Retinal detachment, endophthalmitis and orbital cellulitis Flashcards
What is retinal detachment?
Retinal detachment (RD) involves the neurosensory layer of the retina separating off from the underlying retinal pigment epithelium (RPE).
Most retinal detachments are preceded by a posterior vitreous detachment (PVD), which causes traction on the retina and, potentially, a retinal tear.
The liquefied vitreous can then seep under the retina, causing it to detach. Retinal detachments may initially be localised, but without treatment they may progress and lead to irreversible vision loss. Early recognition and prompt referral are therefore essential
What is the classification of retinal detachment?
Rhegmatogenous RD:
-This follows a retinal break usually caused by PVD. Liquefied vitreous seeps through the break between the sensory retina and the pigment epithelium, lifting the retina off. This is the most common form of RD.
Non-Rhegmatogenous RD:
-Exudative (serous, or secondary RD): primary damage of the underlying RPE allows subretinal fluid to leak into the subretinal space, pushing the retina off.
-Tractional: fibres in the vitreous contract, pulling the sensory retina away. This is an uncommon form of RD.
What is the aetiology of rhegmatogenous RD?
In most cases, RD is preceded by a PVD - usually resulting from age-related degenerative liquefaction and shrinkage of the vitreous. PVD leads to retinal tear in 10-15% of cases.
Of these, asymptomatic new retinal breaks lead to detachment in about 5% of cases but symptomatic new retinal breaks progress to detachment in 50% of cases.
What is the aetiology of exudative RD?
Results from the accumulation of serous and/or haemorrhagic fluid in the subretinal space because of hydrostatic factors (e.g., severe acute hypertension), inflammation (e.g., sarcoid uveitis), or neoplastic effusions.
Exudative RD generally resolves with successful treatment of the underlying disease. Visual recovery is often excellent.
What is the aetiology of tractional RD?
Occurs via mechanical forces on the retina, usually mediated by fibrotic tissue resulting from previous haemorrhage, injury, surgery, infection, or inflammation.
Correction of tractional RD requires disengaging scar tissue from the retinal surface.
What are the risk factors for RD?
Risk factors vary with the type and site of detachment but include:
Myopia: this increases the risk of PVD, as the eyeball is longer and the peripheral retina thinner and more likely to tear. A correction of more than −3 dioptres carries a tenfold risk.
Family history of retinal break or detachment: there may be a tendency towards inherited myopia or degenerative retinal lesions.
Previous history of retinal break or detachment in either eye: about 12% of people with RD develop subsequent detachment in the fellow eye.
What are the risk factors for rhegmatogenous RD?
Age.
Lattice degeneration:
- This condition, present in around 10% of the population, involves the peripheral retina becoming thinned or atrophic in a lattice pattern.
- It may then be prone to tears, breaks, or holes, which may further progress to RD. It is an important cause of RD in young myopic individuals. Lattice degeneration is typically bilateral.
Aphakia.
Age-related retinoschisis.
Previous retinal break.
Marfan’s syndrome.
Previous cataract surgery accelerates PVD. RD occurs in approximately 1% of people in the weeks to years after cataract surgery. Previous complicated cataract surgery substantially increases the risk of subsequent RD.
What are the risk factors for non-rhegmatogenous tractional RD?
Fibrous bands in the vitreous may occur in conditions such as:
- Proliferative diabetic retinopathy.
- Penetrating eye injury.
- Retinal vein occlusion.
- Retinopathy of prematurity.
- Previous giant retinal tear.
- Sickle cell retinopathy.
- Toxocariasis.
- Blunt eye trauma; there may be a latent period of several months to years before RD occurs.
What are the risk factors for exudative RD?
Inflammatory conditions - e.g., uveitis, posterior scleritis.
Vascular disease - e.g., severe hypertension, Coats’ disease.
Toxaemia of pregnancy.
Congenital abnormalities - e.g., coloboma.
Maculopathy - e.g., wet age-related macular degeneration (RD associated with intravitreal anti-vascular endothelial growth factor (anti-VEGF) is very uncommon).
Malignancy (for example, choroidal melanoma or ocular metastasis) - predisposes to exudative RD.
What is the presentation of RD?
New onset of floaters
New onset of flashes.
Sudden-onset painless progressive visual field loss.
Altered red reflex, with a grey or folded appearance.
Poor visual acuity
Poor visual fields
How does the floaters seen in RD differ from floaters from other causes?
