The vasculature of the retina is exposed to systemic and local factors that have the capacity to induce several retinal vascular diseases, each of which may lead to vision loss. Prostaglandin signaling has arisen as a potential therapeutic target for several of these diseases due to the diverse manners in which these lipid mediators may affect retinal blood vessel function. Previous reports and clinical practices have investigated cyclooxygenase (COX) inhibition by nonsteroidal anti-inflammatory drugs (NSAIDs) to address retinal diseases with varying degrees of success; however, targeting individual prostanoids or their distinct receptors affords more signaling specificity and poses strong potential for therapeutic development. This review offers a comprehensive view of prostanoid signaling involved in five key retinal vascular diseases: retinopathy of prematurity, diabetic retinopathy, age-related macular degeneration, retinal occlusive diseases, and uveitis. Mechanistic and clinical studies of these lipid mediators provide an outlook for therapeutic development with the potential to reduce vision loss in each of these conditions.

The medical condition referred to as \"central retinal artery occlusion\" (CRAO) was first documented by Albrecht von Graefe in 1859. Subsequently, CRAO has consistently been identified as a serious medical condition that leads to substantial visual impairment. Furthermore, it is correlated with vascular complications that have the potential to affect crucial organs such as the brain and heart. A considerable amount of research has been extensively published on the various aspects of this topic, which is marked by notable debates and misconceptions, especially regarding its management and outcomes. The primary aim of this review article is to analyze the latest developments in the understanding of CRAO, which includes its causes, techniques for retinal imaging, systemic evaluation, and therapeutic strategies, such as vitrectomy. This review article offers readers a comprehensive learning experience to gain knowledge on the fundamental principles and recent advancements in CRAO.

This case series discusses the presentation, etiologies, and management of retinal artery occlusions in three patients. The first case was diagnosed as right eye central retinal artery occlusion (CRAO) secondary to a hypercoagulable state as the patient had been newly diagnosed with chronic myeloid leukemia. The second case had right branch retinal artery occlusion (RAO) secondary to a thromboembolic event following a percutaneous transluminal coronary angioplasty procedure. The third case involved a right eye CRAO secondary to vasospastic syndrome. The first case had good visual recovery as the patient presented to us within four hours of the onset. In contrast, the second and third cases presented after seven to eight hours, resulting in poor visual recovery. Though several measures have been devised to reverse the occlusion, the final visual prognosis still depends on the degree of occlusion and the time of presentation, as late presentation is usually associated with irreversible visual loss. Detection of RAO may require a multidisciplinary team approach, and proper and timely management may reverse the ischemic state of the retina.

UNASSIGNED: Central retinal artery occlusion (CRAO) presents suddenly causing painless loss of vision that is often significant. Meaningful improvement in vision occurs in only 8% of patients with spontaneous reperfusion. Hyperbaric oxygen treatment (HBOT) is considered to be of benefit if commenced before retinal infarction occurs. The Undersea and Hyperbaric Medical Society (UHMS) guidelines on the management of CRAO were last amended in 2019. This survey questioned Australian and New Zealand (ANZ) hyperbaric medicine units (HMUs) about the incidence of CRAO cases referred and compared their subsequent management against the UHMS guidelines.
UNASSIGNED: An anonymous survey via SurveyMonkey® was sent to all 12 ANZ HMUs that treat emergency indications, allowing for multiple choice and free text answers regarding their management of CRAO.
UNASSIGNED: One-hundred and forty-six cases of CRAO were treated in ANZ HMUs over the last five years. Most (101/146) cases (69%) were initially treated at a pressure of 284 kPa. This was the area of greatest difference noted in CRAO management between the UHMS guidelines and ANZ practice.
UNASSIGNED: Few ANZ HMUs strictly followed the UHMS guidelines. We suggest a more simplified management protocol as used by the majority of ANZ HMUs.

