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PubMed1996

Thrombin-soaked gelatin sponge and brain edema in rats.

Previous work from this laboratory has shown that injection of thrombin into rat basal ganglia causes brain edema. This study investigates the effect on rat brain of thrombin-soaked gelatin sponge (used for intraoperative hemostasis in clinical situations) at a concentration similar to that used in humans. Three models were developed to evaluate this effect. In the first model, a gelatin sponge soaked with vehicle or thrombin (100 U/cm3) was placed on the intact pia of the right frontal lobe in rats without cortical lesions. In the second model, frontal cortex was excised (3 mm3) and the exposed brain was cauterized with electrocoagulation. Gelatin sponge was soaked with vehicle or thrombin (1000, 100, 10, or 1 U/cm3) and placed in the lesion site. In the third model, hirudin, a specific thrombin antagonist, was added to the thrombin-soaked gelatin sponge and placed in a similar cortical lesion to determine if the observed effects were specific to thrombin. The dose-response range for thrombin was determined qualitatively by magnetic resonance (MR) imaging and quantitatively by brain edema formation 24 hours after exposure. We found no edema in the cortically intact rats. The rats given cortical lesions developed significant edema when subjected to 1000, 100, and 10 U/cm3 thrombin as seen on MR imaging and at 100 and 10 U/cm3 thrombin as revealed by wet/dry weight and ion studies of brain tissue. Topical hirudin prevented thrombin-induced edema. It is concluded that thrombin-soaked gelatin sponges cause or enhance significant brain edema in rats at concentrations typically used for human neurosurgery.

Administration, Topical↗
PubMed1997

The importance of pial blood supply to the development of peritumoral brain edema in meningiomas.

In a retrospective analysis, the authors studied the pial and dural blood supplies in 74 intracranial meningiomas and quantified their associated peritumoral brain edema (PTBE). The extent and localization of pial blush in relation to the total tumor volume were determined angiographically. The amount of edema and tumor size were calculated using computerized tomography. The edema-tumor volume ratio was defined as Edema Index (EI). There were 49 meningiomas with PTBE; of those tumors, 46 were supplied by pial vessels, and three were supplied exclusively by dural vessels. Tumors without PTBE showed no pial blush. The mean EI in meningiomas with pial blush was significantly larger (EI = 3) than in meningiomas without pial supply (EI = 1.1; p < 0.0001). Meningiomas with a smaller pial supply than dural supply had a significantly smaller mean EI than tumors with a pial supply equal to or greater than the dural supply (EI = 2.9 vs. EI = 3.7; p < 0.015). In 69.9% of cases with pial blood supply, major portions of the edema were located adjacent to the tumor region supplied by pial vessels. Edema index differences among tumors of different subgroups, as defined by size or histology, were significantly related to the pial supply in each subset. Thus, pial blood supply may be associated with the development of PTBE in meningiomas.

Adult↗
PubMed2001

Expression of matrix metalloproteinases 2 and 9 in meningiomas associated with different degrees of brain invasiveness and edema.

OBJECT: Meningiomas display clinical characteristics that vary from very benign to clearly malignant with rapid invasive growth and metastasis. Benign meningiomas differ in their invasiveness and concomitant edema. This study was undertaken to analyze the expression of matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9, respectively) in meningiomas associated with different degrees of brain invasion and edema. METHODS: Tissue samples from 16 meningiomas were selected according to tumor invasiveness from a consecutive series of patients. Samples were analyzed for expression of both MMP-2 and MMP-9 by using in situ hybridization. The meningiomas consisted of three types: Group I, benign meningiomas that did not interfere with the arachnoid plane and exhibited no edema; Group II, benign meningiomas that invaded the arachnoid plane and caused edema; and Group III, aggressive and malignant meningiomas that caused edema and displayed brain invasion. In all 16 tumors analyzed, MMP-2 mRNA was identified. Levels of expression of MMP-2 mRNA were similar in all samples, and no correlation with increasing tumor invasiveness or associated edema could be detected. Expression of MMP-9 mRNA was identified in 14 of the 16 tumors, and a clear correlation with increasing tumor invasion into the brain was noted. CONCLUSIONS: Meningiomas express both MMP-2 and MMP-9. Tumor invasiveness, which ranged from minor with respect to the arachnoid membrane and progressed to frank brain invasion, correlated with the extent of MMP-9 expression. The findings indicate that MMP-9 expression and brain invasion are relevant mechanisms that must be interfered with in the treatment of aggressive and malignant meningiomas. No such correlation with MMP-2 was found.

