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PubMed2005

[Toxic, allergic, and inflamatory edema].

Edema is defined as the condition in which intraluminal lymph fluid components leak into the tissues and the interstitium fluid is abnormally increased. At the site of edema, toxication, allergy or inflammation occasionally occurs. This paper will focus on local skin and mucosal edema. Toxic edema is locally caused by intake of industrial goods or medical products (pharmaceuticals). Like urticaria, allergic edema is attributed to the increased vascular permeability caused by a chemical mediator. Inflammatory edema is the state in which increased inflammatory reaction in local skin causes increases in osmotic pressure of the tissues and metabolism and then inflammatory effusion accumulate there. It includes burn and cellulites.

Edema↗
PubMed2005

[Intravitreal triamcinolone acetonide for diffuse diabetic macular edema--one year follow-up].

BACKGROUND: Macular edema is the main cause of visual impairment in diabetic patients. Its treatment is mainly based on laser photocoagulation. Intravitreal triamcinolone acetonide (TA) has recently been proposed as a new treatment for eyes with diabetic macular edema resistant to conventional laser photocoagulation. AIM: To evaluate the one year efficacy and safety of a single TA injection administered for diffuse diabetic macular edema unresponsive to prior laser treatment. DESIGN: Interventional case series. METHODS: Setup: University medical center out-patient clinic. PARTICIPANTS: Twenty-one patients with bilateral diffuse diabetic macular edema. INTERVENTION: A single intravitreal injection of triamcinolone acetonide. MAIN OUTCOME MEASURES: Visual acuity measured by ETDRS score, retinal area evaluation clinically and retinal thickness evaluation by Retinal Thickness Analysis (RTA) at 3 and 12 months following injection. Secondary outcomes were intraocular pressure control and cataract progression. RESULTS: Three months following injection, the mean improvement in visual acuity was 4.7 +/- 11.7 letters in the study group as compared to 0.2 +/- 11.4 in the control group (p = 0.18). No difference was noticed one year following injection. Clinical assessment of the retinal area of edema revealed a substantial difference between patients and controls at 3 months (p = 0.0006) and at one year (p = 0.05). RTA evaluation revealed improvement in retinal thickness solely at the 3 months exam. Four eyes developed high intraocular pressure and required treatment (p = 0.054). No difference in cataract progression was noted between the two groups (p = 0.69). CONCLUSIONS: Injection of TA may improve visual acuity for a limited time. Increased intraocular pressure is a frequent side effect. During a one year follow-up, no evidence of ocular toxicity was noted in eyes with diffuse diabetic macular edema.

Anti-Inflammatory Agents↗
PubMed2006

[The intravitreal application of triamcinolone in the treatment of the macular edema].

The aim of this study was to evaluate the efficacy of intravitreal application of triamcinolone in macular edema of different etiology. In this prospective study, 20 eyes were evaluated: 12 with diabetic macular edema, 6 with macular edema due to venous occlusion, 1 with pseudophakic cystoid macular edema, and 1 with cystoid macular edema in case of uveitis. Four milligrams of tramcinolon acetonide were injected in to the vitreous cavity. Before and in one month intervals after the application, the intraocular pressure was measured, visual acuity on the ETDRS optotypes was established, the macula was examined biomicroscopically, examination of the photography of the fundus was performed, and macular thickness was measured by means of optical coherence tomography. The follow-up period was 3 months. The mean visual acuity was 0.16 at the beginning of the study, 1 month after the application 0.32, and after 3 months 0.31. The mean thickness of the macula decreased from the initial value 537 microm by 249 microm after one month (improvement by 46.6%) and by 203 miceom after three month (improvement by 39.7%). As a complication, the elevation of the intraocular pressure was noticed in 20% of eyes, and this was compensated in all cases by means of local therapy. The intravitreal injection of triamcinolon seems to be a promising part of treatment of the macular edema of different origin.

Adolescent↗
PubMed2006

[Pars plana vitrectomy and intravitreal triamcinolone for chronic pseudophakic cystoid macular edema].

