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Patterns of diabetic macular edema with optical coherence tomography.

PURPOSE: We report cross-sectional images of diabetic macular edema and correlation between tomographic features and visual acuity with best correction by means of optical coherence tomography. METHOD: In a prospective study, optical coherence tomography was performed in 59 eyes of 42 patients with diabetic macular edema and in 10 eyes of 10 normal control subjects. RESULTS: Optical coherence tomography showed three patterns of structural changes in diabetic macular edema: sponge-like retinal swelling (52 [88%] of 59 eyes), cystoid macular edema (28 [47%] of 59 eyes), and serous retinal detachment (9 [15%] of 59 eyes). Some eyes had more than one pathologic change. Retinal swelling was more pronounced in the outer rather than the inner retinal layers. Cystoid macular edema was located mainly in the outer retinal layers. In eyes with long-standing cystoid macular edema, cystoid spaces had fused, resulting in a large cystoid cavity involving almost the entire retinal layer. Hard exudates were seen as highly reflective areas located in the outer retinal layers. The retinal thickness at the central fovea and the visual acuity with best correction showed an intermediate negative correlation in eyes without cystoid macular edema (correlation coefficient: -0.61, P < .01). CONCLUSIONS: Diabetic macular edema involved three structural changes, including sponge-like retinal swelling (88%), cystoid macular edema (47%), and serous retinal detachment (15%). Visual acuity with best correction moderately correlated with retinal thickness regardless of the different tomographic features.

Adult↗

Effect of alpha-trinositol on carrageenan-induced rat paw edema and lowering of interstitial fluid pressure.

Alpha-trinositol attenuates edema formation and capillary albumin extravasation and lowering of interstitial fluid pressure (Pif) in several acute inflammatory reactions in rat skin or trachea. The lowering of Pif is an important driving force required to explain the rapid edema formation in acute inflammatory reactions. The lowering of Pif and edema formation are attenuated by alpha-trinositol, which is suggested to act on the cellular adhesion receptor for extracellular matrix components. This would represent a novel therapeutic strategy for acute inflammation. To further clarify the mechanisms behind the anti-inflammatory effects of alpha-trinositol, the effects of pre- and post-treatment with alpha-trinositol on edema formation and lowering of Pif were studied after subdermal injection of carrageenan in the rat. The experiments measuring Pif showed that the lowering of Pif induced by carrageenan was abolished by 10 mg alpha-trinositol when administered either prior to or after injection of 5 microl 1% (w/v) lambda carrageenan in the dorsum of the paw. Edema formation after injection of lambda carrageenan (100 microl, 1.5% w/v) into the foot pad was studied in a separate series. In control animals receiving saline vehicle, the volume of the paw injected with carrageenan increased by approximately 30% after 3-4 h. The only significant effect of infusion of 20 mg kg(-1) h(-1) alpha-trinositol was a reduction of edema to approximately 20% when treatment was started 1 h before carrageenan injection. Therefore, the plasma concentration of alpha-trinositol must already be high when carrageenan is injected in order to prevent edema in the late phase. In conclusion, the present results indicate that the mechanisms involved in the lowering of Pif in the early phase of edema development are different from those responsible for the manifest edema measured 3-4 h after carrageenan.

Animals↗

Clinically significant macular edema in type I diabetes. Incidence and risk factors.

