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PubMed2005

Intraventricular albumin: an optional agent in experimental post-traumatic brain edema.

HYPOTHESIS: Human albumin may be effective in the treatment of posttraumatic brain edema due to its hyperoncotic features. Therefore, the aim of the experimental study presented in this paper has two points: the first is to evaluate the efficacy of intraventricular hyperoncotic human albumin on post-traumatic brain edema and the second is to try to show the appropriate posttraumatic time window for albumin administration. METHOD: Traumatic brain injury and subsequent edema was formed by a model of impact acceleration injury in rats. Human albumin was administered via intraventricular route by using a stereotactic head holder. All animals in each group were decapitated 24 hours after the procedure and the effect of albumin was evaluated by measurement of tissue specific gravity. RESULTS: Tissue specific gravity decreased in edematous tissue (trauma indicator), increased after albumin administration at the 12th (p < 0.001), and both at the 1st and 12th hour of the trauma (edema treatment; p < 0.001). On the other hand, albumin administered at the 12th, and at both the 1st and 12th hours in the rats without trauma has caused the formation of the brain edema. CONCLUSION: We conclude that human albumin is effective in cytotoxic, but not in vasogenic edema and exerts its best anti-edematous effect at the 12th hour of severe head trauma and this study may help future studies that will try to show the effects of albumin with different time modalities after severe head injury.

Analysis of Variance↗
PubMed2004

Differences in temporomandibular joint pain and age distribution between marrow edema and osteonecrosis in the mandibular condyle.

This study investigated the differences of age distribution and temporomandibular joint (TMJ) pain between marrow edema and osteonecrosis in the mandibular condyle. Subjects consisted of 35 TMJs in 35 patients with abnormal bone marrow on MR images who were selected from a consecutive series of 527 patients with TMJ disorders. Proton density and T2-weighted MR images taken in the oblique sagittal and coronal planes were used to diagnose condylar marrow abnormalities and divide them into either edema or osteonecrosis. The differences in TMJ pain and age distribution for these two abnormalities were assessed with the one-sided Wilcoxon rank sum test with 0.05 alpha level. The degree of pain was higher in joints with marrow edema than in joints with osteonecrosis (p = 0.033). The mean age was higher in joints with osteonecrosis (p < 0.001). Our results suggest that there is more severe pain in TMJs with marrow edema of the mandibular condyle than in those with osteonecrosis. Since the patients with marrow edema have lower age, it also appears that marrow edema may be a precursor condition for osteonecrosis of the TMJ.

Adolescent↗
PubMed1999

Biphasic edema after hypoxic-ischemic brain injury in neonatal rats reflects early neuronal and late glial damage.

Magnetic resonance imaging with diffusion- and T2-weighted imaging and 31P magnetic resonance spectroscopy was used to investigate the relationship between development of brain edema and alterations of the brain energy metabolism after hypoxia-ischemia (HI) brain injury in 7-d-old rats. The results were correlated with histologic examinations at various times during recovery up to 5 d. Moderate HI, induced by right common carotid artery ligation and subsequent exposure to 8% O2 for 90 min, produced a cytotoxic edema of 52+/-9% brain volume and depressed the ratio of phosphocreatine to inorganic phosphate from 1.43+/-0.21 to 0.11+/-0.09. Within 1 h of reoxygenation, the edema decreased to 4+/-2% of brain volume, demarcating the core of the lesion. At 5 h of recovery, a secondary cytotoxic edema together with a newly developing vasogenic edema expanded again, reaching its maximal extent of 45+/-10% brain volume at around 24 h. The ratio of phosphocreatine to inorganic phosphate recovered slowly, reaching 1.12+/-0.27 around 13 h. Thereafter it declined again in a manner analogous to the observations made in human newborns after severe perinatal asphyxia, reaching trough values of 0.48+/-0.22 around 24 h after HI. At the cellular level, the vast majority of neuronal death occurred before 15 h. Subsequently, strong glial activation lasted 2-3 d after HI. At 5 d, a cystic infarction of 35+/-12% brain volume was found. We conclude that the biphasic evolution of brain edema and energy metabolism reflects early neuronal and late glial damage in response to moderate HI injury. Therefore, the secondary energy breakdown reflects glial activation and subsequent glial death.

