Bartonella henselae infection associated with peripapillary angioma, branch retinal artery occlusion, and severe vision loss

PURPOSE: To report atypical clinical features of Bartonella henselae neuroretinitis treated with combination antibiotics. METHOD: Case report. RESULTS: A 20-year-old man with a positive B. henselae titer developed a unilateral neuroretinitis, a large peripapillary angiomatous lesion, branch artery occlusion with ischemic maculopathy, and vision loss that failed to improve with clindamycin. Treatment with doxycycline and rifampin led to rapid clinical improvement. The severe vision loss in this case is atypical. CONCLUSIONS: Ocular findings associated with B. henselae infection may include retinal angiomatous lesion and branch retinal artery occlusion. Doxycycline and rifampin were successful in treating the infection.     

Neovascular glaucoma associated with cilioretinal artery occlusion combined with perfused central retinal vein occlusion

BACKGROUND: Cilioretinal artery occlusion rarely results in neovascular glaucoma, especially in cases of extensive cilioretinal infarction and combined retinal vascular occlusion. CASE: A 62-year-old man with diabetes mellitus and essential hypertension showed a visual acuity of counting fingers, retinal whitening temporal to the optic disc with mild dilation and tortuosity of the retinal veins, and retinal hemorrhages in four quadrants of his right eye. Fluorescein angiography demonstrated a delayed filling of the central retinal vein and cilioretinal artery. OBSERVATIONS: Two months later, neovascular glaucoma developed and retinal ablation was performed using an argon laser. Trabeculectomy was also performed due to the intractability of the glaucoma, and central artery occlusion was found. On magnetic resonance angiography, the right distal common carotid artery was irregularly narrowed and the right ophthalmic artery was almost entirely occluded. CONCLUSIONS: In cases of cilioretinal artery occlusion and perfused central retinal vein occlusion with multiple risk factors, close follow-up is advised.     

Intravitreal bevacizumab for neovascular glaucoma following central retinal artery occlusion

PURPOSE: To report a case of neovascular glaucoma due to central retinal artery occlusion treated with a single intravitreal injection of bevacizumab. METHODS: A 68-year-old patient with a 10-week history of central retinal artery occlusion presented with neovascularization of the iris and the angle and intraocular pressure of 30 mm Hg. The patient received a single injection of 1.25 mg bevacizumab in 0.1 mL intravitreally. RESULTS: Iris and angle neovascularization regressed within 48 hours of the injection. Intraocular pressure dropped from 30 to 15 mm Hg, and there was marked improvement in patient comfort. Panretinal photocoagulation was applied 4 weeks after the injection. CONCLUSIONS: Bevacizumab seems to be a useful adjunct to panretinal photocoagulation in the treatment of neovascular glaucoma.     

光凝预防视网膜中央静脉阻塞新生血管性青光眼

目的 评价广泛视网膜光凝预防缺血犁视网膜中央静脉阻塞新牛血管性青光眼的临床效果.方法 为前瞻性随机对照临床研究,共60例(60只眼)经眼底荧光素血管造影证实的缺血型视网膜中央静脉阻塞患者,随机分组,A组30例(30只眼)用药物治疗;B组30例(30只眼)除用药物治疗外,还用氪黄激光进行广泛视网膜光凝(激光波长568nm,功率100～300mw,光斑直径300～500μm,曝光时间0.1s,光凝872-1207点,光斑反应Ⅲ级).随访时间为治疗后1个月、3个月、半年、1年、2年和3年.结果 A组失访7例,B组失访9例;A组23例(23只眼)治疗前平均视力为0.097±0.038,治疗后平均视力为0.102±0.066,两者比较无显著差异(t=0.901,P>0.05);B组21例(21只眼)治疗前平均视力为0.094±0.034,治疗后平均视力为0.10l±0.043,两者比较无显著差异(t=0.887,P>0.05);A组和B组的治疗前平均视力比较无显著筹异(t=0.672.P>0.05);A组和B组的治疗后平均视力比较也无显著筹异(t=0.488,P>0.05);A组发生新生血管性青光眼7例.占30.4%,B组发生新牛血管性青光眼1例,占4.8%,两组比较有显著差异(x2=4.864,P<0.05).结论 氪黄激光广泛视网膜光凝能有效预防缺血型视网膜中央静脉阻塞新生血管性青光眼的发生,但不能提高视力.     

