Treatment of life-threatening hemorrhage due to acquired factor VIII inhibitor. (33/1119)

An otherwise healthy elderly man developed massive, life-threatening, sublingual bleeding associated with an idiopathic factor VIII inhibitor. The patient was treated wtih cyclophosphamide, steroids, factor VIII concentrates, and repeated plasmapheresis (including three times with NCI-IBM blood-cell separator). Rapid clinical and laboratory improvement occurred, with complete disappearance of the inhibitor. The patient has remained well, without evidence of an inhibitor, for 8 mo. The possible role of each of the therapeutic measures in the disappearance of the inhibitor and the possible pathogenetic mechanism of this disorder are discussed. A high mortality rate and a striking incidence of sublingual hematoma have been observed in cases in the literature.  (+info)

Improved functional outcome in patients with hemorrhagic stroke in putamen and thalamus compared with those with stroke restricted to the putamen or thalamus. (34/1119)

BACKGROUND AND PURPOSE: We analyzed the effect of late intensive inpatient rehabilitation on the functional outcome of patients with subcortical hemorrhagic stroke. METHODS: Patients who were nonambulatory with hemorrhagic stroke in the internal capsule and putamen (n=55), the thalamus (n=24), or all 3 regions (n=15) underwent intensive inpatient rehabilitation. Patients with surgical intervention or an episode of ventricular hemorrhage were excluded. Lesion location was evaluated by MRI 4 months after the ictus. RESULTS: Demographic data, initial disability, and impairment measures were comparable in the 3 groups. Functional outcome demonstrated significant differences in mobility subscores (P<0.05) of the Functional Independence Measure such that patients with injury in the 3 regions were more likely to ambulate independently than were patients in the other groups. Lesion location data demonstrated that the ventral anterior nucleus of the thalamus was always spared; the ventral posterior (lateral and medial) nucleus was always damaged, and the ventral lateral nucleus was frequently damaged. Putaminal damage always included the postcommissural area. In addition, the entire posterior half limb of the internal capsule was always damaged. CONCLUSIONS: Subcortical lesions to multiple structures in the basal ganglia-thalamocortical motor circuits permitted enhanced motor recovery. Lesion location predicted the level of independent ambulation and the rate of recovery in patients with stroke who were nonambulatory before neurorehabilitation therapy.  (+info)

Stress-related primary intracerebral hemorrhage: autopsy clues to underlying mechanism. (35/1119)

BACKGROUND: Research into the causes of small-vessel stroke has been hindered by technical constraints. Cases of intracerebral hemorrhage occurring in unusual clinical contexts suggest a causal role for sudden increases in blood pressure and/or cerebral blood flow. CASE DESCRIPTION: We describe a fatal primary thalamic/brain stem hemorrhage occurring in the context of sudden emotional upset. At autopsy, the brain harbored several perforating artery fibrinoid lesions adjacent to and remote from the hematoma as well as old lacunar infarcts and healed destructive small-vessel lesions. CONCLUSIONS: We postulate that the emotional upset caused a sudden rise in blood pressure/cerebral blood flow, mediating small-vessel fibrinoid necrosis and rupture. This or a related mechanism may underlie many small-vessel strokes.  (+info)

A randomized trial comparing heparin initiation 6 h or 24 h after pacemaker or defibrillator implantation. (36/1119)

OBJECTIVES: The purpose of this randomized study was to evaluate the prevalence of pocket hematomas in patients treated with heparin 6 h or 24 h after pacemaker or defibrillator implantation. BACKGROUND: The risks of pocket hematoma and need for evacuation after device implantation have not been defined in patients who require anticoagulation. METHODS: Forty-nine consecutive patients with an indication for anticoagulation with heparin after implantable defibrillator or pacemaker implantation were randomized to receive intravenous heparin either 6 h (n = 26) or 24 h (n = 23) postoperatively. Both groups also received warfarin on a daily basis starting the evening of surgery. Twenty-eight patients who received postoperative warfarin alone and 115 patients who did not receive anticoagulation were followed up in a study registry. RESULTS: A pocket hematoma developed in 6 of 26 patients (22%) who were treated with intravenous heparin 6 h postoperatively, as compared with 4 of 23 patients (17%) who were treated with intravenous heparin 24 h postoperatively (p = 0.7). In total, a pocket hematoma developed in 10 of 49 patients (20%) treated with heparin, 1 of 28 patients (4%) treated with warfarin alone and 2 of 115 (2%) patients who received no anticoagulation (p < 0.001). CONCLUSIONS: Intravenous heparin initiation 6 h or 24 h after pacemaker or defibrillator implantation is associated with a 20% prevalence of pocket hematoma formation. Warfarin therapy or no anticoagulation is associated with only a 2% to 4% risk of pocket hematoma formation.  (+info)

