Retinal Break

Definition

Blood in the vitreous space.

Etiology

Retinal break, posterior vitreous detachment, ruptured retinal arterial macroaneurysm, juvenile retinoschisis, familial exudative vitreoretinopathy, Terson’s syndrome (blood dissects through the lamina cribrosa into the eye due to subarachnoid hemorrhage and elevated intracranial pressure, often bilateral with severe headache), trauma, retinal angioma, retinopathy of blood disorders, Valsalva retinopathy, and neovascularization from various disorders including diabetic retinopathy, Eales’ disease, hypertensive retinopathy, radiation retinopathy, sickle cell retinopathy, and retinopathy of prematurity.

Symptoms

Sudden onset of floaters and decreased vision.

Signs

Differential Diagnosis

Vitritis, asteroid hyalosis, pigment cells, pars planitis.

Evaluation

Prognosis

Usually good.

Treatment of breaks

A major deficiency in the use of cryotherapy is the inability to visualize treated retina for many minutes following thawing. This can lead to over-treatment by treating the same area twice. Alternatively, an inadequate adhesion will be produced if the burns are not contiguous in appropriate areas. Therefore the surgeon must form an optimal visual image of the precise limits of applications of cryotherapy.

Cryotherapy burns should extend only to the edges of medium and large retinal breaks. If the pigment epithelium lying beneath the break is included in the cryotherapy burn, an intravitreal dispersion of pigmented cells capable of proliferation will occur (Fig. 1.3). For the same reason, scleral depression of a treated area at the edge of a break should not be repeated after the treatment, and localization of retinal breaks should always precede cryotherapy.

The development of indirect laser delivery systems has made it possible to treat retinal breaks with photocoagulation, but we do not use this modality except in very unusual circumstances, when breaks in reattached retina are treated postoperatively through a gas bubble.

Prophylaxis:

Scleral dissection

After localization of all retinal breaks requiring support, a lamellar scleral undermining or scleral dissection is performed. The extent of dissection depends on the size of the intended buckle. It is recommended that the lamellar scleral dissection extend 3 mm posterior, 2 mm anterior, and 3 to 4 mm circumferentially beyond the retinal breaks.¹² The dissection is begun with an incision parallel to the limbus at the posterior edge of the retinal breaks. The depth of the incision is considered appropriate if a thin gray layer of sclera remains over the choroid. The lamellar dissection is performed using a blunt dissector with traction on the reflected scleral flaps. Care is taken when dissecting posteriorly to the equator to avoid severing the vortex veins. Modifications of the posterior scleral flap are often necessary to avoid the vortex veins. The size of the scleral dissection is designed to accommodate the width plus the height of the desired implant (Fig. 118-25).

Horseshoe tears

Areas of strong vitreoretinal adhesion cause retinal breaks during traumatic or spontaneous posterior vitreous detachment. These retinal breaks typically take the shape of a horseshoe. Detachments related to horseshoe tears have been reported to account for 11% of traumatic retinal detachments and 45% of spontaneous detachments. Furthermore, a history of trauma was present in 5% and objective evidence of trauma was found in 20% of detachments associated with horseshoe tears. As would be expected, patients with trauma-related horseshoe detachments are younger than those with non-traumatic detachments. However, assigning a traumatic etiology to these cases can be difficult.

When vitreous syneresis leads to a posterior vitreous detachment, horseshoe tears normally occur at sites of vitreoretinal adhesion. A similar mechanism occurs in traumatic horseshoe tear development. Globe deformation and torsion lead to posterior vitreous detachment, and a tear can develop at the site of firm vitreoretinal adhesion. A flap of retina is held open by residual vitreous traction, allowing fluid to continually enter the subretinal space. Unlike retinal dialyses or pars plana tears but similar to giant retinal tears, detachments associated with horseshoe tears tend to progress rapidly and symptomatically to bullous detachments.

Contraction and fibrosis of flap of giant retinal tear

The posterior flap of most giant retinal breaks shows inward curling of the edge because of the normal contractility of the retina. With chronicity and the onset of PVR, this folding may become permanent and prevent reattachment of the edge of the flap (Fig. 108.14A). The inwardly folded retina may become fixed with proliferative membranes, and the edge may be thickened, fibrous, and taut. Even after removal of membranes, the edge may remain folded, requiring retinectomy to allow complete flattening of the flap of the giant break.

There is often both anteroposterior shortening because of inward rolling of the edge of the break and circumferential shortening as a result of fibrous contraction. Membranes are removed on both the anterior and posterior surfaces of the retina. The flap is unfolded mechanically using two instruments. If the flap will not unfold, it is often best to excise the folded edge of the flap.⁴² Alternatively, a series of radial cuts may be placed approximately every 30° along the margin of the flap to allow unfolding.⁴² However, the irregular edge created by this series of cuts is more difficult to manage, and excision of the edge is the preferred approach (Fig. 108.14B).

After removal of posterior membranes, PFCL is injected over the posterior pole and the level is brought to a level posterior to the fibrotic edge of the giant tear (Fig. 108.8B).⁴ The PFCL fixes the retina and makes excision of the organized edge easier. Diathermy is applied to the edge of the flap throughout the extent to be excised. Excision is usually with the vitreous cutting instrument, being careful to apply low suction so that excessive retina is not excised. If radial cuts are to be made, diathermy is applied only locally in the area to be cut.

Definition

Nonrhegmatogenous retinal detachment (not secondary to a retinal break) due to subretinal transudation of fluid from tumor, inflammatory process, vascular lesions, or degenerative lesions.

Etiology

Vogt–Koyanagi–Harada syndrome, Harada’s disease, idiopathic uveal effusion syndrome, choroidal tumors, central serous retinopathy, posterior scleritis, hypertensive retinopathy, Coats’ disease, optic nerve pit, retinal coloboma, and toxemia of pregnancy.

Symptoms

Usually asymptomatic until serous retinal detachment involves macula; may have acute onset of photopsias, floaters (“shade” or “cobwebs”), shadow across visual field, or decreased vision.

Signs

Differential Diagnosis

Retinoschisis, choroidal detachment, rhegmatogenous retinal detachment.

Evaluation

Prognosis

Variable (depends on underlying etiology).

52.5.1 CLINICAL SIGNS AND SYMPTOMS

The ability to make the diagnosis of a traumatic retinal break, retinal dialysis, or retinal detachment may be limited by media opacity. When the ocular media precludes complete posterior segment examination, ultrasonography is performed until a complete examination can be done to rule out the presence of posterior segment retinal breaks or detachment. The presence of a dialysis may be elusive, requiring scleral depression with special attention to the ora serrata. Retinal detachment is rarely present immediately after a contusion injury but can occur weeks to months later, necessitating careful follow-up examination (Figure 52-10). However, retinal breaks or dialysis are often present immediately after the injury, permitting prophylactic treatment if detected.