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PubMed1979

The effect of intracerebral ouabain administration on the composition of edema fluid isolated from cats with cold-induced brain edema.

Brain edema fluid was collected from cats with a freezing lesion in the left parietal cortex by the insertion into the brain of needles containing nylon wicks and connected to polyethylene tubes. The edema fluid samples which accumulated in the polyethylene tubes were regularly analyzed for Na+ and K+ content, colloid osmotic pressure, lactate dehydrogenase and creatine phosphokinase activity, and 99mTc-albumin radioactivity; the albumin tracer being introduced intravenously at the time of cold-injury. One series of cats received an intracerebral injection of ouabain solution, the control series an intracerebral injection of saline, at 100 min after the cold-injury. The ouabain injection was followed by an increase of K+ content, LDH and CPK activities but a decrease of Na+ concentration in the edema fluid, attributable to a concentration of solutes in the edema fluid as presumably water and Na+ were shifted into the cells and hence the extracellular space was reduced.

Animals↗

PubMed1998

Rapid onset pulmonary edema (flash edema) in renal artery stenosis.

Abrupt onset pulmonary edema, that rapidly resolves (flash edema) may be due to renal artery stenosis. We describe two patients with renal artery stenosis who experienced a life-threatening episode of flash edema. Relief of the stenosis prevented recurrence of the flash edema.

Aged↗

PubMed1999

MRI-based quantification of cerebral edema in individual SHRSP rats using averaged criteria determined before the occurrence of edema.

This study evaluated whether it is possible with T2-weighted MRI to quantitatively relate image-outcome in a single, individual case with that of a standardized control group that did not show these pathologies. An animal model of hypertension-related cerebral damage, the salt-loaded, stroke-prone spontaneously hypertensive rat (SHRSP), was applied. Very similar values for cerebral edema were found when using either the individual or the averaged threshold. The values were positively correlated with each, as edema(averaged threshold) = 0.12 + 0.99 x edema(individual threshold) (Pearsons coefficient = 0.99, p < 0.0001). This line was virtually congruent with the line of identity. Thus, by determination of the averaged threshold in the healthy salt-loaded SHRSP, a parameter was obtained to calculate cerebral edema with the specifically used T2-weighted MRI protocol, in any rat.

Animals↗

PubMed1979

Composition of isolated edema fluid in cold-induced brain edema.

Edema fluid isolated from cats with cold-induced brain edema was subjected to analysis of electrolyte content, enzyme activities, colloid osmotic pressure and the radioactivity of intravenously injected 99mTc-labeled albumin. The findings corroborate the essential features of vasogenic edema, such as its origin from the blood plasma, its rapid propagation into the white matter of the brain as contrasted with the delayed spread into gray matter, and its contribution to composition of cerebrospinal fluid. Moreover, the elevated activities of cellular enzymes and K+ content of edema fluid point to the admixture with cellular contents due to the freezing damage.

Albumins↗

PubMed1979

Influence of hypoxia on the composition of isolated edema fluid in cold-induced brain edema.

The isolation of edema fluid from cats with cold-induced cerebral edema allowed the study of changes of Na+ and K+ content, lactate dehydrogenase and creatine phosphokinase activity, colloid osmotic pressure and the level of intravenously administered 99mTc-albumin in the edema fluid during a period of hypoxia. The changes consisted of an increase of all mentioned parameters, except Na+; and could be interpreted as a concentration of solutes (but for Na+) in the extracellular edema fluid, concomitant to a reduction of the extracellular space, as the oxygen deficiency caused improper functioning of the cellular Na+-K+ pump, with a resulting shift of fluid (including Na+) into the cellular elements.

Albumins↗

PubMed1990

Contribution of brainstem edema to neurophysiologic deterioration in the cat infusion edema model.