Animals↗
PubMed1983

Cerebral edema associated with meningiomas.

The cerebral edema, as judged by computed tomographic scan, associated with supratentorial meningiomas was assessed in 55 cases. No relationship to the occurrence or the degree of edema could be established with respect to meningioma location, histological type, tumor vascularity, cellularity, number of mitotic figures, necrosis, calcification, or cortical invasion. The larger the meningioma, the more likely the presence of and the severity of cerebral edema. The edema is a significant factor in the occurrence of clinical signs and symptoms. A biopsy of cerebral cortex and white matter underlying a transitional meningioma in a patient with associated cerebral edema demonstrated perivascular astrocytic end-feet swelling in the cortex and considerable extracellular fluid in the white matter. The ultrastructural appearance is similar to that seen with primary and metastatic brain tumors and with experimental vasogenic cerebral edema.

Brain Edema↗
PubMed1989

Oxygen free radicals in the genesis of traumatic and peritumoral brain edema.

This study evaluates the effect of superoxide dismutase, a scavenger of oxygen free radicals, on peritumoral and cold injury edema. Vasogenic brain edema was produced in 39 cats by a standardized cortical freezing lesion. Peritumoral edema was produced by the transplantation of VX2 carcinoma cells into the brain of New Zealand White rabbits. Detection of superoxide radicals was studied by topical application of nitroblue tetrazolium to the cortical injury and by incubation of the VX2 carcinoma cells. The animals were treated with free superoxide dismutase (SOD) and polyethylene glycol superoxide dismutase (PEG-SOD). The following groups were studied: 1) control, 2) untreated tumor group, 3) tumor group treated with PEG-SOD, 4) a group treated with PEG-SOD before injury, and 5) a group treated with free SOD after injury. Brain edema was evaluated by measurement of specific gravity and planimetry study of the spread of Evans blue dye. Preliminary data indicate that superoxide radicals are present in the brain after cold injury and in the cytoplasm and nucleus of VX2 carcinoma cells. Free SOD and PEG-SOD had no beneficial effect upon the vasogenic brain edema produced in either model. It is concluded that intracellular uptake of SOD may be one of the factors necessary for an effect upon either form of edema.

Animals↗
PubMed2001

The effects of newly synthesized pyrazole derivatives on formaldehyde-, carrageenan-, and dextran-induced acute paw edema in rats.

The antiinflammatory effects of 10 newly synthesized pyrazole derivatives on formaldehyde-induced rat paw edema were investigated. The most effective of them (K-3) was investigated again in dextran- and carrageenan-induced paw edema. In formaldehyde-induced paw edema, K-3 50, 100, and 200 mg/kg p.o. inhibited the edema by 48.9% (p<0.002), 68.7% (p<0.001), and 79.1% (p<0.001), respectively, 3 h after administration. In dextran-induced paw edema, the same dose of K-3 produced 27.1% (p<0.05), 46.8% (p<0.01), and 63.8% (p<0.002) inhibition, respectively. In the carrageenan-induced paw edema test, K-3 100 mg/kg decreased the inflammatory response by 52.0% after 4 h. Acute toxicity studies revealed that K-3 was nontoxic up to an oral dose of 2500 mg/kg.

Animals↗
PubMed1975

Incidence of epinephrine-induced pulmonary edema in rabbits and accompanying metabolic changes.

