Retinal Detachment

Retinal detachment (RD) refers to a separation of the inner neurosensory retina and the outer retinal pigment epithelium (RPE).¹ The space between them becomes filled with subretinal fluid which may come from a number of sources (not all of which are known). Its importance lies in the fact that it is one of the few eye conditions that needs urgent treatment in order to preserve sight (others include chemical burns, retinal artery occlusion and acute angle closure glaucoma)² and so early recognition and prompt referral is essential.³

RD broadly falls into two categories: rhegmatogenous and non-rhegmatogenous.

• Rhegmatogenous RD - this where the sensory retina detaches due to a retinal break: it may get torn as a result of vitreous traction or chronic retinal atrophy may result in a hole. This is the most common form of RD.
• Non-rhegmatogenous RD - there are two types of non-rhegmatogenous RD:
  • Tractional: the vitreous contracts (e.g. due to proliferative diabetic retinopathy) and pulls the sensory retina away with it.
  • Exudative (serous or secondary RD): damage of the underlying RPE (e.g. severe hypertension) allows subretinal fluid to leak into the subretinal space under the sensory retina, so pushing this out and causing a detachment.

• Incidence is about 1 in 10,000 with a prevalence of about 0.3% of the general population and a lifetime risk of 3% by the age of 85.³
• It most commonly occurs in the 40-70 year old age group (average age is 60 years old) although traumatic retinal detachment is more frequently seen in younger patients, particularly males.
• There has recently been an increase in presentation of much younger individuals and in children associated with paint ball injuries.⁴
• There is anecdotal evidence that it is more common in people of Jewish descent and less common in patients of African origin.

RD may be predisposed or caused by a number of conditions, some of which are applicable to all types of RD (see box) and other which tend to occur more specifically in different types of RD. In a large number of people, this is preceded by a posterior vitreous detachment (PVD) - the end point of a life-time of normal, age-related degenerative liquefaction and shrinkage of the vitreous. Patients with a PVD carry a 10-15% risk of going on to developing a RD as the PVD may cause a tear in the retina.

• Age
• Lattice degeneration
• Aphakia (no crystalline lens)
• Age-related retinoschisis
• Previous retinal break
• Marfan's syndrome

• Proliferative diabetic retinopathy
• Penetrating eye injury
• Retinal vein occlusion
• Retinopathy of prematurity
• Previous giant retinal tear
• Sickle cell retinopathy
• Toxocariasis

• Inflammatory conditions e.g. uveitis, Vogt-Koyanagi-Harada syndrome, posterior scleritis
• Vascular disease e.g. severe hypertension, Coats disease
• Neoplasia e.g. multiple myeloma, tumours of the choroid, haemangioma
• Toxaemia of pregnancy
• Congenital abnormalities e.g. coloboma
• Maculopathy e.g. neovascular macular degeneration, idiopathic central serous chorioretinopathy
• Nanophthalmos

Other more unusual reported causes of retinal detachments have been following laser treatment for posterior capsular opacification (a condition that develops months or years after cataract operations that is amenable to laser treatment) and latanoprost use.⁴

History¹

• The classic symptom is photopsia (flashing lights) which occurs in about 60% of patients. This tends to be induced by eye movements and is best seen in dim lighting conditions, particularly in the temporal, peripheral visual field. Where there is a pre-existing PVD, it arises as a result of the vitreous pulling on the retina.
• Photopsia is commonly associated with floaters which may be described as a solitary opacity, a cobweb-like opacity or a shower of little spots. The latter is pathognomonic for vitreous haemorrhage, resulting from disruption of a retinal vessel caused by a retinal tear or mechanical traction of a vitreoretinal adhesion.² Where a PVD has already occurred, they are more visible to the patient as they are more mobile within the globe.³
• Some patients go on to describe a visual field defect apparent as a curtain descending over their vision. This may become worse as the day goes on. If the macula becomes involved, visual acuity is severely reduced and there may be metamorphopsia (distortion of the image).
• A simple tear in the absence of detachment may be completely asymptomatic.⁶

Examination⁷

You may wish to our record on Examination of the Eye for details on carrying out these assessments.

