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PubMed2004

Intravitreal triamcinolone injection for macular edema secondary to increased retinal vascular permeability.

BACKGROUND AND PURPOSE: Macular edema is an important cause of visual loss in various retinal diseases, and may be refractory to conventional treatment. We investigated the efficacy of intravitreal injection of triamcinolone acetonide for the treatment of intractable macular edema. METHODS: A prospective study was conducted in 17 patients (18 eyes) with a diagnosis of macular edema unresponsive to conventional treatment, resulting from inflammatory or retinal vascular diseases. The underlying diseases associated with the development of macular edema were: diabetic retinopathy (6 eyes), branch retinal vein occlusion (5 eyes), Irvine-Gass syndrome (3 eyes), and central retinal vein occlusion (4 eyes). Triamcinolone acetonide 4 mg was injected intravitreally. Ophthalmological examinations, fundus photography, fluorescein angiography, and optical coherence tomography were performed before treatment, 3 months and 6 months after treatment. During the follow-up period, recurrent macular edema was retreated with the same dosage and followed for another 6 months. RESULTS: Sixteen eyes received a single injection and 2 others (11%) underwent reinjection after the 3-month follow-up examination. Among the eyes that received a single injection, 10 (63%) showed visual acuity gain of 2 or more Snellen lines at the 6-month follow-up. The pretreatment central macular thickness averaged 581 microm [corrected] and reduced to 215 microm [corrected] at the 6-month follow-up. In the 2 eyes that received reinjection, macular edema also showed significant reduction 6 months after retreatment. Sterile endophthalmitis was noted in 3 eyes (17%). Two eyes (11%) developed significant cataract. Three eyes (17%) developed high intraocular pressure; 1 of them (5.5%) ultimately required filtering surgery. CONCLUSIONS: Intravitreal injection of triamcinolone temporarily reduced refractory macular edema. Potential complications should be monitored after treatment.

Aged↗
PubMed1992

An experimental model for subclinical edema disease (Escherichia coli enterotoxemia) manifest as vascular necrosis in pigs.

An experimental model for subclinical edema disease was developed in weanling pigs. In multiple experiments, 3-week-old pigs were weaned, then inoculated intragastrically with 10(10) colony-forming units of an SLT-IIv-positive strain of Escherichia coli originally isolated from a pig with edema disease (principals). Control pigs were inoculated with a nonpathogenic E coli strain. Of 39 principals, 8 developed clinical edema disease within 14 days after inoculation. However, 20 of 21 principals that did not develop clinical signs of edema disease, but were submitted for necropsy examination at 14 days after inoculation, had characteristic vascular lesions of edema disease. Vascular lesions, found principally in ileum and brain, consisted of segmental necrosis of myocytes in the tunica media of small arteries and arterioles. None of the pigs inoculated with a nonpathogenic strain of E coli developed edema disease or vascular lesions. None of the principals necropsied at 2 days after inoculation had vascular lesions. Development of vascular lesions by 14 days after inoculation was used as the end point for detecting subclinical edema disease in the model.

Animals↗
PubMed1991

Involvement of PAF-acether and eicosanoids in adrenaline-induced pulmonary edema in mice.

The participation of platelet-activating factor (PAF, PAF-acether) in a mouse model of pulmonary edema was studied using specific antagonists. Mice were treated before induction of edema with the PAF antagonists BN52021 (10 mg/kg, ip), PCA4248 (10 mg/kg, po) or WEB2170 (10 mg/kg, ip), the lipoxygenase inhibitor EP10161 (10 mg/kg, ip), the cyclo-oxygenase inhibitor aspirin (250 mg/kg, po), or with the mixed cyclo-lipoxygenase inhibitor BW755C (50 mg/kg, ip). The test drugs were administered to animals either 30 min (when the ip route was used) or 60 min (when given po) prior to the induction of pulmonary edema. Pulmonary edema was induced by intravenous administration of adrenaline (2 mg/kg). When the lung-body index was used as the criterion for comparison between groups, BN52021, PCA4248 and WEB2170 were found to have no significant effect on pulmonary edema. In contrast, EP10161, aspirin and BW755C significantly inhibited pulmonary edema by 49%, 30% and 27%, respectively. The results suggest that arachidonate metabolites are likely to play a major role in adrenaline-induced pulmonary edema in mice, whereas PAF-acether does not seem to play an important role in this model.