AIM: To report on the results of pars plana vitrectomy and intravitreal triamcinolone in patients with chronic pseudophakic cystoid macular edema unresponsive to medical treatment. PATIENTS AND METHODS: A retrospective analysis of 9 eyes in 9 patients with chronic pseudophakic cystoid macular edema was performed. All patients had cystoid macular edema confirmed on fluorescein angiography, and were unresponsive to medical treatment. In all patients pars plana vitrectomy and intravitreal application of 4 mg of triamcinolone was performed. In one patient with vitreous prolapse into the anterior chamber, anterior vitrectomy was also required. RESULTS: The mean interval between cataract surgery and vitrectomy was 16.28 +/- 2.1 months. The mean preoperative best corrected visual acuity was 0.1 +/- 0.11, and the mean final best corrected visual acuity 0.25 +/- 0.24, after a mean follow up of 6.6 +/- 3.5 months. In all 9 eyes there was a marked reduction of cystoid macular edema, as verified on fluorescein angiography. Intraocular pressure was raised in 4 patients, and it was controlled by topical antiglaucomatous treatment. CONCLUSION: Pars plana vitrectomy and intravitreal triamcinolone in eyes with chronic pseudophakic cystoid macular edema resulted in a reduction of cystoid macular edema, and visual acuity improvement.

Aged↗
PubMed2006

[Effects of Cinnabar and Realgar in Angong Niuhuang powder on heat shock protein, nitric oxide synthase and inflammatory cytokines in contusion cerebral edema].

OBJECTIVE: To explore the pharmacological mechanism of Cinnabar and Realgar in Angong Niuhuang powder (ANP). METHODS: SD rats were randomly divided into six groups (12 rats/group): normal controls group (NS group), contusion cerebral edema model group( CCE group) , cerebral edema rats administrated by cinnabar 0. 15 g/kg 1h (CA group), cerebral edema rats administrated by realgar 0.15 g/kg 1h (RG group), cerebral edema rats administrated by Angong Niuhuang powder 1.5 g/kg 1h (ANP I group), cerebral edema rats administrated by Angong Niuhuang powder substracted cinnabar and realgar 1.2 g/kg 1h (ANP II group). Each group was divided into two subgroups (6 rats/subgroup). The rats in subgroups were killed at 8h and 24h after modeling respectively. Expression of heat shock protein 70 ( HSP 70) mRNA in brain tissues was measured by RT-PCR. Activities of nitric oxide synthase (NOS) and its isoenzymes (iNOS, cNOS) in brain tissues were tested by colorimetry. Levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1beta) in serum were determined by radioimmunoassay (RIA). RESULTS: Expression of HSP 70 mRNA in ANP I group and ANP II group significantly increased as compared with CCE group 8h after being modeled (P < 0.05), and increase range in ANP I group were singificantly higher than that in ANP II group (P < 0.05). Activities of iNOS in CA group, RG group, ANP I group and ANP II group were lower than that in CCE group 8h after being modeled (P < 0.05) , and the activities in ANP I group were the lowest in the four groups. Levels of TNF-alpha in RG group, ANP I group and ANP II group decreased obviously as compared with CCE group 8h after being modeled (P < 0.05) , so did levels of IL-1beta in ANP I group and ANP II group (P < 0.05). But no significant difference was shown between ANP I group and ANP 11 group. CONCLUSION: HSP 70, iNOS, TNF-alpha and IL-1beta are involved in contusion cerebral edema. ANP and CA, RG in ANP are protective against CCE in rats. It may be associated with the increase of HSP 70 mRNA expression, inhibition of iNOS activity, and the decreasae of inflammatory cytokines (TNF-alpha, IL-1beta) levels.

Animals↗
PubMed1991

Myelin basic protein-messenger RNA (MBP-mRNA) expression during triethyltin-induced myelin edema.

Triethyltin (TET) is a neurotoxicant that produces severe but transient cerebral edema, characterized ultrastructurally by vacuolation of the intraperiod line of central nervous system (CNS) myelin. TET has been reported to depress levels of myelin basic protein (MBP), a protein thought to play a critical role in myelin compaction. In the present study, the genomic expression (i.e., mRNA) of MBP was monitored throughout the pathogenesis of TET-induced myelin edema and recovery in Sprague-Dawley rats given a single injection of a neuropathic (8.0 mg/kg) or non-neuropathic (0.8 mg/kg) dose of TET-bromide. Levels of MBP-mRNA from the anterior and posterior brain were collected 1 hr, 3 hr, 2d, and 7d, postexposure. The optic nerve and caudal brainstem, representing anterior and posterior brain sites, respectively, were examined at the same time-points for ultrastructural evidence of edema and recovery. Our data indicate that neuropathic doses (8.0 mg/kg) of TET significantly stimulated MBP transcript throughout the brain at all exposure time-points. The magnitude and time-course of this stimulation differed in the anterior and posterior brain, with the latter region showing higher levels of MBP-mRNA. In the posterior brain, the highest levels of mRNA correlated with the appearance of edema in the caudal brainstem. In the anterior brain, MBP-mRNA levels were only marginally increased over controls. Ultrastructural evidence of myelin edema was confined to the brainstem in rats treated with neuropathic dose of TET. Intralamellar vacuolation appeared at 3 hr and 2d postexposure and could be correlated with peak levels of MBP transcript, whereas, recompacted myelin, which appeared by 7d postexposure, was associated with declining levels of the mRNA. Ultrastructural changes in the oligodendroglia were suggestive of metabolic stimulation and correlated with high MBP-mRNA levels. In summary, these data indicate that an initial genomic event in TET-induced myelin edema is stimulation of MBP transcript.

