Management of retinal detachment: a guide for non-ophthalmologists

What is retinal detachment?

Retinal detachment is separation of the neurosensory retina from the underlying retinal pigment epithelium (fig 1)⇓. In health, the potential “subretinal space” between these two layers is closed by the retinal pigment epithelium actively pumping fluid across the retina and into the choroid.1 Cellular interdigitation and extracellular matrix provide additional adhesion. Retinal detachment occurs when the forces of retinal attachment are overcome and fluid accumulates in the subretinal space.

Fig 1 The retina lines the internal surface of the posterior two thirds of the globe. It is thickest around the optic nerve and ends at the ora serrata, 5-7 mm behind the limbus. The macula lies temporal to the optic nerve, bordered by the vascular arcades; the fovea is a depression at its centre that provides fine visual acuity. The outermost layer of the retina contains photoreceptors (rods and cones), loosely attached to the retinal pigment epithelium; they depend on the retinal pigment epithelium and choroid for support. The vitreous completely fills the vitreous cavity and is firmly attached to the retina near the ora serrata, over the optic nerve and macula, along the blood vessels, and around degenerative retinal lesions

• Download figure
• Open in new tab
• Download powerpoint

How common is retinal detachment and why should it interest non-ophthalmologists?

Large, population based studies of retinal detachment find an annual incidence of around 1 in 10 000, and a familial aggregation study estimated a lifetime risk of 3% at age 85.2 3 White and Asian populations have similar rates, with a lower incidence among blacks.4 5 The average age of presentation is around 60, with the sexes affected equally.2

The modest incidence belies the importance of retinal detachment as a true ophthalmic emergency. Although most detachments can be repaired surgically, only those treated early avoid permanent visual impairment.6 Many patients first present to general practitioners, emergency departments, and optometrists. Retinal detachment is therefore of clinical (and possibly medicolegal) interest to non-ophthalmologists.7

Pathogenesis of retinal detachment

Retinal detachments can be caused by scarring of the vitreous and retina (tractional) or leakage of fluid into the subretinal space (exudative), but most follow the development of breaks in the retina (box 1), which allows fluid in the vitreous cavity to enter the subretinal space (fig 2)⇓. Such detachments are called rhegmatogenous (from the Greek word rhegma, meaning a break, rent, or fissure).

Fig 2 Rhegmatogenous retinal detachment. Hyaluronic acid in the vitreous holds water and keeps insoluble collagen fibrils dispersed in the gel matrix. A—with aging, changes to hyaluronic acid cause pockets of liquefied vitreous, leaving the collagen fibrils to condense into larger fibre bundles, which appear as chronic floaters. B—pockets of liquid vitreous coalesce to form larger spaces. Defects in the vitreous cortex let liquid into the plane between the vitreous cortex and retina, initiating posterior vitreous detachment. C—the collapsing vitreous exerts mechanical traction on the retina and optic nerve, which may be perceived as flashing lights; condensation of the vitreous around the optic nerve may appear as a crescent shaped floater (Weiss ring). Vitreous traction may lead to avulsion of blood vessels or formation of retinal breaks. D—fluid enters the subretinal space through the retinal break and retinal detachment develops

• Download figure
• Open in new tab
• Download powerpoint

Most retinal breaks form when the vitreous separates from the retina as part of the normal ageing process. This event, posterior vitreous detachment, is the result of a lifetime process of degenerative liquefaction and shrinkage of the vitreous (fig 2⇑).8 Although posterior vitreous detachment is benign in most people and may go unnoticed, those with symptoms carry a 10-15% risk of developing retinal breaks.9 10 Posterior vitreous detachment is rare before the age of 40, but the prevalence increases steadily thereafter, to around 40% in the seventh decade. By the ninth decade, up to 86% of the population develop a partial or complete posterior vitreous detachment.11

What symptoms should alert me to a threatened retinal detachment?

Who is at risk of developing retinal detachment?

