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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated liver function and coagulation parameters in 117 patients with spontaneous intracerebral hemorrhage (68 men and 49 women) admitted to our clinic within 24 hours after onset. Liver dysfunction was more common among men than women due to differences in alcohol consumption. Number of thrombocytes and fibrinogen concentrations were lower, especially among men with elevated concentrations of glutamic oxaloacetic transaminase or glutamic pyruvic transaminase and/or elevated gamma-globulin fraction. Five of the 78 patients undergoing stereotactic hematoma aspiration and one of the 39 treated nonsurgically rebled. All six of the patients who rebled were men, heavy alcohol consumers with liver dysfunction. Fibrinogen concentration was abnormally low in four of the six and at the lower end of the normal range in one. Two showed thrombocytopenia and one case showed prolonged prothrombin time. These facts suggest that liver disorders produce a state in which hemorrhage occurs more readily and that this hemorrhagic tendency may be one of the causal factors of spontaneous intracerebral hemorrhage.
Stroke 1988 Jul
PMID:Spontaneous intracerebral hemorrhage and liver dysfunction. 245 66

Pentastarch is a hydroxyethyl starch similar to hetastarch, but with a lower average molecular weight (264,000 versus 450,000) and fewer hydroxyethyl groups (molar substitution ratio = 0.45 versus 0.70). These characteristics result in enhanced enzymatic hydrolysis, faster renal elimination (initial intravascular half-life = 2.5 versus 25.5 hours), and less effect on coagulation. We report on a randomized clinical trial comparing the clinical efficacy and safety of 10% pentastarch (group P) for plasma volume expansion after cardiac operations with that of 5% serum albumin (group A). During the first 24 hours after arrival of the patient in the intensive care unit, colloid was infused to maintain a cardiac index of 2.0 L/m2 or more and a mean arterial pressure within 10% of the preinduction value. Group P (n = 50) received 1706 +/- 393 ml of colloid (mean +/- standard deviation) during this period, and group A (n = 44), 1794 +/- 341 ml (p = no significant difference). Hemodynamic responses to infusion were similar for both groups, although in group P a greater increase in both cardiac index (0.5 +/- 0.5 versus 0.3 +/- 0.5 L/min/m2 in group A, p less than 0.01) and left ventricular stroke work index (10.8 +/- 8.0 versus 5.8 +/- 6.0 gm-m/m2, p less than 0.01) was observed during infusion of the first 500 ml. There were no significant differences in any of the measured respiratory parameters (alveolar-arterial oxygen gradient, estimated shunt fraction, and effective pulmonary compliance). Hemodilution with colloid significantly reduced serum protein levels in group P by 24 hours postoperatively (4.0 +/- 0.6 versus 5.0 +/- 0.7 gm/dl in group A, p less than 0.05), although mean serum colloid osmotic pressure was similar (15.4 +/- 2.6 [P] versus 15.5 +/- 2.7 mmHg [A], p = no significant difference). There were no significant between-group differences in prothrombin time, activated partial thromboplastin time, platelet count, bleeding time, or coagulation factors (fibrinogen, V, VII, VIII, or IX) on postoperative days 1 and 7. Perioperative fluid balance, weight change, chest tube output, red blood, platelet, or fresh frozen plasma usage, reexploration for bleeding, and clinical outcome were also similar. These findings indicate that pentastarch is as safe and effective s 5% albumin for plasma volume expansion after cardiac operations with no apparent adverse effects on coagulation. If commercially available at a lower cost than albumin, it would appear to be a reasonable first choice for colloid therapy in this setting.
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PMID:A randomized clinical trial of 10% pentastarch (low molecular weight hydroxyethyl starch) versus 5% albumin for plasma volume expansion after cardiac operations. 246 78

Tissue plasminogen activator (tPA) dissolves intravascular thrombus and restores blood flow after thromboembolic vascular occlusion. The utility of this agent for treatment of stroke in humans may be limited by post-reperfusion hemorrhagic complications. We studied tPA-mediated thrombolysis in an animal model of cerebrovascular occlusion in order to determine what factors, if any, predispose tPA-treated animals to suffer hemorrhage. Small blood clot emboli were injected into the internal carotid arteries of rabbits. Angiograms confirmed occlusion of the middle cerebral artery or internal carotid artery in 100% of subjects. tPA or saline was administered as a 30-minute infusion at various times after embolization. Hemorrhage rates were similar in all groups regardless of treatment. tPA increased the prothrombin time and the thrombin time but not the partial thromboplastin time. There was no correlation between these changes in blood coagulation and the finding of cerebral hemorrhage. We observed a significant association between stroke severity and cerebral hemorrhage. We conclude that tPA treatment successfully causes thrombolysis of cerebral emboli without causing an increase in the incidence of cerebral hemorrhage in rabbits.
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PMID:Tissue plasminogen activator-mediated thrombolysis of cerebral emboli and its effect on hemorrhagic infarction in rabbits. 249 32

