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PubMed2002

Natural history of perihematomal edema in patients with hyperacute spontaneous intracerebral hemorrhage.

BACKGROUND AND PURPOSE: The natural history of perihematomal edema in human hyperacute spontaneous intracerebral hemorrhage (ICH) has not been well described. METHODS: This study was a secondary analysis of a previously reported prospective, population-based study of hematoma growth in 142 patients with spontaneous ICH. Patients were first imaged within 3 hours of onset, then 1 and 20 hours later. We excluded patients with anticoagulant use (n=7), underlying aneurysm/vascular malformation (n=9), trauma (n=1), incomplete data (n=20), infratentorial ICH (n=17), and no consent (n=2), leaving an overall study population of 86 patients. From this overall group we further excluded patients with intraventricular extension (n=38), subsequent surgery (n=5), or death (n=2) before 20-hour postbaseline CT. This second, "restricted" analysis group of 41 patients was relatively devoid of clinical or radiological variables likely to confound edema measurement. Absolute and relative edema volumes (edema volume divided by hematoma volume) were descriptively summarized. Correlations between baseline edema volumes and relevant clinical and radiological variables were then performed. RESULTS: Overall, median absolute edema volume increased from 6.93 to 14.4 cm(3) during the first 24 hours after ICH, and median relative edema volume increased from 0.47 to 0.81. In the restricted group, median absolute edema volume was 7.4 cm(3) at baseline and 11.0 cm(3) at 24 hours after ICH, and median relative edema volume increased from 0.55 to 0.81. Baseline relative edema volume was significantly negatively correlated with subsequent change in relative edema volume from baseline to 20-hour CT (r=0.57, P=0.0002) but was not significantly correlated with other clinical and radiological variables, including hematoma volume or change in hematoma volume. CONCLUSIONS: Perihematomal edema volume increases by approximately 75% during the first 24 hours after hyperacute spontaneous ICH. Patients with the least amounts of baseline relative edema volume were most likely to develop significant additional amounts of edema during the first 24 hours after spontaneous ICH.

Acute Disease↗
PubMed1998

Proteinuria precedes cerebral edema in stroke-prone rats: a magnetic resonance imaging study.

BACKGROUND AND PURPOSE: Stroke-prone spontaneously hypertensive rats (SHRSP) subjected to high sodium intake develop severe hypertension, cerebral edema, and proteinuria, culminating in organ damage and early death. MRI, which can be applied serially, provides the unique opportunity to study temporal and quantitative relations between these changes and whether diminution of sodium intake can attenuate established cerebral edema. METHODS: SHRSP were subjected to 1% NaCl in drinking water. Cerebral MRI, proteinuria and systolic blood pressure (SBP) were measured serially. After detection of cerebral edema (T2-weighted MRI), 6 rats were killed for histology, to confirm the diagnosis of cerebral edema. The others were followed up for 7 more days while salt loading was continued (n = 10, group 1) or after sodium intake was normalized (n = 7, group 2). RESULTS: SHRSP invariably developed cerebral edema in 30 days (range, 8 to 54 days). At this point neurological signs were absent in 16 of 23 rats. SBP rose until 1 week before detection of cerebral edema, and then stabilized at approximately 265 mm Hg. Proteinuria invariably preceded cerebral edema, with a concentration exceeding 40 mg/d predicting development of cerebral edema in 9 days (range, 3 to 15 days). There was linear correlation (R=.62, P<.0001) between proteinuria and cerebral edema (pixels with an intensity above a defined threshold). Rats in group 1 showed an increase in cerebral edema (from 5.8+/-1.1% to 12.5+/-2.8%; P<.05), and proteinuria remained high (from 305+/-44 to 338+/-29 mg/d); and 2 died spontaneously. Rats in group 2 showed no significant change in edema (from 4.9+/-0.5% to 6.9+/-1.3%) but a marked fall in proteinuria (from 294+/-24 to 119+/-10 mg/d; P<.05), both significantly different from group 1 (P<.05); all survived. SBP remained unaltered in both groups. CONCLUSIONS: Our data establish MRI as a sensitive method for detection of cerebral edema, often prior to neurological signs, in SHRSP. Proteinuria predicts cerebral edema, and these two variables, both obtained noninvasively, are quantitatively related. Moreover, in SHRSP normalizing sodium intake after salt loading attenuates development of cerebral edema and reduces proteinuria.

Animals↗
PubMed2000

Clinical efficacy of micronized purified flavonoid fraction (MPFF) in edema.

