Sustained ocular hypertension following intravitreal injections of 0.5 mg/0.05 ml ranibizumab

To report three cases with sustained ocular hypertension following intravitreal injections of 0.5 mg/0.05 ml ranibizumab and to underline the importance of monitoring intraocular pressure (IOP) following intravitreal injections of ranibizumab (Lucentis). Three patients were found to have high IOP after intravitreal injections of 0.5 mg/0.05 ml ranibizumab. IOP was elevated after the second ranibizumab injection in patients 1 and 2, and after the third injection in patient 3. The increase in IOP was sustained, requiring treatment with anti-glaucoma eye drops in all patients, the addition of systemic carbonic anhydrase inhibitor in one patient, and the application of selective laser trabeculoplasty (SLT) in another patient. None of the patients had a previous history of glaucoma or ocular hypertension. Sustained ocular hypertension may occur after intravitreal injections of 0.5 mg/0.05 ml ranibizumab. Although the precise mechanism of the pressure rise is unknown, three eyes in our series were controlled with topical or oral medication and one with SLT. The necessity of IOP monitoring is strongly emphasized after intravitreal injections of 0.5 mg/0.05 ml ranibizumab.     

反复玻璃体腔注射雷珠单抗与阿柏西普对黄斑水肿患者角膜神经的影响

目的:探讨反复玻璃体腔注射雷珠单抗与阿柏西普对黄斑水肿患者角膜神经的影响。方法:选取2021-06/2022-06在我院进行玻璃体腔注射抗血管内皮生长因子(VEGF)药物治疗的患者64例64眼,其中糖尿病性黄斑水肿20例20眼,湿性年龄相关性黄斑变性19例19眼,视网膜静脉阻塞25例25眼。采取3+PRN治疗方案,注药前和每次玻璃体腔注药后1mo时采用共聚焦显微镜采集角膜上皮基底膜下神经丛图像,测量角膜神经纤维长度和密度。结果:玻璃体腔注射阿柏西普的患者注药前后术眼角膜神经纤维密度无显著变化(P>0.05),但第2、3次注药后角膜神经纤维长度均低于注药前(均P<0.01);玻璃体腔注射雷珠单抗的患者注药前后术眼角膜神经纤维密度和长度均无显著变化(均P>0.05)。第3次注药后,两组患者术眼角膜神经纤维长度和密度均无显著差异(均P>0.05)。结论:反复玻璃体内注射抗VEGF药物会一定程度影响角膜神经,对多次注射抗VEGF药物的患者需关注角膜神经变化。     

Role of nocturnal arterial hypotension in the development of ocular manifestations of systemic arterial hypertension

There are well-known associations between systemic arterial hypertension and a variety of ocular disorders that were previously considered to be primarily manifestations of arterial hypertension. Recent studies with 24-hour ambulatory blood pressure monitoring have shown that the development and progression of nonarteric anterior ischemic optic neuropathy and glaucomatous optic neuropathy are significantly correlated with nocturnal arterial hypotension, particularly in hypertensive patients receiving oral hypertensive therapy. These studies suggest that several of the ocular or optic nerve head ischemic or ocular vascular disorders previously thought to be manifestations of arterial hypertension may, in fact, be due to a combination of systemic arterial hypertension and hypotension, with arterial hypertension acting as a predisposing factor and arterial hypotension actually producing the disorders. This paper reviews this subject in light of recent studies and discusses the physiopathologic bases of the disorders in question. With the development of potent arterial hypotensive medications for arterial hypertension, arterial hypotension (particularly nocturnal hypotension) is increasingly emerging as an important cause of visual disorders. Therefore, it is strongly recommended that when a patient is at risk for ocular or optic nerve head ischemic or ocular vascular disorders, the ophthalmologist should talk to the treating physician about the potential risks of intensive arterial hypotensive therapy, particularly that administered in the evening or at bedtime.     

Abgrenzung der okulären Hypertension

The term ocular hypertension has been used for more than 30 years. It is defined as an elevated intraocular pressure above the statistical norm without detectable optic nerve head or visual field damage. The number of patients with ocular hypertension in Germany is estimated to be approximately 3–5 million. Increased intraocular pressure is a risk factor for conversion to primary open-angle glaucoma. Most patients with ocular hypertension (and no risk factors) can be followed on a regular basis without any treatment. Each visit should include measurement of intraocular pressure, optic nerve head examination with a slit lamp, imaging and perimetric examinations. Currently known risk factors are high intraocular pressure, higher age, myopia, a thin cornea and darkly pigmented skin. If risk factors are present, antiglaucomatous therapy is indicated.     

