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PubMed2000

Dosimetric effects of edema in permanent prostate seed implants: a rigorous solution.

PURPOSE: To derive a rigorous analytic solution to the dosimetric effects of prostate edema so that its impact on the conventional pre-implant and post-implant dosimetry can be studied for any given radioactive isotope and edema characteristics. METHODS AND MATERIALS: The edema characteristics observed by Waterman et al (Int. J. Rad. Onc. Biol. Phys, 41:1069-1077; 1998) was used to model the time evolution of the prostate and the seed locations. The total dose to any part of prostate tissue from a seed implant was calculated analytically by parameterizing the dose fall-off from a radioactive seed as a single inverse power function of distance, with proper account of the edema-induced time evolution. The dosimetric impact of prostate edema was determined by comparing the dose calculated with full consideration of prostate edema to that calculated with the conventional dosimetry approach where the seed locations and the target volume are assumed to be stationary. RESULTS: A rigorous analytic solution on the relative dosimetric effects of prostate edema was obtained. This solution proved explicitly that the relative dosimetric effects of edema, as found in the previous numerical studies by Yue et. al. (Int. J. Radiat. Oncol. Biol. Phys. 43, 447-454, 1999), are independent of the size and the shape of the implant target volume and are independent of the number and the locations of the seeds implanted. It also showed that the magnitude of relative dosimetric effects is independent of the location of dose evaluation point within the edematous target volume. It implies that the relative dosimetric effects of prostate edema are universal with respect to a given isotope and edema characteristic. A set of master tables for the relative dosimetric effects of edema were obtained for a wide range of edema characteristics for both (125)I and (103)Pd prostate seed implants. CONCLUSIONS: A rigorous analytic solution of the relative dosimetric effects of prostate edema has been derived for a class of edema characterized by Waterman et al. The solution proved that the dosimetric effects caused by the edema are universal functions of edema characteristics for a given isotope. It provides an efficient tool to examine the relative dosimetric effects of edema for any given edema characteristics and for any isotopes that may be considered for prostate implants.

Brachytherapy↗
PubMed2002

Edema-induced increase in tumour cell survival for 125I and 103Pd prostate permanent seed implants--a bio-mathematical model.

Edema caused by the surgical procedure of prostate seed implantation expands the source-to-point distances within the prostate and hence decreases the dose coverage. The decrease of dose coverage results in an increase in tumour cell survival. To investigate the effects of edema on tumour cell survival, a bio-mathematical model of edema and the corresponding cell killing by continuous low dose rate irradiation (CLDRI) was developed so that tumour cell surviving fractions can be estimated in an edematous prostate for both 125I and 103Pd seed implants. The dynamic nature of edema and its resolution were modelled with an exponential function V(T) = V(p)(1 + M exp(-0.693T/ T(e))) where V(p) is the prostate volume before implantation, M is the edema magnitude and T(e) is edema half-life (EHL). The dose rate of a radioactive seed was calculated according to AAPM TG43, i.e. D = SkAg(r)phi(an)/r2, where r is the distance between a seed and a given point. The distance r is now a function of time because of edema. The g(r) was approximated as 1/r(0,4) and 1/r(0.8) for 125I and 103Pd, respectively. By expanding the mathematical expression of the resultant dose rate in a Taylor series of exponential functions of time, the dose rate was made equivalent to that produced from multiple fictitious radionuclides of different decay constants and strengths. The biologically effective dose (BED) for an edematous prostate implant was then calculated using a generalized Dale equation. The cell surviving fraction was computed as exp(-alphaBED), where alpha is the linear coefficient of the survival curve. The tumour cell survival was calculated for both 125I and 103Pd seed implants and for different tumour potential doubling time (TPDT) (from 5 days to 30 days) and for edemas of different magnitudes (from 0% to 95%) and edema half-lives (from 4 days to 30 days). Tumour cell survival increased with the increase of edema magnitude and EHL. For a typical edema of a half-life of 10 days and a magnitude of 50%. the edema increased tumour cell survival by about 1 and 2 orders of magnitude for 125I and 103Pd seed implants respectively. At the extreme (95% edema magnitude and an edema half-life of 30 days), the increase was more than 3 and 5 orders of magnitude for 125I and I03Pd seed implants respectively. The absolute increases were almost independent of TPDT and the prostate edema did not significantly change the effective treatment time. Tumour cell survival for prostate undergoing CLDRI using 125I or 103Pd seeds may be increased substantially due to the presence of edema caused by surgical trauma. This effect appears to be more pronounced for 103Pd than 125I because of the shorter half-life of 103Pd. If significant edema is observed post implantation, then a boost to the prostate using external beam radiotherapy may be considered as a part of the treatment strategy.