Aged↗
PubMed2006

Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries.

OBJECT: The edema associated with brain swelling after traumatic brain injury (TBI) has been thought to be vasogenic in origin, but the results of previous laboratory studies by the authors have shown that a cellular form of edema is mainly responsible for brain swelling after TBI. In this study the authors used magnetic resonance (MR) imaging techniques to identify the type of edema that occurs in patients with TBI. METHODS: Diffusion-weighted MR imaging was used to evaluate the apparent diffusion coefficient (ADC) in 44 patients with TBI (Glasgow Coma Scale Score < 8) and in eight healthy volunteers. Higher ADC values have been associated with vasogenic edema, and lower ADC values with a predominantly cellular form of edema. Regional measurements of ADC in patients with focal and diffuse injury were computed. The water content of brain tissue was also assessed in absolute terms by using MR imaging to measure the percentage of water per gram of tissue. Cerebral blood flow (CBF) was measured using stable Xe-computerized tomography (CT) studies to rule out ischemia as a cause of cellular edema. The mean ADC value in the healthy volunteers was 0.82 +/- 0.05 x 10(-3) mm2/second. The ADC values in the patients with diffuse brain injury without swelling were close to the mean for the healthy volunteers. In contrast, the patients with brain swelling had increased brain water content and low ADC values (mean 0.74 +/- 0.05 x 10(-3) mm2/second). The ADC values correlated with CT classifications. In all patients with low ADC values, the CBF values were outside the range for ischemia. CONCLUSIONS: The brain swelling observed in patients with TBI appears to be predominantly cellular, as signaled by low ADC values in brain tissue with high levels of water content.

Adolescent↗
PubMed1995

Incidence and predictors of postextubation laryngeal edema in pediatric patients with congenital heart disease.

Laryngeal edema developed in 10.1% of studied patients with congenital heart disease after cardiac surgery. The 181 patients were divided into two groups; those with laryngeal edema (group 1) and those without laryngeal edema (group 2). The mean ages in group 1 and 2 were 10 and 22.9 months. Group 1 patients were younger on average than those of group 2 (p < 0.05). The differences in the cardiopulmonary bypass time and anesthesia time between the two groups were not statistically significant. The duration of intubations and ventilatory support before and after the onset of laryngeal edema and the period of the ICU stay were longer in group 1 than in group 2 (P < 0.05). A predictor of postextubation laryngeal edema was not found in our patients from above mentioned parameters. We conclude that the higher incidence of laryngeal edema may be due to young age (most were under 1 year of age), and duration of intubation and ventilatory support.

Adolescent↗
PubMedDate not supplied

Serial optical coherence tomography of subthreshold diode laser micropulse photocoagulation for diabetic macular edema.

BACKGROUND AND OBJECTIVE: To use serial optical coherence tomography (OCT) to evaluate low-intensity, high-density subthreshold diode laser micropulse photocoagulation treatment of clinically significant diabetic macular edema. PATIENTS AND METHODS: Eighteen consecutive eyes of 14 patients with clinically significant diabetic macular edema and a minimum foveal thickness of 223 microm or greater were prospectively evaluated by OCT preoperatively and 1, 4, and 12 weeks following treatment. RESULTS: Overall, estimated macular edema 3 months postoperatively (minimum foveal thickness--223 microm) was reduced a mean of 24% (P = .02). Eleven eyes treated for recurrent or persistent clinically significant diabetic macular edema following prior treatment more than 3 months before study entry were most improved, with a mean reduction in estimated macular edema 3 months postoperatively of 59%. No treatment complications were observed. No patient demonstrated laser lesions following treatment. CONCLUSIONS: Low-intensity, high-density subthreshold diode laser micropulse photocoagulation can reduce or eliminate clinically significant diabetic macular edema measured by OCT. Further study is warranted.

Diabetic Retinopathy↗
PubMed2004

Pulmonary edema fluid from patients with early lung injury stimulates fibroblast proliferation through IL-1 beta-induced IL-6 expression.

