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PubMed1991

Effect of edema on segmental vascular resistance in isolated perfused rat lungs.

We have determined the effect of hydrostatic edema on total and segmental vascular resistances in the rat lung. Lungs of 12 adult rats, body weight 515 +/- 42 g, were isolated and perfused with blood. To investigate the role of vasoactivity on edema effects, we studied two groups of lungs; group I (n = 6) were untreated and group II (n = 6) were treated with papaverine hydrochloride to paralyze the vasculature. Initially blood flow was adjusted to keep pulmonary artery pressure approximately 15 cmH2O, left atrial and airway pressures being 8 and 7 cmH2O, respectively, and then kept unchanged thereafter (18 +/- 3 ml/kg/min). Hydrostatic edema was induced by raising venous pressure and pulmonary artery pressure measured continuously. In 4 lungs from each group, during baseline and after the development of severe edema, we partitioned the pulmonary circulation into arteries, microvessels, and veins by measuring pressures in 20-50 microns diameter subpleural arterioles and venules with the micropipette-Servonull method. Baseline total vascular resistance was similar in the two groups. Interstitial and early alveolar edema did not affect pulmonary vascular pressures. With severe edema (W/D ratio: 17 +/- 2), pressures in pulmonary artery and arterioles increased significantly in both groups; venular pressures did not change. Total resistance increased by 250% in group I and by 224% in group II lungs. Arterial resistance increased 3-5-fold in both groups, as did microvascular resistance. Venous resistances also increased in both groups, although to a lesser extent. The increase in total and segmental vascular resistances was not significantly different in the two groups of lungs. We conclude that in isolated rat lungs only severe edema results in an increase in total vascular resistance, mainly due to an increase in arterial and microvascular resistances, with a smaller increase in venous resistance. This appears to be a mechanical effect of edema on the vasculature and not a result of active vasomotion.

Animals↗
PubMedDate not supplied

Effect of nutritional copper deficiency on carrageenin edema in the rat. A quantitative study.

The effects of nutritional copper deficiency on carrageenin edema in the rat were investigated with emphasis on studying the correlation between the degree of copper deficiency and the degree of edema. Carrageenin paw edema in both copper-sufficient and copper-deficient groups of rats was compared after either 20, 40, or 60 d on respective diets. The degree of copper deficiency was quantitated by analyzing total copper concentrations in a number of tissues. Other copper dependent parameters were also determined. Results indicated that: (1) although copper sufficient rats showed relatively little change in the degree of edema, copper-deficient rats showed a steady and significant increase in edema from d 20 to 40 to 60; (2) paw edema in copper-deficient animals was highly and negatively correlated to the concentrations of copper in the liver; the correlation with liver Cu,Zn-superoxide dismutase activity, however, was inconsistent; (3) paw edema was not correlated either to copper concentration in tissues other than liver or to plasma ceruloplasmin activity; and (4) aggravation of carrageenin edema in copper-deficient animals seemed to be mediated via an as yet unknown secondary effect of copper deficiency.

Animals↗
PubMed2002

Value of the plasma protein and hemoglobin concentration in the diagnosis of pulmonary edema in scorpion sting patients.

OBJECTIVE: To investigate the value of measuring total plasma protein and hemoglobin concentrations for the diagnosis of pulmonary edema secondary to scorpion envenomation. DESIGN AND SETTING: Retrospective study over a 4-year period in the medical intensive care unit of a university hospital. PATIENTS: 67 patients older than 3 years admitted in the intensive care unit for scorpion envenomation and stratified into two groups according to the presence of pulmonary edema assessed by a medical committee that took into account clinical, radiological, and blood gas data at admission and after treatment. Total plasma protein and hemoglobin concentrations were analyzed separately. RESULTS: At admission all patients with and without pulmonary edema exhibited polypnea and tachycardia. The mean plasma protein and hemoglobin concentrations were higher in patients with pulmonary edema (74+/-6 and 14.2+/-2.0 g/dl, respectively) than in those without pulmonary edema (64+/-6 and 12.3+/-1.4 g/dl). After 24 h plasma protein and hemoglobin concentrations decreased in the pulmonary edema group (-11 and -1.9 g/dl) despite a negative fluid balance (-500 ml). A plasma protein concentration of 70 g/l or more predicted the presence of pulmonary edema with a sensitivity of 80% a specificity of 96%, a positive predictive value of 97%, and negative predictive value of 77%. CONCLUSIONS: In scorpion-envenomed patients with cardiorespiratory manifestations high plasma protein and hemoglobin concentrations suggest the presence of pulmonary edema.

