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Exudative retinal detachment is characterized by subretinal fluid accumulation between the neurosensory retina and the underlying retinal pigment epithelium. Unlike rhegmatogenous detachment, which involves retinal tears, exudative detachments typically lack retinal breaks and present with a convex configuration due to shifting subretinal fluid. This condition can occur across all age groups and has multiple potential underlying etiologies, ranging from inflammatory conditions to ocular tumors. This activity helps clinicians better understand the clinical presentation and differential diagnosis of exudative retinal detachment. This activity provides a comprehensive overview of the pathophysiology, clinical features, diagnostic modalities, and management strategies for exudative retinal detachment. By improving their knowledge in this area, participants are equipped to recognize and manage exudative retinal detachment promptly, thereby minimizing the risk of associated ocular morbidity and vision loss. Objectives: Apply evidence-based approaches for the prompt diagnosis and medical management of exudative retinal detachments. Assess the clinical features of various types of retinal detachments, with a specific focus on differentiating exudative detachment from other forms. Develop standardized protocols for the collaborative management of exudative retinal detachments within a multidisciplinary healthcare team, ensuring comprehensive patient care. Communicate with the interprofessional team to diagnose, educate, treat, and monitor patients with exudative retinal detachment, optimizing patient outcomes through collaborative care. Access free multiple choice questions on this topic.

In exudative retinal detachment, subretinal fluid accumulates without retinal breaks or tractional forces.[1][2] The underlying cause is a blood-retinal barrier disruption.[1] Processes that either actively or passively allow for excessive fluid accumulation in the subretinal space between the retinal pigment epithelium and neurosensory retina lead to retinal detachment.[3] During a retinal detachment, the retina separates from the underlying retinal pigment epithelium and choroid, resulting in retinal ischemia and photoreceptor degeneration. The subretinal space originates from the remnant of the embryonic optic vesicle.[3] Retinal detachment is classified into three groups based on the etiology of subretinal fluid accumulation: rhegmatogenous, tractional, or exudative.[1][4] Some cases may involve a combination of these categories. Rhegmatogenous retinal detachment occurs when retinal tears or holes allow fluid to seep into the subretinal space.[2] Tractional retinal detachment happens when traction on the retina occurs due to fibrovascular proliferation over the retina, often resulting from ischemic or hypoxic stimuli or other factors.[2] No anatomical adhesion exists between the retinal pigment epithelium and the neurosensory retina.[3] Neural cell adhesion molecules expressed on the apical surface of retinal pigment epithelial cells facilitate adhesion between the retinal pigment epithelium and photoreceptor cells.[3][5] Various etiologic factors, including inflammation, idiopathy, infection, surgery, neoplasia, vascular issues, or drug effects, can trigger ischemic-hypoxic stimuli, compromising the integrity of the blood-retinal barrier.[6][1] Timely diagnosis and treatment offer the possibility of reasonably good vision in patients with exudative retinal detachment.[1] Exudative retinal detachments are primarily managed medically. Surgical intervention with scleral buckling or vitrectomy is rarely considered, typically only if all medical interventions prove ineffective.[1]

Exudative retinal detachment occurs either due to hypersecretion of fluid into the subretinal space or defective fluid transport from the subretinal space. Various factors, such as inflammation, idiopathy, infection, surgery, neoplasia, vascular issues, or drug effects, can compromise the integrity of the blood-retinal barrier, ultimately resulting in exudative retinal detachment.[1][6] Inflammatory Causes Vogt-Koyanagi-Harada syndrome (VKH) [7] Sympathetic ophthalmia [8][9][10] Orbital inflammation Orbital pseudotumor Idiopathic orbital inflammatory disease [11] Posterior scleritis [12] Benign reactive lymphoid hyperplasia [13] Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) [14] Serpiginous choroiditis [15] Behçet disease [16] Intermediate uveitis [17] Relapsing polychondritis [18] Inflammatory bowel disease [19] Sarcoidosis [20] Unilateral acute idiopathic maculopathy [21] HLA-DR53 is associated with VKH syndrome in individuals of Chinese and Japanese descent. VKH syndrome in those of Chinese, Japanese, Native American, Hispanic, and European descent is associated with HLA-DR4.[22] HLA-DR1 is associated with VKH syndrome in individuals of Hispanic descent, while HLA-DQ4 is associated with VKH syndrome in the Japanese population.[23] Mutations in KIF11, observed in 5% to 8% of familial exudative vitreoretinopathy cases, are connected with microcephaly with or without chorioretinopathy, lymphedema, or intellectual disability (MCLID). MCLID is an autosomal dominant condition.[24] Idiopathic Causes Central serous chorioretinopathy [25] Nanophthamic eyes Idiopathic uveal effusion [26] Infectious Causes Tuberculosis [27] Dengue [28] Syphilis [29] Cat-scratch disease [30] Cytomegalovirus (CMV) retinitis [31] Lyme disease [32] Fungal infection [33] Nematode infection Diffuse unilateral subacute neuroretinitis [34][35] Toxoplasmosis [36] Herpes zoster [37] Surgical or Postsurgical Causes Panretinal photocoagulation [38] Scleral buckle [39] Wound leak or ocular hypotony [40] Neoplastic or Paraneoplastic Causes Metastatic disease [41] Choroidal melanoma and nevus [42] Retinoblastoma [43] Choroidal hemangioma [44] Retinal or optic disc capillary hemangioblastoma or Von Hippel-Lindau syndrome [45] Choroidal osteoma [46] Lymphoma [47] Bilateral diffuse uveal melanocytic proliferation [48][49] Multiple myeloma [50] Leukemia [51] Lymphomatoid granulomatosis [52] Cancer-associated retinopathy [53]

