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PubMed1985

Characterization of subcutaneous edema by mechanical impedance measurements.

The mechanical behavior of gels of various water content, normal and edematous tissues have been studied. Static deformations and vibrations at low frequencies were applied to an area of each of these structures. Softer structures, e.g., gel containing a high percentage of water and pitting edema, have lower mechanical impedance (MI), while harder structures, e.g., nonpitting edema have higher MI. A comparison of the static force measured at bilateral sites on normal subjects show lower differences in impedance than do similar comparisons made in subjects having unilateral edema. This difference is more pronounced with greater static compression. The differences in the MI between different structures are greater at the lower frequencies. At the lower frequencies up to around 30 Hz the ratio of the magnitude of MI of edematous skin and that of contralateral normal skin can indicate the degree of edema. The MI of edematous tissues depends on the type of edema and varies with its degree. Thus this study introduces a quantitative method for the diagnostic and therapeutic assessment of unilateral subcutaneous edema.

Adult↗
PubMed1982

Recurrent postictal pulmonary edema: a case report and review of the literature.

A 37-year-old woman with a post-traumatic seizure disorder had four well-documented episodes of postictal acute pulmonary edema and respiratory failure. Subtherapeutic blood concentrations of phenytoin were documented on each admission. Each episode followed one or more grand mal seizures and was characterized by the development of diffuse nodular-appearing alveolar infiltrates, tachypnea, and severe hypoxemia that rapidly resolved with supportive therapy. There was no evidence of gastric acid aspiration, acute lung infection, or underlying heart or lung disease. To determine the frequency of postictal pulmonary edema in our institution, we reviewed the clinical records and chest roentgenograms of 45 consecutive patients who were admitted to our emergency room following a well-documented grand mal seizure. Only one patient (described in this report) had chest roentgenographic evidence of pulmonary edema. A review of the English literature revealed only 11 reported cases of postictal pulmonary edema since 1965 and a total of 42 episodes in 27 patients since 1908. There were no clearly documented cases of postical pulmonary edema following electroconvulsive therapy in 18 published reports totaling more than 38,000 subjects. Our findings suggest that while postictal pulmonary edema may occur repeatedly in the same patient, the overall frequency of this complication is low.

Adult↗
PubMed1997

Effect of hypothermia, dichloroacetate, and deferoxamine in the treatment for cortical edema and functional recovery after experimental cortical impact in the rat.

OBJECTIVE: To investigate the effects of hypothermia alone or in combination with dichloroacetic acid (DCA) and/or deferoxamine (DFO) in reducing cortical edema (CE) and improving neurologic functional recovery after moderate closed and head trauma with controlled cortical impact (CCI). METHODS: Anesthetized rats were randomized to receive right parietal moderate CCI (impact depth 2 mm, speed 3.5 m/sec) or sham operations. Immediately after trauma, the animals underwent selective brain cooling to 30 degrees C (temporalis muscle temperatures). Ten minutes after trauma, the randomized animals received intraperitoneal doses of DCA (25 mg/kg), DFO (50 mg/kg), both DCA and DFO, or equivolume normal saline. For evaluation of cortical edema, some animals (n = 42) were sacrificed 4 hours after trauma and cortical specific gravity (SpG) was determined gravimetrically. The other animals (n = 47) were evaluated for functional recovery beginning 6 days posttrauma. Neurobehavioral performance was assessed in the Morris water maze. RESULTS: Cortical edema was significantly less in the animals treated with hypothermia (SpG = 1.041 +/- 0.001, p < 0.05) compared with the untreated traumatized animals (SpG = 1.037 +/- 0.001). Combination treatment with hypothermia and drug treatment did not reduce cortical edema when compared with no treatment. Hypothermia with and without drug treatment did not improve neurobehavioral performance when compared with no treatment. CONCLUSIONS: In this pilot study with a relatively small sample size, hypothermia alone significantly reduced post-CCI cortical edema as measured by SpG. Hypothermia combined with drug treatment did not reduce posttraumatic cortical edema. Hypothermia with and without drug therapy did not improve functional neurologic recovery in the rats subjected to CCI.

