Intraretinal Hemorrhages Research Articles

Central retinal vein occlusion after liver transplantation

Editor, Central retinal vein occlusion (CRVO) is associated with various systemic abnormalities (McGrath et al. 1978). In organ recipients, however, CRVO has been reported only after heart or heart–lung transplantation (Keller & Linn 1990; Allinson et al. 1993). To our knowledge, this is the first report of CRVO in liver transplant (LT) recipients. From 1995 to 2006, 3656 organ transplantations were performed at Asan Medical Centre (1290 liver, 786 bone marrow, 1445 kidney and 135 heart transplants). Of these patients, 1205 were examined by the Department of Ophthalmology. The medical records of these 1205 patients were reviewed retrospectively. CRVO was diagnosed in five patients, all LT recipients (Table 1). Interestingly, one patient developed sequential CRVO in both eyes following two LTs (1, 2). Fundus photographs of both eyes of patient 4 at first presentation. Features of venous tortuosity, macular thickening and intraretinal haemorrhage were observed in all four quadrants of the fundus of the right eye. There were no specific focal lesions, except small atrophic areas nasal to the macula, in the left eye. (A) Fundus photographs of the same patient at second presentation. There was a new onset of venous tortuosity, cotton-wool spots, retinal haemorrhages and macular oedema with ischaemia in the left eye. (B) Fundus photographs and Fluorescein angrogram (FA) of both eyes 6 months later. Severe ischaemia and non-perfusion were observed in the left eye. CRVO developed 3–40 months (mean 15 months) after LT. Haematological examination showed alterations in blood coagulability secondary to hepatic failure, normalization of absolute platelet count, INR and activated partial thromboplastin time. Increases in factor VIII and activated protein C were observed in the patient with bilateral CRVO (patient 4). A mild increase in factor VIII (195%, reference value 60–120%) was also observed in patient 5. Among the six affected eyes of these five patients, four developed non-perfused CRVO and two developed perfused CRVO, with one of the latter converted to non-perfused CRVO during follow-up. Despite aggressive treatment, including laser photocoagulation, vitrectomy and glaucoma surgery, final visual acuity equal to or worse than 20/200 occurred in three of the six eyes. CRVO has been found to be a complication of heart and lung transplantations (Keller & Linn 1990; Allinson et al. 1993), with cardiopulmonary bypass during heart–lung transplantation associated with factors predisposing to CRVO development. Pulmonary thromboembolism and/or intracardiac thrombus formation have been reported during LT or immediately after graft reperfusion (Gologorsky et al. 2001; Lerner et al. 2005). Among the factors inherent to LT that may be related to these major intraoperative complications are excessive activation of the coagulation system secondary to injury to a large capillary bed, venous stasis during clamping of the portal vein and inferior vena cava, activators released from the grafted liver and massive blood transfusion (Gologorsky et al. 2001). It is unclear, however, why CRVO only developed several months to years after transplantation and exclusively in LT recipients, although CRVO may have been caused by hypertension and/or hyperlipidaemia secondary to the large amount and duration of immunosuppressive therapy administered to LT recipients. Although the absolute levels of serum lipids, including cholesterol, before LT were within reference values in four of our five patients, these serum lipid levels increased markedly after LT. These patients had also received more combination treatments, including prophylaxis for opportunistic infections, and large quantities of transfused blood during the immediate postoperative period. This may be especially applicable to the patient with bilateral CRVO, who was also the only patient treated with interferon α-2b because of chronic hepatitis C. In addition, LT may induce hypercoagulability or relative hypercoagulability, especially because these patients had experienced decreases in platelets and coagulation factors caused by liver failure. The patient with bilateral CRVO was thrombophilic, as evidenced by elevated factor VIII and activated protein C. Factor VIII tested immediately after the onset of CRVO in patient 5 increased slightly. Although her fibrinogen (345 mg/dl) and antithrombin III (96%) levels at the onset of CRVO were within normal limits, they were very low before LT (104 mg/dl and 9%, respectively). CRVO could occur during follow-up in LT recipients. It may be the main cause of morbidity of patients who showed general recovery after successful LT, warranting familiarity with this complication. It is important to determine the risk factors for the development of CRVO in LT recipients, as well as possible preventative measures.

