Continuous haemofiltration in the intensive care unit.
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Continuous renal replacement therapy (CRRT) was first described in 1977 for the treatment of diuretic-unresponsive fluid overload in the intensive care unit (ICU). Since that time this treatment has undergone a remarkable technical and conceptual evolution. It is now available in most tertiary ICUs around the world and has almost completely replaced intermittent haemodialysis (IHD) in some countries. Specially made machines are now available, and venovenous therapies that use blood pumps have replaced simpler techniques. Although, it remains controversial whether CRRT decreases mortality when compared with IHD, much evidence suggests that it is physiologically superior. The use of CRRT has also spurred renewed interest in the broader concept of blood purification, particularly in septic states. Experimental evidence suggests that this is a promising approach to the management of septic shock in critically ill patients. The evolution and use of CRRT is likely to continue and grow over the next decade. (+info)
Systemic complement depletion diminishes perihematomal brain edema in rats.
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BACKGROUND AND PURPOSE: The complement cascade is activated after experimental intracerebral hemorrhage (ICH). It remains unclear, however, whether depleting the complement system will improve injury resulting from ICH. This study investigated the effects of systemic complement depletion on brain edema formation after ICH. METHODS: Fifty-six pentobarbital-anesthetized Sprague-Dawley rats were used. Treatment animals were complement-depleted with cobra venom factor (CVF) (intraperitoneally). Control rats received an equal volume of saline injection (intraperitoneally). In both treatment and control rats, autologous blood (100 microL) was infused stereotaxically into the right basal ganglia. Rats were killed 2, 24, or 72 hours later for brain water, ion, and tumor necrosis factor-alpha (TNF-alpha) measurements, for Western blot analysis, and for immunohistochemical studies. Brain edema was quantitated by wet/dry weight. TNF-alpha levels were measured by enzyme-linked immunosorbent assay. Western blot analysis was applied for C9 semiquantification. Immunohistochemistry was used to detect complement C3d, C5a, C9, and myeloperoxidase. RESULTS: Perihematomal brain edema was reduced by systemic complement depletion at 24 hours (78.8+/-0.6% versus 81.5+/-0.8% in control, P:<0.01) and 72 hours (81.5+/-1.5% versus 83.6+/-0.9% in control, P:<0.05), while cerebellar water content was unaffected (78.2+/-0.3% versus 78.0+/-0. 1%). Complement depletion reduced TNF-alpha production 2 hours after ICH. Immunocytochemistry showed that complement depletion significantly reduced perihematomal C9 deposition, C3d production, and the number of C5a- and myeloperoxidase-positive cells. CONCLUSIONS: Complement depletion by CVF attenuates brain edema in ICH, indicating that complement activation plays an important role in ICH-induced brain edema. Preventing complement activation may be effective in the treatment of ICH. (+info)
Attenuation of ischemic brain edema and cerebrovascular injury after ischemic preconditioning in the rat.
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Ischemic preconditioning (IPC) induces neuroprotection to subsequent severe ischemia, but its effect on the cerebrovasculature has not been studied extensively. This study evaluated the effects of IPC on brain edema formation and endothelial cell damage that follows subsequent permanent focal cerebral ischemia in the rat. Transient (15 minute) middle cerebral artery occlusion (MCAO) was used for IPC. Three days after IPC or a sham operation, permanent MCAO was induced. Twenty-four hours after permanent MCAO, neurologic deficit, infarction volume, and water and ion content were evaluated. Six hours post-ischemia, blood-brain barrier (BBB) permeability was examined using [3H]-inulin. Water, ion contents, and BBB permeability were assessed in three zones (core, intermediate, and outer) depending on their relation to the MCA territory. Heat shock protein 70 (HSP70) was also examined as a potential marker of vascular injury. The model of IPC significantly reduced brain infarction and neurologic deficit. Compared with a sham operation, IPC also significantly attenuated brain edema formation in the intermediate (sham and IPC water contents: 5.99+/-0.65 vs. 4.99+/-0.81 g/g dry weight; P < 0.01) and outer zones (5.02+/-0.48 vs. 4.37+/-0.42 g/g dry weight; P < 0.01) of the ipsilateral hemisphere but not in the core zone. Blood-brain barrier disruption assessed by [3H]-inulin was significantly attenuated in the IPC group and the number of blood vessels that displayed HSP70 immunoreactivity was also reduced. Thus, IPC significantly attenuates ischemic brain edema formation, BBB disruption, and, as assessed by HSP70, vascular injury. Understanding the mechanisms involved in IPC may provide insight into methods for preserving cerebrovascular function during ischemia. (+info)
Does anoxia induce cell swelling in carp brains? In vivo MRI measurements in crucian carp and common carp.