PURPOSE: To examine incidence of and risk factors for clinically significant macular edema in persons with type I diabetes. METHODS: A group of 189 persons with type I diabetes, recruited from a summer camp for children with diabetes and from practices of local physicians, were participants in a longitudinal study with annual follow-up visits which included physical and ophthalmologic examinations and color stereo fundus photographs of each eye, centered on the disc and macula. Subjects were free of proliferative retinopathy at study baseline. Ages ranged from 3 to 40 years, duration of diabetes ranged from 0 to 12 years, mean glycosylated hemoglobin (Hgb A1c) was 12.2% (range, 6.4%-21.5%), and average follow-up was 6.1 years. Presence of clinically significant macular edema was defined as in the Early Treatment Diabetic Retinopathy Study. RESULTS: In a total of 41 persons (62 eyes), clinically significant macular edema developed during study follow-up. Cumulative risk of clinically significant macular edema was 0 until 7 years' duration of diabetes. The cumulative risk of clinically significant macular edema increased linearly for each year of duration between 10 and 20 years, with an average annual increase of approximately 6.7%. Significant risk factors for clinically significant macular edema were older age at diagnosis, male sex, and higher Hgb A1c level. Systolic and diastolic blood pressure, proteinuria, body mass index, race, initial presence of retinopathy, and use of antihypertensives did not significantly affect the risk of clinically significant macular edema. CONCLUSION: Older age at diagnosis of diabetes, male sex, and higher Hgb A1c levels (poorer control of blood glycemic levels) significantly increase the risk of clinically significant macular edema in persons with type I diabetes. These data extend the evidence implicating worse glycemic control as a cause of clinically significant macular edema, even within a population with relatively loose control.

Adolescent↗

Localization of dermal edema in lipodermatosclerosis, lymphedema, and cardiac insufficiency. High-frequency ultrasound examination of intradermal echogenicity.

BACKGROUND: Chronic edema in venous insufficiency is associated with leg ulceration, whereas in lymphedema skin ulceration is less frequent and edema from cardiac failure does not cause major skin changes. The reason for these differences is unclear. OBJECTIVE: Our purpose was to investigate, by means of ultrasound, the distribution of intradermal fluid in patients with edema associated with lipodermatosclerosis, lymphedema, or cardiac insufficiency. METHODS: Sixteen patients with lipodermatosclerosis, 10 with lymphedema, 16 with leg edema from heart insufficiency, and 16 healthy control subjects were studied. Ultrasound images were obtained with a 20 MHz scanner. The echogenicity of the dermis was quantified by image analysis and the echogenicity of the upper (subepidermal) and lower portions of the dermis were measured. RESULTS: In any type of edema the dermal echogenicity was lower than that of the control group, indicating intradermal edema. In normal skin the upper dermis was only slightly less echogenic than the lower dermis. In patients with lipodermatosclerosis a low-echogenic area was present in the upper dermis, which suggests the papillary dermis as a preferential site of edema formation. In contrast, in lymphedema dermal echogenicity was uniformly distributed, whereas in patients with heart failure the lower portion of the dermis was less echogenic than the upper dermis. CONCLUSION: This study demonstrates that intradermal echogenicity shows characteristic patterns in different types of edema, which indicates that localization of fluid varies in the dermis, from subepidermal (lipodermatosclerosis), uniform (lymphedema), to deep dermal (heart failure). These differences may help in understanding the origin of different skin sequelae of edema.

Adolescent↗

Removal of dermal edema with class I and II compression stockings in patients with lipodermatosclerosis.

BACKGROUND: Lipodermatosclerosis is a sequela of deep venous insufficiency and a risk factor for the occurrence of venous leg ulceration. Medical compression stockings facilitate leg ulcer healing and prevent occurrence of ulcers resulting from removal of edema. Although the exact level of compression necessary for removal of dermal edema in patients with deep venous insufficiency has not been established, garments providing high compressive values of 30 to 40 mm Hg have been recommended. Dermal edema can be visualized by high-frequency ultrasonography. OBJECTIVE: We used ultrasound imaging to study whether a lower level of compression (class I 18 to 26 mm Hg vs class II 26 to 36 mm Hg) is effective in removal of dermal edema. This question is important because the use of hosiery with a lower compression class would enhance compliance and enable treatment of patients with mixed arteriovenous disease. METHODS: In 11 patients skin images were obtained with 20 MHz ultrasound from the malleolar region in lipodermatosclerotic skin and corresponding normal skin of the contralateral leg. The ratio of low echogenic pixel number to total pixel number (LEP/TP), which correlates with dermal water, was measured before and after 5 days of applied compression in two treatment courses where classes of compression were switched randomly. Ankle circumference was also measured. RESULTS: We found that LEP/TP was 33% higher in lipodermatosclerotic skin than in the matched normal skin indicating presence of skin edema. Application of class I and II compressive hosiery resulted in LEP/TP decrease by 17% (95% confidence interval, 0.07 to 0.26) and 14% (95% confidence interval, 0.04 to 0.21), respectively, suggestive of dermal edema reduction. No statistically significant difference in efficacy of dermal edema removal between class I and II was found. No changes in ankle circumference after application of both classes of compression was observed. CONCLUSION: Application of light and moderate compression results in a partial edema removal from the dermis in lipodermatosclerosis in the absence of measurable reduction in leg circumference. Class I compression is as effective as class II for elimination of dermal edema. These data indicate that light compression may be a useful modality for patients with deep venous insufficiency and lipodermatosclerosis who are not eligible for treatment with garments having higher compressive forces.

