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

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

Measurement of intestinal edema using an impedance analyzer circuit

BACKGROUND: Acute intestinal edema adversely affects intestinal transit, permeability, and contractility. Current resuscitation modalities, while effective, are associated with development of acute intestinal edema. Knowledge of levels of tissue edema would allow clinicians to monitor intestinal tissue water and may help prevent the detrimental effects of edema. However, there is no simple method to measure intestinal tissue water without biopsy. We sought to develop a tissue impedance analyzer to measure tissue edema, without the need for invasive biopsy. METHODS: Oscillating voltage input was applied to the analyzer circuit and an oscilloscope measured the voltage output across any load. Rats were randomized to three groups: sham, mild edema (80 mL/kg of NS resuscitation), and severe edema (80 mL/kg of NS resuscitation with intestinal venous hypertension). Intestinal edema was measured by wet-to-dry tissue weight ratio. Bowel impedance was measured and converted to capacitance using a standard curve. RESULTS: Acute intestinal edema causes a significant increase in bowel capacitance. This capacitance can be used to predict tissue water concentration. CONCLUSION: Using an impedance analyzer circuit, it is possible to measure intestinal edema reliably and quickly. This may prove to be a useful tool in the resuscitation of critically ill patients.     

Pathophysiological and pathochemical aspects of cerebral edema

Conclusions and summary Cerebral edema is an increase in brain water content causing expansion of cerebral tissue volume. There are two different entities of cerebral edema occurring alone or together. Formation of vasogenic brain edema requires breakdown of the blood-brain barrier, while cytotoxic edema forms by alterations of the permeability of cell membranes, and/or disturbances of active, energy-dependent transport. In primaryvasogenic edema, a secondary cytotoxic component is always observed, while conversely, secondary vasogenic edema is usually not found in primarycytotoxic edema. Ischemic brain edema may be an exception.The mechanism of barrier breakdown in vasogenic edema is still open to debate. Patency of endothelial junctions has rarely been found, whereas enhanced formation of endothelial vesicles is frequently encountered. The problem remains that the direction of vesicular transport in those conditions has not been worked out clearly enough. Nevertheless, this point merits particular efforts because vesicular transport may serve as a target for more effective methods of edema treatment.Investigations to improve the understanding of the role of brain edema factors in edema formation and persistence are in line with this argument. Release of glutamate from damaged cells into the extracellular compartment and activation of the plasma kininogen-kinin system in vasogenic edema are particularly attractive models among the many candidates singled out for investigation. Progress in the brain edema problem can also be expected when the mechanism of glial and nerve cell swelling is better understood.Studies on resolution of vasogenic edema provided insight into the problem of how brain tissue manages to regain control over its extracellular environment. Cellular uptake, retrograde pinocytosis, and probably most important, drainage into the CSF system are the current concepts. Although swelling of nerve and glial cells, myelin splitting, pollution of the extracellular space by an abnormal fluid can be considered to interfere with normal brain function, brain edema is above all a space-occupying process causing rise of intracranial pressure, eventually leading to reduction of cerebral blood flow, and distortion and herniation of vital parts of the brain. Both cerebral ischemia and brain tissue herniation may finally determine whether a patient will survive this condition. It is therefore not surprising that the most powerful methods of brain edema treatment, as for example hypertonic solutions, do not specifically affect the edema proper, but rather the rise in intracranial pressure. We should become aware that, apart from corticosteroids, most of the therapeutic methods currently in use have not been shown to interfere with specific aspects of brain edema, such as permeability of the blood-brain barrier, primary or secondary swelling of cells, edema factors, or resolution of edema. We may be confident, however, that an increased understanding of such aspects will ultimately benefit edema treatment.The technical and secretarial help of Hedwig Kuschke, Beate Komarek and Mechthild Stein is gratefully acknowledged.Dedicated to Professor Anthonie Van Harreveld on the occasion of his 75th birthday.     