Although the fibroproliferative response to lung injury occurs with a high frequency in patients with clinical acute lung injury, the mechanisms that initiate this response are largely unknown. This study was undertaken first to identify fibroblast mitogenic factors in pulmonary edema fluid, and second to examine the human lung fibroblast's gene expression profile in response to pulmonary edema fluid. The edema fluid obtained from patients with early lung injury has an eightfold higher concentration of IL-1beta and a twofold greater IL-1beta-dependent mitogenic effect than does fluid obtained from control patients with hydrostatic pulmonary edema. Furthermore, fibroblasts responded to acute lung injury patient-derived edema fluid through production of soluble mediators that possess an autocrine mitogenic effect. Gene array analysis reveals that acute lung injury edema fluid induces several inflammation-modulating and proliferation-related genes in fibroblasts, whose inductions are similarly dependent on bioactive IL-1beta. Most notably, the 20-fold induction of IL-6 mRNA and protein was completely blocked by IL-1 receptor antagonist. The combined addition of IL-1beta and IL-6 was mitogenic, and the proliferative response to conditioned medium from IL-1beta-exposed cells was blocked by antagonistically acting Abs to IL-6 or to gp130. These novel findings indicate that soluble IL-1beta bioactivity and autocrine IL-1beta-dependent IL-6 up-regulation are critical initiators of fibroblast activation and proliferation and that they likely play a role in the fibroproliferative response seen in human acute lung injury.

Adult↗
PubMed1999

Pulmonary edema after resection of a fourth ventricle tumor: possible evidence for a medulla-mediated mechanism.

A well-recognized fact is that some patients may have development of pulmonary edema in association with disorders of the central nervous system. The origin of this phenomenon, known as neurogenic pulmonary edema, is unclear but may result, in part, from select pulmonary venoconstriction modulated by autonomic outflow from the medulla oblongata. We describe a 21-year-old man who had development of pulmonary edema in association with surgical resection of a brain tumor that was close to the medulla. Other than the possibility of medullary dysfunction, which could have occurred after surgical manipulation, no other risk factor for pulmonary edema was identified. Of note, the patient's blood pressure remained normal throughout the perioperative period, and no fluid overload or primary cardiac dysfunction was evident. This case supports the theory that the medulla is an important anatomic site of origin for neurogenic pulmonary edema and that alterations in medullary function can induce pulmonary edema in humans, independent of systemic hypertension.

Adult↗
PubMedDate not supplied

Hypoglycemia-induced neurogenic-type pulmonary edema: an underrecognized association.

OBJECTIVE: To report a case of hypoglycemia-induced pulmonary edema and to analyze the underlying pathophysiologic processes. METHODS: A case report with clinical and laboratory data is presented, and related studies from the medical literature are discussed. RESULTS: A 23-year-old man with type 1 diabetes was brought to the emergency department because he was found unconscious at home. Despite a morning blood glucose level of 30 mg/dL, he had taken his usual dose of Lente insulin (40 U), and a period of unconsciousness of unknown duration ensued. Intravenous administration of dextrose increased his blood glucose level to 118 mg/dL, but x-ray films of the chest disclosed evidence of pulmonary edema. After 48 hours of supportive care, his respiratory signs and symptoms resolved. The pathophysiologic construct for hypoglycemia-induced pulmonary edema is thought to be the same as for neurogenic pulmonary edema, with a massive sympathetic nervous system discharge being the common denominator in both conditions. CONCLUSION: Clinicians should be aware that severe hypoglycemia can lead to noncardiogenic pulmonary edema as a result of a massive sympathetic nervous system discharge and its associated hemodynamic alterations, in the same manner as occurs in neurogenic pulmonary edema.

Adult↗
PubMed1990

Selective breeding of dogs for segregation of limb edema from microfilaremia as clinical manifestations of Brugia infections.