Adult↗

Cellular edema and alterations in metabolite content in the ischemic and reperfused canine heart following different forms of cardiac arrest.

This study investigates firstly how far cellular edema correlates with parameters of the anaerobic energy turnover independent of the method used for cardiac arrest, and secondly to what extent cellular edema developing during reversible global ischemia is reduced after reperfusion. Canine hearts were arrested 1. by aortic cross clamping (ACC), 2. by coronary perfusion with St. Thomas solution, or 3. HTK (histidine tryptophan ketoglutarate) solution (Custodiol). Samples for biochemical and structural analysis were taken at different times during ischemia and after reperfusion with Tyrode solution. Cellular edema determined morphometrically and given as volume ratio of sarcoplasm and mitochondria to myofibrils (Vvsp + V vmi/Vvmf) varies significantly in the differently arrested hearts. Reperfusion after a decrease in ATP to 4 mumol/gww (revival time) leads to a nearly complete structural recovery. The relationship between cellular edema and defined over-all metabolite tissue concentrations and extracellular pHe values shows: 1. during the decrease of creatine phosphate to 3 mumol/gww, cellular edema does not change; it is, however, significantly higher after ACC and St. Thomas than after HTK perfusion; 2. at each lactate concentration, cellular edema differs significantly depending on the form of cardiac arrest; 3. during the decrease of ATP and pHe cellular edema increases and is comparable at concentrations < 4 mumol/gww and at pHe values < 6.5 independent of the form of cardiac arrest; 4. beyond 10 mumol/gww of inorganic phosphate (Pi), increasing values for cellular edema correspond to defined Pi values in the differently arrested hearts. Thus, the ratio VVSp+ VVMi/VVMf is a powerful parameter for the determination of cellular edema during ischemia, as well as for correlations with metabolic parameters.

Animals↗

The significance of arytenoid edema following radiotherapy of laryngeal carcinoma with respect to residual and recurrent tumour.

We sometimes experience patients with persistent or progressive arytenoid edema, among which residual or recurrent cancer is often accompanied. Because it is difficult to distinguish tumour rest or recurrence from normal tissue sequelae in the early period after irradiation, it is important to know both the contributing factors for arytenoid edema, and the incidence of residual or recurrent tumours in patients with postirradiation laryngeal edema. We therefore reviewed the charts of 67 patients with early laryngeal carcinoma who had received a curative dose of irradiation in the last 5 years. Fourteen patients (20.9%) had moderate or severe laryngeal edema persisting for or developing at more than 3 months after completion of a course of definitive radiotherapy. The incidence was highest in supraglottic T2 disease, followed by glottic T2 tumour. Of the 14 patients with edema, six (42.9%) had persistent or recurrent disease. The primary disease was uncontrolled in 18 patients, 17 of whom received successful salvage surgery. In patients without residual tumours, the edema was usually moderate and resolved within a year, although four patients had chronic edema lasting more than a year after treatment. All four had supraglottic T2 lesions and received 70 Gy of X-ray. We also reviewed, for sake of comparison, the records of 38 patients treated with radiotherapy at doses of more than 40 Gy between 1975 and 1980, when endoscopic microsurgery for laryngeal cancer was introduced as a primary part of treatment. The incidence of persistent or late developed edema over the period, though not significant, was 36.8%: nearly twice that of the last 5 years. Microscopic endolaryngeal surgical procedures seem to have been a causal factor for edema in this period.