OBJECTIVE: To report a fatal case of Susac syndrome in a congenitally deaf patient with a cochlear implant and a history of migraines, emphasizing the diagnostic challenges in patients with preexisting conditions.
METHODS: A 33-year-old male with congenital hearing loss, a cochlear implant, and chronic migraines who presented with mild subacute auditory disturbance and headaches that later progressed to severe encephalopathy.
METHODS: Explantation of a non-magnetic resonance imaging (MRI) compatible cochlear implant followed by MRI, fundoscopy, and the administration of immunosuppressive medications.
METHODS: Diagnosis was confirmed by characteristic MRI appearance and the presence of a hemi-retinal artery occlusion.
RESULTS: After weeks of immunosuppressive treatment, the patient died of a global cerebral ischemic event of unknown origin.
CONCLUSIONS: For patients with preexisting sensorineural hearing loss and cochlear implants, Susac syndrome poses a diagnostic challenge. Auditory disturbances in the absence of cochlear implant failure should prompt further evaluation for visual disturbances and encephalopathy. MRI and fundoscopy should be performed to detect other features of the disease.

OBJECTIVE: To understand the etiology, work-up, and secondary systemic and ocular events of retinal artery occlusion (RAO) in young patients (≤ 45 years old) without typical cardiovascular risk factors.
METHODS: Retrospective longitudinal case series of 18 young patients with RAO and without typical cardiovascular risk factors evaluated at the University of Michigan Medicine Health System between the year 2000 and 2022. Laboratory and imaging studies performed at the time of RAO diagnosis, along with systemic and ocular events during follow-up, were recorded. These data were combined with data from a literature review of 74 similar patients experiencing a RAO.
RESULTS: Fifteen (83%) of patients were female and 10 (56%) suffered a branch retinal artery occlusion (BRAO). 56% of patients had one risk factor associated with cryptogenic stroke, most commonly a migraine history (33%). The most frequent etiology of RAO was vasculitis (28%), followed by idiopathic (22%) and patent foramen ovale (PFO, 17%). Three out of four patients with idiopathic RAOs developed new migraines around the time of RAO diagnosis, whereas none of the patients with a clear etiology had new onset migraines (n = 14). No patients suffered a stroke or myocardial infarction (MI) in the follow-up period (average 3.6 years ± 3.2 years). Two patients (11%) suffered a repeat RAO, both of whom were diagnosed with a vasculitis. Patients with isolated retinal vasculitis required repeat fluorescein angiograms for up to 2 years after the initial event to definitively identify the vasculitic etiology of the RAO. When our data are pooled with similarly healthy patients from previously published RAO series, structural/functional cardiac abnormalities and vasculitides are the most common identifiable etiologies for RAOs in this group.
CONCLUSIONS: The most common identifiable etiologies of RAO in young patients with low cardiovascular risk are structural/functional cardiac abnormalities and vasculitides, with a small range of additional causes/associations accounting for remaining cases. We suggest a focused work-up algorithm to rapidly identify etiologies in this group while minimizing unnecessary testing. The long-term risk of systemic or ocular secondary events in these patients is low regardless of the etiology of their RAO.

OBJECTIVE: To investigate the recurrent non-arteritic retinal artery occlusion (RAO) in the same or opposite eye.
METHODS: We searched the RAO registry at Seoul National University Bundang Hospital and included patients with recurrent RAO in the present study. Ophthalmic and systemic features were analysed to identify risk factors and visual outcomes.
RESULTS: Of the 850 patients in the non-arteritic RAO cohort, 11 (1.3%) experienced a second RAO recurrence, either in the same (5 patients; 0.6%) or opposite (6 patients; 0.7%) eye. The same eye group experienced an earlier recurrence (1-2 months, median 1 month) than the opposite eye group, where the time to recurrence was notably longer (8-66 months, median 22 months). Best corrected visual acuity (BCVA) in the same eye group decreased after the recurrence of RAO. In the same eye group, initial BCVA ranged from 20/200 to counting fingers (CF), while BCVA during RAO recurrence ranged from CF to hand motion. When RAO recurred in the opposite eye, the reduction in visual acuity was less severe than the reduction of the initial episode: initial episode ranged from 20/400 to light perception and recurrent episode ranged from 20/25 to 20/400. Patients exhibited varying degrees of carotid (81.8%) and cerebral (9.1%) artery occlusions. Additionally, one patient in each group (total 2 patients, 18.2%) experienced a stroke 6 months after RAO recurrence.
CONCLUSIONS: Since the RAO recurrences could lead to devastating visual impairment, it is essential to emphasise the importance of risk factor screening to patients while collaborating with neurologists and cardiologists.

