warfarin and Brain-Edema

Topics: Anticoagulants; Antipyrine; Arginine; Aspirin; Brain Edema; Edaravone; Fibrinolytic Agents; Free Radical Scavengers; Glycerol; Humans; Hyperlipidemias; Hypertension; Japan; Methacrylates; Pipecolic Acids; Platelet Aggregation Inhibitors; Practice Guidelines as Topic; Risk Factors; Stroke; Sulfonamides; Thrombolytic Therapy; Time Factors; Warfarin

Little is known about the pathophysiology of oral anticoagulation-associated intracerebral hemorrhage (OAC-ICH). We compared hematoma volume, number of terminal deoxynucleotidyl dUTP nick-end labeling (TUNEL)-positive cells (indicating cell death), MMP-9 levels, and perilesional edema formation between warfarin-treated mice and controls. Intracerebral hemorrhage was induced by an injection of collagenase into the right striatum. Twenty-four hours later, hematoma volume was measured using a photometric hemoglobin assay. Cell death was quantified using TUNEL staining. MMP-9 levels were determined by zymography, and edema formation was assessed via the wet-dry method. Warfarin increased hematoma volume by 2.6-fold. The absolute number of TUNEL-positive cells in the perihematomal zone was lower in warfarin-treated animals (300.5 ± 39.8 cells/mm2) than in controls (430.5 ± 38.9 cells/mm2; p = 0.034), despite the larger bleeding volume. MMP-9 levels were reduced in anticoagulated mice as compared to controls (p = 0.018). Perilesional edema formation was absent in warfarin mice and modestly present in controls. Our results suggest differences in the pathophysiology of OAC-ICH compared to intracerebral hemorrhage occurring under normal coagulation. A likely explanation is that thrombin, a strong inductor of apoptotic cell death and blood-brain barrier disruption, is produced to a lesser extent in OAC-ICH. In humans, however, we assume that the detrimental effects of a larger hematoma volume in OAC-ICH by far outweigh potential protective effects of thrombin deficiency.

Topics: Animals; Anticoagulants; Brain Edema; Cell Death; Cerebral Hemorrhage; Disease Models, Animal; Drug Administration Schedule; Hematoma; In Situ Nick-End Labeling; Male; Matrix Metalloproteinase 8; Matrix Metalloproteinase 9; Mice; Neurologic Examination; Statistics, Nonparametric; Warfarin

Thyroid storm is a rare disorder with a sudden onset, rapid progression and high mortality. We experienced a case of thyroid storm which had a devastating course, including multiple organ failure (MOF), severe hypoglycemia, disseminated intravascular coagulation (DIC), and stroke. It was difficult to make a diagnosis of thyroid storm in the present patient, because she did not have a history of thyroid disease and her serum FT3 level was normal. Clinicians should be aware that thyroid storm can occur even when there is an almost normal level of thyroid hormones, and that intensive anticoagulation is required for patients with atrial fibrillation to prevent stroke after thyroid storm.

Topics: Anti-Inflammatory Agents; Anticoagulants; Antithyroid Agents; Brain Edema; Decompression, Surgical; Disseminated Intravascular Coagulation; Female; Gabexate; Humans; Hydrocortisone; Methimazole; Middle Aged; Multiple Organ Failure; Stroke; Thyroid Crisis; Treatment Outcome; Triiodothyronine; Warfarin

Intracerebral hemorrhage (ICH) associated with warfarin sodium therapy is becoming more common as the use of this medication increases in the aging population.. To delineate factors associated with early mortality, determine variables responsible for poor functional outcome, and evaluate possible reasons for expansion of hemorrhage and associated parenchymal edema.. Retrospective study of clinical and radiologic information for 88 patients with warfarin-associated ICH.. A single hospital. Patients Eighty-eight consecutive patients with warfarin-associated ICH.. Patients were included if the international normalized ratio (INR) at presentation with ICH was 1.5 or greater. Computed tomographic scans were reviewed for volumetric analysis of hematoma and perihematomal edema volume. Outcome variables included 7-day mortality, hematoma enlargement, and functional outcome based on the modified Rankin Scale score.. Seven-day mortality (39.8%) was associated with a lower Glasgow Coma Scale sum score and larger ICH volume at presentation. Univariate analysis revealed that a lower Glasgow Coma Score sum score, larger initial ICH volume, higher initial and 48-hour maximum glucose concentrations, and higher percentage of ICH expansion were significantly associated with poor functional outcome at hospital discharge. At multivariate analysis, only Glasgow Coma Score and ICH volume remained significantly associated with functional outcome measured at hospital discharge and at the last follow-up visit. Conversely, INR at presentation, time to INR correction, initial blood pressure, and enlargement of edema were not associated with functional outcome either at hospital discharge or at the last follow-up. Neither serum glucose concentration at admission nor highest level during the first 48 hours had any correlation with ICH or parenchymal edema enlargement. In addition, neither initial INR nor time to INR correction correlated with expansion of ICH or parenchymal edema.. Lower level of consciousness at presentation and larger initial ICH volume predict poor prognosis in patients with warfarin-associated ICH. In our study population, INR at presentation was not associated with functional outcome.

