Lattice degeneration is a common, atrophic disease of the peripheral retina characterized by oval or linear patches of retinal thinning.[1, 2] The prevalence peaks by the second decade and is believed to be minimally progressive but may be complicated by retinal breaks and retinal detachment.[3] Lattice degeneration elevates the risk for retinal detachment but does not require treatment if it is asymptomatic.
The pathogenesis of lattice degeneration is not well understood, although several theories have been proposed.[4] Regional maldevelopment or absence of the internal limiting membrane versus abnormal vitreoretinal traction dynamics appear to be the most cogent arguments proposed.
Lattice degeneration affects approximately 10% of the population and is bilateral in 30-50% of patients who are affected. A variable familial risk may be present on the basis of various autosomal dominant pedigrees.[5] An increased prevalence exists in myopic eyes, and its prevalence may be associated with increasing axial length, reaching 15% in the longest eyes.
International
No information is available regarding the international occurrence of lattice degeneration.
Mortality/Morbidity
See discussion of retinal detachment in History and Physical.
Race
No reported racial differences exist in lattice degeneration.
Sex
No reported sex differences exist in lattice degeneration.
Age
See History regarding early onset and progression with age.
Educate the patient on signs of retinal detachment.
Encourage annual follow-up for dilated eye examinations.
Patients with lattice degeneration need to be made aware of their condition and should be warned about the increased lifetime risk of retinal tears or detachment. They should be advised to see an eye doctor immediately if they develop symptoms of retinal tears or detachments, including new floaters, flashes of light, decreasing vision, or a "curtain" in their vision.
Patients with lattice degeneration are typically asymptomatic, and the lesions are usually an incidental finding of dilated ophthalmologic examination. A presenting complaint of blurriness in the distance may be the result of myopia, a common association with lattice degeneration. The acute onset of floaters, flashes of light, peripheral field loss, or central vision loss may indicate the presence of a retinal tear or detachment, a complication of lattice lesions.[6]
Lattice degeneration is characterized by oval or linear patches of atrophic retina with a reddish base and is variably located within the equatorial region of the fundus, typically inferotemporal.[2]
Lesions may be isolated or multifocal, variable in dimension, and usually are oriented concentric or slightly oblique to the ora serrata.
Condensed vitreous at the margins of the lattice lesions may appear as vitreous opacities and represent regions of increased vitreoretinal adhesion; overlying vitreal opacities alternatively may be explained by glial proliferation.[7]
Crisscrossing fine white lines that account for the name lattice degeneration are present in roughly only 10% of lesions and most likely represent hyalinized blood vessels; this is shown in the image below.
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Example of a lattice lesion containing white crisscrossing wicker lines, which are seen in about 10% of lattice lesions. This lesion is complicated by....
Various pigmentary disturbances, shown in the image below, occur in more than 80% of lattice lesions. White-yellow occasionally refractile flecks, similar to that seen with degenerative retinoschisis, are an additional common associated feature.
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An example of a heavily pigmented lattice lesion.
Atrophic retinal holes, shown in the image below, and tractional retinal tears may complicate lattice degeneration and increase the risk of retinal detachment.
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Lattice lesion containing small atrophic holes.
Clinical variations
Snail-track degeneration is a morphologic descriptive term for retinal lesions with the same characteristic size, shape, orientation, and location as lattice lesions and is associated with the aforementioned yellowish flecks. Examples of snail-track degeneration are shown in the images below.
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A peripheral lattice lesion demonstrating the typical snail-track appearance, with overlying vitreal opacities, which may represent glial proliferatio....
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Another example of a peripheral lattice lesion with a snail-track appearance.
Vitreous base excavations represent lesions of similar shape, size, and orientations as lattice lesions having a uniform reddish base and located within the vitreous base.
Pigmentary degeneration is a term that most likely represents lattice lesions with prominent but variable pigmentary changes, including clumps of pigment sometimes heavily scattered at the base of lattice lesions and demarcation lines circumscribing cuffs of subretinal fluid.