Swelling is one of the most frequent complaints of patients in daily clinical practice; leg edema is its objective confirmation. It can be associated with several diseases. Micronized purified flavonoid fraction (MPFF) is a phlebotropic drug commonly used to treat the signs and symptoms associated with chronic venous insufficiency (CVI). It has confirmed its clinical efficacy in different groups of patients suffering from edema: idiopathic cyclic edema, CVI-associated edema, postmastectomy lymphedema and might be beneficial in some of drug-induced edema. In a double-blind, placebo-controlled, randomized study including 30 outpatients suffering from idiopathic cyclic edema syndrome, MPFF 1000 mg/day for 6 weeks, normalized the capillary permeability, assessed by the Landis isotope test, in 3 out of 4 patients (p=0.01). The decrease in capillary hyperpermeability led to a clinically significant decrease in weight and edema. In 200 patients with functional or organic venous insufficiency of the lower limbs, a double-blind, placebo-controlled, randomized study with MPFF 1000 mg/day for 2 months provided strong evidence of a marked improvement in symptoms and signs. A significant reduction in supramalleolar edema (assessed by circumference measurement) was observed, whatever the origin of CVI: functional or organic. MPFF efficacy was also demonstrated in another randomized, multicenter controlled trial in 320 patients suffering from chronic venous insufficiency. In this study, a significant decrease in circumference of the most affected leg was observed after 2 months of treatment (p<0.001), whatever the schedule of administration of MPFF (1000 mg once daily or bid). The benefit of MPFF on edema has been further confirmed by the volometer technique (opto-electronic measuring system) which was performed in a population of 30 patients suffering from CVI and treated by MPFF 1000 mg/day over a 6-week period. The mean volume of the more affected lower leg decreased significantly after a 6-week period of treatment, correlating to a significant improvement in clinical symptoms. MPFF has been also tested on another type of edema, upper limb lymphedema secondary to mastectomy, during a double-blind, placebo-controlled, randomized study in 104 patients. MPFF 1000 mg/day improved all lymphoscintigraphic parameters such as half-life and clearance of the labelled colloid. With regard to evolution of lymphedema volume, a tendency in favor of MPFF was observed in the subgroup of patients with more severe lymphedema. Based on its action on capillary hyperpermeability, MPFF has been used with attractive results when combined with classic treatment for a pilot study carried out in patients with advanced breast cancer (n=21) or ovarian carcinoma (n=3), treated with docetaxel, which causes severe edema as a side effect, even when associated with corticoids. Further trials are under way to assess the possible benefit of MPFF in such patients. These results in different types of edema confirm that, by acting on all parameters involved in edema, veins, lymphatics, and microcirculation, MPFF represents a drug of choice for treating CVI-associated edema.

Anthropometry↗
PubMedDate not supplied

The LONFLIT4--Concorde Deep Venous Thrombosis and Edema Study: prevention with travel stockings.

BACKGROUND: The LONFLIT1+2 studies have established that in high risk subjects after long flights (> 10 hours) the incidence of deep venous thrombosis (DVT) is between 4% and 6%. The LONFLIT4 study was designed to evaluate the control of edema and DVT in low-medium risk subjects. The aim of this study was to evaluate edema and its control with specific stockings (ankle pressure between 20 and 30 mm Hg) in long-haul flights. The first part of the study included flights lasting 7-8 hours and the second part included flights lasting 11-12 hours. Ultrasound scans were used to assess thrombosis before and after the flights and a composite edema score was used to evaluate edema and swelling. A group of patients with microangiopathy associated to edema (diabetes, venous hypertension, anti-hypertensive treatment) were also included to evaluate the preventive effects of stockings during flight. Part I: DVT evaluation: Of the 74 subjects in the stocking group and 76 in the control group (150), 144 completed the study. Dropouts were due to low compliance or traveling and connection problems. Age and gender distribution were comparable in the 3 groups as was risk factor distribution. In this part of the study there were no DVTs. Edema Evaluation: The level of edema at inclusion was comparable in the two groups of subjects. After the flight there was an average score of 6.9 (1) in the control group. In the stocking group, the score was on average 2.3 (1), three times lower than in the control group (p < 0.05). Part II: DVT evaluation: Of the 66 included subjects in the stocking group and 68 in the control group (134), 132 completed the study. Dropouts were due to low compliance or connection problems. Age and gender distribution were comparable in the two groups. In the stocking group no DVT was observed. In the control group, 2 subjects had a popliteal DVT and 2 subjects had superficial venous thrombosis (SVT); in total 4 subjects (6%) in the control group had a thrombotic event; the incidence of DVT was 3%. The difference (p < 0.02) is significant. EDEMA EVALUATION: The composite edema score at inclusion was comparable in the two groups. After the flight there was a score of 7.94 (2) in the control group, while in the treatment group the score was 3.3 (1.2). MICROANGIOPATHY STUDY: In all these subjects, the level of edema was very high in the control group and significantly lower in the compression stocking group. Stockings are effective in controlling edema during flights even in subjects with microangiopathy and edema. Compression was well tolerated in normal subjects and in patients. CONCLUSION: The Kendall Travel Socks (Tyco Healthcare, Mansfield, MA, USA) which provide 20-30 mm Hg pressure at the ankle, are effective in controlling edema and reducing the incidence of DVT in both low-medium-risk subjects and in patients with microangiopathy and edema in long-haul flights (7-11 hours).