Adolescent↗
PubMed2005

Edema in the retropharyngeal space associated with head and neck tumors: CT imaging characteristics.

To determine computed tomographic (CT) imaging characteristics of retropharygeal edema, we reviewed CT images in 18 patients with head and neck tumors. Retropharyngeal edema spread craniocaudally between soft palate and upper half of thyroid cartilage in all patients. No edema fluid extended above soft palate and below thyroid cartilage. Horizontally, it spread symmetrically in ten and asymmetrically in eight patients. Predominance in asymmetrical retropharyngeal edema was found on the same side as that of unilateral predominance both in lymph nodes enlargement and jugular vein stenosis/occlusion. All patients had edema also in other cervical spaces. Edema of retropharyngeal and other spaces fluctuated synchronously. In 14 patients, as primary lesion and/or cervical lymph nodes regressed, retropharyngeal edema disappeared or decreased. Retropharyngeal edema had some imaging characteristics. With knowledge of that, we could avoid diagnostic confusion when evaluating head and neck CT images.

Adult↗
PubMed2005

Intravitreal levels of vascular endothelial growth factor and interleukin-6 are correlated with macular edema in branch retinal vein occlusion.

BACKGROUND: To investigate whether vascular endothelial growth factor (VEGF) or interleukin-6 (IL-6) contributes to the pathogenesis of macular edema in eyes with branch retinal vein occlusion (BRVO), the correlations between these factors were investigated. METHODS: We studied 25 patients suffering from macular edema with BRVO and 14 patients with nonischemic ocular disease (control group). The degree of retinal ischemia was evaluated in terms of the area of capillary nonperfusion using Scion Images, and the severity of macular edema was examined using optical coherence tomography. Vitreous fluid samples were obtained at the time of vitreoretinal surgery, and VEGF and IL-6 levels in the vitreous fluid and plasma were determined by means of enzyme-linked immunosorbent assays. RESULTS: Vitreous fluid levels of VEGF and IL-6 were significantly elevated in patients with BRVO compared with control patients (P = 0.0011 and P < 0.0001, respectively). Also, the vitreous level of VEGF was significantly correlated with that of IL-6 (P = 0.0012), and vitreous levels of VEGF and IL-6 were correlated with the size of the BRVO nonperfusion area (P < 0.0001 and P = 0.0033, respectively). Furthermore, vitreous levels of VEGF and IL-6 were correlated with the severity of macular edema (P = 0.0008 and P = 0.0191, respectively) and the severity of macular edema of BRVO was significantly correlated with the size of the BRVO nonperfusion area (P=0.0044). CONCLUSIONS: The levels of VEGF and IL-6 are increased in patients with macular edema with BRVO and are significantly correlated with the size of the nonperfusion area and the severity of macular edema. Therefore, they may play a role in macular edema with BRVO.

Enzyme-Linked Immunosorbent Assay↗
PubMed1985

Acute responses to experimental blunt head trauma: topography of white matter edema.

The location of edema and territory of extravasation of serum protein were examined in the white matter of cats with different forms of intracranial pathology following an impact-acceleration injury to the head. Edema was tested with an organic density gradient and Evans blue dye was used as a marker for breakdown of the blood-brain barrier. Animals with tissue hemorrhage (contusions) involving both cerebral cortex and white matter had a substantial, progressive accumulation of Evans blue-stained edema near tissue hemorrhage during the 6 h following trauma. In addition, this category of cats had a widespread, mild edema at 15 min after injury that was usually unaccompanied by Evans blue stain. Cats with cortical contusions had rather mild edema neighboring tissue hemorrhage; animals with subarachnoid hemorrhage in the absence of cerebral contusions had neither measurable edema nor (usually) visible Evans blue staining. We conclude that: acute traumatic cerebral edema varies considerably in presence, magnitude and territory with different forms of intracranial pathology; and mechanically induced edema can occur that is independent of spread of fluid from areas of tissue hemorrhage.

Acute Disease↗
PubMed1987

The role of pulmonary lymphatics in the clearance of hydrostatic pulmonary edema.