When retinal thinning and pigmentary disturbances are found along retinal vessels, these lattice lesions are referred to as radial perivascular chorioretinal degeneration and are classic findings in Wagner and Stickler disease, a familial vitreoretinal degenerative syndrome. An example of this is shown in the image below.
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Radial perivascular chorioretinal degeneration with retinal tear at the margin. These lesions run along vessels and may be found in Wagner's and Stick....
Clinical examination
Identification of lattice lesions depends largely upon the experience of the examiner and the method of examination used.
In patients with symptomatic lattice degeneration (presence of newly onset flashes or floaters), the retinal periphery must be viewed for 360° of its circumference to identify any retinal breaks, if present. If the general ophthalmologist is unable to do so, referral should be promptly made to a vitreoretinal subspecialist.
The most convenient and frequently used method of examination to detect lattice is with binocular indirect ophthalmoscopy with scleral depression (indentation).
Slit lamp examination with a Goldmann contact lens is used less frequently. This method allows for high magnification of the lattice lesions and the associated vitreoretinal relationships, but evaluation with scleral depression, a critical element of the peripheral examination, becomes technically difficult when using a contact lens.
Clinical course
Lattice lesions are believed to develop early in one's lifetime with minimal progression thereafter. Associated features, such as crisscrossing sclerotic vessels, pigmentation, and atrophic retinal holes, may subsequently develop.
Retinal detachment is a relatively rare complication of lattice degeneration (< 1% of patients with lattice degeneration), but lattice degeneration is associated with as many as 40% of all rhegmatogenous retinal detachments. Lattice degeneration is present in 11% of fellow eyes in patients with rhegmatogenous retinal detachments.[8, 9, 10] Rhegmatogenous retinal detachment is shown in the image below.
A 2015 study reported a higher risk (3.4%) of retinal tears and detachments in myopic eyes (>6 D) over a 10-year period.[11]
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An acute rhegmatogenous retinal detachment that may be associated with lattice degeneration. (Lattice lesion not seen in this image.)
Retinal detachments caused by lattice degeneration occur most commonly by a tractional tear at the cuff or posterior margin of the lattice lesion or less commonly by means of an atrophic hole within the zone of lattice.
Tractional tears
Tractional tears located at the margin of lattice account for 55-70% of retinal detachments in lattice degeneration and are the result of a posterior vitreous detachment (PVD).
These patients are typically older than 50 years, and only 40% of such eyes are myopic.
An acute PVD complicated by retinal tear formation usually is signaled by the complaint of new-onset floaters and/or flashing lights (referred to as photopsia)
As in all retinal tears, preretinal or vitreous hemorrhage may be present if the tear extends through peripheral retinal blood vessel.
Patients with these complaints constitute a true ophthalmologic emergency and need urgent ophthalmic examination.
PVD-related lattice detachments typically are superotemporal and not associated with demarcation lines. Surgical repair is anatomically successful in 90% of such cases.
Atrophic holes
Atrophic holes account for 30-45% of retinal detachments associated with lattice degeneration. In another retrospective case-controlled study, 23.6% of patients with retinal detachments had atrophic holes associated with lattice degeneration.[12]
Seventy percent of patients with rhegmatogenous retinal detachment secondary to round atrophic holes in lattice degeneration occur in patients younger than 40 years, and 70% of these detachments occur in myopic eyes. Sixty percent are found in females.
Fellow eye pathology is found in a significant (96%) portion of these patients. Thus, examination of the fellow eye is important in these cases.
The posterior hyaloid gel usually is attached, excluding a PVD-related mechanism. These detachments are typically inferior, occur slowly, and demonstrate demarcation lines on examination resulting from the slow progressive accumulation of subretinal fluid.
A 98-100% success rate exists in repairing such inferior retinal detachments with demarcation lines with an excellent visual prognosis in the absence of macular detachment.