Aerospace Medicine↗
PubMed1986

[Effects of inhibitors of some mediators on the paw-edema induced by acetyl glyceryl ether phosphorylcholine in rats].

The characterization of acetyl glyceryl ether phosphorylcholine (AGEPC)-induced paw edema in rats was explored. Edema formation was maximum at 45 min after the injection of AGEPC. The dose for maximal response was 1 microgram/site, while edema was suppressed at higher doses. The systemic administration (s.c.) of cyproheptadine (CH, 10 mg/kg) did not inhibit this edema differently from serotonin-induced edema, while the local treatment of CH suppressed AGEPC-induced edema in a dose-dependent manner. The combination of local treatments with pyrilamine and methysergide also suppressed this edema. The s.c. injection of indomethacin (IM, 10 mg/kg) did not inhibit AGEPC edema differently from carrageenin-induced edema, while locally given IM suppressed it partially. The local treatment with caffeic acid and esculetin, lipoxygenase inhibitors, or with FPL 55712, an antagonist of SRS-A, suppressed AGEPC edema slightly. Various combinations of local treatment with IM and lipoxygenase inhibitors gave synergistic suppression of this edema. Dexamethasone strongly suppressed AGEPC edema when given both systemically and locally 3 hr before the injection of AGEPC. However, phospholipase A2 (PLA2) inhibitors, i.e. mepacrine, p-bromophenacyl bromide, chlorpromazine and tetracaine, did not show the same effect as dexamethasone. These results suggest that the edema formation induced by AGEPC may involve not only the combined action of histamine and serotonin but also the synergistic action of cyclooxygenase and lipoxygenase products. Dexamethasone may inhibit this edema by mechanisms other than the inhibitory action of PLA2.

Animals↗
PubMed1990

[A controlled study on edema in elderly inpatients].

The clinical background relating to edema in elderly inpatients was investigated, in terms of various items in elderly (aged greater than or equal to 65) cases with edema (n = 96) and without edema (controls, n = 95). Both groups were matched for sex, age, and underlying diseases. As compared with the control patients, the patients with edema had longer hospital stays with more disabled status, and showed less activity of daily living (ADL). The rates of bed-restricted patients, dementia patients, and patients with decubitus, muscle atrophy, or incontinence were found to be significantly higher in the patients with edema. The measurement of biochemical parameters revealed that the patients with edema had significantly lower levels of serum albumin, Na, Cl, creatinine, and uric acid, in contrast to higher levels of C-reactive protein. According to the classification of the assumed causes of edema, we divided the patients with edema into five groups; group 1 (n = 33): edema associated with immobilization, group 2 (n = 18): edema due to heart failure, group 3 (n = 15): edema on paretic limbs, group 4 (n = 6): edema due to hypoproteinemia, group 5 (n = 5): edema associated with liver cirrhosis. Both group 1 and group 4 patients had lower levels of hemoglobin and albumin, whereas group 3 patients had higher scores of ADL, higher blood pressure, and higher levels of hemoglobin and albumin. These results suggest that immobilization and restriction in bed, as well as malnutrition, were important factors in causing edema in elderly inpatients.

Activities of Daily Living↗
PubMed2003

Neuroprotective effects of nimodipine and MK-801 on acute infectious brain edema induced by injection of pertussis bacilli to neocortex of rats.