Conservative management of documented neuroretinitis in cat scratch disease associated with Bartonella henselae infection

Background: Bartonella henselae has been identified as the causative agent of the neuroretinitis associated with cat scratch disease (CSD). Immunofluorescent antibody tests with good sensitivity and specificity are available to aid in diagnosis. Despite diagnostic advances, optimal management remains controversial. We present a case of documented B. henselae macular neuroretinitis managed without antibiotics and discuss antibiotic use in this condition. Methods: We examined a young woman with macular neuroretinitis and established a diagnosis of CSD. Management consisted of a review of the literature, followed by educating her about the condition and close observation. We documented the course of her disease. Results: We diagnosed neuroretinitis associated with B. henselae infection based on immunofluorescent antibody titres and clinical presentation. Our patient’s neuroretinitis resolved promptly without antibiotic therapy. Conclusions: Macular neuroretinitis in CSD can be satisfactorily diagnosed with the use of fluorescent antibodies in the appropriate clinical setting. Optimal treatment for the disease has not been established and observation combined with patient education remains an appropriate option. The self-limited nature of the disease implies that treatment studies not using controls must be interpreted with great caution. Adverse drug reactions and other iatrogenic complications can be reduced by limiting antibiotic use in settings where a meaningful treatment benefit has not been established.     

Conservative management of documented neuroretinitis in cat scratch disease associated with Bartonella henselae infection.

BACKGROUND: Bartonella henselae has been identified as the causative agent of the neuroretinitis associated with cat scratch disease (CSD). Immunofluorescent antibody tests with good sensitivity and specificity are available to aid in diagnosis. Despite diagnostic advances, optimal management remains controversial. We present a case of documented B. henselae macular neuroretinitis managed without antibiotics and discuss antibiotic use in this condition. METHODS: We examined a young woman with macular neuroretinitis and established a diagnosis of CSD. Management consisted of a review of the literature, followed by educating her about the condition and close observation. We documented the course of her disease. RESULTS: We diagnosed neuroretinitis associated with B. henselae infection based on immunofluorescent antibody titres and clinical presentation. Our patient's neuroretinitis resolved promptly without antibiotic therapy. CONCLUSIONS: Macular neuroretinitis in CSD can be satisfactorily diagnosed with the use of fluorescent antibodies in the appropriate clinical setting. Optimal treatment for the disease has not been established and observation combined with patient education remains an appropriate option. The self-limited nature of the disease implies that treatment studies not using controls must be interpreted with great caution. Adverse drug reactions and other iatrogenic complications can be reduced by limiting antibiotic use in settings where a meaningful treatment benefit has not been established.     

Cilioretinal artery occlusion with central retinal vein occlusion.

BACKGROUND: Combined cilioretinal artery and retinal vein occlusions are infrequently documented retinal vascular disorders of speculative origin. Occlusion of the cilioretinal artery is believed to result from either mechanical compression of the artery as a result of an increase in venous pressure or from a reduction in perfusion pressure in both the cilioretinal and retinal arteries. The ophthalmoscopic and angiographic features of this condition are reviewed. CASE REPORTS: Two cases of cilioretinal artery occlusion after central retinal vein occlusion are presented, one of which evolved to the development of iris neovascularization. DISCUSSION: The incidence of cilioretinal artery occlusions due to central retinal vein occlusions is infrequently reported in the literature. Excluding those with chronic cystoid macular edema, most patients have a favorable visual outcome. It is possible that the incidence of combined cilioretinal artery and central retinal vein occlusions is grossly underestimated.     

康柏西普联合全视网膜激光光凝治疗CRVO继发新生血管性青光眼

目的：探讨康柏西普联合全视网膜激光光凝(panretinal photocoagulation,PRP)治疗视网膜中央静脉阻塞(central retinal vein occlusion,CRVO)继发新生血管性青光眼(neovascular glaucoma,NVG)的疗效。

方法：本组观察对象为2014-05/2017-05于我院眼科治疗的CRVO继发NVG患者100例100眼,现回顾性分析其病历资料,将采用青光眼滤过性手术联合PRP治疗的50例患者设为对照组,在此治疗基础上加用玻璃体腔注射康柏西普的50例患者设为观察组。比较术前、术后7d,1、3、6mo最佳矫正视力(best corrected visual acuity,BCVA),并采用非接触式眼压计比较各时期眼压,裂隙灯检查新生血管消退情况并结合眼压等判断手术效果,随访6mo记录术后复发率及并发症发生情况。

