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PubMed2000

[Post-traumatic lymphatic and venous drainage changes in persistent edema of lower extremities].

Mechanical injury of soft tissues and bones of the lower extremity is followed by chronic edema at the site of trauma and distally to it. This complication affects almost every patient with a fracture of the lower limb. The question is whether posttraumatic edema is due to lymphatic obstruction, venous thrombosis or both, or a local cytokine and growth factor hyperactivity at the fracture site. The aim of study was to assess the venous and lymph outflow in patient with chronic postraumatic edema of the lower limbs. A group of 19 patients with chronic edema lasting for more than 3 months was evaluated. Limb circumference, tissue tone measurements, skin temperature and Doppler enhanced ultrasonography were all taken down for the 19 patients in the evaluated group. Limb circumference was measured at the following level: foot, ankle, calf and thigh. Results showed an increase of circumference in comparison with the healthy extremity at each evaluated level of: 1.20 +/- 1.65 cm, 1.63 +/- 1.41 cm, 1.40 +/- 1.72 cm and 0.30 +/- 1.90 cm. Local temperature increase compared to the healthy extremity was also noted (0.93 +/- 0.81 degree C and 0.37 +/- 0.21 degree C measured at ankle and calf level). Tissue tone measurements and tone index (a quotient of tone measurement values in the extremity with edema and in the healthy extremity) were also increased by 0.86 +/- 0.57, 0.85 +/- 0.34 and 0.86 +/- 0.28, when measured with 40 g, 110 g and 180 g weights respectively. In 17 cases (89.5%) lymphoscintigraphy demonstrated an increased lymphatic outflow compared to the contralateral extremity. A marked increase in the inguinal lymph nodes was also noted. In the remaining 2 cases (10.5%) extravasation of the contrast medium into the skin indicated lymph outflow disorders. Only in 5 cases (26.3%) ultrasonography indicated deep vein thrombosis. The obtained results indicate that the pathophysiology of chronic postraumatic edema is linked with an inflammatory and restorative reaction at the fracture site. Only in a limited number of cases deep vein thrombosis and damaged lymphatic vessels are responsible for postraumatic edema.

Chronic Disease↗
PubMedDate not supplied

99mTc-HSA lymphoscintigraphy and leg edema following arterial reconstruction.

Twelve patients with peripheral arterial occlusive disease were evaluated prospectively in an effort to further investigate the etiology of pedal and lower leg edema that occurs following revascularization (e.g., aorto-iliac or femoropopliteal bypass). Serum total protein, albumin, blood urea nitrogen, and creatinine levels were measured (in addition to peripheral venous pressure), and lymphoscintigraphy of the lower leg was performed. These parameters were assessed just prior to surgery, four weeks postoperatively, and again at follow-up. The serum levels obtained four weeks after surgery and on subsequent follow-ups were significantly higher than the preoperative values. Preoperative peripheral venous pressure was not significantly different from that obtained after surgery. There was no correlation between these pressure measurements and the degree of edema (Grades I to IV correspond to increasing degrees of severity). For both the supine and upright positions, lymphoscintigraphic counts in the inguinal region were significantly higher after surgery. However, the relative increase was dependent upon the severity of edema. The postoperative lymphoscintigraphic count in the upright position was 77 +/- 33 CPS in patients with Grades I and II edema (n = 6) and 20.6 +/- 16.2 CPS in patients with Grades III and IV edema (n = 10) (p less than 0.01). Thus, a lesser degree of postoperative pedal and lower leg edema was associated with higher lymphoscintigraphic counts. We conclude that major contributors to the development of lower extremity edema following arterial reconstruction are failed capillary hydrostatic pressure and interrupted lymphatic drainage.

Aged↗
PubMed1989

Macular edema in branch retinal vein occlusion: types and treatment.

In this study of branch retinal vein occlusion, we distinguished between cystoid macular edema caused by increased capillary pressure and noncystoid edema due to hard exudates in the macula caused by chronic leakage from vascular abnormalities in the posterior pole or midperiphery. We performed laser photocoagulation in 51 eyes with cystoid macular edema to achieve focal narrowing of the retinal arterioles perfusing the macular area affected by the cystoid edema; good anatomic and functional results were achieved in 40 of these eyes (78%). In 25 of the five eyes, the treated segment of the retinal arteriole was outside the area of macular edema; results were successful in 19 of these eyes (76%). In 14 eyes with noncystoid exudative macular edema, we performed laser photocoagulation to the vascular abnormalities; good anatomic and functional results were obtained in 12 of these (86%).

