[Symposium on edema. (2) Clinics of edema. I) Pathogenesis of cardiac edema--with respect to role of hypoproteinemia (author's transl)].
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Animals↗
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[Symposium on edema. (2) Clinics of edema. III) Mechanism of edema in liver cirrhosis (author's transl)].
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Adult↗
[Symposium on edema. (2) Clinics of edema. VI) Treatment--diuretics and refractory edema (author's transl)].
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Bumetanide↗
Etiology of acute pulmonary edema during liver transplantation : a series of cases with analysis of the edema fluid.
STUDY OBJECTIVES: To describe the clinical features of a group of patients who acutely developed pulmonary edema during orthotopic liver transplantation and to determine the nature (transudate vs exudate) of the edema. DESIGN: Retrospective review of clinical records and radiographic studies. SETTING: Operating room and ICU of a tertiary-care medical center hospital. PATIENTS: End-stage liver disease patients undergoing orthotopic liver transplantation under general anesthesia. INTERVENTIONS AND MEASUREMENTS: Pulmonary edema fluid obtained from seven patients within 15 min of first appearance was analyzed for protein content and compared with the protein content of a simultaneously obtained plasma sample. Hemodynamic data, fluid administration totals, and length of postoperative intubation and ICU stay were also collected. RESULTS: Eight patients were identified. Six of the seven patients whose edema fluid was analyzed had edema fluid/plasma protein ratios > or =0.75, characteristic of increased permeability pulmonary edema (the one other patient had a ratio of 0.73). Hemodynamic monitoring at the time of onset of the edema effectively ruled out a cardiogenic etiology. One patient died intraoperatively; at autopsy, the cause of death was determined to be pulmonary fat embolization. In the other seven patients, production of edema fluid resolved within 6 h of admission to the ICU. The duration of ventilatory support ranged from 23 to 96 h, with a mean of 49 h. CONCLUSIONS: The most likely cause of the reaction is transfusion-related acute lung injury (TRALI). An incidence of TRALI that is higher than previously reported in this population indicates that other elements, such as reperfusion of the newly implanted liver, may be contributing factors.
Adult↗
Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners.
BACKGROUND: Noncardiogenic pulmonary edema is often associated with increased intracranial pressure and can be the initial manifestation of hyponatremic encephalopathy. Marathon runners tend to develop conditions that lead to hyponatremia. OBJECTIVE: To describe the development and treatment of noncardiogenic pulmonary edema in marathon runners that was associated with hyponatremic encephalopathy. DESIGN: Case series. SETTING: One university hospital and two community hospitals. PATIENTS: Seven healthy marathon runners who had a history of nonsteroidal anti-inflammatory drug use. The runners collapsed after competing in a marathon and were hospitalized with pulmonary edema. MEASUREMENTS: Plasma sodium levels, chest radiograph, electrocardiogram, cardiac enzyme levels, and magnetic resonance imaging or computed tomographic scans of the brain. RESULTS: Patients had nausea, emesis, and obtundation. The mean (+/-SD) plasma sodium level was 121 +/- 3 mmol/L, and oxygen saturation was less than 70%. Electrocardiograms and echocardiograms were normal. Chest radiographs showed pulmonary edema with a normal heart. Creatine phosphokinase-MB bands, troponin levels, and pulmonary wedge pressure were not elevated. Scanning of the brain showed cerebral edema. All patients were intubated and mechanically ventilated. Treatment with intravenous NaCl, 514 mmol/L, increased plasma sodium levels by 10 mmol/L in 12 hours. Pulmonary and cerebral edema resolved as the sodium level increased. One patient had unsuspected hyponatremic encephalopathy and died of cardiopulmonary arrest caused by brainstem herniation. All six treated patients recovered and were well after 1 year of follow-up. CONCLUSIONS: In healthy marathon runners, noncardiogenic pulmonary edema can be associated with hyponatremic encephalopathy. The condition may be fatal if undiagnosed and can be successfully treated with hypertonic NaCl.
Adult↗
Great Lakes embryo mortality, edema, and deformities syndrome (GLEMEDS) in colonial fish-eating birds: similarity to chick-edema disease.