结果：两组患者术后1、3、6mo BCVA趋于稳定,术后BCVA与术前比较,组间各时间点比较差异无统计学意义(P>0.05); 两组术后7d,1、3、6mo眼压均显著低于术前,术后7d,1mo观察组显著低于对照组,差异有统计学意义(P<0.05),术后3、6mo组间比较差异无统计学意义(P>0.05); 观察组手术成功率为100%,与对照组(92%)比较差异具有统计学意义(P<0.05),观察组手术完全成功率为84%,显著高于对照组(66%), 差异有统计学意义(P<0.05); 观察组前房出血及复发率显著低于对照组,差异有统计学意义(P<0.05),两组患者浅前房、低眼压发生率差异无统计学意义(P>0.05)。

结论：术前玻璃体腔注射康柏西普联合PRP治疗CRVO继发NVG眼压恢复时间更短,手术效果更优,能控制前房出血并降低复发率。     

视网膜中央静脉阻塞后发生新生血管性青光眼的危险因素和预测模型建立

目的:探讨视网膜中央静脉阻塞(CRVO)后发生新生血管性青光眼(NVG)的危险因素,在基础上构建预测模型。方法:选择2016-02/2020-03我院眼科收治的483例527眼CRVO患者临床资料并随访至2021-06,统计CRVO合并NVG情况。采用多因素Logistic回归分析CRVO后发生NVG的危险因素。根据危险因素回归系数构建CRVO后发生NVG的风险预测模型,Hosmer-Lemeshow(H-L)检验、受试者工作特征(ROC)曲线法评价预测模型。结果:患者失访15例23眼,随访15～64(中位数35)mo,其中70例86眼发生NVG(NVG组),398例418眼未发生NVG(非NVG组)。回归分析结果显示缺血型CRVO、首次就诊时IOP≥18mmHg、高血压、首次就诊时相对性瞳孔传入缺陷(RAPD)≥0.75logU、首次就诊时裸眼视力(UCVA)>0.30(LogMAR)是CRVO后发生NVG的危险因素(P<0.01),抗VEGF治疗是CRVO后发生NVG的保护因素(P<0.01)。CRVO后发生NVG的风险预测模型具有较好的符合度(H-L检验P>...     

Electrophysiological evaluation and visual outcome in patients with central retinal vein occlusion,primary open‐angle glaucoma and neovascular glaucoma

Purpose: To evaluate patients with central retinal vein occlusion (CRVO) and neovascular glaucoma (NVG) using electrophysiology in order to gain better understanding of visual outcome and risk factors, such as previously diagnosed primary open‐angle glaucoma (POAG). Methods: Eighty‐three patients (83 eyes) initially presenting with CRVO and examined with full‐field electroretinography (ERG) within 3 months of the thrombotic event were analysed retrospectively regarding treatment, risk factors and visual outcome. In addition, 30 patients initially presenting with NVG caused by CRVO were also investigated regarding risk factors using electrophysiology in order to determine the cause of their visual impairment. Results: Nineteen (23%) of the 83 patients initially presenting with CRVO had been diagnosed previously with POAG. Ninety‐five per cent (18/19) of all the patients with previously diagnosed glaucoma developed ischaemic CRVO. Thirty‐four per cent of the patients initially presenting with CRVO (28/83) developed NVG. Sixty‐eight per cent (13/19) of the patients with previous glaucoma developed NVG, compared to 23% (15/64) of the patients without previous POAG. In the patients who initially presented with NVG, full‐field ERG demonstrated a remaining retinal function of both cones and rods, indicating that the main cause of visual impairment is ischaemia of the ganglion cell layer. Conclusion: Glaucoma is a significant risk factor for developing ischaemic CRVO and subsequent NVG. The presence of POAG in CRVO worsens visual outcome. NVG is associated with preserved photoreceptor function, thus indicating ischaemia of the ganglion cell layer as the primary cause of visual impairment. This emphasizes the importance of prompt treatment of ischaemia and elevated intraocular pressure in these patients.     