OBJECTIVE: To explore the mechanism and type of acute infectious brain edema induced by injection of pertussis bacilli (PB) in rat neocortex, to study the neuroprotective effect of non-competitive antagonist of N-methl-D-aspartate (NMDA) receptor (MK-801) and antagonist of Ca(2+) channels (nimodipine) on brain edema, and to investigate the relationship between percentage of water content and cytosolic free calcium concentration ([Ca(2+) ](i)) in synaptosomes or content of Evans Blue (EB). METHODS: 95 SD rats were randomly divided into five groups, ie, normal control group, sham-operated control group, PB group, nimodipine treatment group and MK-801 pretreatment group. The acute infectious brain edema was induced by injection of PB into the rats. Quantitative measurements of water content and the concentration of EB were performed. [Ca(2+) ](i) was determined in calcium fluorescent indication Fura-2/AM loaded neuronal synaptosome with a spectrofluorophotometer. To observe the effect of MK-801 and nimodipine, we administered MK-801 48 hours and 24 hours before the injection of PB in MK-801 pretreatment group, and nimodipine after the injection of PB in nimodipine treatment group. The specific binding of NMDA receptor was measured with [(3)H]-MK-801 in the neuronal membrane of cerebral cortex. RESULTS: The levels of water content and EB content of brain tissues, and [Ca(2+) ](i) in the neuronal synaptosomes increased more significantly in the PB-injected cerebral hemisphere in the PB group than those of normal control group and sham-operated control group (P<0.05). The water content and [Ca(2+) ](i) increased with the duration of infectious brain edema. Nimodipine administered after the injection of PB could significantly decrease the water content, EB and [Ca(2+) ](i) (P<0.05). MK-801 could significantly decrease the water content, EB and [Ca(2+) ](i) in 4 h and 24 h groups (P<0.05). The Kd values were 30.5 nmol/L+/-3.0 nmol/L and 42.1 nmol/L+/-4.2 nmol/L in PB group and NS group respectively (P<0.05), and Bmax were 0.606 pmol/mg.pro+/-0.087 pmol/mg.pro and 0.623 pmol/mg.pro+/-0.082 pmol/mg.pro respectively, without statistical significance (P>0.05). CONCLUSIONS: The changes in the permeability of blood-brain barrier (BBB) and Ca(2+)-overload may participate in the pathogenesis of infectious brain edema. Treatment with nimodipine can dramatically reduce the damage of brain edema and demonstrate neuroprotective effect on brain edema by inhibiting the excess of Ca(2+) influx and reducing the permeability of BBB. MK-801 pretreatment may inhibit the delayed Ca(2+) influx into the neurons. The infectious brain edema is not only cytotoxic brain edema (intracellular edema) but also vasogenic brain edema (extracellular edema) followed by earlier BBB breakdown, so infectious brain edema is complicated with brain edema.

Acute Disease↗
PubMed1983

Quantitative morphology of permeability lung edema in dogs induced by alpha-naphthylthiourea.

In pulmonary edema, fluid accumulates first in the interstitium, then in the alveoli. However, the relative amounts of interstitial fluid around arteries and veins of different sizes are unknown; in addition, the effects of fixation on the light microscopic quantitation of edema are unclear. To answer these questions, we induced permeability pulmonary edema in seven anesthetized dogs with 27 mg/kg of alpha-naphthylthiourea. Pulmonary artery and wedge pressures were measured. After moderately severe edema, diagnosed by chest x-ray and falling arterial pO2, lobes were fixed by airways instillation or vascular perfusion with glutaraldehyde and formaldehyde or were frozen with liquid nitrogen. With light microscopy, the edema surrounding arteries and veins of different sizes was measured using a computer equipped with a digitizing tablet and expressed as the edema ratio = area of perivascular edema/area of vessel, or as an absolute area of edema. Alveolar edema was graded semiquantitatively, and wet weight to dry weight ratios were calculated. Two control dogs were also studied. During the induction of edema, pulmonary artery and wedge pressures did not change significantly. Mean wet weight to dry weight ratios were 9.3 +/- 1.1. We found that the edema ratio was greater (p less than 0.01) for arteries (2.75, n = 1305) than for veins (1.40, n = 900). The edema ratio was greater for vessels more than 400 micron than less than 400 micron (p less than 0.01) and greater in the instillation- and perfusion-fixed lobes than in the frozen lobes (p less than 0.01). Similar results were obtained for the absolute areas of periarterial and perivenous edema. Less alveolar edema was seen in the lobes fixed by instillation (p less than 0.01). We conclude that, in permeability edema induced by alpha-naphthylthiourea, the fluid accumulates preferentially around arteries compared with veins and around larger compared with smaller vessels. Airways instillation and vascular perfusion fixation appeared to increase interstitial fluid cuffs compared to freezing.

Animals↗
PubMed1994

MR imaging of edema accompanying benign and malignant bone tumors.