These results show that infusion edema produces a significant increase in brainstem tissue water similar to the distribution seen after traumatic injury. The increased brainstem water of 0.24 cc is equivalent to a brainstem volume rise of 7.26% and was sufficient to cause a marked reduction in the PVI and sustained elevation of the ICP. Despite the ICP rise, somatosensory and brainstem potentials are only mildly affected and return to normal within 8 hr. The fact that severe fluid percussion injury results in obliteration of BAER immediately after impact would suggest that the neurologic deterioration seen in the fluid percussion model of injury is due to direct structural damage of the tissue, which was received at the moment of impact, and not to the compressive effect of the developing brainstem edema at levels achieved in these experiments (7.62% swelling). As in other mechanical models, edema results in secondary compression of the tissue and contributes to the general brain swelling, which if unabated could lead to tentorial herniation and death. In these infusion studies, we must conclude that in some cases, mild secondary compression was sufficient to affect other control centers and produce systemic failure at levels of edema that do not result in alteration of evoked potentials. This might explain the deaths of those animals that occurred during the infusion period in which brainstem potentials remained intact.

Animals↗

PubMed2000

[Generalized brain edema in non-purulent meningoencephalitis. The anti-edema effect of therapy with dexamethasone].

We report about two female inpatients aged 58 and 24, suffering from non-purulent meningoencephalitis, in the first case caused by varizella-zoster-virus, in the second case probably due to viral infection. Both patients developed a diffuse brain edema associated with a progressive loss of consciousness. The adjunctive treatment with dexamethasone led to rapid improvement of clinical symptoms. Computed tomography revealed a significant reduction of brain edema. These results of these two cases support the efficacy of corticosteroids as adjunctive treatment of diffuse brain edema caused by non-purulent meningoencephalitis. The pathophysiological mechanisms are discussed.

Adult↗

PubMed1981

Macular edema and cystoid macular edema.

We examined the foveomacular regions from three eyes in which fluorescein angiography had demonstrated the characteristic appearance of cystoid macular edema by light and electron microscopy. Cystoid macular edema was present in two eyes (one of which was from a 63-year-old diabetic man) that contained peripheral choroidal melanomas, and in a third eye from a patient with diabetes only. By light microscopy, cystoid macular degeneration was obvious only in the third eye. The electron microscopic findings common to all three eyes were widespread swelling and necrosis of Müller cell cytoplasm. There was no enlargement of intercellular spaces. There was secondary neuronal degeneration. Retinal vascular changes, consisting mainly of endothelial cell abnormalities, were found in all cases but were far more common in the two eyes from diabetic patients. The retinal vascular changes were probably the cause of the cystoid macular edema.

Aged↗

PubMed1987

Effects of intracarotid hyperosmolar mannitol in triethyl tin (TET)-induced rat brain edema--preservation of blood-brain barrier (BBB) in TET edema.

The effect of intracarotid hyperosmolar mannitol on the blood-brain barrier (BBB) in triethyl tin (TET)-induced rat brain edema was examined by using intravenous Evans blue (EB, MW 68,000) and Adriamycin (ADM, MW 580) as tracers. Three ml of 1.4 M mannitol solution were administered through the right carotid artery during 45 s for BBB opening. The barrier was opened for 60-120 minutes and then re-established. The reversibility was preserved in TET-treated rats and controls. In fact, the intravenous injection of EB stained both TET-treated and non-treated cerebral hemispheres with mannitol-induced transient BBB disruption, but not without BBB disruption. BBB was resistant to both high and low molecular weight substances in TET-induced edema. The importance of this hyperosmotic studies provides the evidence for normal BBB function in TET-induced brain edema.

Animals↗

PubMed2006

MRI findings in the subchondral bone marrow: a discussion of conditions including transient osteoporosis, transient bone marrow edema syndrome, SONK, and shifting bone marrow edema of the knee.

Bone marrow edema signal can be seen in many settings ranging from trauma and arthritis to less common conditions including transient osteoporosis, transient bone marrow edema syndrome, true osteonecrosis, spontaneous osteonecrosis, and shifting bone marrow edema. Terms such as spontaneous osteonecrosis of the knee (SONK) appear frequently in the radiology and orthopedics literature but are rarely described on true, histologic basis. This article reviews the less frequently encountered and less well understood entities and explores their potential pathophysiologies and significance.