Pulmonary lymphatics are believed to play a major role in preventing the formation of pulmonary edema, but their role in clearance of established edema has not been defined. To measure the lymphatic contribution to the clearance of acute hydrostatic pulmonary edema, a lung lymph fistula was established in 16 anesthetized sheep. Pulmonary edema was induced by a rapid volume infusion of Ringer's lactate (six animals) or homologous plasma (six animals). Four control animals received no fluid. Simultaneous measurements of lymph flow and extravascular lung water (EVLW) were made. Data were analyzed for the resolution phase of pulmonary edema. The contribution of the pulmonary lymphatics to resolution was expressed as a percentage of total lung water resolved. Resolution rates for crystalloid and plasma infusion groups were 3.8 +/- 2.4 cc/kg/hr and 2.7 +/- 1.0 cc/kg/hr, respectively. There was no statistically significant difference between the groups in terms of EVLW increases or resolution rates. Net measured pulmonary lymph flow during the resolution phase of pulmonary edema was 0.33 +/- 0.18 cc/kg/hr and 0.39 +/- 0.20 and accounted for only 8.8 and 14.6% of resolved pulmonary edema in these respective groups. These data suggest the pulmonary lymphatic drainage plays a very minor role in the clearance of acute hydrostatic edema. The lungs appear to be capable of resolving as much as 40% per hour of increased extravascular lung water produced under these circumstances.

Animals↗
PubMed1983

Selective action of prostaglandin F2 alpha during paraquat-induced pulmonary edema in the perfused lung.

Lung prostaglandins (PGs) play a key role in normal pulmonary vascular regulation. We investigated PG metabolism during edema formation following paraquat-induced damage with an isolated perfused rat lung preparation. Lungs perfused with paraquat (PQ), 1 X 10(-7) M to 1 X 10(-2) M, showed significant increases in PGF2 alpha prior to detectable functional and pathological changes (increases in airway resistance, vascular resistance, and edema). No changes in PGE were observed. PGF2 alpha in perfused lungs showed a dose-related response following PQ exposure (up to 300% increase over control values). Lungs perfused with PQ and ventilated with high oxygen (95% O2-5% CO2) instead of air-5% CO2 showed a dramatic potentiation in the selective increase of PGF2 alpha, with levels reaching over 1 ng/ml (a 2600% increase over control values). The addition of exogenous PGF2 alpha to the perfusate without PQ initiated edema in a dose-related fashion, indicating the potential of PGF2 alpha as a causative agent in lung edema formation from PQ injury. The addition of ibuprofen (a nonsteroidal anti-inflammatory agent) to the perfusion medium blocked endogenous release of PGF2 alpha in lungs linked to oxidant-induced edema. These data show that in the perfused lung: (1) PQ caused a selective increase of PGF2 alpha; (2) this selective increase occurred prior to the onset of edema; (3) exogenous PGF2 alpha alone induced pulmonary edema; and (4) ibuprofen, in doses which blocked PGF2 alpha, also prevented edema formation.

Animals↗
PubMed1995

Insulin edema in diabetes mellitus associated with the 3243 mitochondrial tRNA(Leu(UUR)) mutation; case reports.

We encountered a patient with diabetes mellitus due to the 3243 mitochondrial tRNA mutation(DM-Mt3243), who developed insulin edema and hepatic dysfunction after starting insulin. Such a rare phenomenon was unlikely to be a fortuitous coincidence in mitochondrial diabetes, as none in 197 non-mutant NIDDM patients had same episode. Moreover, similar leg edema was noticed in another DM-Mt3243 patient, and other two DM-Mt3243 patients had leg edema which responded to coenzyme Q10. These observations suggest further a role of mitochondrial function on leg edema. The mechanism of his insulin edema may involve vasomotor changes induced by the rapidly glycemic control, because our case of insulin edema had a prominent increase of strong succinate dehydrogenase reactive vessels. Alternatively, myocardial dysfunction might have produced leg edema and hepatic dysfunction, because he had subclinical myocardial dysfunction, judged by imaging with beta-methyl-p-(123I)-iodophenyl-pentadecanoic acid. The third explanation is that a rapid improvement of glycemic control might have induced hepatic reoxygenation and the production of reactive oxygen species in the liver that contributed to cell damage. Thus, although we cannot draw definite conclusion, our experiences here suggest that mitochondrial dysfunction is important in the etiology of insulin edema.

