Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Edema”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources
PubMed1985

Increased lung vasoreactivity in children from Leadville, Colorado, after recovery from high-altitude pulmonary edema.

Cardiac catheterization was performed on seven children after recovery from high-altitude pulmonary edema. All were life-long residents at elevations above 10,000 feet. Three of the seven had developed pulmonary edema without antecedent travel to low altitude but had an upper respiratory infection. Response of pulmonary arterial pressure to 16% inspired oxygen in all seven was compared with that in six well children who resided at a similar altitude and had no history of high-altitude pulmonary edema. With hypoxia the susceptible patients had a greater mean pulmonary arterial pressure (56.3 +/- 23.8) than the nonsusceptible children (18.8 +/- 3.9, p less than .05). Comparison with historical hemodynamic responses in children at high altitudes showed a similar greater mean pulmonary arterial pressure in the susceptible children. Thus, in children from high altitudes, increased pulmonary vasoreactivity to hypoxia may play a role in the pathogenesis of high-altitude pulmonary edema. The development of pulmonary edema in high-altitude residents with upper respiratory infections and no antecedent low-altitude journey is consistent with the presence of other factors such as inflammation, which may play a role in the pathogenesis of the edema. The finding of right ventricular hypertrophy on an electrocardiogram in children from high altitudes may be predictive of their susceptibility to high-altitude pulmonary edema.

Altitude↗
PubMed1986

Stimulation of pulmonary vagal afferent C-fibers by lung edema in dogs.

In anesthetized, open-chest dogs we examined the effect of pulmonary edema on the firing frequency of afferent vagal fibers arising from the lung. We recorded impulses from slips of the cervical vagus nerves and infused isotonic Krebs-Henseleit solution (20% of body weight) intravenously to increase net filtration pressure in the lung microvasculature. Measurement of extravascular lung water (6.0 +/- 0.4 g/g dry lung), and morphological examination of lung tissue (revealing various degrees of perivascular and peribronchial cuffing) confirmed that edema was present. At the end of the infusion when the lungs were congested (lung microvascular pressure, 37 cm water) and edematous, the impulse frequency of pulmonary and bronchial C-fibers and rapidly adapting receptors had increased 5-6 times. The only significant change in slowly adapting receptor activity was an increase during deflation. When lung water was still elevated but lung microvascular pressure had been restored to control by withdrawal of blood, impulse activity of rapidly and slowly adapting receptors reverted to or below control. Pulmonary C-fiber activity, although less than during congestion, remained significantly above control, several C-fibers being stimulated by interstitial edema in the absence of alveolar edema. Bronchial C-fibers were stimulated in severely edematous lung showing pronounced peribronchial cuffing and alveolar edema, but were not stimulated in milder grades of edema. Our results support the hypothesis (Paintal, 1969) that pulmonary C-fibers (J-receptors) are stimulated by an increase in interstitial pressure secondary to edema.

Action Potentials↗
PubMedDate not supplied

Ischemic brain edema: comparative effects of barbiturates and hypothermia.

The effect of pentobarbital and hypothermia on the development of ischemic brain edema was studied in 23 rhesus monkeys undergoing transorbital middle cerebral artery occlusion. Fifteen additional animals served as unclipped controls. Regional cortical cerebral blood flow (rCBF), arteriovenous oxygen content difference (AVDO2), and regional cortical metabolic rate of O2 (rCMRO2) were measured hourly until sacrifie 11 hours postocclusion, at which time ischemic cerebral edema was measured. In 8 animals no treatment followed the occlusion, and these developed edema. In 7 animals pentobarbial 14 mg/kg was administered intravenously 30 min after occlusion and 7 mg/kg every 2 hours thereafter. In this group ischemic brain edema was negligible. In 8 animals, hypothermia to 25.9 +/- 0.5 degrees C was started 30 min after occlusion and maintained until sacrifice; ischemic brain edema was not significantly altered from untreated-clipped animals. On the basis that both pentobarbital and hypothermia produced similar changes in rCBF, AVDO2, and rCMRO2, but only pentobarbital prevented edema, it is postulated that the mode of action of barbiturates in preventing ischemic brain edema is not entirely related to their known effect on blood flow and metabolism.