Animals↗
PubMed1983

Edema formation in the lungs and its relationship to neonatal respiratory distress.

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.

Animals↗
PubMed1977

The nature and significance of peribronchial cuffing in pulmonary edema.

So-called "peribronchial cuffing" in acute pulmonary edema appears to be caused by edema involving the bronchila wall as well as the peribronchial interstitial space, and this was confirmed at autopsy in a patient with acute left heart failure. Edema of the bronchial wall indicates transdation from capillaries derived from the bronchial rather than the pulmonary atery, which may well explain all of the radiological manifestations of acute interstitial edema. The possible role of this circulation in the production of acute alveolar edema is also discussed. The significance of the bronchial artery circulation in the production of acute pulmonary edema warrants reevaluation.

Bronchi↗
PubMed2001

Reperfusion edema after lung transplantation: effect of daclizumab.

PURPOSE: To determine if daclizumab, an interleukin-2 antagonist, reduced the severity of reperfusion edema in lung transplant recipients. MATERIALS AND METHODS: Eighty-five patients who were to undergo 86 consecutive lung transplants were included; 43 (50%) received daclizumab in addition to conventional immunosuppression. Patients were assigned to one of the following groups: control, right allograft; control, left allograft; daclizumab treated, right allograft; daclizumab treated, left allograft. Radiographs obtained in the first 5 postoperative days were evaluated for degree of edema. Mean daily edema scores and curves for control and daclizumab-treated groups were compared. Differences in survival at 1, 3, 6, and 12 months after transplantation, days of mechanical ventilation, and the ratio of arterial oxygenation to inspired oxygen level at 1, 3, and 5 days after transplantation were also compared. RESULTS: Mean daily edema scores, edema curves, survival, days of mechanical ventilation, and ratio of arterial oxygenation to inspired oxygen level at 1 and 3 days after transplantation did not significantly differ between daclizumab-treated and control groups. A trend toward improved survival in the daclizumab-treated group was noted. CONCLUSION: Daclizumab had no effect on the radiographic or immediate clinical manifestations of reperfusion edema in lung transplant recipients. Additional follow-up is needed to determine if daclizumab offers any long-term benefit in terms of reduced rejection rates or survival.

Adolescent↗
PubMed2004

Diffusion-tensor MR imaging of intracranial neoplasia and associated peritumoral edema: introduction of the tumor infiltration index.

PURPOSE: To determine whether diffusion-tensor magnetic resonance (MR) imaging metrics of peritumoral edema can be used to differentiate intra- from extraaxial lesions, metastatic lesions from gliomas, and high- from low-grade gliomas. MATERIALS AND METHODS: In this study, diffusion-tensor MR imaging was performed preoperatively in 40 patients with intracranial neoplasms, including meningiomas, metastatic lesions, glioblastomas multiforme, and low-grade gliomas. Histograms of mean diffusivity (MD) and fractional anisotropy (FA) were used to analyze both the tumor and the associated T2 signal intensity abnormality. An additional metric, the tumor infiltration index (TII), was evaluated. The TII is a measure of the change in FA presumably caused by tumor cells infiltrating the peritumoral edema. Student t test and least-squares linear regression analyses were performed. RESULTS: Peritumoral MD and FA values indicated no statistically significant difference between intra- and extraaxial lesions or between high- and low-grade gliomas. Regarding intraaxial tumors, the measured mean peritumoral MD of metastatic lesions, 0.733 x 10(-3) mm(2)/sec +/- 0.061 (SD), was significantly higher than that of gliomas, 0.587 +/- 0.093 x 10(-3) mm(2)/sec (P <.05). There was also a statistically significant difference between the TIIs of the edema surrounding meningiomas and metastases (mean, 0 +/- 35) and the TIIs of the edema surrounding gliomas (mean, 64 +/- 59) (P <.05). CONCLUSION: Peritumoral diffusion-tensor MR imaging metrics enable the differentiation of solitary intraaxial metastatic brain tumors from gliomas. In addition, the TII enables one to distinguish presumed tumor-infiltrated edema from purely vasogenic edema.