Animals↗
PubMed1991

Intermittent pneumatic compression therapy in posttraumatic lower limb edema: computed tomography and clinical measurements.

The purpose of our study was to assess the amount of posttraumatic lower limb edema and its distribution between subcutaneous and subfascial compartments before and after intermittent pneumatic compression (IPC) therapy in patients with fractures of the lower leg immobilized with a cast for six to 12 weeks. Computed tomography (CT) was used as an objective method of measuring the compartmental distribution of edema. Sixteen patients with a mean age of 37 years (range 19 to 64 years) were investigated by clinical measurement of the leg circumference and by CT at the ankle joint and at three equidistant (10cm) levels above it. The unaffected leg served as a control for the evaluation of the amount of edema and density of the tissues. Edema was found primarily in subcutaneous tissue. The IPC treatment decreased relative edema from 23% to 15.9% (p less than 0.01) as measured by CT, and from 23.5% to 13.2% as measured clinically. The density of muscle tissue increased 9% (p less than 0.01) and that of subcutaneous tissue decreased 5.6% (p less than 0.05). The IPC treatment influenced both the amount of edema and the density of tissue compartments.

Adult↗
PubMed1991

The edema inducing activity of phospholipase A2 enzymes.

The edema inducing activity of phospholipase A2 (PLA2) enzymes from snake venoms and porcine pancreas was investigated using mouse paw as experimental model. All ten PLA2 enzymes exhibited potent edema inducing activity. PLA2, however, is generally not the major edema inducing component of snake venom. Chemical modification studies indicated that enzymatic activity of PLA2 was required for its edema inducing activity. All PLA2 enzymes examined displayed a rapid onset edema which was suppressed by pretreatment of the mice with antihistamine. Dexamethasone pretreatment also inhibited edemas elicited by some PLA2 enzymes.

Animals↗
PubMed1991

Contact lens-induced edema in vitro. Pharmacology and metabolic considerations.

The effects of physiologic and pharmacologic manipulations on contact lens-induced edema were studied. In isolated superfused rabbit corneas bathed in Ringer's solution and covered with large-diameter polymethylmethacrylate (PMMA) lenses, corneal swelling rates of 17-26 microns/hr (versus -5-5 microns/hr in paired controls) were observed. Neither the calcium antagonist diltiazem (10(-4) M), the glucocorticoid dexamethasone (10(-7) M), the glucose substitute fructose (20 mM), nor 0.5 mM adenosine and 0.3 mM reduced glutathione mitigated the edema. Lens-induced edema was 25 microns/hr in corneas bathed at pH 8.2 and decreased to 9 microns/hr at pH 7.0. In corneas without lenses, however, decreasing the pH from 7.4-7.0 caused significant swelling (P less than 0.05). The pyruvate dehydrogenase stimulant sodium dichloroacetate (3.2 mM) on the tears side ameliorated the edema, and its congener, 3.2 mM 2-chloropropionate, was less effective. These latter agents are known to relieve lactic acidosis systemically and had no significant effect on corneas without lenses. In tissues bathed with 20 mM lactate Ringer's, normal thickness was maintained in both control and PMMA-treated corneas throughout the 3-hr period. These findings suggest that the contact lens-induced edema does not involve the acute cytotoxic mechanisms seen in severe tissue ischemia or hypoxia. The edema appears to result in part from acidosis but mainly from stromal lactate accumulation.

Animals↗
PubMed1990

Effect of superoxide dismutase in cats with cold-induced edema.

We evaluated the potential role of SOD, an oxygen free radical scavenger, as a probe to cover the trigger period of injury and the prolonged period of development of edema in vasogenic brain edema. Vasogenic brain edema was produced in 34 cats by a standardized cortical freezing lesion. Brain edema and the disruption in the BBB were assessed by SG measurement and spread of Evans blue by planimetry. Detection of superoxide radicals was studied by topical application of NBT within the cranial window. Animals were separated into two groups: (a) controls; and (b) two SOD-treated groups--A was pretreated with 10,000 U/kg PEG-SOD intraperitoneally and sacrificed at 24 and 48 hr after lesions, and B received both a bolus injection of free SOD (4 mg/kg) and then 1 mg/kg/min for 20 min after the lesion and was sacrificed 6 hr later. Our preliminary data indicate that superoxide radicals were detected in the brain after cold-induced injury, but free and PEG-SOD had no beneficial effect on vasogenic brain edema produced by cold-induced injury. It is concluded that intracellular uptake of SOD might be necessary for an effect in the treatment of cold-induced brain edema.

