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PubMed2006

Bilobalide prevents ischemia-induced edema formation in vitro and in vivo.

EGb761, a standardized extract of Ginkgo biloba, has neuroprotective properties in animal models of ischemia, an activity that is partially attributed to its constituent, bilobalide. EGb761 has also been reported to inhibit edema formation induced by toxins such as triethyltin. The goal of this study was to test the activity of pure bilobalide to prevent edema formation in models of ischemia. Oxygen-glucose deprivation (OGD) in rat hippocampal slices served as a model of in vitro-ischemia. OGD caused cellular edema formation as indicated by an increase of slice water contents in 30 min. Bilobalide (1-10 microM) reduced slice water contents in ischemic slices in a concentration-dependent manner. As a model of in vivo-ischemia, we performed middle cerebral artery occlusion (MCAO) in mice. Permanent MCAO caused cell death and swelling of the ischemic hemisphere within 24 h. Pretreatment of the mice with bilobalide (10 mg/kg i.p.) reduced infarct area by 43% (as judged by 2,3,5-triphenyl-tetrazolium chloride (TTC) staining) and edema formation by 70% (as judged by hemispheric enlargement). In parallel experiments, pretreatment with bilobalide also reduced forebrain water contents in the ischemic hemisphere by 57%. As an alternative model of brain edema formation, we used water intoxication to increase brain water content; bilobalide, was, however, inactive in this model. We conclude that bilobalide strongly and specifically attenuates edema formation in models of brain ischemia in vitro and in vivo. Bilobalide may be therapeutically effective in brain edema which occurs secondarily to large hemispheric stroke and traumatic brain injury in humans.

Animals↗
PubMed2001

Aqueous humor and plasma vascular endothelial growth factor in uveitis-associated cystoid macular edema.

PURPOSE: To determine the association between cystoid macular edema and vascular endothelial growth factor concentration in the aqueous humor and plasma of uveitis patients. METHODS: Cross-sectional study. Vascular endothelial growth factor concentrations were measured by enzyme-linked immunosorbent assay in the aqueous humor of 20 uveitis patients (9 with and 11 without cystoid macular edema), and in the plasma of 40 uveitis patients (20 with and 20 without cystoid macular edema) and 20 healthy volunteers. RESULTS: Mean aqueous humor vascular endothelial growth factor concentrations for uveitis patients with and without cystoid macular edema were 152.3 and 109.5 pg/ml, respectively, P =.044. Mean plasma vascular endothelial growth factor concentrations in uveitis patients with and without cystoid macular edema and in healthy volunteers were 32.2, 29.6, and 55.0 pg/ml, respectively. Uveitis patients had lower plasma vascular endothelial growth factor levels than did healthy volunteers, P =.0002. CONCLUSION: In uveitis patients, vascular endothelial growth factor concentration is increased in the aqueous humor of eyes with cystoid macular edema. It may be useful to investigate vascular endothelial growth factor antagonists as a treatment for uveitis-associated cystoid macular edema.

Adolescent↗
PubMed2004

Intravitreal triamcinolone injection for diabetic macular edema: a clinical and fluorescein angiographic case series.

BACKGROUND: A significant number of eyes with diabetic macular edema remain refractory to treatment despite numerous attempts at photocoagulation. Triamcinolone acetonide, a minimally water soluble steroid injected in suspension form, has been reported to be a well-tolerated agent for intravitreal injection, prompting a decrease in diabetic macular edema on optical coherence tomography. We report our experience with this treatment in 19 eyes with persistent diabetic macular edema. METHODS: We reviewed the charts of 16 patients (19 eyes) from a clinical practice with diabetic macular edema persistent after focal or grid laser photocoagulation. All eyes had received 4 mg of triamcinolone, injected into the vitreous cavity 3.5 mm posterior to the limbus. Fluorescein angiography was performed before and about 2 weeks after the injection. Snellen visual acuity and intraocular pressure (as determined with Goldmann applanation tonometry) were also measured before and after the injection. RESULTS: Fluorescein angiography showed marked improvement of macular edema in 4 eyes (21.0%), mild improvement in 10 eyes (52.6%) and no change in 5 eyes (26.3%); no patient had worsening of macular edema. Visual acuity improved by at least 1 line in 13 eyes (68.4%), by 2 or more lines in 5 eyes (26.3%), by 3 or more lines in 2 eyes (10.5%) and by 4 lines in 1 eye (5.3%); visual acuity remained unchanged in 5 eyes (26.3%) and deteriorated by 1 line in 1 eye (5.3%). Intraocular pressure elevation of 10 mm Hg or greater occurred in two eyes (10.5%) and was successfully treated with topical administration of 0.15% brimonidine.The triamcinolone was well tolerated, and there were no other ocular complications. INTERPRETATION: Intravitreal injection of triamcinolone has potential in the treatment of diabetic macular edema and warrants investigation in a randomized prospective clinical trial.

