BASICS

DESCRIPTION

• A full thickness defect in the neurosensory retina.

• May be round/oval (retinal hole), horseshoe shaped (retinal tear), irregularly shaped or semicircular/adjacent to the ora serrata (dialysis).

• Location usually in peripheral retina, although may occur anywhere.

• A retinal break may allow vitreous fluid to pass through the break into the subretinal space leading to rhegmatogenous retinal detachment (RRD) with potential for severe visual loss.

• The etiology, underlying risk factors and shape of the retinal break may increase the risk of progression of a retinal tear to RRD.

• A retinal break does not produce visual loss (exception is a macular hole), but the vitreous hemorrhage or retinal detachment occurring secondarily lead to the loss of vision.

EPIDEMIOLOGY

Incidence

• Incidence of retinal breaks is 6–11% in adult eyes at autopsy.

• Incidence of retinal tears in eyes with symptomatic posterior vitreous detachment (PVD) is 8.2% (1).

• 1.8% of patients develop a retinal tear that was not visualized on initial examination but was noted with follow-up.

• Features associated with delayed-onset diagnosis or development of retinal break associated with PVD include vitreous hemorrhage at initial examination, hemorrhage in the peripheral retina at initial examination, or new symptoms.

• Annual incidence of retinal detachment is 12 per 100,000 per year.

Prevalence

Prevalence of retinal break ranges from 6 to 14%.

RISK FACTORS

• Myopia

• Increased age

• Lattice degeneration

• PVD

• History of intraocular surgery, including cataract surgery

• Trauma

• History of retina break or RRD in the contralateral eye

• Family history

• Stickler syndrome

Genetics

• Genetic syndromes that predispose to myopia or collagen abnormalities may be a risk factor for retinal break.

– These include Stickler’s syndrome, Marfan’s syndrome, Wagner’s syndrome, Ehlers–Danlos syndrome, and homocystinuria.

GENERAL PREVENTION

• Development of PVD is not preventable.

• In most cases progression of PVD to retinal break is not preventable.

• Laser prophylaxis to retinal lesions that predispose to retinal breaks may seal the area and prevent development of retinal detachment.

• Prompt recognition of symptoms of PVD and assessment may prevent the progression of retinal break to retinal detachment.

PATHOPHYSIOLOGY

Retina breaks develop either secondary to peripheral retina stretching and atrophy near the ora serrata (retinal hole) or due to PVD with vitreous traction (horseshoe-shaped tear, operculated hole, dialysis)

COMMONLY ASSOCIATED CONDITIONS

• Myopia

• Lattice degeneration

• See risk factors

DIAGNOSIS

HISTORY

• Symptoms of PVD with attention to photopsia, floaters, visual field disturbance, reduced visual acuity

• Family history

• Prior eye trauma

• Myopia

• History of intraocular surgery, including cataract surgery

PHYSICAL EXAM

• Examination of the peripheral retinal with scleral depression and assessment of the vitreous

• Features may include:

– Retinal hole – round or oval

– Horseshoe-shaped tear – tip of the tear is pointed toward the optic nerve, may be an associated bridging vessel

– Retinal dialysis – may have pigment along its edge if there is associated avulsion of the vitreous base and trauma

• Changes in adjacent retina such as lattice degeneration or pigmentary change

• Peripheral retinal abnormalities

• Pigmented cells in the vitreous (aka tobacco dust, Schafer’s sign)

• Vitreous traction

• Vitreous hemorrhage

• PVD with Weiss ring

DIAGNOSTIC TESTS & INTERPRETATION

Imaging

B-scan ultrasound may demonstrate retinal break if cloudy media obscure visualization of the retina such as with vitreous hemorrhage

Pathological Findings

Full thickness defect in the neurosensory retina

DIFFERENTIAL DIAGNOSIS

• Chorioretinal atrophy or scar

• Pars plana cyst

• Enclosed oral bay

• Meridional folds

• Vitreoretinal tuft

• Peripheral cystoid degeneration

TREATMENT

ADDITIONAL TREATMENT

General Measures

• Goal is to treat retinal breaks that are at a high risk of progression to RRD, thus preventing any secondary visual loss.

• Observation may be recommended when the risk of progression to RRD is extremely low (2) as in the following situations: Asymptomatic retinal holes that do not have vitreoretinal traction, round holes with operculum (relieved vitreous traction) and atrophic round holes, atrophic holes within an area of lattice that is self-sealed by pigment.

Additional Therapies

• Treatment with laser or cryotherapy creates a firm chorioretinal adhesion in the attached retina immediately adjacent to and surrounding the retinal tear.

• Treatment of peripheral breaks should extend anteriorly up to the ora serrata and to completely around the entire break or dialysis.

• Laser prophylaxis to areas of thin retina may be considered in eyes with an increased risk of development in retinal tear or RRD.

• Cryotherapy may be used as an alternative to laser in eyes with cloudy media, if the laser cannot reach the oral serrata, or if the laser is not available.

SURGERY/OTHER PROCEDURES

• May be indicated if media opacity such as asteroid hyalosis, vitreous hemorrhage, or cataract precludes viewing of the retina for laser/cryotherapy or if RRD develops.

• This may include pneumatic retinopexy, vitrectomy, or scleral buckling procedure.

ONGOING CARE

FOLLOW-UP RECOMMENDATIONS

There is an increased risk of retinal break in the same or contralateral eye.

PATIENT EDUCATION

• Individuals at an increased risk of retinal break/detachment should notify their ophthalmologist promptly if they develop or note a change in symptoms such as floaters, photopsia, visual field defect, or reduced acuity.

• Myopic individuals who undergo refractive surgery should be aware of the fact that they remain at a risk of retinal beaks and RRD.

PROGNOSIS

Treatment is usually uncomplicated with a high rate of successfully sealing the break and preventing retinal detachment.

COMPLICATIONS

• Progression of retinal tear to RRD despite the fact that laser/cryotherapy may occur on occasion (3).

• Most common cause of failure is inadequate treatment of the anterior extent of tear. Continued vitreous traction can extend the tear beyond the treated area, allowing fluid to leak into the subretinal space with RRD. Also, continued vitreous traction may produce new tears.

• Vitreous hemorrhage.

• Epiretinal membrane formation may develop after PVD, and it does not appear to have an increased incidence after laser photocoagulation.

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