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PubMed2004

Perihematomal edema in primary intracerebral hemorrhage is plasma derived.

BACKGROUND AND PURPOSE: The mechanisms of perihematomal injury in primary intracerebral hemorrhage (ICH) are incompletely understood. An MRI study was designed to elucidate the nature of edema and blood flow changes after ICH. METHODS: Perihematomal blood flow and edema were studied prospectively with perfusion-weighted MRI (PWI) and diffusion-weighted MRI in 21 ICH patients. MRI and computed tomography (CT) images were coregistered to ensure perfusion and diffusion changes were outside of the hematoma. Edema volumes were measured on T2-weighted images. Apparent diffusion coefficient (ADC) values of the edematous regions were calculated. RESULTS: Mean patient age was 64.2 years (45 to 89), and median National Institutes of Health stroke scale score was 12 (3 to 24). Median time to MRI was 21 hours (4.5 to 110). Average hematoma volume on CT was 26.1 (4 to 84) mL. PWI demonstrated perihematomal relative mean transit time (rMTT) was significantly correlated with hematoma volume (r=0.60; P=0.004) but not edema volume. Perihematomal oligemia (rMTT >2 s) was present in patients with hematoma volumes of >15 mL (average rMTT 4.6+/-2.0 s). Perihematomal edema was present in all patients. ADC values within this region (1178+/-213x10(-6) mm2/s) were increased 29% relative to contralateral homologous regions. Increases in perihematomal ADC predicted edema volume (r=0.54; P=0.012) and this was confirmed with multivariate analysis. CONCLUSIONS: Acute perihematomal oligemia occurs in acute ICH but is not associated with MRI markers of ischemia and is unrelated to edema formation. Increased rates of water diffusion in the perihematomal region independently predict edema volume, suggesting the latter is plasma derived.

Aged↗
PubMed1995

Pulmonary edema during IL-2 therapy: combined effect of increased permeability and hydrostatic pressure.

Systemic administration of recombinant interleukin-2 (rIL-2) has been shown to be promising against certain metastatic cancers. However, major side effects, such as pulmonary edema, have limited its widespread use. Although this pulmonary edema has been attributed to a vascular leak syndrome, this hypothesis has not been verified in humans. The purpose of our study was to determine both the severity and mechanism of pulmonary edema in seven patients treated with rIL-2. The severity of edema was assessed by daily evaluation of chest radiographs, using a semiquantitative scale, as well as by repeated measurements of the alveolar-to-arterial oxygen gradient (A-aDO2) in each patient. To determine the mechanism of pulmonary edema, we serially measured in each patient the lung clearance of technetium 99m-diethylenetriamine pentaacetic acid (DTPA) 99mTc-DTPA), the plasma levels of Von Willebrand factor antigen, and the pulmonary capillary wedge pressure (PCWP). Our results show that there was a gradual increase in the chest radiography edema score that was paralleled by a significant increase in A-aDO2 over its baseline value. During rIL-2 treatment, 99mTc-DTPA clearance was augmented, and the plasma concentration of Von Willebrand factor antigen was elevated. PCWP climbed from 7 to 14 mm Hg and serum total protein fell from 66.1 to 42.1 gm/L. The results obtained indicate that although pulmonary edema associated with rIL-2 treatment is partially dependent on increased permeability of the lung, changes in hydrostatic and oncotic forces may be the principal determinants of edema development.

Blood-Air Barrier↗
PubMed1988

High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure.