Adult↗

Bone marrow edema in the greater tuberosity of the humerus at MR imaging: association with rotator cuff tears and traumatic injury.

UNLABELLED: The purpose of this study was to determine the prevalence of bone marrow edema in the greater tuberosity of the humerus on MR imaging, the association with other findings at MR imaging and the injury mechanism which can lead to this finding. SUBJECTS AND METHODS: MR reports from 863 patients referred for shoulder MRI over 74 months were reviewed to identify patients with marrow edema in the greater tuberosity. The MR images from patients with greater tuberosity marrow edema were reviewed by consensus of two radiologists for the extent of marrow edema and for associated injuries. Marrow edema in the greater tuberosity was seen in 11 of 863 patients (1.3%). Nine patients (82%) had associated rotator cuff tear by MR imaging (four full thickness and five partial thickness), one patient had avulsion of the greater tuberosity from the humerus, and one had no rotator cuff abnormality. History of trauma was reported by eight patients including fall without direct blow to the shoulder (6), car accident (1) and direct blow to the top of the shoulder (1). Marrow edema in the greater tuberosity is an infrequent finding. Marrow edema most often is associated with a history of trauma and with rotator cuff abnormalities including full thickness tears. The history of trauma without direct blow to the shoulder and the location of the edema indicates that marrow edema often results from avulsion injury by the supraspinatus tendon.

Adult↗

Tirilazad prevention of reperfusion edema after focal ischemia in cynomolgus monkeys.

BACKGROUND: The purpose of the present investigation was to determine if post-ischemic treatment with the 21-aminosteroid lipid peroxidation inhibitor tirilazad mesylate (U-74006F) could affect reperfusion brain edema during the first 3h following a 3h period of middle cerebral artery occlusion-induced focal ischemia in cynomolgus monkeys. METHODS: Adult female cynomolgus monkeys (N = 14) were subjected under halothane anesthesia to a 3h period of middle cerebral artery occlusion, followed by 3h of reperfusion. U-74006F, 3.0 mg/kg i.v. or citrate vehicle, was administered 10 min before beginning reperfusion. Multiple spin-echo (8 echoes: TE = 26.3 msec; TR = 3.0 secs; 2.35 Tesla) magnetic resonance imaging was performed every 30 min, beginning at 1h after reperfusion. Transverse relaxation rates (T2) for the caudate, putamen, cortex, insular cortex, parietal cortex and central white matter were calculated as an index of focal brain edema. After the final images, corresponding regions were removed for determination of water content by the wet weight/dry weight method. RESULTS: The T2 measurements strongly suggested the presence of post-reperfusion edema in all gray matter, but not white matter, regions at 1h after reperfusion in vehicle-treated animals. Significant attenuation of edema development was seen in the putamen and insular cortex in U-74006F-treated animals. An effect was also observed in the parietal cortex, but none in the caudate. The measurement of water content at 3h after reperfusion yielded similar results. CONCLUSIONS: These results showing the ability of U-74006F to attenuate post-reperfusion brain edema support the concept that lipid peroxidation is a significant mediator of reperfusion brain edema after focal ischemia. The therapeutic window for U-74006F's anti-edema effect appears to be at least 3h after the onset of focal ischemia since delaying treatment until just before reperfusion largely prevented subsequent edema in cortical regions and the putamen. The effects of U-74006F on edema may play a mechanistic role in the compound's reported neuroprotective efficacy in a variety of focal ischemia models.

Animals↗

Fulminant noncardiogenic pulmonary edema in the critically ill.

