PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Chorioretinitis”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1979

[Central serous retinitis or chorioretinitis (retinopathy or chorioretinopathy) and central hemorrhagic chorioretinitis (juvenile disciform macular detachment; focal hemorrhagic chorioiditis, presumed histoplasmosis) (author's transl)].

There are no clinical or etiological connections between central serous and central hemorrhagic chorioretinitis, Serous chorioretinitis is seen mostly in men; full visual acuity is regained in approx. 80% of all cases. It mainly affects subjects aged between 36 and 45. Hemorrhagic chorioretinitis affects both sexes to about the same extent and causes severe impairment of visual acuity. Both forms should be regarded as genuine inflammations (chorioretinitis centralis serosa, chorioretinitis centralis hemorrhagica), not as "pathies". Whereas the hemorrhagica disease is generally thought to be caused by inflammation, the serous form also often shows signs of inflammation such as varying leakages with inflammatory depigmentation and more frequently inflammatory protein increase (exudate) with precipitation on the posterior surface of the retina/anterior surface of the pigment epithelium.

Adult↗
PubMed2004

A novel TEAD1 mutation is the causative allele in Sveinsson's chorioretinal atrophy (helicoid peripapillary chorioretinal degeneration).

Sveinsson's chorioretinal atrophy (SCRA), also referred to as helicoid peripapillary chorioretinal degeneration or atrophia areata, is an autosomal dominant eye disease, characterized by symmetrical lesions radiating from the optic disc involving the retina and the choroid. Genome-wide linkage analysis mapped the SCRA gene to chromosome 11p15 in 81 patients from a large founder pedigree in Iceland. The parametric LOD score obtained was 18.9 using an autosomal dominant model with high penetrance. Crossover analysis of the linkage region with 51 markers identified a 593 kb segment shared by all patients. Sequencing exons of the only gene in this interval, the transcriptional enhancer TEAD1, revealed a novel missense mutation (Y421H) carried by all patients and none of the 502 controls. The mutation is in a conserved amino acid sequence in the C terminal of the protein, a potential binding site for YAP65 one of TEAD1's cofactors that is expressed in human retina as well as TEAD1 based on RT-PCR experiments. Therefore, we conclude that the mutation in the TEAD1 gene is the cause of Sveinsson's chorioretinal atrophy.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Relentless placoid chorioretinitis: A new entity or an unusual variant of serpiginous chorioretinitis?

OBJECTIVE: To characterize an unusual clinical entity resembling acute posterior multifocal placoid pigment epitheliopathy (APMPPE) and serpiginous choroiditis but with an atypical clinical course. PATIENTS: We describe 6 patients, aged 17 through 51 years, exhibiting this unusual entity who were seen at 6 different centers from 1984 to 1997. RESULTS: The acute retinal lesions in this series were similar to those of APMPPE or serpiginous choroiditis, both clinically and on fluorescein and indocyanine green angiography. However, the clinical course, number of lesions, and location of these lesions were atypical. These patients had evidence of numerous posterior and peripheral retinal lesions predating or occurring simultaneously with macular involvement. Older, healing pigmented lesions were often accompanied by the appearance of new active white placoid lesions. Additionally, these cases all demonstrated prolonged periods of activity resulting in the appearance of more than 50 and sometimes hundreds of lesions scattered throughout the fundus. Growth of subacute lesions and the appearance of new lesions continued for 5 to 24 months after initial examination, and relapses were common. CONCLUSIONS: This entity has clinical features similar to APMPPE and serpiginous choroiditis but has a prolonged progressive clinical course and widespread distribution of lesions. It may represent a variant of serpiginous choroiditis or may be a new entity. We call it relentless placoid chorioretinitis. Arch Ophthalmol. 2000;118:931-938

Acute Disease↗
PubMed1998

Clinical course of newly developed or progressive patchy chorioretinal atrophy in pathological myopia.