Choroidal melanoma and nevus [42] Retinoblastoma [43] Choroidal hemangioma [44] Retinal or optic disc capillary hemangioblastoma or Von Hippel-Lindau syndrome [45] Choroidal osteoma [46] Lymphoma [47] Bilateral diffuse uveal melanocytic proliferation [48][49] Multiple myeloma [50] Leukemia [51] Lymphomatoid granulomatosis [52] Cancer-associated retinopathy [53] Patients suspected of having bilateral diffuse uveal melanocytic proliferation should undergo evaluation for ovarian, lung carcinoma, and urogenital cancer.[54][55][56] These patients should also have regular ophthalmologic monitoring for early detection and management of ocular complications. Vascular or Hematologic Causes Preeclampsia [57][58] Eclampsia Malignant hypertension [59][60][61] Disseminated intravascular coagulation [62] Thrombotic thrombocytopenic purpura [63] Granulomatosis with polyangiitis [64] HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) [65] Systemic lupus erythematosus [66] Antiglomerular basement membrane disease [67] Organ transplantation and hemodialysis [68] Severe diabetic retinopathy Retinal vein occlusion in the systemically unstable patient [69][70] Renal diseases like IGA nephropathy, chronic renal failure, type II membranoproliferative glomerulonephritis, and crescentic membranous nephropathy [71] Choroidal neovascularization due to various causes, including age-related macular degeneration [72] Idiopathic polypoidal choroidal vasculopathy [73] Coats disease [74] Retinal vein occlusion [70] Venous overload choroidopathy due to carotid obstruction [75] Familial exudative vitreoretinopathy [76] Retinopathy of prematurity [77] Norrie disease Retinal artery macroaneurysm [78][79] Norrie disease is a rare X-linked recessive disorder typically manifesting as bilateral leukocoria in children. Ocular findings in Norrie disease include microphthalmos, cataracts, leukokoria, and retinal detachment.[80] Systemic findings encompass intellectual disabilities, behavioral difficulties, growth and developmental delays, hearing loss, peripheral vascular disease, and disruptions in sleep-wake cycles. Miscellaneous Causes Acute exudative polymorphous vitelliform maculopathy [81] Medications like interferon-α, ribavirin, checkpoint inhibitors like atezolizumab and ipilimumab, mitogen-activated protein kinase kinase (MEK) inhibitors, and topiramate [82][83][84][85] Systemic steroids Due to the worsening of central serous chorioretinopathy[86]

Age predilection in exudative retinal detachment varies across different diseases. Retinal detachment due to Coats disease is evident in younger patients, while exudative retinal detachment secondary to malignancy and age-related macular degeneration is more prevalent among older patients. Exudative retinal detachment secondary to preeclampsia, eclampsia, HELLP syndrome, VKH syndrome, and central serous chorioretinopathy tends to occur more frequently in patients who are middle-aged.[87] Choroidal malignancies and exudative age-related macular degeneration are more common in White patients.[88][89] Black patients have a higher incidence of inflammatory ocular diseases.[90] VKH syndrome (see Image. Vogt-Koyanagi-Harada Syndrome) is more common in patients of Asian descent.[6] Due to the multifactorial origin of exudative retinal detachment, previous data lacks data on the frequency. Additionally, sex predilection in exudative retinal detachment varies across different diseases. Central serous chorioretinopathy, Coats disease, and uveal effusion syndrome are more commonly diagnosed in males.[26][91][92] Individuals with a stressful lifestyle, type A personality, and pregnancy have an elevated risk of central serous chorioretinopathy.[86]

Typically, water flows from the vitreous cavity to the choroid. Any excess inflow or insufficient outflow from the vitreous cavity beyond what standard compensatory mechanisms can handle results in fluid accumulation in the subretinal space, culminating in an exudative retinal detachment. The amount of fluid in the subretinal space is influenced by various factors. These include the relative hyperosmolarity of the choroid compared to the vitreous, as well as the active pumping of ions and water from the vitreous into the choroid by the retinal pigment epithelium. Choroidal vascular permeability directly affects the choroidal interstitial fluid content, and damage to the retinal pigment epithelium can disrupt its pumping function, resulting in fluid accumulation in the subretinal space. The retinal pigment epithelium serves as the primary component of the blood-retinal barrier.[93] Comprising a single polarized monolayer of cells, the retinal pigment epithelium forms the outer blood-retinal barrier, crucial for regulating fluid and molecular transport between retinal vasculature and retinal layers.[94][95] The blood-retinal barrier consists of 2 segments: the inner and outer blood-retinal barrier. Tight junctions between the retinal pigment epithelial cells form the outer blood-retinal barrier.[96] No anatomical attachment is present between the retinal pigment epithelium and the neurosensory retina. However, neural cell adhesion molecules expressed on the apical surface of the retinal pigment epithelial cells facilitate attachment between the two structures.[96] Tight junctions between endothelial cells of the capillaries form the inner blood-retinal barrier.[96] The tight junctions formed by cells comprising the blood-retinal barrier play a crucial role in its integrity and function.[95] Disruption of these junctions, whether due to infectious, inflammatory, vascular, infiltrative, neoplastic, or degenerative factors, leads to blood-retinal barrier failure, causing fluid accumulation in the subretinal space.[93][95] Furthermore, the loss of polarity in the retinal pigment epithelium can cause the reversal of pumping mechanisms, contributing to fluid accumulation in the subretinal space.[86]