Aged↗
PubMed2000

Intrinsic prostacyclin contributes to exudation induced by bradykinin or carrageenin: a study on the paw edema induced in IP-receptor-deficient mice.

To prove that prostaglandin I2 (PGI2) is a major prostaglandin involved in bradykinin-induced exudation, we examined carrageenin- or bradykinin-induced paw edema in prostacyclin receptor-deficient mice (IPKO). Paw volume of wild-type mice (IPWT) increased gradually 5-6 hr after the carrageenin injection in a similar manner as in ICR mice, but the swelling in IPKO mice was significantly smaller (about 60% of the IPWT volume). Indomethacin, at 10 mg/kg, suppressed the swelling of the IPWT paw to the level of the non-pretreated IPKO, which was not affected by indomethacin, confirming the previous result that PGI2 is a major prostaglandin involved in the swelling. The paw edema of IPWT and IPKO was significantly attenuated by the nonpeptide bradykinin B2-receptor antagonist FR173657, at 30 mg/kg, to the same level of swelling, indicating kinin involvement. Injection of bradykinin (1.2 nmole) into the paw caused rapid edema, which peaked around 15 min in both mice. However, the edema induced in IPKO was smaller and almost at the same level as that elicited in the indomethacin-treated IPWT, suggesting that edema induced by bradykinin includes the intrinsic effect of PGI2. Concomitant injection of carbacyclin with bradykinin caused enhancement of edema in IPWT mice but not in IPKO mice, indicating that intrinsic PGI2 could cause enhancement of bradykinin- or even carrageenin-induced edema formation. These results clearly demonstrate that bradykinin released by carrageenin may be a key mediator to induce PGI2 formation, and both autacoids work together to induce enhanced inflammatory exudation.

Animals↗
PubMed2003

Acute pulmonary edema in pregnancy.

OBJECTIVE: To describe the incidence, predisposing conditions, and inciting factors culminating in pulmonary edema in the pregnant patient. METHODS: A review of 62,917 consecutive pregnancies delivered at our institution from January 1, 1989 to June 1, 1999 was undertaken for the diagnosis of pulmonary edema. Each chart was reviewed for maternal demographics, admission diagnoses, medication use, gestational age at diagnosis, fluid balance, coexisting maternal illness, tocolytic use, evidence of preeclampsia, and diagnostic criteria. After careful review of the records, the most likely cause of pulmonary edema was assigned. RESULTS: Fifty-one women (0.08%) were diagnosed with acute pulmonary edema during pregnancy or in the postpartum period. The mean patient age at the time of diagnosis was 27.6 +/- 6.4 years. The mean gestational age at the time of diagnosis was 31.5 +/- 6.8 weeks. The diagnosis of pulmonary edema was made during the antepartum period in 24 patients (47%), the intrapartum period in seven (14%), and the postpartum period in 20 (39%). The most common attributable causes were tocolytic use (13 patients [25.5%]), cardiac disease (13 patients [25.5%]), fluid overload (11 patients [21.5%]), and preeclampsia (nine patients [18%]). Those with fluid overload identified as the likely etiology had a significantly greater mean positive fluid balance (6022 +/- 3340 mL). All patients whose pulmonary edema was secondary to tocolytic use received multiple simultaneous tocolytic agents; the most common combination was intravenous magnesium sulfate and subcutaneous terbutaline. Six of the 13 women with cardiac disease were found to have previously undiagnosed structural heart disease. CONCLUSION: The most common causes of pulmonary edema are the use of tocolytic agents, underlying cardiac disease, fluid overload, and preeclampsia.