Regional chorioretinal atrophy in the posterior fundus (patchy chorioretinal atrophy) in pathological myopia impairs vision severely when it covers the macula. The aim of this study was to assess the course of development and progression of patchy chorioretinal atrophy in pathological myopia. The location and progression of patchy chorioretinal atrophy that was either newly developed or had progressed during the follow-up period (mean 5.25 years) were analyzed. A total of 41 lesions of patchy atrophy were newly developed in 30 eyes of 25 patients. These lesions were more likely to occur in marginal regions of a posterior staphyloma but frequency per unit area was highest in the macula. There were 138 lesions of patchy chorioretinal atrophy that progressed in 75 eyes of 53 patients. Sixty percent of the lesions of patchy chorioretinal atrophy in marginal regions of a posterior staphyloma spread toward the center. Seventy percent of the lesions of patchy chorioretinal atrophy in the macula spread in all directions. Fluorescein angiography of newly developed patchy chorioretinal atrophy showed hyperfluorescence in 50% and hypofluorescence in 27%. Fluorescein angiography of progressive lesions of patchy chorioretinal atrophy showed hypofluorescence in 69%. Fluorescein angiography of some progressive areas of patchy chorioretinal atrophy, which showed a change from hyperfluorescence to hypofluorescence within several years, suggested that damage to the retinal pigment epithelium preceded the progression of the patchy chorioretinal atrophy. In conclusion, the patchy chorioretinal atrophy is most likely to occur in the macula and to enlarge in all directions. And it is suggested that the patchy chorioretinal atrophy which shows hyperfluorescence by fluorescein angiography should be kept under observation because our data suggest that this finding indicates progression in the future.

Adult↗
PubMed2000

Lymphocytic choriomeningitis virus: an underdiagnosed cause of congenital chorioretinitis.

PURPOSE: To elucidate the role and clinical spectrum of congenital lymphocytic choriomeningitis virus infection as a cause of chorioretinopathy, congenital hydrocephalus, and macrocephaly or microcephaly in the United States. METHODS: We performed complete ophthalmologic surveys of all residents at Misericordia, a home for the severely mentally retarded in Chicago, and prospectively evaluated all patients with chorioretinitis or chorioretinal scars during a 36-month period at Children's Memorial Hospital, also located in Chicago. Sera for patients demonstrating chorioretinal scars (a sign of intrauterine infection) were tested for Toxoplasma gondii, rubella virus, cytomegalovirus, and herpes simplex virus and lymphocytic choriomeningitis virus antibodies. RESULTS: Four of 95 patients examined at the home had chorioretinal scars, and two of these patients had normal T. gondii, rubella virus, cytomegalovirus, and herpes simplex virus titers and dramatically elevated titers for lymphocytic choriomeningitis virus. Three of 14 cases of chorioretinitis at the hospital had normal T. gondii, rubella virus, cytomegalovirus, and herpes sim-plex virus titers and elevated lymphocytic choriomeningitis virus antibody titers. (A fourth case, diagnosed in 1996, was reported 2 years ago.) CONCLUSIONS: Lymphocytic choriomeningitis virus was responsible for visual loss in two of four children secondary to chorioretinitis in a population of severely retarded children. The six new cases of lymphocytic choriomeningitis virus chorioretinitis identified in these two populations over the last 3 years, compared with the total number ever reported in the United States (10 cases), suggests that lymphocytic choriomeningitis virus may be a more common cause of congenital chorioretinitis than previously believed. Because its consequences for visual and psychomotor development are devastating, we conclude that the workup for congenital chorioretinitis should include lymphocytic choriomeningitis virus serology, especially if T. gondii, rubella virus, cytomegalovirus, and herpes simplex virus titers are negative.

Antibodies, Viral↗
PubMed1996

Choroidal neovascularization secondary to Candida albicans chorioretinitis.