Brachytherapy↗
PubMed1996

Absence of edema in HIV-infected patients with end-stage renal disease.

In attempting to identify variables that might account for the frequent absence of edema in HIV-infected patients with end-stage renal disease, we evaluated 24 consecutive patients at our institution who had HIV infection and developed end-stage renal disease. Clinical and laboratory data prior to the initiation of hemodialysis were recorded and compared between patients with and without edema. Only 11 of the 24 study patients had edema while the remainder did not. The prevalence of diarrhea was significantly less in patients with edema (one of 11 patients compared to eight of 13 with no edema, p < 0.02, odds ratio 0.063). Prior weight loss was significantly less in the patients with edema (9.1 +/- 1.3 kg vs 15.5 +/- 2.2 kg, p < 0.05). Use of antiretroviral therapy was significantly greater in patients with edema (p < 0.05, odds ratio 10.1). None of the patients were receiving diuretics. Blood pressure was significantly higher (p < 0.001) in patients with edema, and serum albumin was low in both groups but did not differ (edema, 24 +/- 2 g/L; no edema, 21 +/- 3 g/L). Four patients had albumin levels as low as 2, 8, 9, and 10 g/L, yet they had no edema. CD4 counts were lower in patients without edema (62 +/- 16 x 10(6) cells/L vs 283 +/- 38 x 10(6) cells/L, p < 0.001). Absence of diarrhea was predictive of the presence of edema with a sensitivity of 91% and specificity of 62% while mean arterial blood pressure > 95 mm Hg was predictive of the presence of edema with a sensitivity of 82% and specificity of 77%. CD4 of > 100 x 10(6) cells/L was predictive of the presence of edema with a sensitivity of 91% and specificity of 77%. These data support the hypothesis that hemodynamic factors may play a role in the frequent absence of edema in patients with HIV infection and renal failure, and variables including diarrhea, low blood pressure, weight loss, and more advanced stage of HIV infection may account for this observation. Hence, the absence of edema should not dissuade the clinician from considering the possibility of advanced renal failure in HIV-infected patients.

Adult↗
PubMed1998

Hepatocyte growth factor and keratinocyte growth factor in the pulmonary edema fluid of patients with acute lung injury. Biologic and clinical significance.

Hepatocyte growth factor (HGF) and keratinocyte growth factor (KGF) are among the most potent mitogens identified for alveolar type II epithelial cells and may have other important functions in repair of the alveolar epithelium in acute lung injury (ALI). However, neither growth factor has been identified in the distal air spaces or plasma of patients with ALI. The goals of this study were to determine: (1) whether HGF and KGF are present in pulmonary edema fluid from patients with ALI and control patients with hydrostatic pulmonary edema; (2) whether HGF and KGF are biologically active in pulmonary edema; and (3) whether HGF or KGF levels are associated with clinical outcome. Pulmonary edema and plasma samples were obtained within 48 h of onset of acute pulmonary edema requiring mechanical ventilation in 26 patients with ALI and 11 control patients with hydrostatic edema. HGF and KGF concentrations were measured with enzyme-linked immunosorbent assays (ELISAs). The median (25th to 75th percentiles) concentration of HGF in pulmonary edema fluid was 21.4 (8.3 to 41.3) ng/ml in ALI and 6.6 (4.8 to 11.4) ng/ml in hydrostatic edema fluid (p < 0.01). The HGF concentration was 7-fold higher in the edema fluid than in the plasma of patients with ALI. In contrast, KGF was detected in low concentrations in edema fluid of patients with ALI and hydrostatic pulmonary edema; the concentration of KGF did not differ in ALI edema (0.6 [0.3 to 2.1] ng/ml) and hydrostatic edema fluid (0.2 [0.0 to 2.6] ng/ml) (p = NS). HGF and KGF were partly purified from four edema-fluid samples by heparin-Sepharose chromatography. Partly purified edema fluids were potent stimuli of DNA synthesis in cultured rat type II alveolar cells; addition of neutralizing antibodies to HGF and KGF attenuated this increase in DNA synthesis by 66% and 53%, respectively. Interestingly, higher edema-fluid levels of HGF were associated with higher mortality in patients with ALI. These novel results show that HGF and KGF are active in the alveolar space early in ALI, probably mediating early events in lung repair, and that increased levels of HGF in edema fluid may have prognostic value early in ALI.

Adolescent↗
PubMed2003

Brain edema -- a new classification.