Three generations of beagles were monitored for microfilaremia (mf) and clinical disease during repeated infection with Brugia pahangi and were selectively bred for offspring manifesting limb edema and low or amicrofilaremia. A high microfilaremic female mated to a high microfilaremic male produced 7 pups, 6 of which maintained mf greater than 1,000/ml for greater than 2 years after 5 monthly infections of 10 infective larvae each. An uninfected female mated to another high mf male produced 5 pups, 4 of which did not exceed 1,000 mf/ml 7 months after initiation of the repeating infection regimen; 1 of these remained amicrofilaremic after 2 additional challenges. Neither the parents nor the offspring from these matings manifested chronic limb edema. Two matings were conducted with offspring from the microfilaremic female by breeding siblings with the lowest mf and breeding siblings with the highest mf. The high mf siblings produced 4/5 offspring manifesting chronic limb edema (greater than or equal to 7 months duration) and either no mf (in 2 dogs) or less than 100 mf/ml after the repeating infection regimen. The lower mf siblings produced 5 offspring, all with greater than 1,000 mf/ml 6 months after the initiation of the repeating infection regimen; none manifested edema. Comparisons of IgG antibody levels, specific for extracts of adult worms, showed no consistent differences between these 2 litters of dogs that could be associated with limb edema or mf when monitored for 16 months; however, the onset of lymph node enlargement was much earlier in the group of dogs manifesting limb edema than in the other litter.

Animals↗
PubMedDate not supplied

[Peripheral nerve lesions of experimental leprosy in monkeys. VII. Intrafascicular-edema and small blood vessels].

Histopathological findings of intrafascicular-edema found in n. ulnaris running at forearm, palmside of hand and fingers of rhesus monkey 8664 and african green monkey 8175 were studied by semithin section method. These two monkeys were inoculated with leprosy bacilli from lepromata of mangabey monkey A022. The mangabey monkey A022 had been experimental leprosy after inoculum of the leprosy bacilli from lepromata of the mangabey monkey A015-natural infection. Period between date of inoculum and sacrifice of the rhesus monkey 8664 was about 2 years, and the african green monkey 8175 was about 5 years. Results found were: 1. Intrafascicular-edema found in n. ulnaris running at forearm, palmside of hand and fingers was remarkable at some of peculiar anatomical areas where were put on mechanical pressure. 2. The intrafascicular-edema inside many fascicles was remarkable around the small blood vessels. 3. Obsruction of the small blood vessels and congestion of blood stream at surrounded of the intrafascicular-edema with fibrous elements and cellular elements were observed inside some of fascicles. 4. Bundles of peripheral nerve fibers inside some of fascicles were pressed by the intrafascicular-edema, and the fibrous elements, especially collagen fibers, were increased around the pressed bundles of nerve fibers and each nerve fiber inside the fascicles. 5. Vacuolar degeneration and swelling of axon were observed at some of myelinated nerve fibers. 6. Not only the intrafascicular-edema but also a large amount of intracytoplasmic foamy structures with solid leprosy bacilli were observed inside many fascicles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Lower-extremity edema associated with gene transfer of naked DNA encoding vascular endothelial growth factor.

BACKGROUND: Vascular endothelial growth factor (VEGF) promotes angiogenesis and vascular permeability. The extent to which VEGF may cause tissue edema in humans has not been established. OBJECTIVE: To evaluate patients undergoing VEGF gene transfer for evidence of lower-extremity edema. DESIGN: Prospective consecutive case series. SETTING: Hospital outpatient clinic. PATIENTS: 62 patients with critical limb ischemia and 28 patients with claudication. INTERVENTION: Gene transfer of VEGF DNA. MEASUREMENTS: Semiquantitative analysis of lower-extremity edema. RESULTS: Lower-extremity edema was observed in 31 of 90 (34%) patients. Edema was less common in patients with claudication than in those with pain at rest (P = 0.016) or ischemic ulcers (P < 0.001), and it was less common in patients with pain at rest than in those with ischemic ulcers (P= 0.017). Treatment was typically limited to a brief course of oral diuretics. CONCLUSIONS: Vascular endothelial growth factor may enhance vascular permeability in humans. At the doses of plasmid DNA used in this study, lower-extremity edema responded to oral diuretic therapy and did not seem to be associated with serious sequelae.

Administration, Oral↗
PubMed1981

Salicylate-induced pulmonary edema. Clinical features and prognosis.

