Jennifer K. Sun,
Lucy H.Y. Young
Retinal detachment occurs when fluid accumulates between the sensory retina and the retinal pigment epithelium. It is different from conditions such as retinoschisis and choroidal detachment, in which the retina is elevated, but the photoreceptor outer segments are not separated from the underlying pigment epithelium.
Retinal detachments are often classified into three major groups, depending on their underlying pathologic mechanism. The most common type is the rhegmatogenous detachment, in which fluid from the vitreous cavity enters the potential subretinal space through a break in the retina and dissects the retina from the retinal pigment epithelium (Fig. 182.1). The second most common type is the tractional retinal detachment which includes detachments caused by vitreoretinal fibroproliferative membranes that mechanically pull the retina away from the underlying retinal pigment epithelium (Fig. 182.2). The detached retina is typically smooth and concave toward the anterior segment, unlike the rhegmatogenous detachments in which the retina is characteristically corrugated or bullous and is convex toward the pupil. In addition, tractional retinal detachment is usually more confied and rarely extends to the ora serrata. In some cases, retinal tears result from increasing vitreoretinal traction, thus resulting in a combined tractional-rhegmatogenous detachment. The third type is the secondary, or exudative, retinal detachment (Fig. 182.3). This group includes retinal detachments caused by retinal or choroidal conditions that disturb the retinal pigment epithelium or blood-retinal barrier, allowing fluid to build up in the subretinal space. A characteristic fiding associated with this type of detachment is the presence of 'shifting fluid', which leads to variations in the location of the detachment as the patient is examined in different positions.
It is crucial to distinguish among different types of retinal detachment, as the management of each type is quite different. An exudative detachment, for example, will usually resolve without surgery if the underlying condition is treated. In tractional retinal detachment, the treatment of choice is to release the vitreoretinal traction, usually through pars plana vitrectomy and membrane dissection, whereas in rhegmatogenous retinal detachment, retinal breaks must be identified and treated in order to successfully reattach the retina.
The remainder of this chapter describes some of the conditions that predispose to retinal detachment.
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FIGURE 182.1 Superotemporal rhegmatogenous retinal detachment with macular involvement caused by a peripheral flap tear. |
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FIGURE 182.2 Severe proliferative diabetic retinopathy with tractional retinal detachment nasal to the disk. |
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FIGURE 182.3 Exudative retinal detachment in a patient with inflammatory uveal effusion. |
RHEGMATOGENOUS RETINAL DETACHMENT
POSTERIOR VITREOUS DETACHMENT
Posterior vitreous detachment (PVD) is commonly found in elderly patients. In an autopsy study, PVD was present in 63% of patients older than 70 years.[1] The incidence of PVD is also much higher in aphakic eyes.[2] The normal aging process that the vitreous gel undergoes is often accelerated by myopia, trauma, cataract surgery, yttrium-aluminum garnet (YAG) capsulotomy, intraocular inflammation, diabetes, vitreous hemorrhage, and certain hereditary conditions.[3, 4] As PVD occurs and the vitreous cortex separates from the retinal internal limiting membrane, vitreous traction on the retina can cause a retinal break and subsequent rhegmatogenous detachment. Approximately 10-15% of all patients with acute, symptomatic PVD have at least one retinal break.[5-9] The incidence of breaks is higher in myopic eyes. In patients with acute PVD and vitreous hemorrhage, the incidence of retinal tears increases to 70%.[4-10]
PERIPHERAL FUNDUS LESIONS
Peripheral lesions that may predispose to retinal detachment include lattice degeneration, atrophic holes, cystic retinal tufts, and zonular traction tufts.