Central retinal vein occlusion associated with cilioretinal artery occlusion

PURPOSE: To describe the clinical characteristics and pathogenesis of central retinal vein occlusion (CRVO) associated with cilioretinal artery occlusion (CLRAO). METHODS: The study included 38 patients (38 eyes) who had CRVO associated with CLRAO and were seen in our clinic from 1974 to 1999. At their first visit to our clinic, all patients provided a detailed ophthalmic and medical history and underwent comprehensive ophthalmic evaluation, color fundus photography, and fluorescein fundus angiography. At each follow-up visit, the same ophthalmic evaluations were performed, except for fluorescein fundus angiography. RESULTS: Of 38 eyes, 30 had nonischemic CRVO, 5 had ischemic CRVO, and 3 had nonischemic hemi-CRVO. Patients with nonischemic CRVO were significantly younger (mean age +/- SD: 45.3 +/- 16.0 years) than those with ischemic CRVO (72.3 +/- 9.2 years; P = 0.001) and those with nonischemic hemi-CRVO (64.7 +/- 7.5 years; P = 0.018). At least one third of the patients gave a definite history of episode(s) of transient visual blurring before the onset of constant blurred vision. Initially, the ophthalmoscopic and fluorescein angiographic findings were similar to those seen in CRVO and hemi-CRVO, except that all these eyes had retinal infarct in the distribution of the cilioretinal artery; its size and site varied widely. Fluorescein angiography typically showed only transient hemodynamic block and not the typical CLRAO. During follow-up, visual acuity improved markedly in nonischemic CRVO (P < 0.001) and nonischemic hemi-CRVO but deteriorated in ischemic CRVO. Retinopathy resolved spontaneously in 22 eyes with nonischemic CRVO (mean duration +/- SD: 42.0 +/- 101.0 months), in 2 eyes with ischemic CRVO (15.4 +/- 4.5 months), and in 1 eye with nonischemic hemi-CRVO. Retinociliary collaterals developed in 30% of eyes with nonischemic CRVO, in 40% of eyes with ischemic CRVO, and in 66% of eyes with nonischemic hemi-CRVO. CONCLUSION: CRVO associated with CLRAO constitutes a distinct clinical entity. The pathogenesis of CLRAO in CRVO is due to transient hemodynamic blockage of the cilioretinal artery caused by a sudden sharp rise in intraluminal pressure in the retinal capillary bed (due to CRVO) above the level of that in the cilioretinal artery.     

Mechanisms of vision loss in eyes with macular edema associated with retinal vein occlusion

Anti-vascular endothelial growth factor agents reduce macular edema and improve vision in eyes with macular edema associated with retinal vein occlusion (RVO), including branch RVO (BRVO) and central RVO. However, not all eyes with resolved macular edema show satisfactory best corrected visual acuity. Photoreceptor impairment can mostly explain the vision loss in these cases. Photoreceptor damage can be caused by subretinal hemorrhage in the central fovea and hard exudates or their precursor derived from concentrated lipoproteins originating from leaky retinal vessel extravasation. The contribution of neuron impairment in the inner retina, including the impairment of bipolar and ganglion cells by ischemia, indicated by the presence of a non-perfusion area (NPA), to vision loss in eyes with BRVO is insignificant. This is because the papillomacular bundle area is usually spared from NPAs in BRVO cases.     

Secondary angle-closure glaucoma after central retinal vein occlusion

A 65-year-old man developed unilateral nonrubeotic secondary angle-closure glaucoma after central retinal vein occlusion. Therapy was nonsurgical and included medical control of the intraocular pressure. The anterior chamber eventually deepened and panretinal photocoagulation was later necessary because of developing rubeosis iridis and neovascularization of the optic disk. Secondary nonrubeotic angle-closure glaucoma from central retinal vein occlusion must be distinguished from rubeotic glaucoma or pupillary-block glaucoma so that inappropriate medical or surgical treatment can be avoided.     

A case of central retinal vein occlusion accompanied by central retinal artery occlusion

A 81-year-old woman developed central retinal vein occlusion (CRVO) in her left eye subsequent to central retinal artery occlusion (CRAO). She noticed sudden visual loss in the left eye. At initial examination, her left visual acuity was 0.03, and only a small visual field was preserved at temporal area. The left fundus showed findings of mild non-ischemic CRVO. In addition white clouded retina was recognized at the left posterior pole which indicated CRAO. FAG showed remarkably prolonged arterial circulation, but no retinal capillary obliteration. Then retinal hemorrhage increased rapidly and her left eye developed hemorrhagic retinopathy. Two weeks after initial examination, FAG showed extensive retinal capillary obliteration. In this case it was supposed that central retinal artery occlusion due to arteriosclerosis produced ischemic capillaropathy and venous thrombosis, after which restoration of arterial circulation caused hemorrhagic retinopathy.