Animals↗
PubMed1991

Anti-inflammatory and immunomodulating effects of the novel agent gamma-(2-aminoethylamino)-2-butyrothienone. 1st communication: inhibitory effects on mouse paw edema.

A series of 4-hydroxy-(or-amino)-ethyl-amino butyrophenones or butyrothienones were synthesized. For detail studies on antiinflammatory effects, gamma-(2-aminoethylamino)-2-butyrothienone (gamma-ABT) was chosen as representative of these new non-steroidal anti-inflammatories (NSAID). The effect on mouse paw edema induced by various phlogistic agents was first investigated. The inhibitory effect of gamma-ABT on carrageenin-induced edema was remarkable and nearly equal to that of indometacin. Similarly to indometacin, gamma-ABT inhibited the early and late stage of yeast-induced edema in contrast to concanavalin A (Con A) induced edema which was only inhibited by gamma-ABT. Both the above induced edema are supposed to be unrelated to prostaglandins in the rat system. gamma-ABT displayed an inhibitory effect on nystatin-induced edema similar to indometacin suggesting that gamma-ABT has significant membrane stabilizing action and a strong blocking action on synthesis of prostaglandins. gamma-ABT inhibited as well the sustained edema induced by mustard. In conclusion gamma-ABT is an effective agent not only on acute but also on subacute and chronic inflammation and its mode of action appears similar to other NSAID. gamma-ABT posses in addition the advantage of antioxidant activity which is not shared by selective cyclooxygenase inhibitors and thus should be potentially effective in autoimmune diseases.

Animals↗
PubMedDate not supplied

[Brain edema as a cause of critical states in neurosurgical patients].

The results of the studies in 120 patients after resection of tumours located in cranial fossa (40 cases), basal-diencephalic area (45 cases), hemispheres (35 cases) have shown the role of brain edema in the onset of critical conditions after neurosurgery (with consideration of a new concept concerning the mechanisms of brain edema development). It has been demonstrated that brain edema at its early stages is a biologically expedient adaptation response to any damage and is manifested in hyperhydration of all the tissues, most marked in the affected focus. Specific (neurogenic, neurohumoral) and non-specific (biochemical, autoimmune, mechanical, etc.) factors of brain edema onset have been identified. It turned out that the location of the affected focus determines the differences in neurogenic and neurohumoral mechanisms of the edema onset. The nearer the affected focus to the stem and diencephalic structures, the more marked the effect of neurogenic and neurohumoral factors and the more distinct the tendency towards edema generalization. Brain edema may be a cause of critical conditions and lethal outcomes only when it leads to dislocation and strangulation of them brain structures, and disturbances of brain metabolism and blood flow.

Brain Edema↗
PubMed1990

Effects of lipoxygenase inhibitor on cerebral edema induced by freezing lesion in rats.

This study was done to examine the effect of the lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA), on cerebral edema and to substantiate the hypothesis that the metabolites of arachidonic acid are involved in the pathogenesis of cerebral edema. The experiment was performed on rats with vasogenic cerebral edema induced by a freezing lesion. Results demonstrate that the permeability of blood-brain barrier to macromolecules, assessed by Evans blue, was progressively increased and reached a maximum at 24 hrs after freezing untreated rats. At 24 hrs following cold injury, the intracranial pressure was significantly increased from 5.6 +/- 0.4 mmHg to 11.1 +/- 0.8 mmHg and water content from 79.9 +/- 0.3% to 82.7 +/- 0.4%. Sodium and calcium contents increased but potassium decreased significantly as found in untreated cerebral edema tissues. In the nordihydroguaiaretic acid pretreatment group, (3 mg/kg & 6 mg/kg, i.p., 48 hrs in advance) intracranial pressure, water, sodium, and calcium contents were significantly decreased but potassium was increased in cerebral edema tissues. There was no significant difference between untreated controls and immediately post-treated animals. Since NDGA substantially alleviated brain edema, the results suggest that the metabolites of arachidonic acid resulting from the lipoxygenase pathway may contribute to the pathogenesis of cerebral edema.