Aged↗
PubMed1986

Edema of the arm as a function of the extent of axillary surgery in patients with stage I-II carcinoma of the breast treated with primary radiotherapy.

Edema of the arm can be a significant complication following treatment of breast cancer. To determine the risk of arm edema and factors associated with this risk in patients treated with primary radiotherapy, we reviewed the records of 475 women with early breast cancer treated between 1968 and 1980. During this period, the use of axillary surgery prior to radiation gradually increased, and all patients received full axillary irradiation until late in the series. Based on the surgeon's report, the extent of axillary surgery was classified as either a sampling, a lower dissection, or a full dissection. Edema of the arm was scored on clinical grounds and ranged from mild hand swelling to an increased arm circumference of 8 cm. At 6 years, the actuarial risk of developing arm edema was 8% for the entire study population. This risk was 13% for 240 patients who had axillary surgery and 4% for 235 patients not undergoing axillary surgery (p = 0.006). For patients undergoing axillary surgery, the risk of arm edema was 37% with full dissection compared to 5% with sampling (p = 0.0003), and 8% with lower dissection (p = 0.03). The risk of arm edema at 6 years was 28% if more than ten nodes were removed, and 9% if one to ten nodes were removed (p = 0.03). However, the extent of axillary dissection was stronger predictor of subsequent edema than was the number of nodes obtained. The role of axillary irradiation could not be evaluated since 91% of patients received axillary irradiation. The use of chemotherapy, the site or size of the primary tumor, clinical nodal status, patient age and weight, type of suture, the use of a drain, and subsequent local or distant failure did not appear to be significant risk factors. We conclude that the combination of full dissection and full axillary irradiation results in an unacceptably high risk of arm edema.

Arm↗
PubMed2006

Resistance to motion of flexor tendons and digital edema: An in vivo study in a chicken model.

PURPOSE: Tissue edema contributes to resistance to motion of flexor tendons during postsurgical exercises. We assessed edema formation and resistance of injured subcutaneous tissue and sheath to motion of the digital flexor tendon in a chicken model. METHODS: Ninety-four toes of 47 white Leghorn chickens were divided into 6 surgical groups and 1 nonsurgical control. Subcutaneous tissue and the sheath were incised, and the skin incision and the subcutaneous tissue were closed surgically. The toes were evaluated morphologically for severity of edema and tested for the force and work required to move the tendon. The evaluation time points were 1, 2, 3, 4, 5, and 7 days after surgery. Edema in the toes was scored according to severity and extent. The force and energy required to move the tendon were measured at the first and sixth cycles after cyclic loading in a testing machine with customized software and were statistically analyzed. RESULTS: The force and work increased progressively for the first 4 days, and were relatively consistent from days 4 to 7. The severity of edema peaked at the third and fourth days. At each postsurgical day, edema scores corresponded to increases in the force and work. The force and work were reduced drastically (30%-50%) after the first 6 cycles of toe motion. CONCLUSIONS: Resistance to tendon motion increased for the initial 4 days after surgery and remained comparatively consistent from the fourth to the seventh days. The severity of digital edema peaks at the third and fourth postoperative days. Motion of the digits for several cycles greatly reduces the resistance to the subsequent movement. We believe that tendon mobilization should not necessarily be started within the initial postoperative days, the optimum time to begin probably is the period from the fourth to the seventh day after surgery, and that judgment of edema helps to determine how aggressive exercise should be.

Animals↗
PubMedDate not supplied

Macular edema.

Macular edema is the final common pathway of many intraocular and systemic insults. It may develop in a diffuse pattern where the macula appears generally thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with protean underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, diabetic retinopathy, and posterior segment inflammatory disease. As well as clinical suspicion, a wide range of investigations may lead to the diagnosis of macular edema. Fluorescein angiography and optical coherence tomography provide enhanced visualization of the geometry and distribution of macular edema. A variety of approaches to the treatment of macular edema have been attempted, with a variable degree of success. These options have included topical and systemic steroids, topical and oral non-steroidal anti-inflammatory agents and laser photocoagulation treatment. More recently other therapeutic modalities, including immunomodulators, intravitreal injection of triamcinolone, and pars plana vitrectomy have also been employed. Clinical trials are currently looking into the use of a steroid slow-release intravitreal device for the management of macular edema secondary to uveitis and diabetes. This article reviews the clinical entity of macular edema focusing on the current therapeutic strategies for its management.

