Mini course: hemostasis. Unit four: hemostasis--thrombosis.
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Hemostasis↗
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[Hemostasis in patients with acute leukemia treated with high doses of cytosine-arabinoside: the effect of chemotherapy and infectious complications on hemostasis].
Haemostatic parameters were studied in 12 adult patients with acute myeloid leukaemia and acute lymphoblastic leukaemia in complete remission using high-dose cytosine arabinoside regiments together with with other drugs. Increased tissue plasminogen activator (t-PA:Ag) antigen 4 hours after AraC application (p < 0.05) as well as increased levels of plasminogen activator inhibitor activity (PAI) (p < 0.05) and fibrinopeptide A (FPA) antigen (p < 0.05) were observed on day 2. All patients during bone marrow aplasia suffered from infectious complications (7 from sepsis and 5 from fever of undetermined origin). During that period of infection the increased levels of FPA on day 21 (p < 0.05), PAI on days 15 and 21 (p < 0.05) and fibrinogen on day 21 (p < 0.05) as well as decreased values of antithrombin III (p < 0.05) on day 21 and protein C on day 15 (p < 0.05) were measured. t-PA:Ag, plasminogen, alpha 2 antiplasmin and fibrin(ogen) degradation products were within normal throughout infectious complications. None of the patients experienced clinically manifest thrombotic complication. Though the results demonstrate that changes found were not clinically important (even if they were statistically significant), and that haemostasis was compensated as well as that thrombosis was not serious problem, authors recommend routine haemostasis monitoring in acute leukaemia patients, especially at diagnosis, in association with chemotherapy and during infectious complications.
Acute Disease↗
[Hemostasis in patients operated on for abdominal hemorrhage. 3. Boundary deviations of hemostasis].
The fibrinolytic process in the plasma of patients operated for abdominal haemorrhages have been investigated. The results allowed to conclude that the blockade of fibrinolysis did not effect on the course of the disease. The high level of the inhibitors and of the platelets hypoaggregation can be considered as a cause increased of the recurring gastrointestinal haemorrhages. It was demonstrated that the probability of DIC-syndrome development increased at the aggravation of the patient's state after the operation.
Abdomen↗
[Hemostasis in patients operated on for abdominal hemorrhage. 4. Conception of hemostasis changes].
Studies of haemostasis changes in the dynamics of early post-operational period permitted revealing the tendency to the growth of fibrinogen concentration, decrease in the fibrinogen self-assembling rate, weakening of thrombinemia, disturbances in fibrinogen degradation products (FDP) elimination, increase of inhibitors activity and/or weakening of blood coagulation factors activity, intensification thrombocytes aggregation. Hypercoagulation has been registered under acute haemorrhage and the haemorrhage time exceeding 24 h before the operation, the weakening of hypercoagulation response was observed, notwithstanding the possibility of haemorrhage continuation. The letter is underlined by the changes in the balance between the coagulation factors and inhibitors up to the absence of typical hypercoagulation response to surgical interference.
Abdomen↗
[Endoscopic hemostasis using laser beams. Use of laser beams for endoscopic hemostasis in the gastrointestinal tract].
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Endoscopy↗
[Clinical guidelines for inhibitors of hemostasis and locoregional neuraxial anesthesia. Spanish Society of Anesthesiology-Resuscitation and Pain Therapy, Division of Hemostasis, Transfusion Medicine, and Perioperative Fluid Therapy].
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Anesthesia, Epidural↗
Hemostasis: Part I. Screening tests to evaluate abnormal hemostasis.
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Adolescent↗
[Surgical hemostasis in recurrent peptic ulcer hemorrhage after endoscopic hemostasis--indications and results].
The identification of prognostic factors in patients with bleeding peptic ulcer is an important step for improving the outcome. Besides of age, concomitant diseases and bleeding activity, recurrent bleeding is the principal determinant of mortality in peptic ulcer bleeding. Obviously, there is still a considerable proportion of patients who cannot be successfully managed by endoscopic treatment alone. Therefore the identification of high-risk patients before rebleeding, an adequate early surgical intervention during a stable period after endoscopic haemostasis can prevent recurrent haemorrhage. Emergency endoscopy and, possibly, Doppler ultrasound provide prognostic relevant information allowing 'prospective' therapeutic decisions. By using this strategy in a clinical trial (291 patients) the overall mortality rate could be reduced markedly from 14% (139 patients) to 5% (152 patients). The results were mainly reproducible under clinical routine circumstances.
Adult↗
Role of femoral vessel catheterization and altered hemostasis in the development of extraperitoneal hematomas: CT study in 44 patients.
