Risk factors for epiretinal membrane surgery after initial pars plana vitrectomy for rhegmatogenous retinal detachment.

OBJECTIVES: The purpose of this study was to examine the incidence of, and risk factors for, epiretinal membrane (ERM) surgery after an initial pars plana vitrectomy (PPV) for rhegmatogenous retinal detachment (RRD). METHODS: The records of consecutive patients (3,495 eyes of 3,387 patients) who underwent RRD repair at Fujita Health University Hospital between January 1, 2008, and February 28, 2019, were retrospectively reviewed. A total of 1,736 eyes without an ERM in preoperative optical coherence tomography were included in this study. RESULTS: The incidence of ERM surgery after RRD repair was 2.4%. The mean time from RRD repair to ERM surgery was 19.5±27.2 months. The odds ratios after adjusting for age and sex were as follows: the preoperative visual acuity (logarithm of the minimum angle of resolution, logMAR), 2.17 (p=0.02; 95% confidence interval [CI], 1.11-5.16); axial length, 1.38 (p=0.002; 95% CI, 1.12-1.72); 20-gauge vitreous surgery instruments, 3.82 (p<0.0001; 95% CI, 2.02-7.16); internal limiting membrane (ILM) peeling, 0.28 (p=0.033; 95% CI, 0.05-0.92). ERM surgery improved visual acuity from 0.36 to 0.01 logMAR, even at ≥1.5 years after RRD repair. CONCLUSIONS: Careful follow-up is required in the following cases: long axial length before RRD repair, low visual acuity, use of 20-gauge vitreous surgery instruments, and a lack of ILM peeling.

Asymmetric extent of distortion measured using the Watzke-Allen Test in patients with macular hole.

Visual dysfunction in patients with macular hole is believed to occur because of cone cell displacement, often measured by the Watzke-Allen test (WAT). However, it is unknown if the horizontal and vertical measurements recorded by WAT reflect the true extent of photoreceptor displacement. This study aimed to measure the extent of photoreceptor displacement in patients with macular hole using WAT and compare the displacement value with the hole diameter measured by optical coherence tomography (OCT). This prospective, observational study at a single tertiary referral center included 43 patients with macular hole. WAT thresholds were assessed for their ability to detect macular hole. The slit was presented vertically and horizontally, and the brightness of the monitor screen was 180 cd/m2. Horizontal and vertical WAT thresholds for distortion were measured. Correlations and performance evaluations were assessed by Pearson's correlation analysis and Wilcoxon rank-sum test, respectively, between WAT threshold values and hole diameters. Horizontal and vertical WAT thresholds and diameters were compared using paired t-tests. The mean vertical WAT threshold (1.95° ± 0.87°) was significantly higher than the mean horizontal threshold (1.71° ± 0.73°; P < 0.0001). The mean minimum horizontal hole diameter (303.42 ± 111.16 mm; visual angle, 1.01°) was significantly greater than the mean minimum vertical diameter (264.12 ± 107.88 mm; visual angle, 0.88°; P = 0.0149). The minimum vertical and horizontal macular hole diameters were positively correlated with the vertical and horizontal WAT threshold values (r = 0.514, P < 0.01; r = 0.447, P < 0.01, respectively). The WAT threshold values were greater than the respective minimum macular hole diameters, indicative of cone cells displacement over an area larger than that of the hole. The difference in the extent of vertical and horizontal distortions suggests asymmetric hole formation. Hence, WAT threshold values may help evaluate visual function in patients with macular hole.

Influence of hyperbaric oxygen therapy on thrombus formation ability in humans.

Background: Hyperbaric oxygen (HBO2) therapy was introduced nearly 300 years ago. However, its effect on thrombus formation is unclear. This may be because platelet and coagulation functions are unstable, yielding variable results; hence, accurate measurement is difficult. Our study aimed to analyze changes in thrombus formation before and after HBO2 therapy by using a total thrombus formation analysis system (TTAS). Methods: Six patients were prescribed HBO2 therapy for skin and soft tissue ulcers, and necrotic fasciitis. Blood samples were collected immediately before and after treatment. Then samples were put into a reservoir that connected to AR-chip to assess changes in the thrombus formation ability of both platelets and coagulation factors. We examined the differences in the thrombus formation ability using T-TAS. Time until the onset of white thrombus formation (T10) and complete occlusion of the capillary (T80) were analyzed by a two-way repeated measure analysis of variance (ANOVA). Results: The duration to pressure increase of samples after HBO2 therapy was longer than the duration before HBO2 therapy (p<0.05). This suggests decreased clot adhesiveness to the inner surface of the simulated blood vessel and reduced clot formation ability. Conclusions: The results for T10 and T80 suggest that HBO2 therapy reduced thrombus formation ability in the enrolled patients. We believe that T-TAS is a promising method to predict the efficacy of HBO2 therapy.

Effects of hyperbaric exposure on thrombus formation.

BACKGROUND: Hyperbaric oxygen (HBO2) therapy has a long history of use. However, its effect on thrombus formation is unclear. Many reports have indicated that it accelerates platelet aggregation, which suggests that it may increase thrombotic events. However, clinical trial results are inconsistent, and no previous reports have demonstrated that HBO2therapy does in fact increase thrombotic events. Here, we used a total thrombus formation analysis system (T-TAS) to analyze changes in thrombus formation in a specimen group exposed to constant hyperbaric pressure in vitro, and a control group. METHODS: Blood samples were collected from two sets of 10 healthy volunteers (mean age, 28.8 years) with no underlying disease. In the pressurized group, a constant pressure was applied to specimens in temperature-controlled test tubes; the non-pressurized group served as the control. Thrombus formation in samples from both the pressurized and control groups were measured using the T-TAS immediately, 20 minutes, and 40 minutes after pressurization. RESULTS: In the pressurized group, the onset of thrombus formation was significantly delayed, confirming a reduction in thrombus formation ability. However, the reduced ability for thrombus formation in the pressurized group recovered to the level of the control group. That is, the change in thrombus formation ability caused by pressure was proven to be reversible. CONCLUSIONS: We are the first to ascertain a decrease in the thrombus formation ability in specimens exposed to hyperbaric pressure using a T-TAS, which is capable of measuring thrombus formation in an environment similar to that in vivo.