Humans↗
PubMed2003

Early postoperative retinal thickness changes and complications after vitrectomy for diabetic macular edema.

PURPOSE: To determine the early postoperative changes in retinal thickness and complications after pars plana vitrectomy for diabetic macular edema. DESIGN: Consecutive interventional case series. METHODS: Studied retrospectively, pars plana vitrectomy was performed on 65 consecutive eyes of 63 patients with diabetic macular edema. The follow-up interval ranged from 6 to 36 months (12.6 +/- 7.4 months [mean +/- standard deviation (SD)]). The indications of pars plana vitrectomy in this study were (1) diffuse diabetic macular edema, (2) preoperative visual acuity less than 20/40, and (3) noneffective macular photocoagulation therapy. Preoperative and postoperative examinations by stereoscopic biomicroscopy, color fundus photography of the macula and optical coherence tomography (OCT) were performed on all eyes. Preoperatively, direct photocoagulation to microaneurysms in the macula had been performed in 48 eyes, and focal/grid photocoagulation had been performed in five eyes. Preoperative examination showed that epiretinal membranes were observed in 20 eyes, cystoid macular edema in 40 eyes, and 23 eyes had a complete posterior vitreous detachment (PVD). Epimacular membranes, removed during surgery, were examined histopathologically. RESULTS: The postoperative mean best-corrected visual acuity (logarithm of the minimum angle of resolution [logMAR] = 0.696 +/- 0.491 [mean +/- SD]) was significantly better than the preoperative mean best-corrected visual acuity (0.827 +/- 0.361; P <.0001; Wilcoxon signed-rank test). The final visual acuity improved by 2 or more lines in 32 of 65 eyes (45%), remained unchanged in 32 of 65 eyes (49%), and exacerbated after the surgery in 4 of 65 eyes (6%) due to neovascular glaucoma (2 eyes) and residual cystoid macular edema (2 eyes). The postoperative foveal retinal thickness (224.9 +/- 116.9 microm) at the last visit was significantly thinner than the preoperative foveal retinal thickness (463.7 +/- 177.3 microm; P <.0001; Wilcoxon signed-rank test). The foveal retinal thickness did not decrease linearly but fluctuated: The mean postoperative retinal thickness had decreased significantly 7 days after surgery, then remained unchanged for approximately 1 month, and thereafter gradually decreased until 4 months. The intraoperative and postoperative complications included peripheral retinal tear in 3 of 65 (4.6%) eyes, postoperative rhegmatogenous retinal detachment in 1 of 65 (1.5%) eyes, neovascular glaucoma in 3 of 65 (5%) eyes, recurrent vitreous hemorrhage in 1 of 65 (1.5%) eyes, hard exudates in the center of the macula in 3 of 56 (4.6%) eyes, postoperative epiretinal membrane formation in 9 of 65 (13.8%) eyes, and a lamellar macular hole in 1 of 65 (1.5%) eyes. CONCLUSIONS: Vitrectomy for diabetic macular edema is an effective procedure for reducing the edema and improving visual acuity. Because the postoperative reduction in retinal thickness is not complete until 4 months, the assessment of vitrectomy on foveal thickness should not be made until this time. In addition, there are severe complications from vitrectomy for diabetic macular edema, and careful preoperative and postoperative examinations and surgical methods are required.

Adult↗
PubMed1998

Volumetric analysis of early macular edema with the Heidelberg Retina Tomograph in diabetic retinopathy.