Adolescent↗
PubMed1986

Clinical and experimental vasogenic edema: in vivo sodium MR imaging. Work in progress.

To investigate the sodium magnetic resonance (MR) imaging characteristics of acute vasogenic edema, an experimental canine model was developed. Vasogenic edema was produced in the hemisphere of the dogs by the intraarterial infusion of hypertonic mannitol (25%). This solution opens the blood-brain barrier, allowing the influx of water, electrolytes, and proteins into the brain. The main advantage of this model over the established "cold injury" model is the lack of associated brain necrosis. Two patients with chronic vasogenic edema secondary to well-circumscribed meningiomas also underwent MR imaging. The sodium signal was markedly elevated in both clinical and experimental studies of vasogenic edema fluid compared with signal in healthy brain tissue. Extracellular sodium associated with vasogenic edema displayed MR imaging characteristics similar to that of sodium in serum. There was a trend toward a shortened T2 in edema fluid secondary to the presence of serum macromolecules.

Animals↗
PubMed1997

Knee and shoulder fractures: association of fracture detection and marrow edema on MR images with mechanism of injury.

PURPOSE: To assess the value of magnetic resonance (MR) imaging for enabling the classification of fracture mechanisms and to compare marrow edema caused by compressive forces with that caused by tensile forces. MATERIALS AND METHODS: In 62 knees or shoulders, 78 fractures were identified prospectively on MR images or plain radiographs; compressive or tensile forces were determined retrospectively to have caused impaction or distraction fractures, respectively. Edema was measured on T1-weighted images. Frequencies of fracture detection on MR images or plain radiographs were compared. RESULTS: Forty-nine (63%) and 29 (37%) fractures were attributed to compressive and tensile forces, respectively. Edema measured 31 mm +/- 10 in impaction fractures and 2.5 mm +/- 2.4 in distraction fractures (P < .001). MR images and plain radiographs of 63 fractures were compared. On MR images, distraction fractures, including four of seven Segond fractures, were missed more often than impaction fractures (P < .008). Fractures overlooked on MR images were associated with less edema (P < .003). CONCLUSION: On MR images, impaction fractures demonstrate prominent marrow edema, and distraction fractures demonstrate minimal edema. Impaction fractures are more often missed on plain radiographs, and distraction fractures are more often missed on MR images. Segond fractures should be suspected if MR images show lateral capsular ligamentous injury in the knee; in these cases, evaluation with plain radiography is warranted.

Adult↗
PubMed1994

Leukocyte adhesion, edema, and development of postischemic capillary no-reflow.

The aim of this study was to determine whether the formation of edema that occurs secondary to the neutrophil-dependent increase in microvascular permeability contributes to the genesis of no-reflow in postischemic skeletal muscle. To address this issue, four experimental approaches were used. In the first group, capillary perfusion was assessed in nonischemic canine gracilis muscles in which interstitial fluid volume was increased to a level similar to that in postischemic muscle. In the second and third groups, edema formation was prevented in postischemic skeletal muscles by administration of phalloidin or a hypertonic hyperosmotic saline-dextran solution (HSD; 7.5% saline-6% Dextran 70), and the extent of capillary no-reflow was assessed. In the final group of experiments, a monoclonal antibody (MAb) that binds to the common beta-subunit of the leukocyte integrin CD11/CD18 (MAb IB4) was administered after the development of postischemic edema, and capillary perfusion was determined. Formation of edema in nonischemic preparations and ischemia-reperfusion (I-R) were associated with marked reduction in the number of patent capillaries per fiber (1.2 +/- 0.1 and 0.4 +/- 0.1, respectively) compared with nonedematous nonischemic controls (2.5 +/- 0.3). Treatment with phalloidin or HSD prevented edema formation and attenuated the reduction in the number of patent capillaries per fiber (1.62 +/- 0.2 and 1.71 +/- 0.2, respectively) induced by I-R, whereas administration of MAb IB4 after the formation of edema in reperfused muscles failed to limit capillary no-reflow (0.5 +/- 0.1 patent capillaries/fiber).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed2006

Recombinant human VEGF treatment transiently increases lung edema but enhances lung structure after neonatal hyperoxia.