During the acute phases of exudative retinal detachment, patients experience a loss of photoreceptor outer segments. In chronic cases, notable findings include proliferation of retinal pigment epithelium, formation of cysts, increased leakage into the subretinal space, and retinoschisis.[1]

A retinal detachment patient may present with various symptoms and a pertinent medical history. They may report decreased visual acuity, floaters, eye pain, visual field defects, redness, leukocoria, and metamorphopsia. It is essential for the clinician to note the duration of symptoms, inquire about any prior intraocular surgeries or systemic illnesses, and review the patient's use of systemic or topical medications. Additionally, excessive weight loss or loss of appetite may raise concerns about malignancy, warranting a thorough evaluation. A history of a flu-like illness during the prodromal phase may indicate the acute uveitis phase of VKH syndrome.[97] A comprehensive physical examination is crucial for assessing potential systemic causes of exudative retinal detachment.[1] Measuring the patient's blood pressure is essential. The ophthalmic examination should include the best-corrected visual acuity, intraocular pressure, and evaluation for longstanding amblyopia. Ptosis, proptosis, and pain with ocular movements may indicate posterior scleritis and orbital inflammation.[98][99] Anterior Segment Examination Anterior segment examination may be unremarkable, but in cases of inflammatory etiologies, specific manifestations may include circumcorneal congestion, aqueous cells, anterior chamber flare, posterior synechiae, complicated cataracts, keratic precipitates, hypopyon, and retrolental or anterior vitreous cells on slit-lamp examination.[100] Raised intraocular pressure may be observed due to secondary angle closure associated with ciliary congestion and anterior rotation of the ciliary body, as seen in conditions such as scleritis, panretinal photocoagulation, and VKH syndrome.[14] Neovascularization of the iris and angle may occur in patients with VKH syndrome.[101] Evaluating the pupil for a relative afferent pupillary defect is important, as it can provide insight into the severity of posterior segment involvement.[102] Additionally, features indicative of rhegmatogenous retinal detachment, such as retrolental pigments or Shafer sign, as well as hypotony, should also be noted during the examination.[103] Posterior Segment Examination

Neovascularization of the iris and angle may occur in patients with VKH syndrome.[101] Evaluating the pupil for a relative afferent pupillary defect is important, as it can provide insight into the severity of posterior segment involvement.[102] Additionally, features indicative of rhegmatogenous retinal detachment, such as retrolental pigments or Shafer sign, as well as hypotony, should also be noted during the examination.[103] Posterior Segment Examination Shifting fluid across the retina is a characteristic feature of exudative retinal detachment.[104] As the patient changes position, the subretinal fluid accumulates in the most dependent area of the retina. Previously, shifting fluid was the hallmark finding associated with exudative retinal detachment.[105] However, shifting fluid is also present with aphakic and longstanding rhegmatogenous retinal detachment in patients with small retinal holes.[106] Other characteristic features of exudative retinal detachment include a smooth retinal surface without retinal folds or corrugations, and the presence of vitreous cells. In cases with inflammatory etiologies, optic disc hyperemia may be observed.[105] Additionally, choroidal neovascularization can develop in chronic nonresolving cases of exudative retinal detachment.[107] Choroidal metastases can present as an exudative retinal detachment, with the metastases typically being small while the detachment appears relatively larger.[41][108] Unlike rhegmatogenous retinal detachment, exudative retinal detachment lacks associated Shaffer sign, posterior vitreous detachment, and vitreous hemorrhage.[1] Detailed discussion on the distinctions between exudative and rhegmatogenous retinal detachments is provided in the "Differential Diagnosis" section. Assessing for Retinal Break or Tractional Bands

Choroidal metastases can present as an exudative retinal detachment, with the metastases typically being small while the detachment appears relatively larger.[41][108] Unlike rhegmatogenous retinal detachment, exudative retinal detachment lacks associated Shaffer sign, posterior vitreous detachment, and vitreous hemorrhage.[1] Detailed discussion on the distinctions between exudative and rhegmatogenous retinal detachments is provided in the "Differential Diagnosis" section. Assessing for Retinal Break or Tractional Bands Exudative retinal detachment is a diagnosis of exclusion. A thorough central and peripheral fundal examination is necessary to exclude the presence of any fibrovascular proliferation causing traction over the retina, resulting in a tractional retinal detachment, or the presence of any retinal tear, hole, or dialysis that may lead to a rhegmatogenous retinal detachment.[109][110] In cases of inferior bullous retinal detachment with shifting fluid, evaluating for superior small breaks is crucial.[109] The presence of proliferative vitreoretinopathy suggests a likely rhegmatogenous retinal detachment. This differentiation is essential as both rhegmatogenous and tractional retinal detachments require surgical management.[111]

