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PubMed1992

Ischemic macular edema. Recognition and favorable natural history in branch vein occlusion.

Eyes with macular edema caused by retinal branch vein occlusion underwent masked evaluation of fluorescein angiography to determine complete macular perfusion vs incomplete macular perfusion (capillary dropout, ischemia). Cases evaluated as incomplete macular perfusion showed a greater frequency of improvement (91%) in visual acuity than did perfused cases (29%) (P = .003) after a mean follow-up of 39 months. Ischemic edema is often transient, and is associated with a good outcome in visual acuity (median final visual acuity was 20/30). Perfused macular edema has a poorer prognosis for visual acuity (median final visual acuity was 20/80). Macular ischemia is usually associated with a broken foveal capillary ring. Previous animal research on ischemic brain edema has shown that following brain ischemia, an intracellular and an extracellular hypertonic environment lead to intracellular and extracellular edema (cytotoxic edema), which is often followed by vascular protein leakage (vasogenic edema). A similar occurrence in ischemic retina could explain the transient edema reported herein, with good outcome in visual acuity following the spontaneous resolution of edema.

Aged↗
PubMed1983

Induction of brain edema following intracerebral injection of arachidonic acid.

The effects of polyunsaturated fatty acids on brain edema formation have been studied in rats. Intracerebral injection of polyunsaturated fatty acids (PUFAs), including linolenic acid (18:3) and arachidonic acid (20:4), caused significant increases in cerebral water and sodium content concomitant with decreases in potassium content and Na+- and K+- dependent adenosine triphosphatase activity. There was gross and microscopic evidence of edema. Saturated fatty acids and monounsaturated fatty acid were not effective in inducing brain edema. The [125I]-bovine serum albumin spaces increased twofold and threefold at 24 hours with 18:3 and 20:4, respectively, indicating vasogenic edema with increased permeability of brain endothelial cells. Staining of the brain was observed five minutes after injection of Evans blue dye followed by arachidonic acid perfusion. A major decrease in brain potassium content was evidence of concurrent cellular (cytotoxic) edema as well. The induction of brain edema by arachidonic acid was dose dependent and maximal between 24 and 48 hours after perfusion. Dexamethasone (10 mg/kg) was effective in ameliorating the brain edema, whereas a cyclooxygenase inhibitor, indomethacin (10 mg/kg), was not. These data indicate that arachidonic acid and other PUFAs have the ability to induce vasogenic and cellular brain edema and further support the hypothesis that the degradation of phospholipids and accumulation of PUFAs, particularly arachidonic acid, initiate the development of brain edema in various disease states.

Animals↗
PubMedDate not supplied

Discrimination between different types of white matter edema with diffusion-weighted MR imaging.

Brain edema can be classified into three categories: vasogenic, cytotoxic, and interstitial. The mechanism of edema is thought to be different in each type. The authors studied the movement of water molecules in each type of white matter edema in a rat model by using diffusion-weighted magnetic resonance imaging. Conventional T2-weighted imaging did not allow distinction between the three types of white matter edema; the three types of edema were, however, distinguished by using diffusion-weighted imaging. The apparent diffusion coefficient (ADC) of water was different in each type of edema. Water molecules in cytotoxic edema induced by triethyl-tin intoxication showed a smaller and less anisotropic ADC than in normal white matter. In contrast, water in vasogenic edema induced by cold injury had a larger and more anisotropic ADC than in normal white matter. Water in interstitial edema due to kaolin-induced hydrocephalus had an anisotropic and very large ADC.

Animals↗
PubMed1997

Complement component C5 deficiency reduces edema formation in murine ligation-induced acute pancreatitis.