The respective roles of high pressure and high tidal volume to promote high airway pressure pulmonary edema are unclear. Positive end-expiratory pressure (PEEP) was shown to reduce lung water content in this type of edema, but its possible effects on cellular lesions were not documented. We compared the consequences of normal tidal volume ventilation in mechanically ventilated rats at a high airway pressure (HiP-LoV) with those of high tidal volume ventilation at a high (HiP-HiV) or low (LoP-HiV) airway pressure and the effects of PEEP (10 cm H2O) on both edema and lung ultrastructure. Pulmonary edema was assessed by extravascular lung water content and microvascular permeability by the drug lung weight and the distribution space of 125I-labeled albumin. HiP-LoV rat lungs were not different from those of controls (7 cm H2O peak pressure ventilation). By contrast, the lungs from the groups submitted to high volume ventilation had significant permeability type edema. This edema was more pronounced in LoP-HiV rats. It was markedly reduced by PEEP, which, in addition, preserved the normal ultrastructural aspect of the alveolar epithelium. This was in striking contrast to the diffuse alveolar damage usually encountered in this type of edema. To our knowledge, this constitutes the first example of a protective effect of PEEP during permeability edema.

Animals↗
PubMed1981

Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits.

In order to study the mechanism(s) underlying re-expansion edema, we measured the concentration of labeled albumin (RISA) in the extravascular, extracellular water (EVECW) of the lung as a measure of pulmonary vascular permeability. Re-expansion edema was first induced by rapid re-expansion of rabbit lungs that had been collapsed for 1 wk by pneumothorax. The RISA in EVECW was expressed as a fraction of its plasma concentration: (RISA)L/(RISA)PL. The volume of EVECW (ml/gm dry lung) was measured using a 24Na indicator. Results in re-expansion edema were compared with normal control lungs and with oleic acid edema as a model of permeability edema. In re-expanded lungs, EVECW (3.41 +/- SD 1.24 ml/g) and (RISA)L/(RISA)PL 0.84 +/- SD 0.15) were significantly increased when compared with normal control lungs (2.25 +/- 0.41 ml/g and 0.51 +/- 0.20, respectively). Results in oleic acid edema (5.66 +/- 2.23 ml/g and 0.84 +/- 0.23) were similar to re-expansion edema. This suggested that re-expansion edema is due to increased pulmonary vascular permeability caused by mechanical stresses applied to the lung during re-expansion.

Animals↗
PubMed1981

Treatment of acute low pressure pulmonary edema in dogs: relative effects of hydrostatic and oncotic pressure, nitroprusside, and positive end-expiratory pressure.

Severe pulmonary edema sometimes develops despite normal pulmonary capillary wedge pressure (Ppw). The equation describing net transvascular flux of lung liquid predicts decreased edema when hydrostatic pressure is reduced or when colloid osmotic pressure is increased in the pulmonary vessels. We tested these predictions in a model of pulmonary capillary leak produced in 35 dogs by intravenous oleic acid. 1 h later, the dogs were divided into five equal groups and treated for 4 h in different ways: (a) not treated, to serve as the control group (Ppw = 11.1 mm Hg); (b) given albumin to increase colloid osmotic pressure by 5 mm Hg (Ppw = 10.6 mm Hg); (c) ventilated with 10 cm H(2)O positive end-expiratory pressure (Peep) (transmural Ppw = 10.4 mm Hg); (d) phlebotomized to reduce Ppw to 6 mm Hg; (e) infused with nitroprusside, which also reduced Ppw to 6 mm Hg. Phlebotomy and nitroprusside reduced the edema in excised lungs by 50% (P< 0.001), but Peep and albumin did not affect the edema. Pulmonary shunt decreased on Peep and increased on nitroprusside, and lung compliance was not different among the treatment groups, demonstrating that these variables are poor indicators of changes in edema. Cardiac output decreased during the treatment period in all but the nitroprusside group, where Ppw decreased and cardiac output did not. We conclude that canine oleic acid pulmonary edema is reduced by small reductions in hydrostatic pressure, but not by increased colloid osmotic pressure, because the vascular permeability to liquid and protein is increased. These results suggest that low pressure pulmonary edema may be reduced by seeking the lowest Ppw consistent with adequate cardiac output enhanced by vasoactive agents like nitroprusside. Further, colloid infusions and Peep are not helpful in reducing edema, so they may be used in the lowest amount that provides adequate circulating volume and arterial O(2) saturation on nontoxic inspired O(2). Until these therapeutic principles receive adequate clinical trial, they provide a rationale for carefully monitored cardiovascular manipulation in treating patients with pulmonary capillary leak.