Ocular involvement in paediatric haemolytic uraemic syndrome

The aim of this study was to estimate the frequency and severity of ocular involvement in paediatric patients with haemolytic uraemic syndrome (HUS). The study was designed as an institutional, retrospective, observational case series. Charts for all 87 paediatric patients with HUS treated at the University Children's Hospital Zurich between 1995 and 2007 were reviewed. Patients with ocular involvement were identified and clinical findings presented. Three of 69 examined patients with HUS showed ocular involvement. Ophthalmic findings in two children were consistent with bilateral Purtscher retinopathy, showing multiple haemorrhages, exudations and superficial retinal whitening. The third child presented with bilateral isolated central intraretinal haemorrhages as a milder form of ocular involvement. In one of the children with Purtscher retinopathy, laser photocoagulation was required for bilateral rubeosis irides and development of disc neovascularization. Longterm outcomes in the two severely affected children showed decreased visual acuity caused by partial atrophy of the optic nerves. In the milder case visual acuity was not impaired at any time. A minority of paediatric patients with HUS developed ocular involvement. Acute ocular findings varied in severity from isolated intraretinal haemorrhages to Purtscher-like retinopathy with retinal ischaemia. Longterm complications included the development of neovascularizations and consecutive optic nerve atrophy. Although ocular involvement in HUS seems to be rare, physicians should be aware of this complication because of its possible vision-endangering consequences.

Eales' disease: The great masquerader

Background Eales' disease, also known as idiopathic retinal periphlebitis, is a diagnosis of exclusion, mainly affecting men in the second through fourth decades of life. Although less common in the United States, Eales' disease is widespread in India and certain areas of the Middle East. Case Report A healthy, 42-year-old Filipino man presented with reduced vision in the right eye of 2 days' duration and had recently had a nonrhegmatogenous retinal detachment diagnosed. Clinical findings included angle neovascularization, posterior vitritis, intraretinal hemorrhages, and retinal vascular sheathing in that eye. Systemic evaluation did not disclose an underlying etiology. Eales' disease was diagnosed. Treatment included topical steroids and cycloplegia, along with intravitreal triamcinolone acetonide injection, which yielded an improvement in the vasculitis and vitritis with subsequent visual improvement and stabilization. Conclusion Eales' disease should be considered as a differential diagnosis in patients with vasculitis and vitritis.

Optical Coherence Tomographic Hyperreflective Foci: A Morphologic Sign of Lipid Extravasation in Diabetic Macular Edema

To analyze hyperreflective foci typically seen in diabetic macular edema (DME) in optical coherence tomography (OCT). Prospective clinical trial. Twelve consecutive patients with treatment-naïve, clinically significant DME. During a same-day examination, a standardized visual acuity assessment (Early Treatment of Diabetic Retinopathy Study protocol), infrared fundus imaging, color fundus photography, and biomicroscopy were performed. Additionally, all patients were scanned using Stratus, Cirrus, and Spectralis OCT and results correlated. Morphologic changes secondary to DME. In all eyes with DME, distinct hyperreflective foci distributed throughout all retinal layers were found in the OCT scans of all 3 OCT devices. These deposits could not be identified by infrared imaging, fundus photography, or biomicroscopy as long as they were not confluent. Accumulations of such foci at the border of the outer nuclear and in the outer plexiform layer were recognizable clinically as hard exudates showing the same hyperreflective features in OCT. The hyperreflectivity of these foci did not correspond with intraretinal hemorrhage, nor did the lesions cause the characteristic OCT laser beam scattering phenomena typically seen secondary to intraretinal bleedings or microaneurysms. Further, they were detected within the walls of intraretinal microaneurysms. Well-demarcated, hyperreflective foci were identified in the retina of patients with DME. The deposits were located within walls of intraretinal microaneurysms and scattered throughout all retinal layers, forming confluent plaques in the outer plexiform layer. It is suggested that the foci represent extravasated lipoproteins and/or proteins being a very early subclinical barrier breakdown sign in DME.

Retinal Angiomatous Proliferations: When Should We Suspect Them and How Should We Detect Them?

