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PubMed1986

Increased vascular pedicle width preceding burn-related pulmonary edema.

Widening of the vascular pedicle on the chest roentgenogram is a recently identified sign of increased circulating blood volume. To determine whether vascular pedicle enlargement can be detected during the initial day of burn resuscitation and whether this change correlates with the early development of pulmonary edema, we reviewed the serial chest roentgenograms of 42 patients with cutaneous burns and risk factors for inhalation injury. Although no patient had pulmonary edema at the time of vascular pedicle measurements, 18 (42.9 percent) developed this complication during the 3.3 +/- 1.5 days after injury. These patients were significantly older (p less than 0.025) and had received more resuscitative fluid (P less than 0.005) than those without pulmonary edema. Initial vascular pedicle width was similar in both groups (5.9 +/- 0.9 vs 6.0 +/- 1.0 cm) and did not change in patients without pulmonary edema (5.8 +/- 0.7 cm). Vascular pedicle width increased (6.9 +/- 1.2 cm, p less than 0.01) in patients who subsequently developed pulmonary edema, and 12 of the 13 patients who had changes exceeding +1.0 cm had this problem. Enlargement of the vascular pedicle is associated with early burn-related pulmonary edema and might provide a clinically useful predictor of this cardiopulmonary complication.

Adult↗
PubMed2005

Cerebral edema during treatment of diabetic ketoacidosis in an adult with new onset diabetes.

INTRODUCTION: Diabetic ketoacidosis (DKA) continues to be a medical emergency, in part because of a rare and devastating complication associated with its treatment, cerebral edema. In children, cerebral edema is the principal cause of mortality, but clinically significant cerebral edema in adults is rare. METHODS AND RESULTS: We report the case of a 27-year-old male (not previously known to be diabetic) who presented with a first episode of DKA complicated by the development of fatal cerebral edema despite medical treatment. CONCLUSION: The pathophysiological mechanisms for cerebral edema associated with DKA occurring in children and adults are believed to be similar and are discussed in this report. However, patients who develop cerebral edema may deteriorate rapidly, and experience with successful treatment has been limited.

Adult↗
PubMed2005

Relationship between plasma hANP level and pretibial edema by pioglitazone treatment.

Pioglitazone is an insulin-sensitizer with a thiazolidinedione structure. It is used to reduce hyperglycemia and is frequently prescribed to type 2 diabetic patients. However, it causes edema as an adverse effect in some patients. Although the mechanism of edema is unclear, it may bring an increased risk of congestive heart failure. We investigated whether pioglitazone correlates with the level of plasma human atrial natriuretic peptide (hANP), a marker for congestive heart failure. We administered 15 mg/day of pioglitazone for 3 months to 49 patients (34 men and 15 women; mean age: 64+/-12 years) with type 2 diabetes and no history of pretibial edema. Three of the patients complained of pretibial edema during the 3-month period, and their plasma hANP levels were higher than those of the other 46 before and during the treatment. We therefore suspect that pretibial edema appearing after administration of low-doses of pioglitazone coincides with the level of plasma hANP, and that the appearance of pretibial edema may reflect an increase in circulating blood volume induced by pioglitazone.

Aged↗
PubMedDate not supplied

Retinal thickness assessed by optical coherence tomography (OCT) in pseudophakic macular edema.

PURPOSE: To evaluate the usefulness of the optical coherence tomography (OCT) retinal map in angiographic pseudophakic macular edema (ACME). METHODS: This is a prospective analysis of a group of 36 pseudophakic eyes at the fifth postoperative week, submitted to optical coherence tomography 2 macular map and fluorescein angiography on the same day and, a control group of twenty-two 20/20 vision eyes with a minimum 6-month postoperative period, submitted to optical coherence tomography 2 macular map only. Exclusion criteria were diabetes, any macular pathology and unreadable optical coherence tomography or angiogram. The angiograms were divided into three groups according to the edema intensity: Group I: level 0 (absence of angiographic pseudophakic macular edema); group II: levels 1 and 2 (incomplete and complete perifoveal angiographic pseudophakic macular edema respectively) and group III: levels 3 and 4 (up to one disc diameter and greater than one disc diameter angiographic pseudophakic macular edema area respectively). The nine zones of the optical coherence tomography macular map were compared between the control and the three subgroups of the study group and, between group I and groups II and III. RESULTS: Among the 36 eyes, 23 (64%) were classified as group I, 10 (28%) as group II and three (8%) as group III. The mean thickness of the fovea zone was 185+/-15 microm for the control group, 189+/-24 microm for group I, 213+/-33 microm for group II and 455+/-38 microm for group III. Significant differences: between group III and the control or group I for all zones (p<0.01) and, between group II and control or group I for the fovea and temporal inner zones (p<0.05). CONCLUSION: The optical coherence tomography retinal map is useful in angiographic pseudophakic macular edema diagnosis.