• Visual acuity - this should be checked in all patients, before dilating the pupil. If you strongly suspect a retinal detachment and the visual acuity is normal, referral is all the more urgent as the macula has not yet been involved and surgery can prevent it from becoming detached. A poor visual acuity suggests that the macula has already become detached - these patients do need urgent referral but their outcome is less promising. It may also suggest a vitreous haemorrhage.
• Visual fields - confrontational visual field testing will give you an idea of any gross visual defects corresponding to the area of detached retina - defects may not be picked up this way if they are small.
• Dilated fundal examination (check for an RAPD first) - once you have assessed the visual acuity and ruled out the presence of a relative afferent pupillary defect - RAPD (this indicates extensive RD), dilate the pupils. 1% tropicamide is suitable - warn the patient that their vision will become blurred (this settles over 2-3 hours) and that they will not be able to drive. A large detachment can be seen as a sheet of sensory retina billowing towards the centre of the globe, over which the vessels pass like paths over a hill. There may be an associated tear visible. Note that the location of the photopsia in the patient's visual field bears no relation to where the tear is but the location of the field loss does.²

If you cannot see a RD on ophthalmoscopy but suspect it, refer the patient on for a slit-lamp examination (direct ophthalmoscopy offers only a narrow field of view). If you have access to a slit-lamp, look for cells in the anterior chamber and the presence of 'tobacco dust', seen as grey-red specks just behind the pupil. This is associated with a 90% risk of a retinal break. A vitreous haemorrhage is associated with a 70% risk of a retinal break.

Ultimately, these patients will be fully re-examined in the Eye casualty department. This will involve a slit-lamp examination, indirect ophthalmoscopy (a head-mounted ophthalmoscope shines light through a wide-angled lens to allow a more peripheral look) or they will have a Goldmann triple mirror examination (which involves a slit-lamp and a contact lens applied against the anaesthetised cornea for a few minutes as the peripheral retina is examined).

Some patients may also have an ultrasound performed where they simply have to lie back with their eyes closed as the probe is applied over the eyelid. Ophthalmologists will be assessing the type and extent of the detachment, the type, extent and number of any associated tears and any ocular co-morbidity.

Conditions with similar symptoms:

1. Photopsia
   • Posterior vitreous detachment: this may lead to a retinal detachment (see above).
   • Atypical/ocular migraine
   • Optic nerve pathology e.g. optic neuritis
   • Cerebrovascular event/transient ischaemic attacks
   • Choroidal tumours
2. Floaters³
   • Age-related macular degeneration
   • Posterior vitreous detachment
   • Vitreous haemorrhage (e.g. diabetic retinopathy)
   • Asteroid hyalosis
   • Uveitis (particularly posterior)
   • Retinitis pigmentosa

Conditions with similar signs:

• Retinoschisis: usually benign condition where the retina is split into layers.
• Choroidal detachment: detachment of the vascular layer of the eye.
• Uveal effusion syndrome: rare idiopathic condition characterised by self-limiting choroidal and retinal detachment.

Additionally, when the diagnosis is confirmed, there will be efforts to rule out any underlying predisposing factors that need to be treated e.g. tumour (see list above).

Diagnosis is confirmed on examination and any further investigations relate to the suitability of the patient to have a general anaesthetic. Occasionally, an ultrasound (simple procedure done in outpatient clinic) or optical coherence tomography are needed to confirm the diagnosis or further assess the eye in order to prepare for surgery. CT and MRI scans only have a role if there is a tumour or suspected foreign body.

Medical treatment

Generally, retinal breaks and detachment are treated with lasers and surgically respectively. However, a small number of exudative RDs caused by inflammatory conditions may respond best to treatment of the underlying condition. All other forms of RD need active intervention.

Laser treatment

This is performed if there is a retinal break but a full-blown RD hasn't yet developed (or if it is very small). The idea is to encircle the lesion with laser burns. The subsequent scar tissue prevents the tear from extending or subretinal fluid from leaking in or out of it. This can be done within a clinic setting.

Cryotherapy

This treatment modality may be selected in preference to laser treatment if the tear is in certain locations around the fundus, if the view is a little hazy or the pupil is small.

