Retinal detachment

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Retinal detachment
Slit lamp photograph showing retinal detachment in Von Hippel-Lindau disease EDA08.JPG
Slit lamp photograph showing retinal detachment.
Classification and external resources
Specialty Ophthalmology
ICD-10 H33
ICD-9-CM 361
DiseasesDB 11417
MedlinePlus 001027
eMedicine oph/504
Patient UK Retinal detachment
MeSH D012163
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Retinal detachment (also known as amotio retinae) is a disorder of the eye in which the retina peels away from its underlying layer of support tissue. Initial detachment may be localized or broad, but without rapid treatment the entire retina may detach, leading to vision loss and blindness. It is almost always classified as a medical emergency.[1] Permanent damage may occur if the detachment is not repaired within 24–72 hours.[2]

The retina is a thin layer of light sensitive tissue on the back wall of the eye. The optical system of the eye focuses light on the retina much like light is focused on the film or sensor in a camera. The retina translates that focused image into neural impulses and sends them to the brain via the optic nerve. Occasionally, posterior vitreous detachment, injury or trauma to the eye or head may cause a small tear in the retina. The tear allows vitreous fluid to seep through it under the retina, and peel it away like a bubble in wallpaper.

Signs and symptoms

A retinal detachment is commonly preceded by a posterior vitreous detachment which gives rise to these symptoms:

  • flashes of light (photopsia) – very brief in the extreme peripheral (outside of center) part of vision
  • a sudden dramatic increase in the number of floaters
  • a ring of floaters or hairs just to the temporal (skull) side of the central vision
  • a slight feeling of heaviness in the eye

Although most posterior vitreous detachments do not progress to retinal detachments, those that do produce the following symptoms:

  • a dense shadow that starts in the peripheral vision and slowly progresses towards the central vision
  • the impression that a veil or curtain was drawn over the field of vision
  • straight lines (scale, edge of the wall, road, etc.) that suddenly appear curved (positive Amsler grid test)
  • central visual loss

In the event of an appearance of sudden flashes of light or floaters, an eye doctor needs to be consulted immediately.[2] A shower of floaters or any loss of vision, too, is a medical emergency.

Risk factors

Risk factors for retinal detachment include severe myopia, retinal tears, trauma, family history, as well as complications from cataract surgery.[3][4]

Retinal detachment can be mitigated in some cases when the warning signs[5] are caught early. The most effective means of prevention and risk reduction is through education of the initial signs, and encouragement for people to seek ophthalmic medical attention if they have symptoms suggestive of a posterior vitreous detachment.[6] Early examination allows detection of retinal tears which can be treated with laser or cryotherapy. This reduces the risk of retinal detachment in those who have tears from around 1:3 to 1:20. For this reason, the governing bodies in some sports require regular eye examination.

Trauma-related cases of retinal detachment can occur in high-impact sports or in high speed sports. Although some recommend avoiding activities that increase pressure in the eye, including diving and skydiving, there is little evidence to support this recommendation, especially in the general population. Nevertheless, ophthalmologists generally advise people with high degrees of myopia to try to avoid exposure to activities that have the potential for trauma, increase pressure on or within the eye itself, or include rapid acceleration and deceleration, such as bungee jumping or roller coaster rides.

Intraocular pressure spikes occur during any activity accompanied by the Valsalva maneuver, including weightlifting.[7] An epidemiological study suggests that heavy manual lifting at work may be associated with increased risk of rhegmatogenous retinal detachment, but this relationship is not strong.[8][9] In this study, obesity also appeared to increase the risk of retinal detachment.

Genetic factors promoting local inflammation and photoreceptor degeneration may also be involved in the development of the disease.[10]

Diagnosis

A physician using a "three-mirror glass" to diagnose retinal detachment

Retinal detachment can be examined by fundus photography or ophthalmoscopy. Fundus photography generally needs a considerably larger instrument than the ophthalmoscope, but has the advantage of availing the image to be examined by a specialist at another location and/or time, as well as providing photo documentation for future reference. Modern fundus photographs generally recreate considerably larger areas of the fundus than what can be seen at any one time with handheld ophthalmoscopes.