Adult↗
PubMedDate not supplied

[Edema in leprosy: the clinical and therapeutic aspects].

Edema, which is commonly described as a symptom of reactional states, may occur during the course of leprosy. Both diagnosis and adequate treatment measures are often difficult to achieve and failure to do so may result in permanent damage to the lower limbs. In a one-year follow-up study of leprosy patients--ten multibacillary and one paucibacillary--who had been submitted to a clinical protocol for diagnosis and pathological classification, a clinical pattern of localized and/or systemic edema was observed. Among these patients, five simultaneously presented other symptoms related to reactional states, 4 were diagnosed as Type I, and one as Type II. On the other hand, while three of the patients did not present reaction at the time when edema was diagnosed, they did develop some aspects of reactional disease later on (two had neuritis e one had Type I reaction). The edemas that preceded or were associated with reactional episodes showed clinical regression as a result of specific treatment against reactions (corticosteroids and/or pentoxifylline and/or thalidomide) in the absence of another treatment normally used for edemas. Although these data need to be confirmed by controlled studies, they strongly suggest that immunological mechanisms are involved in the physiopathology of edema in leprosy.

Adolescent↗
PubMed1985

Cerebral edema associated with acute hepatic failure.

The clinicopathological findings of cerebral edema were investigated in patients with acute hepatic failure autopsied at Okayama University Hospital between 1970 and 1980 retrospectively. Nine (64%) of 14 hepatic failure cases were found to have cerebral edema during a post-mortem examination of the brain. Clinical features of the patients with cerebral edema were not significantly different from those of the patients without cerebral edema. However, general convulsions were observed more frequently in patients later found to have cerebral edema. Moreover, the length of time from deep coma to death was much shorter in the brain edema cases with cerebral herniation than without herniation.

Acute Disease↗
PubMed1996

Magnetic resonance imaging of cold injury-induced brain edema in rats.

The chronological changes of blood-brain barrier disruption, and diffusion and absorption of edema fluid were investigated in rats with cold-induced brain injury (vasogenic edema) using magnetic resonance imaging. Contrast medium was administered intravenously at 3 and 24 hours after lesioning as a tracer of edema fluid. Serial T1-weighted multiple-slice images were obtained for 180 minutes after contrast administration. Disruption of the blood-brain barrier was more prominent at 24 hours after lesioning than at 3 hours. Contrast medium leaked from the periphery of the injury and gradually diffused to the center of the lesion. Contrast medium diffused into the corpus callosum and the ventricular system (cerebrospinal fluid). Disruption of the blood-brain barrier induced by cold injury was most prominent at the periphery of the vasogenic edema. Edema fluid subsequently extended into the center of the lesion and was also absorbed by the ventricular system. Magnetic resonance imaging is a useful method to assess the efficacy of therapy for vasogenic edema.

Animals↗
PubMed2006

Relationship between bone marrow edema and development of symptoms in patients with osteonecrosis of the femoral head.