Bone Marrow↗

PubMed2002

Lung edema clearance: 20 years of progress: invited review: alveolar edema fluid clearance in the injured lung.

Resolution of pulmonary edema involved active transepithelial sodium transport. Although several of the cellular and molecular mechanisms involved are relatively well understood, it is only recently that the regulation of these mechanisms in injured lung are being evaluated. Interestingly, in mild-to-moderate lung injury, alveolar edema fluid clearance is often preserved. This preserved or enhanced alveolar fluid clearance is mediated by catecholamine-dependent or -independent mechanisms. This stimulation of alveolar liquid clearance is related to activation or increased expression of sodium transport molecules such as the epithelial sodium channel or the Na(+)-K(+)-ATPase pump and may also involve the cystic fibrosis transmembrane conductance regulator. When severe lung injury occurs, the decrease in alveolar liquid clearance may be related to changes in alveolar permeability or to changes in activity or expression of sodium or chloride transport molecules. Multiple pharmacological tools such as beta-adrenergic agonists, vasoactive drugs, or gene therapy may prove effective in stimulating the resolution of alveolar edema in the injured lung.

Animals↗

PubMed1998

Edema, oncotic pressure, and free entropy: novel considerations for the treatment of edema through attention to thermodynamics.

Over 170 years after Richard Bright and a century after Ernest H. Starling, the development, location, and severity of edema in patients with renal impairment continue to baffle the predictions of most nephrologists. While much of the phenomenon can be explained by levels of serum proteins, or hydrostatic pressures, there are stunning exceptions well known to any practicing nephrologist. Some of the derangement is undoubtedly due to unmeasured but well-known variables, such as membrane permeability; however, other factors such as free entropy of plasma are also clearly involved. The study of other polyelectrolyte colloids, similar to plasma proteins, for industrial purposes has led to the identification of various phenomena such as counterion condensation that can result in loss of entropy and consequently osmotic pressure. Variables known to result in a loss of free entropy, such as pH, oxidation products and ligand binding, are discussed. Older equations developed by van't Hoff and Donnan might require replacement by newer mathematical models such as the nonlinear Poisson-Boltzmann equation or the Monte Carlo simulator. Attempts to restore free entropy to plasma would be a more physiological treatment of edema than diuretic use. Implications are noted for future drug development to treat edema.

Blood Proteins↗

PubMed1997

Spreading of vasogenic edema and cytotoxic edema assessed by quantitative diffusion and T2 magnetic resonance imaging.

BACKGROUND AND PURPOSE: The apparent diffusion coefficient (ADC) of water should be sensitive to the cytotoxic edema triggered by energy failure during ischemia. Elevated values of T2. the nuclear MR transverse relaxation time of water, seen on T2 nuclear MR images detect vasogenic edema and infarcted areas. The temporal and spatial changes in ADC and T2 abnormalities after occlusion of the middle cerebral artery (MCAO) were therefore estimated by these two quantitative techniques. METHODS: Permanent MCAO was performed on rats. Quantitative ADC and T2 maps of brain water were obtained, from which the ischemic volumes were calculated at various times up to 48 hours after MCAO. RESULTS: The areas of decreased ADC represented 36 +/- 7% of the final infarct volume (24 hours) at 0.5 hours and 64 +/- 4% at 5 hours after MCAO, suggesting that there is recruitment of peripheral areas with disturbed energy metabolism and cytotoxic edema. The ADC and T2 contours closely matched at 3.5, 24, and 48 hours after MCAO. CONCLUSIONS: T2 imaging can assess ischemic insults as well as ADC imaging, but only 3.5 hours after the onset of ischemia. Assessment of edematous swelling (approximately 24.5% of total infarcted volume) demonstrates that ADC and therefore T2 imaging detect all the tissue that will become infarcted approximately 7 hours after occlusion. The spread of ADC and T2 abnormalities would therefore stop at approximately 7 hours, and any further increase in volume observed on the images would be mainly due to edematous swelling.