Ultrasound has diagnostic accuracy similar to that of examination by an ophthalmologist.[21] The recent meta-analysis shows the diagnostic accuracy of emergency department (ED) ocular ultrasonography is high. The sensitivity and specificity ranged from 97% to 100% and 83% to 100%. The typical feature of ultrasound is "flying angel sign". It shows the detached retina moving with a fixed point under the B mode, liner probe 10mhz.[22]

retinal detachment, flying angel sign

Types

  • Rhegmatogenous retinal detachment – A rhegmatogenous retinal detachment occurs due to a break in the retina (called a retinal tear) that allows fluid to pass from the vitreous space into the subretinal space between the sensory retina and the retinal pigment epithelium. Retinal breaks are divided into three types – holes, tears and dialyses. Holes form due to retinal atrophy especially within an area of lattice degeneration. Tears are due to vitreoretinal traction. Dialyses are very peripheral and circumferential, and may be either tractional or atrophic. The atrophic form most often occurs as idiopathic dialysis of the young.
  • Exudative, serous, or secondary retinal detachment – An exudative retinal detachment occurs due to inflammation, injury or vascular abnormalities that results in fluid accumulating underneath the retina without the presence of a hole, tear, or break. In evaluation of retinal detachment it is critical to exclude exudative detachment as surgery will make the situation worse, not better. Although rare, exudative detachment can be caused by the growth of a tumor on the layers of tissue beneath the retina, namely the choroid. This cancer is called a choroidal melanoma.
  • Tractional retinal detachment – A tractional retinal detachment occurs when fibrous or fibrovascular tissue, caused by an injury, inflammation or neovascularization, pulls the sensory retina from the retinal pigment epithelium.

A minority of retinal detachments result from trauma, including blunt blows to the orbit, penetrating trauma, and concussions to the head. A retrospective Indian study of more than 500 cases of rhegmatogenous detachments found that 11% were due to trauma, and that gradual onset was the norm, with over 50% presenting more than one month after the inciting injury.[23]

Treatment

There are several methods of treating a detached retina, each of which depends on finding and closing the breaks that have formed in the retina. All three of the procedures follow the same three general principles:

  1. Find all retinal breaks
  2. Seal all retinal breaks
  3. Relieve present (and future) vitreoretinal traction

Cryopexy and laser photocoagulation

Cryotherapy (freezing) or laser photocoagulation are occasionally used alone to wall off a small area of retinal detachment so that the detachment does not spread.

Scleral buckle surgery

Scleral buckle surgery is an established treatment in which the eye surgeon sews one or more silicone bands (or tyres) to the sclera (the white outer coat of the eyeball). The bands push the wall of the eye inward against the retinal hole, closing the break or reducing fluid flow through it and reducing the effect of vitreous traction thereby allowing the retina to re-attach. Cryotherapy (freezing) is applied around retinal breaks prior to placing the buckle. Often subretinal fluid is drained as part of the buckling procedure. The buckle remains in situ. The most common side effect of a scleral operation is myopic shift. That is, the operated eye will be more short sighted after the operation. Radial scleral buckle is indicated for U-shaped tears or Fishmouth tears, and posterior breaks. Circumferential scleral buckle is indicated for multiple breaks, anterior breaks and wide breaks. Encircling buckles are indicated for breaks covering more than 2 quadrants of retinal area, lattice degeneration located on more than 2 quadrant of retinal area, undetectable breaks, and proliferative vitreous retinopathy.

Pneumatic retinopexy

This operation is generally performed in the doctor's office under local anesthesia. It is another method of repairing a retinal detachment in which a gas bubble (SF6 or C3F8 gas) is injected into the eye after which laser or freezing treatment is applied to the retinal hole. The patient's head is then positioned so that the bubble rests against the retinal hole. Patients may have to keep their heads tilted for several days to keep the gas bubble in contact with the retinal hole. The surface tension of the gas/water interface seals the hole in the retina, and allows the retinal pigment epithelium to pump the subretinal space dry and "suck the retina back into place". This strict positioning requirement makes the treatment of the retinal holes and detachments that occurs in the lower part of the eyeball impractical. This procedure is usually combined with cryopexy or laser photocoagulation. Pneumatic retinopexy has significantly lower success rates compared to scleral buckle surgery and vitrectomy. Some initially successful cases will fail during the weeks and months after surgery. In some of the failed cases, an area of the retina which was healthy and attached prior to the initial pneumatic retinopexy repair procedure develops new tears and/or becomes detached.