Searching for an experimental condition to produce pulmonary edema of uniform high grade severity in rabbits, five different doses of epinephrine (38,60, 100, 160 and 260 mug/ml) were infused at a rate of 0.29 ml/min for 20 min into the femoral vein of fed and fasted animals. Body temperature was maintained at 38 to 40 degrees C. The incidence of pulmonary edema was not dose-dependent, and was approx. 70% by the administration of 60 to 260 mug/ml of epinephrine solutions. In general, the edema was more severe in the fed group than in the fasted. The highest dose of epinephrine was often fatal in the fasted group. One hundred mug/ml (approx. 10 mug/kg/min), fed was regarded as a favourable condition for the experiment. The amounts of lung lipids increased in edema (+) cases of the fed groups. The plasma potassium level was elevated in proportion to the dose of epinephrine. The clotting time of blood was markedly prolonged in edema (+) rabbits. The significance of these observations was discussed in regard to the mechanism of epinephrine-induced pulmonary edema.

Animals↗
PubMed1996

Inhibitory effect of glycyrrhetinic acid derivatives on capsaicin-induced ear edema in mice.

We examined the effect of glycyrrhetinic acid (Ia) and its derivatives on ear edema induced by topical application of capsaicin in mice. Three dihemiphthalate compounds: di-sodium salt of 18 beta-olean-12-ene-3 beta,30-diol (deoxoglycyrrhetol, IIa) di-O-hemiphthalate (IIb); 18 beta-olean-9(11),12-diene-3 beta, 30-diol di-O-hemiphthalate (IIIa); and olean-11,13(18)-diene-3 beta,30-diol di-O-hemiphthalate (IVa) inhibited capsaicin-induced edema with ED50 values of 52.6, 41.0 and 51.8 mg/kg (p.o.), respectively. However, glycyrrhetinic acid and deoxoglycyrrhetol at a dose of 200 mg/kg (p.o.) had no effect. Compound IIIa (100 mg/kg, p.o.) also inhibited the edema response to capsaicin in mast cell-deficient mice. Furthermore, compounds IIb, IIIa and IVa (25-100 mg/kg, p.o.) prevented ear edema in response to intradermal injection of substance P (SP) and compound 48/80. In addition, these compounds at a high dose of 100 mg/kg (p.o.) produced a significant inhibition of the plasma extravasation in ear skin induced by i.v. administration of SP. The above results suggest that the effect of these compounds on capsaicin-induced ear edema is due at least in part to an inhibition of the increase of vascular permeability induced by vasoactive agents released from mast cells. Moreover, it seems likely that these compounds at a high dose can suppress vasodilatation and plasma extravasation induced by SP involved in capsaicin-induced edema.

Administration, Topical↗
PubMed1993

Right upper lobe pulmonary edema caused by acute mitral regurgitation. Diagnosis by transesophageal echocardiography.

Unilateral pulmonary edema is a distinctly unusual clinical entity, often misdiagnosed initially as one of the more common causes of focal lung disease. Predominantly lobar pulmonary edema is rarer still. We report a case of right upper lobe pulmonary edema caused by the acute onset of severe mitral regurgitation. In addition, we briefly review the other causes of unilateral pulmonary edema, focusing on the cases that have been reported in association with heart failure and valvular heart disease. The majority of cases of right upper lobe pulmonary edema have been associated with mitral regurgitation. In addition to confirming the presence of mitral regurgitation, transesophageal echocardiography proved useful in delineating the mechanism for edema formation. It detected differential gradients between the right and left pulmonary venous systems and documented the direction of the regurgitant flow.

Acute Disease↗
PubMed1994

Pulmonary hemodynamics in patients with chronic obstructive pulmonary disease before and during an episode of peripheral edema.

