8.1 Treatment of Peripheral Retinal Lesions

Select peripheral retinal lesions are considered to be a risk factor for rhegmatogenous retinal detachment and treatment can be considered (Figure 8.1.1).

Indications for Treatment of Peripheral Retinal Lesions

The guidelines on which retinal breaks require treatment are debatable and vary among physicians and regions. Treatment should be based on the risk of a break or lesion to progress to retinal detachment.[1] The correct management is on the configuration of the break(s) and the presence of symptoms. Table 1 lists types of lesions and the typical recommendation.

Adrean SD, Elliot D. Prophylaxis for retinal detachment. Review of Ophthalmology. 2005;5(6).

Table 1. Management Recommendations for Peripheral Retinal Lesions

Type of Lesion

Treatment

Acute Symptomatic Horseshoe Tears

Treat promptly

Acute Symptomatic Operculated Holes

Treatment may not be necessary

Acute Symptomatic Dialyses

Treat promptly

Traumatic Retinal Breaks

Usually treated

Asymptomatic Horseshoe Tears (Without Subclinical RD)

Consider treatment unless there are signs of chronicity such as pigmentation

Asymptomatic Operculated Tears

Treatment is rarely recommended

Asymptomatic Lattice Degeneration Without Holes

Not treated unless PVD causes a horseshoe tear

Asymptomatic Lattice Degeneration with Holes

Usually does not require treatment

Asymptomatic Dialyses

No consensus on treatment and insufficient evidence to guide management

Eyes with Atrophic Holes or Lattice Degeneration Where the Fellow Eye has had an RD

No consensus on treatment and insufficient evidence to guide management

Prophylaxis of Asymptomatic Retinal Breaks for Patients Undergoing Cataract Surgery

No consensus on treatment and insufficient evidence to guide management

Table modified after: Posterior vitreous detachment, retinal breaks, and lattice degeneration preferred practice patterns. AAO 2019

The primary method of treatment for these peripheral degenerations involves:

  1. Laser photocoagulation
  2. Cryotherapy

Laser Photocoagulation

The goal of laser photocoagulation is to generate regions of firm chorioretinal adhesion completely surrounding a retinal lesion. Melanin pigment is located in the retinal pigment epithelium (RPE) and choroid, and it is the absorption by this pigment to which most of retinal photocoagulation is attributed.[2] Green light has emerged as the predominant wavelength owing largely to its excellent absorption by melanin and hemoglobin with relatively poor absorption by xanthophylls thus sparing potential macular damage and being less painful. Red wavelengths are also poorly absorbed by xanthophyll and well absorbed by melanin but with the added benefit of being better suited for treating retinal tears associated with media opacity such as cataracts or vitreous hemorrhages.[3] Its longer wavelength, however, makes it more prone to deeper, and more unpredictable absorption by the choroid which can result in pain and even focal damage to Bruch’s membrane.

Intraocular fluids affect the laser spot size in silicone oil-filled eyes, yielding spot size enlargement while intraocular air or gas will decrease spot size. Such variations should be used to titrate laser settings as smaller spot sizes (as well as longer-duration applications) require less energy than larger spot sizes (and those of shorter-duration). In gas-filled eyes an additional consideration is the effective insulation of retinal tissue by the intraocular gas. This serves to augment laser power by reducing heat dissipation at the treatment site and results in more intense photocoagulation.

It is difficult to be prescriptive regarding laser settings, as they need to be individualized. It is better to know the outcome of laser burns depending on the aim: grey-white burns for laser retinopexy and panretinal photocoagulation and minimal colour change for macular laser (e.g. for macular oedema). Laser retinopexy is generally performed using a power of 200-500mW and a pulse duration of 0.1 to 0.2 seconds with higher powers required for shorter duration treatments (Figure 8.1.2). Higher powers and/or longer exposure may be required in cases with media opacity, shallow sub-retinal fluid and pale, myopic fundi. Smaller spot sizes yield a higher power per unit of area than larger spot sizes. Therefore, care needs to be taken to avoid rupture of Bruch’s membrane.[4] When performing laser retinopexy with an argon laser or a solid-state YAG laser with doubled frequency, the continuous mode is used with spot diameter of 200–500 μm. In cases when a diode laser (infrared: 810 nm) is used, burn diameter is 200–300 μm. The results of treatment are evaluated after 2 weeks.

Possible complications after laser retinopexy include inadvertent foveal burns, epiretinal membranes, peripheral visual field defects, nyctalopia, intraretinal and preretinal hemorrhages, late choroidal neovascularization due to rupturing of Bruch’s membrane, necrotic retinal tears and rarely choroidal detachment or exudative retinal detachment.

Laser delivery can be done either with slit lamp or indirect ophthalmoscopy (LIO):

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