Aged↗
PubMed1983

[Non-cardiogenic pulmonary edema].

Non-cardiac pulmonary edema comprises all types of pulmonary edema not caused by increase of left ventricular filling pressure and elevated pulmonary capillary pressure. In one year 42 patients at our intensive care unit developed non-cardiac pulmonary edema. In a retrospective study the clinical, radiological and functional changes in patients with non-cardiac pulmonary edema were determined. 76% of the patients had multiple causes for development of non-cardiac pulmonary edema. Sepsis was the most frequent predisposing disease. Over-all mortality reached up to 69%. Additional organ failure caused an increase in mortality. Patients without complications had the best prognosis. Mechanical ventilation (69%), high-dose corticosteroids (50%), hemodialysis with ultrafiltration (33.3%) and hemofiltration (7.1%) were used for treatment of non-cardiac pulmonary edema.

Acute Disease↗
PubMed2001

Treatment of 193 episodes of laryngeal edema with C1 inhibitor concentrate in patients with hereditary angioedema.

BACKGROUND: Hereditary angioedema (HAE) is an autosomal dominant disease (Mendelian Inheritance in Man 106100) caused by an inherited deficiency of C1 inhibitor (C1-INH) function. The clinical symptoms include skin swelling, abdominal pain, and life-threatening episodes of upper airway obstruction. We evaluated the efficacy of C1-INH concentrate for treating sudden airway compromise. METHODS: A series of 95 patients with HAE and a functional deficiency of C1-INH belonging to 59 families underwent screening for laryngeal edema. Double-blind treatment of randomized patients was not justifiable because of the life-threatening nature of this condition. Efficacy was evaluated by determining the interval from injection of C1-INH concentrate to the beginning of resolution of symptoms. The mean duration of episodes of laryngeal edema was compared in treated and untreated patients. Clinical information was obtained from emergency department physicians, the hospitals involved, reports of the general practitioners, and patients and their relatives. RESULTS: Forty-two patients had 517 episodes of laryngeal edema. Eighteen patients received 500- or 1000-U injections of C1-INH concentrate in 193 episodes. The C1-INH concentrate was effective in all laryngeal edemas. The interval from injection to interruption in progress of symptoms ranged from 10 minutes to 4 hours (mean +/- SD, 42.2 +/- 19.9 minutes). The mean +/- SD duration of laryngeal edema was 15.3 +/- 9.3 hours in patients who received C1-INH concentrate and 100.8 +/- 26.2 hours in those who did not. CONCLUSIONS: Injected C1-INH concentrate is highly and rapidly effective in the treatment of laryngeal edema of HAE. Relief and resolution of symptoms begins 30 to 60 minutes after injection, and duration of the upper airway obstruction is substantially reduced.

Adult↗
PubMed2002

Diffusion-weighted imaging abnormalities in wernicke encephalopathy: reversible cytotoxic edema?

BACKGROUND: Wernicke encephalopathy (WE) is a metabolic disorder of the central nervous system resulting from vitamin B(1) deficiency. The exact mechanisms underlying the pathogenesis of the lesions in WE are not completely understood. Vitamin B1 deficiency is associated with intracellular and extracellular edema by glutamate(N-methyl-D-aspartate) receptor-mediated excitotoxicity. Conventional magnetic resonance imaging (MRI) cannot differentiate the types of edema. Diffusion-weighted imaging (DWI) has been reported to detect early ischemic damage (cytotoxic edema) as bright areas of high signal intensity (SI) and vasogenic edema as areas of heterogeneous SI. OBJECTIVES: To describe the DWI findings and to characterize the types of edema in WE using DWI. SETTING: Tertiary referral center. DESIGN AND METHODS: Two patients with WE underwent DWI and conventional MRI with gadolinium enhancement. Wernicke encephalopathy was diagnosed with salient conventional MRI findings (high SIs in the paramedian thalamus, periaqueductal gray matter, and mamillary bodies) and typical clinical history and symptoms. Apparent diffusion coefficient (ADC) values were measured in abnormal lesions by visual inspection of DWIs and T2-weighted echo planar images. RESULTS: T2-weighted and fluid-attenuated inversion recovery MRIs showed high SIs in the bilateral paramedian thalamus, mamillary bodies, and periaqueductal gray matter. The DWIs showed bright high SI in the corresponding lesions, and ADC values were decreased (patient 1: 512-545 x 10(-6)mm2/s; patient 2: 576-612 x 10(-6)mm2/s). The ADC decrease and the DWI high SI were normalized in 2 weeks with administration of thiamine hydrochloride. CONCLUSIONS: Abnormalities on DWI and ADC decrease became normalized with adequate therapy. The MRI abnormalities in WE might be owing to the "reversible cytotoxic edema" caused by vitamin B1 deficiency.