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Although both common and crucian carp survived 2 h of anoxia at 18 degrees C, the response of their brains to anoxia was quite different and indicative of the fact that the crucian carp is anoxia tolerant while the common carp is not. Using in vivo T(2) and diffusion-weighted magnetic resonance imaging (MRI), we studied anoxia induced changes in brain volume, free water content (T(2)), and water homeostasis (water diffusion coefficient). The anoxic crucian carp showed no signs of brain swelling or changes in brain water homeostasis even after 24 h except for the optic lobes, where cellular edema was indicated. The entire common carp brain suffered from cellular edema, net water gain, and a volume increase (by 6.5%) that proceeded during 100 min normoxic recovery (by 10%). The common carp recovered from this insult, proving that the changes were reversible and suggesting that the oversized brain cavity allows brain swelling during energy deficiency without a resultant increase in intracranial pressure and global ischemia. It is tempting to suggest that this is a function of the large brain cavity seen in many ectothermic vertebrates. (+info)
Diffusion-weighted imaging patterns of brain damage associated with cerebral venous thrombosis.
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BACKGROUND AND PURPOSE: Apart from cases studies, little is known regarding diffusion-weighted imaging of brain lesions associated with human cerebral venous thrombosis (CVT). Our aim was to describe the initial diffusion-weighted imaging patterns observed in brain areas with MR signal changes associated with CVT and to compare them with those of follow-up imaging. METHODS: The cases of nine patients with brain lesions associated with CVT who underwent CT and diffusion-weighted imaging 3 hours to 4 days after sudden neurologic onset were retrospectively reviewed. The apparent diffusion coefficient (ADC) in abnormal brain was compared with that of contralateral normal regions using z score analysis. MR images obtained during 3 to 6 months of follow-up were available for seven patients. RESULTS: All patients had nonhemorrhagic T2-hyperintense brain regions. These were associated with partially hemorrhagic areas on the CT scans of four patients. In nonhemorrhagic edematous areas, ADC was heterogeneous (coexistence of increased, normal, or decreased ADC) in five patients and homogeneous in four. In the latter four patients, ADC values were within normal range in three, whereas a large homogeneous hyperintensity with decreased ADC values (0.3-0.4 10(-3)mm2/s, <-3 z scores) was observed in one. When available, follow-up images always showed hemorrhagic sequelae in initially hemorrhagic areas. Nonhemorrhagic edematous areas with initially increased ADC values returned to normal. Initially normal or decreased ADC values were predictive of reversibility, although imaging sequelae were rarely observed. CONCLUSION: The diffusion-weighted imaging/ADC pattern of venous stroke is more heterogeneous than previously thought. Large brain regions of reduced ADC values that are not predictive of ultimate infarction in cases of CVT can be observed. (+info)
Sonographic monitoring of midline shift in space-occupying stroke: an early outcome predictor.
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BACKGROUND AND PURPOSE: Transcranial color-coded duplex sonography (TCCS) allows bedside imaging of intracranial hemodynamics and parenchymal structures. It provides reliable information regarding midline shift (MLS) in space-occupying hemispheric stroke. We studied the value of MLS measurement to predict fatal outcome at different time points after stroke onset. METHODS: Forty-two patients with acute, severe hemispheric stroke were enrolled. Cranial computed tomography (CCT) and extracranial duplex sonography were performed on admission. TCCS was carried out 8+/-3, 16+/-3, 24+/-3, 32+/-3, and 40+/-3 hours after stroke onset. Lesion size was determined from follow-up CCT. RESULTS: Twelve patients died as the result of cerebral herniation (group 1); 28 survived (group 2). Two patients received decompressive hemicraniectomy and were therefore excluded from further evaluation. MLS was significantly higher in group 1 as early as 16 hours after onset of stroke. Specificity and positive predictive values for death caused by cerebral herniation of MLS >/=2.5, 3.5, 4.0, and 5.0 mm after 16, 24, 32, and 40 hours were 1.0. CONCLUSIONS: TCCS helps to estimate outcome as early as 16 hours after stroke onset and thus facilitates identification of patients who are unlikely to survive without decompressive craniectomy. Because of its noninvasive character and bedside suitability, sonographic monitoring of MLS might be a useful tool in management of critically ill patients who cannot undergo repeated CCT scans. (+info)
Human albumin therapy of acute ischemic stroke: marked neuroprotective efficacy at moderate doses and with a broad therapeutic window.