Several species of colonial fish-eating birds nesting in the Great Lakes basin, including herring gulls, common terns and double-crested cormorants, have exhibited chronic impairment of reproduction. In addition to eggshell thinning caused by high levels of DDT and metabolites, the reproductive impairment is characterized by high embryonic and chick mortality, edema, growth retardation, and deformities, hence the name Great Lakes embryo mortality, edema, and deformities syndrome (GLEMEDS). The hypothesis has been advanced that GLEMEDS in colonial fish-eating birds resembles chick-edema disease of poultry and has been caused by exposure to chick-edema active compounds that have a common mode of action through the cytochrome P-448 system. Detailed evidence has been collected from the following three groups of studies on herring gulls in the lower Great Lakes during the early 1970s; Forster's terns in Green Bay, Wisconsin in 1983; and double-crested cormorants and Caspian terns in various locations in the upper Great Lakes from 1986 onwards. It has proved difficult to establish not only the onset of the disease in the various species at various locations but also the period in which chick-edema active compounds were released. Anecdotal evidence suggested that serious egg mortality in Lake Ontario herring gulls first occurred in 1966, through the signs of chick-edema disease were not looked for until 1974. Only indirect evidence is available on the date of the release of one of the presumed causal agents, 2,3,7,8-tetrachlorodibenzo-p-dioxin, but highest levels may have occurred in the early to mid 1960s. More reliable data show that the onset of the improvement of reproduction of Lake Ontario herring gulls coincided with the declines in organochlorine compounds and particularly 2,3,7,8-TCDD and PCB. Similarly, information on the onset of the disease and exposures in the Forster's tern and double-crested cormorants in Green Bay is uncertain but bird banders did not observe deformities until the 1970s, which corresponds with the onset of high levels of PCB. If the disappearance of the Caspian tern from Saginaw Bay in the mid 1960s corresponds with the onset of GLEMEDS at that location, then there is a close temporal relationship to the onset of high PCB levels. Chick-edema disease is difficult to diagnose because there is no specific lesion, but rather there is a suite of lesions.(ABSTRACT TRUNCATED AT 400 WORDS)
Abnormalities, Drug-Induced↗
Fibromatosis and massive edema of the ovary, possibly related entities: a report of 14 cases of fibromatosis and 11 cases of massive edema.
Twenty-five cases of ovarian enlargement secondary to massive edema, to a hitherto undescribed lesion that we have designated fibromatosis, or to both processes were reviewed to explore the possibility of a relation between them. The patients ranged in age from 13 to 39 years. The 14 patients with pure or predominant fibromatosis usually presented because of menstrual abnormalities; two had evidence of androgen excess and three had abdominal pain. At laparotomy two involved ovaries were observed to have twisted on their pedicles. There was definite bilateral ovarian involvement in two cases and probable bilateral involvement in two others. The excised specimens measured up to 12 cm in diameter and typically had firm, white sectioned surfaces. Microscopic examination showed a proliferation of spindle cells usually separated by dense collagen, which surrounded normal follicular structures. Lutein cells were present in the fibromatous areas in one patient, who was masculinized, and in the adjacent ovarian stroma in another patient, who was hirsute; a proliferation of cells of sex cord type was observed in the fibromatous areas in three cases. Six of the specimens contained focal areas of edema similar in appearance to that seen in cases of massive edema. The features of the 11 cases of massive edema were, in general, similar to those of the 40 examples of this entity reported in the literature. Six of the 11 patients had menstrual abnormalities and/or evidence of androgen excess, but most of them presented because of abdominal pain. At operation an involved ovary was observed to have undergone torsion in five of the cases; bilateral ovarian enlargement due to massive edema was present in two cases. The excised specimens, which measured up to 15 cm in diameter, typically had a watery appearance on sectioning. Microscopic examination showed edematous stroma surrounding residual normal ovarian structures. Lutein cells were identified in the edematous stroma in four cases and in the adjacent ovarian stroma in three of these cases. One of these patients was masculinized and another was hirsute. Small foci of fibromatosis similar to that seen in cases of pure fibromatosis were present in eight cases. The similar age range and clinical manifestations of these two processes and the overlap in their histologic features suggest that they are closely related and may reflect differing morphologic expressions of the same underlying disorder. Some of the cases of massive edema, however, may result from the development of stromal edema in ovaries involved by hyperthecosis.
Abdomen↗
Clearance of edema fluid into cerebrospinal fluid. A mechanism for resolution of vasogenic brain edema.