Animals↗
PubMed1993

Effect of brain edema on infarct volume in a focal cerebral ischemia model in rats.

BACKGROUND AND PURPOSE: Infarct volume is one of the common indexes for assessing the extent of ischemic brain injury following focal cerebral ischemia. Accuracy in the measurement of infarct volume is compounded by postischemic brain edema that may increase brain volume in the infarcted region. We evaluated the effect of brain edema on infarct volume determined by triphenyltetrazolium chloride and hematoxylin and eosin stains in a focal cerebral ischemia model in rats. METHODS: In a middle cerebral artery occlusion model in rats, infarction is confined to the cerebral cortex. The infarct was delineated by triphenyltetrazolium chloride stain and, in selected samples, by hematoxylin and eosin stain. We determined infarct size at different times after the ischemic insult (6 hours to 7 days) in relation to the evolution of brain edema by the direct measurement of infarct volume. Indirect measurement to reduce the effect of edema on infarct volume was also conducted in the same brain samples. RESULTS: Direct measurement showed that infarct volume fluctuated with the evolution of brain edema (one-way analysis of variance, p < 0.0001). Infarct volume determined by indirect measurement was independent of the extent of brain edema and remained stable from 6 hours to 3 days after ischemia. There was a good correlation between triphenyltetrazolium chloride and hematoxylin and eosin stains in delineating infarct volume with both direct and indirect measurement. CONCLUSION: Traditional direct measurement of infarct volume is associated with an overestimation of infarct volume during the development of brain edema in the first 3 days after ischemia. This artifact can be reduced with indirect measurement, which is based on noninfarcted cortex volume.

Animals↗
PubMed1999

Dopamine restores lung ability to clear edema in rats exposed to hyperoxia.

Exposure to hyperoxia causes lung injury, decreases active sodium transport and lung edema clearance in rats. Dopamine (DA) increases lung edema clearance by stimulating vectorial Na+ flux and Na, K-ATPase function in rat alveolar epithelium. This study was designed to test whether DA (10(-)5 M) would increase lung edema clearance in rats exposed to 100% O2 for 64 h. Active Na+ transport and lung edema clearance decreased by approximately 44% in rats exposed to acute hyperoxia (p < 0.001). DA increased lung edema clearance in room air breathing rats (from 0.50 +/- 0.02 to 0.75 +/- 0.06 ml/h) and in rats exposed to 100% O2 (from 0.28 +/- 0.03 to 0. 67 +/- 0.03 ml/h). Disruption of cell microtubular transport system by colchicine blocked the stimulatory effect of DA on active Na+ transport in control and hyperoxic rats, whereas the isomer beta-lumicolchicine, which does not affect cell microtubular transport, did not inhibit the stimulatory effects of dopamine. The Na,K-ATPase alpha1-subunit protein abundance increased in the basolateral membranes of alveolar type II (ATII) cells incubated with 10(-)5 M DA for 15 min, probably by recruiting Na+ pumps from intracellular pools. Colchicine, but not beta-lumicolchicine, prevented the recruitment of alpha1 subunits to the plasma membrane by DA. Accordingly, DA restored lung ability to clear edema in hyperoxic-injured rat lungs. Conceivably, dopamine induces recruitment of Na+ pumps from intracellular pools to the plasma membrane of alveolar epithelial cells and thus increases lung edema clearance.

Acute Disease↗
PubMed2001

Increased levels of nitrate and surfactant protein a nitration in the pulmonary edema fluid of patients with acute lung injury.