OBJECTIVE: This study describes a new method for the quantification of diabetic macular edema by volumetric analysis with the Heidelberg Retina Tomograph (HRT) scanning laser ophthalmoscope. DESIGN: Topographic images of the macula were obtained in 25 consecutive patients who fitted the inclusion criteria. Twenty age-matched control subjects were randomly selected for a similar examination. PARTICIPANTS: Twenty normal control eyes and 32 eyes of 25 patients with diabetes mellitus were studied. INTERVENTION: Patients with diabetes were examined by HRT and slit-lamp biomicroscopy with a contact lens. On HRT, the volumes above reference plane bound by three consecutive circles centered at the fovea (diameter, 1, 2, and 3 mm) were measured. Measurements were repeated three times in a masked fashion, and the mean measurements were used for the analysis. MAIN OUTCOME MEASURES: Visual acuity, macular edema, and volume above reference plane were measured. RESULTS: There were 19 diabetic eyes with clinical macular edema (deemed positives) and 13 without edema (deemed negatives). Diabetic eyes with macular edema had statistically greater volumes above reference plane than did diabetic eyes without edema (P < 0.001) and greater than the control eyes (P < 0.001) for all three circles. There was no statistically significant difference between volumes measured in eyes without macular edema and control eyes (P = 0.42 for the 1-mm diameter circle; P = 0.72 for the 2-mm diameter circle; and P = 0.19 for the 3-mm diameter circle). For the two smallest circles only, the sensitivity of the HRT was 78.94%, and the specificity was 84.61%. None of the patients missed on the two smallest circles would have been positively identified on the 3-mm diameter circle. CONCLUSION: The HRT can detect and quantify macular edema in diabetes by volumetric analysis with the method the authors have described. It is sufficient to measure the volumes above reference plane of two circles centered on the fovea and measuring 1 and 2 mm in diameter because the 3-mm diameter circle does not increase the system's sensitivity.

Aged↗
PubMed1998

Modulation of kinin B1 but not B2 receptors-mediated rat paw edema by IL-1beta and TNFalpha.

The modulatory effects of IL-1beta and TNF alpha on the rat paw edema induced by B1 agonists have been analyzed. In naive rats, i.d. injection of B1 agonists, des-Arg9-bradykinin and des-Arg10-kallidin (up to 300 nmol), causes a minimal increase in paw volume, while the B2 agonist tyrosine8-bradykinin (0.3-10 nmol) induces graded paw edema. The injection of des-Arg9-bradykinin (10-100) nmol or des-Arg10-kallidin (1-100 nmol), in paws pre-treated with IL-1beta or TNF alpha (both 5 ng/paw; 60 and 30 min prior, respectively), caused a graded edema formation. The edemas induced by des-Arg9-bradykinin (100 nmol) were evident at 15 min, reaching the maximum 60 and 30 min after treatment with IL-1beta (0.64 +/- 0.06 ml) or TNF alpha (0.47 +/- 0.05 ml), respectively, being reduced at 360 min. The B1 antagonist des-Arg9-NPC 17731 (1-30 nmol), but not the B2 antagonist Hoe 140 (10 nmol), produced marked inhibition of des-Arg9-bradykinin-induced paw edema. Dexamethasone (0.5 mg/kg, s.c., 4 h) or cycloheximide (1.5 mg/kg, s.c., 6 h) significantly prevented the edema caused by des-Arg9-bradykinin (100 nmol) in rats treated with IL-1beta (81 +/- 5% and 59 +/- 3%) or TNF alpha (78 +/- 4% and 43 +/- 2%). Indomethacin (2 mg/kg, i.p.) or meloxicam (3 mg/kg, i.p.), 1 h prior, significantly reduced the edema induced by des-Arg9-bradykinin (100 nmol) in IL-1beta (40 +/- 6% and 69 +/- 8%) or TNF alpha (43 +/- 3% and 53 +/- 9%) treated rats. It is suggested that i.d. injection of the IL-1beta or TNF alpha, produced up-regulation of B1 receptor-mediated paw edema, being this effect sensitive to dexamethasone and cycloheximide and to cyclo-oxygenase pathway.

Animals↗
PubMed2000

High-frequency ultrasound for quantitative characterization of myocardial edema.

Myocardial edema has been associated with impaired ventricular compliance and diastolic filling. To determine the sensitivity of high-frequency (40 MHz) ultrasound to myocardial edema, we employed a model in which myocardial edema was induced by immersion of tissue in isotonic saline. The effect of freezing tissue on edema formation was also evaluated. Rat hearts were arrested at end-diastole and insonified fresh within 15 min of excision (n = 5) or following being frozen for 24 h and thawed (n = 4). Measurements of attenuation, backscatter, tissue thickness and speed of sound were performed at baseline and hourly for 4 h, and compared with direct measurements of myocardial edema. Fresh tissue demonstrated a greater propensity for the development of edema than frozen tissue. Integrated backscatter increased in both tissues, whereas the magnitude and slope of attenuation decreased as edema evolved. We conclude that high-frequency ultrasound sensitively detects myocardial edema, and we propose that the extension of these methods to clinical frequencies may prove useful for monitoring and treatment of cardiac edematous disease states.