The authors present the results of an investigation studying the resolution of vasogenic brain edema using cold injury in cats. The appearance of RISA-I131 and sucrose-C14 lebeled edema fluid in the ventricular cerebrospinal fluid (CSF) was assessed by means of ventriculocisternal perfusion. The effect of low- or high-pressure perfusion on edema spread was determined by measuring the water, sodium, RISA-I131, and sucrose-C14 content of serial tissue blocks taken from the injured cortex through the white matter to the ventricular ependyma. The findings indicate that increasing the hydrostatic pressure gradient between edematous brain and CSF enhances the clearance of edema fluid into the ventricular CSF. This was conclusively demonstrated with low-pressure ventricular perfusion which markedly diminished the amount of edema close to the ventricles compared to the controls. The concentration of albumin, sodium, and potassium to the fluid removed from the tissue during low-pressure perfusion indicates that bulk flow was the primary method of edema movement through the extracellular space. With high-pressure perfusion the concentration profiles suggested alternative mechanisms of edema resolution, such as diffusion and reabsorption into capillaries.
Animals↗
Dynamics of cerebral edema. The role of an intact vascular bed in the production and propagation of vasogenic brain edema.
Brain edema was produced in cats by a standardized cortical freezing lesion. With a careful microsurgical tehnique, the injured cortex was removed as a single piece, either immediately after induction or at 2, 4, or 8 hours after lesion production. The injured brain was either discarded or replaced in its bed. Brain edema and the defect in the blood-brain barrier were assessed by determining percent dry weight, increase in volume of white matter, and spread of Evans' blue by planimetry. The results indicate that 1) if the lesion is removed immediately after production, formation of the expected vasogenic brain edema is completely abolished; 2) replacement of the frozen brain is unable to induce significant increase in permeability of the surrounding blood-brain barrier or a significant amount of brain edema; and 3) if the lesion is removed at 2, 4, or 8 hours with or without replacement, advancement of the edema front and increase in the amount of edema is stopped. It appears that an intact vascular bed is necessary for the extracellular fluid component of brain edema, and that no edemagenic factors exist within the injured brain in this model that influence either the production or propagation of the increased extracellular fluid volume.
Animals↗
[Study of brain edema by an infusion edema Model--the method and characteristics of the model].
In this report, we have described the way of making the infusion edema model, physiological changes of various parameters during this procedure, distribution of water content in white and gray matter and the light and electron microscopic findings of this edema model, for the further understanding of vasogenic edema of the brain. To make the infusion edema model, 25-G needle was stereotaxically inserted into the left frontal white matter of the cat brain. Through the polyethylene catheter with three way stop cock, this catheter was connected to the pressure transducer and slow infusion pump. By this way, we can monitor the pressure of infusing fluid into the white matter. Normal saline was infused with initial rate of 0.75 microliter/min for the first 2 hours. The inflow rate was increased to 1.5 microliter/min for the next one hour, and then changed to 3.0 microliters/min for maintenance inflow rate. The total amount of infused volume was 0.5 ml in this study. During making the infusion edema model, blood pressure and PaCO2 changed little. Intracranial pressure slightly increased from 5.8 to 15.1 mmHg. Pressure volume index (PVI) changed from 0.74 to 0.64, suggesting the changes of intracranial compliance. The water content measured by specific gravimetric technique showed nearly the same water contents and distribution of edema fluid in the white matter of the cat as in the cryogenic injury model. Pathological findings of this infusion edema model demonstrated that the infused liquid was accumulated in the extracellular space of white matter without damaging the tight junction, and endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Use of the Gamow Bag by EMT-basic park rangers for treatment of high-altitude pulmonary edema and high-altitude cerebral edema.
As part of an emergency medical system protocol, national park service rangers certified at the level of an emergency medical technician-basic (EMT-B) are taught to recognize and treat high-altitude pulmonary edema and high-altitude cerebral edema. In Sequoia and Kings Canyon National Parks, this is done with the assistance of physician on-line medical control as a backup. High-altitude pulmonary edema and high-altitude cerebral edema are both potentially fatal altitude illnesses that can be particularly problematic in the backcountry, where evacuation may be delayed. We report a case of high-altitude pulmonary edema and high-altitude cerebral edema occurring at moderate altitude that was successfully treated by park rangers with the Gamow Bag.
Adult↗
Biomechanical characteristics of brain edema: the difference between vasogenic-type and cytotoxic-type edema.