Acute Disease↗
PubMed1999

Thoracic-fluid conductivity in peripartum women with pulmonary edema.

OBJECTIVE: To measure the level of thoracic-fluid conductivity associated with pulmonary edema in peripartum women by noninvasive thoracic electrical bioimpedance. METHODS: Between March 1994 and August 1996, 134 women were selected for thoracic electrical bioimpedance monitoring. Among them, 12 had pulmonary edema, 33 had severe preeclampsia, 17 had mild preeclampsia, and 72 were in uncomplicated early labor. Each subject's highest thoracic-fluid conductivity measurement was related to her clinical presentation. The Kruskal-Wallis one-way analysis of variance was used to compare groups' means. A receiver operating characteristic curve was used to identify thoracic-fluid conductivity values associated with pulmonary edema. RESULTS: Pulmonary edema was associated with severe preeclampsia in ten cases, urosepsis in one case, and postoperative volume overload in one case. Other than gestational age, there were no significant differences in maternal demographics between groups. Thoracic-fluid conductivity values in women with pulmonary edema (80.6+/-18.3 kohm(-1)) were significantly higher than those in women with severe preeclampsia (62.8+/-16.3 kohm(-1)), mild preeclampsia (53.3+/-11.2 kohm(-1)), or early labor (41.3+/-6.7 kohm(-1)). Thoracic-fluid conductivity of at least 65 kohm(-1) best identified pulmonary edema (sensitivity 83.3%; specificity 86.9%; positive predictive value 38.5%; negative predictive value 98.1%). CONCLUSION: Preeclampsia was associated with increased thoracic-fluid conductivity stratified between mild and severe disease. Thoracic-fluid conductivity of at least 65 kohm(-1) was strongly associated with peripartum pulmonary edema. Women with values above 65 kohm(-1) might be candidates for medical intervention even without overt clinical symptoms.

Adult↗
PubMed1997

Vagal and sympathetic denervation in the development of oleic acid-induced pulmonary edema.

This study investigates the effects of autonomic denervation on extravascular lung water, pulmonary hemodynamics, the filtration coefficient of pulmonary vasculature and oxygenation in the development of pulmonary edema. Thirty seven dogs were divided into seven groups. No experimental treatment was conducted in group Nc (n = 4, sham operation) or group Nv (n = 6, bilateral vagotomy) during a 3 h observation period. In the following groups, oleic acid (0.06 ml/kg) was injected into a central vein to induce pulmonary edema: group OAc (n = 6, intact innervation); group OAv (n = 6, bilateral vagotomy); group OAa (n = 6, alpha-blockade by phentolamine); group OAs (n = 6, alpha- and beta-blockade by sympathectomy); and group OAvs (n = 3, vagosympathectomy). The results showed that in the dogs with normal lungs, bilateral vagotomy per se did not cause lung injury during 3 h of observation. However, in oleic acid pulmonary edema, vagotomy significantly deteriorated pulmonary edema by increasing pulmonary intravascular pressures; Alpha- or alpha- and beta- sympathetic inhibition deteriorated pulmonary edema by increasing pulmonary microvascular permeability. The severity of oleic acid-induced pulmonary edema was same in the dogs with vagosympathectomy as in the dogs with intact innervation. These results suggest the inhibition of vagal or sympathetic innervation will aggravate pulmonary edema in the dog.

Animals↗
PubMed1988

The role of the vitreous in diabetic macular edema.