The relationship between the serum colloid osmotic pressure (COPs), pulmonary artery wedge pressure (PWP), and pulmonary edema fluid colloid osmotic pressure was studied in six critically ill patients with fulminant noncardiogenic pulmonary edema. The relationship between COPs and PWP was also studied in 36 critically ill patients without pulmonary edema. The COPs-PWP gradient was normal in those patients without pulmonary edema. Three patients with noncardiogenic pulmonary edema had markedly reduced COPs-PWP gradients secondary to decreases in COPs. Their pulmonary edema fluid colloid osmotic pressure averaged 61% that of their serum colloid osmotic pressure. Three patients with noncardiogenic pulmonary edema had normal COPs-PWP gradients. Their pulmonary edema fluid colloid osmotic pressure averaged 92% that of their COPs. Noncardiogenic pulmonary edema in the critically ill patient may be caused by either a decrease of COPs-PWP gradient or an increase in capillary membrane permeability.

Adult↗

Electron microscopic study of capillary wall in human cerebral edema.

Cortical biopsies of 17 patients with diagnoses of congenital malformation, cerebral tumor or brain trauma complicated by subdural hematoma or hygroma were studied with the electron microscope; the alterations of the blood-brain barrier in moderate and severe perifocal cerebral edema were observed. Moderate edema was found associated with central nervous system malformations, while severe edema was seen accompanying brain tumors and serious head injuries. The peripheral cytoplasm of endothelial cells displayed increased formation of microvilli and clear or amorphous electron-dense vacuoles, as well as pinocytotic and coated vesicles. In severe edema, the formation of elongated or chained vacuoles forming transendothelial channels was observed. In moderate edema, endothelial junctions exhibited a tortuous pathway, with a luminal portion sealed by tight junctions and dilated, open, basal portions ending at the basement membrane. In severe edema, the zonulae accludentes partially disappeared and the endothelial junction basal segments became irregularly dilated. The basement membrane showed enlargement, rarefaction, vacuolization, and the presence of collagen fibers. Fine expansion of the basement membrane was distinguished, showing matrix loss and clear, irregularly-dilated channels. Capillaries with reduplicated basement membrane were also observed. The pericytes exhibited edema, vacuolization, and phagocytic activity. In moderate cerebral edema, the clear or dense edematous and vacuolated perivascular end-feet of astrocytes appeared closely applied to the basement membrane, while in severe cerebral edema, they were separated from the basement membrane and showed gradual disappearance of the gap junctions. In all cases, moderately or markedly dilated extracellular spaces were observed in the pericapillary neuropil.

Adolescent↗

Triamcinolone acetonide with vitrectomy for treatment of macular edema associated with branch retinal vein occlusion.

PURPOSE: To review the efficacy of a combination of triamcinolone acetonide (TA) injection and pars plana vitrectomy (PPV) for the treatment of macular edema associated with branch retinal vein occlusion (BRVO). METHODS: Seventeen eyes with macular edema associated with BRVO underwent PPV with an intraoperative injection of TA (10 mg) into the vitreous cavity. Residual or recurrent macular edema was treated with postoperative sub-Tenon capsule injections of TA (20 mg). RESULTS: With PPV and an intraoperative injection of TA, 82% of eyes showed rapid reduction of macular edema; foveal thickness decreased from 507 +/- 115 microm preoperatively to 261 +/- 123 microm 2 months after surgery (P = 0.0041). However, 59% of eyes showed recurrence of macular edema during the follow-up period. Twelve eyes with residual or recurrent macular edema received sub-Tenon capsule injections of TA; of these eyes, 9 showed substantial reduction of macular edema. Foveal thickness decreased from 381 +/- 102 microm to 256 +/- 56 microm (P = 0.0076) 2 weeks after postoperative injections of TA. At the final visit, visual acuity (logMAR) improved from 0.74 +/- 0.40 preoperatively to 0.40 +/- 0.34 (P = 0.010). CONCLUSION: An intraoperative injection of TA in combination with PPV has the potential to facilitate the absorption of macular edema associated with BRVO. In addition, residual or recurrent macular edema can be treated with additional sub-Tenon capsule injections of TA.