New onset of floaters (perception of mobile dots, lines, or haze due to blood and pigment cells entering the vitreous cavity casting shadows on the retina):
-Floaters caused by acute PVD, especially in the presence of a retinal tear, occur more abruptly and dramatically than the floaters that people experience for much of their lifetime. Similar floaters occur with other causes of intraocular bleeding, such as proliferative diabetic retinopathy, trauma and ocular inflammation (uveitis).
What is the presentation of flashes in RD?
New onset of flashes (seen as recurrent, brief flashes, often more noticeable in low light conditions, caused by traction on the retina as the vitreous pulls away):
Light flashes may precede migraine headaches but these typically occur bilaterally (although often in one area of the visual field). Photopsia induced by eye movements may indicate optic neuritis. Light flashes also may occur with postural hypotension and vasovagal reactions; these are bilateral and often accompanied by temporary dimming of vision and light-headedness.
What is the presentation of visual field loss?
Sudden-onset painless, usually progressive, visual field loss. This may be described as a dark curtain or shadow, which usually starts in the periphery and progresses towards the centre over hours, days, or weeks. If the macula detaches, central visual acuity is severely reduced:
- Visual field loss begins suddenly, usually in the periphery; it progresses towards the central visual axis over hours to weeks.
- Field loss caused by stroke or other central nervous system processes is always bilateral, stable, and homonymous, due to crossing of nasal retinal projections at the optic chiasm.
- Even in patients with severe field loss caused by cerebral disease, the macula is spared and central vision persists.
- Visual loss from a transient ischaemic attack may be unilateral; however, it is not persistent or progressive and may be accompanied by other neurological symptoms.
- Fixed field defects of variable size occur in patients with retinal vascular occlusion; these patients lack acute flashes and floaters.
What are the differentials of RD?
PVD Migraine Optic neuritis Choroidal tumours Cerebrovascular event Uveitis Age-related macular degeneration Vitreous haemorrhage Retinoschisis
What are the investigations for RD?
Examination in the eye department will involve a slit-lamp examination, indirect ophthalmoscopy or 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).
Ultrasound or optical coherence tomography may be used to assess the type and extent of the detachment, any associated tears and any ocular comorbidity.
CT and MRI scans have a role if there is a tumour or suspected foreign body.
Patients with an exudative RD benefit from a full systemic examination, owing to its association with systemic disease.
When should patients with suspected RD be referred to a specialist?
Patients with a suspected RD should be seen by a specialist on the same day.
The urgency of specialist assessment depends on your assessment and clinical suspicion, whether there are changes in visual acuity, visual field loss, or signs seen on fundoscopy.
If there is a visual field defect but visual acuity is good, referral is urgent, as it is likely to be a ‘macula-on’ RD (the macula is still adherent to the underlying RPE) as opposed to a ‘macula-off’ detachment (where surgery is a rescue procedure rather than a protective one).
What is the management of RD?
Cryotherapy/laser photocoagulation:
- Retinal tears and holes are treated with cryotherapy or laser photocoagulation.
- This achieves permanent adhesion between the retina and RPE. In around 95% of cases this prevents further accumulation of fluid through retinal breaks and stops progression to RD.
Surgery
- The rate of evolution of RD is a key factor when scheduling emergency surgery, and where there is imminent danger that the fovea is about to detach, surgery must be carried out urgently. Where there is a low risk of progression to involve the fovea, it may be better to use posturing and bed rest, organising surgery for when the appropriate skill mix of the theatre team can be assembled
- Strict bedrest is to prevent progression of the detachment.
Three surgical techniques are used:
- Vitrectomy: This is performed to relieve traction. Air, gas or silicon oil injected into the vitreous to help flatten the retina, commonly used in Rhegmatogenous RD.
- Scleral buckling: A piece of silicone material on the scleral surface pushes the wall of the eye closer to the detached retina. This allows fluid formed under the retina to be pumped out and helps the retina to re-attach.
- Pneumatic retinopexy: A small expansile gas bubble is injected into the vitreous cavity. It expands over 1-3 days, and can be positioned to close the retinal break, again allowing the fluid to be pumped out and encouraging reattachment.
What is the postoperative care after surgery for RD?
Topical antibiotics and corticosteroids are prescribed postoperatively.
Occasionally, patients also need cycloplegic drugs and ocular hypotensive drugs.
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).