Diagnosis of exudative retinal detachment is primarily clinical, relying on a thorough ophthalmic examination. However, additional testing may be necessary to determine the underlying etiology. Laboratory and General Imaging The evaluation is tailored to each patient based on medical history, associated symptoms, and examination findings. Depending on clinical presentation, tests may include a combination of the following: Complete blood cell count with a differential Erythrocyte sedimentation rate Mantoux test Chest radiography Rheumatoid factor Antinuclear antibody Interferon-gamma release assay Venereal disease research laboratory (VDRL) test and fluorescent treponemal antibody absorption test (FTA-ABS) test Serum homocysteine levels Serum cortisol levels Renal function tests Liver function test Toxoplasma, rubella, cytomegalovirus, herpes (TORCH) markers Prothrombin time, bleeding time, and clotting time Fasting blood sugar, postprandial blood sugar, and glycosylated hemoglobin [112] The Amsler grid provides a simple method for detecting metamorphopsia and scotoma.[113] It is a valuable tool for monitoring changes in central vision over time and can aid in assessing retinal function. Ocular  Imaging Imaging studies, such as optical coherence tomography (OCT), fundus fluorescein angiography (FFA), and ultrasonography, may be necessary to investigate the etiology and guide the management of an exudative retinal detachment. These imaging modalities provide detailed information about the retinal anatomy, vascular perfusion, and underlying pathology, aiding in accurate diagnosis and treatment planning (see Image. Exudative Retinal Detachment). Optical coherence tomography of the macula OCT scanning is invaluable for delineating the macula's serous detachment, assessing the septae's presence, and measuring choroidal thickness. Additionally, it allows for the precise visualization of any associated structural changes in the retina and choroid. Choroidal thickness decreases as the primary inflammatory insults subside with or without treatment.[114][115] Hence, choroidal thickness is a useful OCT biomarker for disease prognostication.[116] Increased choroidal thickness is noted on enhanced depth imaging OCT in patients affected with various conditions, such as the following: VKH syndrome Posterior scleritis Uveal effusion syndrome Central serous chorioretinopathy [117]

Choroidal thickness decreases as the primary inflammatory insults subside with or without treatment.[114][115] Hence, choroidal thickness is a useful OCT biomarker for disease prognostication.[116] Increased choroidal thickness is noted on enhanced depth imaging OCT in patients affected with various conditions, such as the following: VKH syndrome Posterior scleritis Uveal effusion syndrome Central serous chorioretinopathy [117] Patients with bacillary layer detachment may present symptoms such as metamorphopsia, scotoma, and decreased visual acuity. Additionally, they may exhibit characteristic findings on OCT, including disruption or elevation of the outer retinal layers and detachment of the photoreceptor outer segments from the retinal pigment epithelium (see Image. Bacillary Layer Detachment). This can be seen in conditions such as: VKH syndrome Sympathetic ophthalmia Acute posterior multifocal placoid pigment epitheliopathy Hematological disorders Posterior scleritis Choroidal metastases Central serous chorioretinopathy [118] Fundus fluorescein angiography FFA utilizes intravenous fluorescein to examine the choroid and retinal vascular supply. Patients with an exudative retinal detachment may have areas of hyper- and hypofluorescence, multiple window defects, dye pooling in serous retinal detachment areas, and disc staining.[119] Angiography is also beneficial for detecting choroidal and disc neovascularization, neovascularization elsewhere, retinochoroidal and arteriovenous anastomoses, and identifying the peripheral ischemic zone, aiding in further management planning.[120] In patients with VKH syndrome, FFA imaging reveals hypofluorescent dots in the early phase (see Image. Early Phase Vogt-Koyanagi Harada Syndrome), followed by multiple focal areas of leakage and subretinal fluid accumulation in the late phase (see Image. Late Phase Vogt-Koyanagi Harada Syndrome).[115] These findings indicate the choroidal inflammatory process and associated disruption of the blood-retinal barrier seen in VKH syndrome.