Lattice degeneration is characterized by areas of retinal thinning. The borders of the thinned retina are strongly adherent to the overlying vitreous. Although lattice degeneration occurs in up to 10% of nonselected patients,[11] and is the leading fundus lesion that predisposes to retinal breaks, only 22-30% of retinal detachments are associated with lattice degeneration.[12, 13] The risk of lattice degeneration developing into retinal detachment is estimated to be ?0.3-0.5%.[12, 14] Approximately 55-70% of detachments associated with lattice degeneration are caused by tears that develop posterior to or at the edge of a lattice bed.[12, 13] The remaining 30-45% of detachments are associated with small, round atrophic holes that are seen within lattice lesions in ?25% of eyes with lattice degeneration.[12, 13, 15-18] Up to 70% of patients with retinal detachment caused by atrophic holes in the lattice lesions are myopic and younger than 40 years of age.[13, 17] This fiding is in contrast to patients with retinal detachments caused by tears at the edge of lattice lesions. Ninety percent of these individuals are 50 years of age or older and only 43% of the detachments are associated with myopia.[13]
Cystic retinal tufts are generally round or oval white, elevated vitreoretinal lesions that are present in 5% of individuals. Their exaggerated adherence to the vitreous gel can lead to retinal tears with or without a PVD.[19] Retinal breaks associated with peripheral cystic retinal tufts may account for up to 10% of rhegmatogenous detachments.[20]
Zonular traction tufts are congenital malformations of zonules that are displaced posteriorly, sometimes leading zonular traction on the anterior retina. They are responsible for ?6% of retinal breaks, but these tears rarely lead to significant retinal detachments.[11]
MYOPIA
Patients with myopia are at a much higher risk of experiencing rhegmatogenous retinal detachment.[21-23] The lifetime incidence of retinal detachment among myopic patients is estimated to be 0.7-6%, compared with an incidence of 0.06% for emmetropic patients.[23] Myopia is present in at least 30% of patients with retinal detachment.[21, 23, 24] It predisposes to retinal detachment for a combination of reasons, including premature and higher rates of PVD, increased incidence of lattice degeneration, and possibly thinner peripheral retina.[25-28]
SENILE RETINOSCHISIS
Retinoschisis describes the splitting of the retina into inner and outer layers. The histopathologic types of degenerative, or senile retinoschisis are the reticular and typical forms. The reticular form is more frequently associated with outer layer holes, which are necessary for the development of rhegmatogenous retinal detachment. In an autopsy study, 23% of eyes with senile retinoschisis had outer layer holes.[29] Byer found outer layer holes in 16% of 218 eyes with retinoschisis in a long-term follow-up study.[30] The reported incidence of retinal detachment with outer layer holes and retinoschisis varies considerably. In Byer's study, 58% of eyes with outer layer breaks had a localized detachment.[30] Natural history studies have shown that this type of localized detachment rarely progresses to symptomatic rhegmatogenous retinal detachments, possibly because the viscous nature of the schisis cavity contents prevents the rapid passage of fluid into the subretinal space.[30, 31] When retinal detachments do occur in conjunction with retinoschisis cavities, they are often marked by the following clinical signs: a nonuniform appearance of the schisis cavity, the presence of a yellow line deep to the inner layer that demonstrates the position of the outer layer, and linear hyperpigmentation of the retinal pigment epithelium demarcating the extent of the retinal detachment.[32] Because posterior extension of schisis detachments is often very slowly progressive, and extension into the macula is rare, surgical intervention can often be deferred indefiitely.[32-34]
CATARACT EXTRACTION
Cataract extraction is a major cause of retinal detachment. Up to 40% of retinal detachments occur in aphakic and pseudophakic eyes.[35-37] The clinical features of pseudophakic or aphakic retinal detachments are different from detachments in phakic eyes. Retinal detachments after cataract extraction typically have small flap tears along the posterior margin of the vitreous base. They are usually more extensive and often involve the macula. Multiple breaks are found in more than 50% of retinal detachments after cataract extraction.[24] The incidence of retinal detachment varies after differing types of cataract procedures. It is ?1.1-6.7% after intracapsular cataract extraction, 0-3.6% after extracapsular cataract extraction, and 0.4-1.2% after phacoemulsification.[38-49]