Levels of nitrite (NO2-) and nitrate (NO3-) were measured in pulmonary edema fluid and plasma from 34 patients with early acute lung injury (ALI) and 20 patients with hydrostatic pulmonary edema. Pulmonary edema fluid from patients with ALI had significantly higher levels of NO2- + NO3- compared with pulmonary edema fluid from patients with hydrostatic pulmonary edema (108 +/- 13 microM versus 66 +/- 9 microM; means +/- SEM; p < 0.05). In addition, patients with shock had higher plasma NO2- + NO3- levels than those without shock (79 +/- 11 microM versus 53 +/- 12 microM, p < 0.05). Acidemia and increased anion gap, markers of systemic hypoperfusion, were also associated with twofold higher plasma NO2- + NO3- levels (p < 0.01). Increased levels of NO2- + NO3- in edema fluid samples were associated with slower rates of alveolar fluid clearance. Nitrated pulmonary surfactant protein A (SP-A) was also detected in the edema fluid of patients with ALI after immunoprecipitation with a specific antibody against this protein. Previously, we have shown that nitration of SP-A impairs its host- defense properties. In aggregate, the results of this study indicate that reactive oxygen-nitrogen species may play a role in the pathogenesis of human ALI.

Body Fluids↗
PubMed1987

Delirium and pulmonary edema after completing a marathon.

Pulmonary edema is a rare complication of distance running. All 4 previously reported cases occurred after triathalons or ultramarathons. We report the first case of pulmonary edema in a healthy but untrained runner after a conventional 42-km marathon race. This is also the first reported case of pulmonary edema complicating distance running in which hemodynamic measurements have been made. The pulmonary capillary wedge pressure was low. The cardiac index was initially depressed, and the arterial-venous oxygen tension difference was high, but the latter abnormalities disappeared after volume infusion. These hemodynamic data suggest that pulmonary edema in this distance runner was predominantly noncardiogenic. The etiology of the edema is uncertain, but concurrent hyponatremia and cerebral edema were present in this patient, as in 2 previously reported cases, suggesting that neurogenic pulmonary edema caused by water intoxication may be a contributing factor in pathogenesis.

Adult↗
PubMed1989

The role of activation of neutrophils and microvascular pressure in acute pulmonary edema.

Activated polymorphonuclear neutrophils (PMN) can mediate vascular injury in the lung. This study compared activated aggregate PMN (emboli) to activated PMN that were previously adhered to the microvasculature (non-embolic) in the isolated perfused rat lung. Permeability and microvascular pressure (Pmv), components of PMN-induced edema, were examined by continuous measurement of wet weight, pulmonary arterial and left atrial pressures, and by intermittent determination of double occlusion pressure. PMN that were activated with phorbol myristate acetate and then perfused into the lung formed aggregates that lodged primarily in the precapillary bed, increasing arterial resistance. Although these PMN had minimal direct contact with the capillary endothelium, edema rapidly developed and Pmv was progressively elevated. If PMN were allowed to adhere in the capillary bed, a minimal and nonprogressive increase in Pmv and lung weight occurred. When these adherent PMN were then activated, there was a progressive rise in both Pmv and lung weight. The free radical scavenger catalase prevented this edema formation but not the rise in pressure. In control lungs with matched elevation of Pmv, edema did not develop. In another group of lungs with activation of pre-adherent PMN in which Pmv was maintained at control levels, edema formation was greatly delayed. These data show that: (1) the activated PMN free radical products alone caused permeability injury in the lung because neither contact of the PMN with the capillary endothelium nor embolization was necessary, and (2) increased Pmv does not cause edema but greatly increases the rate of edema formation when the endothelium is injured.

Animals↗
PubMed1993

Experimental hydrostatic pulmonary edema in rabbit lungs. Morphology.