Topics: Aged; Aged, 80 and over; Anticoagulants; Brain Edema; Cerebral Hemorrhage; Female; Glasgow Coma Scale; Humans; Longevity; Male; Middle Aged; Predictive Value of Tests; Prognosis; Retrospective Studies; Risk Assessment; Treatment Outcome; Venous Thromboembolism; Warfarin

The pathophysiology and clinical significance of perihematomal edema (PHE), a cause of secondary neuronal injury after intracerebral hemorrhage (ICH), is poorly understood. A leading theory proposes that early PHE results from activation of the clotting cascade. We sought to test this theory by examining the relationship between early PHE and warfarin use in ICH patients.. ICH and PHE volumes were measured in consecutive patients with warfarin-related ICH and compared to those of controls with non-coagulopathic ICH. Subjects were identified from a prospective database of ICH patients. Clinical and radiological predictors of PHE volume and relative PHE (PHE volume/ICH volume) were identified. The relationship between PHE volume and 90-day mortality was determined.. For the 49 consecutive warfarin-related ICH patients and 49 matched controls: median INRs (interquartile ranges) were 3.2 (2.3, 4.1) and 1.1 (1.08, 1.2); median hematoma volumes were 37.8 cm(3) (6.7, 102.9) and 18.1 cm(3) (9, 51) (P = 0.18); median PHE volumes were 12 cm(3) (3.7, 36.7), and 11 cm(3) (4.1, 24) (P = 0.87); and median relative PHE was 0.38 (0.28, 0.52) and 2 (1.37, 3.06), respectively. In multivariable analysis, ICH volume and warfarin use independently predicted PHE volume. There was an association between higher PHE volume and decreased 90-day mortality.. Warfarin-related ICH is associated with less early relative edema than non-coagulopathic ICH. This is consistent with the theory that coagulation contributes to early edema. Early edema may be associated with improved functional outcome.

Topics: Aged; Aged, 80 and over; Anticoagulants; Blood Coagulation; Brain Edema; Cerebral Hemorrhage; Humans; Middle Aged; Radiography; Retrospective Studies; Severity of Illness Index; Time Factors; Warfarin

The goal of medical treatment during acute cerebral infarction is to enhance thrombolysis and inhibit the chemical alterations associated with cell death. Treatment includes avoidance of blood pressure reduction, blood glucose control, possible anticoagulation with IV heparin, and sometimes reduction of cerebral edema. Optimal treatment thereafter depends on the result of patient evaluation. Uncontrolled vascular risk factor (eg, hypertension, smoking, and diabetes) should be treated. Aspirin and ticlopidine reduce the risk of recurrent ischemic stroke. In patients with nonrheumatic atrial fibrillation, anticoagulation with warfarin reduces the risk of embolic events. Carotid endarterectomy is superior to medical management alone in reducing the risk of stroke in patients with > 70% symptomatic extracranial carotid stenosis.

Topics: Aged; Aspirin; Brain Edema; Brain Ischemia; Cerebral Infarction; Heparin; Humans; Recurrence; Risk Factors; Ticlopidine; Warfarin

Topics: Adult; Aged; Angiography; Brain Edema; Cerebral Hemorrhage; Cerebral Ventriculography; Corpus Striatum; Diagnosis, Computer-Assisted; Female; Hematoma; Humans; Hypertension; Infant, Newborn; Infant, Newborn, Diseases; Intracranial Arteriovenous Malformations; Male; Phlebitis; Thalamus; Tomography, X-Ray; Warfarin