A number of risk factors have been identified for aphakic and pseudophakic retinal detachments. Retinal detachment is more common in patients with younger age, high myopia, and a history of detachment in the fellow eye. Most reports suggest that the incidence of detachment in myopic eyes is ?6%, and the rate goes up with higher degrees of myopia.[40, 41, 43, 44, 46,50-52] One study showed that the incidence of detachment was as high as 40% for eyes with myopia greater than 10 D.[50] After intraoperative vitreous loss or posterior capsulotomy, detachment rates may approach 20%,[39, 45, 47, 53] and postoperative capsulotomy (surgical or Nd:YAG) is associated with an approximately threefold increased incidence of retinal detachment.[46, 47, 54-57] Several reports indicate that at least 50% of detachments occur within the first year after cataract surgery, and thereafter the incidence remains higher than in phakic eyes.[24, 38, 44,58-62]
Retinal detachment is also a well-known complication of congenital cataract extraction. However, the interval between surgery and the development of retinal detachment is much longer in children (20-30 years) than in adults.[63-68] The incidence of retinal detachment after surgery for congenital cataract is not well established. One review in the literature reported incidences ranging from 2% to 8%, and another reported incidences of 5-25%.[69, 70] A more recent study looked at patients who had cataract extraction using newer surgical techniques and found that 3.2% of the patients experienced later retinal detachment. However, the incidence is probably higher because the mean follow-up period in this study was only 6.8 years.[71] An important fact to remember when dealing with retinal detachments after congenital cataract extraction is that 70% of these patients will experience detachment in the fellow eye, and therefore require careful follow-up.[67]
OTHER OCULAR SURGERY
The development of retinal detachments is also associated with other surgical procedures such as penetrating keratoplasty and pars plana vitrectomy. After keratoplasty, detachments have been reported to occur in between 2% and 4% of cases, with higher risk in eyes requiring anterior vitrectomy.[72-74] After pars plana vitrectomy, later detachments occur between 3% and 6% of the time. They are usually due to breaks located pos-terior to pars plana sclerotomies, probably caused by traction on the vitreous base or by the repeated introduction of instruments.[75-80] An even higher rate of detachment (12.8%) is associated with vitrectomy performed for removal of retained lens fragments.[81]
Several studies have examined detachment rates after laser in situ keratomileusis (LASIK). Results suggest that post-LASIK patients do not have a higher risk of detachment than myopes who have not had the procedure,[82] but further, large-scale prospective studies are needed to confirm this fiding.
INADVERTENT SCLERAL PERFORATION
Inadvertent perforation of the sclera may occur during retinal reattachment surgery, retro- or peribulbar injection of an anesthetic agent prior to ocular surgery,[83] strabismus surgery,[84] and placement of a bridal suture through the superior rectus muscle.[85] Scleral perforation is frequently accompanied by a retinal break, and subsequent vitreoretinal changes can lead to rhegmatogenous retinal detachment. Fortunately, these are rare complications.
TRAUMA
Retinal detachment is a frequent complication of ocular trauma. Studies have shown that up to a third of retinal detachments may be attributed to trauma.[86, 87] In children and young adults, ocular contusion is the leading cause of retinal detachment.[88, 89] Traumatic detachments typically occur in males, and boxers are at much higher risk.[88, 90, 91] The majority of traumatic detachments are caused by blunt trauma.[87, 92, 93]
Retinal dialyses constitute 75% of retinal breaks found after blunt trauma, and in eyes with traumatic detachments retinal dialyses are present in up to 85% of cases.[88, 90, 92, 94-96] Approximately 25% of giant retinal tears occur in association with trauma.[97] Detachments after penetrating injuries are usually characterized by the presence of transvitreal fibroproliferative membranes.