Persisent ocular hypertension following intravitreal ranibizumab

BACKGROUND: To describe the occurrence of ocular hypertension in four patients following injection of ranibizumab intravitreally. METHODS: Case series. RESULTS: Four patients had high intraocular pressure after intravitreal ranibizumab 0.5 mg. Ocular hypertension occurred 1 month after the second ranibizumab injection in patients 1 and 3, and 1 month after the first ranibizumab in patient 2. In patient 4, it occurred several hours after the first ranibizumab injection. In all patients, the IOP increase was sustained across several visits, requiring control with topical glaucoma therapy, and in two cases the addition of a systemic carbonic anhydrase inhibitor. None of the patients had a previous history of glaucoma, ocular hypertension or IOP asymmetry and the IOP was as high as 30, 34, 46, and 50 mmHg in the four patients. CONCLUSION: Severe and sustained ocular hypertension may occur after intravitreal ranibizumab. Although the mechanism of the pressure rise is unknown, all eyes in our series were controlled with medical therapy.     

颅内压与青光眼及其无创测量技术的研究进展

青光眼是世界上第二位致盲性眼病,第一位不可复性致盲性眼病。尽管眼压增高被认为是青光眼性视神经损害的主要危险因素,但是50%的原发性开角型青光眼患者的日常眼压正常,还有一些患者尽管眼压控制良好,但青光眼性视神经损害仍继续发展。这些现象无法用高眼压理论来解释,青光眼患者视神经损害的发病机制仍待探讨。目前国内外的一些研究表明：（1）视神经周围的生物力学的解剖结构包括眼内压,筛板和球后的脑脊液压力在原发性开角型青光眼的发病机制中发挥重要的作用;（2）正常眼压性青光眼患者的脑脊液压力比正常人低,而跨筛板压力差比正常人高;（3）高眼压症患者的脑脊液压力比正常人群高,而跨筛板压力差和正常人之间没有统计学意义。基于以上研究,本文就颅内压与青光眼性视神经损害之间关系的相关研究进展及临床上可行的无创颅内压测量方法作一综述。     

Intraokulare Bevacizumab-Injektionen bei seltenen Indikationen – zwei Kasuistiken

Intravitreal anti-VEGF injections are currently the most effective treatment option for neovascular age-related macular degeneration. The anti-VEGF treatment of other, more common ocular diseases, such as diabetic retinopathy and vascular occlusions with neovascularization and retinal edema, is currently described in numerous studies and cases. Rare neovascular ocular diseases, such as Eales disease, presumed ocular histoplasmosis syndrome (POHS), retinopathy of prematurity, and idiopathic telangiectasia, may be future areas for anti-VEGF therapy. In our case report we describe intravitreal bevacizumab (Avastin) therapy for central serous chorioretinopathy and for pseudoxanthoma elasticum with angioid streaks and choroidal neovascularization. In both cases the intravitreal injection resulted in morphological and functional rehabilitation.     

地塞米松玻璃体内植入剂联合抗VEGF药物治疗视网膜静脉阻塞

目的：比较地塞米松玻璃体内植入剂联合抗VEGF药物与抗VEGF药物单药治疗视网膜静脉阻塞继发黄斑水肿(RVO-ME)的疗效和安全性。

方法：选取2019-06/2020-12在厦门大学附属厦门眼科中心确诊为视网膜中央静脉阻塞(CRVO)或视网膜分支静脉阻塞(BRVO)继发黄斑水肿的患者133例133眼,其中CRVO-ME患者48眼,BRVO-ME患者85眼。将纳入患者随机分组,其中单药治疗组66眼接受每月注射康柏西普1次,连续3mo,之后每月复诊; 联合治疗组67眼接受地塞米松玻璃体内植入剂注射1次,1wk后注射康柏西普1次,之后每月复诊。随访6mo,观察两组患者最佳矫正视力(BCVA)和中央视网膜厚度(CRT)改善情况,记录康柏西普注射次数及与玻璃体腔注射治疗相关的眼部及全身不良事件发生情况。