In patients with VKH syndrome, FFA imaging reveals hypofluorescent dots in the early phase (see Image. Early Phase Vogt-Koyanagi Harada Syndrome), followed by multiple focal areas of leakage and subretinal fluid accumulation in the late phase (see Image. Late Phase Vogt-Koyanagi Harada Syndrome).[115] These findings indicate the choroidal inflammatory process and associated disruption of the blood-retinal barrier seen in VKH syndrome. In patients with central serous chorioretinopathy, characteristic patterns such as the inkblot or, less commonly, the smokestack pattern may be observed. The inkblot pattern begins as a pinpoint leakage in the early phase, which concentrically enlarges in the late phase. Conversely, with the smokestack pattern, leakage from the choroid begins as a pinpoint and gradually expands to form an umbrella- or tree-like appearance.[86] In patients with posterior scleritis, FFA typically reveals blocked fluorescence during the initial arteriovenous phase and diffuse hyperfluorescence in the late phase without any evident leak. Choroidal folds appear as alternating hyperfluorescent and hypofluorescent bands.[121][122] Uveal effusion syndrome appears as hyperfluorescence in a leopard-spot pattern on FFA.[123] In patients with acute posterior multifocal placoid pigment epitheliopathy, early-phase FFA typically demonstrates hypofluorescence due to choroidal fluorescence blockage. Subsequently, staining of the lesions becomes evident later in the angiogram. As the disease becomes inactive, hyperfluorescence corresponding to window defects in the mottled retinal pigment epithelium develops.[124] The early phase of FFA early phase reveals a reticular pattern of hypofluorescence surrounded by a background of choroidal hyperfluorescence in patients with bilateral diffuse uveal melanocytic proliferation.[125] Indocyanine green angiography Indocyanine green (ICG) angiography uses indocyanine green dye instead of fluorescein. Unlike fluorescein, indocyanine green fluoresces in the infrared or nonvisible light spectrum. The infrared wavelengths can penetrate the retinal layers, rendering the circulation in deeper layers visible when photographed with an infrared-sensitive camera.

Indocyanine green (ICG) angiography uses indocyanine green dye instead of fluorescein. Unlike fluorescein, indocyanine green fluoresces in the infrared or nonvisible light spectrum. The infrared wavelengths can penetrate the retinal layers, rendering the circulation in deeper layers visible when photographed with an infrared-sensitive camera. In patients with central serous chorioretinopathy, early-phase indocyanine green angiography (ICG) typically reveals hypocyanescence, suggesting nonperfusion or delayed choriocapillaris filling. Subsequently, mid-phase hypercyanescence is observed, indicating choroidal vessel hyperpermeability. The hypercyanescence gradually diminishes in the late phase.[126][127][128] In VKH syndrome, ICG typically demonstrates early hyperfluorescence accompanied by leakage and hypofluorescent dark dots at the choroid level.[129][130] These findings indicate choroidal inflammation and disruption of the blood-retinal barrier seen in VKH syndrome. In idiopathic polypoidal choroidal vasculopathy, ICG typically reveals interconnecting channels with an abnormal vascular network that becomes visible within 1 minute of dye injection. Additionally, the polyp and feeder vessels associated with the lesion are often identified on ICG imaging.[131][132] In acute posterior multifocal placoid pigment epitheliopathy, the early lesions typically exhibit hypofluorescence on fluorescein angiography. As the angiogram progresses into the late phases, these lesions become more defined in shape and size, often appearing larger than the placoid lesions seen clinically. As the lesions heal, the hypofluorescence in the late phases tends to become smaller and less distinct.[133][134][135][136] Ultrasonography Ultrasound is invaluable for detecting choroidal thickness, assessing the presence or absence of choroidal masses, determining the size and location of choroidal masses, and evaluating scleral thickness.[98] It mainly benefits patients with hazy media that preclude a precise posterior segment examination. Autofluorescence

Ultrasound is invaluable for detecting choroidal thickness, assessing the presence or absence of choroidal masses, determining the size and location of choroidal masses, and evaluating scleral thickness.[98] It mainly benefits patients with hazy media that preclude a precise posterior segment examination. Autofluorescence Fundus autofluorescence maps naturally and pathologically occurring fluorophores in the posterior pole. In patients with cancer-associated retinopathy, a parafoveal ring of hyper-autofluorescence is typically observed, with normal autofluorescence within the ring and hypo-autofluorescence outside the ring.[137] In bilateral diffuse uveal melanocytic proliferation, ultra-widefield color fundus photography often reveals greater pigmentary changes and lesions in the periphery. Ultra-widefield autofluorescence imaging demonstrates the characteristic giraffe-pattern fundal changes associated with bilateral diffuse uveal melanocytic proliferation.[138] In acute central serous chorioretinopathy, observers often detect focal areas of hypoautofluorescence, which may correspond to the leakage observed on FFA. In chronic central serous chorioretinopathy, hyperautofluorescent tracks are present due to the accumulation of photoreceptor pigments.[86] In Best disease, autofluorescence imaging shows uniform hyperfluorescence of vitelliform lesions, while sub-retinal pigment epithelium fibrosis or atrophy shows hypofluorescence.[139][140] The increased autofluorescence is attributed to the lipofuscin content.[141][142][143] Electrophysiological tests Electroretinography (ERG) measures the retina's electrical response to light stimuli. In patients with cancer-associated retinopathy, full-field ERG may reveal attenuated or absent photopic and scotopic responses, indicating dysfunction of both cones and rods. However, in some cases of cancer-associated retinopathy, only the cones are affected, and full-field ERG may appear normal. In contrast, multifocal ERG is typically abnormal in cancer-associated retinopathy, reflecting localized retinal dysfunction.[144][145]