Assessment of edema volume in skin upon injury in a mouse ear model with optical coherence tomography

Accurate measurement of edema volume is essential for the investigation of tissue response and recovery following a traumatic injury. The measurements must be noninvasive and repetitive over time so as to monitor tissue response throughout the healing process. Such techniques are particularly necessary for the evaluation of therapeutics that are currently in development to suppress or prevent edema formation. In this study, we propose to use optical coherence tomography (OCT) technique to image and quantify edema in a mouse ear model where the injury is induced by a superficial-thickness burn. Extraction of edema volume is achieved by an attenuation compensation algorithm performed on the three-dimensional OCT images, followed by two segmentation procedures. In addition to edema volume, the segmentation method also enables accurate thickness mapping of edematous tissue, which is an important characteristic of the external symptoms of edema. To the best of our knowledge, this is the first method for noninvasively measuring absolute edema volume.     

Effect of heparin on edema after second- and third-degree burns

Heparin has been reported to decrease wound edema as well as improve the clearance of excess fluid after thermal injury. No quantitative data on burn edema are available to support these statements. We studied the effect of heparin in therapeutic doses on edema formation and resorption in the sheep hind limb after deep second (85°C)- or third (95°C)-degree burns. Heparin was given as a continuous infusion for 24 hr to increase clotting time 2.5-fold. We used dichromatic absorptiometry, a noninvasive, sensitive method for measuring tissue fluid, to quantitate edema. We found that heparin did not decrease the quantity of edema produced after a second-degree burn or increase the rate of resorption. In a variable third-degree burn, heparin treatment resulted in a significant increase in tissue edema (P < 0.005). Clearance of edema was markedly decreased after a third-degree burn as compared to second degree. Heparin did not improve this process.     

Peritumoral brain edema associated with meningiomas

Although generally benign, meningiomas may be associated with extensive peritumoral brain edema, as visualized on computed tomographic (CT) scans. An analysis of 38 meningiomas indicated that severity of edema on CT scans positively correlated with tumor size and also with evidence of disruption of the cortical layer, which initially separates the tumor from the white matter, in which edema tends to accumulate. The various histological subtypes also seemed to be distinct in their tendency to induce edema, with the transitional and meningotheliomatous subtypes associated with the more severe grades of edema. There was no correlation between grade of edema and location of the tumor. Contact of the edematous area or the tumor itself with the ventricle, which is relevant to the possibility of drainage of edema fluid into the ventricle, seemed to occur in cases of the more severe grades of edema rather than in cases showing slight or no edema.     

Cerebral edema associated with meningiomas

The cerebral edema, as judged by computed tomographic scan, associated with supratentorial meningiomas was assessed in 55 cases. No relationship to the occurrence or the degree of edema could be established with respect to meningioma location, histological type, tumor vascularity, cellularity, number of mitotic figures, necrosis, calcification, or cortical invasion. The larger the meningioma, the more likely the presence of and the severity of cerebral edema. The edema is a significant factor in the occurrence of clinical signs and symptoms. A biopsy of cerebral cortex and white matter underlying a transitional meningioma in a patient with associated cerebral edema demonstrated perivascular astrocytic end-feet swelling in the cortex and considerable extracellular fluid in the white matter. The ultrastructural appearance is similar to that seen with primary and metastatic brain tumors and with experimental vasogenic cerebral edema.     

Edema after intracerebral hemorrhage: correlations with coagulation parameters and treatment

OBJECT: Development of edema is known to contribute to poor outcome after spontaneous intracerebral hemorrhage (ICH). Recent research has identified thrombin as a key mediator in the development of edema in animal models; however, little has been published correlating the coagulation cascade and edema in humans. METHODS: In this retrospective clinical study of 80 patients with spontaneous supratentorial ICH, the authors sought to identify factors associated with edema development and outcome, including lesion imaging parameters, anticoagulant use, international normalized ratio and platelet count on hospital admission, and treatment with mannitol and steroid medications. A multivariate model was used to identify edema volume, use of mannitol, elevated blood glucose, and the presence of intraventricular hemorrhage as predictors of poor outcome at the time patients were discharged from the hospital. The authors developed a quadratic model for predicting edema volume against time by using a random coefficients model, and found that edema peaks between Days 5 and 6 after onset of ICH. The volume of the hemorrhage and the platelet count correlated significantly with edema volume within the first 24 hours post-ICH in the multiple regression analysis (p < 0.0001, r2 = 0.75). Edema growth during the first 5 days post-ICH also correlated with the platelet count, with an increasing platelet count associated with an increasing growth of edema (p = 0.0013). CONCLUSIONS: The authors propose that factors released from activated platelets at the site of hemorrhage, for example vascular endothelial growth factor, may interact with thrombin to increase vascular permeability and contribute to the development of edema.     