Several imaging techniques have improved or can replace traditional methods for diagnosing lattice degeneration (LD) from a clinical perspective.[13] Techniques like ultra-widefield imaging (UWFI) simplify and standardize the diagnosis process as they are less dependent on the examiner's skill compared to traditional methods using 90 D or Goldman three-mirrors lenses. However, UWFI may not provide detailed information on the vitreoretinal interface, such as subclinical retinal detachments and vitreous tractions, which are crucial for assessing the risk of rhegmatogenous retinal detachment (RRD) and determining the need for laser prophylaxis. For these details, peripheral optical coherence tomography (OCT) or retro-mode scanning laser ophthalmoscopy (SLO) are more effective, with peripheral OCT being particularly precise for detailed examination but limited to post-capture analysis.
From a scientific standpoint, these imaging advancements also enhance understanding of LD's etiology, which remains largely unknown.[13] Despite the prevalence of LD and its straightforward diagnosis via indirect ophthalmoscopy, the underlying causes—whether inflammatory, vascular, or anatomic—remain speculative. Vascular theories suggest involvement of retinal vessels, but LD lesions typically do not follow specific vascular patterns and are not confined to areas supplied by individual vessels. Mechanical stress from eye elongation, particularly in moderately myopic eyes, is another proposed cause, supported by the prevalence of LD in these conditions. Additionally, while retinal non-perfusion is a noted feature, choroidal infarction leading to neurosensory retina degeneration has been observed, indicating that changes in choroidal circulation might contribute to LD. This is further supported by OCT and OCTA data showing choroidal involvement, suggesting that factors like scleral status and altered collagen synthesis in myopic eyes might play roles in LD pathophysiology.
Fluorescein angiography
Fluorescein angiography (FA) is not commonly used in the routine diagnosis of LD due to its limitations in providing clinically relevant information, particularly because it does not show the vitreoretinal interface status.[13] Early studies using FA have shown that mild LD lesions typically do not exhibit significant changes. However, moderate to severe lesions display decreased retinal perfusion or non-perfusion within the lesion area. In these cases, retinal arterioles appear narrow and poorly differentiated within the lesion and are completely obstructed along the posterior border in severe cases. Interestingly, arteriolar branches that supply the surrounding undamaged retina show normal filling, indicating that the vascular involvement is localized. Retinal venules generally mirror these changes, with no perfusion within the lesions but maintained perfusion around them. Additionally, no dye leakage is observed within the lesions, although some studies have reported microaneurysms, leakage from borderline vessels, and arterio-venous shunts in the affected areas.
In terms of imaging characteristics, background granular hyperfluorescence aligns with the lesion area as observed through ophthalmoscopy, indicating its consistency with the extent of the lesions.[13] About 41.2% of cases showed dyeing of the vessels, and 17.6% exhibited leakage from the vessels within the lesion. Among lesions with sheathing and whitening of the vessels, 27.3% still had perfused vessels. Notably, some lesions (17.6%) demonstrated leakage not only within but also around the lesions, suggesting a broader area of impact. The formation of microaneurysms was noted in a single case. These findings highlight the localized vascular involvement in LD and the potential for FA to reveal underlying choroidal patterns, especially in areas of RPE loss, despite its limited use in routine diagnostics.
Optical coherence tomography
Optical coherence tomography (OCT) plays a crucial role in both clinical and scientific realms for imaging LD lesions.[13] Clinically, OCT is advantageous for diagnosing the majority of LD lesions, except those in extreme peripheral locations or in patients with small pupils or non-compliance. It provides detailed insights into the vitreoretinal interface around the lesion, detects subclinical retinal detachments, and identifies retinal holes, which can influence the approach to laser prophylaxis. Scientifically, OCT is unique in its ability to offer pathology-like information on a diverse cohort of otherwise healthy individuals, a feat difficult to achieve in postmortem studies. The process of peripheral OCT imaging involves the patient sitting in front of the device, with possible head tilting towards the area of interest, and using manual adjustments on the device to capture high-resolution images of the lesions. Despite its utility, OCT imaging faces challenges such as the frequent occurrence of inverted images, especially with far-peripheral lesions.