The complement cascade is activated in humans and animals with acute pancreatitis. Activation of complement component C5 liberates C5a, C5a-desarg, and terminal complement complexes (TCCs) that increase capillary permeability, edema, and leukocyte chemotaxis at injured sites. Complement activation plays a major role in pathogenesis of capillary leak and edema formation in severe acute pancreatitis; however, the contribution of C5 (C5a/C5a-desarg, TCCs) has not been defined. Using He gene mutant mice lacking circulating C5, the role of C5 in ligation-induced acute pancreatitis was evaluated. We performed the following experiments: C5-sufficient (Hc1/Hc1) and C5-deficient (Hc0/Hc0) mice had bile and pancreatic ducts ligated. Sham-operated mice had ducts dissected but not ligated. Mice were killed at 4, 8, and 24 hr after bilepancreatic duct ligation. Serologic and morphologic evidences of acute pancreatitis were evaluated. Pancreatic edema was assessed using analysis of pancreatic water content, histologic edema score, and determination of wet weight ratio. After 4, 8, and 24 hr of bile-pancreatic duct ligation, hyperamylasemia and histologic changes of acute pancreatitis were observed in both C5-deficient and C5-sufficient mice. Edema developed in all mice with acute pancreatitis. However, when compared to C5-sufficient mice, mice deficient in C5 developed significantly less pancreatic edema at both 8 and 24 hr of bile-pancreatic duct ligation. This difference was not observed 4 hr after induction of acute pancreatitis. We conclude that C5 contributes to edema formation in murine ligation-induced acute pancreatitis. The presence of an early C5-independent phase, in conjunction with the observation of significant edema in mice deficient in C5, suggests there are other mediators of edema formation in this acute pancreatitis model.

Amylases↗
PubMed2000

Heterogeneous mechanisms of early edema formation in cerebral contusion: diffusion MRI and ADC mapping study.

Severe cerebral contusion is sometimes associated with early edema formation within 24-48 hours post-trauma, and this frequently results in progressive ICP elevation and clinical deterioration. To investigate the underlying mechanisms of such severe contusion edema, diffusion imaging and ADC mapping were performed in 20 patients with cerebral contusion, employing 1.5 T echo planar MRI. Within 24 hours post-trauma, the diffusion images demonstrated a low intensity core in the central area and a high intensity rim in the peripheral area of contusion. The ADC value increased in the central area (ADC ratio (contusion/normal brain) = 1.13 +/- 0.13) and decreased in the peripheral area (ADC ratio = 0.83 +/- 0.13). This suggested that intra- and extracellular components underwent disintegration and homogenization within the central area, whereas cellular swelling was predominant in the peripheral area. A crescent-shaped zone of very high ADC value (ADC ratio = 1.38-1.61) was observed at the border between these two areas during the period of 24-48 hours post-trauma in some cases, apparently indicating that edema fluid was accumulated within a space formed by homogenization. The ADC values in the peripheral area shifted to an increase after 48-72 hours post-trauma. These findings imply that multiple mechanisms operate in early edema formation in cerebral contusion. It appears that the capacity for edema fluid accumulation increases in the central area and resistance for edema fluid propagation is elevated by cellular swelling in the peripheral area. We suggest that a combination of such events facilitates edema fluid accumulation in the central area and contributes, together with the cellular swelling in the peripheral area, to the mass effect of contusion edema. Diffusion MRI and ADC mapping represent powerful tools for investigating spatially as well as temporally heterogeneous mechanisms of contusion edema.

Brain↗
PubMed2000

The permissive nature of blood brain barrier (BBB) opening in edema formation following traumatic brain injury.

The contribution of blood brain barrier opening to traumatic brain edema is not known. This study compares the course of traumatic BBB disruption and edema formation, with the hypothesis that they are not obligately related. Sprague-Dawley rats were divided into three groups: Group A (n = 47)--Impact Acceleration (IAM); Group B (n = 104)--lateral cortical impact (CCI); Group C (n = 26)--IAM + hypoxia & hypotension (THH). BBB integrity was assessed using i.v. markers (Evan's Blue, or gadolinium-DTPA). Edema formation was evaluated with gravimetry, and T1-weighted MRI. In IAM, BBB opened immediately but closed rapidly, and remained closed for at least the next 36 hours whilst 24-hour hemispheric water content (HWC) rose by 0.9% (p < 0.01). In CCI, BBB opened in both hemispheres for up to 4 hours; four hour HWC in the uninjured hemisphere was indistinguishable from Sham, where HWC in the injured hemisphere rose by approximately 1.5% (p < 0.005). We distinguished two THH animals based on Apparent Diffusion Coefficient (ADC) recovery: in ADC-recovery animals 4 hour cortical water content (CWC) was 80.4 +/- 0.6%, cf 81.4 +/- 1.3% in ADC-non-recovery (p < 0.05). In all animals the BBB was open, however two populations of permeability were seen which likely related to flow-limited extravasation of gadolinium. In IAM edema forms despite only brief BBB opening. Although there is diffuse BBB opening with lateral contusion, edema only forms in the injured hemisphere. In THH, edema formation in the face of a widely permeable barrier is driven by ADC changes or cell swelling. Edema formation clearly does not correspond with BBB opening and an open BBB is clearly not required for edema formation. However we hypothesize that a permeable BBB permissively worsens the process, by acting as a low resistance pathway for ion and water movement. These findings are consistent with our general hypothesis that edema formation after TBI is mainly cytotoxic.