Aged↗
PubMed2004

Detection of diabetic foveal edema: contact lens biomicroscopy compared with optical coherence tomography.

OBJECTIVE: To compare contact lens biomicroscopy with optical coherence tomography (OCT) for the detection of diabetic foveal edema. METHODS: Study participants consisted of a convenient cohort of consecutive patients with diabetes mellitus seen at the Wilmer Eye Institute's Retinal Vascular Center, Baltimore, MD. Case characteristics were recorded and eyes were examined by 1 of 4 retina specialists by means of contact lens biomicroscopy. Edema involving the center of the macula was assessed as definitely present, questionably present, or definitely not present. The OCT testing was performed and interpreted by trained technicians, masked to the physicians' assessment of foveal edema. Agreement between OCT and contact lens examination for the absence or presence of foveal edema was evaluated. RESULTS: One hundred seventy-two eyes of 95 patients with diabetes were enrolled in August and September 2002. Foveal thickness was objectively measured by OCT in 170 (99%) of 172 cases. We found excellent agreement between OCT and contact lens examination for the absence or presence of foveal edema when OCT thickness was normal ( 300 microm). However, agreement was poor when foveal thickness was mildly increased on OCT (201-300 microm). CONCLUSIONS: Agreement between contact lens examination and OCT for the detection of diabetic foveal edema is poor when OCT thickening is mild. This suggests that contact lens biomicroscopy is relatively insensitive for the detection of mild foveal thickening apparent on OCT. Additional studies are needed to investigate the natural course of cases with mildly increased foveal thickness on OCT that do not appear thickened clinically.

Adult↗
PubMed1995

Quantitative assessment of macular edema with optical coherence tomography.

OBJECTIVE: To evaluate optical coherence tomography, a new technique for high-resolution cross-sectional imaging of the retina, for quantitative assessment of retinal thickness in patients with macular edema. DESIGN: Survey examination with optical coherence tomography of patients with macular edema. SETTING: Referral eye center. PATIENTS: Forty-nine patients with the clinical diagnosis of diabetes or diabetic retinopathy and 25 patients with macular edema secondary to retinal vein occlusion, uveitis, epiretinal membrane formation, or cataract extraction. MAIN OUTCOME MEASURES: Correlation of optical coherence tomograms with slit-lamp biomicroscopy, fluorescein angiography, and visual acuity. RESULTS: Optical coherence tomograms of cystoid macular edema closely corresponded to known histopathologic characteristics. Quantitative measurement of retinal thickness is possible because of the well-defined boundaries in optical reflectivity at the inner and outer margins of the neurosensory retina. Serial optical coherence tomographic examinations allowed tracking of both the longitudinal progression of macular thickening and the resolution of macular edema after laser photocoagulation. In patients with diabetic retinopathy, measurements of central macular thickness with optical coherence tomography correlated with visual acuity, and optical coherence tomography was more sensitive than slit-lamp biomicroscopy to small changes in retinal thickness. CONCLUSIONS: Optical coherence tomography appears useful for objectively monitoring retinal thickness with high resolution in patients with macular edema. It may eventually prove to be a sensitive diagnostic test for the early detection of macular thickening in patients with diabetic retinopathy.

Adult↗
PubMed1995

The effect of intradermal corticosteroids on skin flap edema.