INTRAOCULAR INFLAMMATION AND INFECTION
Intraocular inflammatory and infectious conditions are often complicated by retinal detachments caused by vitreoretinal traction from PVD. In the cohort of patients from the Endophthalmitis Vitrectomy Study, the incidence of retinal detachment was 8.3%. Anatomic success after surgical repair as well as fial visual acuity outcomes were lower in these patients than in patients with uncomplicated primary rhegmatogenous detachment.[98]
A retrospective study of 1387 patients with uveitis likewise found a higher prevalence of retinal detachment than in the general population. Risk factors for detachment included the presence of panuveitis or infectious uveitis, such as acute retinal necrosis syndrome (ARN).[99] In patients with ARN, rhegmatogenous retinal detachment occurs in 50-75% of afflicted eyes.[100, 101] Retinal breaks are usually found within or adjacent to areas of necrosis. Proliferative vitreoretinopathy (PVR) is a common fiding in ARN.[102] Exudative detachments may also occur during the acute phase of this condition. Rhegmatogenous retinal detachment is also a common complication in patients with cytomegalovirus retinitis. However, it is less frequent when compared with ARN.[103-105] The incidence of retinal detachment is reported in the range of 15-35%, although these numbers appear to be decreasing in the era of highly active antiretroviral therapy.[106] Both decreased CD4+ T cell count and increasing retinal surface involvement have been correlated with higher risk for detachment.[103-109]
Ocular toxocariasis, toxoplasmosis, and pars planitis are also known to be associated with an increased incidence of retinal detachment from vitreoretinal changes initiated during the acute phase of inflammation.[110-112] Both traction and rhegmatogenous retinal detachments have been reported. Hagler and coworkers analyzed 100 cases of ocular toxocariasis and found retinal detachments in 11%.[112]Friedmann and Knox found rhegmatogenous retinal detachments in 5% of 63 patients with ocular toxoplasmosis.[110] Smith and colleagues reported rhegmatogenous retinal detachments in 5.5% of 182 eyes with pars planitis.[111]
WAGNER-JANSEN-STICKLER SYNDROME
A wide range of familial vitreoretinal disorders is associated with retinal detachment. The Wagner-Jansen-Stickler syndrome (also known as Wagner's or Stickler's syndrome) is associated with eyes having an optically empty vitreous cavity and lattice retinal degeneration. The frequency of retinal detachment varies among pedigrees. Hirose and associates reported retinal detachment in 47% of 79 eyes diagnosed as having Wagner's syndrome; 42% of these patients had bilateral detachments.[113]
GOLDMANN-FAVRE SYNDROME
Goldmann-Favre vitreoretinal degeneration is an autosomal recessive condition characterized by a combination of night blindness, cataract, optically empty vitreous cavity, peripheral pigmentary retinal changes, peripheral and macular retinoschisis, lattice degeneration, and characteristic changes on electroretinography. Recent studies have found a genetic link between Goldmann-Favre syndrome, enhanced s-cone syndrome, and clumped pigmentary retinal degeneration in that all three entities may share mutations in the NR2E3 gene.[114] Rhegmatogeneous retinal detachment can be a complication of this rare entity.
X-LINKED JUVENILE RETINOSCHISIS
In X-linked juvenile retinoschisis, the retinal splitting occurs within the nerve fiber layer. In the periphery, the inner layer may be elevated, simulating a retinal detachment. Holes in the inner layer are common but do not cause detachment. However, the outer layer holes can allow fluid to enter the subretinal space, resulting in retinal detachment. Retinal detachment secondary to a macular hole has also been reported in a patient with X-linked juvenile retinoschisis.[115] True retinal detachment associated with juvenile retinoschisis is rare.[116]
MARFAN'S SYNDROME
The ocular features of Marfan's syndrome are characterized by axial myopia, ectopia lentis, and retinal detachment. Retinal detachment in this disorder is related to a combination of factors, including axial length, lens subluxation, and aphakia.[117, 118] Maumenee analyzed a group of 160 patients with Marfan's syndrome and found that rhegmatogenous retinal detachment did not occur in eyes with normal axial length.[118] In one study, detachment occurred in 9% of phakic eyes and 19% of aphakic eyes.[117] Retinal detachment was found only in aphakic eyes or in eyes with subluxed lenses. The rate of vitreous loss is high during lens removal in these patients, thus putting them at higher risk for the development of retinal detachment.[119] Fortunately, success rates of surgical reattachment in Marfan's patients are high, and comparable to those in patients without Marfan's syndrome.[120, 121]