The aim of this study was to identify the clinical and angiographic features of retinal angiomatous proliferations (RAPs) in patients with age-related macular degeneration. 26 eyes of 24 patients with RAPs were retrospectively reviewed. All patients had colour and red-free photographs, and fluorescein (FA) and indocyanine-green angiography (ICGA). The biomicroscopic and angiographic characteristics were evaluated and video-angiograms were analysed for staging the RAPs. The total number of RAPs was 29. Stage 1 was present in 3/29, stage 2 in 3/29 and stage 3 in 23/29 with a chorio-retinal anastomosis identified in 21 of these 23 eyes. The total number of retinal vessels involved were 83, 35 were arteries and 48 were veins. RAPs were seen in ICGA as hot spots in all but one case where it appeared as a plaque. A retinal pigment epithelial detachment (PED) was observed in 22/26 eyes. Cystoid macular oedema was observed in 13/26 eyes in FA and intraretinal ICG leakage in 6/26 eyes. Hard exudates were present in 21/26 eyes. Retinal haemorrhages were present in 23/26 eyes; all but one were intraretinal and had a size of less than half of the optic disc diameter. The RAP was bilateral in 2/24 patients. Clinicians should suspect the diagnosis of RAP when hard exudates, small intraretinal haemorrhages, PED or a hot spot in ICGA are present. Both fluorescein and ICG video-angiography provide adequate temporal resolution and vascular flow examination leading to easier RAP staging and identification of the anastomosis.

Visual Disturbance as Initial Presentation of Hairy Cell Leukemia

Hairy cell leukemia (HCL) is a rare disorder that occasionally has visual symptoms after diagnosis. The authors present a case of HCL in which bilateral visual symptoms led to the initial diagnosis. Observational case report. Bilateral decreased vision to 20/30 in the right eye and 20/40 in the left due to intraretinal and preretinal hemorrhages with no other systemic signs or symptoms prompted a hematologic evaluation in which HCL was found to be the causative disorder in a previously healthy 41-year-old man. The authors present a rare case in which bilateral visual complaints led to the diagnosis of HCL. Thus, though uncommon, HCL should be considered in the differential diagnosis of otherwise unexplained retinal hemorrhages.

Outcome of Retinopathy in Chronic Hepatitis C Patients Treated with Peginterferon and Ribavirin

The purpose of this study is to evaluate the incidence and outcome of retinopathy in chronic hepatitis C patients treated with peginterferon and ribavirin. A total of 74 hepatitis C patients with baseline eye exams and eye exams during therapy were included. Retinopathy was defined as development of cotton wool spots and/or intra-retinal hemorrhage. Demographics, hepatitis C viral characteristics, treatment and laboratory data, and eye exam findings were compared in groups with and without retinopathy. Retinopathy developed in 28 (38%), early in therapy. Pre-treatment eye exams did not predict risk of retinopathy. Therapy was continued in all but one; cotton wool spots resolved in 24 of 26. All nine patients with intra-retinal hemorrhage had resolution. No patient had retinopathy-related visual deterioration. Retinopathy is common with peginterferon therapy, but the outcome is favorable. Cessation of therapy for retinopathy is not warranted. Severe visual disturbances and scotomas deserve further evaluation.