We have investigated pulmonary hemodynamics in 16 patients with COPD with respiratory insufficiency, exhibiting marked peripheral edema. All the patients had previously undergone, within the last 6 months (T1), a right heart catheterization, in a stable state of their disease, when they were free of edema. Patients were subdivided into two groups according to the level of right ventricular end-diastolic pressure (RVEDP) during the episode of edema (T2): patients with a markedly elevated RVEDP (> 12 mm Hg) indicating the presence of right ventricular failure (RVF) = group 1, n = 9; patients with a normal or slightly elevated RVEDP (< 12 mm Hg) = group 2 (no RVF), n = 7. In group 1 pulmonary artery mean pressure (PAP) increased very significantly from T1 (27 +/- 5) to T2 (40 +/- 6 mm Hg, p < 0.001) as did RVEDP, from 7.5 +/- 3.9 to 13.4 +/- 1.2 mm Hg (p < 0.001). These hemodynamic changes paralleled a marked worsening of arterial blood gases, PaO2 falling from 63 +/- 4 to 49 +/- 7 mm Hg (p < 0.01) and PaCO2 increasing from 46 +/- 7 to 59 +/- 14 mm Hg (p < 0.01). On the other hand, in group 2, PAP was stable during the episode of edema (from 20 +/- 6 to 21 +/- 5 mm Hg), as was RVEDP (from 5.5 +/- 2.4 to 5.1 +/- 1.5 mm Hg), and changes in arterial blood gases from T1 to T2 were small and nonsignificant. It is concluded that RVF is effectively present in at least some patients with COPD with peripheral edema and is associated with a significant increase of PAP from baseline, probably accounted for by hypoxic vasoconstriction. Thus, pressure overload may contribute to the development of RVF. In other patients there are no hemodynamic signs of RVF, PAP is stable, and the origin of edema is not well understood.

Aged↗
PubMed1995

Pulmonary complications of hyponatremic encephalopathy. Noncardiogenic pulmonary edema and hypercapnic respiratory failure.

OBJECTIVE: To determine the causes of hypoxia in patients with hyponatremic encephalopathy. DESIGN: Retrospective cohort study. SETTING: Consultation and referral service of two university medical centers and community hospitals. PATIENTS: Forty adults with postoperative hyponatremic encephalopathy and hypoxia of whom 30 had noncardiogenic pulmonary edema and 10 had hypercapnic respiratory failure. MAIN MEASUREMENTS: We evaluated the chest radiographs and measured plasma electrolytes, arterial blood gas values, pulmonary artery pressure, pulmonary capillary wedge pressure (PCWP), cardiac output, and net fluid retention. RESULTS: Forty patients with hyponatremic encephalopathy had hypoxia (arterial PO2 below 70 mm Hg), of whom 30 had pulmonary edema and 10 had hypercapnia (PCO2 above 50 mm Hg). Among the 30 patients with pulmonary edema, the serum sodium (+/- SD) was 114 +/- 7 mmol/L, arterial pH was 7.24 +/- 0.16, PCO2 was 45 +/- 15 mm Hg, and PO2 was 42 +/- 16 mm Hg. The cardiac index was 3.6 +/- 0.4 L/min/M2, pulmonary artery pressure was 26/16 mm Hg, and PCWP was 12 +/- 6 mm Hg. There was pulmonary edema, with normal heart size. The hypoxic patients who did not have pulmonary edema had significant hypercapnia (PCO2 = 91 +/- 29 mm Hg, p < 0.001). CONCLUSIONS: Patients with postoperative hyponatremic encephalopathy can develop hypoxia by at least two different mechanisms: noncardiogenic pulmonary edema or hypercapnic respiratory failure.

Adult↗
PubMed1996

Early diagnosis and estimation of pulmonary congestion and edema in patients with left-sided heart diseases from histogram of pulmonary CT number.