磁疗对兔脑水肿影响的研究

报道将兔背部制造Ⅱ°烫伤的创伤后,大剂量快速补入不含盐的糖水,造成稀释性低钠、脑水肿动物模型。在不同时期,分别用磁疗与不用磁疗,对照观察磁疗对稀释性低钠、脑水肿的产生与治疗影响。结果发现旋磁场可减轻兔脑水肿的程度,有利于脑水肿的治疗而提高治疗效果。     

Delayed resolution of high-pressure pulmonary edema or capillary leak

Both clinical and experimental evidence suggest that the time course of edema formation is different from that of edema resolution. To better describe and quantify this difference, we followed the accumulation of high-pressure pulmonary edema in live dogs with the thermal-green dye (TGD) double-indicator technique at steady-state levels of lung liquid. We raised left atrial pressure (PLa) in steps of 5 to 10 mm Hg as high as 25 mm Hg and followed edema to steady-state levels. Lung water was then measured as PLa was lowered to initial values. By plotting steady-state edema against PLa, pressure-volume relationships were constructed. There was little change in edema until PLa reached approximately 15 mm Hg, at which point further changes in PLa were associated with large increases in lung liquid. At PLa = 25 mm/kg, the average lung water had increased by 10 ml/kg. In each animal there was slow resolution of edema with decreases in PLa from its peak back to its initial value, but in no animal was edema fully reabsorbed even though PLa was maintained at about 5 mm Hg for as long as 10 hours. Several possible explanations account for these observations. Water could be trapped in alveolar and central interstitial spaces. In addition, vessel closure in edematous lung units could further influence water reabsorption. These observations raise the possibility that pulmonary edema in the presence of normal filling pressures may represent resolution of a transient high-pressure edema as opposed to a capillary leak syndrome.     

The role of the coagulation cascade in brain edema formation after intracerebral hemorrhage

Summary The coagulation cascade has a potential role in brain edema formation due to intracerebral hemorrhage. In this study blood and other solutions were injected stereotactically into the right basal ganglia in rats. Twenty-four hours following injection, brain water and ion contents were measured to determine the amount of brain edema. Intracerebral blood resulted in an increase in brain water content. The amount of brain edema surrounding the intracerebral hematoma was reduced by a thrombin inhibitor Na-(2-Naphthalenesulfonylglycyl)-4-amidino-DL-phenylalaninepiperidide, (-NAPAP) infused into the hematoma after the clot had been allowed to solidify. The inhibitor did not alter the actual size of the clot mass. An artificial clot composed of fibrinogen, thrombin, and styrene microspheres also produced brain edema. A fibrin clot led to edema formation even in the absence of mass effect provided by the microspheres. The single component responsible for production of brain edema in all these models was thrombin. The edema was formed in response to a fibrinogen-independent pathway. These results indicate that the coagulation cascade is involved in brain edema that develops adjacent to an intracerebral hematoma.     

Severe cerebral edema in a patient with anasarca and hypernatremia.

We describe a woman whose fatal post-liver transplantation cerebral edema was unexpected and of unusual pathogenesis. Her severe cerebral edema is of considerable pathophysiologic interest: 1) it developed in the setting of marked anasarca and persistent hypernatremia, and 2) although hepatic function was poor, it was not considered sufficiently deranged to induce cerebral edema. Furthermore, there was no histologic evidence of hepatic rejection or antemortem hepatic necrosis. We postulate that an impairment of the blood brain barrier in association with a degree of hepatic dysfunction insufficient by itself to cause cerebral edema permitted the brain interstitial fluid volume to increase pari passu with ECF expansion. Cytotoxic cerebral edema and vascular engorgement may also have contributed to a life-threatening increase in intracranial pressure.     