Exudative retinal detachment has a multifactorial origin, and the management approach is individualized depending on the type, severity, and presentation stage. Medical management is the primary approach for treating exudative retinal detachment. Surgical intervention is rarely necessary unless all other measures fail.[76] Inflammatory diseases like VKH syndrome and posterior scleritis should be treated with intravenous methylprednisolone pulse therapy at 1 g/d for 3 to 5 days, followed by a shift to oral corticosteroids according to weight.[97] The involvement of inflammation and the use of steroids in the management of uveal effusion may be subject to debate.[26][146] In successfully treating VKH syndrome, clinicians have utilized immunosuppressive agents such as methotrexate, azathioprine, cyclosporine A, mycophenolate mofetil, and alkylating agents, alongside corticosteroids.[147][148][149][150] These immunosuppressive therapies aim to suppress the autoimmune response and reduce inflammation associated with VKH syndrome. The American Uveitis Society and the International Uveitis Study Group recommend immunosuppressive agents as mandatory in treating VKH syndrome to prevent recurrences. While high-dose corticosteroids also affect recurrences, as outlined above, careful consideration must be given to balance the initial treatment with the subsequent need for immunosuppressive agents.[97] Oral nonsteroidal anti-inflammatory medications can be effective with various appropriate regimens, such as ibuprofen 600 to 800 mg 4 times daily, piroxicam 20 mg daily, and naproxen 375 mg twice daily. In cases unresponsive to oral nonsteroidal anti-inflammatory medications, high-dose systemic corticosteroids are often used, with typical doses of 1 mg/kg/d.[151][152][153] These steroids are tapered slowly over several weeks, carefully considering potential side effects such as weight gain, mood instability, blood-sugar abnormalities, and adrenal insufficiency. If the patient continues to demonstrate active disease or cannot tolerate corticosteroids, prompt corticosteroid-sparing immunosuppression is warranted.

These steroids are tapered slowly over several weeks, carefully considering potential side effects such as weight gain, mood instability, blood-sugar abnormalities, and adrenal insufficiency. If the patient continues to demonstrate active disease or cannot tolerate corticosteroids, prompt corticosteroid-sparing immunosuppression is warranted. Antimetabolites such as methotrexate and mycophenolate mofetil are employed, often to their maximal doses of 25 mg/week of methotrexate or 1,500 mg twice daily of mycophenolate.[154][152] These medications may take up to 6 months for full effect, and some patients may require a faster-acting solution. Biologics such as tumor necrosis factor inhibitors (TNF-inhibitors) like adalimumab and infliximab may be necessary in these cases.[155][156] The management of malignant hypertensive retinopathy involves controlling blood pressure and addressing any secondary causes of hypertension. Timely intervention and close monitoring of blood pressure levels are crucial to prevent further retinal damage and preserve visual function in patients with malignant hypertensive retinopathy. Management Options of Central Serous Chorioretinopathy Management of central serous chorioretinopathy includes observation, laser, photodynamic therapy, and anti-vascular endothelial growth factor (anti-VGEF) agents. Laser photocoagulation can treat the retinal pigment epithelium leakage sites identified on angiography, effectively sealing the leakage point and promoting the resolution of subretinal fluid.[157] Central serous chorioretinopathy with a subfoveal leak, juxtafoveal leak, multiple leaks, and chronic cases with diffuse decompensation of the retinal pigment epithelium often benefit from laser photodynamic therapy as a management strategy.[158][159] Anti-VEGF therapy has been proposed to reduce choroidal hyperpermeability by upregulating the tight junctions between endothelial cells and reducing vascular fenestrations.[160][161][162] Surgical intervention is considered the last resort for managing exudative retinal detachment after exhausting all medical treatment options.[4] Surgical management options include:[163] Scleral buckling with external drainage of the subretinal fluid with laser of the nonperfused retina

Central serous chorioretinopathy with a subfoveal leak, juxtafoveal leak, multiple leaks, and chronic cases with diffuse decompensation of the retinal pigment epithelium often benefit from laser photodynamic therapy as a management strategy.[158][159] Anti-VEGF therapy has been proposed to reduce choroidal hyperpermeability by upregulating the tight junctions between endothelial cells and reducing vascular fenestrations.[160][161][162] Surgical intervention is considered the last resort for managing exudative retinal detachment after exhausting all medical treatment options.[4] Surgical management options include:[163] Scleral buckling with external drainage of the subretinal fluid with laser of the nonperfused retina Pars plana vitrectomy with internal drainage of the subretinal fluid with laser delimitation of the nonperfused retina with or without endotamponade with expansile gases or silicone oil [164][165] Management of Familial Exudative Vitreoretinopathy The management of familial exudative vitreoretinopathy depends on the stage at the time of presentation: Stage 1: Observation Stage 2: Laser photocoagulation of the areas with abnormal vessels and ischemia or the avascular zone [166] Advanced stage: In cases of retinal detachment, a surgical approach is necessary. Scleral buckling, vitrectomy, and lasering of the avascular zone are recommended.[167] Screening family members for genetic predisposition to certain retinal conditions is advisable. The use of anti-VEGF therapy remains a topic of debate in the management of retinal neovascularization. According to a study by Tagami M et al, regression of neovascularization occurs after a single intravitreal injection of bevacizumab.[168] A study by Henry CR et al reveals favorable results with intravitreal bevacizumab use along with laser or surgical treatment.[169] There is a risk of worsening tractional forces, potentially causing tractional retinal detachment with the administration of anti-VEGF injections. Therefore, clear guidelines are essential for appropriately using anti-VEGF as an adjunct to laser or surgical therapy.[167][169] Management of Coats Disease The management of Coats disease varies depending on the stage of the condition. Care for these patients is outlined as follows: Mild cases are often observed without exudation.[18]