OBJECTIVE: The purpose of this study was to determine the significance of risk factors on MR images for predicting the outcome of patients with osteonecrosis of the femoral head. SUBJECTS AND METHODS: Eighty-three asymptomatic or minimally symptomatic hips in 61 consecutive patients were followed up prospectively. Inclusion criteria included osteonecrosis of the femoral head identified by typical MRI findings, with no radiographic evidence of progression of collapse, and Harris hip score of 85 points or more. Every 3 months, the patients underwent clinical and radiographic examination, and MR images were obtained at 6- to 12-month intervals. Follow-up continued until worsening of hip pain with Harris hip score of less than 70 points or surgery. Asymptomatic hips were followed up for at least 24 months. The mean clinical and radiographic follow-up period after the initial diagnosis was 60 months (range, 3-168 months). RESULTS: Thirty-six (43%) of the 83 hips were symptomatic at the last follow-up. Bone marrow edema was present in 28 hips (34%) during the follow-up period. Twenty-seven (96%) of the 28 hips were symptomatic, and bone marrow edema significantly correlated with worsening of hip pain (p < 0.0001). The necrotic volume of hips with bone marrow edema was significantly larger than those without bone marrow edema (p < 0.0001). Bone marrow edema was found to be the most significant risk factor for worsening of pain (p < 0.0001). CONCLUSION: Bone marrow edema strongly correlated with necrotic volume and was the most significant risk factor for worsening of hip pain. A large necrotic volume of 30% or more may be the second useful indicator for predicting future worsening of hip pain.

Adolescent↗
PubMed1991

Pathogenesis of pulmonary edema during interleukin-2 therapy: correlation of chest radiographic and clinical findings in 54 patients.

The pathogenesis of pulmonary edema that occurs during interleukin-2 therapy has often been attributed to an increase in pulmonary capillary permeability. However, renal insufficiency, fluid overload, and hypotension also develop in many patients. These manifestations of systemic toxicity may contribute to the development of pulmonary edema during therapy. Understanding the cause of pulmonary edema during interleukin-2 therapy could directly affect patients' care. Therefore, we reviewed the chest radiographs and clinical course of 54 patients who received high-dose interleukin-2 therapy and lymphokine-activated killer cells for advanced carcinoma. The type, frequency, and course over time of pulmonary abnormalities were recorded and correlated with clinical measures of renal function, fluid status, and blood pressure. Focal or diffuse parenchymal lung opacities were found on radiographs in 43 (80%) of 54 patients. Findings of interstitial pulmonary edema were most common, occurring in 76% of patients. Weight gain, hypotension, and elevation of the serum creatinine level were not associated statistically with interstitial edema. Diffuse air-space disease developed in 20% of patients. Focal consolidation, which was associated with positive central venous catheter cultures (p less than .03), developed in 28% of patients. Pleural effusion occurred in 48% of patients and was associated with all types of parenchymal disease. These data suggest that the frequent development of pulmonary edema during interleukin-2 therapy is not due to renal insufficiency, fluid overload, or hypotension, but is more likely the result of an interleukin-2-related increase in pulmonary capillary permeability.

Adult↗
PubMed2001

Subtendinous bone marrow edema patterns on MR images of the ankle: association with symptoms and tendinopathy.

OBJECTIVE: We sought to describe a pattern of subtendinous bone marrow edema on MR images of the ankle and to determine if there is an association with location of symptoms and overlying tendinopathy. MATERIALS AND METHODS: At 1.5 T, 141 MR examinations of the ankle (116 clinical examinations of patients with chronic pain, 25 of asymptomatic control patients) were performed using T1-weighted, proton density-weighted fast spin-echo, and T2-weighted fat-suppressed fast spin-echo sequences. Images were retrospectively reviewed by two musculoskeletal radiologists for presence of bone marrow edema occurring in a subcortical location associated with the course of the medial or lateral tendon groups, as well as focal thickening or increased T2 signal within the tendons. These findings were correlated with clinical information regarding symptom location. The association of subtendinous marrow edema with tendinopathy and symptom location was statistically analyzed. RESULTS: Subtendinous bone marrow edema was present at 26 sites on 24 ankle MR examinations (17%) (at the medial malleolus [n = 17] associated with the posterior tibialis tendon, at the lateral malleolus [n = 6] and the calcaneus [n = 2] associated with the peroneus longus and brevis tendons, and at the cuboid [n = 1] associated with the peroneus longus tendon). These subtendinous bone marrow edema patterns were significantly associated with overlying tendon abnormality medially (p = 0.001) and laterally (p = 0.001), and with symptoms medially (p = 0.0016) but not laterally (p = 0.078). CONCLUSION: On MR images of the ankle, bone marrow edema localized in a subtendinous location is associated with overlying tendinopathy medially and laterally and with ankle pain medially.