Animals↗
PubMed2006

[Differential diagnosis of bone marrow edema of the knee joint].

Bone marrow edema of the knee joint is a frequent clinical picture in MR diagnostics. It can be accompanied by symptoms and pain in the joint. Diseases that are associated with bone marrow edema can be classified into different groups. Group 1 includes vascular ischemic bone marrow edema with osteonecrosis (synonyms: SONK or Ahlbäck's disease), osteochondrosis dissecans, and bone marrow edema syndrome. Group 2 comprises traumatic or mechanical bone marrow edema. Group 3 encompasses reactive bone marrow edemas such as those occurring in gonarthrosis, postoperative bone marrow edemas, and reactive edemas in tumors or tumor-like diseases. Evidence for bone marrow edema is effectively provided by MRI, but purely morphological MR information is often unspecific so that anamnestic and clinical details are necessary in most cases for definitive disease classification.

Bone Marrow Diseases↗
PubMed2002

Aerosolized beta(2)-adrenergic agonists achieve therapeutic levels in the pulmonary edema fluid of ventilated patients with acute respiratory failure.

OBJECTIVE: Experimental studies demonstrate that beta-adrenergic agonists markedly stimulate alveolar fluid clearance if concentrations of 10(-6) M are achieved in alveolar fluid. However, no studies have determined whether aerosolized beta-adrenergic agonists are delivered to the distal air spaces of the lung in therapeutic concentrations in patients with pulmonary edema. DESIGN AND SETTING: This retrospective study measured albuterol levels in the pulmonary edema fluid and plasma from mechanically ventilated patients with pulmonary edema from a hydrostatic mechanism ( n=10) or from acute lung injury ( n=12). MEASUREMENTS AND RESULTS: After a total aerosolized albuterol dose of 4.2+/-3.2 mg in the prior 6 h the median pulmonary edema fluid albuterol level was 1,250 ng/ml (10(-6) M) in patients with hydrostatic pulmonary edema; after 3.5+/-2.6 mg the figure was 1,240 ng/ml (10(-6) M) in patients with pulmonary edema from acute lung injury. Plasma albuterol levels were much lower, with a median of 5.2 ng/ml (0.01 x 10(-6) M) in patients with hydrostatic pulmonary edema and 3.1 ng/ml (0.01 x 10(-6) M) in patients with pulmonary edema from acute lung injury. CONCLUSIONS: These results provide the first evidence that levels of beta-adrenergic agonists that are physiologically efficacious in experimental models can be achieved with conventional delivery systems in ventilated, critically ill patients with acute respiratory failure from pulmonary edema.

APACHE↗
PubMed2001

Morphological and functional analyses of diabetic macular edema by optical coherence tomography and multifocal electroretinograms.