Aged↗

Prostatic edema in 125I permanent prostate implants: dynamical dosimetry taking volume changes into account.

The purpose of this study is to determine the impact of edema on the dose delivered to the target volume. An evaluation of the edema characteristics was first made, and then a dynamical dosimetry algorithm was developed and used to compare its results to a standard clinical (static) dosimetry. Source positions and prostate contours extracted from 66 clinical cases on images taken at different points in time (planning, implant day, post-implant evaluation) were used, via the mean interseed distance, to characterize edema [initial increase (deltar0), half-life (tau)]. An algorithm was developed to take into account the edema by summing a time series of dose-volume histograms (DVHs) with a weight based on the fraction of the dose delivered during the time interval considered. The algorithm was then used to evaluate the impact of edema on the dosimetry of permanent implants by comparing its results to those of a standard clinical dosimetry. The volumetric study yielded results as follows: the initial prostate volume increase was found to be 1.58 (ranging from 1.15 to 2.48) and the edema half-life, approximately 30 days (range: 3 to 170 days). The dosimetric differences in D90 observed between the dynamic dosimetry and the clinical one for a single case were up to 15 Gy and depended on the edema half-life and the initial volume increase. The average edema half-life, 30 days, is about 3 times longer than the previously reported 9 days. Dosimetric differences up to 10% of the prescription dose are observed, which can lead to differences in the quality assertion of an implant. The study of individual patient edema resorption with time might be necessary to extract meaningful clinical correlation or biological parameters in permanent implants.

Algorithms↗

Pulmonary edema: an MR study of permeability and hydrostatic types in animals.

Permeability pulmonary edema was induced in ten rats by intravenous injection of oleic acid. Hydrostatic pulmonary edema was induced in another ten rats by continuous infusion of saline. Permeability pulmonary edema was detected as increased signal intensity in all animals on images obtained with repetition times (TR) of 2.0 sec and echo times (TE) of 28 and 56 msec. Hydrostatic pulmonary edema was perceivable only in seven of ten rats. It was best seen on spin-echo TR = 2.0 sec, TE = 28 msec images as increased intensity either throughout the whole lung or in a predominant central distribution. The slopes of the relationships between the mean signal intensity and water content of both lungs were lower for hydrostatic pulmonary edema than for permeability pulmonary edema. Hydrostatic pulmonary edema demonstrated similar T1 but markedly shorter T2 relaxation times than permeability edema. Magnetic resonance imaging can be used to estimate severity of hydrostatic and permeability pulmonary edemas.

Animals↗

Differentiation of capillary leak and hydrostatic pulmonary edema with a macromolecular MR imaging contrast agent.

The ability of a macromolecular contrast agent (polylysine-[gadopentetate dimeglumine]40) to allow distinction of pulmonary capillary leak from hydrostatic pulmonary edema was investigated. Capillary leak edema was induced in 12 rats by means of venous injection of oleic acid; hydrostatic pulmonary edema was induced in 10 rats by means of continuous infusion of 0.9% sodium chloride. In the oleic acid pulmonary edema model, the signal intensity continued to increase for 12 minutes after administration of contrast material, indicating a leak of paramagnetic molecules from the intravascular to the extravascular spaces. Conversely, lung enhancement remained virtually constant after injection of contrast material in the hydrostatic edema model, as would be expected in the absence of endothelial damage. Hydrostatic edema tended to be distributed homogeneously throughout the lung, while capillary leak edema tended to occur predominantly in the peripheral portions of the lung. These findings indicate that macromolecular contrast agents can facilitate differentiation between edema caused by elevated intravascular pressure and edema induced by abnormal capillary permeability.

Animals↗

Can running cause the appearance of marrow edema on MR images of the foot and ankle?