To evaluate the incidence, quantity, and presentation of intra- and extraosseous edema accompanying benign and malignant primary bone lesions, the magnetic resonance (MR) studies of 63 consecutive patients with histologically proven primary bone tumors were reviewed. MR scans were assessed for the presence and quantity of marrow and soft tissue edema and correlated with peroperative findings, resected specimens and follow-up data. The signal intensity and enhancement of tumor and edema prior to and after intravenous administration (if any) of gadolinium-labeled diethylene triamine pentaacetate (Gd-DTPA) was analyzed. Marrow edema was encountered adjacent to 8 of 39 malignant tumors and 14 of 24 benign lesions. Soft tissue edema was found accompanying 28 of 39 malignancies and 10 of 24 benign disorders. On unenhanced T1-weighted MR images tumor and edema were difficult to differentiate. Tumor inhomogeneity made this differentiation easier on T2-weighted sequences. In 36 patients the contrast medium Gd-DTPA was used. Edema was present in 27 of these patients and the respective enhancement of tumor and edema could be compared. Edema always enhanced homogeneously, and in most cases it enhanced to a similar degree as or more than tumor. Marrow and, more specifically, soft tissue edema is a frequent finding adjacent to primary bone tumors. The mere presence and quantity of marrow and soft tissue edema are unreliable indicators of the biologic potential of a lesion. Unenhanced MR scans cannot always differentiate between tumor and edema, but the administration of Gd-DTPA is of assistance in differentiating tumor from edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Rapid diuresis in patients with ascites from chronic liver disease: the importance of peripheral edema.

Serial measurements of plasma volume and ascites volume were made during treatment with large doses of oral diuretics in 14 patients with stable chronic liver disease. Eight patients had pitting edema in addition to ascites. Reproducibility of ascites and plasma volume measurements was verified in 10 control subjects not receiving diuretics. Six patients without edema undergoing rapid diuresis lost a mean of 1.2 +/- 0.2 L of ascites and an equivalent amount of weight (1.3 +/- 0.4 kg) per day. All had a rise in blood urea nitrogen or creatinine, or both, and a fall in creatinine clearance. Eight patients with edema undergoing rapid diuresis lost more weight (1.8 +/- 0.5 kg/day, p = 0.06) but less ascites (0.7 +/- 0.35 L/day, p less than 0.05) than those without edema, and none developed renal insufficiency. After edema disappeared, ascites mobilization increased (1.4 +/- 0.7 L/day) and renal dysfunction occurred. Plasma volume fell an average of 24% +/- 9% in patients without edema but did not change in patients with edema (-0.4% +/- 3%). When edema disappeared, plasma volume fell significantly (28% +/- 8%, p less than 0.001). Electrolyte changes including hyponatremia, hyperkalemia, and hypochloremia were seen only in the group without edema. Patients with ascites and no edema are able to mobilize more than 1 L/day during rapid diuresis, but at the expense of plasma volume contraction and renal insufficiency. Patients with peripheral edema appear to be protected from these effects because of the preferential mobilization of edema and may safely undergo diuresis at a rapid rate (greater than 2 kg/day) until edema disappears.

Amiloride↗
PubMed2006

Risk factors for udder edema and its association with lactation performance on primiparous Holstein cows in a large Florida herd, U.S.A.

The objective of this study was to determine risk factors for udder edema (case-control study) and to evaluate the association of udder edema in primiparous Holstein cows with their lactation performance (cohort study). Values for the first 10 test day for milk yield, fat, protein, and somatic cell counts (SCC) linear score as well as mature equivalent (ME) 305 days milk yield, fat, protein, SCC linear score, and incidences of periparturient diseases from a computerized farm recording system were compared between primiparous cows with and without udder edema. Data consisted of 118 dairy heifers with udder edema, induced for parturition, and treated with diuretics and 889 control heifers that received no treatment. Primiparous cows giving birth to male calves, were 1.72 (1.01, 3.24; 95% CI) times more likely to develop udder edema than cows giving birth to female calves. Primiparous cows calving in winter season were 3.68 (1.09, 12.5; 95% CI) times more likely to develop udder edema than cows calving in summer. For each extra 10cm in height the odds of udder edemas was 1.23 (1.03, 1.47; 95% CI). The first test day DHIA milk yield was lower in cows that developed udder edema (3.6kg/day) than in normal cows. However, the subsequent test days and ME measurements were not statistically different between groups. Cows with udder edema were 1.62 (1.18, 2.14; 95% CI) times more likely to develop udder edema in the second lactation than control animals. It is concluded that the gender of the offspring, calving season and height at parturition were significant risk factors for udder edema. Only milk yield on the first DHIA test day was lower in cows with udder edema than in cows without udder edema.