To assess the course and prognosis of salicylate-induced pulmonary edema, we reviewed the records of 36 consecutive patients admitted with serum salicylate levels greater than 30 mg/dL. Pulmonary edema developed in eight patients, and pulmonary infiltrates were never seen in 28 patients. Several features distinguished the two patient groups. Persons with pulmonary edema were older, ingested salicylates chronically, and had a history of smoking. They also were more likely to present with neurologic abnormalities. proteinuria, and serum salicylate levels greater than 40 mg/dL. The severity of pulmonary edema ranged from moderate (no assisted ventilation) to severe (characteristics of adult respiratory distress syndrome requiring assisted ventilation with positive end-expiratory pressure). Pulmonary edema resolved concomitant with a decline in serum salicylate levels. We conclude that certain patients are at increased risk for salicylate pulmonary edema, which responds to measures that lower serum salicylate levels.

Adult↗
PubMed1999

Ultrastructural pathology of Golgi apparatus of nerve cells in human brain edema associated to brain congenital malformations, tumours and trauma.

The alterations induced by ischemia and anoxia upon smooth endoplasmic membranes are studied in 38 patients with congenital malformations, brain tumours and brain trauma. The effects of vasogenic and cytotoxic brain edema are examined in the Golgi apparatus of nerve and endothelial cells. Samples of cortical biopsies were conventionally processed for transmission electron microscopy. Cortical biopsies were performed according to the basic principles of Helsinki declaration. Slices of 2 to 5 mm were immediately fixed in the surgical room in 4% glutaraldehyde-0.1 M sodium phosphate buffer, pH 7.4 at 4 degrees C, and postfixed in 1% osmium tetroxide in similar buffer. The pathological alterations of the Golgi complex were studied in samples with moderate and severe brain edema. Moderate edema was mainly found in congenital malformations and severe edema in brain trauma and tumours. In some severely edematous neurons, observed in hydrocephalus associated to Arnold-Chiari malformation, small vesicular type Golgi complexes and atrophic ones were observed, characterized mainly by partial or total disappearance of stacked Golgi cisternae and presence of congregated vesicular profiles. In brain trauma and tumours the Golgi complex showed enlargement and fragmentation of the stacked cis- medial- and trans-Golgi cisternae and vacuolization of trans-Golgi network. In addition, an increased formation of Golgi and coated vesicles was observed in the cis- and trans-Golgi regions. Most Golgi and clathrin coated vesicles were observed throughout the cytoplasm suggesting an increased vesicular transport. In severe edema the nerve cell plasma membranes appeared fragmented, presumably due to an interference of the protein insertion process into the plasma membrane. In brain trauma, a hypertrophic Golgi complex was observed in some nerve cells and endothelial cells of cortical capillaries, with increased formation of Golgi and coated vesicles. The ischemia and anoxia associated to the vasogenic and cytotoxic brain edema induced enlargement, fragmentation and disappearance of stacked Golgi cisternae.

Adolescent↗
PubMed2000

Laser treatment and the mechanism of edema reduction in branch retinal vein occlusion.

PURPOSE: To test a hypothesis on the physiological mechanism of the disappearance of macular edema after laser treatment. The hypothesis is based on the effect grid laser treatment has on retinal oxygenation and hemodynamics. It predicts that laser-induced reduction of macular edema is associated with shortening and narrowing of retinal vessels in patients with branch retinal vein occlusion (BRVO). METHODS: The study included 12 subjects, treated with argon laser photocoagulation for BRVO and macular edema. Fundus photographs taken at the time of diagnosis and again after laser treatment, were digitized, and diameter and segment length of retinal vessels was measured using NIH-Image program. RESULTS: Macular edema disappeared or was dramatically reduced in all cases after laser treatment. The diameter of occluded venules constricted to 0.81+/-0.02 (mean +/- SD, P = 0.019) of the prelaser diameter and adjacent arterioles constricted to 0.78+/-0.01 (P = 0.008). The laser treatment also led to shortening of the affected vessels. The final segment length of the occluded venules was 0.95+/-0.17 (P = 0.005) of the length before treatment. The corresponding value for the adjacent arterioles is 0.95+/-0.14 (P = 0.008). Control arterioles and venules in the same fundus did not change in either length or width. CONCLUSIONS: These results do not reject the authors' hypothesis that the disappearance of macular edema in BRVO can be explained by the effect the laser photocoagulation has on retinal oxygenation. Increased oxygenation causes vessel constriction and shortening and lower intravascular pressure, which reduces edema formation according to Starling's law.