PURPOSE: To determine if runners have an increased prevalence of marrow edema in the foot and ankle compared with nonrunners at magnetic resonance (MR) imaging. MATERIALS AND METHODS: Ankles and feet were imaged in 20 runners and 12 nonrunners with a fast short inversion time inversion-recovery sequence at 1.5 T. Edema within each bone was graded from 0 (no edema) to 3 (severe edema). Total scores for each subject equaled the sum of the grades. RESULTS: Reader 1 found edema in 16 of 20 runners and four of 12 nonrunners (P < .04); runners had a mean score of 4.7 and nonrunners had a mean score of 0.9 (P < .006). The average number of bones with edema was 3.4 for runners and 0.7 for nonrunners (P < .005). Reader 2 found edema in 16 of 20 runners and two of 12 nonrunners (P < .002); runners had a mean score of 4.5 and nonrunners had a mean score of 0.3 (P < .001). The average number of bones with edema was 3.6 for runners and 0.3 for nonrunners (P < .001). CONCLUSION: When the fast short inversion time inversion-recovery sequence is performed, edema seen within the marrow of runners on MR images may be due to exercise alone.

Adult↗

Intracranial meningiomas: factors that influence the development of cerebral edema after stereotactic radiosurgery and radiation therapy.

PURPOSE: To evaluate causative factors of cerebral edema after stereotactic radiosurgery or stereotactic radiation therapy in intracranial meningiomas. MATERIALS AND METHODS: Of 43 adult patients with intracranial meningiomas, three received 13.5-18-Gy single-fraction stereotactic radiosurgery; one received 19.8 Gy in three fractions, one received 42 Gy in six fractions, and 31 received 32-36 Gy in six to eight fractions of stereotactic radiation therapy; and seven received 45-54-Gy external-beam radiation with 20-28 Gy in five to seven fractions as concomitant stereotactic boosts. Brain edema was estimated by calculating the edema index. RESULTS: After irradiation, all 11 patients with parasagittal and four patients with nonparasagittal tumors developed worsening cerebral edema that necessitated the administration of steroids (P < .001). The statistically significant factors for the development of edema were parasagittal location, presence of pretreatment edema, sagittal sinus occlusion, and the use of more than 6 Gy per fraction. Five patients with parasagittal tumors developed life-threatening panhemispheric edema, which was fatal in one. The causative factors of panhemispheric edema were a large tumor, single-fraction stereotactic radiosurgery, or use of more than 6 Gy per fraction. CONCLUSION: A smaller dose per fraction and aggressive use of steroids may help prevent life-threatening complications due to worsening edema.

Brain Edema↗

Increase of lung sodium-potassium-ATPase activity during recovery from high-permeability pulmonary edema.

Previous studies have suggested that recovery from pulmonary edema may be dependent on active sodium ion transport. Most of the data supporting this concept came from work done in isolated type II cells, isolated lung preparations, or in models of alveolar flooding. There is a limited amount of information regarding the role of active sodium ion transport in vivo. Furthermore, most of this information was obtained in one model of pulmonary edema, the hyperoxic lung injury model. The purpose of these experiments was then to measure the activity of the sodium-potassium-adenosinetriphosphatase (Na(+)-K(+)-ATPase), the active component of the sodium transport process and an indirect marker of active sodium transport, during recovery from thiourea-induced pulmonary edema in rats. Na(+)-K(+)-ATPase activity was significantly increased during recovery from lung edema. This increase could not be accounted for by the Na(+)-K(+)-ATPase activity present in inflammatory cells recruited in the lung by the injury process or by a direct impact of thiourea on the enzyme. Alveolar flooding, induced by instillation of a protein-containing solution into the airways of ventilated rats also increased the activity of Na(+)-K(+)-ATPase, suggesting that activation of the enzyme is probably secondary to either the presence of edema or the physiological consequences associated with edema. The quantity of lung Na(+)-K(+)-ATPase protein was also elevated during edema resolution, indicating that augmented synthesis of this enzyme underlies the increased enzyme activity observed. The quantity of Na(+)-K(+)-ATPase protein in alveolar type II cells was also significantly enhanced during recovery from edema, suggesting that these cells contribute to active sodium transport in vivo. The results of this study suggest that active sodium transport could participate in the resolution of pulmonary edema.

Animals↗