Albumins↗
PubMedDate not supplied

The LONFLIT4-Venoruton Study: a randomized trial--prophylaxis of flight-edema in venous patients.

The aim of this independent study was to evaluate the protective effects, on the development of flight edema, of Venoruton. The study included patients with venous disease traveling in economy in long-haul flights (9 hours). Edema is a relevant aspect of long-haul flights affecting both patients with venous disease and normal subjects. Microcirculatory variations during flights cause a microangiopathy and biochemical and coagulation alterations. This condition may be defined as flight microangiopathy. A group of 203 subjects with chronic venous disease (uncomplicated varicose veins) at low-medium risk for DVT were contacted; 43 subjects were excluded for several nonmedical, travel-related problems or inconvenient evaluation time; the remaining 160 were randomized, after informed consent, into 2 groups to evaluate 2 prophylaxes in 7-8-hour, long-haul flights: The treatment group received Venoruton (hydroxyethyl rutosides) 1 g twice daily for 3 days (2 days before the flight and the day of the flight). The control group received comparable placebo. The edema score was based on the edema tester, ankle circumference, volume measurements, subjective swelling, and discomfort score. Items 1, 4, and 5 are based on an analogue scale line (1 to 10) directly defined by the subjects before and after the flights. Of the 160 included subjects 139 completed the study. Dropouts (21) were due to poor compliance, traveling, and/or connection problems (11 in the control group, 10 in the treatment group). Age and sex distribution were comparable in the 2 groups as were risk factors distributions. The level of edema at inclusion was comparable in the 2 groups of subjects. After the flight there was an average score of 7.2 (sd 2) in the control group, while in the Venoruton group the score was on average 3.2. (sd 1.1) (p < 0.05), 2.25 times lower than in the control group (p < 0.05). In the control group 89% of the subjects had an evident increase in ankle circumference and volume, which was clearly visible at inspection and associated with discomfort. In the Venoruton group edema was clearly present in 12% of subjects (associated with discomfort between 5 and 7 on the analogue scale line) and it was mild-moderate, not associated with symptoms (pain, discomfort between 2 and 4 on the analogue scale line). Therefore, the control of flight edema with Venoruton was clear both considering parametric data (circumference and volume) and nonparametric (analogue scale lines) measurements. The combined evaluation of the edema score is significantly favorable for patients treated with Venoruton. No deep vein thrombosis or superficial vein thrombosis was observed in this study.

Adult↗
PubMed2002

Pulmonary edema during pregnancy: unilateral presentation is not rare.

Information regarding pulmonary edema in obstetric patients is limited, especially its natural history as most cases are from tertiary care centers. The incidence, etiology, and course of pulmonary edema in all obstetric patients at a primary-secondary care center was studied prospectively among 29,621 obstetric cases in the past 3.5 years. Pulmonary edema developed in 18 cases (0.06%) of all obstetric patients that were associated with pre-eclampsia-eclampsia and tocolysis with beta-mimetics. The onset of pulmonary edema was 1-8 days postpartum in 12 patients, 1 day antepartum in 3 patients, and 26-32 gestational weeks in 3 patients. The cause was mainly cardiogenic, and the mean time taken for resolution was 2.2 days. Unilateral pulmonary edema occurred in 4 patients and there was delayed resolution compared with bilateral pulmonary edema because of delayed treatment. Pulmonary edema associated with pregnancy developed in 0.06% of cases, mainly during the peripartum, and resolved rapidly. Unilateral pulmonary edema was not uncommon.

Adult↗
PubMed2005

Anasarca edema with amlodipine treatment.