Some of the basic biomechanical properties of edematous brain tissue have yet to be clarified. Therefore we measured regional tissue compliance and swelling isotropy/anisotropy in cat brain during development of vasogenic-type and cytotoxic-type edema. In vasogenic-type edema induced by cryogenic injury, the edematous white matter showed an increase of regional tissue compliance (indentation method), which paralleled the increase in the regional tissue water content (gravimetry). Swelling of the white matter due to edema was anisotropic, in which expansion transverse to the neuronal fibers caused by their dissociation was 91.1%, whereas longitudinal expansion was 2.3%. In cytotoxic-type edema induced by cerebral ischemia for 3 h, regional tissue compliance was decreased in the area suffering energy failure, which was visualized as an area of reduced succinic dehydrogenase activity. The ischemic gray matter showed isotropic swelling, and morphologically, prominent swelling of neuroglial cells. These marked differences in basic biomechanical properties between vasogenic-type and cytotoxic-type edema should be taken into account when analyzing the mechanism of edema-mediated tissue injury.
Animals↗
Histamine paw edema of mice was increased and became H2-antagonist sensitive by co-injection of nitric oxide forming agents, but serotonin paw edema was decreased.
Nitric oxide (NO) surprisingly caused the opposite effect on histamine and serotonin edema. The local injection of acidified nitrite (0.3-30 micrograms/paw which correspond 10 micrograms-1 mg/kg) increased histamine edema of mice up to 45 +/- 4% and suppressed serotonin edema to 90 +/- 3%. Other NO-generators (nitroprusside sodium and hydroxylamine) showed similar effects. These results were in accordance with our previous data on endogenous NO. Methylene blue (MB, 30 ng/paw which corresponds to 1 microgram/kg) suppressed histamine edema (62 +/- 3%) and increased serotonin edema (43 +/- 3%) in normal mice, being reversed by acidified nitrite. This suggests the involvement of guanosine 3',5'-cyclic monophosphate (cGMP) formation for the action of NO. Histamine edema became sensitive to H2-antagonist, cimetidine, by co-injection of 30 micrograms/paw (which corresponds to 1 mg/kg) acidified nitrite (ED50 = 30 micrograms/kg versus >> 1 mg/kg). NO seemed to modify the histamine receptor(s) or tautomeric form of histamine. NO, O2- and other oxyradicals might finely control the vascular permeability together with inflammatory mediators.
Animals↗
Importance of protein content in the edema fluid for the resolution of brain edema.
This study shows that there is a quantitative relation between the protein content of edema fluid and the rate of fluid clearance. Minimal clearance takes place during the first 3 days in the high albumin group. Thereafter, the majority of the fluid is cleared, and tissue water returns to normal values by 8 days. This appears to support an idea that the rate of clearance is in direct proportion to protein concentration. This also supports the findings of Kuroiwa et al. who showed a direct relation between protein extravasation and the increase of water in extracellular vasogenic edema. However, the rate of clearance does not in fact appear to be linear with time as the greater percentage of protein edema fluid is cleared after 3 days. This may be explained by the observations of Rasmussen and Klatzo and Bodsch and Hossmann who indicate that the composition of the extracellular protein may undergo various changes, similar to fragmentation, hence increasing the number of osmotically active particles so the pre-existing edema would remain stable or slightly increase. In conclusion, this study demonstrates that the infusion model of edema can be applied to the rat for study of resolution dynamics. We have also shown that in this model, there is a proportional relation between protein concentration of the edema fluid and time necessary for clearance.
Albumins↗
Unilateral pulmonary edema following acute subglottic edema.
Presented here is a case of unilateral pulmonary edema following acute subglottic edema after removal of an endotracheal tube. A 3-year-old boy, diagnosed as having nondiphtheric croup and pectus excavatum deformity, was scheduled for repair of a cleft lip. No complication occurred during the operation. After removal of the endotracheal tube, he showed dyspnea and cyanosis and was later found to have acute subglottic edema. After reintubation of the trachea, frothy pink fluid was discharged from the tube, and chest roentgenogram showed a right-sided alveolar infiltrate. Many factors may cause unilateral pulmonary edema, but it is suggested that acute subglottic edema and unilateral bronchial fragility strongly affected this episode.
Acute Disease↗
Effect of steroid on ischemic brain edema. Analysis of cytotoxic and vasogenic edema occurring during ischemia and after restoration of blood flow.
Mongolian gerbils were observed for the effects of beta-methasone on ischemic brain edema which developed during ischemia or after blood flow restoration. The severity of brain edema was determined by measuring water content of the ischemic cerebral hemisphere, using the wet and dry methods. Sodium and potassium ions were extracted from homogenized brains with 0.75N HNO2 and ion concentration measured by flame photometry. Passage of RISA from blood into the cerebral parenchyma, as an indicator of blood-brain barrier change, was determined with a gamma-scintillation counter. In the cytotoxic edema model, animals were killed after 9 h permanent ischemia or 3 h after 1 h ischemia. In the simultaneous cytotoxic and vasogenic edema model, the animals were killed either 20 h or 3 days following 1 h ischemia, or 3 h after blood flow restoration following 6 h ischemia. Steroid treatment was ineffective in ischemic brain edema of the cytotoxic or vasogenic type.