Adult↗
PubMed2005

Bumetanide reduces cerebral edema formation in rats with diabetic ketoacidosis.

The mechanisms responsible for cerebral edema formation in diabetic ketoacidosis (DKA) are not well understood, although evidence suggests ischemia as a contributing factor. Previous studies have shown that the Na-K-Cl cotransporter of cerebral microvascular endothelial cells and astrocytes is a major participant in ischemia-induced cerebral edema in stroke. The present study was conducted to test the hypothesis that the Na-K-Cl cotransporter also contributes to cerebral edema in DKA. Sprague-Dawley rats were administered streptozotocin to induce DKA, and then cerebral edema was assessed by determination of apparent diffusion coefficients (ADC) with magnetic resonance diffusion-weighted imaging. Cerebral ADC values in DKA rats were significantly reduced in both cortex and striatum compared with non-DKA control rats, indicating the presence of cerebral edema. Intravenous administration of bumetanide to DKA rats abolished the drop in cortical ADC values, while having no significant effect in the striatum. Insulin and saline treatment had no effect when given after bumetanide but increased both cortical and striatal ADC values when given before bumetanide. Evidence is also presented here that acetoacetate and beta-hydroxybutyrate stimulate brain microvascular Na-K-Cl cotransporter activity. These findings suggest that the Na-K-Cl cotransporter contributes to brain edema in DKA.

Animals↗
PubMed2000

Criterion-related validity of the figure-of-eight method of measuring ankle edema.

STUDY DESIGN: Single-session, prospective, repeated-measures design. OBJECTIVE: To determine intratester reliability and criterion-related validity of the figure-of-eight method of measuring ankle edema. BACKGROUND: The measurement of edema is often necessary when physical therapists assess patients with ankle injuries. The figure-of-eight method has been shown to be a reliable method in measuring the size of ankles in subjects without edema but not in subjects with ankle swelling. The validity of this method of measurement has not been established. METHODS AND MEASURES: The subjects (mean age, 22.7 +/- 4.4 years) were 7 men and 8 women with observable ankle edema secondary to acute or chronic ankle sprains or injury to the lower extremity. Three figure-of-eight measurements were taken by one tester. These measurements were correlated to measurements taken by another tester using a foot volumeter. RESULTS: The intraclass correlation coefficient (ICC [2,1]) for the figure-of-eight measurements was 0.99. The Pearson Product Moment correlation coefficients between the figure-of-eight measurements and the first volumetric measurement were 0.89 (first figure-of-eight), 0.88 (second figure-of-eight), 0.91 (third figure-of-eight), and 0.90 (mean of all 3 figure-of-eight measurements). CONCLUSION: The figure-of-eight method was demonstrated to be a reliable and valid indirect method of measuring ankle edema in individuals with edema secondary to sprains or other lower-extremity musculoskeletal disorders.

Adolescent↗
PubMed1998

Surgical management of macular edema.

Macular edema, often a component of diabetic retinopathy, can be complicated by many other diseases. It is considered to be multifactorial and difficult to treat. The relation of the vitreous and macular edema is discussed. We examined many eyes of patients with diabetic macular edema that improved after spontaneous posterior vitreous detachment or vitrectomy for proliferative diabetic retinopathy. Recent advances in vitreous surgery have enabled us to treat surgically eyes with good visual acuity. We began surgical treatment for macular edema without the fibrous membrane in 1990. Here we discuss our experience in surgical treatment of macular edema as contrasted to photocoagulation therapy. This review is based on the published and unpublished results of our cases of more than 100 eyes that underwent vitrectomy for diabetic macular edema.

Diabetic Retinopathy↗
PubMed1976

Effect of dexamethasone on experimental brain edema in cats.