Serial determinations of beta-thromboglobulin (BTG), platelet factor 4 (PF4), fibrinopeptide A (FPA), antithrombin III (ATIII), protein C (PC), fibrin (ogen) degradation product (FDP), FDP D-dimer, activated partial thromboplastin time (APTT), prothrombin time (PT), and euglobulin lysis time (ELT) were performed in 18 patients with non-progressing stroke and 14 patients with progressing stroke in order to predict the development of progressing stroke. Increasing levels of BTG, PF4 and FDP with frequent fluctuation were noted in both kinds of stroke. Fluctuation of FPA levels was also noted but was less pronounced. PC levels were found to be slightly decreased with fluctuation but the mean was still in the lower normal limit. BTG, PF4 and PC all elevated at the time of deterioration of physical condition in patients with progressing stroke, whereas FPA had no definite change at that time. From our study, we conclude that both platelet activation and coagulation process do occur in both kinds of stroke. But the latter plays a minor role in the formation of thrombosis. The hemostasis change, especially concerning the thrombosis formation, probably plays a role in the development of progressing stroke, but we cannot predict their development even by the detections of the newly known molecular substances appearing in various steps of the hemostatic mechanism. Development of new tests for understanding the whole dynamic change of the thrombosis process is necessary for accurate prediction of the progressing stroke in the future.
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PMID:The serial hemostasis-related changes in patients with cerebral infarction: comparison between progressing and non-progressing stroke. 253 1

Polymeric drug delivery systems that allow the application of substances to a localized region for specified periods of time have been developed. A model for intravascular thrombosis in the rat common carotid artery was established using a combination of balloon catheter endothelial injury with 1-hour occlusion of the vessel. After endothelial injury in 11 Sprague-Dawley rats, the adventitial surface of the carotid artery was exposed to the polymer polyvinyl alcohol (PVA) containing heparin and was compared with exposure to PVA alone in the contralateral (control) vessel. Subsequent determinations of the coagulation parameters systemic prothrombin and partial thromboplastin times showed no systemic effect of heparin. All 11 control vessels demonstrated complete or partial thrombosis, whereas only one of 11 heparin/PVA-treated vessels showed a small thrombus. Morphometric analysis of the cross-sectional thrombus: lumen ratio in 10 rats showed a significant reduction (p less than 0.005) in thrombus size for treated vessels (4.1 +/- 9.6%) compared with control vessels (60.2 +/- 25.8%). Scanning electron microscopy verified the absence of thrombus in the treated vessels despite complete endothelial desquamation. In a second group of eight rats, endothelial injury without occlusion did not cause thrombosis in treated or control arteries. The coagulation parameters for this group of eight unoccluded rats were similarly unaffected by heparin/PVA treatment. Our observations suggest that a localized antithrombotic effect of heparin can be achieved without systemic anticoagulation using a polymeric drug delivery system. This technique may be applied to a variety of surgical and nonsurgical clinical conditions.
Stroke 1988 Dec
PMID:Local anticoagulation without systemic effect using a polymer heparin delivery system. 320 3

Six alcoholic patients developed extensive cerebral hemispheric hemorrhages with both intraventricular and subarachnoid blood. All patients had evidence of liver damage, low platelet counts, and abnormal prothrombin and partial thromboplastin times. Four patients presented with seizures; in two of the four, these seizures were initially diagnosed as alcohol withdrawal seizures. Four patients were comatose with lateralizing neurologic deficit; two patients were comatose without lateralizing neurologic deficit, suggesting a metabolic encephalopathy. In one patient there was delayed neurologic deterioration. In all six patients, computed tomography showed large diffuse cerebral hemispheric hemorrhages, prominent intraventricular blood, and breakthrough into the subarachnoid spaces, which was confirmed by necropsy findings. There was marked mass effect but minimal surrounding edema. All six patients died. In three, autopsy showed no evidence of aneurysm, vascular malformation, neoplasm, or amyloid angiopathy and no arteriolar hypertensive changes.
Stroke 1988 Dec
PMID:Alcoholic intracerebral hemorrhage. 320 17