The authors assessed retrospectively clinical records of 76 patients (125 eyes) 60 years of age or older with diabetic retinopathy who had undergone a vitreous examination. The groups consisted of 105 eyes (63 patients) with macular edema and 20 eyes (13 patients) without macular edema. Vitreous studies were done using the El Bayadi-Kajiura lens to determine whether or not the posterior vitreous was attached to the retina in the macula. Twenty-one of 105 eyes (20.0%) in the edema group and 11 of 20 eyes (55.0%) in the no-edema group had a detached posterior vitreous. This difference was found to be statistically significant, indicating that diabetic cases without macular edema have a significantly higher rate of posterior vitreous detachment than those with macular edema. This study demonstrates that the vitreous may play a role in diabetic macular edema.

Aged↗
PubMed1997

Diode laser (810 nm) versus argon green (514 nm) modified grid photocoagulation for diffuse diabetic macular edema.

OBJECTIVE: To compare argon green (514 nm) versus diode laser (810 nm) modified grid laser photocoagulation treatment in diffuse diabetic macular edema (DDME). DESIGN: Randomized, prospective clinical trial. PARTICIPANTS: Patients with DDME and diabetic retinopathy of fewer than two high-risk characteristics in severity, no previous laser photocoagulation for diabetic macular edema, and no other ocular condition that could interfere with assessment of treatment results. INTERVENTION: One hundred seventy-one eyes of 91 patients were randomized to either argon green (514 nm) or diode laser (810 nm) modified grid laser photocoagulation for DDME. Follow-up was conducted for a minimum of 12 months (16.55 +/- 3.52 months). Retreatment was performed for residual edema involving the foveal avascular zone. MAIN OUTCOME RESULTS: Visual improvement, visual loss, reduction-elimination of macular edema, and the number of supplemental treatments. RESULTS: A comparison of visual improvement, visual loss, reduction-elimination of macular edema, and the number of supplemental treatments showed no statistical difference between the groups (P > 0.05 for all groups). Reduction-elimination of DDME was better in the group without cystoid macular edema than the group with cystoid macular edema, but visual outcome appeared to be similar in both groups. History of hypertension or poor initial visual acuity (< or = 20/80) at entry into the study had no significant effect on the outcome. However, the patients without systemic vascular disease have improved more than those with systemic vascular disease regardless of the type of the laser used. CONCLUSIONS: Diode laser (810 nm) modified grid laser photocoagulation for DDME is equivalent to argon green (514 nm) and patients without systemic vascular disease are more likely to improve after laser treatment with either wavelength.

Adult↗
PubMed1999

The natural history of macular edema after cataract surgery in diabetes.

OBJECTIVE: To determine the natural history of macular edema after cataract surgery in diabetes to provide a rational basis for laser therapy. DESIGN: Prospective clinical and angiographic trial. PARTICIPANTS: Thirty-two patients with diabetes undergoing cataract surgery. INTERVENTION: Phacoemulsification surgery with intraoperative fluorescein angiography, and postoperative clinical and angiographic assessment without macular laser therapy for 1 year after surgery. MAIN OUTCOME MEASURES: Clinically significant macular edema, postoperative macular and optic disc hyperfluorescence relative to the intraoperative angiogram, and logarithm of the minimum angle of resolution (LogMAR) visual acuity. RESULTS: In the first postoperative year, macular fluorescence remained at its intraoperative level in 2 (6%) of 32 eyes and increased in 30 (94%) of 32 eyes, returning to its intraoperative level within 1 year of surgery in 13 (43%) of 30 eyes. Optic disc fluorescence remained at its intraoperative level in 2 (6%) of 32 eyes, was not graded in 3 (9%) of 32 eyes, and increased in 27 (84%) of 32 eyes, returning to its intraoperative level within 1 year of surgery in 19 (70%) of 27 eyes. Clinically significant macular edema was identified in the first postoperative year in 18 (56%) of 32 eyes, being present at the time of surgery in 5 eyes and arising de novo within 1 year of surgery in 13 eyes. It resolved spontaneously within 1 year of surgery in 0 of 5 eyes in which it had been present at the time of surgery and in 9 (69%) of 13 eyes in which it arose in the first 6 months after surgery (P = 0.05). Angiographic and clinical resolutions of macular edema were less likely in eyes with more severe retinopathy at the time of surgery (P = 0.03, 0.005). One-year LogMAR acuity of 0.3 or less (> or = 20/40) was achieved in 27 (84%) of 32 eyes. Clinically significant macular edema at the time of surgery was associated with poorer 1-year visual acuity in multivariate analysis (P = 0.005, r2 = 0.5). CONCLUSIONS: Clinically significant macular edema present in diabetic eyes at the time of cataract surgery is unlikely to resolve spontaneously, but clinically significant macular edema arising after surgery commonly resolves, particularly if retinopathy is mild. These findings have implications for the timing of cataract surgery in diabetes and postoperative macular laser therapy. Ophthalmology 1999;106:663-668