Gemcitabine‐induced retinopathy in a diabetic patient

Editor, Gemcitabicine, a nucleoside analogue, has been approved for the treatment of a variety of cancers (bladder, ovarian, pancreatic, etc). The major dose-limiting side-effect seems to be myelosuppression (Noble & Goa 1997). We report the case of a 58-year-old white man suffering from a bladder carcinoma who developed a retinal microangiopathy after being treated with gemcitabine (Gemzar®, Lilly, France). The patient was given a combination of gemcitabine and a platinium salt after surgical management from March to June 2006 with good response. Past medical history included insulin-dependent diabetes and hypertension, which were well controlled. In July 2006, visual acuity decreased to 20/40 in both eyes after four cycles of chemotherapy. Dilated fundus examination showed mild retinal oedema associated with cotton-wool spots and haemorrhages in both eyes (Fig. 1A). Fluorescein angiogram demonstrated microaneurysms, and capillary vascular leakage (Fig. 1D). Optical coherence tomography (OCT) revealed thickening of the macula [right eye (OD) = 319 μm; left eye (OS) = 282 μm] and of the retinal nerve fibre layer (RNFL) of both eyes (OD = 133.48 μm; OS = 126.31 μm) (not shown). Retinopathy induced by chemotherapy was diagnosed. Gemtabicine was discontinued and carboplatine was maintained. Gemcitabine-induced retinopathy of the right eyes after four cycles of chemotherapy with cotton-wool spots, intraretinal haemorrhages and microaneurysms (A) and capillary vascular leakage at late phase of fluorescein angiogram (D). One month after discontinuation of gemcitabine, cotton-wool spots and haemorrhages have mostly reabsorbed (B). Late phase of fluorescein angiogram showed persistence of microaneurysms and resolution of vascular leakage (E). Retinopathy reappeared one month after re-exposure to gemcitabine with cotton-wool spots, intraretinal haemorrhages (C) and capillary vascular leakage (F). In August 2006, visual acuity improved to 20/25 OD and 20/30 OS. Fluorescein angiogram showed resolution of vascular leakage and persistence of microaneurysms (Fig. 1E). Macular and RNFL thickness decreased on OCT. A follow-up retinal examination in September showed that retinopathy had improved and cotton-wool spots and haemorrhages had mostly reabsorbed (Fig. 1B). The patient remained asymptomatic and was monitored every 4 weeks until his bladder cancer relapsed in February 2007. Reintroduction of gemcitabine was attempted. One month later, retinopathy appeared with cotton-wool spots, intraretinal haemorrhages (Fig. 1C) and mild vascular leakage on fluorescein angiogram without change in visual acuity (Fig. 1F). Discontinuation of gemcitabine was decided and the patient died 4 months later. Retinal changes found in this case included aneurysms, cotton-wool spots, intraretinal haemorrhages and vascular leakage on fluorescein angiogram. Clinical improvement after gemcitabine withdrawal and relapse of retinopathy from re-exposure to the drug strongly suggest gemtabicine to be causative for the retinopathy. The retinopathy occurs within 1 month at reintroduction of gemcitabine and may be asymptomatic. Our patient presented decreased vision caused by macular involvement (haemorrhages, oedema) after four cycles of chemotherapy when he was first treated, and retinopathy appeared without vision change when gemcitabine was reintroduced. The prognosis is good with resolution of retinal changes after gemcitabine discontinuation. Banach & Williams first reported a Purtscher retinopathy and necrotizing vasculitis after gemcitabine therapy in a diabetic patient. This retinopathy was associated with digital necrosis, ESR and antinuclear antibody elevation (Banach & Williams 2000). In our patient, diabetes and hypertension may be the risk factors to develop gemcitabine-induced retinopathy. The direct drug-induced endothelial damage suggested by some authors (Moake 2002) may be the pathogenic mechanism, leading to retinal capillary changes including capillary dilatation and capillary closure. Exudative phenomena resulting from retinal vascular incompetence may occur, as in our case. Damage to mitotically active endothelial cells eventually leads to occlusive vascular disease (Archer et al. 1995), causing necrotizing retinopathy, as reported previously (Banach & Williams 2000). Carboplatine is known to cause optic neuritis (Caraceni et al. 1997), and might not be responsible for the retinopathy because improvement was observed when the treatment was maintained. However, the possibility that carboplatine combination is pathogenic for the development of this retinopathy cannot be excluded completely. To the best of our knowledge, this is the first report of gemcitabine-induced retinal microangiopathy with causative evidence. This case highlights the need for fundus examination during gemcitabine therapy, especially in patients with diabetes and hypertension. Early diagnosis and careful follow-up are recommended in order to avoid progression to irreversible changes.

PURTSCHER-LIKE RETINOPATHY ASSOCIATED WITH PRIMARY HYPEREOSINOPHILIC SYNDROME

To describe a patient with undiagnosed primary hypereosinophilic syndrome (HES) who presented with Purtscher-like retinopathy and to review the literature. Observational case report. A 25-year-old man presented with a 1-week history of bilateral visual blur. Examination revealed multiple peripapillary cotton-wool spots and few intraretinal hemorrhages. Clinical history was obtained and fluorescein angiography, systemic evaluation, laboratory studies, and histopathologic analysis of a bone marrow biopsy specimen were performed. The patient was diagnosed with primary HES. No previous description was found in the literature. HES should be considered in the differential diagnosis of Purtscher retinopathy. This case supports the microembolic theory of Purtscher retinopathy.