A hemiplegic patient with severe upper extremity spasticity 2 years after a cerebrovascular accident received a diagnostic median nerve block below the elbow with bupivacaine. He had been placed on Coumadin as prophylaxis for cerebrovascular arteriosclerotic disease, and prothrombin time was kept at twice the control value. Less than 48 hours after the procedure, a compartment syndrome developed in the volar forearm. Compartment syndrome has not previously been reported as a complication resulting from a nerve block procedure. We conclude that (1) compartment syndrome may develop after a peripheral nerve block procedure for spasticity, (2) prophylactic anticoagulation may increase the risk for hemorrhagic events resulting from percutaneous injection and (3) early recognition is essential and appropriate decompressive fasciotomy may be indicated if a compartment syndrome develops after a nerve block procedure.
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PMID:Diagnostic peripheral nerve block resulting in compartment syndrome. Case report. 335 80

The plasma concentrations of protein C, an anticoagulant protein, and fibrinopeptide A were measured in 37 patients with acute hemispheric stroke and in age-matched controls with nonvascular neurologic diseases. In 11 stroke patients who died within 15 days after the onset (nonsurvivors) protein C antigen concentration on admission was lower than in the control group (p less than 0.005), with a mean value of 63% of the concentrations found in the 26 survivors (p less than 0.001). The difference in protein C concentrations was not associated with different prothrombin time ratios and serum albumin concentration in survivors and nonsurvivors of stroke and was independent of the size of the cerebral lesion. Increased fibrinopeptide A concentration on admission was found in all stroke patients (p less than 0.001), but it was higher in nonsurvivors than in survivors (p less than 0.01), suggesting that lower protein C concentrations in nonsurvivors might be due to increased thrombin-dependent protein C activation. In survivors, protein C concentration was slightly but significantly higher than in controls (p less than 0.05) and was unchanged 2 months after stroke, a time when fibrinopeptide A concentrations had returned to normal. These results show that protein C is involved in the hemostatic derangement caused by stroke and provide a rationale for clinical trials evaluating the therapeutic supplementation with protein C of patients with acute ischemic stroke.
Stroke 1988 May
PMID:Protein C in acute stroke. 336 90

We analysed 103 episodes of upper gastrointestinal bleeding in 88 elderly patients (age 76 +/- 7.7 years) to determine which of a group of 52 clinical and laboratory variables, measured on admission, best predicted continued or rebleeding, and death in these patients. Variables which related directly to the size of the bleed (blood urea, haemoglobin, pulse rate, systolic blood pressure) were all strongly predictive of both outcomes (P less than 0.001). Of the variables unrelated to the size of the bleed, prolonged prothrombin time and elevated serum creatinine were most strongly predictive of a poor outcome, suggesting that haemostatic dysfunction may be a major contributor to death from upper gastrointestinal haemorrhage in elderly patients. Other variables with strong predictive potential were age (P less than 0.001), the presence of multiple disease states (P less than 0.01), therapy with multiple drugs (P less than 0.01) and acute stroke or obtundation on admission (P less than 0.01). In general terms the size of the bleed was as significant as the premorbid condition of the patient in predicting the outcome. This, together with the fact that half the patients died of hypovolaemia, suggests that death from upper gastrointestinal bleeding in the elderly is not inevitable and that further reduction in mortality from this cause is attainable.
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PMID:Prognostic factors for continued or rebleeding and death from gastrointestinal haemorrhage in the elderly. 349 10

The primary risk of anticoagulant therapy in cardiac embolic stroke is hemorrhage--particularly cerebral hemorrhage in the elderly. Improving the benefit/risk ratio for indicated anticoagulation involves consideration of the following: hemostatic competence, blood pressure, drug interactions, falls, interval surgery, diet, aspirin and last but not least, the intensity of anticoagulant prophylaxis. For the present it would be prudent to limit heparin administration to a low-dose regimen not exceeding 20,000 units/24 hours and warfarin maintenance to a low-dose prothrombin time ratio of 1.5.
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PMID:Prophylactic anticoagulants in managing embolic stroke. 381 82


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