Recent studies suggest that VEGF may worsen pulmonary edema during acute lung injury (ALI), but, paradoxically, impaired VEGF signaling contributes to decreased lung growth during recovery from ALI due to neonatal hyperoxia. To examine the diverse roles of VEGF in the pathogenesis of and recovery from hyperoxia-induced ALI, we hypothesized that exogenous recombinant human VEGF (rhVEGF) treatment during early neonatal hyperoxic lung injury may increase pulmonary edema but would improve late lung structure during recovery. Sprague-Dawley rat pups were placed in a hyperoxia chamber (inspired O(2) fraction 0.9) for postnatal days 2-14. Pups were randomized to daily intramuscular injections of rhVEGF(165) (20 microg/kg) or saline (controls). On postnatal day 14, rats were placed in room air for a 7-day recovery period. At postnatal days 3, 14, and 21, rats were killed for studies, which included body weight and wet-to-dry lung weight ratio, morphometric analysis [including radial alveolar counts (RAC), mean linear intercepts (MLI), and vessel density], and lung endothelial NO synthase (eNOS) protein content by Western blot analysis. Compared with room air controls, hyperoxia increased pulmonary edema by histology and wet-to-dry lung weight ratios at postnatal day 3, which resolved by day 14. Although treatment with rhVEGF did not increase edema in control rats, rhVEGF increased wet-to-dry weight ratios in hyperoxia-exposed rats at postnatal days 3 and 14 (P < 0.01). Compared with room air controls, hyperoxia decreased RAC and increased MLI at postnatal days 14 and 21. Treatment with VEGF resulted in increased RAC by 181% and decreased MLI by 55% on postnatal day 14 in the hyperoxia group (P < 0.01). On postnatal day 21, RAC was increased by 176% and MLI was decreased by 58% in the hyperoxia group treated with VEGF. rhVEGF treatment during hyperoxia increased eNOS protein on postnatal day 3 by threefold (P < 0.05). We conclude that rhVEGF treatment during hyperoxia-induced ALI transiently increases pulmonary edema but improves lung structure during late recovery. We speculate that VEGF has diverse roles in hyperoxia-induced neonatal lung injury, contributing to lung edema during the acute stage of ALI but promoting repair of the lung during recovery.

Animals↗
PubMed2003

Elevated levels of plasminogen activator inhibitor-1 in pulmonary edema fluid are associated with mortality in acute lung injury.

The alveolar fibrinolytic system is altered in acute lung injury (ALI). Levels of the fibrinolytic protease inhibitor, plasminogen activator inhibitor-1 (PAI-1), are too low in bronchoalveolar lavage to address its prognostic significance. This study was performed to assess whether PAI-1 antigen in undiluted pulmonary edema fluid levels can identify patients with ALI and predict their outcome. PAI-1 antigen levels in both plasma and edema fluid were higher in ALI compared with hydrostatic edema, and edema fluid PAI-1 values identified those with ALI with high sensitivity and specificity. Both the high plasma and edema fluid PAI-1 antigen values were associated with a higher mortality rate and fewer days of unassisted ventilation in patients with ALI. Differences in PAI-1 activity were concordant with levels of PAI-1 antigen. Although the fibrin-derived alveolar D-dimer levels were strikingly similar in both groups, ALI patients had a higher relative proportion of D-monomer. In conclusion, PAI-1 levels in edema fluid and plasma identify those with ALI that have a poor prognosis. The data indicate that fibrin turnover in early ALI is a consequence of a rapid fibrinogen influx and fractional fibrinolytic inhibition.

