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intracranial hemorrhages/œdème
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Dialysis-induced worsening of cerebral edema in intracranial hemorrhage: a case series and clinical perspective.
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BACKGROUND
Intracranial hemorrhage (ICH) is not an uncommon complication of end-stage renal disease (ESRD), and may be complicated by cerebral edema. Hemodialysis (HD) may induce rapid osmolar and fluid shifts, increasing brain water content with the potential to worsen cerebral edema. The dangers
Pulmonary edema following intracranial hemorrhage.
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Hemodynamic changes and samples of fluid from pulmonary edema were studied in a 50-year-old woman who developed florid pulmonary edema following intracranial hemorrhage. Marked systemic and pulmonary arterial hypertension were associated with the rapid production of edema fluid that contained red
Nonimmune hydrops and hydrocephalus secondary to fetal intracranial hemorrhage.
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Our case demonstrates that nonimmune hydrops and hydrocephalus may be associated by the common pathway of intracranial hemorrhage and the development of anemia. The anemia apparently resulted in cardiomegaly with pericardial effusion and ascites as well as marked extramedullary hematopoiesis.
Fatal cerebral edema and intracranial hemorrhage associated with hypernatremic dehydration.
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We report neuroimaging findings of intracranial hemorrhage and cerebral edema in an infant with obtundation and seizures, initially suspected to be secondary to non-accidental trauma but finally attributed to hypernatremic dehydration. Neuroimaging findings due to hypernatremic dehydration have not
Haptoglobin is associated with increased early perihematoma edema progression in spontaneous intracranial hemorrhage.
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Intracranial hemorrhage and hydrops in the fetus of a mother with thrombocytosis: implications for possible pathogenetic factors and therapy.
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We report a case of prenatally diagnosed intracranial hemorrhage and hydrops in the fetus of a mother with a past history of surgical and medical treatment for gastric lymphoma and having high platelet counts thereafter. To the best of our knowledge, such a complication of maternal thrombocythemia
Remitting seronegative symmetrical synovitis with pitting edema following acute intracranial hemorrhage.
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Remitting seronegative symmetrical synovitis with pitting edema (RS3PE) is an unusual inflammatory arthritis with unknown pathogenic mechanism, and is characterized by an acute onset of symmetrical synovitis with pitting edema of the hands or feet. Numerous diseases are associated with RS3PE,
Plasma kallikrein mediates brain hemorrhage and edema caused by tissue plasminogen activator therapy in mice after stroke.
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Thrombolytic therapy using tissue plasminogen activator (tPA) in acute stroke is associated with increased risks of cerebral hemorrhagic transformation and angioedema. Although plasma kallikrein (PKal) has been implicated in contributing to both hematoma expansion and thrombosis in stroke, its role
Tissue plasminogen activator induced delayed edema in experimental porcine intracranial hemorrhage: reduction with plasminogen activator inhibitor-1 administration.
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Hematoma puncture and subsequent clot lysis with recombinant tissue plasminogen activator (rtPA) emerged as an alternative therapy for spontaneous intracerebral hemorrhage (ICH) and is associated with delayed edema possibly counteracting the beneficial effects of hematoma volume reduction. We
Sonographic Demonstration of Intracranial Hemorrhage in a Fetus with Hydrops Fetalis due to Rh Alloimmunization after Intrauterine Intravascular Transfusion: A Case Report and Review of the Literature.
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Intrauterine transfusion is the most common and successful intrauterine procedure for the treatment of fetal anemia due to red cell alloimmunization. Fetal intracranial hemorrhage is a very rare complication of intrauterine transfusion in patients with Rh(D) alloimmunization and it has been
Human brain hemorrhage: quantification of perihematoma edema by use of diffusion-weighted MR imaging.
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OBJECTIVE
Animal models have clearly shown a critical role for extravascular blood in the initiation of the vasogenic edema associated with intracerebral hemorrhage (ICH). Nevertheless, the relevance of these observations to the human disease process has not been evaluated. With a prospectively
Astrocytic induction of matrix metalloproteinase-9 and edema in brain hemorrhage.
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We tested the hypothesis that astrocytic matrix metalloproteinase-9 (MMP-9) mediates hemorrhagic brain edema. In a clinical case of hemorrhagic stroke, MMP-9 co-localized with astrocytes and neurons in peri-hematoma areas. In a mouse model where blood was injected into striatum, MMP-9 was
Cerebral hemorrhage, brain edema, and heme oxygenase-1 expression after experimental traumatic brain injury.
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Intracranial bleeding is a common and serious consequence of traumatic brain injury (TBI). In the present study, we investigated cerebral hematoma occurrence, brain edema formation, blood-brain barrier (BBB) disruption, and heme oxygenase-1 (HO-1) expression after TBI. Moderate severity (1.8-2.2
Attenuation of Acute Phase Injury in Rat Intracranial Hemorrhage by Cerebrolysin that Inhibits Brain Edema and Inflammatory Response.
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The outcome of intracerebral hemorrhage (ICH) is mainly determined by the volume of the hemorrhage core and the secondary brain damage to penumbral tissues due to brain swelling, microcirculation disturbance and inflammation. The present study aims to investigate the protective effects of
[Dexamethasone in treatment of brain edema and intracranial hemorrhage].
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