Vitrectomy

Vitrectomy is an increasingly used treatment for retinal detachment. It involves the removal of the vitreous gel and is usually combined with filling the eye with either a gas bubble (SF6 or C3F8 gas) or silicone oil (PDMS). An advantage of using gas in this operation is that there is no myopic shift after the operation and gas is absorbed within a few weeks. PDMS, if used, needs to be removed after a period of 2–8 months depending on surgeon's preference. Silicone oil is more commonly used in cases associated with proliferative vitreo-retinopathy (PVR). A disadvantage is that a vitrectomy always leads to more rapid progression of a cataract in the operated eye. In many places vitrectomy is the most commonly performed operation for the treatment of retinal detachment.

Prognosis

85 percent of cases will be successfully treated with one operation with the remaining 15 percent requiring 2 or more operations. After treatment patients gradually regain their vision over a period of a few weeks, although the visual acuity may not be as good as it was prior to the detachment, particularly if the macula was involved in the area of the detachment.

Up until the early 20th century, the prognosis for rhegmatogenous retinal detachment was very poor, and no effective treatments were available. Currently, about 95 percent of cases of retinal detachment can be repaired successfully.[24] Treatment failures usually involve either the failure to recognize all sites of detachment, the formation of new retinal breaks, or proliferative vitreoretinopathy.[24]

Involvement of the macula portends a worse prognosis. In cases where the macula is not involved (detached), 90 percent of patients have 20/40 vision or better after reattachment surgery.[24] Some damage to vision may occur during reattachment surgery, and 10 percent of patients with normal vision experience some vision loss after a successful reattachment surgery.

Epidemiology

The incidence of retinal detachment in otherwise normal eyes is around 5 new cases in 100,000 persons per year.[25] Detachment is more frequent in middle-aged or elderly populations, with rates of around 20 in 100,000 per year.[26] The lifetime risk in normal individuals is about 1 in 300.[3] Asymptomatic retinal breaks are present in about 6% of eyes in both clinical and autopsy studies.[27]

  • Retinal detachment is more common in people with severe myopia (above 5–6 diopters), in whom the retina is more thinly stretched. In such patients, lifetime risk rises to 1 in 20.[28][not in citation given] About two-thirds of cases of retinal detachment occur in myopics. Myopic retinal detachment patients tend to be younger than non-myopic ones.
  • Retinal detachment is more frequent after surgery for cataracts. The estimated long-term prevalence of retinal detachment after cataract surgery is in the range of 5 to 16 per 1000 cataract operations,[29] but is much higher in patients who are highly myopic, with a prevalence of up to 7% being reported in one study.[30] One study found that the probability of experiencing retinal detachment within 10 years of cataract surgery may be about 5 times higher than in the absence of treatment.[31]
  • Tractional retinal detachments can also occur in patients with proliferative diabetic retinopathy[32] or those with proliferative retinopathy of sickle cell disease.[33] In proliferative retinopathy, abnormal blood vessels (neovascularization) grow within the retina and extend into the vitreous. In advanced disease, the vessels can pull the retina away from the back wall of the eye, leading to tractional retinal detachment.

Although retinal detachment usually occurs in just one eye, there is a 15% chance of it developing in the other eye, and this risk increases to 25–30% in patients who have had a retinal detachment and cataracts extracted from both eyes.[28]

See also

References

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  5. Detachment – NHS Choices
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  11. 11.0 11.1 11.2 11.3 Yanoff & Duker 2008, pp. 724
  12. Yanoff & Duker 2008, pp. 492
  13. Goldman 2011, pp. e236-13
  14. 14.0 14.1 Goldman 2011, pp. 2467
  15. Goldman 2011, pp. 1362
  16. Goldman 2011, pp. 2442
  17. Goldman 2011, pp. 2441
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  20. Goldman 2011, pp. 2390–2391
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  24. 24.0 24.1 24.2 Yanoff & Duker 2008, pp. 725
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Notes
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External links