伴上肢局部水肿的颈椎病与颈椎减压术的关系

[目的]探讨伴有上肢局部水肿的颈椎病患者的发病机理和与手术颈椎减压的关系。[方法]总结分析4a来收治的10例伴有上肢局部水肿的颈椎病人，其中脊髓型颈椎病7例，神经根型颈椎病2例，后纵韧带骨化型1例，7例行前路椎体次全切减压植骨内固定，1例行前路椎体次全切＋单间隙间盘摘除植骨内固定，2例行后路减压植骨内固定，术后观察患者水肿消退情况。[结果]10例病人上肢局部水肿不同程度消退，前路手术者较后路手术者消退快。[结论]颈椎病患者上肢水肿的发生与颈交感神经受激惹有关，通过前路或后路颈椎管减压，去除颈椎不稳、椎间盘突出、骨赘等交感神经受激惹因素，水肿可逐步消退。     

Pulmonary Edema in Patients After Liver Transplantation

The aim of this study is to determine the incidence of radiological pulmonary edema in elective liver transplant recipients and its relationship to perioperative factors and postoperative course. We reviewed 102 chest radiographs from 34 patients who had undergone orthotopic liver transplantation (OLT). Films were assessed by 2 trained radiologists for evidence of pulmonary edema using a standardized system. Clinical and outcome data from the 34 patients were also recorded. There was a high incidence (47%) of postoperative radiological pulmonary edema that was associated with deterioration in gaseous exchange, elevated pulmonary artery pressure, and increased duration of ventilator dependence and intensive care stay. Eighteen percent of the patients developed edema immediately after surgery, which was associated with greater pulmonary artery pressure and transfusion requirements during surgery. An additional 29% developed edema during the next 16 to 20 hours, but there was no association with fluid replacement. We conclude that pulmonary edema is common after OLT and will influence postoperative recovery in a substantial proportion of transplant recipients. Excess perioperative fluid replacement is unlikely to be the sole mechanism of edema in these patients. (Liver Transpl 2000;6:466-470.)     

Increase in glutamate as a sensitive indicator of extracellular matrix integrity in peritumoral edema: a 3.0-tesla proton magnetic resonance spectroscopy study

OBJECT: The authors of previous studies based on diffusion tensor imaging have indicated that there are two types of peritumoral edema-namely, edema with preserved structural integrity of the glial matrix and edema with compromised glial matrix. The authors of this study hypothesized that functionality of the glutamate (Glu)-glutamine shuttle, a vital neuron-glia interaction, may be differentially affected by peritumoral edema. They tested this hypothesis using proton magnetic resonance (MR) spectroscopy on a 3.0-tesla system that is capable of quantifying Glu without need of editing. METHODS: Twenty-three patients, each with a single brain tumor mass and peritumoral edema (nine high-grade gliomas, eight metastatic brain tumors, and six meningiomas), and nine healthy individuals participated in this study. Single-voxel proton MR imaging targeting the region of peritumoral edema was performed using a 3.0-tesla system. Glutamate levels in the peritumoral edema of nonglial tumors was significantly elevated (p < 0.01) compared with edema associated with glial tumors or normal white matter. The finding confirmed that peritumoral edema in nonglial tumors is distinct from that of glial tumors, as previously indicated in diffusion tensor imaging studies. The authors hypothesized that the former condition represents a compensatory increase in activities of the Glu-glutamine shuttle brought about by simple expansion of the extracellular space due to edema. CONCLUSIONS: The assessment of Glu concentrations in peritumoral edema using 3.0-tesla proton MR spectroscopy may be developed into an objective index of the structural integrity of the glial matrix.     