Brain edema is a reaction to any brain injury and can be the first stage in the beginning of intracranial hypertension. This paper puts forth a modern classification of brain edema types, based on a etiopathogenic interpretation. The hydroelectrolitic and/or proteinic buildup can occur within cells and/or in the extracellular space and differentiates three types of brain edema: cellular brain edema; extracellular brain edema and combined brain edema. Cellular brain edema (cytotoxic brain edema) occurs through intracellular hyperosmolarity or extracellular hypotonicity. Extracellular brain edema (interstitial) appears as a result of the buildup of edema fluid in the extracellular space of the brain parenchyma and can be: hydrostatic extracellular brain edema (through ultrafiltration), oncotical extracellular brain edema (vasogen brain edema) and hydrocephalic extracellular brain edema. Combined brain edema includes in variable ratios both types of brain edema, cellular and extracellular; they can be present together from the beginning or can appear successively.

Animals↗
PubMed1993

Contribution of edema to the sensitization of high-threshold mechanoreceptors of the goat palatal mucosa.

1. Carrageenan has been shown to alter transduction capacities of high-threshold mechanoreceptors of the goat palatal mucosa. Assessments were made of the contributions of carrageenan-induced edema to the sensitization of mechanonociceptors (mechanically insensitive afferents) and intense pressure receptors of the palatal mucosa of the goat. The degree of edema was assessed by measurement of changes in tissue compliance produced by carrageenan. The impact of a simulated edema on both dynamic and static aspects of transduction were examined. The following observations were made. 2. Tissue compliance of the ventral zone of the incisal papilla (IP) was decreased after carrageenan treatment (0.042-0.014 mm/g). Tissue compliance changes were large for small displacements (< 1.4 mm), where displacement curves were substantially linear. For large displacements (> 1.4 mm), there was an exponential relationship between displacement and reactive force, and the compliance was unchanged. The exponential component may have represented the contribution of the maxillary bone compliance measures. 3. A simulated edema was created to assess the effects of edema on afferent reactivity. Saline was used to create the simulated edema by using changes in tissue compliance as a means of matching simulated to carrageenan-induced edema. An analysis of linear and exponential phases of saline or carrageenan-induced changes in tissue compliance indicated that saline injections produced a good approximation of the changes in linear properties, but diverged from a match of the exponential phase of carrageenan edema. 4. Assessments were made of modifications in nociceptor reactivity after simulated edema or retested controls (n = 47). There was little indication that edema influenced quantitative aspects of either static or dynamic force transduction. Mechanonociceptors, but not intense pressure receptors, sensitized after repeated intense stimulation (mean decline of dynamic activation threshold of 42 +/- 16 g/mm2, mean +/- SE). Artificial edema did not further contribute to this sensitization. 5. Qualitative features of stimulus transduction were modified by simulated edema. Eleven of 17 afferents without initial static or dynamic transduction capacity acquired the capacity after artificial edema. 6. Although most aspects of force transduction were unaffected by artificial edema, displacement transduction was considerably shifted. Artificial edema decreased the threshold and shifted the displacement range over which nociceptors transduced dynamic and static aspects of force (threshold decreased from 1,894 +/- 229 to 1,456 +/- 194 microns; range decreased 239 +/- 99 microns). 7. It was concluded the contribution of edema to allodynia and hyperalgesia is best understood in terms of its contribution to population-coding mechanisms that are brought about by changes in transmission properties.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1998

Edema associated with I-125 or Pd-103 prostate brachytherapy and its impact on post-implant dosimetry: an analysis based on serial CT acquisition.

PURPOSE: To characterize the magnitude and duration of post-implant edema following the implantation of I-125 or Pd-103 seeds into the prostate and to investigate its effect on the CT-based calculation of the total dose delivered by the implant. MATERIALS AND METHODS: A pre-implant CT scan and 3 to 5 serial post-implant CT scans were obtained on 10 patients who received either I-125 or Pd-103 seed implants. None of the patients received hormone therapy. The magnitude and duration of edema were determined from the change in the spatial distribution of the implanted seeds as the edema resolves. Dose volume histograms were compiled to determine the percentage of the prostate volume that received a dose equal to, or greater than, the prescribed dose. RESULTS: The magnitude of the edema, expressed as the ratio of the post- to pre-implant volume on the day of the procedure, ranged from 1.33 to 1.96 (mean 1.52). The edema decreased exponentially with time; however, the edema half-life (time for the edema to decrease by 1/2) varied from 4 to 25 days (mean 9.3 days). As the edema resolved, the percentage of the prostate that received a dose equal to or greater than the prescribed dose increased by at least 7% in 7 of the 10 patients and increased by more than 15% in 2. In those patients in whom dose coverage was unaffected by the resolution of edema, more than 90% of the prostate was covered by the prescribed dose in the initial CT scan. CONCLUSION: Post-implant edema increased the prostate volume by factors which ranged from 1.33 to 1.96 (mean: 1.52). The edema resolved exponentially with an edema half-life which varied from 4 to 25 days (mean: 9.3 days). Edema had a significant effect on the post-implant dosimetry in 7 of 10 cases. Factors that affect the impact of edema on the dosimetry are the magnitude of the edema and the planned margin between the prescribed isodose line and the periphery of the prostate.