Structurally, OCT has revealed various changes in LD lesions such as retinal thinning, vitreoretinal adhesion, and less commonly, retinal breaks with subretinal fluid.[13] These findings suggest underlying vascular abnormalities and tight vitreous adhesions that may shape the lesion's appearance. OCT has also been instrumental in monitoring the effects of treatments like laser photocoagulation, showing that vitreous tractions can blunt but not always release post-treatment. Additionally, OCT can detect structural changes beneath the lesions, such as scleral indentations and choroidal thinning, which are critical in understanding the lesion's impact on the eye's anatomy. Despite the effectiveness of OCT in capturing these details, the variability in scan patterns and the limitations of certain OCT devices mean that not all lesions are successfully imaged, and further studies are needed to optimize OCT's use in routine clinical practice.
Optical coherence tomography angiography
Optical coherence tomography angiography (OCTA) is traditionally used for assessing the central retina, but recent advancements in OCT technology now allow for the imaging of equatorial regions, including LD lesions located there.[13] The 3-mm pattern is preferred for OCTA as it provides more consistent images without truncating the scan edges. However, the application of wide-field OCTA in LD imaging remains unexplored, and concerns exist about the low resolution of wide-field OCTA scans. OCTA is effective in producing readable images, particularly for lesions in the mid-periphery, although its clinical significance is considered less critical than that of structural OCT due to the complexities of using OCTA in the retinal periphery.
Optical coherence tomography angiography has confirmed that retinal non-perfusion is a characteristic of LD lesions, with only a few vessels visible within the lesions and larger white vessels remaining perfused.[13] This scattered pattern of vessel loss suggests that vascular changes might be secondary. OCTA also enhances visualization of the choriocapillaris in the LD region, revealing a rarefication of the choriocapillaris meshwork and the presence of choroidal venous collectors beneath the lesions. Interestingly, in the macular region, LD eyes show a higher perfusion area of the choriocapillaris compared to healthy controls, suggesting a potential role of choroidal microcirculation in LD pathophysiology. These findings, while preliminary, highlight the need for further research to confirm these observations and to explore their implications, particularly in relation to conditions like central serous chorioretinopathy (CSCR) which shows impaired choriocapillaris perfusion. Additionally, the association of LD lesions with venous vessels and their significant pigmentary changes compared to peripheral lesions suggest a specific pattern that merits further study, especially concerning their role in rhegmatogenous retinal detachment.
Combined UWF and OCT imaging
An alternative method for imaging LD using OCT involves the use of single-capture ultra-widefield (UWF) confocal scanning laser ophthalmoscopy (SLO) integrated with swept-source OCT.[13] This technology pinpoints the location of peripheral retinal degenerations on UWF fundus images, which facilitates concurrent retinal tomography through horizontal 23-mm or 6.0x3.5 mm volume scans. This technique effectively correlates clinical observations with morphological data, enabling the detection of subretinal fluid, retinal detachments, and vitreous tractions associated with LD.
Spectral imaging and scanning laser ophthalmoscopy
Red-free and green-free imaging indicate that internal hyperpigmentation in LD lesions is confined to the RPE layer without choroidal involvement.[13] Infrared imaging reveals irregular reflectivity and shows that the orientation of the lesions is largely parallel to the ora serrata. Infrared SLO is advantageous for evaluating peripheral lesions as it offers imaging similar to conventional ophthalmoscopy but without intense light exposure, making it suitable for light-sensitive patients. Although confocal SLO provides limited new information, primarily about vitreous floaters over areas of lattice degeneration, it is useful in cases with decreased optical media transparency, such as cataracts and vitreous hemorrhage.
Two additional SLO techniques, dark-field SLO and retro-mode SLO, offer further insights into LD morphology.[13] Retro-mode SLO, using a 790 nm laser and a side-deviated aperture, produces pseudo three-dimensional images that enhance visualization of a wide range of retinal lesions, including holes and RPE alterations. It has revealed 31.5–55.0% more peripheral findings compared to indirect ophthalmoscopy, including new lesions and details within known lesions. Dark-field SLO, which utilizes a confocal aperture with a central stop, generates images based on backscattering of infrared light from the sclera, clearly displaying pigmentary changes. This method shows regional hypo-/hyperintense signals within and around LD lesions, suggesting possible scleral involvement beneath the lesions. These imaging techniques, combined with OCT findings, enhance the diagnostic capabilities for assessing LD.
