-year span).12-17

In some eyes (predominantly myopic ones), a slow build-up of fluid can occur in conjunction with posterior vitreous detachment (PVD).17 These eyes seem to be at greatest risk of developing rhegmatogenous retinal detachment.17 If a PVD occurs, vitreoretinal traction along the posterior edge of the lattice degeneration lesion may result in a tractional tear adjacent to the lesion. When these tears develop, they are typically created at the posterior boundary of the lesion.17 This greatly increases the risk of rhegmatogenous retinal detachment.17,18


The main concern with lattice degeneration is the risk of progression to rhegmatogenous retinal detachment.1-19 When lattice degeneration with holes is detected, several factors can be used to determine if prophylactic treatment is required. These include a history of retinal detachment from lattice degeneration in the same or fellow eye, a family history of retinal detachment, axial myopia of greater than six diopters, presence of significant subretinal fluid under the edges of the hole and concurrent photopsia. Additionally, if the holes are large, the patient is pseudophakic or is planning to undergo cataract surgery, or the patient has an active, high-impact lifestyle, prophylactic treatment can be recommended.7-23

However, most lattice cases, even those presenting with associated retinal holes, are simply monitored, with visits every six to 12 months. Atrophic holes within lattice degeneration in phakic eyes without any complicating factors as previously mentioned do not generally require prophylactic treatment as the risk of progression to detachment is small.2-20 These lesions need only periodic monitoring, with the patient educated on the signs and symptoms of retinal detachment.

When high-risk tractional retinal breaks associated with lattice degeneration are detected, the area can be prophylactically sealed with barrier laser photocoagulation or cryoretinopexy.2,4,20,21 Cryoretinopexy uses an externally applied transscleral/conjunctival probe to deliver directed cold pressure to the area contacted, destroying the integrity of the choriocapillaris, RPE and outer retina. This induces RPE hyperplasia, creating an adhesion between the area of the tear and the healthy, attached, adjacent retina.2,19-21 This prevents liquid vitreous from gaining access to the subretinal space.2,19-21

Advantages of cryoretinopexy over laser photocoagulation are that it can be applied to the retina of an eye with media opacities that preclude the use of laser photocoagulation (cataract or vitreous hemorrhage), ease of procedure performance and its suitability if the pupil size cannot be adequately enlarged. It is also the treatment of choice if the retinal lesion is anteriorly located in the eye close to the ora serrata.19 Retinal adhesion with cryoretinopexy takes up to three weeks to mature.19 Adverse effects of cryoretinopexy include inflammation, choroidal detachment, reduced accommodation, discomfort and raised intraocular pressure.19

Laser photocoagulation applies varying wavelengths of light (argon green, argon blue-green, krypton red) via a biomicroscope or binocular indirect delivery system to the retina to create a similar tissue adhesion. Unlike cryoretinopexy, the adhesion is immediate and matures within 10 days.2,19 Laser photocoagulation, which is more commonly employed than cryoretinopexy, has fewer side effects, can be applied to more posterior lesions and can be more accurately placed.2,19

Clinical Pearls

Lattice degeneration with or without atrophic holes is generally benign and often simply monitored.

Tractional tears at the posterior border of lattice lesions can be difficult to see ophthalmoscopically. These tears can become apparent upon scleral depression, making the procedure a prudent exercise in the examination of these individuals.

When unsure, use three-mirror or a non-contact fundus lens and biomicroscope to more closely evaluate the lesion.

Patients should be educated regarding the signs and symptoms of retinal detachment.

Standard follow-up in asymptomatic patients should be at six- to 12-month intervals for a dilated exam.

Any tears along lattice lesions should be referred for further evaluation and treatment.

While both cryoretinopexy and laser photocoagulation of retinal breaks are efficacious, most patients today are treated with the latter.

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