Brachytherapy↗
PubMed2003

Clinical relevance of time of onset, duration, and type of pulmonary edema after liver transplantation.

We investigated the clinical significance of time of onset, duration, and type of pulmonary edema after orthotopic liver transplantation by retrospectively reviewing 93 consecutive recipients. Pulmonary edema was diagnosed by means of radiographic criteria and Pao(2)/Fio(2) ratio <300. Type was identified by pulmonary artery wedge pressure (hydrostatic, >18 mm Hg; permeability, < or =18 mm Hg). Of 91 evaluable patients, 44 (48%) had no pulmonary edema, 23 (25%) had immediate pulmonary edema resolving within 24 hours, 8 (9%) had late pulmonary edema (developing de novo in the first 16 to 24 hours), and 16 (18%) had persistent pulmonary edema (developing immediately and persisting for at least 16 hours). At 16 to 24 hours, mean arterial pressure was lower with persistent permeability-type edema than without pulmonary edema (75 versus 87 mm Hg, P <.01). Patients with persistent permeability-type edema had higher mean pulmonary arterial pressure (23 versus 16 mm Hg, P <.01) and higher pulmonary vascular resistance (103 versus 53 dyn. second. m(-5), P <.05), consistent with a resistance-dependent mechanism. Patients with persistent hydrostatic-type edema did not differ from those without edema in mean arterial pressure (84 versus 87 mm Hg, P >.05) or pulmonary vascular resistance (67 versus 53 dyn. second. m(-5), P >.05), but had increased mean pulmonary arterial pressure (27 versus 16, P <.01), suggesting a flow volume-dependent mechanism. Duration of mechanical ventilation, intensive care, and hospital stay were prolonged in patients with late or persistent permeability-type edema but not in patients with immediate pulmonary edema of any type. In conclusion, immediate pulmonary edema resolving within 24 hours after liver transplantation had little clinical consequence; persistent permeability-type pulmonary edema portended a worse outcome.

Adolescent↗
PubMedDate not supplied

Thiazolidinediones, peripheral edema, and type 2 diabetes: incidence, pathophysiology, and clinical implications.

OBJECTIVE: To present an objective, evidence-based review of edema associated with thiazolidinedione use in patients with type 2 diabetes. METHODS: We review the incidence, pathophysiology, and clinical significance of edema associated with the use of thiazolidinediones, with specific emphasis on the two currently available thiazolidinediones, rosiglitazone and pioglitazone. RESULTS: Both pioglitazone and rosiglitazone have been associated with increased development of edema in clinical trials. The incidence of edema in these trials varies from about 3.0 to 7.5% with the thiazolidinediones compared with 1.0 to 2.5% with placebo or other oral antidiabetic therapy. The highest incidence of edema has been reported when thiazolidinediones are used in combination with insulin. In clinical studies, these patients have an incidence of edema of 15.3% when treated with insulin plus pioglitazone and 14.7% when treated with insulin plus rosiglitazone (compared with 7.0% and 5.4% in the insulin-only groups, respectively). In addition to peripheral edema, reports have described pulmonary edema associated with thiazolidinedione therapy. In all such reports, patients failed to respond to diuretics during use of thiazolidinediones. Clinical improvement ensued only after discontinuation of thiazolidinedione therapy. Therefore, thiazolidinediones either may have some effect on the delivery of diuretics to the lumen of the nephron or may induce tubular alterations that impair the ability of the nephrons to respond to diuretics. Several potential causes have been postulated to precipitate edema in patients with diabetes who are treated with these agents: increased plasma volume, increased renal sodium reabsorption, reflex sympathetic activation, alteration of intestinal ion transport, and increased production of vascular endothelial growth factor. CONCLUSION: Available evidence suggests that edema is a class effect of the thiazolidinediones and is multifactorial in origin. Thiazolidinedione-associated edema seems to be dose related and occurs most frequently when thiazolidinediones are used in combination with insulin. Hence, therapy with these agents should be initiated at low doses, and patients should undergo assessment for edema and congestive heart failure during the first few weeks of treatment. Caution should be exercised when thiazolidine-diones are used in those at risk for or with a history of heart failure. Options for management thiazolidinedione-associated edema include dose reduction, drug discontinuation, and symptomatic therapy with diuretics. Further studies are needed to elucidate the mechanisms responsible for the cause of edema in patients with type 2 diabetes treated with thiazolidinediones and to determine whether certain factors might predict susceptibility to development of edema and congestive heart failure.