Animals↗
PubMed1990

Hydrostatic pressure versus osmotic pressure in the development of vasogenic brain edema induced by cold injury.

The role of hydrostatic pressure and osmotic pressure gradient in the development of vasogenic brain edema induced by cold lesion made in the parietal cortex was studied in cats under ketamine anesthesia and blood pressure monitoring. The animals were divided into a hypertensive group and a normotensive group and were kept alive for 6 hr. The brain was removed and cut coronally at the lesion for tissue sampling from various areas of edematous white matter to measure both the SG and the amount of extravasated serum albumin in the same samples. Our result showed that the edema confined in the area containing extravasated serum albumin and the increase of water content correlated linearly with the amount of extravasated serum albumin both in the normotensive group and hypertensive group. However, the slope of the regression line indicated albumin content in the edema fluid was significantly different between the two groups. The slope became lower as the MABP during the experiment became higher, indicating that protein concentration in the edema fluid became lower when hypertension sustained. Thus, both hydrostatic and osmotic pressure gradient regulate the extravascular accumulation of edema fluid in the cold lesion edema.

Albumins↗
PubMed1990

Evaluation of brain edema using magnetic resonance proton relaxation times.

Experimental and clinical studies on the evaluation of water content in cases of brain edema were performed in vivo, using MR proton relaxation times (longitudinal relaxation time, T1; transverse relaxation time, T2). Brain edema was produced in the white matter of cats by the direct infusion method. The correlations between proton relaxation times obtained from MR images and the water content of white matter were studied both in autoserum-infused cats and in saline-infused cats. The correlations between T1 as well as T2 and the water content in human vasogenic brain edema were also examined and compared with the data obtained from the serum group. T1 and T2 showed good correlations with the water content of white matter not only in the experimental animals but also in the clinical cases. The quality of the edema fluid did not influence relaxation time and T1 seemed to represent almost solely the water content of the tissue. T2, however, was affected by the nature of existence of water and was more sensitive than T1 in detecting extravasated edema fluid. It seems feasible therefore to evaluate the water content of brain edema on the basis of T1 values.

Animals↗
PubMed1990

Relation between macrophage infiltrates and peritumoral edema.

Peritumoral edema is one of the most serious complications of intracranial neoplasms. However, the exact pathogenesis of peritumoral edema is still unknown. To explore the role of macrophages and LTs in brain tumors, we examined macrophage infiltrates in the brain tumors by immunohistological method using anti-Leu M3 monoclonal antibody and measured tissue LTC4 and LTD4 by HPLC with ODS column and UV spectrophotometer in the wavelength of 280 nm. Nine of 14 gliomas, 10 of 14 meningiomas, and all six metastatic brain tumors had macrophage infiltrates. The correlation was good between macrophage infiltration and peritumoral edema detected on CT. In many cases with peritumoral edema, LTC4 was detected. In most cases without peritumoral edema and many cases with preoperative steroid treatment, LTC4 was not detected. These data suggest that macrophages and LTs may play an important role in the formation of peritumoral edema.

Adrenal Cortex Hormones↗
PubMed1989

Influence of thermal stress and various agents on the brain edema formation in rats following a cryogenic brain lesion.

The influence of cold stress, heat stress, or various agents on the development of brain edema were assessed in rats following a cryogenic brain lesion. Brain edema was induced by local cold injury to the cortex. Cerebral edema was assessed 0.5, 3.0 or 24 h after a cryogenic brain lesion by measuring the water content of two hemispheres. Pretreatment of animals with sodium pentobarbital (15 or 30 mg/kg, i.p.) or lidocaine (15 mg/kg, i.p.) did not influence the development of brain edema. In addition, pretreatment with an external heat stress (heat exposure of 32 degrees C for 6 h) exaggerated significantly the development of brain edema in the rat following a cryogenic brain lesion. On the other hand, pretreatment of animals with either external cold stress (cold exposure of 8 degrees C for 6 h), glycerol (10% 10 ml, i.p.), mannitol (15% 10 ml, i.p.), gamma-hydroxybutyric acid (300 mg/kg, i.p.), metiamide (5 mg/kg, i.p.), dexamethasone (4 mg/kg, i.p.), aminophylline (100 mg/kg, i.p.), or ketamine (30 mg/kg, i.p.) inhibited significantly the brain edema formation.