OBJECTIVE: To report a case of anasarca edema associated with amlodipine use. CASE SUMMARY: A 77-year-old woman with essential hypertension who had not been treated with any other drug was prescribed amlodipine 10 mg/day to control her blood pressure. She developed anasarca edema soon after amlodipine treatment was initiated. Laboratory test results for possible etiologies were negative. Discontinuation of amlodipine resulted in dramatic improvement. DISCUSSION: To our knowledge, as of February 3, 2005, there have been no other reports of amlodipine-related anasarca edema in the English literature, and only one case was described in the Japanese literature. Pretibial edema is the most common adverse effect of amlodipine. Periocular and perioral edema have occurred less frequently, but anasarca edema has not emerged as a problem. An objective causality assessment revealed amlodipine to be a probable cause of anasarca edema. CONCLUSIONS: In rare instances, amlodipine may cause generalized edema, which will resolve upon discontinuation of the drug.

Aged↗
PubMed1999

Exacerbation of acute pulmonary edema during assisted mechanical ventilation using a low-tidal volume, lung-protective ventilator strategy.

STUDY OBJECTIVES: To assess the magnitude of negative intrathoracic pressure development in a patient whose pulmonary edema acutely worsened immediately following the institution of a low-tidal volume (VT) strategy. DESIGN: Mechanical lung modeling of patient-ventilator interactions based on data from a case report. SETTING: Medical ICU and laboratory. PATIENT: A patient with suspected ARDS and frank pulmonary edema. INTERVENTIONS: The patient's pulmonary mechanics and spontaneous breathing pattern were measured. Samples of arterial blood and pulmonary edema fluid were obtained. MEASUREMENTS: A standard work-of-breathing lung model was used to mimic the ventilator settings, pulmonary mechanics, and spontaneous breathing pattern observed when pulmonary edema worsened. Comparison of the pulmonary edema fluid-to-plasma total protein concentration ratio was made. RESULTS: The patient's spontaneous VT demand was greater than preset. The lung model revealed simulated intrathoracic pressure changes consistent with levels believed necessary to produce pulmonary edema during obstructed breathing. A high degree of imposed circuit-resistive work was found. The pulmonary edema fluid-to-plasma total protein concentration ratio was 0.47, which suggested a hydrostatic mechanism. CONCLUSION: Ventilator adjustments that greatly increase negative intrathoracic pressure during the acute phase of ARDS may worsen pulmonary edema by increasing the transvascular pressure gradient. Therefore, whenever sedation cannot adequately suppress spontaneous breathing (and muscle relaxants are contraindicated), a low-VT strategy should be modified by using a pressure-regulated mode of ventilation, so that imposed circuit-resistive work does not contribute to the deterioration of the patient's hemodynamic and respiratory status.

Adult↗
PubMed1977

Colloid osmotic pressure as a prognostic indicator of pulmonary edema and mortality in the critically ill.

The relationship of colloid osmotic pressure (COP) to pulmonary edema and mortality in 128 critically ill patients was investigated in our critical care unit, and confirms previously reported observations. The COP in the 86 survivors was 22.0 (+/- 0.4 SEM) mm Hg versus 17.2 (+/- 0.6 SEM) mm Hg in the 42 who died (P less than 0.001). The patients were divided into three groups: 71 with no pulmonary edema, COP of 21.5 (+/- 0.5 SEM) mm Hg; 40 with cardiogenic pulmonary edema, COP of 21.4 (+/- 0.4 SEM) mm Hg; and 17 with noncardiogenic pulmonary edema, COP OF 13.6 (+/- 0.8 SEM) mm Hg. Colloid osmotic pressure was significantly lower in patients with noncardiogenic pulmonary edema (P less than 0.001). In 36 patients in whom pulmonary artery wedge pressures (PWP) were available, a COP-PWP gradient of 4.0 mm Hg or less was always associated with pulmonary edema, while a COP-PWP gradient greater than 4.0 mm Hg was never associated with pulmonary edema. Colloid osmotic pressure is a useful prognostic indicator of pulmonary edema and mortality in the critically ill.