Retinal detachment occurs more commonly with age as posterior vitreous detachment becomes more prevalent. Cataract surgery is thought to accelerate vitreous liquefaction and posterior vitreous detachment.14 A retrospective, population based study found that the eight year cumulative risk of retinal detachment approached 1% after cataract surgery, almost nine times higher than expected.15 The risk increases further if vitreous is lost during surgery.16

Myopic patients (with increased axial length) are more likely to develop posterior vitreous detachment at a younger age.11 The peripheral retina in these eyes is less robust and commonly habours degenerative lesions, such as lattice, where the retina is thinned and firmly adherent to the vitreous.17 Retinal detachment from atrophic holes, without posterior vitreous detachment, is relatively common in highly myopic people.18 Cataract surgery in very myopic patients carries a particularly high risk of detachment.19

Many retrospective studies have shown that trauma is an important cause of retinal detachment in young patients.20 21 A direct blow to the eye induces breaks in the retina, usually in the form of retinal dialysis (lifting of the retinal edge at the periphery), and tears and atrophic holes from retinal contusion can also develop. Ocular trauma induces premature posterior vitreous detachment, possibly through liquefaction of the vitreous from leakage of blood and protein.22

Prospective and retrospective case series report retinal detachment in up to 23% of second eyes as the features that played a role in the previous detachment are replicated.23 24 Family history is also a risk factor because features such as increased axial length and degenerative retinal lesions are heritable traits.25

How to assess a patient with suspected retinal detachment

If the presenting symptoms and risk factor profile suggest retinal breaks or detachment, further ophthalmic assessment is indicated. The completeness of the assessment will depend on the availability of equipment and the skills of the examiner (fig 3)⇓.

Fig 3 Management of retinal detachment

• Download figure
• Open in new tab
• Download powerpoint

Visual acuity should be assessed before the pupil is dilated. Decreased visual acuity usually indicates macular detachment, but vitreous haemorrhage may also reduce vision. A confrontational visual field test may show an asymptomatic peripheral field defect. Extensive retinal detachment will produce a relative afferent pupillary defect. This can be tested by shining a bright torch alternately on one eye for two seconds, then rapidly swinging it on to the other eye. This can be tested by shining a bright torch on each eye for two seconds, several times in quick succession. The pupils will dilate when the torch is swung on to the affected eye and constrict when it shines on the unaffected eye, as a result of less “brightness signal” being sent to the brain from the eye with the detachment.

Dilating the pupil with a short acting mydriatic (tropicamide 1%, for example) is safe, and the risk of inducing acute angle closure glaucoma is extremely low. The red reflex should be examined with a direct ophthalmoscope at 1 metre for loss caused by retinal detachment or vitreous haemorrhage. If a detachment is near the macula it may be visible through the direct ophthalmoscope; the detached retina will appear pale, opaque, and wrinkled, with masking of the underlying choroidal pattern (fig 4)⇓.

Fig 4 Funduscopic appearance of rhegmatogenous retinal detachment. The patient noticed blurred vision in her left eye three days earlier. A sector of retina is attached superiorly; shallow retinal detachment over the macula and nasally appears pale and featureless owing to the masking of the choroidal pattern. The fovea appears dark against the pallor of detached macula, and the bullous retinal detachment inferiorly appears pale, opaque, and wrinkled. The detachment was caused by a single superotemporal retinal tear

• Download figure
• Open in new tab
• Download powerpoint

Retinal detachment cannot be excluded by direct ophthalmoscopy owing to the narrow field of view. Slit lamp or indirect ophthalmoscopy with a consdensing lens is needed to examine the peripheral retina and locate retinal breaks. A slit lamp is needed to assess the anterior vitreous for pigment granules (“tobacco dust”), which correlate with a 90% risk of retinal breaks.26 The anterior vitreous is best visualised with an oblique slit beam through a dilated pupil.

Macroscopic vitreous haemorrhage is associated with a 70% risk of retinal breaks.27 When dense vitreous haemorrhage precludes examining the fundus, ultrasonography can identify the detachment. Because ultrasound does not image the retinal periphery well, retinal breaks there cannot be diagnosed with certainty by this method.