PURPOSE: To determine the correlation between the tomographic features and the visual functions of eyes with diabetic macular edema. METHODS: Optical coherence tomographic (OCT) images and multifocal electroretinograms were obtained from 45 eyes of 25 patients with diabetic macular edema and from 21 eyes of 21 normal subjects. RESULTS: The OCT images showed cystoid macular edema in 18 eyes and diffuse retinal swelling without cystoid edema in the other 27 eyes. The fovea was significantly thicker in eyes with cystoid macular edema and in those with diffuse retinal swelling than in normal eyes. The fovea of eyes with cystoid edema was significantly thicker than the fovea of eyes with diffuse swelling. The best-corrected visual acuity and the electrical response density from the macular area were significantly reduced in eyes with diabetic macular edema, particularly in those with cystoid edema. The best-corrected visual acuity and macular response density of the multifocal ERGs were inversely correlated, and the implicit times were directly correlated with foveal thickness. CONCLUSION: The visual acuity was correlated significantly with morphological changes revealed by OCT and with multifocal ERGs. The combination of OCT and multifocal ERGs may provide objective criteria for the evaluation and assessment of diabetic macular edema.

Adult↗
PubMed1984

The role of brain edema in epileptic brain damage induced by systemic kainic acid injection.

Edema formation and blood-brain barrier permeability was studied in animals with epileptic seizures induced by subcutaneous injection of kainic acid. Brain edema was most pronounced between 3 and 24 h after kainic acid injection. It was reflected by massive swelling of perineuronal and perivascular astroglia. Three hours after kainic acid perivascular astroglia swelling resulted in disturbance of local microcirculation in the affected brain areas. In addition, compression of drainage veins by the edematous brain induced focal perivenous hemorrhages similar to herniation damage in human brain edema. Tracer studies with sodium fluorescein, Evans blue, albumin and horseradish peroxidase revealed only a mild increase in the permeability of cerebral vessels, topographically unrelated to areas of brain edema. This finding indicates the presence of cytotoxic brain edema in kainic acid-induced epileptic brain damage. Treatment of brain edema with dexamethasone did not influence the incidence and severity of kainic acid-induced epileptic brain damage. However, in 54% of animals injected with kainic acid, lesions were completely prevented by treatment of brain edema with mannitol. The present results indicate that brain edema plays an important role in the pathogenesis of epileptic brain damage following systemic kainic acid intoxication. It is suggested that in this model of limbic epilepsy the brain edema is due to the massive ionic imbalance elicited in the affected brain regions by the kainic acid-induced persistent neuronal excitation.

Animals↗
PubMed1986

Comparative study of the edema-forming activity of Costa Rican snake venoms and its neutralization by a polyvalent antivenom.

The edema-forming activity of eight Costa Rican crotaline snake venoms and its neutralization by a polyvalent antivenom were studied using the mouse footpad test. All of the venoms induced edema, the highest activity being present in the venoms of Bothrops lateralis and Bothrops picadoi. When experiments were performed with preincubation of venom and antivenom, neutralization of edema was poor. Moreover, it was observed that, with some venoms, edema increased when large doses of antivenom were used. This effect was also observed when some venoms were incubated with coral snake antivenom, suggesting that venoms may release some pharmacologically active component(s) from antivenom, since the latter contains traces of alpha-2 and beta globulins. Based on these findings, an alternative approach to the study of the neutralization of edema was used; in this new method, antivenom was injected i.v. before venom administration, thereby avoiding preincubation. With this technique, a much better neutralization of edema was observed, although with some venoms it was still poor. Venoms contain low molecular weight factors which induce edema, suggesting that lack of immunogenicity of some components may cause a poor neutralization. However, such components are responsible for only a minor portion of the edema induced by crude venoms. It is suggested that experiments in which venom and antivenom are preincubated preincubated in testing the neutralization of edema should be avoided, and that a more adequate approach may be an independent inoculation of venom and antivenom.

Animals↗
PubMedDate not supplied

Nature, time-course, and extent of cerebral edema in perinatal hypoxic-ischemic brain damage.