Animals↗
PubMed1990

Enhancement of infusion-induced brain edema by mediator compounds.

Mediator compounds such as bradykinin, arachidonic acid, and LT are released in the brain in conditions causing cerebral swelling. The potential of these compounds to enhance this process was studied in the infusion-induced model of brain edema. Cats subjected to chloralose anesthesia were infused with 400 microliters of artificial CSF into the right and left frontal white matter within 2.5 hr. CSF infused into the left hemisphere contained either bradykinin (40 microM), arachidonic acid (3 mM), LTB4 (15 microM), or LTC4 (16 microM), respectively. Evans blue was administered as blood-brain barrier indicator. Water content of gray and white matter was microgravimetrically determined in serial coronal brain slices. Infusion of CSF only led to an increase in water content from 69 to between 75% and 79%. Addition of bradykinin effectively enhanced the infusion edema but did not open the barrier to Evans blue. Arachidonic acid even more effectively led to an increase in water content and opened the barrier to Evans blue, in addition. Infusion of LT (LTB4, as well as LTC4) was not found to increase further the infusion edema and did not open the blood-brain barrier to Evans blue. It is concluded that the infusion edema model is suitable for studying the edema-enhancing potential of mediator compounds. Marked enhancement of vasogenic brain edema by bradykinin or arachidonic acid again demonstrates a pathophysiological function of these compounds as mediators of secondary brain damage, although LT are unlikely to be specifically involved in vasogenic edema formation.

Animals↗
PubMed1990

Comparative studies of edema produced by fluid percussion injury with lateral and central modes of injury in cats.

Earlier studies by our laboratories indicated that severe fluid percussion injury in cats results in the development of significant brain edema. In this study we measured the spatial distribution of edema developed after both central and lateral modes of impact with the objective of determining the degree to which the edema volume may contribute to ICP elevation and neurologic deterioration. All animals developed a marked increase in tissue water, particularly in the brainstem. In laterally injured cats, the increase in brainstem water equaled the edema produced supratentorially. Adding the increase of brainstem edema and the edema volume of the supratentorial compartment, we found an average water increase of 1.125 cc in survivors and 2.492 cc in nonsurvivors. This represents a significant volume increase when it is considered that the average PVI of the normal cat is approximately 0.9 cc (6). However, we observed that the PVI was reduced soon after injury and at a time when it has been reported that water content was near normal levels (7). Taking these studies in concert, we believe that the early reduction in PVI is most probably due to vascular swelling. The developing edema further contributes to reductions in PVI, thus setting the stage for elevated ICP and the tissue impaction observed in nonsurvivors.

Animals↗
PubMed1989

Macular edema and vitreous detachment.

To determine if vitreous changes play a role in macular edema, 197 eyes were selected, 113 with macular edema (68 diffuse and 45 cystoid) associated with different pathologies. We studied the vitreoretinal relationship in all cases. Photocoagulation was done in 21 eyes and vitreous examination before and after treatment. The difference between complete and incomplete posterior vitreous detachment (PVD) between the control and pathologic groups was statistically significant (P less than .0005). This shows that incomplete PVD is related to macular edema. The difference between complete and incomplete PVD and diffuse or cystoid macular edema was not statistically significant. It was significant between incomplete PVD without collapse and with contraction and diffuse and cystoid macular edema (P less than .0005). That is cystoid macular edema is associated with incomplete PVD with vitreous contraction. The vitreous usually collapses with laser treatment. Complete PVD before treatment seems to be associated with a good prognosis after photocoagulation. Cases with incomplete PVD and cystoid macular edema show worsening of the visual field after laser treatment.

Adult↗
PubMed1989

Pseudophakic corneal edema. An 11-year study of its development, incidence, and treatment.

