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Intraparenchymal Hemorrhage (intraparenchymal + hemorrhage)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Morphological changes induced in the pig kidney by extracorporeal shock wave lithotripsy: Nephron injury

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 1 2003
Youzhi Shao
Abstract While shock wave lithotripsy (SWL) is known to cause significant damage to the kidney, little is known about the initial injury to cells along the nephron. In this study, one kidney in each of six juvenile pigs (6,7 weeks old) was treated with 1,000 shock waves (at 24 kV) directed at a lower pole calyx with an unmodified HM-3 lithotripter. Three pigs were utilized as sham-controls. Kidneys were fixed by vascular perfusion immediately after SWL or sham-SWL. Three of the treated kidneys were used to quantitate lesion size. Cortical and medullary samples for light (LM) and transmission electron microscopy (TEM) were taken from the focal zone for the shock waves (F2), the contralateral kidney, and the kidneys of sham-SWL pigs. Because preservation of the tissue occurred within minutes of SWL, the initial injury caused by the shock waves could be separated from secondary changes. No tissue damage was observed in contralateral sham-SWL kidneys, but treated kidneys showed signs of injury, with a lesion of 0.2% ± 0.1% of renal volume. Intraparenchymal hemorrhage and injury to tubules was found at F2 in both the cortex and medulla of SWL-treated kidneys. Tubular injury was always associated with intraparenchymal bleeding, and the range of tissue injury included total destruction of tubules, focal cellular fragmentation, necrosis, cell vacuolization, and membrane blebbing. The initial injury caused by SWL was cellular fragmentation and necrosis. Cellular vacuolization, membrane blebbing, and disorganization of apical brush borders appear to be secondary changes related to hypoxia. Anat Rec Part A 275A:979,989, 2003. © 2003 Wiley-Liss, Inc. [source]

Utility of an Initial D-dimer Assay in Screening for Traumatic or Spontaneous Intracranial Hemorrhage

ACADEMIC EMERGENCY MEDICINE, Issue 9 2001
Mark E. Hoffmann MD
Abstract Objective: To evaluate the sensitivity of a D-dimer assay as a screening tool for possible traumatic or spontaneous intracranial hemorrhage. If adequately sensitive, the D-dimer assay may potentially permit omission of a more expensive computed tomography (CT) scan of the head when such hemorrhage is clinically suspected. Methods: Prospective, consecutive, blinded study of patients (age > 16 years) requiring a CT scan of the head for suspected intracranial hemorrhage over a five-month period at a university, Level I trauma center. All study patients had a serum D-dimer assay obtained prior to their CT scans. Sensitivity and specificity, with 95% confidence intervals (95% CIs), of the enzyme-linked immunosorbent assay (ELISA) D-dimer assay for the detection of intracranial hemorrhage were calculated. Results: Of the 319 patients entered in the study, 25 (7.8%) had a CT scan positive for intracranial hemorrhage. Patients with intracranial hemorrhage were more likely to have a positive D-dimer assay (chi-square ? 13.075, p < 0.001). The D-dimer assay had 21 true-positive and four false-negative tests, resulting in a sensitivity of 84.0% (95% CI ? 63.7% to 95.5%) and a specificity of 55.8% (95% CI ? 55.5% to 55.9%). The four false-negative cases included one small intraparenchymal hemorrhage, one small subarachnoid hemorrhage, one moderate-sized intraparenchymal hemorrhage with mid-line shift, and one large subdural hematoma requiring emergent surgery. Conclusions: Due to the catastrophic nature of missing an intracranial hemorrhage in the emergency department, the D-dimer assay is not adequately sensitive or predictive to use as a screening tool to allow routine omission of head CT scanning. [source]

Systemic lupus erythematosus complicated with posterior reversible encephalopathy syndrome and intracranial vasculopathy

INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 4 2010
Hung-An CHEN
Abstract Posterior reversible encephalopathy syndrome (PRES) is a neurotoxic condition characterized by reversible vasogenic edema on neuroimaging. It is associated with various neurological manifestations, including headaches, vomiting, seizures, visual loss, altered mental status and focal neurological deficits. PRES mainly occurs in the setting of eclampsia, hypertension, uremia, malignancy, transplantation, autoimmune diseases and/or use of immunosuppressive drugs. This syndrome has been described in patients with systemic lupus erythematosus (SLE). PRES is a potentially reversible clinical,radiological entity; however, it can be complicated with vasculopathy, infarction or hemorrhage. Vasculopathy has been demonstrated to be a common finding in patients with SLE. We report the case of a woman with lupus nephritis and PRES whose diffuse vasculopathy was present on initial neuroimaging. Subsequent brain computed tomography scan demonstrated interval development of intraparenchymal hemorrhage and subarachnoid hemorrhage. To our knowledge, this unique brain image pattern has not been reported in SLE patients. [source]

Intracranial hemorrhage following allogeneic hematopoietic stem cell transplantation,

AMERICAN JOURNAL OF HEMATOLOGY, Issue 5 2009
Yuho Najima
Charts and radiographs of 622 allogeneic hematopoietic stem cell transplant (HSCT) recipients, over a 20-year period, were retrospectively reviewed for intracranial hemorrhage (ICH) following transplant. A total of 21 cases of ICH were identified (3.4%) including 15 cases of intraparenchymal hemorrhage (IPH), two cases of subarachnoid hemorrhage (SAH), and four cases of subdural hematoma (SDH). The median time from transplantation to the onset of ICH was 63 days (range, 6,3,488 days). The clinical features of post-transplant ICH patients were similar and included hypertension, diabetes mellitus, chronic graft-versus-host disease (GVHD), systemic infection, and veno occlusive disease (VOD), recently referred to as sinusoidal obstruction syndrome, in addition to severe thrombocytopenia. Mortality rate was especially high (89%) after IPH with a median survival of 2 days (range, 0,148 days). In contrast, all patients with SAH or SDH following HSCT survived. The cause of post-transplant ICH appears to be multifactorial, including thrombocytopenia, hypertension, acute GVHD, VOD, and radiation therapy. Most patients in our series displayed severe thrombocytopenia at the onset of ICH, even though adequate prophylactic platelet transfusions were given. By univariate analysis, cord blood transplantation, acute GVHD, systemic infection, and VOD were related to the incidence of ICH, whereas prior CNS episodes and radiation therapy did not reach statistical significance. A multivariate analysis with logistic regression identified acute GVHD as the only factor that significantly influenced ICH occurrence. Am. J. Hematol. 2009. © 2009 Wiley-Liss, Inc. [source]