Diabetes Mellitus, Type 2↗
PubMed2006

[A comparative study of various diagnostic procedures in macular edema].

OBJECTIVE: To compare the results for diagnosis of macular edema between Heidelberg retina tomography (HRT-II macular edema module) and optical coherence tomography (OCT). METHODS: Two hundred and twelve eyes of 106 macular edema patients were diagnosed with fundus fluorescein angiography (FFA). HRT-II was used to obtain Edema Index and OCT was used to measure the retina thickness in the fovea. The results were compared with FFA. RESULTS: As FFA for gold standard, we compared with other diagnosis method. With regard to the diagnosis of macular edema by OCT, the Kappa value was 0.553, the odds ratio (OR) was 8.519. The Kappa value of HRT-II was 0.403 and OR was 3.210. In two groups of patients with and without macular edema, which were diagnosed by FFA, the difference of Macular edema Index P assayed by HRT-II between these two groups was significant (P = 0.00); while the difference of fovea retina thickness P assayed by OCT between these two groups was significant, too (P = 0.00). The best critical value of E was 2.00 and the ROC curve's area was 0.673 in the detection of macular edema by HRT-II. The best critical value of retina thickness for the diagnosis of macular edema was 170 microm and the ROC curve's area was 0.774 in the detection of macular edema by OCT. CONCLUSIONS: In regard to the diagnosis of macular edema, the sensitivity of HRT-II is better than that from OCT, with a lower false-negative result. However, HRT-II has a relatively low specialty with a higher false- positive result. As for the localization of macular edema, HRT-II has its advantage. Compared with FFA, the consistence of OCT for the diagnosis of macular edema is better than that of HRT-II. We can conclude from the OR value that OCT has greater influence than HRT-II in the diagnosis of macular edema. In addition, as for the diagnosis and different diagnosis, the clinical value of OCT is higher than that of HRT-II. Combination of these two different diagnostic methods might provide an accurate quantitative analysis of macular edema.

Adolescent↗
PubMed1987

[Physiopathology of brain edema].

Brain edema (BE), defined as an increase in tissue water content leading to an increase in tissue volume, is a common histopathologic response associated with a number of acute and subacute brain lesions. In some cases BE is a result of an unbalance of physical forces, hydrostatic or osmotic gradients driving the water in the tissue (hypertensive encephalopathy, hydrocephaly, plasma hypoosmolarity). In most cases however BE is associated with complex brain tissue alterations. According to Klatzo (1967) two physiopathological types can be described: vasogenic edema follows a breakdown of blood brain barrier to proteins. Edema fluid enlarges the extra-cellular space and spreads within the white matter; cytotoxic edema is an intra-cellular retention of water due to various disorders of ionic balance across the plasmic cell membrane. In both cases the hydrostatic gradient between the vascular lumen and the tissue plays a major role in the amount and spread of the edema fluid. In both cases also, toxic substances produced by tissue destruction act as factors of secondary damage causing more blood brain barrier lesions and/or cellular membrane alterations and eventually enhance edema. In various pathological conditions vasogenic and cytotoxic edema are associated: edema around circumscribed lesions such as hematomas, traumatic contusions, tumors, abscesses is basically a vasogenic edema with a secondary cytotoxic component. Ischemic edema is initially a pure cytotoxic phenomenon with a secondary osmotic edema and lately a vasogenic component. The formation of BE leads to an increase in tissue pressure which may reduce local cerebral blood flow. If blood supply is already impaired this can lead to energy shortage and further tissue destruction. If the bulk of edema is large enough intracranial pressure rises up, brain shifts and herniations may occur. Hypertonic solutions and corticoids are the more widely used drugs against brain edema. Hypertonic solutions remove water from the normal brain and hence may reduce intracranial pressure rather than treat edema. Corticoids, through various discrete mechanisms interfere with some toxic substances, enhance energetic metabolism and allow tissue restitution with a rather limited effect on edema itself.

Brain Edema↗
PubMed2005

Is intra-articular pathology associated with MCL edema on MR imaging of the non-traumatic knee?