To study the accumulation and distribution of edema fluid and the associated changes in alveolar microarchitecture, edema was induced in excised rabbit lungs perfused with 6% albumin solution. The lungs, including the edema fluid, were then fixed by vascular perfusion with glutaraldehyde, osmium tetroxide, and uranyl acetate. Tissue samples were analyzed by light microscopy and transmission and scanning electron microscopy. We found (1) fixation was successful in that the albumin in the edema fluid formed coherent webs indicating the location and arrangement of the extravascular fluid accumulations; (2) regardless of the filtration pressure (about 29 mm Hg in one set of experiments and about 14 mm Hg in the other), an apical to basal gradient of fluid accumulation was found. This gradient was absent in lungs held in the inverse position, suggesting that the regional distribution of pulmonary edema is not simply gravity dependent. At the same lung height, there was a remarkable inhomogeneity of interstitial and alveolar edema. (3) Both the inhomogeneous distribution of fluid and the resulting changes in surface tension affected the entire alveolar architecture. (4) Within interstitial and alveolar spaces, there were striking inequalities in the density of the proteinaceous fluid pools that suggest local differences in the sieving properties of the barriers, that is, in the reflection coefficients for albumin. In conclusion, our findings suggest that the formation of pulmonary edema cannot be explained solely by uniform membrane models for fluid exchange.

Animals↗
PubMed1993

Experimental hydrostatic pulmonary edema in rabbit lungs. Barrier lesions.

In excised rabbit lungs perfused with a 6% albumin solution, hydrostatic pulmonary edema was induced by moderate (about 14 mm Hg) and high increases (about 29 mm Hg) of capillary transmural pressure. Thereafter, lung tissue and proteinaceous edema fluid were fixed by vascular perfusion and analyzed by electron microscopy for possible lesions of the blood-gas barrier. The following observations appear noteworthy: (1) There were distinct and numerous lesions of the epithelial cell layer. In high-pressure edema, frank disruptions on the thin and thick sides of the blood-gas barrier were prominent. In moderate pressure edema epithelial blebs were more conspicuous. (2) In contrast, endothelial lesions were rare in both high- and moderate-pressure experiments. (3) Epithelial Type I cells revealed an enormous plasticity as illustrated by the formation of large epithelial blebs. (4) Although the entire microvasculature was subjected to high pressures, barrier lesions were exclusively seen in regions with alveolar edema. These findings suggest that barrier leaks play a role in both hydrostatic and permeability lung edema and that the differences between both types of edema rather reflects the type and extent of injury to the alveolar epithelial barrier and the associated inflammatory reaction.

Animals↗
PubMed1983

Dynamic insufficiency of lung lymph flow from the right lymph duct in dogs with acute filtration edema.

Using 14 anesthetized dogs with lymph flowing through right lymph duct, we observed dynamic insufficiency of lung lymph flow during acute left atrial pressure loading. Net pulmonary microvascular fluid filtration pressure (sigma p) was defined as the difference between pulmonary microvascular pressure (Pmv) and oncotic gradient through the capillaries (pi mv - pi pmv). Pulmonary extravascular water content (PEVW) was well correlated with sigma p in either mild edema or gross edema (PEVW = 0.19 sigma p + 2.15, r = 0.813, 0.001 less than p less than 0.002). Percent increase in lymph flow (% Qlym) was well correlated with both PEVW (% Qlym = 130.8 PEVW - 376.5, r = 0.886, 0.005 less than p less than 0.01) and sigma p (% Qlym = 11.0 sigma p + 34.7, r = 0.853, 0.02 less than p less than 0.05) in mild edema. However, in gross edema compared with mild edema, % Qlym as a function of PEVW or sigma p was significantly low. We concluded that in gross edema with PEVW, over 6 g/g of bloodless dry lung and sigma p over 20 mmHg, lymph flow from right lymph duct becomes dynamically insufficient and can neither transport enough fluid from the pulmonary interstitium nor tracheobronchial trees to relieve the edema process.

Animals↗
PubMed2006

Diabetic macular edema: correlation between microperimetry and optical coherence tomography findings.