Edema: a silent but important factor

Edema is a normal response to injury. Even the smallest injury is associated with some inflammation, and initial edema is part of the normal inflammatory process. However, edema becomes a concern when it persists beyond the inflammatory phase. Once we have progressed into the rebuilding, or fibroplastic phase of healing, edema will delay healing and contribute to complications such as pain and stiffness. Early prevention and management to prevent this progression are therefore critical. This article discusses edema in relation to stages of healing and presents the research behind techniques available to the clinician to manage localized extracellular upper extremity edema in the patient with an intact lymphatic system.     

Breast edema in patients undergoing breast-conserving treatment for breast cancer: assessment via high frequency ultrasound

To identify factors that can influence breast edema in women undergoing breast-conserving therapy. Breast edema was assessed clinically and via high frequency ultrasound (HFUS) prior to, during and following radiotherapy. Fifty-four women were assessed. Breast edema was present prior to radiotherapy in patients who had undergone level 2 node dissection or had wound infection after sentinel node dissection. Edema increased during and after radiotherapy and peaked at 4-6 months. The time course of breast edema was related to the extent of nodal dissection, postoperative wound infection and regional radiotherapy. HFUS prior to irradiation was found to be no better than clinical assessment in predicting prolonged parenchymal breast edema but was significantly better at the end of irradiation. Breast edema levels are minimal in patients who do not undergo axillary node dissection or have an uncomplicated sentinel node dissection. Most edema is due to compromise of the draining lymphatics, which relates largely to the extent of axillary node dissection. HFUS appears to be a useful in the research setting in quantifying the effect of techniques that aim to reduce complications such as edema.     

Unilateral pulmonary edema following acute subglottic edema

Presented here is a case of unilateral pulmonary edema following acute subglottic edema after removal of an endotracheal tube. A 3-year-old boy, diagnosed as having nondiphtheric croup and pectus excavatum deformity, was scheduled for repair of a cleft lip. No complication occurred during the operation. After removal of the endotracheal tube, he showed dyspnea and cyanosis and was later found to have acute subglottic edema. After reintubation of the trachea, frothy pink fluid was discharged from the tube, and chest roentgenogram showed a right-sided alveolar infiltrate. Many factors may cause unilateral pulmonary edema, but it is suggested that acute subglottic edema and unilateral bronchial fragility strongly affected this episode.     

Aquaporin-4 and traumatic brain edema

Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist： ＂vasogenic＂ and ＂cytotoxic/cellular＂. However, the cellular and molecular mechanisms contributing to the development/resolution of traumatic brain edema are poorly understood and no effective drugs can be used now. Aquaporin-4 （AQP4） is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments,including cerebrospinal fluid and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 has been proposed as a novel drug target in brain edema. These findings suggest that modulation of AQP4 expression or function may be beneficial in traumatic brain edema.     

Correlation of tumor plasminogen activator with peritumoral cerebral edema. A CT and biochemical study

Extracts from 15 human cerebral tumors were tested by a fibrin-plate plasminogen-dependent assay for levels of tumor plasminogen activator (TPA) activity. The TPA activity was correlated with the amount of perineoplastic edema as quantified on computerized tomography (CT) brain scanning. Analysis of the results showed a correlation coefficient of 0.72 when all tumors were included. Analysis of the nine tumors with the highest TPA levels showed a correlation coefficient of 0.96. One metastatic tumor had the highest level of TPA activity, equivalent to a pure 100-micrograms/ml solution of urokinase, and the greatest amount of cerebral edema on CT. Meningiomas generally had the next highest levels of TPA activity and edema, followed by astrocytomas of varying grades, which generally had the lowest level of TPA activity. However, three astrocytomas that had low TPA activity also had significant edema surrounding the tumor, indicating that more than one mechanism may be producing peritumoral edema. There was no correlation between tumor size and the amount of perineoplastic edema. These preliminary results suggest that TPA's may be involved in the production of perineoplastic cerebral edema and that treatment of patients with currently available plasminogen activator inhibitors may be successful in reducing peritumoral edema.