To establish an early diagnosis and have a quantitative estimation of congestion or edema, pulmonary CT scans were performed to detect the increase of regional lung water volume of patients with congestive heart failure. CT scanning of the upper, middle, and lower lung fields at maximum inspiration and hemodynamic analysis to ensure a hemodynamically chronic stable condition after the heart failure therapy for 5 weeks by cardiac catheterization within 2 weeks before CT scanning were performed in 10 normal subjects and 25 patients with left-sided heart failure. Patients were divided into two groups according to the presence or absence of pulmonary congestion or edema on chest radiographs, and the mean pulmonary wedge pressure (mPWP). The pulmonary congestion group (14 patients) had pulmonary congestion or edema, and mPWP was greater than 13 mm Hg despite the heart failure therapy. The nonpulmonary congestion group (11 patients) had no pulmonary congestion or edema, and mPWP was lower than 10 mm Hg. Histograms of pulmonary CT numbers were graphed to a set region of interest (ROI) on transverse CT images in all subjects; then changes of pulmonary CT numbers when pulmonary congestion or edema occurred were estimated from those histograms. We found that when severe pulmonary congestion or edema occurred in 6 patients with severe left heart failure, the pulmonary CT numbers within the ROI rapidly increased from -650 to -750 Hounsfield units (HU). We defined the amount ratio between the pixels (pixel counts between -650 and -750 HU within these R0Is) and the pixels (pixel counts between -300 and -950 HU) of the CT number (which were all pixels composing these R0Is) x100(%) as "%PXL." %PXL showed a linear correlation with mPWP. Compared with the %PXL in the normal group, the %PXL in the pulmonary congestion group was significantly higher than that in the normal group (p<0.05, p<0.01, p<0.001) in all lung fields. Similarly, compared with the %PXL in the normal group, %PXL in the nonpulmonary congestion group was significantly higher than that in the normal group in the middle and lower lung fields (p<0.05, p<0.01) in the posterior field. From these results, we concluded that %PXL was a good index to identify abnormal water content usually not recognizable by routine chest radiograph in the lungs.

Adult↗
PubMed2001

Evaluation of blood vessels and edema in the airways of asthma patients: regulation with clarithromycin treatment.

BACKGROUND: Although airway angiogenesis and edema have been proposed to contribute to the airway remodeling process in patients with asthma, there are few studies looking at these structural components in the airway tissue of asthma patients. Mycoplasma infection may be associated with chronic asthma and has been shown to induce angiogenesis and edema in a murine model. PARTICIPANTS AND MEASUREMENTS: We evaluated blood vessels and edema by immunohistochemistry in endobronchial biopsy samples from 10 normal control subjects and 15 patients with mild-to-moderate asthma before and after a 6-week treatment with clarithromycin (n = 8) or placebo (n = 7). Type IV collagen and alpha(2)-macroglobulin were used to identify blood vessels and edema in the tissue, respectively. Mycoplasma pneumoniae was evaluated by polymerase chain reaction. SETTING: National Jewish Medical and Research Center. RESULTS: At baseline, the vascularity, the number of blood vessels, and the edematous area in the airway tissue were not significantly different between asthmatic patients and normal control subjects. However, asthmatic patients demonstrated increased blood vessel size compared with normal control subjects (p = 0.03). After clarithromycin treatment in asthmatic patients, the number of blood vessels was increased (p = 0.02), while edema decreased (p = 0.049). Asthmatic patients who tested positive for M pneumoniae showed a significant increase in vascularity than asthmatic patients who tested negative for M pneumoniae (p = 0.02). CONCLUSION: Our data suggest that angiogenesis and edema may not be significant features of airway remodeling in patients with chronic, mild-to-moderate asthma. Clarithromycin treatment in asthmatic patients could reduce the edematous area as identified by alpha(2)-macroglobulin staining, which may lead to airway tissue shrinkage and cause an artificial increase in the number of blood vessels.

Adult↗
PubMed2003

High-altitude pulmonary edema at moderate altitude (< 2,400 m; 7,870 feet): a series of 52 patients.

STUDY OBJECTIVES: To describe a group of patients who acquired pulmonary edema at a moderate altitude of 1,400 to 2,400 m. DESIGN: Observational, retrospective chart review (1992-2000) of a series of 52 consecutive patients admitted for high-altitude pulmonary edema (HAPE) that occurred at 1,400 to 2,400 m. SETTING: Emergency department of a community hospital in the French Alps (altitude, 500 m). PATIENTS: Vacationing skiers who met criteria for altitude-related pulmonary edema, and in whom other causes (infectious, cardiogenic, neurogenic, and toxic) were excluded. MEASUREMENTS AND RESULTS: All patients presented with signs of pulmonary edema. Diagnoses of infectious, cardiogenic, neurogenic, or toxic edema were ruled out in each patient. All patients were hypoxemic and had radiographic signs of pulmonary edema. Virtually all patients (96%) had dyspnea, and most (77%) had moist rales. All patients were treated with supplemental oxygen (3 to 12 L/min), bed rest, moderate fluid restriction, and continuous positive airway pressure. All recovered fully and were discharged after 4 +/- 2 days (mean +/- SD). CONCLUSION: This study suggests that HAPE at moderate altitudes is more frequent than usually reported. Patients are likely to be young, vacationing men, with no history of prior disease. The disease has a favorable prognosis, and requires simple treatment and a short hospital stay.