PURPOSE: To compare the changes in macular sensitivity (microperimetry) and macular thickness with different degrees of diabetic macular edema. METHODS: Sixty-one eyes of 32 consecutive diabetic patients were included in this cross-sectional study. All included eyes underwent functional and morphologic examination of the macular area. Best corrected visual acuity (ETDRS charts), macular sensitivity, and macular thickness were quantified. Lesion-related macular sensitivity and retinal fixation were investigated with an advanced, automatic microperimeter. Optical coherence tomography (OCT) was used to quantify macular thickness. RESULTS: The 61 included eyes were graded, by two retinal specialists, for diabetic macular edema as follows: 16 were graded as no macular edema (NE), 30 as non-clinically significant macular edema (NCSME), and 15 as clinically significant macular edema (CSME). Macular thickness significantly increased from the NE to the CSME group (P<0.0001), whereas macular sensitivity significantly decreased from the NE to the CSME group (P<0.0021). A significant correlation coefficient was noted between retinal sensitivity and normalized macular thickness (r=-0.37, P<0.0001). Linear regression analysis showed a decrease of 0.83 dB (P<0.0001) for every 10% of deviation of retinal thickness from normal values. Visual acuity and central macular sensitivity correlated significantly in the NCSME group (r=-0.6, P=0.0008), but not in the NE (r=-0.144, P=0.6) or in the CSME (r=-0.46, P=0.11) groups. CONCLUSIONS: Macular edema may be better documented by adding macular sensitivity mapping by microperimetry to macular thickness measurement by OCT and visual acuity determination because macular sensitivity seems to be a relevant explanatory variable of visual function, independent of macular thickness data. Moreover, microperimetry may be of value in predicting the outcome of diabetic macular edema, because it incorporates a functional measure that may supplement the predictive value of OCT and visual acuity.

Adult↗
PubMed1983

Acetyl glyceryl ether phosphorylcholine-stimulated human platelets cause pulmonary hypertension and edema in isolated rabbit lungs. Role of thromboxane A2.

Macrophages, neutrophils, and platelets may play a role in acute edematous lung injury, such as that seen in the adult respiratory distress syndrome (ARDS), but their potential actions and interactions are unclear. Because stimulated human macrophages and neutrophils can release acetyl glyceryl ether phosphorylcholine (AGEPC), a potent platelet activator, we hypothesized that in ARDS, leukocyte release of AGEPC might stimulate platelets to release thromboxane A2 (TXA2), which then produces pulmonary hypertension and lung edema. In support of this premise, we found that pulmonary hypertension and edema occurred in isolated rabbit lungs perfused with human platelets and AGEPC, but not with platelets or AGEPC alone. Infusion of a vasodilator (nitroglycerin) to maintain base-line pulmonary artery pressures in lungs perfused with platelets and AGEPC prevented the development of lung edema suggesting that platelet and AGEPC-induced edema was hydrostatic in nature. Additional experiments suggested that the increased pressure was a result of TXA2 release from platelets stimulated by AGEPC. Specifically, preincubation of platelets with imidazole, a thromboxane synthetase blocker, prior to infusion with AGEPC significantly diminished pulmonary hypertension and prevented lung edema. Furthermore, pretreating lung preparations with 13-azaprostanoic acid, a TXA2 antagonist, before infusion of AGEPC and untreated platelets also reduced the pulmonary hypertension and blocked the lung edema. The role of TXA2 was further suggested when perfusates from lungs infused with platelets and AGEPC developed high levels of TXA2, whereas perfusates from controls did not. These results suggest that platelet aggregation induced by AGEPC may contribute to ARDS by releasing TXA2, which raises microvascular pressure and increases edema formation, especially when an underlying permeability defect is present.

Animals↗
PubMed2000

Pharmacologic aspects of a phlebotropic drug in CVI-associated edema.