This paper studies the appearance and development of pseudophakic corneal edema (PCE) in a series of 840 patients referred for keratoplasty for corneal edema. There were no cases of PCE in 100 eyes with corneal edema studied between 1960 and 1970. In 200 cases of corneal edema studied between 1978 and 1980, there were 30 eyes with PCE (15%). The disease has gradually increased to 56% of all cases of corneal edema seen in 1986. A tendency of PCE to decrease has been noted in the last 2 years. The high incidence of PCE in recent years, which is the main reason for keratoplasty today, seems to be related to the use of closed loop anterior chamber lenses. Fuchs' dystrophy, which formed the bulk of cases of corneal edema, may be present in many cases of PCE. results of keratoplasty with intraocular lens (IOL) removal or exchange provided better than 80% good results in a group of 230 cases followed from 1 to 7 years with visual improvement better than 20/100 in over 50% of cases. The removal of an intraocular lens causing progressive visual symptoms is advised even at the risk of causing corneal edema.

Anterior Chamber↗
PubMed1985

[The pathomechanism underlying ischemic brain edema: the role of Na+, K+-ATPase of the brain microvessels].

In the present study, the anti-edema effect of AVS [1,2-bis (nicotineamide)-propane] was evaluated using the cat MCA occlusion model with or without recirculation. In the prolonged ischemia (PI) group, cortical edema as assessed by the changes in specific gravity, developed in those cortical areas where the mean 1-CBF was less than 25-30 ml/100 g/min during MCA occlusion (4 hours). In the recirculation group (2 hours' ischemia followed by 2 hours' recirculation: RC group), the ischemic threshold for edema development was almost the same as in the PI group. In both groups, the drop in cortical specific gravity was significantly suppressed by AVS. Regarding the time-course of 1-CBF, there was no difference between the PI-AVS-treated and PI-saline-treated groups. In the RC group, however, the postischemic hypoperfusion was significantly ameliorated by AVS. Based on the present and previous data showing the antiedema effect of AVS, the mechanism of action of AVS was discussed in relation to the pathomechanism underlying ischemic brain edema. Our new concept of ischemic brain edema is briefly stated below. Related in vitro studies have shown the followings: (i) the influx of sodium not of proteins is the principal cause of ischemic brain edema: (ii) the eicosanoid synthetic capacity of the brain microvessel (MV) is increased simultaneous to edema development (iii) an elevation in the level of hydroperoxides enhances the activities of Na+, K+-ATPase as well as the arachidonate cascade of MV. These data suggest that free fatty acids and free radicals liberated following cerebral ischemia stimulate the activity of the MV-Na+, K+-ATPase, which results in increased sodium influx across the BBB. AVS was shown to scavenge hydroxyl radicals and to inhibit the stimulatory effects of a lipid hydroperoxide (15-HPAA) on the activities of Na+, K+-ATPase and the arachidonate cascade of the MV. These actions of AVS may be linked to its antiedema effect.

Animals↗
PubMed1988

[Photocoagulation with the argon laser in cystoid macular edema in retinal venous occlusions. Apropos of 68 cases].

Sixty-eight consecutive eyes with cystoid macular edema due to venous occlusion were treated by grid laser photocoagulation. The diagnosis of cystoid macular edema was based on both the biomicroscopic and angiographic findings. The treatment was applied with blue-green or green argon laser. The criteria for treatment were the presence of cystoid macular edema, visual acuity of 0.5 or less and duration of the venous occlusion for more than 6 months. The technique of treatment included direct photocoagulation of certain microaneurysms and of collateral dilatations exhibiting fluorescein leakage in the macular area, followed by grid photocoagulation applied to the area of cystoid edema. No laser burn was placed within 300 microns of the center of the macula. The patients were followed for periods of 6 to 24 months with a mean follow-up of 15 months. Forty-five eyes presented with a branch vein occlusion. Photocoagulation resulted in the decrease or disappearance of macular edema in 42 of these eyes (93%) and the improvement of visual acuity by 0.2 or more in 12 (27%). Twenty-three eyes presented central vein occlusion. In these cases, photocoagulation resulted in the decrease or disappearance of macular edema in 20 eyes (87%), and visual acuity improved by 0.2 or more in 4 (17%). These results indicate that grid laser photocoagulation is an effective method, reducing persistent cystoid macular edema due to venous occlusion. However, visual results were better in the branch vein occlusions than in the central vein occlusions.