PURPOSE: To study the clinical histories and courses of six patients with choroidal neovascularization secondary to endogenous Candida albicans chorioretinitis. METHODS: The medical records, fundus photographs, and fluorescein angiograms of six patients who developed C. albicans chorioretinitis secondary to candidemia and who subsequently developed choroidal neovascularization in one or both eyes were reviewed. RESULTS: The six patients ranged in age from 18 to 79 years. Four were women and two men; all but one showed evidence of bilateral chorioretinal scarring secondary to C. albicans chorioretinitis. All patients had been treated successfully with systemic antifungal therapy (amphotericin B). Two weeks to two years after the chorioretinitis, choroidal neovascularization developed in one eye (four cases) or both eyes (two cases). The neovascularization on initial examination was subfoveal in four eyes, extrafoveal in three eyes, and juxtafoveal in one eye. Laser photocoagulation was used in four of the eight involved eyes. In these cases, the active choroidal neovascularization was brought under control. In one eye, the patient had submacular surgery for excision of the choroidal neovascular membrane. Final visual acuities ranged from 20/20 to 20/200 in treated eyes and from 20/50 to 20/400 in untreated eyes. CONCLUSION: Choroidal neovascularization is a potential cause of late visual loss in patients who have had C. albicans sepsis and endogenous C. albicans chorioretinitis. Eyes that have chorioretinal scarring from C. albicans chorioretinitis should be watched for the development of choroidal neovascularization. Laser photocoagulation or perhaps surgical excision of the neovascular complex may be of benefit in selected cases.

Adolescent↗
PubMed1989

Herpes simplex virus type-1 strain influence on chorioretinal disease patterns following intracameral inoculation in Igh-1 disparate mice.

We have previously shown that the Igh-1 locus on chromosome 12 of the mouse influences contralateral disease patterns in the modified von-Szily model. Following intracameral injection with 1.5 X 10(4) PFU of HSV strain KOS (HSV-KOS), 75% of BALB/cByJ (Igh-1a), 30% of C.AL-20 (Igh-1d) and 5% of C.B-17 (Igh-1b) mice develop contralateral chorioretinal necrosis. In contrast, Igh-1 congenic mice do not develop contralateral chorioretinal necrosis following anterior chamber inoculation of the same dose of an HSV-KOS mutant lacking surface glycoprotein-C (HSV-GC-KOS). Similarly, injection of wild type HSV strain mP (HSV-mP) into the anterior chamber of susceptible BALB/cByJ mice induces destructive contralateral chorioretinitis whereas injection of the same dose of the mutant HSV strain MP (HSV-MP) lacking surface glycoprotein-C does not induce a destructive contralateral chorioretinitis. In addition, higher doses of HSV-mP inoculum abrogate the Igh-1-associated contralateral chorioretinal protection seen in C.B-17 mice; protection is restored in C.B-17 mice at lower HSV-mP doses that still cause contralateral chorioretinitis in BALB/cByJ mice. These data demonstrate the influence of the viral isolate on the modified von-Szily model and specifically the requirement for the presence of glycoprotein-C on the surface of HSV for the development of contralateral destructive chorioretinitis.

Animals↗
PubMed2003

Factors associated with the development of chorioretinal atrophy around choroidal neovascularization in pathologic myopia.

PURPOSE: To examine the influencing factors on the development of chorioretinal atrophy, which is the main cause of long-term visual decrease in myopic choroidal neovascularization (CNV), in a large series of highly myopic patients. METHODS: Sixty-five patients (81 eyes) with myopic CNV were studied retrospectively. The influence of the patient's age, refractive error, axial length, visual acuity at onset of CNV, size of CNV, and grade of myopic retinopathy on the extent of chorioretinal atrophy more than 3 years after CNV onset was investigated by means of multiple linear regression analysis. RESULTS: Seventy-seven of 81 eyes (95.1%) developed chorioretinal atrophy around myopic CNV during the follow-up period. Multiple linear regression revealed that age was the most influencing factor for the development of chorioretinal atrophy in all the subjects. When we divided the subjects into two groups according to their age, however, CNV size was the only factor to influence the development of chorioretinal atrophy in the patients younger than 40 years, whereas age was still the only influencing factor in those older than 40 years. CONCLUSIONS: The factors influencing the development of chorioretinal atrophy differ according to patient age. Local factors, such as CNV size, determine the tendency to develop chorioretinal atrophy in young patients. Systemic factors, such as patient age, play a greater part in older subjects.