To ascertain the nature, time-course, and extent of the cerebral edema that accompanies perinatal hypoxic-ischemic brain damage, 7-day postnatal rats were subjected to unilateral right common carotid artery ligation followed by exposure to hypoxia with 8% oxygen for up to 3 hours. Some rat pups were sacrificed during hypoxia-ischemia or recovery for determination of cerebral hemispheric water content and percentage of brain swelling. Other animals were sacrificed and their brains processed either for determination of cerebral cortical edema and infarct volume or for horseradish peroxidase staining. The results indicated that cerebral edema occurs even during the course of hypoxia-ischemia and that the extent and duration of edema formation during the recovery period is dependent upon the severity of tissue injury. The data also disclosed a direct, linear correlation between infarct volume and the extent of cerebral edema. Accordingly, the greater the severity of cerebral edema, the proportionately greater the extent of infarction. Horseradish peroxidase staining, a reflection of vasogenic edema, occurred in 17 of 19 brains in a distribution which corresponded closely to the distribution of neuropathologic alterations observed histologically. The findings indicate that cerebral edema can occur in the absence of consequent infarction and that when infarction does occur, the associated edema contributes little or nothing to the severity of the ultimate brain damage.

Analysis of Variance↗
PubMed2006

Hemorrhagic corpus luteum is associated with ovarian edema.

BACKGROUND: Most cases of ovarian edema are thought to result from intermittent ovarian/adnexal torsion. This study describes how, in some cases, this etiology was ruled out even though the edema was unexplained. STUDY OBJECTIVE: To evaluate the association between ovarian edema and hemorrhagic corpus luteum. SETTING: Department of gynecology in an urban medical center. PARTICIPANTS: Five patients admitted to the department of gynecology with a sonographic diagnosis of ovarian edema of unexplained etiology. RESULTS: Laparoscopy performed on three of five patients in whom a diagnosis of unexplained ovarian edema revealed hemorrhagic corpus luteum and ovarian edema. The remaining two patients displayed typical sonographic imaging of hemorrhagic corpus luteum and ovarian edema and they were managed expectantly. The affected ovaries were between 4.8 and 10 times larger than the unaffected ovaries. During follow-up, the affected ovaries returned to their normal size and appearance. CONCLUSIONS: Hemorrhagic corpus luteum can cause ovarian edema without interrupting the blood flow supply. The outcome of expectant management without any surgical intervention is the gradual disappearance of the ovarian edema in these patients and the return of ovaries to a normal sonographic appearance.

Adolescent↗
PubMed2005

Inhibition of intestinal transit by resuscitation-induced gut edema is reversed by L-NIL.

BACKGROUND: Post-resuscitation gut edema and associated gut dysfunction is a common and significant clinical problem that occurs after traumatic injury and shock. We have shown previously that gut edema without ischemia/reperfusion injury delays intestinal transit [1]. We hypothesized that gut edema increases expression of inducible nitric oxide synthase (iNOS) protein, and that selective iNOS inhibition using L-NIL reverses the delayed intestinal transit associated with gut edema. MATERIALS AND METHODS: One hour prior to laparotomy, rats were pretreated with 10 mg/kg body weight of intraperitoneal L-NIL or saline vehicle and underwent 80 ml/kg body weight of 0.9% saline + superior mesenteric venous pressure elevation (Edema) or sham surgery (Sham). A duodenal catheter was placed to allow injection of a fluorescent dye for the measurement of intestinal transit. At 6 h, the small bowel was divided and the mean geometric center (MGC) of fluorescent dye was measured to determine transit. Ileum was harvested for histological assessment of mucosal injury, evaluation of iNOS protein expression by Western blotting, and MPO activity. Tissue water was determined using the wet-to-dry weight ratio to assess gut edema. Data are expressed as mean +/- SEM, n = 3-6 and * = P <0.05 using ANOVA. RESULTS: Gut edema, expressed as increased wet-to-dry ratio, was associated with decreased intestinal transit and elevated iNOS protein expression. Pretreatment with l-NIL improved intestinal transit and decreased expression of iNOS protein without decreasing intestinal tissue water compared to edema animals. There was no difference in mucosal injury or MPO activity among groups. CONCLUSION: Gut edema delays intestinal transit via an iNOS-mediated mechanism.

Animals↗
PubMed2004

Edema and brain trauma.

Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury (TBI) as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist: "vasogenic" due to blood-brain barrier (BBB) disruption resulting in extracellular water accumulation and "cytotoxic/cellular" due to sustained intracellular water collection. A third type, "osmotic" brain edema is caused by osmotic imbalances between blood and tissue. Rarely after TBI do we encounter a "hydrocephalic edema/interstitial" brain edema related to an obstruction of cerebrospinal fluid outflow. Following TBI, various mediators are released which enhance vasogenic and/or cytotoxic brain edema. These include glutamate, lactate, H(+), K(+), Ca(2+), nitric oxide, arachidonic acid and its metabolites, free oxygen radicals, histamine, and kinins. Thus, avoiding cerebral anaerobic metabolism and acidosis is beneficial to control lactate and H(+), but no compound inhibiting mediators/mediator channels showed beneficial results in conducted clinical trials, despite successful experimental studies. Hence, anti-edematous therapy in TBI patients is still symptomatic and rather non-specific (e.g. mannitol infusion, controlled hyperventilation). For many years, vasogenic brain edema was accepted as the prevalent edema type following TBI. The development of mechanical TBI models ("weight drop," "fluid percussion injury," and "controlled cortical impact injury") and the use of magnetic resonance imaging, however, revealed that "cytotoxic" edema is of decisive pathophysiological importance following TBI as it develops early and persists while BBB integrity is gradually restored. These findings suggest that cytotoxic and vasogenic brain edema are two entities which can be targeted simultaneously or according to their temporal prevalence.

Acidosis, Lactic↗
PubMed2004

Patterns of macular edema in patients with uveitis: qualitative and quantitative assessment using optical coherence tomography.

PURPOSE: To describe the morphologic characteristics of uveitic macular edema by the use of optical coherence tomography (OCT) and to investigate the correlation between tomographic features and visual acuity (VA). DESIGN: Cross-sectional study. PARTICIPANTS: Seventy consecutive patients with uveitis in a university-based practice with a clinical diagnosis of macular edema in at least one eye. Inclusion criteria were: (1) verification of macular edema by OCT, (2) adequate media clarity for fundus visualization, and (3) absence of coexisting ocular disease limiting visual potential. METHODS: Complete ophthalmic examination: best-corrected Snellen VA, slit-lamp examination, fundus biomicroscopy, indirect ophthalmoscopy, and OCT. Fluorescein angiography was performed in selected cases. MAIN OUTCOME MEASURES: Best-corrected Snellen VA and tomographic features of the macula, including macular thickness measurement and correlation of macular thickness with VA. RESULTS: Eighty-four eyes of 60 patients met the inclusion criteria. The mean VA (Snellen test) was 20/36. There were 3 patterns of macular edema: diffuse macular edema (DME), cystoid macular edema (CME), and serous retinal detachment (RD). Serous retinal detachment was detected in 17 eyes (20.2%). Patients were classified into the following groups: DME (46 eyes, 54.8%), CME (21 eyes, 25%), DME and RD (5 eyes, 5.9%), CME and RD (12 eyes, 14.3%). Epiretinal membrane was detected by OCT in 34 eyes (40.5%). Eight eyes (9.5%) demonstrated vitreomacular traction. The mean retinal thickness at the central fovea was 333+/-171 microm (mean +/- standard deviation). Macular edema was located mainly in the outer retinal layers. Eyes with CME had significantly greater retinal thickness measurements than eyes with DME (P<0.001). Multivariate analysis revealed that VA was negatively correlated with increased macular thickness, presence of CME, and RD (P<0.05). CONCLUSIONS: Optical coherence tomography demonstrated 3 patterns of macular edema in patients with uveitis: DME, CME, and RD. Epiretinal membrane coexisted in a significant percentage of patients. In patients with uveitis with clear media, the morphologic features of macular edema and macular thickness correlated with VA.

Adolescent↗
PubMed2006

Relationship between macular microcirculation and progression of diabetic macular edema.