OBJECTIVE: Edema surrounding the medial collateral ligament (MCL) is seen on MR imaging in patients with MCL injuries and in patients with radiographic osteoarthritis in the non-traumatic knee. Because we noted MCL edema in patients without prior trauma or osteoarthritis, we studied the association between intra-articular pathology and MCL edema in patients without knee trauma. DESIGN AND PATIENTS: We evaluated the MR examinations of 247 consecutive patients (121 male, 126 female with a mean age of 44 years) without recent trauma for the presence of edema surrounding the MCL, meniscal and ACL tears, medial meniscal extrusion, medial compartment chondromalacia, and osteoarthritis. The percentages of patients illustrating MCL edema with and without each type of pathology were compared using Fisher's exact test to determine if there was a statistically significant association. RESULTS: We found MCL edema in 60% of 247 patients. MCL edema was present in 67% of patients with medial meniscal tears, 35% with lateral meniscal tears, 100% with meniscal extrusion of 3 mm or more, 78% with femoral chondromalacia, 82% with tibial chondromalacia, and 50% with osteoarthritis. The percentage of patients with edema increased with the severity of the chondromalacia. These associations were all statistically significant (p <0.02). The mean age of those with MCL edema was 49.7 years compared with 34.9 years without MCL edema ( p <0.001). Patient gender and ACL tear did not correlate with MCL edema. Nine (4%) of the 247 patients had MCL edema without intra-articular pathology. None of these 9 patients had MCL tenderness or joint laxity on physical examination. CONCLUSIONS: We confirmed that MCL edema is associated with osteoarthritis, but is also associated with meniscal tears, meniscal extrusion, and chondromalacia. In addition, MCL edema can be seen in patients without intra-articular pathology, recent trauma or MCL abnormality on physical examination.

Adult↗
PubMed2005

Investigation of resistance of digital subcutaneous edema to gliding of the flexor tendon: an in vitro study.

PURPOSE: Although edema generally is considered to contribute to resistance to tendon mobilization and is a cause of tendon overload during postoperative motion exercise, it is unclear exactly how edema of the peritendinous tissues affects tendon mobilization. We assessed the effects of simulated subcutaneous edema on the gliding resistance of the flexor tendon in an in vitro model using chicken toes. METHODS: Thirty long toes of white Leghorn chickens were used. Twenty-two toes were divided into 2 groups and another 8 toes were used to determine the preconditions needed. In group 1 we produced 3 levels of edema severity in the subcutaneous tissue over a 1-cm segment by means of saline injection. In group 2 we created moderate tissue edema over 1-cm, 2-cm, or 3-cm segments of the toes. The work required to move the flexor digitorum profundus tendon over a fixed excursion and ultimate force were recorded with a testing machine after each run of flexion. RESULTS: Work and ultimate force increased significantly in the toes with simulated tissue edema in proportion to the severity and area of the edema. Even the least severe edema increased the work and force; a further increase to moderate edema tripled the energy needed to flex the toes. Increases in edema from 1-cm to a 2-cm and then to a 3-cm toe segment increased the work and force for each increment of extension. CONCLUSIONS: Simulated edema significantly increases energy and force required to move the tendons. The increase in resistance was proportionate to the severity and area of the edema. These results suggest that postoperative edema may increase significantly the resistance to tendon motion and that limiting both the severity and size of edema likely will reduce the resistance.

Animals↗
PubMed2001

Pharmacological characterization of the rat paw edema induced by Bothrops lanceolatus (Fer de lance) venom.

The inflammatory response induced by Bothrops lanceolatus venom (BLV) in the rat hind-paw was studied measuring paw edema. Non-heated BLV (75microg/paw) caused a marked paw edema accompanied by intense haemorrhage whereas heated venom (97 degrees C, 30s; 12.5-100microg/paw) produced a dose- and time-dependent non-haemorrhagic edema. The response with heated BLV was maximal within 15min disappearing over 24h. Heated venom was then routinely used at the dose of 75microg/paw. The prostacyclin analogue iloprost (0.1microg/paw) potentiated by 125% the venom-induced edema. The histamine H(1) receptor antagonist mepyramine (6mg/kg) or the serotonin/histamine receptor antagonist cyproheptadine (6mg/kg) partially inhibited BLV-induced edema whereas the combination of both compounds virtually abolished the edema. The lipoxygenase inhibitor BWA4C (10mg/kg), but not the cyclooxygenase inhibitor indomethacin (10mg/kg), significantly inhibited the edema (35% reduction; P<0.05). Dexamethasone (1mg/kg) also markedly (P<0.001) reduced venom-induced edema. The bradykinin B(2) receptor antagonist Hoe 140 (0.6mg/kg) reduced by 30% (P<0.05) the venom induced edema, whereas the angiotensin-converting enzyme inhibitor captopril (300microg/paw) potentiated by 42% (P<0.05) the edema. Bothrops lanceolatus antivenon (anti-BLV) reduced by 28% (P<0.05) the venom-induced edema while intravenous administration of antivenom failed to affect the edema. In conclusion, BLV-induced rat paw edema involves mast cell degranulation causing local release of histamine and serotonin, a phenomenon mediated mainly by kinins and lipoxygenase metabolites. Additionally, the use of a specific Bothrops lanceolatus antivenom, given subplantarily or intravenously, revealed to be little effective to prevent BLV-induced edema.