Atrophy↗
PubMed1992

[Idiopathic and secondary chorioretinal folds].

Chorioretinal folds may be observed in many choroidal or retinal diseases. In age-related macular degeneration, they are usually associated with retraction of a neovascular membrane and a typically radial pattern of the folds can be seen. In this disease, pigment epithelium folds were recently described. Their clinical and angiographical characteristics are different from chorioretinal folds and the two diseases should not be confused. A 74-old patient presented, in the left eye, with sub foveal new vessels situated at the center of a pigment epithelial detachment (PED). Radial chorioretinal folds surrounded the PED, as frequently observed during follow-up in subretinal neovascular membranes. Nevertheless, right eye fundus examination revealed roughly horizontal, regular and parallel chorioretinal folds. Ultrasonography demonstrated characteristics of idiopathic chorioretinal folds: flattening and thickening of the posterior sclera and choroid. No sign of posterior scleritis was found. These ultrasonographic elements were observed in the left eye away from the central neovascular membrane. The chorioretinal folds therefore seemed to be idiopathic, in a hyperopic patient. The shape of the folds was modified in one eye by a subfoveal neovascular membrane. Chorioretinal folds may occur in different retinal diseases. The associations with many different aetiologies with modification of the shape of the folds, as described in this clinical case, should be emphasized.

Aged↗
PubMed2001

Effect of Fas and Fas ligand deficiency in resistance of C57BL/6 mice to HSV-1 keratitis and chorioretinitis.

PURPOSE: To investigate the effect of Fas and Fas ligand (FasL) deficiency on the development of herpes stromal keratitis and on the von Szily model of herpes retinitis in C57BL/6 mice, which are ordinarily resistant to development of both of these herpetic diseases. METHODS: Anterior chamber inoculation of the right eye of each mouse with various titers of HSV-1 (KOS strain) was performed. Both eyes of each mouse were enucleated on postinoculation day 15 and processed for histopathologic examination. HSV-1 was inoculated into one cornea of other mice, and the severity of stromal keratitis was scored. RESULTS: Contralateral destructive chorioretinitis developed in susceptible Balb/cByj mice (19/23); ipsilateral chorioretinitis did not occur (0/23). Stromal keratitis developed in susceptible C.AL-20 mice (15/16). None of the C57BL/6 (0/10 for keratitis or 0/20 for retinitis) developed inflammation. Neither did B6.SMN.C3H.gld (FasL deficient; 0/12 or 0/28) or B6.MRL.lpr (Fas deficient; 0/11 or 0/34) mice (keratitis or contralateral chorioretinitis). Minimal scattering of inflammatory cells in the contralateral retina but not destructive chorioretinitis was observed in two C57BL/6, three B6.SMN.C3H.gld, and five B6.MRL.lpr mice. Few inflammatory cells were also found in the ipsilateral vitreous and vitreoretinal interface (but not destructive chorioretinitis) of all C57BL/6, two gld, and three lpr mice. CONCLUSIONS: Immune dysregulation secondary to deficiency in Fas or FasL system does not influence the resistance of the C57BL/6 mice to develop herpes simplex keratitis or destructive herpes simplex chorioretinitis.

Animals↗
PubMed2003

Evaluation of vitrectomy specimens and chorioretinal biopsies in the diagnosis of primary intraocular lymphoma in patients with Masquerade syndrome.