结果：治疗后1、2、3、6mo,两组患者BCVA和CRT均较治疗前显著改善,但两组间BCVA和CRT改善程度均无差异(P>0.05)。首次玻璃体腔注射至治疗6mo时,单药治疗组和联合治疗组康柏西普玻璃体腔注射次数分别为3.56±0.12、2.96±0.17次,联合治疗组注射次数显著低于单药治疗组(P=0.004)。随访期间,联合治疗组高眼压和白内障发生率均高于单药治疗组。

结论：地塞米松玻璃体内植入剂联合抗VEGF药物是治疗RVO-ME的有效方法,可显著改善视力,降低CRT,该治疗方案可在减少抗VEGF药物注射次数的同时达到与抗VEGF药物单药治疗相似的疗效,但需要监控眼压变化及白内障进展情况。     

Iris colour, optic disc dimensions, degree and progression of glaucomatous optic nerve damage

PURPOSE: To evaluate whether iris colour influences size and shape of the optic nerve head and risk for glaucoma progression. METHODS: The hospital-based observational study included 1973 eyes of 1012 Caucasian subjects with ocular hypertension or chronic open-angle glaucoma. For all patients, colour stereo optic disc photographs were evaluated, and corneal pachymetry and achromatic perimetry were performed. Main outcome measures were optic nerve head parameters, the development or progression of visual field defects and iris colour. RESULTS: In most of the study groups, size of the optic disc, neuroretinal rim, alpha zone and beta zone of parapapillary atrophy, retinal vessel diameter and central corneal thickness did not differ significantly between eyes with blue, green, brown and mixed iris colour. In the normal-pressure glaucoma group, neuroretinal rim area was smallest in the population with mixed-coloured eyes and largest in the group of eyes with brown irides (P = 0.001 after correction for inter-eye dependency and multiple testing). For the ocular hypertensive subjects and glaucoma patients with follow-up examinations, the rate of development or progression of glaucomatous visual field loss was not significantly associated with iris colour (P = 0.060). CONCLUSIONS: In Caucasian subjects, iris colour does not have a major association with the size of the optic nerve head structures, central corneal thickness and retinal arterial diameter. In Caucasian patients with ocular hypertension or chronic open-angle glaucoma, an influence of iris colour on the risk for development or progression of glaucomatous visual field defects could not be confirmed.     

Electrophysiological evaluation of retinal photoreceptor function after repeated bevacizumab injections

Bevacizumab (Avastin, Genentech) was one of the first anti-VEGF substances used to treat macular edema or choroidal neovascularization in patients with vascular ocular pathologies. However, only few studies evaluate the safety of intravitreal bevacizumab injections in regard to retinal photoreceptor function. We evaluated retinal function after repeated (2-3) monthly injections of bevacizumab in a prospective case series of 10 patients with various retinal diseases. Study endpoints were visual acuity (VA) using ETDRS charts and 3 full-field electroretinography sessions with a flash intensity range of 0.0005-2 cds/m(2). V-log-I b-wave amplitudes were fitted by a Naka-Rushton model. No significant changes in scotopic or photopic ERG measures were observed between baseline ERG and last follow-up ERG. Individual patients showed transient alterations of ERG measures on the first follow-up visit. Mean visual acuity was stable over the time course of the study (logMAR = 0.42 at baseline and logMAR = 0.48 at last follow-up). In conclusion, three monthly repeated injections of bevacizumab do not affect mid-term electrophysiological retinal function. Transient alterations in ERG readings of individual patients 1 week after intravitreal bevacizumab injection may be attributed to short-term disruption of the retinal equilibrium through the trauma of injection. Evaluation of patients receiving more than three injections of anti-VEGF substances should be the focus of future studies.     

The “no treatment” approach to ocular hypertension

Should patients with ocular hypertension be treated to prevent glaucomatous visual field loss? Three considerations suggest that for most patients the answer is no. First, the average risk of visual field loss in untreated ocular hypertension is small. Population surveys and prospective studies indicate that no more than about one of every nine persons with intraocular pressures higher than 20 mm Hg will develop a visual field defect. Secondly, treatment of ocular hypertension to lower intraocular pressure is of unproven efficacy in preventing visual field defects. Thirdly, adverse reactions to glaucoma therapy occur frequently and are sometimes serious. Although pressure reduction may be indicated for some patients who possess certain risk factors which make them especially susceptible to glaucomatous damage, for most patients “no treatment” is the best management. Untreated patients must be observed carefully with periodic visual field and optic disc examinations.     