Bilateral periorbital ecchymosis in a case with dengue fever

Dear Editor, Dengue is caused by one of four closely related, but antigenically distinct, virus serotypes of the genus Flavivirus and spreads by Aedes aegypti, a domestic, day-biting mosquito that prefers to feed on humans.[1] Infections produce a spectrum of clinical illness ranging from a nonspecific viral syndrome to severe and fatal hemorrhagic disease resulting from increased vascular permeability and decreased platelet count.[1] Varying ocular findings in dengue, though rare are known,[24] petechial hemorrhages in conjunctiva being the commonest.[2] Maculopathy is another common manifestation.[5] We hereby, report a case of bilateral periorbital ecchymosis in a case of dengue hemorrhagic fever. A 22-year-old male patient admitted with the diagnosis of dengue hemorrhagic fever was referred from the medicine department of our hospital with complaints of bilateral periorbital swelling and bruising of one-day duration. There was no history of any blunt trauma to the orbit or the head. On examination, both the eyes had periorbital ecchymosis significantly worse in the right eye [Fig. 1]. Both the ocular globes were normal with no restriction of motility and a visual acuity of 20/20 in both eyes. Pupils were reactive to light in both eyes with no relative afferent pupillary defect. Intraocular pressure was 18 mm Hg in both eyes as measured by applanation tonometry. A dilated fundus examination revealed normal fundus with no evidence of hemorrhages or exudates. There was no evidence of ecchymosis elsewhere in the body. Complete blood counts of patient showed a significantly reduced platelet count of 16000/μL (normal range 150000 – 400000/μL). The diagnosis of dengue fever was confirmed by the detection of dengue IgM antibodies.Figure 1: Bilateral periorbital ecchymosis in a patient with dengue feverThe patient received six units of platelet concentrate and supportive therapy was given in the form of antipyretics and volume replacement. No specific treatment was added from the ophthalmic point of view. He was followed up after one week, and there was no change in the periorbital ecchymosis. Platelet count was 28000/μL at this point. Subsequently the patient was lost to follow-up. Dengue fever is considered to be rarely associated with ocular manifestations. The onset of symptoms appears to coincide with the resolution of fever and the nadir of thrombocytopenia.[6] Reported ocular manifestations of dengue fever include subconjunctival hemorrhage, vitreous hemorrhage, choroidal effusions, relative central scotoma, intraretinal hemorrhages, Roth spots, cotton-wool spots, retinal edema, blurring of the optic disk and maculopathy. Platelet count less than 50000/μL predisposes to ocular hemorrhages.[2] Nevertheless, periorbital ecchymosis has not been described as part of the clinical spectrum of dengue fever or any other viral fever. As it occurred with a significantly low platelet count, it appears to be related to thrombocytopenia. Patients with dengue fever who report visual symptoms should be evaluated promptly. Although there is no specific therapy, retinal hemorrhage may be an indication for early and aggressive correction of thrombocytopenia. Ocular alterations in dengue are usually self-limiting. Most of the findings resolve without specific treatment, but occasionally visual recovery may be prolonged or vision may remain permanently impaired in patients with a severe maculopathy.[4] To the best of our knowledge this is the first reported case of bilateral periorbital ecchymosis in a case of dengue hemorrhagic fever.

Macular ischemia associated with imatinib mesylate therapy for chronic myeloid leukemia.

Imatinib mesylate (Gleevec, East Hanover, NJ) is a drug approved for the treatment of patients with Philadelphia chromosome-positive chronic myeloid leukemia (CML) or Kit-positive gastrointestinal stromal tumors. A case of ischemic maculopathy associated with imatinib mesylate therapy is reported. A 62-year-old woman with a 16-year history of CML was treated with imatinib mesylate, initially at a daily dose of 400 mg that was decreased to 300 mg due to systemic side effects. Several weeks after beginning imatinib mesylate therapy, she developed blurred vision (greater in the left eye than in the right eye). Fundus examination of both eyes revealed retinal telangiectasia with intraretinal hemorrhages and perifoveal retinal telangiectasia. Fluorescein angiography showed macular ischemia (greater in the left eye than in the right eye). Late perifoveal leakage was present surrounding the macular ischemic zone. Visual acuity was reduced to 20/30 in the right eye and 20/100 in the left eye, which did not improve over 10 months of follow-up. Imatinib mesylate may be associated with ischemic maculopathy that can severely compromise vision. It may be necessary for patients receiving this therapy to be monitored for associated visual symptoms and funduscopic abnormalities.