Animals↗
PubMedDate not supplied

Quantitative MR analysis of glucocorticoid effects on peritumoral edema associated with intracranial meningiomas and metastases.

OBJECTIVE: The purpose of our study was to quantify peritumoral brain edema (PTE) in vivo using NMR relaxation time imaging, as the longitudinal relaxation time T1 is proportional to tissue water content, and to use the method for monitoring the effects of glucocorticoids (GCCs) on PTE in brain tumor patients as a function of time. MATERIALS AND METHODS: Relaxation time imaging (T1 maps) was done on a 1.5 T MR scanner on 23 brain tumor patients [13 cerebral metastases (METs), 10 intracranial meningiomas (MMs), and 9 benign and 1 anaplastic MM] before, and 1, 3, and 7 days after initiation of GCC treatment (dexamethasone 0.26-0.64 mg/kg bw). In addition, 7 patients were studied for 14-63 days of treatment. Imaging analysis included mean T1 of the edema area as a function of time, and an image histogram evaluation technique, which measures 50% of the edema area, where T1 is highest (corresponding to the highest water content of the area), termed the "super-edema." Using a conversion equation, mean T1 in the edema area was recalculated into a percent of tissue water content. RESULTS: After 7 days of GCC treatment total edema area was reduced by 10.3% in the MET patients. The average reduction in mean T1 was 4.6% after 24 h of treatment and 13.5% after 7 days. Expressed in terms of percent tissue water content, the average edema resorption rate in the MET patients was 0.4 +/- 0.1% H2O/day (p < 0.02). Super-edema area was reduced by 64% after 7 days (p < 0.0001). None of the benign MMs responded to GCC treatment, either in edema size or in mean T1, unlike the anaplastic type, in which there was a response comparable to that in the MET patients. The effect of GCCs in up to 63 days of treatment is demonstrated. It is shown that after 40-63 days of GCC treatment, PTE water content is close to the upper normal range for white matter. CONCLUSION: PTE is heterogeneous in terms of the spatial distribution of T1 and, thereby, water content. GCCs reduce T1 in PTE around cerebral metastases significantly after a few days of treatment, possibly through a mechanism that reduces edema production below the level of edema resorption. PTE surrounding benign MM was not affected by GCC treatment, contrary to one anaplastic MM, which leads to the speculation that malignant tumors may produce substances that are affected by GCCs and are prerequisites for a GCC effect. Significant reductions in the highest T1 area (super-edema area) were observed after 24 h of treatment. The anti-edema effect of GCC may last at least 63 days. A lower dose-dependent threshold for the effect seems to exist. The possible mechanisms of actions of the GCCs on PTE are discussed.

Adult↗
PubMed1998

Quantitative analysis of edema in the dorsal nerve roots induced by acute mechanical compression.

STUDY DESIGN: Edema in the dorsal nerve roots caused by acute compression was assessed quantitatively in the lumbar spine of the adult dog. OBJECTIVE: To establish quantitative evaluation of edema in the dorsal nerve roots and to observe changes after acute compression with time. SUMMARY OF BACKGROUND DATA: Mechanical compression induces an increase in microvascular permeability of the endoneurial capillaries and results in intraneural edema. However, there are no quantitative studies on edema in the nerve roots. METHODS: The seventh lumbar nerve root was compressed with a 60-g force clip for 10 minutes. The nerve roots were removed immediately and at 24 hours, 1 week, and 3 weeks after compression. Nerve roots from the control and the sham groups were also obtained. Before removing the nerve roots, Evans blue albumin was injected intravenously. Changes in edema were examined using fluorescence microscopy. Evans blue albumin emits a bright red fluorescence. The relative red fluorescent area was calculated using computer image analysis, and the data were used to indicate the degree of edema. RESULTS: In the compressed segment, edema was most pronounced just after decompression and reduced in nerves removed at 24 hours. In nerves removed at 1 week, edema was pronounced but was reduced at 3 weeks. In the segments closest to the spinal cord, edema was seen after 1 week and was significant after 3 weeks. In the segments closest to the dorsal root ganglion, edema was not detected at any time. CONCLUSION: In the dorsal nerve roots the degree and the area of edema changed with time elapsed after acute compression. The degree of edema 24 hours after decompression was one third the degree immediately after decompression. These results show that edema induced by mechanical compression can recover after decompression.

Animals↗
PubMed1999

The impact of edema on planning 125I and 103Pd prostate implants.

