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. Caused by chronic traction from scars on the retinal surface and across the vitreous cavity. Most retinal breaks form when the vitreous separates from the retina as part of the normal ageing process. Photopsia and floaters can occur in conditions other than posterior vitreous detachment box 2.
Photopsia associated with posterior vitreous detachment results from traction on the retina as the vitreous pulls away. It is usually described as recurrent, brief flashes in the temporal peripheral field, but can occur anywhere. Floaters are caused by vitreous opacities casting shadows on the retina.
Posterior vitreous detachment makes them more mobile and thus more noticeable. Symptomatic posterior vitreous detachment carries a considerable risk of breaks that are likely to progress to retinal detachment.
When the retina is separated from the retinal pigment epithelium, the visual field defect is opposite the site of the detachment because of the optical inversion of images. It is commonly described as a dark curtain or shadow, appearing first in the periphery and moving to the centre over hours, days, or even weeks as the detachment extends. Visual acuity decreases when the macula becomes detached, and the patient may notice distortion of images. Without prompt treatment, total retinal detachment and blindness are almost inevitable.
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. Myopic patients with increased axial length are more likely to develop posterior vitreous detachment at a younger age.
Many retrospective studies have shown that trauma is an important cause of retinal detachment in young patients. Ocular trauma induces premature posterior vitreous detachment, possibly through liquefaction of the vitreous from leakage of blood and protein. If the presenting symptoms and risk factor profile suggest retinal breaks or detachment, further ophthalmic assessment is indicated. 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 red reflex should be examined with a direct ophthalmoscope at 1 metre for loss caused by retinal detachment or vitreous haemorrhage. 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.
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. Because ultrasound does not image the retinal periphery well, retinal breaks there cannot be diagnosed with certainty by this method.
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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.
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. 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.
Pneumatic retinopexy can be performed in some cases, but enthusiasm for this technique outside North America has been minimal. 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.
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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 comment faire un regime blog 123siteweb 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. 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.
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Management of retinal detachment: a guide for non-ophthalmologists
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