Animals↗
PubMed1997

Oncotic pressure and edema formation in hypoalbuminemic HIV-infected patients with proteinuria.

Human immunodeficiency virus nephropathy (HIVN) continues to challenge nephrologic consultative services at major urban institutions. Although noted in the literature, the decreased incidence of peripheral edema in HIVN has been unexplained to date. In HIV patients, total proteins frequently are found to be elevated due to an elevated globulin fraction. The impact that plasma proteins, specifically globulins, have on the total oncotic pressure has not been reported in HIVN, but may play a role in the paucity of edema noted in this proteinuric population. To evaluate the contributions of serum globulin to the total oncotic pressure and the presence or absence of edema in HIVN, we randomly selected 27 patients with proteinuria greater than 2.5 g/24 hr and serum albumin less than 3.1 g/dL from patients presenting to the nephrology outpatient clinic at the University of Miami/Jackson Memorial Hospital. Seventeen of the patients (63%) had a known diagnosis of HIV infection (group 1). These patients were subdivided into two subgroups: those presenting with clinically evident edema on physical examination (n = 7 [41%]; group 1A) and those who had an absence of edema (n = 10 [59%]; group 1B). Conversely, group 2 comprised 10 patients without known HIV infection, of whom six (60%) had edema (group 2A) and four (40%) did not (group 2B). Blood pressures were noted, and mean arterial pressure was calculated using standard formulas. Serum albumin, serum total proteins, and urine total proteins were measured using standard laboratory methods. Oncotic pressures for albumin (alpha), globulin (beta), and total protein (c) were calculated using the following formula: COPpl = alpha(2.8c + 0.18c2 + 0.012c3) + beta(0.9c + 0.12c2 + 0.004c3). We used Student's t-test to analyze the data. There is no significant difference between the albumin concentrations of HIV patients without edema (group 1B) and non-HIV patients with edema (group 2A), with mean concentrations of 2.3 +/- 0.1 g/dL versus 2.3 +/- 0.15 g/dL, respectively (P = NS). Group 1B, however, has a total oncotic pressure of 17.1 +/- 1.5 mm Hg, whereas both groups with edema (groups 1A and 2A) have statistically significant lower total oncotic pressures (12.1 +/- 2.3 mm Hg and 12.9 +/- 1.1 mm Hg, respectively; P < 0.05). The globulin oncotic pressures may account for some of the differences in total oncotic pressures, being significantly higher for those patients without edema in group 1B compared with group 2A (7.1 +/- 0.9 mm Hg v 3.9 +/- 0.4 mm Hg, respectively; P < 0.05). In patients with HIV, however, the presence or absence of edema is mandated by albumin concentration because both groups have similar globulin concentrations (group 1A 3.1 +/- 0.1 g/dL v group 1B 3.8 +/- 0.3 g/dL; P = NS). Mean arterial pressure does not play a role in edema formation in this study because the HIV patients without edema had the higher blood pressures (group 1B 97.8 +/- 4.7 mm Hg v group 2A 84.7 +/- 5.5 mm Hg; P < 0.05). We conclude that globulins play an important role in maintaining oncotic pressure in low albumin states. HIVN patients with increased serum immune globulin may benefit from higher globulin oncotic pressure, delaying the onset of clinical edema in the setting of proteinuria.

AIDS-Associated Nephropathy↗
PubMed1994

Hydrostatic versus oleic acid-induced pulmonary edema: high-resolution computed tomography findings in the pig lung.

RATIONALE AND OBJECTIVES: We evaluated the differences between combined hydrostatic and hypervolemic edema and oleic acid-induced edema on high-resolution computed tomography (HRCT) scans. METHODS: Twelve anesthetized and ventilated pigs were studied. Hydrostatic edema was induced by ligation of the abdominal aorta and infusion of normal saline (n = 4); permeability edema was induced by intravenous injection of oleic acid (n = 4). Four pigs were studied as normal controls. Serial scans were obtained before and after induction of edema at a constant position in the caudal lobe of the lung. The distribution of edema was assessed visually. Cross-sectional areas (CSAs) of the pulmonary artery and vein were measured both at the lobar and segmental levels. RESULTS: Gravity-dependent opacity, peribronchovascular fluid collection, prominent centrilobular core, thickening of the interlobular septa, and air-space consolidation at the dependent site were the sequential HRCT findings of hydrostatic edema. Randomly distributed, diffuse patchy high attenuation areas with a tendency for predilection in the subpleural and peripheral areas of the secondary lobule were the findings of oleic acid-induced edema. Hydrostatic edema increased the mean CSAs of the lobular vein by 137.8% +/- 78.7, but oleic acid edema decreased the mean CSAs by 33.2% +/- 22.7. Changes in the mean CSAs of the pulmonary arteries were not significant. The mean vein-to-artery ratio increased significantly in hydrostatic edema but decreased in oleic acid edema. CONCLUSION: HRCT findings for hydrostatic and oleic acid-induced pulmonary edema differed both in distribution of edema and in pulmonary vascular response.