Permanent transperineal interstitial 125I and 103Pd prostate implants are generally planned to deliver a specific dose to a clinically defined target volume; however, the post-implant evaluation usually reveals that the implant delivered a lower or higher dose than planned. This difference is generally attributed to such factors as source placement errors, overestimation of the prostate volume on CT, and post-implant edema. In the present work we investigate the impact of edema alone. In routine prostate implant planning, it is customary to assume that both the prostate and seeds are static throughout the entire treatment time, and post-implant edema is not taken into consideration in the dosimetry calculation. However, prostate becomes edematous after seed implantation, typically by 50% in volume [Int. J. Radiat. Oncol., Biol., Phys. 41, 1069-1077 (1998)]. The edema resolves itself exponentially with a typical half-life of 10 days. In this work, the impact of the edema-induced dynamic change in prostate volume and seed location on the dose coverage of the prostate is investigated. The total dose delivered to the prostate was calculated by use of a dynamic model, which takes edema into account. In the model, the edema resolves exponentially with time, as reported in a separate study based on serial CT scans [Int. J. Radiat. Oncol., Biol., Phys. 41, 1069-1077 (1998)]. The model assumes that the seeds were implanted exactly as planned, thus eliminating the effect of source placement errors. Implants based on the same transrectal ultrasound (TRUS) images were planned using both 125I and 103Pd sources separately. The preimplant volume and planned seed locations were expanded to different degrees of edema to simulate the postimplant edematous prostate on day 0. The model calculated the dose in increments of 24 h, appropriately adjusting the prostate volume, seed locations, and source strength prior to each time interval and compiled dose-volume histograms (DVH) of the total dose delivered. A total of 30 such DVHs were generated for each implant using different combinations of edema half-life and magnitude. In addition, a DVH of the plan was compiled in the conventional manner, assuming that the prostate volume and seeds were static during treatment. A comparison of the DVH of the static model to the 30 edema corrected DVHs revealed that the plan overestimated the total dose by an amount that increased with the magnitude of the edema and the edema half-life. The maximum overestimation was 15% for 125I and 32% for 103Pd. For more typical edema parameters (a 50% increase in volume and a 10 day half-life) the static plan for 125I overestimated the total dose by about 5%, whereas that for 103Pd overestimated it by about 12%.

Brachytherapy↗
PubMed2002

Global cerebral edema after subarachnoid hemorrhage: frequency, predictors, and impact on outcome.

BACKGROUND AND PURPOSE: Cerebral edema visualized by CT is often seen after subarachnoid hemorrhage (SAH). Inflammatory or circulatory mechanisms have been postulated to explain this radiographic observation after SAH. We sought to determine the frequency, causes, and impact on outcome of early and delayed global cerebral edema after SAH. METHODS: We evaluated the presence of global edema on admission and follow-up CT scans in 374 SAH patients admitted within 5 days of onset to our Neurological Intensive Care Unit between July 1996 and February 2001. Using multivariate analysis, we identified predictors of global cerebral edema and evaluated the impact of global edema on outcome 3 months after onset with the modified Rankin Scale. RESULTS: Global edema was present on admission CT scans in 8% (n=29) and developed secondarily in 12% (n=44) of the patients. Global edema on admission was predicted by loss of consciousness at ictus and increasing Hunt-Hess grade. Delayed global edema was predicted by aneurysm size >10 mm, loss of consciousness at ictus, use of vasopressors, and increased SAH sum scores. Thirty-seven percent (n=137) of the patients were dead or severely disabled (modified Rankin Scale 4 to 6) at 3 months. Death or severe disability was predicted by any global edema, aneurysm size >10 mm, loss of consciousness at ictus, increased National Institutes of Health Stroke Scale scores, and older age. CONCLUSIONS: Global edema is an independent risk factor for mortality and poor outcome after SAH. Loss of consciousness, which may reflect ictal cerebral circulatory arrest, is a risk factor for admission global edema, and vasopressor-induced hypertension is associated with the development of delayed global edema. Critical care management strategies that minimize edema formation after SAH may improve outcome.

Adolescent↗
PubMed1990

Intact epithelial barrier function is critical for the resolution of alveolar edema in humans.