The authors studied the effects of dexamethasone, 0.3 mg/kg/hr administered intravenously beginning 1 hour before injury, in adult cats with brain edema secondary to cold-induced cortical lesions. Edema was quantitatively measured in cortex, gyral white matter, and central (deep) white matter at 3, 24, 48, and 72 hours, with and without dexamethasone, by determining specific gravity (density) of samples in a continuous gradient column. Cold-induced lesions resulted in edema, which was greatest in the white matter of the injured hemisphere but also present in the contralateral hemisphere. Except for a slight but significant increase in density (decreased edema) of cortex at 24 hours, dexamethasone therapy resulted in no reduction of cold-induced edema, and in some cases increased the edema.

Animals↗
PubMed1978

Experimental neurogenic pulmonary edema in cats.

Hemorrhagic pulmonary edema was produced consistently in 19 of 20 anesthetized, paralyzed, ventilated cats when intracranial pressure (ICP) was raised for 30 minutes by intraventricular infusion of mock CSF to 150 mm Hg in 14, or 200 mm Hg in six. However, under identical conditions, except that ICP was raised to only 100 mm Hg, three of seven animals did not develop hemorrhagic edema of the lungs and the remaining four had spotty hemorrhage. Thirteen control animals with normal ICP had normal lungs. Gravimetric lung water analysis by Pearce's method confirmed gross and microscopic appearance of hemorrhagic pulmonary edema. Extravascular lung water (p less than 0.05) and lung blood (p less than 0.05) were significantly greater than control values when ICP was raised to or exceeded 150 mm Hg. Despite hemorrhagic edema, pulmonary gas exchange (O2, CO2) remained unaffected. This animal model allows quantitative measurement of neurogenically-mediated hemorrhagic edema of the lungs before gas exchange is impaired. The model may facilitate clarification of the pathogenesis of neurogenic pulmonary edema and, consequently, refine evaluation of therapy.

Animals↗
PubMed1991

Evidence against leukotrienes as mediators of brain edema.

Leukotrienes are powerful metabolites of arachidonic acid which are known to increase the permeability of peripheral blood vessels. These substances are found in brain tissue in association with cerebral ischemia, and in brain tumors. Therefore, it has been proposed that leukotrienes have a mediator function in brain edema. This hypothesis was subjected to further experimental analysis in this study, in which the authors investigated whether: 1) superfusion of the exposed brain surface with leukotrienes increases the permeability of extraparenchymal blood vessels in vivo; 2) intraparenchymal infusion of leukotrienes induces brain edema; and 3) pharmacological inhibition of leukotriene formation by BW755C, an inhibitor of leukotriene synthesis, reduces formation of brain edema from a standardized traumatic insult. The pial vessels of the parietal cortex of cats were examined by fluorescence microscopy during cerebral superfusion with the leukotrienes C4 (LTC4), D4 (LTD4), or E4 (LTE4) by using an open cranial window preparation. Intravenous Na(+)-fluorescein served as an in vivo blood-brain barrier (BBB) indicator. Superfusion of the pia with leukotrienes (up to 2 microM) did not open the barrier to fluorescein, but was associated with a significant constriction (up to 25%) of arterial and venous vessels. In experiments with slow infusion of leukotriene B4 (LTB4) or LTC4 into the white matter of feline brain, the tissue water content was subsequently determined in serial brain slices using the specific gravity method. Tissue water profiles obtained after a 15-microM infusion of either LTB4 or LTC4 were virtually identical with those of control animals infused with mock cerebrospinal fluid. Thus, neither LTB4 nor LTC4 led to an augmentation of infusion-induced brain edema. In a final series, a cold lesion of the left parietal cortex was induced in rabbits. Twenty-four hours later, swelling of the exposed hemisphere was quantified by gravimetrical comparison of its weight with that of the contralateral nontraumatized hemisphere. Eight animals received BW755C intravenously prior to and after trauma to inhibit formation of leukotrienes. Seven rabbits were infused with an equivalent volume of saline as a control study. The resulting hemispheric swelling was 7.7% +/- 0.6% (mean +/- standard error of the mean) 24 hours later in animals receiving BW755C and 7.8% +/- 1.2% in the control group, indicating that inhibition of leukotrienes was ineffective in preventing formation of vasogenic brain edema. The findings demonstrate that leukotrienes administered to the brain in concentrations occurring under pathological conditions do not open the BBB nor do they induce brain edema.(ABSTRACT TRUNCATED AT 400 WORDS)

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1994

Vascular permeability factor in brain metastases: correlation with vasogenic brain edema and tumor angiogenesis.