Haemorrhagic lumbar synovial cyst. A cause of acute radiculopathy. (37/1119)

A total of 254 cases of synovial cysts of the spine have been reported in the English literature, but only eight have been associated with haemorrhage. We describe a 55-year-old man with acute radiculopathy resulting from haemorrhage involving a synovial cyst at a lumbar facet joint. Traumatic factors could have caused bleeding around or into the synovial cyst. Treatment by resection of the cyst and evacuation of the haematoma led to complete neurological recovery.  (+info)

Noninvasive in vivo magnetic resonance imaging of experimental coronary artery lesions in a porcine model. (38/1119)

BACKGROUND: The ability to characterize and quantify coronary artery atherosclerotic lesions accurately, reproducibly, and noninvasively may allow the stratification of risk for future acute coronary syndromes and help direct therapeutic management. MRI has been shown to accurately characterize and quantify atherosclerosis; however, because of the combination of cardiac and respiratory motion artifacts, nonlinear course, and relatively small size of the coronary arteries, these techniques have not been able to be translated to the coronary system in vivo. METHODS AND RESULTS: Coronary lesions were induced in Yorkshire albino swine (n=6) with balloon angioplasty, and 4 weeks later MRI of the coronary artery lesions was performed. High-resolution in vivo images of the coronary artery wall and lesions were obtained with a double-inversion-recovery fast-spin-echo sequence in a 1.5-T MR system. There was good agreement between measurements of vessel wall thickness and area from MR images of the coronary arteries and the matched histopathology sections (n=43). The mean difference (MRI minus histopathology +/- SD) for mean wall thickness was 0.26+/-0.18 mm, and for vessel wall area, 5.65+/-3.51 mm(2). MRI was also able to visualize intralesion hematoma (sensitivity 82%, specificity 84%). CONCLUSIONS: Using a clinical MR system, we were able to image coronary artery lesions in vivo in an experimental porcine model. Further studies are needed to assess the ability of MRI to characterize coronary atherosclerotic lesions in vivo.  (+info)

Intracortical hemorrhage injury in rats : relationship between blood fractions and brain cell death. (39/1119)

BACKGROUND AND PURPOSE: Intracerebral hemorrhage is associated with stroke and head trauma. The purposes of this study were to investigate the effect of intracortical injections of autologous whole blood and blood components on inflammatory cell infiltration and brain cell death and to determine if nonhemorrhagic lesions differ in these respects. METHODS: Eighty-seven adult rats were subjected to intracortical injections of autologous whole blood or allogeneic plasma, erythrocytes, leukocytes, "activated" leukocytes, and serum. Injections of saline or mineral oil were controls. Blood injections were compared with cortical freeze injury and pial devascularization. Rats were perfusion-fixed 48 hours after injection or lesioning. Eosinophilic neurons, TUNEL-positive cells, brain damage area, infiltrating neutrophils, and CD8a-immunoreactive lymphocytes were quantified. RESULTS: Damage area, dying cells, and inflammatory infiltrate were significantly greater after autologous whole blood, leukocyte, and "activated" leukocyte injections than injection of other fractions. CONCLUSIONS: These results suggest that extravasated whole blood causes a greater degree of cortical cell death and inflammation than ischemic lesions of similar size. Leukocytes "activated" by systemic illness might exacerbate the injury. Secondary hemorrhagic phenomena suggest that the harmful effect is directed toward both brain cells and the vasculature. Further studies are required to delineate the mechanism(s).  (+info)

Immediate surgery reduces mortality in deeply comatose patients with spontaneous cerebellar hemorrhage. (40/1119)

Cerebellar hemorrhage is regarded as a neurosurgical emergency. However, patients with deteriorating consciousness are very likely to die irrespective of the choice of therapy, and it is not clear if surgical intervention can benefit patients in a deeply comatose state. We reviewed 20 patients with a Glasgow Coma Scale score of 3 at admission to ascertain the salvage rate and determine the prognostic factors. Four patients who were managed conservatively died within 2 days. Sixteen patients underwent decompressive suboccipital craniectomy and hematoma evacuation. At discharge, three patients were moderately disabled, three were severely disabled, four were persistently vegetative, and six had died. The overall mortality was 50%. The mean interval between the onset of symptoms and the operation was 1.67 +/- 0.29 hours in patients with favorable outcome, and significantly longer at 2.42 +/- 0.49 hours in patients with an unfavorable outcome (p = 0.025). Immediate evacuation of the hematoma reduces morbidity and mortality even in deeply comatose patients, especially if the time interval between the onset and surgery is within 2 hours.  (+info)