Aged↗
PubMed1989

Ulcerated edematous limbs: effect of edema removal on transcutaneous oxygen measurements.

We studied the effect of edema removal on transcutaneous oxygen tension (TcPO2) in eight patients with leg ulcers. An external pneumatic compression device was effective in removing edema from the ulcerated limbs over a 5-day course of treatment, at which time all treated limbs were clinically free of edema. TcPO2 levels at room air at the ulcer site were markedly reduced when compared with the control chest site, both before and after external pneumatic compression device therapy (p less than 0.001). Edema removal, however, did not significantly alter TcPO2 values (p greater than 0.9). No significant positional effects on TcPO2 values were noted with patients supine, sitting, or with the affected limbs elevated. Five patients (63%) had increased TcPO2 values adjacent to the ulcer site when receiving supplemental oxygen. For these patients, TcPO2 values increased after oxygen inhalation, both before and after edema removal (p less than 0.05). We conclude that TcPO2 values are markedly reduced in ulcerated edematous limbs. Edema, however, may not constitute a barrier to oxygen diffusion through the skin and does not account for the low TcPO2 values in the ulcerated edematous limb. Therefore the positive therapeutic effect of removing edema is unlikely to be related to better oxygenation of the tissues.

Aged↗
PubMed1999

Receptor subtypes involved in tachykinin-mediated edema formation.

Intradermal (ID) injection of the natural tachykinins substance P (SP), neurokinin A (NKA), and neurokinin B (NKB) (0.3-30 nmol) resulted in a marked and dose-related rat paw edema, with mean ED50 values of 2.68 nmol, 1.17 nmol, and 0.80 nmol, respectively. The ID injection of the selective NK1, SP methyl-ester (1-30 nmol), NK2, [beta-Ala8]-neurokinin A4-10) (beta-Ala, 0.3-30 nmol), or NK3, senktide (1-10 nmol) agonists, caused extensive edema formation with mean ED50s of 0.48 nmol, 0.41 nmol, and 0.18 nmol, respectively. The ID injection of the selective NK1 antagonist FK888 (0.1-3 nmol) produced marked inhibition (94%, 52%, and 66%, respectively) of rat paw edema induced by SP, NKA, or SP methyl-ester. The ID co-injection of the NK2 receptor antagonist SR 48968 elicited a graded inhibition (52%, 67%, and 35%, respectively) of rat paw edema induced by NKA, beta-Ala and, to a lesser extent, the edema caused by SP. Finally, the ID co-injection of the NK, receptor antagonist SR 142801 significantly inhibited (53%, 76%, 53%, and 100%, respectively) the edema formation caused by NKB and NKA or by SP and senktide. Together, the data of the present study suggest that tachykinin-mediated rat paw edema depends on the activation of NK1, NK2 and NK3 receptor subtypes, with apparent major involvement of NK1 receptors subtypes.

Animals↗
PubMed2002

Prediction of macular edema exacerbation after phacoemulsification in patients with nonproliferative diabetic retinopathy.