Decisions to refer: when, to whom, and how urgently?

All patients with a recent onset of retinal detachment should be referred immediately. Time can be saved by referring the patient directly to the ophthalmologist who will perform the surgery. In some countries, retinal detachments are mostly repaired by specialist vitreoretinal surgeons. If immediate referral is not possible, the patient should be instructed to lie down with the face on the side of the detachment to the pillow (opposite the field defect) to minimise the detachment extending towards the macula.

There is no general consensus on how soon patients presenting with a symptomatic posterior vitreous detachment and no other visual symptoms should be referred for a definitive examination. The referral should be made as soon as possible, certainly within days, in view of the considerable risk of retinal breaks associated with the presentation. The patient should be instructed to return earlier if symptoms worsen or a visual field defect develops.

Treatment of retinal break and detachment

Retinal breaks caused by posterior vitreous detachment are treated using laser therapy or cryotherapy to create a scar adhesion between the retina and retinal pigment epithelium. This treatment is almost 100% successful, but new breaks can develop elsewhere.28 Prophylactic treatment of asymptomatic breaks or degenerative retinal lesions has not been shown to reduce the risk of retinal detachment.29

Once the retina is detached, additional surgical procedures are required to reattach it and seal the breaks. Most retinal detachments not involving the macula are repaired on the same day or the following day. For patients presenting with the macula already detached, the macula should be reattached within five days, but the urgency of the surgery is influenced by individual factors such as the duration of symptoms, the height of macular detachment, and visual acuity.6

Scleral buckling and vitrectomy with gas tamponade are the most common surgical approaches to repairing retinal detachment (fig 5)⇓. Pneumatic retinopexy can be performed in some cases, but enthusiasm for this technique outside North America has been minimal. In 95% of cases the retina will be reattached, sometimes after more than one operation.30 Successful reattachment of the retina does not always correlate with a good visual outcome, and patients presenting with poorer vision are less likely to achieve good final visual acuity.6 Macular detachment has a poorer visual outcome, and the chance of regaining good vision diminishes with the duration of detachment.6 Results are best when the detachment is repaired before the macula becomes involved, and this can be achieved only through early diagnosis and urgent referral.

Fig 5 Surgery for retinal detachment. A—in scleral buckle surgery, the retinal break is treated with cryotherapy or laser therapy, and an explant (usually a silicone band or strip) is sutured on the outer surface of the sclera to indent the wall of the globe. This interrupts the flow of fluid through the break, allowing it to close. Subretinal fluid is drained through a small sclerotomy or left to be absorbed into the choroid. B—the vitrectomy approach involves removing the vitreous through sclerotomies made in the pars plana. Subretinal fluid is drained internally, and laser therapy or cryotherapy is applied around the flattened retinal break. The vitreous cavity is filled with a tamponade (usually gas but occasionally silicone oil) to hold the retina in place while scarring develops around the break. In some cases, pneumatic retinopexy may be less invasive: a bubble of gas is injected into the vitreous cavity, and the patient’s head is positioned to place the bubble on the retinal break; once the retina is flattened, the break can be treated with laser therapy or cryotherapy

• Download figure
• Open in new tab
• Download powerpoint

Postoperative care

After the operation, topical antibiotics and corticosteroids are routinely prescribed, and cycloplegics and ocular hypotensive agents may be prescribed in some patients. If intraocular gas has been instilled, vision will be poor. As the gas is resorbed over weeks to months, the gas-fluid interface will become apparent to the patient as an undulating line that moves downward. Worsening vision is not expected and should be reported to the surgeon immediately. Severe pain is also unusual and should be reported. Headache and nausea suggest an acute rise in intraocular pressure. Patients with intraocular gas are usually asked to maintain a certain head posture, typically for one week. Air travel must be avoided while the gas remains, and intraocular gas is a contraindication for volatile gas anaesthesia.