There is a risk of worsening tractional forces, potentially causing tractional retinal detachment with the administration of anti-VEGF injections. Therefore, clear guidelines are essential for appropriately using anti-VEGF as an adjunct to laser or surgical therapy.[167][169] Management of Coats Disease The management of Coats disease varies depending on the stage of the condition. Care for these patients is outlined as follows: Mild cases are often observed without exudation.[18] Direct laser photocoagulation of the telangiectatic vessels is a beneficial treatment option in mild to moderate cases of exudation.[92] Laser therapy will not be effective in cases of massive subretinal exudation and exudative retinal detachment. In such cases, practitioners perform cryotherapy over the diseased retina using a double freeze-thaw technique.[170] Anti-VEGF medications and intravitreal corticosteroids can be used as adjunctive therapy before laser or surgical management, as they also help to reduce macular edema associated with exudation.[171][172] Advanced stages of Coats disease are associated with inferior visual prognosis. Treatment in advanced stages focuses on avoiding a painful blind eye and enucleation. Scleral buckling with external drainage or pars plana vitrectomy with or without endotamponade may save the eye.[173][163] Transscleral diode laser photocoagulation is a treatment option for neovascular glaucoma. If all measures to save the eye fail, practitioners should enucleate an endstage painful blind eye.[92][170] Exudative retinal detachment due to wound leak or hypotony after ocular surgery responds satisfactorily with timely wound suturing and anti-inflammatory agents.[1] Similarly, exudative detachments secondary to panretinal photocoagulation or scleral buckling may benefit from topical and systemic anti-inflammatory or steroid therapy.[38] In cases where the scleral buckle exerts excessive pressure, readjustment is required to alleviate stress on the vascular system.[39]

Exudative retinal detachment due to wound leak or hypotony after ocular surgery responds satisfactorily with timely wound suturing and anti-inflammatory agents.[1] Similarly, exudative detachments secondary to panretinal photocoagulation or scleral buckling may benefit from topical and systemic anti-inflammatory or steroid therapy.[38] In cases where the scleral buckle exerts excessive pressure, readjustment is required to alleviate stress on the vascular system.[39] Radiation therapy, particularly proton beam radiation, is frequently employed in the treatment of malignant uveal melanoma.[42][174] However, post-radiation therapy, there is an elevated risk of exacerbating retinal detachment, particularly with proton beam radiation.[174] Treatment of choroidal tumors with exudative retinal detachment includes proton beam radiation or brachytherapy using a plaque, transretinal tumor biopsy for prognostication of the disease, and surgical intervention as the last measure with may entail pars plana vitrectomy and drainage of subretinal fluid with endotamponade.[42] A variety of treatment options exist for choroidal hemangioma, including laser photocoagulation, low-dose external beam radiation, proton beam irradiation, gamma knife radiosurgery, radiotherapy, cryotherapy, photodynamic therapy with verteporfin, transpupillary thermotherapy, oral β-blockers, or intravitreal anti–VEGF.[175] Patients with metastatic tumors should receive chemotherapy or focal radiation therapy.[176] Patients with infectious causes leading to exudative retinal detachment should be promptly treated with appropriate antibiotics.[177] Tuberculous exudative detachment requires a comprehensive approach involving antitubercular drugs in conjunction with glucocorticoids to manage the infection effectively.[178] Syphilitic exudative detachment necessitates treatment with the regimen typically used for neurosyphilis, while viral etiologies warrant urgent initiation of antiviral drugs alongside corticosteroids to mitigate inflammation and viral replication.[179][180][181] Pregnancy-induced hypertension can lead to marked vision loss, but these changes are typically reversible in the postpartum period.[59] Adequate blood pressure control is the most critical intervention. Compared to malignant hypertension, the visual prognosis is generally more favorable in cases of pregnancy-induced hypertension.[59]

Pregnancy-induced hypertension can lead to marked vision loss, but these changes are typically reversible in the postpartum period.[59] Adequate blood pressure control is the most critical intervention. Compared to malignant hypertension, the visual prognosis is generally more favorable in cases of pregnancy-induced hypertension.[59] Secondary exudative retinal detachment in patients with systemic hematologic and vascular diseases like disseminated intravascular coagulation, malignant hypertension, anti-glomerular basement membrane disease, thrombotic thrombocytopenic purpura, organ transplant recipients, renal failure, systemic lupus erythematosus, and granulomatosis with polyangiitis can resolve once the underlying systemic condition is controlled and treated.[182][183][184] Timely and comprehensive management of the primary systemic disease is crucial in achieving resolution of secondary exudative retinal detachment in these patients. Exudative retinal detachment in hepatitis C patients treated with interferon-α and ribavirin improves upon discontinuation of the offending medications and initiation of corticosteroid treatment.[85] Close monitoring of visual symptoms and prompt intervention are essential to managing exudative retinal detachment in patients undergoing these treatments.