Animals↗
PubMed2003

Bone marrow edema of the mandibular condyle related to internal derangement, osteoarthrosis, and joint effusion.

PURPOSE: The purpose of this prospective study was to evaluate whether common magnetic resonance imaging (MRI) variables such as temporomandibular joint (TMJ) internal derangement, osteoarthrosis, and effusion may predict the diagnostic group of bone marrow edema of the mandibular condyle. MATERIALS AND METHODS: The relationship between bone marrow edema and TMJ disc displacement, osteoarthrosis, and effusion was analyzed in MRIs of 120 TMJs in 73 consecutive patients with TMJ pain and/or a clinical diagnosis of TMJ internal derangement type III (disc displacement without reduction). The diagnostic bone marrow edema group was comprised of 54 TMJs in 40 patients with a unilateral or bilateral MRI diagnosis of bone marrow edema. The control group consisted of 66 non-bone marrow edema TMJs in 33 patients with a bilateral MRI finding of an absence of bone marrow edema. A logistic regression analysis was used to compute the odds ratios for internal derangement, osteoarthrosis, and effusion for non-bone marrow edema TMJs (n = 66) versus TMJs with bone marrow edema (n = 54). RESULTS: Using Chi;(2) analysis for pair-wise comparison, the TMJ-related data showed a significant relationship between the MR imaging findings of TMJ bone marrow edema and those of internal derangement (P = .000), osteoarthrosis (P = .000), and effusion (P = .010). Of the MRI variables considered simultaneously in the multiple logistic regression analysis, osteoarthrosis (P = .107) and effusion (P = .102) dropped out as nonsignificant in the diagnostic bone marrow edema group when compared with the control group. The odds ratio for individuals with an internal derangement showing bone marrow edema was strong (3.6:1) and highly significant (P = .000). Significant increases in risk of bone marrow edema occurred with disc displacement without reduction and osteoarthrosis (9.2:1) (P = .000) and disc displacement without reduction and effusion (6.4:1) (P = .002). CONCLUSIONS: The results suggest that the MR imaging findings for TMJ bone marrow edema are related to those of internal derangement, osteoarthrosis, and effusion. However, the data re-emphasize the aspect that internal derangement, osteoarthrosis, and effusion may not be regarded as the unique and dominant factors in defining TMJ bone marrow edema instances.

Adolescent↗
PubMed1999

Mesenteric, omental, and retroperitoneal edema in cirrhosis: frequency and spectrum of CT findings.

PURPOSE: To determine the frequency and CT imaging spectrum of mesenteric, omental, and retroperitoneal edema in patients with cirrhosis. MATERIALS AND METHODS: Eighty patients were identified with liver cirrhosis and no other cause of edema. Five radiologists jointly reviewed the abdominal CT scans of these patients to assess, by majority decision, the presence, severity, distribution, and configuration of mesenteric edema and the presence of omental and retroperitoneal edema. Subcutaneous edema, ascites, pleural effusion, splenomegaly, varices, portal venous thrombosis, and serum albumin levels were also documented. RESULTS: Mesenteric edema was present in 69 (86%) patients. Mesenteric edema occurred alone in 26 (38%) and with omental or retroperitoneal edema in 40 (58%) of the 69 patients with edema. No patient had omental or retroperitoneal edema alone. Mesenteric edema was mild in 51 (74%) and moderate to severe in 18 (26%), patchy in 47 (68%) and diffuse in 22 (32%), purely infiltrative in 60 (87%) and infiltrative with superimposed masslike nodules in nine (13%) patients. These parameters had significant associations among themselves and with ascites, pleural effusions, subcutaneous edema, and low mean serum albumin levels but not with splenomegaly or varices. CONCLUSION: Mesenteric, omental, and retroperitoneal edema occur commonly in patients with cirrhosis. The appearance of mesenteric edema varies from a mild infiltrative haze to a severe masslike sheath that engulfs the mesenteric vessels.

Adult↗