Histologic studies of autopsy cases demonstrate that lattice lesions are characterized by three invariable features: thinning or atrophy of the inner retinal layers, vitreous liquefaction overlying the area of thinned retina, and vitreous condensation and exaggerated vitreoretinal attachments at the borders of the lesions.
The blood vessels within the lesions are usually patent, but they often show fibrous thickening of their walls, which correlates to the white lattice lines seen clinically. Melanin-laden macrophages may explain the pigmentation seen clinically. Glial proliferations may represent overlying preretinal opacities.
Electron microscopic studies have demonstrated retinal thinning, loss of retinal neurons, internal limiting lamina absence, fibrosis of blood vessels, and accumulation of pigment and/or glial elements.
The presence of uncomplicated lattice does not interfere with visual function and does not constitute a high risk for future development of retinal detachment. Prophylactic treatment is clearly indicated only in the context of specific circumstances.[14, 15, 16]
Indications for prophylactic treatment
Lattice degeneration complicated by tractional tears as the result of an acute, symptomatic posterior vitreous detachment represents a high-risk situation for future retinal detachment and is an urgent indication for laser retinopexy. Lattice and atrophic holes complicated by progressively increasing subretinal fluid represent an additional indication for surgical intervention.
The presence of lattice lesions in fellow eyes of patients who have sustained retinal detachment in the first eye may be treated prophylactically. Exceptions may include eyes with greater than 6 clock hours of lattice lesions and eyes with myopia greater than 6 diopters (D). Strong evidence suggests that subsequent retinal detachments may occur as a result of lesions developing in previously healthy retina.[17] Moreover, laser scars may increase vitreoretinal adhesion and increase the risk of future retinal tears. Therefore, this indication is controversial. In the absence of the aforementioned features, convincing evidence does not exist to clearly indicate prophylactic laser treatment of fellow eye lattice lesions.
Although prophylactic laser treatment may not convincingly prevent subsequent retinal detachment, some authors believe that laser demarcation may limit the extent of future detachments and help preserve the macula.
Researchers found that prophylactic treatment (PTx) significantly reduced the incidence of retinal tear and rhegmatogenous retinal detachment (17% in PTx cohort vs 41% in No-PTx cohort) in the fellow eyes of patients who had undergone primary RRD repair.[18] Additionally, there was no significant difference in final visual acuity between the two groups.
Methods of prophylactic treatment
Subclinical retinal detachment (>1-disc diameter of subretinal fluid but < 2-disc diameters posterior to the equator) may be treated more effectively with a scleral buckle approach versus a laser barrier.
Laser photocoagulation is the primary method of prophylactic treatment.[19] Recommended laser settings include the following: green, yellow, or red wavelengths via biomicroscope/contact lens or indirect ophthalmoscope delivery systems, duration of 0.1-0.2 seconds, and spot size of 100-200 micrometers. Apply laser in 3 confluent 360° rings around the lesion. Care should be taken to avoid bare retinal pigment epithelium.
Cryotherapy may be a necessary alternative in cases in which significant hemorrhage prevents laser administration.
Retinal detachment treatments
Frank rhegmatogenous retinal detachment may be treated with a scleral buckling procedure and/or pars plana vitrectomy with gas administration.[20] All areas of lattice and retinal breaks should be meticulously sought after and barricaded with laser or cryotherapy.
Educating patients about the symptoms (eg, new-onset floaters, flashes, visual field defects) of a retinal tear or detachment is critical. The necessity of being examined on an emergent basis if symptoms of flashes or floaters occur should be stressed.
Hemang K Pandya, MD, FACS, Vitreoretinal Specialist, Dallas Retina Center; President, American Retina Forum
Disclosure: Nothing to disclose.