Within 15 min of endotracheal intubation, the resolution of pulmonary edema was studied over the next 12 h in 34 mechanically ventilated patients by (1) serial measurements of the alveolar-arterial oxygen difference, (2) the extent of edema on the initial and follow-up chest radiograph, and (3) by an initial and final measurement of total protein and albumin concentration in sequential samples of pulmonary edema fluid. Based on the oxygenation and chest radiographic data, 24 patients clinically improved and 10 patients did not improve. In the 10 patients who did not clinically improve (3, hydrostatic edema; 7, permeability edema), there was no change in the final edema fluid protein concentration (4.1 +/- 1.1 g/100 ml) compared with the initial edema fluid protein concentration (4.2 +/- 1.0 g/100 ml) (p = ns). However, in the 24 patients who clinically improved (15, hydrostatic edema; 9, permeability edema), there was an increase in every patient's final edema protein concentration (5.6 +/- 2.3 g/100 ml) compared with their initial edema protein concentration (3.8 +/- 1.2 g/100 ml) (p less than 0.01). In 13 of these 24 patients, the final edema fluid concentration (7.3 +/- 1.6 g/100 ml) exceeded the final plasma protein concentration (5.6 +/- 0.8 g/100 ml) by a mean value of 1.7 g/100 ml protein. The data provide the first evidence in humans to support the hypothesis that active ion transport across the alveolar epithelial barrier is the primary mechanism for clearance of edema fluid from the air spaces of the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Biological Transport, Active↗
PubMed1994

Experimental intracerebral hemorrhage: relationship between brain edema, blood flow, and blood-brain barrier permeability in rats.

There have been few investigations of brain edema formation after intracerebral hemorrhage (ICH), despite the fact that mass effect and edema are important clinical complications. The present study was designed to investigate the time course for the formation and resolution of brain edema and to determine how changes in cerebral blood flow (CBF) and blood-brain barrier (BBB) permeability are temporally related to edema formation following ICH. Anesthetized adult rats received a sterile injection of 100 microliters of autologous blood into the caudate nucleus. Water and ion contents were measured immediately, at 4 and 12 hours, and daily to Day 7 (10 time points, six rats at each time) after experimental ICH. The water content of the ipsilateral basal ganglia increased progressively (p < 0.002) over the first 24 hours, then remained constant until after Day 5, when the edema began to resolve. Edema was most severe in the tissue immediately surrounding the hemorrhage; however, it was also present in the ipsilateral cortex, the contralateral cortex, and the basal ganglia. Measurements of local CBF (using [14C]-iodoantipyrine) and BBB permeability (using [3H]-alpha-aminoisobutyric acid) were obtained in separate groups of six to eight rats at various time intervals between 1 and 48 hours after ICH. Cerebral blood flow was reduced to 50% of control at 1 hour, returned to control values by 4 hours, but then decreased to less than 50% of control between 24 and 48 hours after ICH. The BBB permeability increased significantly prior to the occurrence of significant edema in the tissue surrounding the clot. However, BBB permeability in the more distant structures remained normal despite the development of edema. These results demonstrate a time course for the formation and resolution of brain edema following ICH similar to that observed during focal ischemia. Brain edema forms in the immediate vicinity of the clot as a result of both BBB disruption and the local generation of osmotically active substances and then spreads to adjacent structures. While local ischemia, due to the mass effect of the hemorrhage, may play a role in producing cytotoxic and vasogenic edema, the release of toxic substances from the clot should also be considered. Since edema is nearly maximal by 24 hours after ICH, therapy directed at reducing edema formation must be instituted within the 1st day.

Aminoisobutyric Acids↗
PubMed1998

A new view of pulmonary edema and acute respiratory distress syndrome.

The old division of lung edema into two categories--cardiogenic (hydrostatic) and noncardiogenic (increased permeability)--is no longer adequate. For instance, it fails to distinguish between the capillary leak caused by acute respiratory distress syndrome from that caused by interleukin-2 treatment. Further, it fails to account for the capillary leak ('stress-failure') that may accompany edema. A modern view of edema must recognize the natural barriers to the formation and spread of edema. These barriers are the capillary endothelium and the alveolar epithelium. Varying degrees of damage to them can account for the varying radiographic and clinical manifestations of lung edema. Thus, interleukin-2 administration causes increased endothelial permeability without causing alveolar epithelial damage. The result is lung edema that is largely confined to the interstitium, causing little hypoxia and clearing rapidly. However, acute respiratory distress syndrome, which is characterized by extensive alveolar damage, causes air-space consolidation, severe hypoxia, and slow resolution. Thus, a reasonable classification of lung edema requires at least four categories: 1) hydrostatic edema; 2) acute respiratory distress syndrome (permeability edema caused by diffuse alveolar damage); 3) permeability edema without alveolar damage; and (4) mixed hydrostatic and permeability edema. The authors emphasize the importance of the barriers provided by the capillary endothelium and the alveolar epithelium in determining the clinical and radiographic manifestations of edema. In general, when the alveolar epithelium is intact, the radiographic manifestations are those of interstitial (not air-space) edema; this radiographic pattern predicts a mild clinical course and prompt resolution.

Acute Disease↗