Acoustics↗
PubMed1996

The role of pain from veins for the formation of perivenous edema in humans.

To test the hypothesis that nociception from veins plays a role in the formation of perivenous edema, we looked at edema along hand veins of humans during painful noxious stimulation in the presence and absence of nerve conduction block. Pain from vascularly isolated hand vein segments was evoked by perfusion with hyperosmolar saline and rated with the help of an electronically controlled visual analogue scale. Perivenous edema measured as changes in skin altitude was continuously recorded by means of infrared reflection. To alternately block the innervation of skin and vein segment we used a perivenous block (vein but not skin numbed), a distal ulnar nerve block (skin but not vein numbed), and a proximal ulnar nerve block (both vein and skin numbed). Without nerve block, hyperosmolar saline always evoked both pain and a continuous increase in perivenous edema to a maximum of 2.0-3.2 mm after 30 min. On painless control perfusions with isoosmolar saline, edema increased slightly (0.2-0.8 mm) to a plateau which was maintained until the end of perfusion. When the vein was denervated by perivenous or proximal ulnar nerve block, hyperosmolar saline evoked a slight increase in edema which resembled that of control perfusions in both extent and time course. On distal ulnar nerve block, which numbed the skin but not the vein, both pain and substantial edema were evoked. These observations show that nociception from veins is a prerequisite for perivenous edema to occur.

Adult↗
PubMed2002

Impact of postimplant edema on V(100) and D(90) in prostate brachytherapy: can implant quality be predicted on day 0?

PURPOSE: To determine the effect of edema on the dosimetric parameters V(100) (percentage of prostate volume that received a dose equal to or greater than the prescribed dose) and D(90) (minimal dose delivered to 90% of prostate volume) in 125I prostate brachytherapy and to determine whether the edema can be used to predict implant quality on the day of the implant (Day 0). METHODS AND MATERIALS: Fifty consecutive patients treated with (125)I implants who had two postimplant CT scans were selected for this study. The mean interval between the studies was 46 +/- 23 days. The implants were preplanned to deliver 150 Gy to the prostate plus a 3-5-mm symmetric dose margin using peripherally loaded 0.4-0.6-mCi (NIST-99) (125)I seeds. A dose-volume histogram was compiled for each postimplant CT scan. The V(100) and D(90) from the first and second CT scans were compared to determine the effect of edema on these parameters. A multivariate regression analysis was performed to define the linear relationships for predicting the V(100) or D(90) at 30-60 days after implant from the magnitude of the edema and the values of V(100) and D(90) on Day 0. RESULTS: V(100) and D(90) increased by 5% +/- 6% and 15% +/- 17%, respectively, during the interval between the first and second postimplant CT scans. The mean edema was 1.53 +/- 0.20. The increases in V(100) and D(90) were found to be proportional to the edema and the values of V(100) and D(90) on Day 0. The increase in V(100) was also found to depend on the width of the preplan dose margin. Linear relationships were derived that predict the V(100) and D(90) at 30-60 days after implant with a standard error of +/-4% and +/-24 Gy, respectively. CONCLUSION: V(100) and D(90) increased by 5% +/- 6% and 15% +/- 17%, respectively, during the first 30-60 days after implant. The results of a multivariate linear regression analysis showed that the increases in V(100) and D(90) were proportional to both the magnitude of the edema and the values of these parameters on Day 0. The relationships derived by linear regression analysis predict V(100) and D(90) at 30-60 days after implant to within +/-4% and +/-24 Gy, respectively. However, predicting the 30-60-day V(100) and D(90) on Day 0 is a poor substitute for obtaining a 30-60-day CT scan, because the uncertainty in the predicted values is greater by a factor of > or =2. Nevertheless, on average, the predicted values should provide a more reliable estimate of the actual V(100) and D(90) than the Day 0 values that ignore the effect of edema altogether. The increase in V(100) was also found to depend on the width of the preplan dose margin; therefore, our results for V(100) are only valid for implants planned with a 3-5-mm margin.

Algorithms↗