Coauthor(s)
Ilya (Eli) M Sluch, MD, Fellow in Cornea, Bascom Palmer Eye Institute
Disclosure: Nothing to disclose.
Specialty Editors
Simon K Law, MD, PharmD, Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine
Disclosure: Nothing to disclose.
Steve Charles, MD, Founder and CEO of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine
Disclosure: Received royalty and consulting fees for: Alcon Laboratories.
Chief Editor
Andrew A Dahl, MD, FACS, Assistant Professor of Surgery (Ophthalmology), New York College of Medicine (NYCOM); Director of Residency Ophthalmology Training, The Institute for Family Health and Mid-Hudson Family Practice Residency Program; Staff Ophthalmologist, Telluride Medical Center
Disclosure: Nothing to disclose.
Additional Contributors
Alex Yuan, MD, PhD, EyeSTAR Resident and Postdoctoral Fellow, Department of Ophthalmology, Jules Stein Eye Institute at University of California, Los Angeles
Disclosure: Nothing to disclose.
David Sarraf, MD, Associate Clinical Professor of Ophthalmology, Retinal Disorders and Ophthalmic Genetics Division, Jules Stein Eye Institute, UCLA Geffen School of Medicine, Greater Los Angeles Veterans Affairs Healthcare System
Disclosure: Nothing to disclose.
Stanley M Saulny, MD, Consulting Staff, Department of Ophthalmology, Ophthalmology Associates of the Valley
Disclosure: Nothing to disclose.
V Al Pakalnis, MD, PhD, Professor of Ophthalmology, University of South Carolina School of Medicine; Chief of Ophthalmology, Dorn Veterans Affairs Medical Center
Disclosure: Nothing to disclose.
Acknowledgements
This review was partly supported by a Research to Prevent Blindness Grant #OP 31 for David Sarraf, MD.
Ho TC, Ho A. Long-term natural course of lattice degeneration of the retina in high myopic eyes - A ten-year long term study. Investigative Ophthalmology & Visual Science. 2015. 56 (7):
Example of a lattice lesion containing white crisscrossing wicker lines, which are seen in about 10% of lattice lesions. This lesion is complicated by an extensive retinal tear at the cuff of the lesion.
An example of a heavily pigmented lattice lesion.
Lattice lesion containing small atrophic holes.
A peripheral lattice lesion demonstrating the typical snail-track appearance, with overlying vitreal opacities, which may represent glial proliferations or regions of increased vitreoretinal condensation.
Another example of a peripheral lattice lesion with a snail-track appearance.
Radial perivascular chorioretinal degeneration with retinal tear at the margin. These lesions run along vessels and may be found in Wagner's and Stickler's disease.
An acute rhegmatogenous retinal detachment that may be associated with lattice degeneration. (Lattice lesion not seen in this image.)
Example of a lattice lesion containing white crisscrossing wicker lines, which are seen in about 10% of lattice lesions. This lesion is complicated by an extensive retinal tear at the cuff of the lesion.
Another example of wicker lines seen within a lattice lesion. Prophylactic retinopexy has been performed around this lesion.
An example of a flap tear at the edge of a lattice lesion and three adjacent holes. This area of lattice degeneration has been barricaded by laser retinopexy.
A large horseshoe tear at the opposite edge of the lattice lesion pictured above. Laser retinopexy surrounds the tear and lattice lesion.
A peripheral lattice lesion demonstrating the typical snail-track appearance, with overlying vitreal opacities, which may represent glial proliferations or regions of increased vitreoretinal condensation.
An example of a heavily pigmented lattice lesion.
An acute rhegmatogenous retinal detachment that may be associated with lattice degeneration. (Lattice lesion not seen in this image.)
Another example of a peripheral lattice lesion with a snail-track appearance.
Lattice lesion containing small atrophic holes.
Radial perivascular chorioretinal degeneration with retinal tear at the margin. These lesions run along vessels and may be found in Wagner's and Stickler's disease.
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