HOMOCYSTINURIA AND THE EHLERS-DANLOS SYNDROME
Homocystinuria is also characterized by ectopia lentis, and can result in secondary glaucoma, optic atrophy, and retinal detachment.[122] The incidence of retinal detachment is similar to that associated with Marfan's syndrome. In contrast, both myopia and retinal detachment are associated with the autosomal dominant syndrome of Ehlers-Danlos, but the prevalence of retinal detachment is low.[123]
COLOBOMAS OF THE CHOROID AND RETINA
Retinal detachments associated with colobomas of the choroid and retina can be caused by retinal breaks within or outside the coloboma. The incidence of undetected breaks is high, especially when breaks occur at the border of the coloboma where the outer retina becomes disorganized and fused with the retinal pigment epithelium.[124-127] Retinal detachment may also result as a complication of lens colobomas and is usually due to giant tears.[128]
OPTIC NERVE PIT
Serous detachment of the macula associated with optic nerve pit has been reported by many authors.[129] Recently, migration of gas and silicone oil from the vitreous cavity into the subretinal space has been described in association with surgical repair of detachments due to optic pit.[130] These data suggest that the etiology of retinal detachments in optic pit patients may lie in tissue defects that allow communication between the vitreous and subretinal space. Brown and co-workers reviewed 75 eyes with congenital pits of the optic nerve head and found that less than 20% of small pits (i.e., <0.25 disk diameter) were associated with retinal detachment. However, the incidence of detachment approached 90% in eyes with pits larger than 0.4 disk diameter.[131] Spontaneous reattachment occurs in more than 25% of patients with optic nerve pits, but it may take months to years, after which time cystic degeneration of the macula may have taken place.
MORNING GLORY SYNDROME
The most frequent complication associated with morning glory syndrome is retinal detachment. In three reports, a third of patients with this disk anomaly were found to have detachment of the posterior pole.[132-134] Many pathogenic mechanisms have been suggested to explain the origin of the subretinal fluid, but the pathophysiology of retinal detachment associated with this malformation has yet to be conclusively established.[133, 135, 136] Recent reports describe the development of rhegmatogenous detachments from tissue breaks within the abnormal disc.[137-139]
TRACTIONAL RETINAL DETACHMENT
PROLIFERATIVE DIABETIC RETINOPATHY
Diabetes mellitus is the most common systemic disease associated with retinal detachment. Proliferative diabetic retinopathy is characterized by neovascular proliferations arising from the retinal vessels, typically in the posterior pole. As the process of vitreous detachment proceeds, vitreous attachments to areas of neovascularization can result in vitreous hemorrhage and traction retinal detachment. If the fovea is elevated, a loss of central vision will result. Retinal breaks may develop with continued vitreoretinal traction, resulting in a combined tractional-rhegmatogenous detachment. A recent review of studies reporting vitrectomy results for diabetic traction detachment suggests that retinal reattachment rates have improved over the last 25 years, likely due to improved surgical techniques and equipment. However, visual outcomes after traction detachment repair have not changed markedly over the last quarter century.[140]
SICKLE-CELL RETINOPATHY
Of the sickling disorders (hemoglobins AS, SS, SC, S-thalassemia), proliferative retinopathy is most commonly found in patients with hemoglobin SC[141] or hemoglobin S-thalassemia disease. In contrast to diabetic retinopathy, retinal arteriolar occlusion in sickle-cell retinopathy is more prominent in the peripheral retina. Peripheral fibrovascular proliferation occurs on the posterior vitreous surface, which causes vitreoretinal traction, which in turn results in vitreous hemorrhage or tractional retinal detachment. With continued traction, breaks may develop adjacent to the neovascular fronds, causing a combined tractional-rhegmatogenous detachment. Retinal detachment rates among patients with SC disease are ?8%.[142] Retinal breaks may also develop at the edge of laser scars.[143] In one study, 8.7% of 46 eyes treated with argon laser for proliferative sickle-cell retinopathy experienced retinal breaks.[143]