Aged↗
PubMed1988

Pattern of fluid accumulation in NO2-induced pulmonary edema in dogs. A morphometric study.

To ascertain whether the pattern of fluid accumulation could be altered by an agent introduced through the airways, the authors studied the physiology and morphology of 11 dogs exposed to 150-494 ppm.hr NO2 and compared them with 3 new and 5 previously reported control dogs. NO2 caused a partly reversible decrease in systemic arterial pressure and cardiac output, a fall in arterial PO2, and rapid shallow breathing, while pulmonary arterial and wedge pressures remained normal. Post mortem, lower (LL) and middle (ML) lobes were frozen, sections fixed for light microscopy by freeze-substitution, and wet weight/dry weight (W/D) ratios were measured. Alveolar edema was graded, and the distribution of interstitial edema around arteries and veins and within bronchovascular bundles was studied with morphometry: edema ratios (ER) were calculated as area of interstitium/area of vessel or airway. We found that NO2 produced an exposure-dependent increase in lung water (r = 0.73), and that both LL and ML had similar W/D ratios (7.77 and 8.39, respectively) and percent alveolar edema (30% and 34%). Morphometry of interstitial edema showed that the ER for vessels and airways of edematous LL were essentially similar to controls, while those of the ML were markedly increased. It is concluded that NO2 produces exposure-related lung edema and preferential alveolar flooding with probable secondary interstitial accumulation. The discrepancies in interstitial edema between middle and lower lobes may be due to differences in lung volume or in ventilation.

Animals↗
PubMed1986

Pharmacological investigations of the new antiinflammatory agent 2-(10,11-dihydro-10-oxodibenzo[b,f]thiepin-2-yl)propionic acid. 1st communication: inhibitory effects of rat paw edema.

In the development process of a new nonsteroidal antiinflammatory drug (NSAID) with less toxicity and side-effects, 2-(10,11-dihydro-10-oxodibenzo[b,f]thiepein-2-yl) propionic acid (CN-100) was chosen as the most excellent NSAID from synthetic tricyclic compounds after screening test. For the series of studies on antiinflammatory effects of this compound in detail, its effect on rat paw edema induced by various phlogists was first investigated. The inhibitory effect of CN-100 on carrageenin-induced edema was remarkable and nearly equal to that of indometacin. The effect was not affected by continuous administration for 2 weeks or adrenalectomy. Similarly to indometacin, CN-100 had no significant effect on yeast-induced edema mediated by 5-hydroxytryptamine and concanavalin-A-induced edema unrelated with prostaglandins. However, CN-100 displayed a weaker inhibitory effect on nystatin-induced edema than indometacin, suggesting that CN-100 has a low membrane stabilizing action and a strong blocking action on synthesis of prostaglandins. CN-100 inhibited the sustained edema induced by mustard, but the drug did not interfere with the increase in body weight of rats. Indometacin in the same dose caused decrease in body weight and death. The toxicity of CN-100 was definitely less than that of indometacin, although both drugs were similar in antiinflammatory activity and mode of action on rat paw edema. Results suggest that CN-100 is an effective drug on not only acute but also subacute and chronic inflammation.

Adrenalectomy↗
PubMed1974

Experimental edema disease of swine (E. coli enterotoxemia). 3. Pathology and pathogenesis.

Experimental colibacillary (Escherichia coli) enterotoxemia as described in this report mimics natural edema disease both clinically and in gross pathology. The histopathology is characterized by accumulations of non-inflammatory edema and by arteriopathy. The smaller arterial and arteriolar changes recorded here are similar to those described in natural edema disease. The vascular changes described in recovered cases of experimental colibacillary enterotoxemia concur with those reported in so-called subacute and chronic edema disease. The arteriolar changes that occur in colibacillary enterotoxemia of swine are comparable to those associated with hypertension. Thin sections of cerebral cortex from four pigs with acute experimental edema disease were examined by electron microscopy in an attempt to demonstrate brain edema. Sections from one pig taken during the convulsive phase of disease revealed dilatation of perivascular glial processes. However, examination of sections taken from three other pigs during an earlier phase of the neurological disturbance revealed no significant lesions. We were unable to ascertain the role of brain edema in the pathogenesis of the nervous system disturbance in these experiments.