Aged↗
PubMed2000

A nomogram to compensate for intraoperative prostate edema during transperineal brachytherapy.

PURPOSE: Prostate edema during and following prostate brachytherapy may have a negative impact on implant dosimetry. The purpose of this study was to assess the magnitude of prostate edema during the operative procedure and to develop a nomogram of isotope activity required for compensation of such intraoperative prostate volume changes. MATERIALS AND METHODS: Twenty-five consecutive patients with early-stage, localized adenocarcinoma of the prostate underwent ultrasound-guided transperineal interstitial permanent prostate brachytherapy with either iodine 125 or palladium 103. Transrectal ultrasound volume studies of the prostate were performed before and during the implant procedure. Computed tomography-based postimplant dosimetry was performed 3-4 weeks after surgery. RESULTS: A median intraoperative prostate volume increase after insertion of applicator needles of 10.4% (range 1.2-32.5%) was identified. A correlation of -0.55 (95% confidence interval -0.78 to -0.19) between the minimum dose covering 90% of the prostate volume (%D90) and the amount of edema was identified. An algorithm and nomogram was developed to calculate the extra isotope activity necessary to compensate for intraoperative edema. CONCLUSIONS: Prostate edema occurs at the time of transperineal needle placement. A negative correlation was found between the amount of edema and dose coverage of the prostate (%D90). Therefore, to cover the prostate volume adequately, additional isotope activity is required when preoperative treatment planning is performed. This nomogram can be used to compensate for such volume changes.

Adenocarcinoma↗
PubMed2000

Edema factor from the venom of Trimeresurus elegans (Sakishimahabu).

An edema factor was isolated from the venom of Trimeresurus elegans using HW-55, CM-Cellulose, and Mono S column chromatographies. Homogeneity was demonstrated by the formation of a single band in polyacrylamide gel electrophoresis (pH 8.3). The edema factor has a molecular weight of 25,500, an isoelectric point of 7.5, and express edema, proteolytic and capillary permeability-increasing activities. Edema, proteolytic and capillary permeability-increasing activities are inhibited by ethylenediaminetetraacetic acid (EDTA), o-phenanthroline, and N-bromosuccinimide. Additionally, this factor exhibits kinin-releasing activity. The edema factor possesses proteolytic activity as shown by hydrolyzing the Val(3)-Asn(4), His(5)-Leu(6), Ser(9)-His(10), Ala(14)-Leu(15), Leu(15)-Tyr(16), Tyr(16)-Leu(17), and Glu(21)-Arg(22) bonds of oxidized insulin B chain. The A alpha, B beta, and gamma chains of human fibrinogen were also hydrolyzed. The edema factor was found to contain 1 mol of zinc and 2 mols of calcium per mol of protein and the amino-terminal sequence was determined.

Amino Acid Sequence↗
PubMed2001

Macular edema and retinal hard exudates in African Americans with type 1 diabetes: the New Jersey 725.

OBJECTIVE: To determine frequency and associated risk factors for macular edema and retinal hard exudates in hospitalized African Americans with type 1 diabetes. SUBJECTS AND METHODS: Included were 725 African Americans with type 1 diabetes who participated in the New Jersey 725. Clinical evaluations consisted of a structured clinical interview, ocular examination, stereoscopic fundus photographs, and blood pressure measurements. Presence of macular edema and hard exudates was determined via masked grading of fundus photographs. Biological evaluations included blood and urine assays. RESULTS: Of the 725 patients, 89 (12.3%) had macular edema and 149 (20.6%) had retinal hard exudates in at least 1 eye. The presence of macular edema and hard exudates was significantly associated with older age at examination, longer duration of diabetes, and severity of diabetic retinopathy. Presence of proteinuria, missing insulin injections at least once a week, and longer duration of diabetes were significantly and independently associated with macular edema. Presence of proteinuria, male sex, higher low-density lipoprotein cholesterol levels, and longer duration of diabetes were significantly and independently associated with severity of retinal hard exudates. CONCLUSION: Macular edema and hard exudates are common in African Americans with type 1 diabetes, particularly in patients with evidence of renal disease.

Adolescent↗