OBJECTIVE: To validate a model for skin flap edema in the piglet and determine whether intraoperative and postoperative intradermal corticosteroids reduce the edema created. DESIGN: Prospective, randomized, matched-control animal model. SETTING: Animal laboratory. PARTICIPANTS: Twenty-five weight-matched purebred Yorkshire piglets. INTERVENTION: Intraoperative and postoperative injections of intradermal triamcinolone. MAIN OUTCOME MEASURED: Flap edema. RESULTS: A reproducible skin flap edema model was validated in the piglet. Intraoperative intradermal corticosteroids decreased flap edema but postoperative corticosteroids did not. CONCLUSION: Clinical improvement in skin flap and supratip fullness may result from mechanisms other than edema.

Animals↗
PubMed1982

Breast edema following staging axillary node dissection in patients with breast carcinoma treated by radical radiotherapy.

Seventy-four patients with carcinoma of the breast were treated by irradiation without a mastectomy at Stanford between May 1973 and March 1980. Seventy-six breasts were treated because two patients had bilateral simultaneous cancers. Breast edema was noted in 41% of these cases. Analysis of potential predisposing factors revealed that this complication occurred primarily in patients who received a staging axillary lymph node dissection. Lymphedema occurred in 26 of 33 breasts (79%) in patients who had staging axillary dissections; this complication developed in only three of 12 (25%) with axillary samplings and two of 31 (6%) with no axillary surgery. Two groups of patients were identified: (1) 28 patients whose breast edema occurred early (prior to or during radiation therapy), and (2) three patients with late onset edema that developed several months postirradiation. The early edema, which is clearly related to axillary lymph node dissection, gradually improved during the follow-up period with complete or near complete resolution expected by three years. Late onset edema was rare, appears to be related to an axillary radiation dose greater than 5500 rad, and may be irreversible. There was no correlation of breast edema with tumor stage, radiation time/dose factors, the use of bolus, patient weight, or breast size.

Adult↗
PubMed1996

Distal extremity swelling with pitting edema in polymyalgia rheumatica. Report on nineteen cases.

OBJECTIVE: To determine the frequency and clinical characteristics of diffuse distal extremity swelling with pitting edema occurring in polymyalgia rheumatica (PMR). METHODS: Clinical features and laboratory findings were recorded for all 245 residents of Olmsted County, Minnesota who developed PMR over a 22-year period (1970-1991). Those who exhibited > or = 1 episode of diffuse distal extremity edema with pitting were selected for this study, and were evaluated further. RESULTS: Thirteen women and 6 men in this incidence cohort of PMR had > or = 1 episode of distal extremity swelling with pitting edema. Giant cell arteritis was also identified in 5 patients. In 11 patients, the swelling and edema development concurrently with proximal PMR symptoms. In 2 patients, the distal swelling was the initial manifestation, and in 6 patients, the distal symptoms developed during relapses or recurrences of PMR. Both upper and lower extremities were affected, usually in a symmetric manner. Other peripheral manifestations were also common. The distal swelling and pitting edema responded promptly to corticosteroids, and slowly or incompletely to nonsteroidal anti-inflammatory drugs; a similar response was observed in the proximal symptoms. The distal swelling appeared to represent tenosynovitis and synovitis of regional structures. CONCLUSION: Distal extremity swelling with pitting edema represents a manifestation of PMR that has not been well described in previous studies. Awareness of this finding will help facilitate the proper diagnosis and institution of appropriate therapy for this disease.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Muscle edema in musculoskeletal tumors: MR imaging characteristics and clinical significance.

To determine the frequency and clinical significance of tumor-associated muscle edema, magnetic resonance (MR) imaging findings in 46 consecutive patients with benign or malignant musculoskeletal lesions were reviewed. Increased muscle signal intensity on T2-weighted, STIR (short-inversion-time inversion-recovery), and gadopentetate dimeglumine-enhanced T1-weighted images was present in 41 cases, with the clearest delineation of tumor margins seen on T2-weighted images. Typical peri/paratumoral edema (PTE) was present in equal proportions of malignant (25 of 37) and benign lesions (six of nine). Massive edema involving the entirety of at least one contiguous muscle--to the authors' knowledge, a previously undescribed finding--was identified on MR images of eight malignant and two benign lesions (22% of both groups). All cases of massive edema had a substantial soft-tissue component and involved muscles disrupted by tumor at the point of attachment to bone. Malignant tumors associated with massive edema were larger than those with typical or no PTE, showed a poorer response to initial chemotherapy, and had a higher frequency of metastases at diagnosis. Thus, the presence of massive muscle edema appears to be an ominous clinical finding in patients with malignant musculoskeletal lesions.