Acute Disease↗
PubMed1999

Use of NK(1) knockout mice to analyze substance P-induced edema formation.

The mechanisms involved in tachykinin-induced neurokinin-1 (NK(1)) receptor-mediated edema formation have been studied in anesthetized wild-type and NK(1) knockout mice. Intradermally injected substance P (30-300 pmol), NK(1) agonists septide (3-30 pmol) and GR-73632 (3-30 pmol), and the mast cell-degranulating agent, compound 48/80 induced dose-dependent edema in wild-type skin, measured by the accumulation of intravenously injected (125)I-labeled albumin. Septide was 3-10x more potent than substance P. The tachykinins were inactive in knockout mice, but compound 48/80 induced a significantly greater edema (P < 0.05) than that observed in paired wild-type mice. Capsaicin (which releases endogenous neuropeptides) and exogenous tachykinins induced edema formation, which was reduced by the mast cell amine histamine H(1) antagonist mepyramine (P < 0.05). These findings confirm that tachykinins mediate edema formation via the NK(1) receptor and provide direct evidence that the septide-sensitive binding site is on the NK(1) receptor. Furthermore, results suggest that edema induced by the tachykinins, although totally dependent on NK(1) receptor-mediated mechanism, contains a mast cell-dependent component. The evidence is in keeping with an NK(1) receptor on mast cells.

Animals↗
PubMed1980

Effect of edema on pulmonary blood flow in the isolated perfused dog lung lobe.

We determined the relationship between the amount of edema and changes in blood flow in the isolated, perfused, and ventilated lower lobe of dog lung. We held vascular pressure constant and measured lobe weight and flow continuously. Vascular pressures were set to produce minimal weight gain in four lobes (controls) and large weight gain in six lobes (edema). In all lobes, the outflow pressure exceeded alveolar pressure at end expiration (zone III conditions). The control lobes gained an average of 20% in weight over 4 h, but blood flow remained constant. They showed interstitial edema histologically and extravascular lung water was increased 38%. The edema lobes gained weight rapidly, ultimately tripling their weight. In these lobes, blood flow remained constant until lobe weight had doubled; then flow decreased progressively to low levels. These lobes showed extensive alveolar edema histologically and extravascular lung water was increased 238%. Pulmonary blood flow is not affected by interstitial edema, but is markedly reduced when alveolar flooding occurs.

Animals↗
PubMed1981

Pulmonary microvascular clearance of radiotracers in human cardiac and noncardiac pulmonary edema.

We examined the integrity of the alveolocapillary membrane in human cardiac (hydrostatic) (group 1) and noncardiac (permeability) (group 2) edema by measuring the clearance of two intravenously administered radiotracers from the blood to suctioned bronchoalveolar secretions (BAS), representing pulmonary edema fluid, and compared the clearances to simultaneously measured pulmonary capillary wedge pressure (PCWP) and colloid osmotic pressure (COP), representing the intravascular Starling forces, Pmv and pimv. 111In-labeled diethylenetriamine pentaacetic acid (DTPA), mol wt 504, a hydrophilic radiotracer that equilibrates with extracellular water, and 125I-labeled human serum albumin (HSA), mol we 69,000, were injected intravenously. Samples of blood and BAS were then collected hourly for 405 h, and clearances were calculated. We found the clearance of both radiotracers to be greater in group 2 than in group 1 patients, despite a low mean PCWP-COP gradient, indicating greater alveolocapillary membrane permeability membrane in noncardiac, than in cardiac edema. Furthermore, 111In-DTPA clearance was linearly correlated with the PCWP-COP gradient in both groups (group 1, R2 = 0.726, P less than 0.001; group 2, R2 = 0.879, p less than 0.001 as was the clearance of 125I-HSA in group 2 (R2 = 0.35, P less than 0.027). Clinically, the data suggest that in cardiac and noncardiac pulmonary edema the transmicrovascular flux of small and large solutes may be favorably influenced by therapeutic alterations aimed at widening the intravascular PCWP-COP gradient. However, the greater permeability of the alveolocapillary membrane in noncardiac edema would prohibit any major resolution of edema by simple therapeutic alterations of this gradient.