RETINOPATHY OF PREMATURITY
Retinopathy of prematurity (ROP), or retrolental fibroplasia, is a PVR that commonly causes retinal detachment in newborns and young adults. Retinal detachment occurs as a result of tractional forces caused by the neovascular proliferation, and its presentation can range from a mild peripheral tractional retinal detachment to total tractional detachment. Coats et al. reported a 13.7% rate of retinal detachment in 262 eyes with ROP, and found that detachment risk was correlated with the presence of clinically important vitreous organization and hemorrhage.[144] In this study, clinically important vitreous organization was defied as white, fibrous opacification of the vitreous that spanned two or more contiguous clock hours and was dense enough to reduce visualization of the underlying retina. Clinically important vitreous hemorrhage was defied as hemorrhage that completely obscured the underlying retina from view.[144] In ROP patients, retinal detachments that develop shortly after birth are usually due to mechanical traction or exudation from the retinal vessels in the active stage of proliferation. Those that develop later in life are usually of the rhegmatogenous type and may or may not be associated with cicatricial ROP changes.[145, 146]
FAMILIAL EXUDATIVE VITREORETINOPATHY
Familial exudative vitreoretinopathy (FEVR) is an autosomal dominant or X-linked condition that is associated with a wide spectrum of retinal changes, including avascularity of the retinal periphery, neovascularization, exudation, vitreous bands, retinochoroidal atrophy, hemorrhage, neovascularization, and tractional dragging of retinal vessels. Retinal detachment is not an uncommon complication of this condition, and it can be rhegmatogenous in nature,[147] although it is usually tractional or exudative.[148] One series reporting ocular fidings in 52 eyes affected by FEVR reported a 73% prevalence of retinal detachments, the majority of which were tractional.[149]
PROLIFERATIVE VITREORETINOPATHY
Approximately 5-10% of primary rhegmatogenous retinal detachments,[150] and 75% of post-surgical detachments[151] are complicated by the development of contractile membranes within the vitreous and along the retinal surface, that are known as PVR. The risk of developing PVR is higher in patients with uveitis; giant, large or multiple retinal tears; aphakia; vitreous hemorrhage; pre or postoperative choroidal detachment; multiple previous surgeries; and retinal detachments involving two or more quadrants.[152, 153] Large amounts of cryopexy, air or gas tamponade, repeated surgical procedures, the presence of preoperative PVR, and high concentrations of vitreous protein have also been identified as risk factors for PVR.[154, 155] As they contract, PVR membranes exert traction on retinal tissue, causing detachments that are often challenging to repair surgically. Surgical success rates for PVR-related detachments range from 60% to 80%, with rates lower for more severe stages of PVR.[156] However, only 40-80% of cases with anatomic success achieve ambulatory (5/200 or better) vision.[157]
EXUDATIVE RETINAL DETACHMENT
CHOROIDAL TUMORS
Choroidal lesions such as uveal melanoma, metastatic carcinoma, and hemangioma are frequently associated with exudative retinal detachment. In these conditions, it is postulated that leakage of proteinaceous fluid occurs from the neoplasm, and this fluid accumulates under the retina. In ocular melanoma patients, large tumor size is the most important predictor of retinal detachment, although other risk factors include may include posterior location, rupture of Bruch's membrane, and the presence of microvascular loops and networks.[158] Treatment of the neoplasm by irradiation, photocoagulation, or cryotherapy may permit resorption of the subretinal fluid.[158-160] Photodynamic therapy has also been shown to be effective in treatment of exudative retinal detachments associated with choroidal hemangiomas.[161]
HARADA'S DISEASE
This entity is a autoimmune disorder that leads to bilateral panuveitis often accompanied by systemic manifestations that include neurologic, auditory, and integumentary fidings.[162] Patients with Harada's (also known as Vogt-Koyanagi-Harada) disease may experience rapid loss of vision in one or both eyes because of extensive bullous serous retinal detachment.[163-165] The serous detachment in this disease is caused by a diffuse choroiditis, and it typically shifts with positioning of the patient.