PURPOSE: To correlate the histopathological diagnoses established by diagnostic vitrectomy and chorioretinal biopsy in patients with clinically suspected primary intraocular lymphoma (PIOL) or chronic idiopathic uveitis, and the clinical follow-up data. METHODS: Eighty-four consecutive pars plana vitrectomy (PPV) specimens, three chorioretinal biopsies and two enucleated eyes taken from 80 patients were evaluated. All PPV specimens were unfixed; these were centrifuged, the "cytospins" being stained conventionally (May-Grünwald-Giemsa) and using immunocytology (CD79a, CD3, CD68, immunoglobulin (Ig) light chains). An extended immunohistochemical panel, as well as polymerase chain reaction (PCR) for rearrangements of the Ig heavy chain gene (IgH-PCR), were used to investigate the chorioretinal biopsies and the enucleated eyes. Diagnoses, made on the basis of morphology and immunophenotype, included "reactive cellular infiltrate", "malignant lymphoma", "suspicious of neoplastic disease", and "insufficient for diagnosis". The corresponding clinical data were collected and compared with the diagnosis. RESULTS: The 80 patients consisted of 46 women and 34 men. The patients' age range varied from 21 to 100 years (mean age 62 years). Sixty-two (74%) of the 84 vitrectomy specimens were diagnosed as "reactive cellular infiltrate", 12 (14%) as definite "malignant lymphoma", 5 (6%) as "suspicious of neoplastic disease" and 5 (6%) specimens were considered "insufficient for diagnosis". An additional chorioretinal biopsy enabled an unequivocal diagnosis of PIOL to be reached in 3 patients. All PIOL were diffuse large cell B-cell lymphoma (DLBCL), with the immunophenotype CD79+, CD20+, BCL-2+, BCL-6+, MUM1+ and monotypical expression for IgM+. A monoclonal IgH-PCR amplification product was obtained in four vitrectomy specimens, two chorioretinal biopsies and one of the enucleated eyes. Comparison of the diagnoses with long-term follow-up clinical data resulted in concordance in 77 (96%) cases and discrepancies ("false-negative" diagnoses) in 3 patients (4%). The patients diagnosed with lymphoma were treated with either radiotherapy, chemotherapy or both. At final follow-up (mean 35 months), 5 patients (6%) had developed cerebral lymphomatous manifestation, and 7 (9%) had succumbed to their disease. CONCLUSION: The diagnosis of PIOL is often extremely difficult, requiring sufficient rapidly transported good-quality material, and experienced interpretation. Although cytological examination of vitreal aspirates remains the gold standard in diagnosis, examination of chorioretinal biopsies increase the reliability of diagnosing or excluding a PIOL that involves the retina or choroid. Most PIOL are DLBCL with an immunophenotype suggesting a cellular origin from germinal centre cells.

Adult↗
PubMedDate not supplied

Chorioretinal topography and histopathology in laser-induced choroidal neovascularization.

OBJECTIVE: To investigate the correspondence between topographic mapping of the vitreoretinal and chorioretinal surfaces in vivo and histopathology findings. MATERIALS AND METHODS: Choroidal neovascularization was induced in the retina of a primate by an argon laser. Serial optical section images of the retina were obtained using an optical imaging system based on the Retinal Thickness Analyzer. Topography of the vitreoretinal and chorioretinal surfaces was mapped. The animal was killed and the eyes enucleated for histopathologic examination. RESULTS: In the normal retina, the topography of the vitreoretinal surface showed a depression at the center of the fovea while the chorioretinal surface was relatively flat, corresponding to normal anatomy. In the retina with choroidal neovascularization, the topography of the vitreoretinal surface indicated a smooth elevation while there were irregular elevations in the topography of the chorioretinal surface. Histological sections displayed focal serous retinal detachment, metaplasia of retinal pigment epithelium, and choroidal neovascularization. CONCLUSION: Topographic mapping of the vitreoretinal and chorioretinal surfaces in vivo corresponds with histological findings and shows promise for quantitative evaluation of pathologic alterations caused by chorioretinal diseases.

Animals↗
PubMed2004

Chorioretinal involvement in patients with West Nile virus infection.