Animals↗
PubMed1984

[Post-traumatic cerebral edema. Physiopathology and treatment].

Severe head injury often produces complex intracranial displacements of the brain, resulting in widespread, often microscopic lesions. These are responsible for two types of edema: vasogenic edema, with outflow of molecules and fluid into the extracellular spaces by rupture of the blood-brain barrier and vasoplegia, and cytotoxic edema, with swelling of astrocytes due to membrane lesions. The connexions between these two types of edema are still obscure. Alterations in membrane phospholipids may impede function of Na-K pump enzymes, causing accumulation of water in the cell. Cerebral edema is responsible for intracranial hypertension and tentorial herniation, which in turn increase edema through venous compression, ischemia, and hypoxia. The least controversial anti-edema therapeutic measures include relative fluid and salt restriction, mannitol if called for, neuroplegia, in particular with diazepam and Gamma-OH, and assisted ventilation.

Alfaxalone Alfadolone Mixture↗
PubMed1984

Distribution of fluid in bronchovascular bundles with permeability lung edema induced by alpha-naphthylthiourea in dogs. A morphometric study.

We utilized light microscopic morphometry to examine the distribution of fluid in bronchovascular bundles of different sizes. Permeability edema was induced in 10 anesthetized dogs with 27 mg/kg of alpha-naphthylthiourea. Eight dogs served as controls. After moderately severe edema, diagnosed on chest radiographs and with decreasing arterial pO2, lobes were fixed with glutaraldehyde and formaldehyde or by freeze substitution. Postmortem wet weight to dry weight ratios were 7.82 +/- 0.62 (mean +/- SE) in the edematous lungs and 4.38 +/- 0.25 in the controls. Bronchovascular bundles were photographed and grouped as follows: bundles composed of separated arteries and bronchioles, bundles with connected arteries and bronchioles, and bundles with connected arteries and bronchi. The transparencies were projected on a tablet interfaced to a computer and the following areas were determined: T, the total bundle area; V, the vessel (artery) area; B, the airway (bronchiole or bronchus) area; A1, the tight periarterial adventitial sheath area; A2, the loose periarterial interstitial area; and A3, the bronchiolar/bronchial interstitial area. In addition, edema ratios for arteries (A2/V) and airways (A3/B) were calculated. We found that (a) A1 was very small and did not change with edema; (b) A2 in all bundles increased 10-fold with edema (p less than 0.01), whereas A3 increased 2- to 3-fold; (c) A2/V increased 9- to 15-fold in the edematous bundles (p less than 0.01) and (d) A3/B did not change in separated bundles (p greater than 0.05) but was approximately double after edema in the connected bundles with bronchioles and bronchi (p less than 0.01). We conclude that edema in bronchovascular bundles accumulates preferentially in the loose periarterial interstitium and does not appear to accumulate around smaller bronchioles. These data may be explained by anatomical factors and by gradients of interstitial pressure.

Animals↗
PubMed1984

Permeability pulmonary edema caused by venous air embolism.

A 22-yr-old man developed severe pulmonary edema after blowing air into tubing connected to a catheter inserted in a vein in his forearm. Pulmonary edema was rapid in onset, peaking in intensity about 12 h after the air had been insufflated. The patient's edema fluid to plasma protein concentration ratio of 0.79 showed that the edema fluid was rich in protein. Vascular pressures were normal except for mild pulmonary arterial hypertension and systemic hypotension. The patient's clinical course, edema fluid protein concentration, and vascular pressures were characteristic of an increased microvascular permeability type of pulmonary edema. The patient recovered fully within 48 h of the air infusion. His response to venous air embolism was similar to findings in an experimental model of pulmonary edema in sheep infused with venous air emboli. As long as air is not infused continuously for long periods or in very large amounts, this disorder is probably self-limiting, and supportive care may be the only treatment necessary.

Adult↗