Animals↗

PubMed1974

Experimental edema disease of swine (E. coli enterotoxemia). II. The development of hypertension after the intravenous administration of edema disease principle.

The intravenous inoculation of edema disease principle induced profound hypertension in pigs. The increase in blood pressure occurred approximately 40 hours after inoculation and coincided with the development of the characteristic neurological disturbance of edema disease. Therefore hypertension may play a pathogenetic role in the neuropathy of experimental edema disease.

Animals↗

PubMedDate not supplied

The use of manual edema mobilization for the reduction of persistent edema in the upper limb.

Management of persistent edema with the common treatment methods reported in the literature is not always successful. Manual edema mobilization (MEM) is a relatively new treatment regimen derived from established European and Australian lymphedema reduction regimens. It includes the use of exercises, light skin-tractioning massage techniques following the lymphatic pathways, and the use of low-compression garments. The typical patient who may benefit from the use of MEM has a presumed healthy lymphatic system, is an active participant, and performs some of the techniques independently between therapy sessions. This case report describes the use of MEM on a patient with multiple trauma, which resulted in a significant reduction--78%--of the persistent edema in the affected upper limb. A theoretic rationale is offered for each MEM technique.

Adult↗

PubMed1988

Synthesis of 11C-methylated inulin as a radiopharmaceutical for imaging brain edema and pulmonary edema.

11C-methylated inulin, supposedly useful for imaging of brain edema and pulmonary edema, was prepared using cyclotron produced 11CO2. The synthesis consists of the production of 11C-methyl iodide and its coupling with inulin alkoxide sodium in dimethylsulfoxide as solvent. 11C labeled inulin was purified by alcohol precipitation. The radiochemical yield of pure 11C-inulin was 34% of 11CO2 30 min after the end of bombardment. The blood clearance and body distribution of 11C was observed in rabbits after i.v. injection of 11C-inulin. The blood clearance curve was composed of a sum of three exponential functions. The gamma camera image showed that the 11C activity in blood moved quickly to kidneys and urine and a small dose of radioactivity remained persistently in edematous tissues, i.e. the edematous lung tissues produced by oleic acid treatment.

Animals↗

PubMed1986

Medulla oblongata edema associated with neurogenic pulmonary edema. Case report.

Neurogenic pulmonary edema (NPE) occurs in association with central nervous system disease without underlying cardiopulmonary problems. It is characterized by profound pulmonary vascular congestion and a fulminant clinical course. Although several reports document a role for experimental brain-stem lesions in the production of NPE, there have been only two studies in man correlating specific brain-stem lesions with NPE. The authors report a case of NPE occurring in a patient with von Hippel-Lindau disease and a dorsal medullary syrinx with postoperative dorsal medullary edema. The anatomical location of this patient's lesion is reviewed in the context of alternative theories of the pathogenesis of NPE.

Adult↗

PubMed1981

Role of platelets in vasogenic brain edema. II. Contribution of platelet serotonin in brain edema.

In this study of the function of platelets after CNS injury, platelets were treated with serotonin labeled with radioactive carbon (14C) in animals subjected to a freezing lesion of the cerebrum. The distribution of platelet serotonin was measured by counting the specific activity of 14C-labeled serotonin in tissue and by autoradiography. Some of the animals were treated with RA-233, which inhibits the formation of platelet plugs after endothelial damage and the release of serotonin from platelets. Platelet serotonin accumulated near the surface of the cortex at the site of injury in all animals. More cerebral edema developed in animals treated with the platelet inhibitor than in untreated animals, probably because platelet aggregates were inhibited from forming and were not available to plug leaks in the traumatized vessels. Serotonin did not appear to facilitate the spread of edema.

Animals↗