Clinical Review: Lattice Degeneration

A Review of Lattice Degeneration

Introduction:

  • Aka equatorial, circumferential, or palisade retinal degeneration
  • Prevalence: 8-11% of population, usually younger patients, evident in 2nd decade of life
  • Unclear genetic link; no gender or racial predilection
  • Tends to be bilateral & fairly symmetric

Pathogenesis:

It’s a slow progressive disease with an unclear pathogenesis. Based on eyes at autopsy, the sequence of events begins with thinning of the innermost retinal layers secondary to ischemia resulting from dropout of peripheral retinal capillaries. Pocket of vitreous liquefaction (lacuna) overlying the lesion then forms. This is followed by glial cells proliferation along the vitreal surface, which causes increased vitreoretinal adhesions at margins of lesion, further causing vitreoretinal traction, and ultimately resulting in more retinal thinning of deeper sensory layers. Finally, the RPE atrophies & pigment hyperplasia occurs.

Physical appearance of lesions:

  • Lesions vary from ½ to 6 DD in size and 1-19 in number. They are usually located temporally and in the vertical meridians (11-1 & 5-7 o’clock). They tend to be adjacent to each other on the same equatorial line or lined up in rows parallel to the ora.
  • White lines in criss-cross pattern (hence the name Lattice); these lines are uncommon in young and increase in frequency with age.
  • RPE hyperplasia which migrates into the overlying sensory retina > most common finding.
  • White/yellow flecks located beneath the retinal surface > 2nd most common finding.
  • Vessels can be surrounded by glial proliferation or hyaline deposits, or replaced with cords of connective tissue, forming sclerosis or fibrosis of vessels over the lesion.
  • Area of vitreoretinal adhesion appearing as a thin translucent membrane
  • Occasionally, can see white-without-pressure along the lesion’s borders (secondary to vitreous traction), chorioretinal atrophy, & snowflake-like opacities adjacent to the lesion.
  • Retinal breaks (atrophic holes or tractional tears) and rhegmatogenous retinal detachments can be associated with lattice degeneration.
Atrophic holesLoss of all sensory retina

Prevalence in LD: ~18-28%

Occur within lesion or adjacent to it

Red, round or oval

Usually small & solitary

Asymptomatic & occur earlier than tractional tears

Tractional tearPrevalence in LD: ~2%

Most frequently occur at posterior and lateral edges of lesion

Linear or horseshoe

Small or large

Don’t occur across lesion due to strength of fibrotic area

When tear is associated with LD, common to find PVD at posterior margin of lesion

Tear probably secondary to sudden tractional forces caused by PVD (symptomatic)

 

Rhegmatogenous Retinal Detachment:

  • Occur in ~0.3-0.5% of patients with Lattice Degeneration; secondary to a retinal break.
  • In cases of an atrophic hole, liquefied vitreous passes through into the subretinal space and causes a slowly progressing detachment; thus can have an associated demarcation line.
  • In cases of a tractional tear, the detachment progresses rapidly and thus no associated demarcation line. If PVD is present, more fluid and vitreous traction is present, increasing the prevalence of the detachment to ~37% of the cases.

Management:

In absence of breaks:

  • Record findings & monitor annually (or every 6 months if patient has symptoms of floaters/flashes)
  • Prophylactic treatment can be given only if the eye with lattice has symptomatic tears, is highly myopic or aphakic, and if there’s a strong family history of retinal detachments or if fellow eye had a detachment secondary to lattice in the past.

In presence of breaks:

  • For holes, just monitor if no symptoms.
  • Prophylactic treatment for tears? Unclear.
  • For significant breaks but no detachment, need laser photocoagulation & cryoretinopexy.
  • For retinal detachment, scleral buckling with or without an encircling band.

References: (OptometryStudents.com and the author recommend obtaining a comprehensive understanding of this subject by reviewing it’s sources)

1. Jones, William. Peripheral Ocular Fundus. Missouri: Butterworth Heinemann Elsevier, 1998.

2. Lattice Degeneration with and without Atrophic Holes. Handbook of Ocular Disease Management.

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