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BACKGROUND AND PURPOSE: We examined the neuroprotective efficacy of moderate-dose human albumin therapy in acute focal ischemic stroke and defined the therapeutic window after stroke onset, within which this therapy would confer neurobehavioral and histopathological neuroprotection. METHODS: Sprague-Dawley rats were anesthetized with halothane/nitrous oxide and received 2-hour middle cerebral artery occlusion (MCAo) by a poly-L-lysine-coated intraluminal suture. Neurological status was evaluated during occlusion (60 minutes) and daily for 3 days after MCAo. In the dose-response study, human albumin doses of either of 0.63 or 1.25 g/kg or saline vehicle (5 mL/kg) were given intravenously immediately after suture removal. In the therapeutic window study, a human albumin dose of 1.25 g/kg was administered intravenously at 2 hours, 3 hours, 4 hours, or 5 hours after onset of MCAo. Three days after MCAo, brains were perfusion-fixed, and infarct volumes and brain swelling were determined. RESULTS: Moderate-dose albumin therapy significantly improved the neurological score at 24 hours, 48 hours, and 72 hours and significantly reduced total infarct volume (by 67% and 58%, respectively, at the 1.25- and 0.63-g/kg doses). Cortical and striatal infarct volumes were also significantly reduced by both doses. Brain swelling was virtually eliminated by albumin treatment. Even when albumin therapy (1.25 g/kg) was initiated as late as 4 hours after onset of MCAo, it improved the neurological score and markedly reduced infarct volumes in cortex (by 68%), subcortical regions (by 52%), and total infarct (by 61%). CONCLUSIONS: Moderate-dose albumin therapy markedly improves neurological function and reduces infarction volume and brain swelling, even when treatment is delayed up to 4 hours after onset of ischemia. (+info)
Apparent diffusion coefficients in the evaluation of high-grade cerebral gliomas.
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BACKGROUND AND PURPOSE: Preliminary data indicate that apparent diffusion coefficient (ADC) values may be useful in identifying and grading primary cerebral tumors. We tested the hypothesis that ADC values can be used to differentiate tumor, edema, and normal brain tissue. METHODS: Fifteen patients with high-grade cerebral astrocytomas underwent conventional MR imaging, diffusion-weighted MR imaging, and proton MR spectroscopy. We defined tumor as an area containing the highest choline/creatine and choline/N-actetyl aspartate ratios, contrast enhancement, and abnormal T2 signal intensity. Edema was defined as tissue with normal proton MR spectra, no enhancement, and high T2 signal intensity. Normal brain was assumed if tissue had normal proton MR spectra, no enhancement, and normal T2 signal intensity in the hemispheres ipsilateral or contralateral to tumor. ADC maps were calculated and regions of interest were manually placed over areas of tumor, edema, and normal tissue. Comparisons were made by analysis of variance. For post hoc testing, the Tukey method was used to correct for the effect of multiple comparisons, and significance was accepted if P was less than .05. RESULTS: When ADC values were analyzed as a group, significant differences were found between tumor (131 + 45) and normal brain tissue (ipsilateral to tumor, 92 + 22; contralateral to tumor, 78 + 5) but not between tumor and adjacent edema (129 + 45). A plot of individual data points showed considerable overlapping among the three types of tissue sampled. CONCLUSION: As a group, ADC values helped to distinguish high-grade glioma from normal tissue but could not be used to separate high-grade glioma from surrounding edema. Individually, ADC values overlapped considerably and were not useful in our patients. The utility of ADC values (as obtained in this relatively small study) is questionable in patients with high-grade cerebral astrocytomas. (+info)