Adolescent↗
PubMed1987

Decreasing hydrostatic pressure does not uniformly decrease high-pressure pulmonary edema.

Pulmonary artery wedge pressure (PAWP) of 30 mm Hg with left atrial balloon inflation for 1 1/2 hours produced pulmonary edema in eight dogs. PAWP was then decreased to 10 mm Hg for two hours, and shunt, lung water (extravascular thermal volume, or ETV, by thermal dye), and perfusion distribution (radiomicrosphere technique) were measured and compared with four other dogs (group 1) whose PAWP was maintained at 10 mm Hg. The eight dogs with PAWP of 30 mm Hg for 1 1/2 hours were retrospectively subdivided into two groups of four based on ETV (group 2, double baseline ETV; group 3, triple baseline ETV). Baseline ETV and shunt were similar for all groups and remained unchanged for group 1. At 1 1/2 hours, 2 hours (1/2 hour after decreasing PAWP), 2 1/2 hours, and 3 1/2 hours, respectively, ETV were: 13.9 +/- 1.9, 12.8 +/- 2.0, 9.3 +/- 1.5, and 8.5 +/- 1.0 ml/kg in group 2; and 21.9 +/- 2.1, 22.7 +/- 2.2, 22.5 +/- 2.0, and 22.2 +/- 2.0 ml/kg in group 3. A more variable rate of edema formation was detected in eight additional dogs, but failure to resolve higher levels of edema after decreasing PAWP was also demonstrated in this group. Edema was greatest in lower lobes and decreased lobar perfusion. Shunt was higher in group 3 than in group 2 at 1 1/2 hours and decreased in group 2 but not in group 3 at 3 1/2 hours. Changes in colloid osmotic pressure may account for the differences in edema formation and resolution, but our data suggest that, independent of the rate of edema formation, a decrease in vascular exchange surface area at higher levels of edema may inhibit edema resolution when PAWP is decreased.

Animals↗
PubMed1985

The radiologic distinction of cardiogenic and noncardiogenic edema.

Improvement in the ability to determine the specific cause of any given case of pulmonary edema would lead to more rapid and definitive treatment. "Wedge" pressures and measurements of cardiac output derived from Swan-Ganz catheterization assist in making this determination, but the procedure is invasive, expensive, associated with complications, and not infrequently inaccurate. A plain chest film is, however, almost invariably available in all patients with pulmonary edema, and as shown in this study, the cause of the edema can be determined with a high degree of accuracy by careful attention to certain radiographic features. An independent two-observer study was performed on 216 chest radiographs of 61 patients with cardiac disease, 30 with renal failure or overhydration, and 28 with capillary permeability edema. Three principal and seven ancillary features have been identified, all of which are statistically significant and permit the cause of the edema to be determined correctly in a high percentage of cases. The three principal features are distribution of pulmonary flow, distribution of pulmonary edema, and the width of the vascular pedicle. The ancillary features are pulmonary blood volume, peribronchial cuffing, septal lines, pleural effusions, air bronchograms, lung volume, and cardiac size. Differing constellations of these features occur, each of which is characteristic of a specific type of edema. Overall accuracy of diagnosis in this study ranged from 86% to 89%. The highest accuracy was obtained in distinguishing capillary permeability edema from all other varieties (91%), and the lowest in distinguishing chronic cardiac failure from renal failure (81%).

Blood Volume Determination↗
PubMed2000

Correlation between bone marrow edema and collapse of the femoral head in steroid-induced osteonecrosis.