Metastatic brain tumors are almost always associated with vasogenic brain edema, which in turn plays a pivotal role in the evolution of neurological morbidity associated with these lesions. Attention has recently focused on a group of proteinaceous vascular permeability factors (VPF's) that are capable of inducing angiogenesis and promoting increased capillary permeability. To test the hypothesis that metastatic brain tumors expressing VPF's are associated with peritumoral cerebral edema, a rabbit polyclonal immunoglobulin (Ig) G anti-VPF was used to immunostain pathological specimens of metastatic cerebral tumors obtained from 22 patients who underwent surgery at Yale-New Haven Hospital. Magnetic resonance (MR) imaging was used to correlate VPF staining in tumor tissue with the occurrence of peritumoral brain edema. A histological study of the microvasculature was then conducted by immunostaining the specimens for endothelial cell factor VIII surface antigen, using two gliosis specimens as controls. Results revealed 21 of 22 tumors stained positively for VPF's; the negative-VPF tumor was a melanoma that exhibited no peritumoral edema. Twenty of 22 tumors had MR imaging-evident vasogenic edema. The presence and intensity of VPF immunostaining of microvascular features were noted and compared. Factor VIII staining demonstrated tumor vascularity to be most abundant in VPF-rich regions of tumor. The authors therefore report a high correlation between the presence of VPF's and the occurrence of peritumoral brain edema associated with cerebral metastases.

Brain Edema↗
PubMed1995

Brain edema and neurological status with rapid infusion of lactated Ringer's or 5% dextrose solution following head trauma.

Rapid infusion of 0.25 ml/g of 0.9% saline over 30 minutes has been shown to have no effect on electrolyte balance, neurological severity score (NSS), or brain edema, following closed head trauma (CHT). Rapid infusion of the same volume of 5% dextrose solution decreased blood sodium concentration, increased edema, and decreased NSS following CHT. In the present study the authors examined the effect of rapid infusion (30 minutes) of smaller volumes of 5% dextrose (0.08 ml/g and 0.16 ml/g) and of 0.25 ml/g lactated Ringer's solution on blood electrolyte concentrations, plasma osmolality, brain edema, and NSS. The purposes of this study were to determine whether rapid infusion of a large volume of lactated Ringer's solution could be given after CHT without increasing mortality or brain edema or producing electrolyte disturbances, and whether small volumes of 5% dextrose could be infused with few or none of the deleterious effects expected from large volumes of 5% dextrose. One hundred eighteen rats, which survived halothane anesthesia and CHT, were randomly assigned to one of 15 experimental groups. Fluids were administered beginning 1 hour after scalp incision or CHT. The NSS, extent of edema, blood electrolyte concentrations, and plasma osmolality in the groups treated with lactated Ringer's solution were not significantly different from those values in the nontreated groups. In addition, the mortality rate after CHT was not increased by administration of lactated Ringer's solution. The groups treated with 5% dextrose solution showed a significantly higher mortality rate, but the NSSs of the surviving rats were not different from controls. None of the groups treated with 0.16 ml/g 5% dextrose solution survived 24 hours. Although blood glucose concentration increased to 1126 +/- 102 g% (mean +/- standard deviation) and 1568 +/- 283 g% and blood sodium concentration decreased to 110.4 +/- 4.6 mEq/L and 92.0 +/- 5.2 mEq/L in the groups treated with 0.08 ml/g and 0.16 ml/g of 5% dextrose solution, respectively, plasma osmolality was normal and no significant difference could be found between the brain tissue specific gravity of animals in the nontreated and 5% dextrose treatment groups. It is concluded that in the CHT model used in this study, the large volume of lactated Ringer's solution did not affect blood electrolyte concentration, neurological outcome, or formation of brain edema, whereas smaller volumes of 5% dextrose solution increased blood glucose and decreased blood sodium concentrations, did not affect plasma osmolality, and had a deleterious effect on neurological outcome.

Animals↗