Exudative retinal detachments can arise from various causes, including inflammatory, infectious, neoplastic, and other conditions. Clinicians must rule out rhegmatogenous and tractional retinal detachments during the diagnostic process. Exudative retinal detachment, rhegmatogenous retinal detachment, and tractional retinal detachment have distinct underlying causes. Therefore, it is essential to differentiate exudative retinal detachment from rhegmatogenous retinal detachment and tractional retinal detachment (see Table. Comparison of Different Forms of Retinal Detachment). Table Table. Comparison of Different Forms of Retinal Detachment. Patients with a hemorrhagic retinal detachment are distinguished from those with an exudative retinal detachment by subretinal blood instead of serous fluid. Causes of hemorrhagic retinal detachment include conditions such as peripheral exudative hemorrhagic chorioretinopathy, often considered a variant of idiopathic polypoidal choroidal vasculopathy, trauma, leukemia, and age-related macular degeneration, particularly in individuals taking blood thinners.

The prognosis of exudative retinal detachment depends on the underlying condition. Exudative retinal detachment secondary to uveal effusion and VKH syndrome may improve with high-dose systemic steroids. However, the recurrence risk is high.[97][185] Recurrence risk is also high in patients with acute central serous chorioretinopathy. Once central serous chorioretinopathy becomes chronic, the permanent loss of cones leads to a less promising visual recovery.[186] Exudative retinal detachment in patients with preeclampsia and eclampsia is usually self-limiting and resolves entirely with time.[187] The prognosis for other underlying conditions like Coats disease, choroidal tumors, infection, uveitis, retinal vein occlusion, and retinopathy of prematurity depends on the severity of the underlying condition, the response to treatment, the amount of macular involvement, and complications secondary to treatment.[42][86][166][185][188][189] Long-standing pathology causes permanent damage to photoreceptors and the retinal pigment epithelium, often leading to a poor prognosis despite comprehensive treatment efforts.[86][185][188][185][86][190]

If not treated promptly, secondary complications may develop in patients with an exudative retinal detachment. The following is a list of potential complications: Phthisis bulbi [191] Neovascular glaucoma Subretinal fibrosis Choroidal neovascularization Pigmentary changes of the fundus Festooned pupil Vitreous hemorrhage Complicated cataract [192]

A retinal detachment is the separation of the retina from the underlying retinal pigment epithelium and choroid, resulting in retinal ischemia and photoreceptor degeneration. Without treatment, a retinal detachment can lead to blindness. Retinal detachments occur when a retinal hole or tear allows fluid accumulation between the layers, with vitreous traction or an exudative process. Patients with an exudative retinal detachment have fluid that enters the subretinal space from retinal or choroidal blood vessels. The adhesive forces between the neurosensory retina and retinal pigment epithelium become overwhelmed. Potential causes are choroidal tumors, uveitis, hypertension, ocular vascular disorders, medications, other systemic inflammatory conditions, collagen vascular diseases, or infectious diseases. The differential diagnosis for exudative retinal detachment is extensive. Differentiating exudative, tractional, and rhegmatogenous retinal detachment is paramount and can be a clinical diagnosis. Patients with exudative retinal detachment should undergo a thorough history and physical examination to determine the underlying etiology of their retinal detachment. Diagnostic laboratory studies and imaging are individualized based on the patient's history and examination findings. Appropriate and timely intervention by the treating clinician may improve the visual and systemic status of the patient.

Key points to keep in mind about exudative retinal detachments include the following: Exudative retinal detachment refers to the accumulation of fluid in the subretinal space without the presence of retinal breaks or tractional forces. It can be caused by various factors, including inflammatory conditions, infectious diseases, systemic diseases (such as hypertension), ocular vascular disorders, medications, and ocular tumors. Patients may present with decreased visual acuity, floaters, visual field defects, and metamorphopsia. They may have signs of retinal detachment on fundoscopic examination. Diagnosis is primarily clinical, but additional testing, such as OCT, FFA, and ICG, may be necessary to determine the underlying etiology. Treatment depends on the underlying cause and may include medical management with corticosteroids or immunosuppressive agents, laser photocoagulation, photodynamic therapy, anti-VEGF therapy, or surgical intervention in refractory cases. Prognosis varies depending on the underlying condition, treatment response, and macular involvement extent. Prompt diagnosis and treatment are crucial to prevent permanent vision loss.

Caring for patients with an exudative retinal detachment necessitates a collaborative approach among healthcare professionals to ensure patient-centered care and improve overall outcomes. Ophthalmology, primary care, emergency medicine, oncology, rheumatology, hematology, dermatology, genetics, and infectious disease clinicians, along with any other healthcare professionals involved in the care of these patients, must possess the essential clinical skills and knowledge to diagnose and manage exudative retinal detachments. This knowledge includes the ability to differentiate exudative retinal detachments from other retinal detachment forms and recognize the multitude of potential underlying etiologies. A strategic, evidence-based evaluation is necessary to promptly diagnose the retinal detachment and any underlying condition to prevent morbidity, vision loss, and recurrence. Each healthcare professional should contribute their expertise and participate in seamless interprofessional communication to enable collaborative decision-making among the team members. By embracing the principles of skill, strategy, responsibilities, and interprofessional communication, healthcare professionals can deliver patient-centered care, enhancing overall quality of life and decreasing morbidity, ultimately improving patient outcomes and team performance in managing exudative retinal detachment.