POSTERIOR SCLERITIS
Posterior scleritis is an inflammation of the posterior sclera with associated vascular leakage, and it is often difficult to diagnose. Approximately 50% of patients with posterior scleritis have a history of rheumatoid arthritis. Exudative retinal detachment is one of the most common fidings in patients with this disease. Other fundus changes include choroidal detachments, a subretinal mass, chorioretinal folds, disk edema, and cystoid macular edema.[166-168]
IDIOPATHIC CENTRAL SEROUS CHORIORETINOPATHY
Multiple foci of serous detachment of the retina may occur in eyes with central serous chorioretinopathy. An extensive bullous retinal detachment may develop when these foci coalesce.[169-172] Patients with this atypical presentation may be mistakenly thought to have other types of retinal detachment, but fluorescein angiography is usually helpful in making the correct diagnosis. Laser treatment may hasten the resolution of subretinal fluid in this disease, but even large bullous retinal detachments are generally self-limited, and resolve without treatment over the course of a few months.[172]
IDIOPATHIC UVEAL EFFUSION SYNDROME
This syndrome usually presents in healthy middle-aged men as an insidious, progressive, often bilateral serous detachment of the choroid, ciliary body, and retina. There is striking shifting of the subretinal fluid, which is attributed to its high protein content.[173-175] Many patients with uveal effusion syndrome have abnormally thick sclera which compresses the vortex veins and impedes intraocular fluid outflow. Intraocular fluid builds up and creates a ciliochoroidal detachment with secondary retinal detachment.[176, 177]
NANOPHTHALMOS
Exudative retinal detachments may also result from compression of the vortex veins by the thickened sclera in nanophthalmic eyes.[177, 178] The treatment of choice in this condition is decompression of the vortex veins[179] or subscleral sclerectomy.[177]
MALIGNANT HYPERTENSION
Patients with malignant hypertension may experience exudative detachment of the retina caused by ischemic infarction of the underlying retinal pigment epithelium from occlusion of the choroidal circulation.[180-182] Sites of choroidal damage may be marked by characteristic pigment changes called Elschnig's spots. Improvement in blood pressure control usually leads to rapid resolution of the serous retinal detachments.[183]
PREECLAMPSIA (TOXEMIA OF PREGNANCY)
Serous retinal detachment occurs in 0.2-2% of patients with severe preeclampsia, and in 0.9% of patients with HELLP syndrome (hemolysis, elevated liver enzymes, low platelets), usually shortly before or immediately after childbirth.[184, 185] Patients with severe toxemia may experience total serous retinal detachment.[186] Given the severe hypertension experienced by these patients along with fluorescein angiographic and indocyanine green observations, it is likely that detachments result from choroidal ischemia.[187] In most cases, the retinal detachments associated with preeclampsia are self-limited and resolve with return of normal visual function.[185]
DISSEMINATED INTRAVASCULAR COAGULOPATHY
Disseminated intravascular coagulation is a widespread process that results in the formation of thrombi in the small vessels throughout the body. It has been reported in gram negative bacterial sepsis, cancer, obstetrical complications, after transplantation and other surgeries, and after burn and crush injuries.[188] Bilateral serous detachment of the retina is secondary to fibrin-platelet clots in the choroidal vessels, and is one of the many ocular manifestations associated with this condition.[189, 190]
COLLAGEN VASCULAR DISEASE
Various collagen vascular diseases, including systemic lupus erythematosus, rheumatoid arthritis, and polyarteritis nodosa may be complicated by serous retinal detachment.[191-194] Detachments are caused by fibrinoid necrosis of the choroidal vessels and subsequent ischemic infarction of the overlying retinal pigment epithelium.
RETINAL TELANGIECTASIA
The abnormal vessels leak in retinal telangiectasia, resulting in the accumulation of exudate in and under the retina. A wide spectrum of telangiectasia exists, ranging from minimal retinal vascular malformation to massive areas of telangiectasia and extensive exudation. Generally, the phrase Leber's military aneurysm is used to describe the more mild forms of retinal telangiectasia whereas Coats' disease is used to refer to telangiectasia accompanied by exudative retinopathy.[195, 196] Vitreoretinal traction is rare in these entities. Total retinal detachment is common, occurring in ?47% of eyes.[196]
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