PURPOSE: To characterize and analyze the chorioretinal manifestations of West Nile virus (WNV) infection. DESIGN: Prospective, noncomparative case series. PARTICIPANTS: Twenty-nine consecutive patients with serologically confirmed WNV infection in the setting of an outbreak of the disease. METHODS: The average duration of systemic symptoms before ophthalmic examination was 10 days (range, 2-30 days). All participants underwent a detailed ophthalmic examination at presentation and regularly throughout follow-up, including dilated biomicroscopic fundus examination, fundus photography, and fluorescein angiography. RESULTS: A typical multifocal chorioretinitis was observed in 20 of 29 patients (69%) bilaterally at presentation and developed later during follow-up in 3 patients (10.3%), bilaterally (n = 1) or unilaterally (n = 2). Multifocal chorioretinitis was associated with mild vitreous inflammatory reaction in all cases. Other findings included intraretinal hemorrhages (21 patients [72.4%]), white-centered retinal hemorrhages (7 patients [24.1%]), focal retinal vascular sheathing (3 patients [10.4%]), marked diffuse retinal arterial sheathing (1 patient [3.4%]), retinal vascular leakage (5 patients [17.2%]), optic disc swelling (2 patients [6.9%]), optic disc staining (6 patients [20.7%]), segmental zones of retinal pigment epithelium changes (1 patient [3.4%]), and nonproliferative diabetic retinopathy (7 patients [24.1%]). The posterior segment findings related to WNV disease had a self-limited course in all patients. CONCLUSIONS: Chorioretinal involvement, frequently asymptomatic and self-limited, is common in patients with acute WNV infection. The unique pattern of multifocal chorioretinitis in patients with systemic symptoms suggestive of WNV can help to establish the diagnosis while serologic testing is pending. Therefore, a systematic ocular evaluation, including dilated fundus examination and fluorescein angiography in selected cases, is recommended in patients with clinically suspected WNV infection.

Adult↗
PubMed2006

Linear pattern of West Nile virus-associated chorioretinitis is related to retinal nerve fibres organization.

PURPOSE: To clarify the reason for the linear pattern of West Nile virus (WNV)-associated chorioretinitis. METHODS: The study included 12 patients (24 eyes) with WNV-associated chorioretinitis. All the patients underwent a complete ophthalmic evaluation, including dilated fundus examination, fundus photography, fluorescein angiography, and indocyanine green angiography. Characteristics of linear streaks, particularly their relationship to the course of retinal and choroidal vessels, and pattern of retinal nerve fibres, were analysed. RESULTS: All patients had bilateral multifocal chorioretinitis with linear clustering of chorioretinal lesions associated with a variable number of scattered lesions. Linear streaks, variable in number and length, originated from the optic disc or its vicinity in most cases. Their course in all cases appeared to closely follow the course of retinal nerve fibres, rather than that of retinal or choroidal vessels. CONCLUSIONS: Results of our study show that the linear pattern of WNV-associated chorioretinitis is related to retinal nerve fibres organization, suggesting a contiguous spread of WNV virus from central nerve system via the optic nerve fibres to the outer retina, retinal pigment epithelium, and choroid.

Adult↗
PubMed1989

Chorioretinal disease patterns in congenic mice following intraocular inoculation with HSV-1.

Disease patterns and immunologic parameters were studied employing inbred and Igh-1 disparate congenic mice to determine the role of host genetics and Igh-1-linked gene products in the von Szily model of viral chorioretinitis. Following intracameral inoculation of 1.5 x 10(4) PFU HSV-1 (KOS), 100% of BALB/c (Igh-1a), 62% of A/J (Igh-1e) and none of the C57BL/6J (Igh-1b) inbred mice developed contralateral necrotizing chorioretinitis. Multigenic differences between inbred mice prohibit conclusions about the specific role of Igh-1-linked immune regulation in this model. In order to more exactly define Igh-1-specific restriction of HSV-1-mediated chorioretinitis, Igh-1-disparate, congenic BALB/c mice were studied following both anterior chamber and intravitreal inoculation protocols. Anterior chamber inoculation resulted in contralateral retinal necrosis in 75% of BALB/c (Igh-1a) mice, 30% of C.AL-20 (Igh-1d) and 5% of the C.B-17 (Igh-1b) congenic mice; all strains showed ipsilateral retinal sparing. Following intravitreal inoculation of HSV-1 a similar restricted disease pattern was found in contralateral eyes. Contralateral chorioretinitis developed in 30% of BALB/c, 15% of C.AL-20 and 6% of C.B-17 mice. Ipsilateral disease, however, was found in all murine strains. These disease patterns developed despite equivalent suppression of systemic DTH and equivalent RPE permissivity to viral replication. These data demonstrate that host genetics strongly regulates contralateral HSV-1-mediated chorioretinal disease patterns by a mechanism unrelated to the development of systemic suppression of DTH and specifically support a dominant role for gene products linked to the Igh-1 locus in the immunomodulation of ocular disease.