Several phlebotropic drugs, or edema-protecting drugs, are available, the most important of which are found in the gamma-benzopyrone family (flavonoids). gamma-Benzopyrones can be plant extracts, semisynthetic preparations, or synthetic preparations. This family is divided into two different groups: flavones and flavonols, and flavanes (flavanones). The flavone group contains various types of molecule and includes diosmin. Here we discuss the pharmacologic aspects in edema associated with chronic venous insufficiency (CVI) of one of the reference phlebotropic drugs, micronized purified flavonoid fraction (MPFF), a semisynthetic preparation from the diosmin group, which represents the latest improvement in flavonoid formulation. Before we detail the pharmacologic aspects, a brief summary of the pathophysiology of edema in CVI is necessary. Several factors are implicated: the veins, which create the conditions favorable to edema; the microcirculation, which is the site of fluid transfer into the interstitial tissue; and the lymphatics, which have a limited possibility to reduce edema. Major discoveries are currently being made in CVI and the microcirculation. Results of studies show that MPFF decreases capillary permeability and increases capillary resistance, which could partly be explained by inhibition of leukocyte activation, migration, and adhesion. This inhibition is linked to a significant decrease in plasma levels of endothelial adhesion molecules (VCAM-1 and ICAM-1) after MPFF treatment. Thus, the CVI-induced damage to the microcirculation is counteracted by MPFF. The lymphatic system is also improved by MPFF treatment. The lymphagogue activity of MPFF has been demonstrated in experimental animal models and confirmed by microlymphographic measurement in patients suffering from severe CVI. The pharmacologic activity of MPFF in lymphedema was observed in a study using an animal model of acute lymphedema and in a study in patients with upper limb lymphedema secondary to breast cancer treatment. All these findings point to the importance of acting on each factor involved in the formation and maintenance of edema. This pharmacologic activity is indeed reflected by the clinical efficacy on edema observed during treatment with MPFF.

Animals↗
PubMedDate not supplied

Vitrectomy results for diffuse diabetic macular edema with and without inner limiting membrane removal.

PURPOSE: To determine whether vitrectomy for diffuse diabetic macular edema with and without internal limiting membrane (ILM) peeling is equally effective in reducing edema. METHODS: The authors retrospectively analyzed the surgical outcomes in 73 eyes of 52 patients with diffuse diabetic macular edema. Eighteen eyes (Group A) underwent three-port pars plana vitrectomy with posterior hyaloid membrane (PHM) removal, while 55 eyes (Group B) had pars plana vitrectomy with additional ILM peeling after PHM removal. RESULTS: Intraoperatively, the posterior hyaloid was found to be attached to the macula in all eyes. In Group A, macular edema resolved completely in 8 eyes (44.4%) with improvement of visual acuity (VA). In Group B, VA improved in 38 eyes (69.1%) with complete resolution of edema. The results of this study indicated that vitrectomy effectively reduced macular edema but eyes with ILM peeling (Group B) presented better results than those without ILM peeling. Another important factor related to the outcome seems to be the level of glycosylated hemoglobin (HbA1c). CONCLUSIONS: In eyes with diffuse diabetic macular edema vitrectomy seems to be effective, but additional ILM peeling presented better results.

Aged↗
PubMed2006

Biochemical and morphological changes in endothelial cells in response to hypoxic interstitial edema.