Adolescent↗
PubMedDate not supplied

Relative quantification of pulmonary edema with noncontrast-enhanced MRI.

Pulmonary edema is a debilitating effect of acute respiratory distress syndrome. The ability to measure it noninvasively with high sensitivity and in three dimensions could be useful in not only detection but also in assessment and guidance of treatment. To this end, a three-dimensional MRI pulse sequence to measure the formation of edema was developed and tested. Another sequence was tested to measure blood flow in distal pulmonary arteries. Pulmonary edema was induced in nine dogs via venous injections of oleic acid. Edema was verified by wet-to-dry weight ratio (5.30 +/- .38) and extra-vascular lung water at baseline (2.03 +/- 1.12 ml/g dry lung weight) versus postinjury (3.00 +/- 1.45 ml/g) (P < .005). The signal-to-noise ratio within the lungs increased from 5.47 +/- 1.00 at baseline to 7.51 +/- 1.96 (P < .005), and the time course of edema formation was resolved. Results from MR phase-contrast blood flow measurements were variable. The authors conclude that the three-dimensional scan provides a sensitive relative quantification of pulmonary edema formation without the use of contrast agents or ionizing radiation.

Animals↗
PubMed1996

Nitric oxide plays a role as a mediator of conjunctival edema in experimental allergic conjunctivitis.

The role of nitric oxide in allergic conjunctivitis was studied in a guinea pig model. The eyes of sensitized guinea pigs were challenged with ovalbumin (20 micrograms per eye) or histamine (20 micrograms per eye). Synthesis of nitric oxide (NO) was inhibited using L-NAME (200 micrograms per eye) or aminoguanidine (200 micrograms per eye). The formation of conjunctival edema was graded and levels of nitrite, a breakdown product of nitric oxide were measured in lavage fluid. Conjunctival vasopermeability was determined by measuring the albumin concentration in the fluid on the surface of the eye (lavage fluid). Animals were treated with sodium nitroprusside (SNP) or phenylephrine after which histamine induced conjunctival vasopermeability changes were measured. Drugs were administered topically with the other eye serving as a control. Both ovalbumin and histamine produced a marked inflammatory response including hyperaemia and edema. At the top of the inflammatory response occurring 30 min after challenge, increased levels of nitrite, a breakdown product of NO, were measured in lavage fluid. Prophylactic treatment with L-NAME or aminoguanidine resulted in a significant inhibition of the NO synthesis. Both L-NAME and aminoguanidine decreased conjunctival vascular permeability and edema formation significantly. Administration of SNP resulted in a marked dilatation of conjunctival blood vessels and produced a dose-dependent increase of vascular permeability. Addition of SNP to histamine significantly enhanced conjunctival edema and potentiated vascular permeability. These results indicate that NO is produced in the acute phase of allergic conjunctivitis and mediates vasodilatation after topical provocation with ovalbumin or histamine in sensitized guinea pigs. The resulting increase of the conjunctival blood flow subsequently increases the vascular permeability and enhances conjunctival edema formation. Inhibition of NO synthesis leads to a reduction of conjunctival hyperaemia and subsequently reduces the formation of edema.

Animals↗
PubMed1996

Progesterone rapidly decreases brain edema: treatment delayed up to 24 hours is still effective.

Cerebral edema is a serious side effect of traumatic brain injury. We have previously established that progesterone injections, initiated within 1 h after cortical contusion injury, reduced edema when assessed 3 days later. To determine how rapidly progesterone can reduce edema, male and female rats were given the hormone 1 h after damage to the medial frontal cortex, and edema levels were assessed between 2 h and 7 days postinjury. Progesterone decreased edema with 6 h of the injury and continued to be effective for the duration of treatment. In addition, we assessed whether progesterone injections are effective when delays are imposed between injury and initiation of treatment. Male and female rats received progesterone after postinjury delays 6, 24, or 48 h. Progesterone was effective in reducing edema when treatment was delayed until 24 h after injury.