Diabetic retinopathy – An update

Management of diabetes should involve both systemic and ocular aspects. Control of hyperglycemia, hypertension and dyslipidemia are of major role in the management of diabetic retinopathy. In the ocular part; laser treatment remains the cornerstone of treatment of diabetic macular edema (focal/grid), severe non-proliferative and proliferative diabetic retinopathy (panretinal photocoagulation). There is a strong support to combination therapy. Using one or two intravitreal injections such as anti-VEGF and or steroid to reduce central macular thickness followed by focal or grid laser to give a sustained response may offer an alternative to treatment in diabetic macular edema. Anti-VEGF were found to be effective as an adjunct therapy in proliferative diabetic retinopathy patient who is going to have vitrectomy for vitreous hemorrhage with neovascularization, panretinal photocoagulation, and other ocular surgery such as cases with neovascular glaucoma and cataract with refractory macular edema.     

非动脉炎性前部缺血性视神经病变的临床治疗现状

非动脉炎性前部缺血性视神经病变（NAION）是50岁以上人群常见的急性视神经病变,以突发、单眼、无痛性视力下降为特征。多种治疗方法被尝试用于治疗NAION,包括药物治疗和手术治疗,但是迄今为止尚无一种治疗方案被证实明确有效。近年的一项非随机前瞻性研究显示,患者急性期口服糖皮质激素可改善视力和视野,减轻视盘水肿,然而其确切疗效仍待证实。对于NAION患者进行的玻璃体腔内注射曲安奈德、抗血管内皮生长因子抗体、促红细胞生成素治疗的试验结果令人鼓舞,然而其所带来的风险不容忽视。目前,NAION的治疗尚缺乏有力的证据,有待更深入的研究,尤其要加强临床前的基础研究。     

Prophylaxis with intraocular pressure lowering medication and glaucomatous progression in patients receiving intravitreal anti-VEGF therapy

AIM: To investigate whether pretreatment with pressure-lowering medication prior to anti-vascular endothelial factor (VEGF) injections had an effect on glaucomatous progression in patients with preexisting glaucoma or ocular hypertension (OHT). METHODS: A total of 66 eyes from 54 patients with a preexisting diagnosis of glaucoma or OHT, treated with six or more anti-VEGF injections were selected for chart review. Primary outcome measures were rate of visual field loss in dB/year, rate of change in retinal nerve fiber layer (RNFL) thickness in microns/year, and need for additional glaucoma intervention. RESULTS: The number of eyes requiring additional glaucoma medication was 5 of 20 (25.0%) and 14 of 46 (30.4%) for the pretreated and non-pretreated groups, respectively. The number of eyes requiring glaucoma laser or surgery was 4 of 20 (20.0%) and 13 of 46 (28.3%) for the pretreated and non-pretreated groups, respectively. Estimated mean rate of pattern standard deviation decline was not significant in either group (P>0.073), with no difference between groups (P=0.332). Although both groups showed significant RNFL change from baseline (P<0.011), no difference was detected between groups (P=0.467). CONCLUSION: Pretreatment has no detectable effect on structural or functional glaucomatous progression. Patients receiving repeated injections may be at risk for glaucomatous complications requiring invasive intervention.     

Apoptotic retinal ganglion cell death in the DBA/2 mouse model of glaucoma

The DBA/2 mouse has been used as a model for spontaneous secondary glaucoma. We attempted to determine the in vivo time course and spatial distribution of retinal ganglion cells (RGCs) undergoing apoptotic death in DBA/2 mice. Female DBA/2 mice, 3, 9-10, 12, 15, and 18 months of age, received intravitreal injections of Annexin-V conjugated to AlexaFluor 1h prior to euthanasia. Retinas were fixed and flat-mounted. Annexin-V-positive RGCs in the hemiretina opposite the site of injection were counted, and their locations were recorded. Positive controls for detection of apoptotic RGCs by Annexin-V labeling included rats subjected to optic nerve ligation, and C57BL/6 mice subjected to either optic nerve ligation or intravitreal injection of NMDA. To verify that Annexin-V-labeled cells were RGCs, intravitreal Annexin-V injections were also performed on retinas pre-labeled retrogradely with FluoroGold or with DiI. Annexin-V-positive RGC locations were analyzed to determine possible clustering and areas of preferential loss. Annexin-V labeled apoptotic RGCs in eyes after optic nerve ligation, intravitreal NMDA injection, as well as in aged DBA/2 animals. In glaucomatous DBA/2 mice 95-100% of cells labeled with Annexin-V were also FluoroGold- and DiI-positive. This confirms that Annexin-V can be used to specifically detect apoptotic RGCs in rodent retinas. In DBA/2 mice, apoptotic RGC death is maximal from the 12th to the 15th month of age (ANOVA, p<0.001, Fisher's post hoc test) and occurs in clusters. These clusters are initially located in the midperipheral retina and progressively occur closer to the optic nerve head with increasing age. Retrograde axonal transport of FluoroGold in the glaucomatous mouse retina is functional until at least 2-3days prior to initiation of apoptotic RGC death.     