BACKGROUND: A correlation between interstial pulmonary matrix disorganization and lung cellular response was recently documented in cardiogenic interstitial edema as changes in the signal-cellular transduction platforms (lipid microdomains: caveoale and lipid rafts). These findings led to hypothesize a specific "sensing" function by lung cells resulting from a perturbation in cell-matrix interaction. We reason that the cell-matrix interaction may differ between the cardiogenic and the hypoxic type of lung edema due to the observed difference in the sequential degradation of matrix proteoglycans (PGs) family. In cardiogenic edema a major fragmentation of high molecular weight PGs of the interfibrillar matrix was found, while in hypoxia the fragmentation process mostly involved the PGs of the basement membrane controlling microvascular permeability. Based on these considerations, we aim to describe potential differences in the lung cellular response to the two types of edema. METHODS: We analysed the composition of plasma membrane and of lipid microdomains in lung tissue samples from anesthetized rabbits exposed to mild hypoxia (12 % O2 for 3-5 h) causing interstitial lung edema. Lipid analysis was performed by chromatographic techniques, while protein analysis by electrophoresis and Western blotting. Lipid peroxidation was assessed on total plasma membranes by a colorimetric assay (Bioxytech LPO-586, OxisResearch). Plasma membrane fluidity was also assessed by fluorescence. Lipid microdomains were isolated by discontinuous sucrose gradient. We also performed a morphometric analysis on lung cell shape on TEM images from lung tissue specimen. RESULTS: After hypoxia, phospholipids content in plasma membranes remained unchanged while the cholesterol/phospholipids ratio increased significantly by about 9% causing a decrease in membrane fluidity. No significant increase in lipid peroxidation was detected. Analysis of lipid microdomains showed a decrease of caveolin-1 and AQP1 (markers of caveolae), and an increase in CD55 (marker of lipid rafts). Morphometry showed a significant decrease in endothelial cell volume, a marked increase in the cell surface/volume ratio and a decrease in caveolar density; epithelial cells did not show morphological changes. CONCLUSION: The biochemical, signaling and morphological changes observed in lung endothelial cell exposed to hypoxia are opposite to those previously described in cardiogenic edema, suggesting a differential cellular response to either type of edema.

Animals↗
PubMed1981

Biological features of meningiomas that determine the production of cerebral edema.

Although meningiomas are known to cause varying degrees of cerebral edema, the relative importance of their location, size, histological subtype, and other histological features in the production of cerebral edema has not been studied adequately. Therefore, we undertook a retrospective analysis of 43 meningiomas excised between 1975 and 1980. The results indicate that histological subtype has no relationship to the production of cerebral edema, with one exception. Meningiomas containing partly or completely a hemangiopericytic component were the only histological subtype associated consistently with cerebral edema. The location of a meningioma per se may not determine the production of cerebral edema. A relationship between size, aggressive histological features, vascular proliferative changes, and the production of cerebral edema was seen. The need for and the nature of further studies required to explain the cerebral edema that may be associated with small meningiomas are discussed.

Brain Edema↗
PubMed2006

Extended bifrontal craniotomy for midline anterior fossa meningiomas: minimization of retraction-related edema and surgical outcomes.

OBJECTIVE: Meningiomas of the anterior cranial base can be approached with a variety of techniques. The extended bifrontal approach is often thought to be associated with increased morbidity because of the need for extensive removal of the bone and longer surgical times. The authors have attempted to quantitate retraction-related edema occurring after surgery to determine whether the extra bone removal limits retraction and reduces the chance of brain injury. METHODS: Charts were reviewed for patients who underwent extended bifrontal craniotomies performed for meningiomas at the University of California, San Francisco, between 1997 and 2005. Magnetic resonance imaging scans obtained before and after surgery were reviewed for brain edema as indicated by fluid-attenuated inversion recovery/T2 abnormality and grouped into four categories: A, no edema; B, edema restricted to the gyrus rectus; C, edema beyond the gyrus rectus; and D, extensive bifrontal edema. RESULTS: Forty-five patients were identified. Fifty-four percent of patients had tumors with a diameter of more than 4 cm. Simpson Grade 2 or 3 resection was achieved in 82% of patients, and the average operative time was 12.3 hours. Vision outcome was favorable in 74% of patients. Extent of fluid-attenuated inversion recovery abnormality remained unchanged in 87.5%, with 91% of patients in categories A or B edema remaining in those categories after surgery. There were no infections and there were two cerebrospinal fluid leaks. CONCLUSION: The extended bifrontal approach is a safe surgical procedure with limited morbidity that the authors think: 1) prevents secondary brain injury from excessive retraction; 2) offers great flexibility of view for the surgeon; and 3) should be considered the preferred approach compared with the standard bifrontal craniotomy for large tumors of the anterior cranial base.

Adult↗