Surgical treatment

There are three approaches to surgical treatment, the first two of which are the most commonly used:⁸

1. Scleral buckle - a silicone sponge or solid silicone is placed on the outside of the globe at the site of retinal breaks. The breaks themselves are treated with cryotherapy. The idea is to create an inward indentation of the sclera in order to close off the breaks and to reduce any associated vitreal traction. The explants may be short stumps placed locally or longer structures encircling the circumference of the globe. The choice depends on the nature of the break(s).
2. Vitrectomy - the vitreous may be removed in the case of a tractional RD. This technique is also sometimes used in rhegmatogenous RD.
3. Pneumatic retinopexy - a gas bubble (sometimes a silicone bubble) is injected inside the globe, over the site of the break (which has either previously been repaired with cryotherapy or is subsequently repaired with laser therapy) and pushes the flaps of retina against the periphery. If it stays in position, it permits the subretinal fluid to be resorbed over 24-48 hours. The bubble itself will very gradually be resorbed over weeks/months.This procedure is favoured in North America and less commonly used in the UK.³

There are a few things that are helpful to know about surgical repair of RD:⁹

• It is carried out by specialist vitreoretinal surgeons (so a patient may find themselves being referred on from a DGH).
• Most RDs not involving the macula are repaired the same day and those involving the macula are repaired within 5 days.³
• It is usually performed under a general anaesthetic.
• It may involve 'posturing' (the gas or silicone bubble has to stay in the right place by keeping the head very still). This can be for up to 10 days.
• It usually involves a few nights stay (2 or 3 is common) at the hospital.
• Topical antibiotics and corticosteroids are routinely prescribed post-operatively; occasionally, patients may also need cycloplegics and ocular hypotensive drugs.³
• Following discharge, patients should report excessive pain, worsening vision or an increasingly red eye to the team. Headaches and nausea should also be reported (this could be rising intraocular pressure).
• Patients who have had pneumatic retinopexy should not travel by air and should advise anaesthetists that they have intraocular gas prior to any subsequent general anaesthetic. (The team will inform the patient when these activities are safe). They will notice a gas-fluid interface in their lie of vision (an undulating line) that moves downwards over weeks/months.
• Unfortunately, a successful reattachment doesn't always result in a good visual outcome.³

• Untreated retinal detachment Some retinal breaks and RDs are long-standing problems that are incidentally picked up. These are more likely to be stable but should be monitored and depending on the site and size, repair is carried out on an elective basis. All new problems should be treated as they may lead to extensive detachment and ultimately, sight loss.
• Laser treatment Complications are uncommon. If these do occur, they may include maculopathy (such as oedema), choroidal detachment, a secondary tear or haemorrhage.
• Cryotherapy There is often an associated transient lid chemosis. Other complications include transient diplopia, vitritis (inflammation of the vitreous) and rarely, maculopathy.
• Complications of surgical treatment¹ These are relatively uncommon and patients will be advised individually depending on the nature of their RD. Generic complications include haemorrhage, iatrogenic retinal break during the procedure, retinal incarceration (where the retina folds and gets pulled up into the break) and a paradoxical gaping of certain types of retinal break. Poor visual recovery and the need for a further procedure (due to re-detachment of the retina) are also possible. Rarely, a silicone explant may dislodge or even ulcerate out through the conjunctiva or the skin.

• Patients who have simply needed laser treatment or cryotherapy for a tear without detachment should expect a full recovery.
• For those requiring surgery, the outcome depends upon the time the retina is detached, the underlying mechanism of the RD and whether the macula is involved: prognosis is related inversely to the degree of macular involvement and the length of time the retina has been off. Recovery depends on the site and extent of the RD.
• A patient presenting late with a 'macula-off' RD has a very bleak outlook. Early and prompt presentation/treatment should ensure good recovery with restoration of most of the vision. It may take several weeks for the vision to improve after surgery (particularly if there is a gas/silicone bubble in situ) and patients may go on to need additional spectacles or other visual aids.
• There is about 10% chance of a RD developing in the fellow eye.
• Only a very small number of patients have a recurrence of the original detachment.¹⁰

A rhegmatogenous RD can be prevented if the retinal break is diagnosed and treated prior to the accumulation of subretinal fluid.