OBJECTIVE: The purpose of this study was to clarify whether bone marrow edema is detectable on initial MR imaging of steroid-induced osteonecrosis of the femoral head. SUBJECTS AND METHODS: Forty-eight hips with osteonecrosis were examined consecutively with MR imaging and radiography. In a previously reported screening program, osteonecrosis was diagnosed on MR imaging when subchondral bands of abnormal signals were present. In the screening program, the MR images of 200 hips of 100 patients receiving high-dose steroid therapy were examined prospectively. Subchondral bands were detected in 48 hips at a mean of 14 weeks after the initiation of steroid therapy. RESULTS: On follow-up MR imaging of 47 hips (one hip excluded) bone marrow edema was initially observed in 13 hips after the onset of hip pain. MR imaging of the remaining 34 hips did not reveal bone marrow edema and the patients were all asymptomatic. MR imaging of 31 of the 34 hips continued to show subchondral bands and MR imaging of the other three hips indicated that the subchondral bands had disappeared. When bone marrow edema was detectable, abnormal findings on radiography were slight but 11 (85%) of the 13 hips progressed to advanced osteonecrosis. Bone marrow edema was highly correlated with the subsequent collapse of the femoral head (p<0.0001). CONCLUSION: Bone marrow edema was not present on initial MR imaging of osteonecrosis. Bone marrow edema should be considered a marker for potential progression to advanced osteonecrosis, and careful examinations for osteonecrosis are necessary when bone marrow edema is seen.

Adolescent↗
PubMed2003

MR imaging of the lumbar spine: relation of posterior soft-tissue edema-like signal and body weight.

OBJECTIVE: Our purpose was to determine the association between posterior lumbar spine subcutaneous edema, fluid collections, and body weight on lumbar spine MR imaging. MATERIALS AND METHODS: MR images of the lumbar spine obtained at 1.5 T of 307 consecutive outpatients (191 female, 116 male) were reviewed on the basis of MR imaging signal characteristics for the presence, degree, size, and location of presumed subcutaneous posterior soft-tissue edema and fluid collections. The patients were divided into three weight groups (<70, 70-85, or > 85 kg) and two age groups (<50 or >/=50 years old). Edema was graded on a scale of 0-5 according to its length relative to the vertebral bodies. When present, the fluid collection volumes were calculated. The vertical epicenter of the signal abnormality was noted by vertebral body level. RESULTS: Lumbar soft-tissue edema was seen in 121 patients (39%), and discrete fluid collections were seen in 53 patients (17%). Both degree of edema and volume of fluid collection were associated with increasing weight (p < 0.001 and p = 0.002, respectively) and increasing age (p < 0.001 and p = 0.01, respectively). The degree of edema in females was significantly greater than in males (p = 0.003). However, the sex of the patient did not correlate with frequency of fluid collections (p = 0.12) or volume of collections (p = 0.08). The mean epicenters of edema in females and males were at similar levels (L3.4 and L3.9, respectively, p = 0.54). CONCLUSION: The severity of posterior lumbar subcutaneous edema and the volume of fluid collections on MR imaging are associated with increased weight.

Adolescent↗
PubMed1977

Role of pressure gradients and bulk flow in dynamics of vasogenic brain edema.

The authors present the results of an investigation of the vasogenic type of brain edema using cold injury in cats as a model. Their findings indicate that bulk flow and not diffusion should be considered the main mechanism for the spread of edema through the white matter. This conclusion is based on: 1) comparison of the distances actually traveled by various substances during edema spread with those calculated theoretically for migration of the substances by diffusion; 2) coincidence in the speed of movement by two substances (sucrose and albumin) with widely different diffusion coefficients; 3) measurement of interstitial fluid pressure (IFP) at various distances from the lesion showing the presence of increased IFP in the lesion area and decreasing pressures along the edema pathway toward the normal tissue; and 4) the fact that spreading of edema can be significantly impeded by inducing before the cold lesion an intracellular type of brain edema that reduces the size of the extracellular space (ECS) and increases the resistance to flow of edema fluid. The pressure-volume curve of the brain ECS, as derived from determinations of IFP and tissue water content, indicates that initial steep slope in IFP probably represents the high resistance to fluid mobility through the small diameter extracellular channels and the counteracting resistance of the intermingled structures of brain parenchyma to be separated. Once the IFP exceeds these opposing forces, the ECS dilates, fluid mobility increases, and the edema front advances.