Animals↗
PubMed2006

Spontaneous intracerebral hemorrhage in humans: hematoma enlargement, clot lysis, and brain edema.

Early hematoma enlargement and delayed clot lysis contribute to brain injury after intracerebral hemorrhage (ICH). We investigated hematoma growth, clot lysis, and brain edema formation in patients with spontaneous ICH. A total of 17 spontaneous ICH patients who received regular medication were chosen for this study. All patients had their first CT scan within 5 hours of onset of symptoms (day 0). The patients then underwent second, third, and fourth CT scans at 1, 3, and 10 days later. Hematoma size and absolute and relative brain edema volumes were measured. Hematoma enlargement was defined as a > 33% increase in volume. Relative brain edema volume = absolute brain edema volume/hematoma size. Hematoma enlargement occurred in 4 of the 17 ICH patients (24%) within the first 24 hours. The hematoma sizes were reduced significantly at day 10 (p < 0.05) because of clot lysis. However, both absolute and relative brain edema increased gradually with time (p < 0.01). These results suggest that delayed brain edema following ICH may result from hematoma lysis. This study also shows that early hematoma enlargement occurs in Chinese patients with ICH. Reducing early hematoma growth and limiting clot lysis-induced brain toxicity could be potential therapies for ICH.

Brain Edema↗
PubMed2006

Zinc protoporphyrin IX attenuates closed head injury-induced edema formation, blood-brain barrier disruption, and serotonin levels in the rat.

The role of heme oxygenase (HO) in closed head injury (CHI) was examined using a potent HO and guanylyl cyclase inhibitor, zinc protoporphyrin (Zn-PP) in the rat. Blood-brain barrier (BBB) permeability to Evans blue and radioiodine, edema formation, and plasma and brain levels of serotonin were measured in control, CHI, and Zn-PP-treated CHI rats. CHI was produced by an impact of 0.224 N on the right parietal bone by dropping 114.6 g weight from a height of 20 cm in anesthetized rats. This concussive injury resulted in edema formation and brain swelling 5 hours after insult that was most pronounced in the contralateral hemisphere. The whole brain was edematous and remained in a semi-fluid state. Microvascular permeability disturbances to protein tracers were prominent in both cerebral hemispheres and the underlying cerebral structures. Plasma and brain serotonin showed pronounced increases and correlated with edema formation. Pretreatment with Zn-PP (10 mg/ kg, i.p) 30 minutes before or after CHI attenuated edema formation, brain swelling, plasma and brain serotonin levels, and microvascular permeability at 5 hours. Brain edema, BBB permeability, and serotonin levels were not attenuated when the compound was administered 60 minutes post-CHI suggesting that HO is involved in cellular and molecular mechanisms of edema formation and BBB breakdown early after CHI.

Animals↗
PubMed2006

Inflammation and brain edema: new insights into the role of chemokines and their receptors.

Brain edema is associated with a variety of neuropathological conditions such as brain trauma, ischemic and hypoxic brain injury, central nervous system infection, acute attacks of multiple sclerosis, and brain tumors. A common finding is an inflammatory response, which may have a significant impact on brain edema formation. One critical event in the development of brain edema is blood-brain barrier (BBB) breakdown, which may be initiated and regulated by several proinflammatory mediators (oxidative mediators, adhesion molecules, cytokines, chemokines). These mediators not only regulate the magnitude of leukocyte extravasation into brain parenchyma, but also act directly on brain endothelial cells causing the loosening of junction complexes between endothelial cells, increasing brain endothelial barrier permeability, and causing vasogenic edema. Here we review junction structure at the BBB, the effects of pro-inflammatory mediators on that structure, and focus on the effects of chemokines at the BBB. New evidence indicates that chemokines (chemoattractant cytokines) do not merely direct leukocytes to areas of injury. They also have direct and indirect effects on the BBB leading to BBB disruption, facilitating entry of leukocytes into brain, and inducing vasogenic brain edema formation. Chemokine inhibition may be a new therapeutic target to reduce vasogenic brain edema.

Animals↗