To evaluate the predictive and prognostic value of fibroblast growth factor 21 (FGF21) levels in retinal artery occlusion (RAO) patients. In this case-control study, serum FGF21 levels were detected by using the ELISA method. Multivariable logistic regression analyses were performed to evaluate the significance of FGF21 in assessing the risk of developing RAO and its impact on vision and concurrent ischemic stroke. Compared with control group, serum FGF21 levels were significantly higher (median [IQR] = 230.90[167.40,332.20] pg/ml) in RAO patients. Multivariate logistic regression analysis showed that elevated serum FGF21 levels were associated with a higher risk of RAO occurrence (P = 0.025, OR [95%CI] = 9.672 [2.573, 36.359]) after adjustment for multiple confounding factors. Higher serum FGF21 levels were negatively associated with visual acuity improvement (P = 0.029, OR [95%CI] = 0.466[0.235, 0.925]) and positively correlated with concurrent ischemic stroke (P = 0.04, OR [95% CI] = 1.944[1.029, 3.672]) in RAO patients. Elevated serum FGF21 levels could promote the development of RAO and indicate worse visual prognosis and increase the risk of concurrent ischemic stroke, which might help clinicians early diagnose and treat RAO patients.

UNASSIGNED: Eosinophils have widespread procoagulant effects. In daily practice, eosinophil-related cardiovascular toxicity consists of endomyocardial damage, eosinophilic vasculitis and arterial or venous thrombosis. Here we aim to report on the clinical features and treatment outcomes of patients with unexplained ophthalmic vascular manifestations and eosinophilia.
UNASSIGNED: We conducted a retrospective, multicenter, observational study and a literature review of patients with eosinophilia (≥0.5 x109/L) and concomitant ophthalmic vascular manifestations independent of the underlying eosinophilic disease but with no alternative cause for ophthalmic manifestations.
UNASSIGNED: Fifty-seven patients were included (20 from the observational study and 37 from the literature review). Ophthalmic vascular features were the initial manifestation of eosinophil-related disease in 34 (59%) patients and consisted of 29 central retinal artery occlusions, six branch retinal artery occlusions, five central retinal vein occlusions, two branch retinal vein occlusions, seven retinal vasculitides, two retinal vasospasms, 12 Purtscher\'s retinopathies, 13 anterior ischemic optic neuropathies and two posterior ischemic optic neuropathies. The median [IQR] absolute eosinophil count at onset of ophthalmic vascular manifestations was 3.5 [1.7-7.8] x109/L. Underlying eosinophil-related diseases included eosinophilic granulomatosis with polyangiitis (n=32), clonal hypereosinophilic syndrome (HES) (n=1), idiopathic HES (n=13), lymphocytic HES (n=2), adverse drug reactions (n=3), parasitosis (n=2), polyarteritis nodosa (n=1), IgG4-related disease (n=1), eosinophilic fasciitis (n=1) and primary sclerosing cholangitis (n=1). Other extra-ophthalmologic arterial or venous thromboses related to eosinophilia were reported in four (7%) and nine (16%) patients, respectively. Visual prognosis was poor: only eight (10%) patients achieved full recovery of ophthalmologic symptoms. After a median follow-up of 10.5 [1-18] months, one patient (3%) had a recurrence of an ophthalmic vascular manifestation, and three patients (10%) had a recurrence of other vascular symptoms (deep vein thrombosis in two and pulmonary embolism in one patient). At the time of recurrence, absolute eosinophil counts were above 0.5 x109/L in all cases (n=4).
UNASSIGNED: This study broadens the spectrum of vascular manifestations associated with hypereosinophilia by adding ophthalmic vascular manifestations. In patients with ophthalmological vascular manifestations and hypereosinophilia, aggressive treatment of the underlying pathology (and normalization of blood count) should be implemented.

暂无摘要。