Current intravitreal therapy and ocular hypertension: A review

To determine the effect of commonly used intravitreal agents on immediate and long-term IOP elevations and their association, if any, with glaucoma. Literature searches in PubMed and the Cochrane databased in January 2020 yielded 407 individual articles. Of these, 87 were selected for review based on our inclusion criteria. Based on the evidence provided, 20 were assigned level I, 27 level II, and 22 level III. Eight articles were rejected because of poor quality, insufficient clarity, or irrelevance based on standardized protocols set out by the American Academy of Ophthalmology. The studies that reported on short-term IOP elevation (i.e., between 0 and 60 min) showed that an immediate increase in IOP is seen in all patients who receive anti-VEGF agents or triamcinolone acetonide when measured between 0 and 30 min of intravitreal injection and that the IOP elevation decreases over time. The data on long-term IOP elevation were mixed; Pretreatment with glaucoma medications, anterior chamber tap, vitreous reflux, longer intervals between injections, and longer axial lengths were associated with lower IOP elevations after injection of anti-VEGF agents, while the position of the implant vis-à-vis, the anterior chamber was important for steroid therapy. Data were mixed on the relationship between IOP increase and the type of intravitreal injection, number of intravitreal injections, preexisting glaucoma, and globe decompression before injection. There were no data on the onset or progression of glaucoma in the studies reviewed in this assessment. However, some studies demonstrated RNFL thinning in patients receiving chronic anti-VEGF therapy. Most, if not all, intravitreal agents cause ocular hypertension, both in the short term and long term. The functional consequences of these observations are not very clear.     

Local and Systemic Complications after Intravitreal Administration of Anti-Vascular Endothelial Growth Factor Agents in the Treatment of Different Ocular Diseases: A Five-Year Retrospective Study

Abstract

Purpose: To observe the frequency of complications in patients undergoing intravitreal anti-VEGF injections for different ocular diseases in a five-year period. Materials and Methods: Charts of patients receiving intravitreal anti-VEGF were retrospectively reviewed. Out of 1173 eyes, 762 were treated with bevacizumab, 382 with ranibizumab, and 29 with pegaptanib. Data recorded included demographic information, clinical findings, total injections received, and info about the onset of adverse effects. Results: 12.86% of the eyes treated with bevacizumab presented side-effects, while ratings in the ranibizumab and pegaptanib groups were 15.97% and 20.69%, respectively. Odds ratios calculated comparing incidences after each anti-VEGF are 0.78 (bevacizumab versus ranibizumab, p?=?0.152), 0.57 (bevacizumab versus pegaptanib, p?=?0.227), and 0.73 (ranibizumab versus pegaptanib, p?=?0.508). A total of 185 complications were detected (62.16% after bevacizumab). Ocular side-effects registered were 40 cases of sustained intraocular pression (IOP) elevation, one infectious uveitis, one retinal detachment, and one sub-retinal hemorrhage. Other cases were related to transient IOP elevation immediately after injection. Systemic complications registered were one case of nausea, one episode of chest pain with acute vision loss, and one case of acute blood hypertension. Conclusions: The majority of significant complications occurred in patients receiving multiple bevacizumab administrations. However, results may be affected by the difference in the utilization amount for each drug. AMD patients were the most represented, probably due to greater indication to treatment.     