Animals↗
Effects of pulmonary edema on regional blood volume and red blood cell transit time. Comparison of high pressure and oleic acid-induced edema.
The present study was designed to determine the effects of pulmonary vascular pressure, vascular injury, and pulmonary edema on regional blood volume (Vr) and regional red blood cell (RBC) transit time (Tr) in the lung. The experiments were carried out in 15 dogs. Six served as controls, six had oleic acid-induced pulmonary edema (OAPE), and three had high pressure pulmonary edema (HPPE). Regional blood flow (Qr) was measured with 99mTc macroaggregates, Vr with 51Cr homologous RBC, and regional transit time was calculated (Vr/Qr). The dogs were killed, and the lungs removed and sampled completely. Regional extravascular lung water (EVLW) was measured in grams per gram of dry lung and ranged from 3.7 +/- 1.1 in the control group to 6.0 +/- 1.3 in OAPE and 5.6 +/- 0.6 in HPPE. The data show that in normal lungs, increased Qr was associated with a recruitment of blood volume. In OAPE, data show that regional blood volume was decreased and that vascular injury and edema formation interfered with a further increase in Vr as Qr increased. In HPPE, Vr has already fully distended and it changed little with increased blood flow. We conclude that oleic acid-induced pulmonary injury and edema interfere with vascular recruitment and shorten regional RBC transit times. HPPE, on the other hand, is associated with normal regional RBC transit times because the vessels are fully recruited.
Animals↗
Blood pressure, edema and proteinuria in pregnancy. 7. Edema-plus-proteinuria relationships.
1. A total of 488 pregnancies had the combination of two-plus or more proteinuria and edema of the hands and face. Of these, 208 were white and 280 were black gravidas. In the white gravidas, 8 fetal and neonatal deaths occurred with a perinatal mortality of 38.5 per 1,000. There were 13 perinatal deaths in the black subgroup with a perinatal mortality rate of 46.4 per 1,000. The overall perinatal mortality rate was 43.0 per 1,000, which could be compared to the overall perinatal mortality rate of 32.8 per 1,000 for the segment of the study population without edema or proteinuria. This underscored the implication of increased hazard to fetal outcome of these clinical signs in combination. 2. The analysis of the matrix data showed scattered rates throughout gestation in white median-age nulliparas. Their black counterparts had comparable increased mortality rates. In the white multiparas of ages 20 to 34 years, the highest rates were found at relatively low blood pressure levels. The black median-age multiparas had rates associated with higher pressure readings, especially at or above 125/75. In teenage mulliparas with edema and proteinuria, perinatal mortality rates were similar for both subgroups and were found in somewhat lower blood pressures. 3. The incremental analysis was remarkable in that rates were scattered widely in the white subgroups, but tightly clustered in the black subgroups. The black median-age nulliparas had perinatal mortality concentrated about 115 to 134 mm. Hg systolic and 65 to 84 mm. Hg diastolic. The overall mortality rates of this subgroup were the highest of the subgroups studied. The black 20 to 34 year old multiparas had highest coassociated deaths in the 134-154 mm. Hg systolic levels throughout pregnancy. The clustering effect was most pronounced in black teenage nulliparas in both systolic and diastolic blood pressure groups at much lower levels. 4. The use of a critical cut-off blood pressure level of 125 mm. Hg systolic and 75 mm. Hg diastolic emphasized the combination factor effect, especially by the increased perinatal mortality rates in the black median-age subgroups of both nulliparas and multiparas. In the white median-age subgroups the rates were not uniformly affected. The teenage nulliparas as a group showed increased mortality rates with lower pressure levels in general. This was seen when the diastolic level was above 75 mm. Hg. 5. Perinatal mortality rates of nulliparas were increased by proteinuria and edema. This increase was great in the case of the 20 to 34 year old black nulliparas, particularly in association with increased blood pressure. Trends are not so apparent for the white median-age nulliparas. Nulliparas of 19 years of age or less have higher perinatal loss with edema and proteinuria, but this is not necessarily augmented with blood pressure elevation. This is notably so in teenage black nulliparas in the early periods of gestation and at term.
Adolescent↗