RETINAL NEOVASCULARIZATION ASSOCIATED WITH A RETINAL ARTERIAL MACROANEURYSM

This case report describes an uncommon presence of a retinal arterial macroaneurysm complicated by retinal neovascularization. This is a case history of a 49-year-old woman presenting with preretinal, intraretinal, and subretinal hemorrhage with an adjacent retinal arterial macroaneurysm complicated by the development of retinal neovascularization. The neovascularization, intraretinal lipid, and retinal and preretinal hemorrhage resolved after laser photocoagulation, topical steroids, and nonsteroidal antiinflammatory agent treatment. The rapid development of a large frond of neovascularization is atypical for retinal arterial macular aneurysms and has not been previously reported.

Chronic Retinal Detachment with Secondary Retinal Macrocyst and Peripheral Neovascularization

Purpose: To report the association of a retinal macrocyst with peripheral retinal neovascularization that occurred secondary to a chronic, subclinical rhegmatogenous retinal detachment and to illustrate the utility of wide-field fundus photography. Methods: Case Report Results: A 37 year-old male was diagnosed with chronic retinal detachment on routine eye examination. Further evaluation revealed intraretinal hemorrhages and a retinal macrocyst. Diagnosis was confirmed with wide-field fundus photography and fluorescein angiography. Surgery was recommended to repair the retinal detachment, to allow spontaneous resolution of the macrocyst. Conclusion: Chronic, subclinical retinal detachments may rarely be associated with retinal macrocysts and retinal neovascularization. This altered retinal morphology can be delineated on wide-field fundus imaging, which aids in diagnosis and management.

Ischaemic change after intravitreal bevacizumab (Avastin®) injection for macular oedema secondary to non‐ischaemic central retinal vein occlusion

Editor, A 65-year-old male patient with a 12-year history of diabetes presented with decreased visual acuity in his right eye of 3 months duration. Best-corrected visual acuity (BCVA) was 0.4 in the right eye (RE) and 1.0 in the left eye (LE). A slit-lamp examination showed grade two bilateral nucleosclerosis with no further abnormalities of the anterior segment. Fundus examination and fluorescein angiography showed flame-shaped retinal haemorrhages in four quadrants and optocillary shunt vessels. These ocular findings were consistent with non-ischaemic central retinal vein occlusion (CRVO). Optical coherence tomography (OCT) showed submacular fluid and macular elevation with a central macular thickness of 533 μm in the RE (Fig. 1). An intravitreal off-label bevacizumab injection was recommended. The patient was informed about the treatment beforehand and provided written informed consent. The injection was performed in a sterile setting and prophylactic topical antibiotics and carbonic anhydrase inhibitor were given for 1 week pre- and post-injection. The intravitreal dosage of bevacizumab was 1.25 mg (0.05 ml). Repeat examinations of visual acuity, intraocular pressure and fundus examinations were scheduled at 1 day, 1 week and 1 month after injection. Three weeks after injection, the patient reported a deterioration of visual acuity in the RE. His visual acuity in the RE was 0.02 and a fundus examination showed disc oedema with extensive flame-shaped retinal haemorrhages in the four retinal quadrants (Fig. 2). A fluorescein angiogram of the RE demonstrated severe non-perfusion including the fovea with blocked hypofluorescence. OCT imaging showed a central macular thickness of 560 μm (Fig. 2). Six months after the injection, his visual acuity in the RE was 0.02 and panretinal photocoagulation was performed. Fundus photography (A), fluorescein angiography (B) and optical coherence tomography (OCT) (C) images at initial presentation. (A) Fundus photograph showing multiple intraretinal haemorrhages and dilated retinal veins with optociliary shunt vessels. (B) Fluorescein angiograph in the late phase showing blocked hypofluorescence with patelloid pattern of dye leakage in the fovea in the right eye. (C) A vertical OCT image of the right eye showing cystoid macular oedema with a central macular thickness of 533 μm. Fundus photography (A), fluorescein angiography (B) and optical coherence tomography (OCT) (C) images 3 weeks after intravitreal bevacizumab administration. (A) Fundus photograph showing extensive flame-shaped retinal haemorrhages and disc swelling. (B) Fluorescein angiograph in the late phase showing severe non-perfusion and dye leakage at the optic disc. (C) Vertical OCT image showing subretinal fluid with a central macular thickness of 560 μm. Bevacizumab represents a new treatment option for early intervention against the formation of macular oedema in various disease conditions. Several short-term results have been published on intravitreal bevacizumab for macular oedema secondary to retinal vein occlusion with CRVO (Iturralde et al. 2006; Spandau et al. 2006; Pai et al. 2007). These reports suggest that intravitreal bevacizumab may reduce macular oedema and increase visual acuity in CRVO. But because a physiological level of vascular endothelial growth factor (VEGF) may be necessary for retinal homeostasis, precautions may have to be taken to avoid the possible negative effects of a complete blockade of VEGF, particularly in primarily ischaemic diseases. However, no report has been issued regarding complications associated with intravitreal bevacizumab except for endophthalmitis. Here, we present a case of non-ischaemic CRVO conversion to ischaemic CRVO after injecting bevacizumab intravitreally. The formation of a new blood flow balance is presumably supported by the formation of collateral vessels with a new drainage route. Spandau et al. (2006) suggested the possibility of complete blockage of VEGF by intravitreal bevacizumab. Although 11–34% of non-ischaemic CRVO cases convert to ischaemic CRVO over a natural course of 3–5 years, we suggest that intravitreal bevacizumab injection affected the outcome in this case (TCVOS 1997). This is because ischaemic CRVO occurred 3 weeks after the injection, when bevacizumab has its peak effect and relatively good initial visual acuity and perfusion status. There were no other patient factors that might cause the ischaemic conversion of CRVO except diabetes. The causes and mechanisms of treatment failure associated with bevacizumab administration must be elucidated further in vitro and by clinical studies. Furthermore, the possibility that bevacizumab has a negative long-term effect on collateral vessel formation because of its anti-VEGF action requires investigation.