Intravitreal triamcinolone acetonide for treatment of intraocular proliferative, exudative, and neovascular diseases

Within the last three years, triamcinolone acetonide has increasingly been applied intravitreally as treatment option for various intraocular neovascular edematous and proliferative disorders. The best response in terms of gain in visual acuity after the intravitreal injection of triamcinolone acetonide was found in eyes with intraretinal edematous diseases such as diffuse diabetic macular edema, branch retinal vein occlusion, central retinal vein occlusion, and pseudophakic cystoid macular edema. Visual acuity increased and degree of intraocular inflammation decreased in eyes with various types of non-infectious uveitis including acute or chronic sympathetic ophthalmia and Adamantiadis-Behcet's disease. Intravitreal triamcinolone may be useful as angiostatic therapy in eyes with iris neovascularization and proliferative ischemic retinopathies. Possibly, intravitreal triamcinolone may be helpful as adjunct therapy for exudative age-related macular degeneration, possibly in combination with photodynamic therapy. In eyes with chronic, therapy resistant, ocular hypotony, intravitreal triamcinolone can induce an increase in intraocular pressure and may stabilize the eye. The complications of intravitreal triamcinolone therapy include secondary ocular hypertension in about 40% of the eyes injected, cataractogenesis, postoperative infectious and non-infectious endophthalmitis, and pseudo-endophthalmitis. Intravitreal triamcinolone injection can be combined with other intraocular surgeries including cataract surgery. Cataract surgery performed some months after the injection does not show a markedly elevated rate of complications. If vision increases and eventually decreases again after an intravitreal triamcinolone acetonide injection, the injection can be repeated. The duration of the effect of a single intravitreal injection of triamcinolone depended on the dosage given. Given in a dosage of about 20mg to non-vitrectomized eyes, the duration of the effect and of the side-effects was 6-9 months. Intravitreal triamcinolone acetonide may offer a possibility for adjunctive treatment of intraocular edematous and neovascular disorders. One has to take into account the side-effects and the lack of long-term follow-up observations.     

Administration of Repeat Intravitreal Anti-VEGF Drugs by Retina Specialists in an Injection-only Clinic for Patients with Exudative AMD: Patient Acceptance and Safety

Purpose: To report patient acceptance and safety of repeated intravitreal injections of anti-VEGF agents for exudative AMD, by retina specialists, without an eye examination before every injection.

Methods: Retrospective chart review. 115 eyes (110 patients) with exudative AMD underwent repeated intravitreal anti-VEGF injections with limited interval examination and diagnostic testing. Medication, laterality, number of injection cycles started and completed, number of injections per injection cycle, subjective visual changes, pre- and post-injection visual acuity (VA), pre- and post-injection intraocular pressure (IOP), nurse- and patient-initiated phone calls, emergency (non-scheduled) clinic visits, complications, new diagnoses, and patient complaints after each injection were recorded. The main outcome measures were complications and patient complaints.

Results: 396 injections were administered in the injection clinic to 110 patients in 175 injection cycles (range: 0 to 5 injections per cycle). Of 175 injection cycles, there were 134 uninterrupted cycles and 41 interrupted cycles where an eye exam was performed. Fourteen new diagnoses were made: six during emergency visits, three at injection clinic appointments, and five at the next full examination after completion of a prescribed injection clinic cycle.

Conclusions: Administration of anti-VEGF injections in a designated injection clinic, by retina specialists, according to a prescribed schedule, and with limited pre-injection testing, for patients with wet AMD, is well-tolerated.     

Normal tension glaucoma, sleep apnea syndrome and nasal continuous positive airway pressure therapy--case report with a review of literature

BACKGROUND: In the pathogenesis of glaucoma, besides an elevated intraocular pressure (IOP), cardiovascular risk factors, such as arterial hypotension and hypertension, vasospasms, autoregulatory defects, atherosclerosis, and diabetes mellitus are of increasing importance, especially in normal tension glaucoma. Recently, there have been several reports of an additional risk factor: obstructive sleep apnea syndrome. METHODS: Literature review (Medline) and case report. RESULTS: The authors report on a 8 1/2 years follow-up of a 60-year-old patient with normal tension glaucoma. Despite successful pharmacological and surgical lowering of intraocular pressure a progressive glaucomatous damage with optic nerve atrophy and increasing visual field defects occurred. As a result of intensive investigations of possible cardiovascular risk factors, an obstructive sleep apnea syndrome was diagnosed. Since the beginning of therapy with nCPAP (nasal continuous positive airway pressure) more than 3 1/2 years ago, no further progression of glaucomatous optic nerve damage or visual field defects have been observed. CONCLUSIONS: In clinical practice, obstructive sleep apnea syndrome often is underdiagnosed. In patients suffering from glaucoma and obstructive sleep apnea syndrome, intraocular pressure lowering therapy may not be enough, whereas an additional nCPAP-therapy potentially could prevent the beginning/progression of glaucomatous optic nerve damage.