Capillary Permeability↗
PubMed1983

Alveolar pressure in fluid-filled occluded lung segments during permeability edema.

In a model of increased hydrostatic pressure pulmonary edema Parker et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 267-276, 1978) demonstrated that alveolar pressure in occluded fluid-filled lung segments was determined primarily by interstitial fluid pressure. Alveolar pressure was subatmospheric at base line and rose with time as hydrostatic pressure was increased and pulmonary edema developed. To further test the hypothesis that fluid-filled alveolar pressure is determined by interstitial pressure we produced permeability pulmonary edema-constant hydrostatic pressure. After intravenous injection of oleic acid in dogs (0.01 mg/kg) the alveolar pressure rose from -6.85 +/- 0.8 to +4.60 +/- 2.28 Torr (P less than 0.001) after 1 h and +6.68 +/- 2.67 Torr (P less than 0.01) after 3 h. This rise in alveolar fluid pressure coincided with the onset of pulmonary edema. Our experiments demonstrate that during permeability pulmonary edema with constant capillary hydrostatic pressures, as with hemodynamic edema, alveolar pressure of fluid-filled segments seems to be determined by interstitial pressures.

Animals↗
PubMed1986

Factors affecting perfusion distribution in canine oleic acid pulmonary edema.

Factors affecting perfusion distribution in oleic acid pulmonary edema were examined in 28 anesthetized open-chest dogs. Sixteen had unilobar oleic acid edema produced by left lower lobe pulmonary artery infusion of 0.03 ml/kg of oleic acid, and 12 had the same amount of edema produced by left lower lobe endobronchial instillation of hypotonic plasma. Lobar perfusion (determined from flow probes) and lobar shunt (determined from mixed venous and lobar venous blood) were measured at base line, 1.5 h after edema, and 10 min after 10 cmH2O positive end-expiratory pressure (PEEP). Fourteen dogs (8 oleic acid, 6 plasma) received sodium nitroprusside (11.72 +/- 7.10 micrograms X kg-1 X min-1). Total and lobar shunts increased to the same extent in all animals. Lobar perfusion decreased by 49.8 +/- 4.8% without nitroprusside and 34.0 +/- 3.6% with nitroprusside in the oleic acid group, corresponding values being 40.3 +/- 0.8% and 26.4 +/- 1.7% in the hypotonic plasma group. PEEP returned perfusion and shunt to base line. In oleic acid edema, most of the decreased perfusion results from mechanical effects of the edema, a smaller fraction results from other vascular effects of the oleic acid, and approximately 30% is reversible by nitroprusside. PEEP normalizes the perfusion distribution.

Animals↗
PubMed1987

Analysis of airway fluid protein concentration in neurogenic pulmonary edema.

Intracisternal administration of veratrine (40 micrograms/kg) in the alpha-chloralose-anesthetized dog produces fulminant neurogenic pulmonary edema (NPE). To determine whether the edema resulted from increased microvascular pressure or from increased permeability, the airway fluid-to-plasma protein (A/P) concentration ratios were compared for both total proteins and endogenous protein fractions of known molecular radii (37-114 A) from dogs with edema produced by either veratrine, alloxan (permeability edema), or combined left atrial pressure and volume overload (hemodynamic edema). High A/P ratios (0.98 +/- 0.05) were observed after alloxan administration, whereas lower values (0.54 +/- 0.04) were observed in hemodynamic edema. A/P ratios were observed after veratrine administration that formed a continuum (0.48-0.84) between these extremes. Veratrine animals with high overall A/P ratios exhibited elevated A/P ratios for all protein fractions, whereas animals with lower overall A/P ratios exhibited A/P protein fraction ratios similar to those observed in the hemodynamic group. These data indicate that both hemodynamic and increased permeability mechanisms may play a role to varying degrees in the development of this form of NPE.

Animals↗