Risk Factors for Retinal Hemorrhage after Photodynamic Therapy in Age-Related Macular Degeneration

Background: Subretinal or intraretinal hemorrhage may occur after photodynamic therapy (PDT). However, risk factors for post-PDT hemorrhage have not yet been investigated. Methods: We reviewed the medical records of patients who had undergone PDT for subfoveal choroidal neovascularization secondary to age-related macular degeneration. Primary outcomes were the occurrences of hemorrhages at 2 and 12 weeks after PDT. To identify the risk factors of hemorrhages after treatment, ocular and systemic factors were investigated. The secondary outcome was visual acuity. Results: Ninety-two eyes from 92 patients were analyzed. New hemorrhages developed in 9 (9.8%) within 2 weeks and in 8 (8.3%) between 2 and 12 weeks after PDT. Hypertension [odds ratio (OR) 356.9, 95% confidence interval (CI) 3.7–34,487.1], minimally classic lesion (OR 53.4, 95% CI 2–1,429) and advanced age (OR 1.2, 95% CI 1–1.5) were related to hemorrhagic events within 2 weeks after PDT. A tendency toward recurrent hemorrhage was noted after repeat treatments (p < 0.05). Forty-four percent of the patients with a hemorrhagic event within 2 weeks after PDT experienced decreased vision. Conclusion: Hypertension, minimally classic lesion, advanced age and a previous hemorrhagic event were associated with the development of hemorrhage within 2 weeks after PDT.

Secondary vasoproliferative retinal tumor associated with Usher syndrome type 1

Vasoproliferative retinal tumors are benign tumors of unknown origin that generally affect healthy persons between their fourth and sixth decades and may lead to severe vision loss as a result of intraretinal hemorrhages and exudates. They must be differentiated from retinal capillary hemangiomas of von Hippel-Lindau disease, retinal astrocytoma, Coats disease, peripheral exudative hemorrhagic chorioretinopathy, choroidal melanomas, and retinal/choroidal metastasis. We describe a case of unilateral vasoproliferative retinal tumor associated with retinitis pigmentosa in a patient with Usher syndrome type 1.