PURPOSE: To ascertain whether the aqueous humor levels of vascular endothelial growth factor (VEGF), interleukin-6 (IL-6), and protein can predict the postoperative exacerbation of macular edema in patients with nonproliferative diabetic retinopathy (NPDR) after phacoemulsification surgery for cataract. SETTING: Department of Ophthalmology, Diabetes Center, Tokyo Women's Medical University, Tokyo, Japan. METHODS: This prospective study included 104 consecutive patients (104 eyes) with NPDR who had cataract surgery. The concentrations of VEGF and IL-6 in aqueous humor specimens obtained during cataract surgery were measured by enzyme-linked immunosorbent assay. Patients were followed for 6 months to assess the postoperative exacerbation of macular edema. RESULTS: Ninety patients (87%) achieved a visual acuity of 20/40 or better. Exacerbation of macular edema was seen in 30 eyes (29%) after 6 months. Hypertension and the aqueous levels of VEGF, IL-6, and protein were significantly correlated with the exacerbation of macular edema (odds ratio 1.16, 1.33, 1.27, and 1.28, respectively). In contrast, there was no correlation between the exacerbation of macular edema and other systemic factors. Multivariate logistic regression analysis showed that the aqueous VEGF level increase of 100 pg/mL increased the macular edema after phacoemulsification surgery (odds ratio 1.53). CONCLUSIONS: A high VEGF level in the aqueous humor predicted a significant risk for the postoperative exacerbation of macular edema. A model was developed to predict the risk exacerbation.

Aged↗
PubMed2001

Pilot study to evaluate a water displacement technique to compare effects of diuretics and ACE inhibitors to alleviate lower extremity edema due to dihydropyridine calcium antagonists.

Combination therapy is required in many patients to achieve goal blood pressure (BP). Calcium antagonists are highly effective antihypertensive drugs in a broad range of demographic groups. Yet, higher doses are associated with an increased frequency of lower extremity edema. The purpose of our open label, single-center clinical trial was to evaluate the use of concomitant pharmacologic therapies to attenuate the lower extremity edema associated with dihydropyridine calcium antagonists therapy using a water displacement technique. Forty-seven patients received 5 mg/day of oral amlodipine for a period of 6 weeks after a 4-week wash-out off of all antihypertensive medications to establish baseline BP. They were then randomized to receive either an additional 5 mg of amlodipine, 25 mg of hydrochlorothiazide (HCTZ), or 20 mg of benazepril for an additional 6 weeks. Blood pressure determinations and water displacement measurements were obtained at the end of the 4-week placebo wash-out period, after 6 weeks of 5 mg/day of oral amlodipine therapy, and after an additional 6 weeks of 5 mg of amlodipine and randomized drug therapy. Adjusted BP reductions (based on pretreatment BP) were -6.8/-3.8 mm Hg for the 10-mg amlodipine group, -9.9/-8.2 mm Hg for the amlodipine (5 mg)/HCTZ (25 mg) group, and -26.2/-16.4 mm Hg for the amlodipine (5 mg)/benazepril (20 mg) group (P < .0167, group 3 v group 1 diastolic BP, which was statistically significant by the improved Bonferroni method). Seventeen of the 47 patients developed at least a 10% increase in lower extremity edema water displacement in response to 5 mg/day of oral amlodipine therapy (36.2%). Adding 5 mg of amlodipine to a baseline of 5 mg of amlodipine resulted in no net change in lower extremity edema (+58.0 mL,+ 0.6% change, n=5). Adding 25 mg of HCTZ reduced lower extremity edema by a mean of 136.3 mL (-11.1% change, n=4). Benazepril reduced water displacement by 204.4 mL (-14.3% change, n=8). Our pilot study indicates that adding an angiotensin converting enzyme inhibitor to a dihydropyridine calcium channel blocker is the most effective way to not only reduce systolic and diastolic BP but also attenuate lower extremity edema. Due to the inherent daily variability of lower extremity edema, power calculations indicate many patients (n=702, 356 in each group) would be needed to compare the antiedema efficacy of the angiotensin converting enzyme inhibitor and the thiazide diuretic.

Adult↗
PubMedDate not supplied

Meningiomas with brain edema: radiological characteristics on MRI and review of the literature.