Adolescent↗
PubMed1978

Pulmonary edema: physiologic approaches to management.

The integrity of the normal endothelial barrier is responsible for two of the three major safety factors preventing pulmonary edema. This is why edema due to increased pressure is usually not as severe as edema due to increased permeability. Management ought to follow sound physiologic principles. These principles are to lower microvascular hydrostatic pressure and to provide adequate supportive therapy. Positive end-expiratory pressure may improve arterial oxygen transport, but there is no evidence that it improves the balance of pulmonary fluid in edema. Raising the microvascular protein osmotic pressure may be beneficial in edema due to increased pressure but has no demonstrated rationale in edema due to increased permeability.

Blood Proteins↗
PubMed1979

Pulmonary edema following intracranial hemorrhage.

Hemodynamic changes and samples of fluid from pulmonary edema were studied in a 50-year-old woman who developed florid pulmonary edema following intracranial hemorrhage. Marked systemic and pulmonary arterial hypertension were associated with the rapid production of edema fluid that contained red blood cells, but had a lower protein content than plasma. After restoration of pulmonary vascular pressures to a normal range, the production of fluid ceased, and clinical signs of edema resolved. These findings point to the sudden increase in pulmonary microvascular pressure as the cause of pulmonary edema in this patient. Our findings contrast with those of previous reports and with speculations on the extent of a defect in permeability accounting for pulmonary edema following injury to the brain.

Albumins↗
PubMed1982

The relationship of the colloid osmotic-pulmonary artery wedge pressure gradient to pulmonary edema and mortality in critically ill patients.

The relationship of serum colloid osmotic pressure (COP) and pulmonary artery wedge pressure (PAWP) to pulmonary edema and mortality was investigated in 76 critically ill patients. Forty patients suffered from circulatory shock and 36 did not. The COP-PAWP gradient and radiographic evidence of pulmonary edema were measured at the time of diagnosis. The COP-PAWP gradient was markedly decreased in both shock and non-shock patients with pulmonary edema. Decrease of the COP-PAWP gradient correlated with mortality only in those patients with shock. The shock patients who died had a significantly higher incidence of pulmonary edema than those who survived, whereas there was no difference in the incidence of pulmonary edema for surviving or dying non-shock patients. We conclude that marked decreases of the COP-PAWP gradient predict pulmonary edema in the critically ill, but predict mortality only for patients with circulatory shock.

Adult↗
PubMed1985

Small solute clearance from the lungs of patients with cardiogenic and noncardiogenic pulmonary edema.

The regional clearance of 99mTc-diethylenetriamine penta-acetate (99mTc-DTPA) from the lungs was measured in 14 patients with noncardiogenic pulmonary edema, six patients with acute pulmonary edema secondary to heart failure, and 29 normal subjects. The radionuclide was delivered in an aerosol which was inhaled for 120 seconds, and the subsequent decline of radioactivity from the lungs was monitored for seven minutes over each of six peripheral regions of interest with a computerized scintillation camera. The average 99mTc-DTPA clearance of these regions was accelerated above the 98 percent confidence limits in all but three of the patients with noncardiogenic edema. The mean clearance value in this group of patients was significantly greater than those in normal subjects or patients with cardiogenic pulmonary edema. Clearances returned toward normal in each of seven subjects who improved clinically. Only one of the patients with cardiogenic pulmonary edema had an elevated average clearance rate, and the mean clearance for this population was not statistically greater than normal. This procedure appears to detect increased epithelial permeability caused by lung injury and may help distinguish between cardiogenic and noncardiogenic pulmonary edema.

Adult↗