Prospective Study of Intravitreal Ranibizumab as a Treatment for Decreased Visual Acuity Secondary to Central Retinal Vein Occlusion

To evaluate intravitreal injection of ranibizumab as a potential treatment for decreased visual acuity (VA) secondary to central retinal vein occlusion (CRVO). Prospective, interventional case series. Patients with CRVO prospectively recruited from a practice were administered intravitreal ranibizumab 0.5 mg (Lucentis; Genentech Inc, South San Francisco, California, USA) at baseline and monthly for two additional doses. The patients were given additional ranibizumab if they had macular edema as determined by optical coherence tomography or any new intraretinal hemorrhage. Patients were evaluated for number of required injections, side effects, changes in VA, and macular thickness. There were 20 eyes of 20 patients who at baseline had a mean age of 72.1 years, a mean VA of 45.8 Early Treatment of Diabetic Retinopathy letters, and a mean central macular thickness of 574.6 microm. Of the 20 eyes, five previously had received intravitreal triamcinolone and 11 had received intravitreal bevacizumab (Avastin; Genentech Inc). At 12 months of follow-up, the mean VA improved to 64.3 letters and the central macular thickness decreased to 186 microm (both different than baseline values; P < .001) using a mean of 8.5 injections. The change in macular thickness was not correlated with the change in VA. In one patient with a history of transient ischemic attack, an ischemic stroke developed but no sequela resulted. In another patient, vitreomacular traction developed, but the patient had improved acuity as compared with baseline. There were no infections, retinal tears, or detachments. Intravitreal ranibizumab used over a period of one year improved mean VA, with low rates of adverse events, in patients with CRVO.

Combined therapy for retinal angiomatous proliferation with intravitreal triamcinolone and argon laser photocoagulation

The occurrence of retinal neovascularisation at the macula in age-related macular degeneration (AMD) was described by Hartnett et al.1 Yannuzzi et al coined the term “retinal angiomatous proliferation” (RAP) to...

Comparison of diabetic retinopathy phenotype between Latinos and Blacks

Objective The objective of this study was to delineate the difference in the phenotype of diabetic retinopathy (DR) in Latinos versus Blacks using characteristics shown on fundus photography (FP) and fluorescein angiography (FA). Research Design and Methods This was a retrospective chart review of 203 adult Black and Latino diabetic patients from the King–Drew Medical Center eye clinic from January 1998 to March 2005. Systemic risk factors such as HbA 1c and kidney function data were collected. FP and FA were analyzed and graded according to Early Treatment of Diabetic Retinopathy Study criteria. Statistical analysis was performed to determine whether a given lesion type was more characteristic of a particular racial group. Results Gender, age, median microalbumin-to-creatinine ratio (ACR), and average HbA 1c values were not significantly different between the groups. The presence of clinically significant macular edema (CSME), focal or diffuse, was very high in both groups (44% in Latinos and 46% in Blacks), and the overall DR grades were similar. However, upon individual lesion analysis, the Latinos were noted to have more prevalent intraretinal hemorrhages involving a greater area of the retina ( P=.046). Conclusions Although Latinos and Blacks of comparable age and glycemic control are equally at risk for CSME and proliferative retinopathy, Latinos may be at greater risk for a specific phenotype of DR characterized by extravasation of intraretinal hemorrhages, which is associated with poor prognosis. Further prospective studies may uncover racial differences that may have implications for prognosis and therapy.

Clinical features of hypoperfusion retinopathy induced neovascular glaucoma

To analyze the clinical features of hypoperfusion retinopathy induced neovascular glaucoma This retrospective case series included 18 cases (18 eyes) with hypoperfusion retinopathy induced neovascular glaucoma Among them, there were 15 male and 3 female; 10 right eye and 5 left eye. The average age was 40-year-old (ranged from 18- to 78-year-old). Visual acuity and fundus were examined using fundus fluorescein angiography (FFA), Color Doppler Flow Imaging (CDFI), magnetic resonance angiography (MRA), and Digital subtraction angiography (DSA) etc in all patients. The visual acuity was ranged from light perception to 0. 8 in all patients. The clinical features in hypoperfusion retinopathy induced neovascular glaucoma were characterized by midperipheral intraretinal hemorrhages, narrowed retinal arteries, dilated retinal veins, neovascularisation in iris and anterior chamber angle, ocular hypertension, excavation and atrophy of optic disk, and visual field defects when glaucoma progressed. All eyes have either ipsilateral common carotid artery obstruction or severe bilateral obstruction of the internal carotid arteries. Neovascular glaucoma is a rare and severe complication of hypoperfusion retinopathy associated with either ipsilateral common carotid artery obstruction or severe bilateral obstruction of the internal carotid arteries. Fundus degeneration is commonly involved in one eye. The characteristic clinical features are presented during the process of the disease.