OBJECT: Despite their benign characteristics, meningiomas are often accompanied by perifocal brain edema. The aims of this study are to determine what kind of characteristics on magnetic resonance (MR) image are indicative of a meningioma that produces brain edema and to investigate the mechanism responsible for brain edema accompanying meningiomas. METHODS: Fifty-one patients with meningioma were examined by magnetic resonance imaging (MRI), and tumor size, tumor location, shape of tumor margin, peritumoral rim, and signal intensity of tumor on T2-weighted image (T2WI) were compared and correlated with the presence versus absence of brain edema. Surgical histopathology was also examined and correlated with the MRI findings and brain edema. RESULTS: Shape of tumor margin, peritumoral rim, and signal intensity of tumor on T2WI correlated with brain edema on multivariate analyses. CONCLUSION: Invasive pattern of brain-tumor interface and hyperintensity on T2WI were indicative factors of meningiomas producing brain edema.

Brain↗
PubMed1987

Massive cerebral edema associated with meningioma.

Cerebral edema is a well-known complication of malignant astrocytoma and metastatic brain tumour. Though far less frequent, the association of cerebral edema with meningioma is also recognized; this is unpredictable and sometimes out of proportion to tumour size. We describe three cases where the mass effect was due to severe edema, rather than the tumour itself and was responsible for a catastrophic clinical presentation. The mechanisms responsible for the development of severe edema with meningioma which have been previously proposed are reviewed. They include tumour size, location, histologic subtype, cellularity, mitotic activity, vascularity and the presence of excretory-secretory activity. None of these consistently correlate with cerebral edema. Our cases suggest that spontaneous hemorrhage into the tumour may be the common factor responsible for severe cerebral edema. It is stressed that though a decidedly rare complication, cerebral edema secondary to meningioma should be entertained in the differential diagnosis of acute neurologic deterioration of these patients.

Adult↗
PubMed1999

The historical discovery of macular edema.

The occurrence of macular edema, or of intraretinal fluid in general, was largely unknown prior to the invention of the ophthalmoscope. One of the first reports on 'Retinitis in Glycosuria', a disease complex, which today would partly be described as diabetic maculopathy, was published in 1856 by Jaeger. His observations were confirmed less than twenty years later by Nettleship in London, and in 1875 Appolinaire Bouchardat from Paris described fluid and lipid accumulation in the macula which led--in his words--to a glucose induced amblyopia. The first pathophysiological hypotheses of fluid accumulation in the posterior pole were then put forward in 1882 by Tartuferi, who thought the edema represented swelling of photoreceptor sheaths. In 1896, the Frenchman Nuel coined the term 'oedème maculaire' which he had observed in a retinitis pigmentosa patient. However, it was not until the end of the first World War, that the Swiss ophthalmologist Alfred Vogt observed macular edema in a variety of other ocular conditions such as iridocyclitiOFF macular edema to a macular hole. A quarter of a century later Bangerter coined the German term 'Zystoides Makulaödem', and in 1950, Hruby was the first to draw attention to the development of macular edema after cataract extraction. Three years later this was followed by Irvine's classical paper on cystoid macular edema after intra- and extracapsular cataract extraction which had been complicated by incarceration of the vitreous in the anterior segment with consecutive tugging on the macula. A decade later, the phenomenon of cystic fluid accumulation in the macula after cataract extraction was further characterised by Gass and Norton using fluorescein angiography. The ensuing years saw the emergence of new concepts regarding the blood-retinal barrier and the paramount role of its dysfunction in the development of macular edema.

Fluorescein Angiography↗
PubMed1999

Mechanisms of fluid accumulation in retinal edema.

This paper reviews the anatomic and physiologic conditions which predispose to fluid accumulation within the retina. Retinal edema has its inception in disease that causes a breakdown of the blood-retinal barrier in retinal capillaries and/or the retinal pigment epithelium (RPE). Edema develops not only because protein and fluid enter the extracellular space, but because the external limiting membrane and the convoluted extracellular pathway within the retina limit the clearance of albumin and other large osmotically-active molecules. These molecules bind water to cause edema. Recognition of edema clinically is complicated by the facts that angiographic markers (fluorescein and ICG) do not match albumin in size, and that clinical leakage does not always correlate closely with tissue swelling or functional loss. Active water transport across the RPE is efficient at removing subretinal water, but the flow resistance of the retina limits RPE access to the water of retinal edema. Consideration of the pathophysiology of retinal edema may aid in the development of better strategies for managing retinal edema.

Animals↗