Animals↗
PubMedDate not supplied

[Postoperative edema in brain tumors].

CT examination of postoperative edema of the brain in 251 neurosurgical patients showed edema to be determined by the location and histostructure of the tumor. The data obtained suggested that the pathogenesis of edema differs. Thus, vasogenous edema develops predominantly after removal of hemispheric gliomas, cytotoxic (hypoxic) edema--after removal of basal-diencephalic tumors, and hydrostatic edema--after removal of subtentorial tumors. It is shown that operative trauma causes hyperhydration of all brain structures.

Adult↗
PubMed1988

Ultrastructural alterations of human cortical capillary basement membrane in perifocal brain edema.

The fine structural alterations of cortical capillary basement membrane have been studied in 16 patients with perifocal edema associated to brain tumors, traumatic injuries complicated with subdural or epidural hematoma or hygroma and congenital malformations, such as hydrocephalus, Arnold-Chiari and Alport's syndromes and vascular anomalies. The basement membrane displayed homogeneous and nodular thickening, vacuolization, rarefaction and reduplication. Its average thickness varied according to the etiology and severity of brain edema. In nine patients with moderate brain edema the thickness ranged from 71.97 to 191.90 nm and in the remaining seven patients with severe brain edema it varied from 206.66 to 404.22 nm. The basement membrane complex appeared apparently intact in moderate edema and showed glio-basal dissociation in severe edema. In areas of highly increased cerebro-vascular permeability, the basement membrane showed matrix disorganization and bifurcations acting as abluminal transcapillary channels. In regions of total brain necrosis, its structural stability was lost showing loosening, dissolution and rupture. Proliferation of collagen fibers was also found in three cases. Basement membrane swelling was interpreted as an overhydration of its matrix. The thickening, rarefaction and vacuolization seem to be induced by the increased vacuolar and vesicular transendothelial transport. The degenerated areas feature a finely granular precipitate interpreted as a protein or glycoprotein degraded matrix.

Adolescent↗
PubMed1986

[Altitude edema in the Swiss Alps. Observations on the incidence and clinical course in 50 patients 1980-1984].

In the Swiss Alps 50 patients with high altitude edema (high altitude pulmonary edema and/or high altitude cerebral edema) had to be rescued by helicopter during the period 1980-1984. The development, clinical picture and clinical course have been analyzed retrospectively. The patients were 49 men and one woman, generally in good health and well trained. They had ascended from the low-lands to an altitude above 2500 m and subsequently climbed higher. The climbers developed symptoms of acute mountain sickness on the second to third day of high altitude exposure and had to be evacuated by air on the fourth to fifth day. 70% of the cases occurred in the Valais Alps and the rest in the region of the Bernese Alps and the Bernina. The highest incidence of high altitude edema was observed in the Capanna Margherita (4559 m), where one of 588 climbers who stayed overnight had to be air-rescued. This ratio was about one in 4000 mountaineers at the Finsteraarhorn hut (3050 m) and the Monte Rosa hut (2795 m). Evacuation by air was the most successful therapeutic measure and resulted in immediate amelioration of clinical symptoms in 16 patients. 34 climbers had to be admitted to local hospitals due to severe high altitude pulmonary and/or cerebral edema. The pulmonary edema was bilateral in two thirds of these patients and unilateral in one third. Arterial blood gases showed moderate to severe limitation of oxygen diffusion capacity. All patients recovered completely within a few days.

Adult↗
PubMed1979

Pathogenesis of pulmonary edema associated with the adult respiratory distress syndrome.

Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the development of acute pulmonary edema in any clinical situation can usually be explained alterations in the forces governing the transvascular flux of fluid in the pulmonary microvasculature, according to the Starling equation. "Cardiac" pulmonary edema is primarily due to an increase in the capillary hydrostatic pressure of sufficient magnitude to overcome the forces maintaining fluid within the vessel and the ability of the lymphatics to drain the transudated fluid. On the other hand, pulmonary edema occurring in association with noncardiac disease (e.g., sepsis, aspiration or shock) is secondary to an increase in the permeability of the pulmonary microvasculature and is referred to as noncardiogenic pulmonary edema or the adult respiratory distress syndrome. This article examines the mechanisms for the development of pulmonary edema and discusses the differences between the cardiac and noncardiac types.

Animals↗