Animals↗
PubMed1987

Correlation of tumor plasminogen activator with peritumoral cerebral edema. A CT and biochemical study.

Extracts from 15 human cerebral tumors were tested by a fibrin-plate plasminogen-dependent assay for levels of tumor plasminogen activator (TPA) activity. The TPA activity was correlated with the amount of perineoplastic edema as quantified on computerized tomography (CT) brain scanning. Analysis of the results showed a correlation coefficient of 0.72 when all tumors were included. Analysis of the nine tumors with the highest TPA levels showed a correlation coefficient of 0.96. One metastatic tumor had the highest level of TPA activity, equivalent to a pure 100-micrograms/ml solution of urokinase, and the greatest amount of cerebral edema on CT. Meningiomas generally had the next highest levels of TPA activity and edema, followed by astrocytomas of varying grades, which generally had the lowest level of TPA activity. However, three astrocytomas that had low TPA activity also had significant edema surrounding the tumor, indicating that more than one mechanism may be producing peritumoral edema. There was no correlation between tumor size and the amount of perineoplastic edema. These preliminary results suggest that TPA's may be involved in the production of perineoplastic cerebral edema and that treatment of patients with currently available plasminogen activator inhibitors may be successful in reducing peritumoral edema.

Brain Edema↗
PubMed1993

Contributions of ions and albumin to the formation and resolution of ischemic brain edema.

Changes in brain water, sodium, potassium, and albumin contents and blood-brain barrier (BBB) permeability were determined at various times between 1 hour and 6 weeks following occlusion of the middle cerebral artery (MCA) in rats. In the center of the infarct, brain edema increased to a maximum level by 12 hours, remained elevated for 7 days, and then returned to normal. The change in water content was accompanied by a parallel increase in sodium and decrease in potassium contents; however, the increase in sodium always exceeded the decrease in potassium, resulting in a net gain in brain cations during edema formation which returned to normal with edema resolution. The BBB permeability to 3H-alpha-aminoisobutyric acid was increased by 24 hours after MCA occlusion and returned to normal by 1 week after the edema had resolved. The time course for changes in brain albumin content was different than that for brain edema formation. Large increases in brain albumin content were not apparent until 6 hours after the onset of ischemia, rose to a peak at 3 days after occlusion of the MCA, and returned to normal several weeks after the edema had resolved. Albumin appeared to spread from the central infarct zone to surrounding, less ischemic areas. The relative contributions of the osmotic force produced by the increase in brain cations and the oncotic force produced by the increase in brain albumin to the observed change in water content were calculated. At all time points, the increase in brain cations accounted for nearly all of the observed brain edema, while the increase in albumin played essentially no role in edema development.

Albumins↗
PubMed1994

Cerebrospinal fluid edema associated with shunt obstruction.

The authors report four hydrocephalic children with cerebrospinal fluid (CSF) edema extending along the ventricular catheter of an obstructed CSF shunt. Three of the patients exhibited massive CSF edema along the ventricular catheter, yet they manifested neither ventricular enlargement nor apparent periventricular CSF edema despite increased intraventricular pressure. These findings suggested ventricular tautness. The remaining patient, who had dilated ventricles with periventricular CSF edema, displayed CSF edema in a limited area along the ventricular catheter. Replacement of the obstructed peritoneal catheter of the shunt resulted in rapid improvement of the edema in all patients. In the three patients with massive CSF edema, however, a small lesion remained in the subcortical white matter along the ventricular catheter as demonstrated by computerized tomography and/or magnetic resonance imaging 3 to 5 years after shunt revision. It is concluded that shunt obstruction may result in massive CSF edema along the ventricular catheter in hydrocephalic children who have ventricular tautness after installation of the shunt causing irreversible although usually asymptomatic damage to the affected area of the brain.

Adult↗