PURPOSE: To investigate the relationship between blood flow velocity in perifoveal capillaries and retinal thickness at the central fovea in diabetic patients with clinically significant macular edema to elucidate the pathogenesis of diabetic macular edema. DESIGN: Comparative, cross-sectional, prospective study. PARTICIPANTS: Participants included diabetic patients with clinically significant macular edema (n = 22), matched diabetic patients without clinically significant macular edema (n = 22), and healthy volunteers (n = 16). METHODS: Perifoveal capillary blood flow velocity was measured with fluorescein angiography using a scanning laser ophthalmoscope and was analyzed by the tracing method. The severity of perifoveal capillary abnormalities among diabetic patients without clinically significant macular edema was classified by the size and outline of the foveal avascular zone and extent of foveal capillary loss at the baseline by the use of fluorescein angiograms. Retinal thickness at the central fovea was measured by optical coherence tomography. MAIN OUTCOME MEASURES: Relationship between perifoveal capillary blood flow velocity and retinal thickness at the central fovea. RESULTS: Perifoveal capillary blood flow velocity was significantly slower in the patients with clinically significant macular edema (0.94+/-0.09 mm/second) compared with the patients without clinically significant macular edema (1.22+/-0.20 mm/second) and the healthy volunteers (1.49+/-0.11 mm/second; P<0.0001). Capillary blood flow velocity negatively correlated with retinal thickness at the central fovea (r = -0.4018, P<0.0001). Capillary blood flow velocity varied among diabetic patients without clinically significant macular edema, and there were significant negative correlations between capillary blood flow velocity and the size of the foveal avascular zone (r = -0.52, P = 0.01), the outline of the foveal avascular zone (r = -0.44, P = 0.04), and the extent of foveal capillary loss (r = -0.51, P = 0.01). CONCLUSIONS: The reduction of perifoveal capillary blood flow velocity may occur before the increase of retinal thickness at the central fovea in the diabetic patients. It is possible that long-term reduction of blood flow velocity increases retinal thickness of the macula and may play an important role in the development and the progression of diabetic macular edema.

Aged↗
PubMed2003

Randomized clinical trial of topical betaxolol for persistent macular edema after vitrectomy and epiretinal membrane removal.

PURPOSE: To report the efficacy and safety of topical betaxolol for treatment of persistent macular edema. DESIGN: Randomized clinical trial. METHODS: Thirty-seven eyes (37 patients) with best-corrected visual acuity between 20/200 and 20/50 and macular edema that remained for 3 months after vitrectomy and removal of epiretinal membrane were prospectively, randomly assigned to receive betaxolol or placebo. Nineteen eyes of 19 patients received betaxolol twice daily, and 18 eyes of 18 patients received placebo as a randomized comparison group. The patients were followed up for 6 months. This study evaluated the effect of betaxolol on best-corrected visual acuity and area of macular edema, which was digitally measured on serial fluorescein angiogram. Calculations of mean best-corrected visual acuity were based on logarithm of the minimal angle of resolution (logMAR). To assess changes in area of edema, the initial (pretreatment) size of the edema was set to 100%, and all posttreatment measurements were normalized relative to the initial size. RESULTS: Mean best-corrected visual acuity at baseline was 0.216 (20 of 92.6) and 0.244 (20 of 82.0) in the treatment and control group, respectively. Mean area of macular edema was 2.271 +/- 1.629 mm(2) and 2.273 +/- 1.209 mm(2) in the treatment and control group; there was no significant difference. The visual acuity at 6 months after the start of the follow-up was 0.471 (20 of 42.5) in the treatment group and 0.236 (20 of 84.7) in the control group. Mean changes in logMAR of visual acuity for 3- and 6-month follow-up were -0.282 +/- 0.191 and -0.337 +/- 0.197 in the treatment group, and -0.016 +/- 0.186 and +0.015 +/- 0.267 in the control group; a significant difference was found (P <.0001; P <.0001). Areas of macular edema at 6 months after the start of the follow-up were 1.492 +/- 1.357 mm(2) in the treatment group and 2.125 +/- 1.434 mm(2)in the control group. Mean change in area of the edema for 6 months were 76.5% +/- 24.1% and 63.4% +/- 28.3% in the treatment group and 92.9% +/- 15.4% and 87.4% +/- 25.6% in the control group; treated patients showed a significantly larger reduction than untreated patients at each examination (P =.0193; P =.0102). No complication associated with treatment or placebo was found. CONCLUSIONS: Topical betaxolol appeared to have a favorable treatment effect in eyes with macular edema that remained after vitrectomy and removal of epiretinal membrane. Further investigation of more cases and longer follow-up are needed.

Administration, Topical↗