Animals↗
PubMed2003

[Chorioretinal anastomosis as unfavourable prognostic factor during photodynamic therapy].

BACKGROUND: The aim of this study was the documentation of chorioretinal anastomosis in neovascular age-related macular degeneration (AMD) and correlation with functional and angiographic results following photodynamic therapy (PDT). METHOD: A total of 100 patients presenting with neovascular AMD and indication for PDT based on the presence of predominantly classic choroidal neovascularization (CNV), underwent ophthalmoscopic and angiographic screening for chorioretinal anastomosis. Conventional PDT using verteporfin was performed according to the recommended standard procedure. The pre- and post-treatment status at 3 and 6 months post-PDT in all patients and at 1 week in selected patients was documented with respect to the central visual acuity test (ETDRS), ophthalmoscopy as well as fluorescein (FA) and indocyanine green angiography (ICGA). RESULTS: A primary chorioretinal anastomosis was found in 6% ( n=12) of all eyes with CNV and classic PDT indication. Mean visual loss within the first 6 months after therapy was 3 lines indicating lack of visual stabilization according to the PDT study criteria.Furthermore, an increase in visual acuity could not be documented in any case. Angiography demonstrated continuous progression of CNV size although PDT had been uneventful. The characteristic initial occlusion of the CNV with homogeneous hypofluorescence was absent angiographically at 1 week post-PDT. The anastomosis was detected by ICGA in all eyes and by ophthalmoscopy or optical coherence tomography (OCT) in most eyes. DISCUSSION: Chorioretinal anastomosis is not a rare finding associated with predominantly classic CNV. The presence of anastomosis appears to be an unfavourable prognostic factor during PDT. If a chorioretinal shunt is suspected evaluation by ICGA and/or OCT should be performed and the indication for PDT should be rediscussed.

Aged↗
PubMed2002

Intentional complete interruption of a retinal vein after vitrectomy might improve the rate of successful chorioretinal venous anastomosis formation in central retinal vein occlusion.

BACKGROUND: Laser or surgical chorioretinal venous anastomosis has not become widespread as suitable treatment for central retinal vein occlusion (CRVO). We report here the effectiveness of cutting off a retinal vein with vitrectomy in making a chorioretinal venous anastomosis in CRVO. METHODS: We performed a vitrectomy accompanied by a chorioretinal venous anastomosis procedure for seven consecutive patients with CRVO. These patients had shown no improvement in their visual acuity in the month following their first visit to our hospital and had a visual acuity of less than 20/200. Their preoperative visual acuity ranged from counting fingers to 20/300. The procedure included the complete cutting of the affected retinal vein, and the making of a small incision at both sides of the vein interruption through the full thickness of the retina, the retinal pigment epithelium and Bruch's membrane. RESULTS: In five of the seven patients, successful chorioretinal venous anastomosis was observed. All five patients showed an improvement of two or more lines in visual acuity 6 months postoperatively. In three of the five, visual acuity was 20/100 or better. A postoperative complication of recurrent vitreous hemorrhage and fibrous proliferation was observed in one patient, and a second operation was necessary. CONCLUSIONS: Surgical interruption of an affected vein was a feasible procedure and could raise the rate of successful chorioretinal venous anastomosis in CRVO.

Aged↗