OBJECTIVE: To ascertain the role of femoral vessel catheterization and altered hemostasis in the development of extraperitoneal hematomas, we evaluated CT scans to study the locations of extraperitoneal hematomas in three distinct clinical settings: (1) after femoral vessel catheterization with concurrent altered hemostasis due to anticoagulant, thrombolytic, and/or antiplatelet therapy (catheterized-altered hemostasis group); (2) after femoral vessel catheterization without altered hemostasis (catheterized group); and (3) with no history of femoral vessel catheterization, with or without altered hemostasis caused by a bleeding diathesis or pharmacotherapy (uncatheterized group). MATERIALS AND METHODS: Forty-four patients were identified who had CT evidence of extraperitoneal hematomas. Twenty-four were in the catheterized-altered hemostasis group, one was in the catheterized group, and 19 were in the uncatheterized group. CT scans were evaluated for anatomic subspace involvement by hemorrhage and for the presence or absence of contiguity between the hematoma and the femoral vessels. RESULTS: Bilateral hematomas were present in six of 24 patients in the catheterized-altered hemostasis group and in four of 19 patients in the uncatheterized group. We found no significant difference between the catheterized-altered hemostasis and the uncatheterized groups regarding the proportion of cases involved at any individual retroperitoneal site (p > .05). The mean number of hematoma sites in the catheterized-altered hemostasis group (4.3) was not significantly different from the mean number in the uncatheterized group (3.7) (p > .05). Contiguity between the sites of hematoma and the punctured femoral vessels was present in 75% of the patients in the catheterized-altered hemostasis group; contiguity between the hematoma and a groin was seen in 58% in the uncatheterized group. Twenty-two of 24 patients in the catheterized-altered hemostasis group had CT findings of subcutaneous fat infiltration in the groin; however, six of 19 patients in the uncatheterized group also had this finding, indicating that its presence does not always represent changes caused by catheterization. CONCLUSION: Retroperitoneal hematomas in patients with altered hemostasis and femoral vessel catheterization do not show a unique distribution attributable solely to contiguous spread of blood from the vessel puncture site. Many of these hematomas probably arise at sites distant from the femoral vessel puncture. When the hematoma is not contiguous with the punctured femoral vessels, altered hemostasis is most likely the cause of the hemorrhage.
Catheterization, Peripheral↗
Arginine inhibits hemostasis activation.
BACKGROUND: The diagnosis and the therapy of in vivo hemostasis activation is of great clinical importance. Artefactual changes of the hemostasis (i.e., coagulation or fibrinolysis) in vitro have to be prevented. Usual in vitro anticoagulation by sodium citrate does not fully inhibit coagulation--or fibrinolysis--activation. Therefore, there is need for a simple physiologic inhibitor of hemostasis activation both in diagnosis and therapy of hemostasis activation. METHODS: Whole blood clotting time (WBCT), prothrombin time (PT), activated partial thromboplastin time (APTT), in vitro bleeding test closure time (IVBT-CT), and whole blood aggregometry (WBA) were determined in normal human blood or plasma, supplemented with increasing concentrations of L-arginine or guanidine. RESULTS: Arginine in concentrations of 5-100 mM inhibited the WBCT, PT, APTT, IVBT-CT, and WBA. Arginine (50 mM) resulted in a two-fold prolongation of WBCT, PT, or IVBT-CT (the anti-epinephrine action is superior to the anti-ADP action), a four-fold prolongation of APTT or a 60% inhibition of WBA. CONCLUSION: L-Arginine (or guanidine) inhibited the activation of hemostasis. Arginine might be used as hemostasis stabilizer both in the diagnosis and therapy of hemostasis activation. The usage of arginine as an in vitro hemostasis inhibitor might be indicated in the diagnosis of hemostasis activation, as occurring in pharmacological thrombolysis or disseminated intravascular coagulation (DIC). The storage of blood or blood products might be improved by arginine stabilization. The amino acid (and nitric oxide precursor) L-arginine could be an interesting new pharmacologic agent to inhibit a pathologic hemostasis activation.
Arginine↗
Zebrafish: a tool to study hemostasis and thrombosis.
PURPOSE OF REVIEW: In the past eight years our laboratory has developed the zebrafish model to study hemostasis and thrombosis. The purpose of this review is to explore current developments involving the zebrafish model in the study of hemostasis and thrombosis because the time is now ripe to apply this model to identify novel players that participate in hemostasis and thrombosis. RECENT FINDINGS: In the past twelve months, three papers appeared in the hemostasis and thrombosis area using the zebrafish model. The first one is a review article that summarizes establishment of the zebrafish model to study hemostasis and thrombosis. The second study is a methodological paper describing assays for measuring hemostasis and thrombosis by inducing vascular occlusion in zebrafish larvae. The third paper describes a knockdown of prothrombin in zebrafish, which recapitulates knockout studies in mouse, and marks the beginning of studies in the hemostasis and thrombosis area by this new knockdown technology. In addition to the above papers, there is one abstract that describes kinetics of thrombocyte and thrombocyte-microparticle recruitment in laser-induced arterial thrombus formation in zebrafish. SUMMARY: With the above advances, the zebrafish model has now matured to the point that it can address more important questions in the hemostasis and thrombosis area using genetic approaches. This review therefore summarizes the issues described in the above papers along with thoughts about future progress of the zebrafish model as a tool to study hemostasis and thrombosis.
Animals↗
Achieving femoral artery hemostasis after cardiac catheterization: a comparison of methods.
BACKGROUND: Cardiac catheterization is a common procedure that involves the introduction of a small sheath (5F-8F) into the femoral artery for insertion of other diagnostic catheters. After cardiac catheterization, local compression of the femoral artery is required to prevent bleeding and to achieve hemostasis. Traditional methods of achieving hemostasis require significant time and close supervision by medical personnel and can contribute to patients' discomfort. VasoSeal is a recently developed device that delivers absorbable collagen into the supra-arterial space to promote hemostasis. OBJECTIVES: To compare outcomes between patients receiving a collagen plug and patients in whom a traditional method of achieving hemostasis was used after diagnostic cardiac catheterization. METHODS: An outcomes tracking tool was used to analyze the medical records of 95 patients in whom a traditional method was used (traditional group) and 81 patients in whom VasoSeal was used (device group) to achieve hemostasis. Complications at the femoral access site, patients' satisfaction, and times to hemostasis, ambulation, and discharge were compared. RESULTS: Hematomas of 6-cm diameter occurred in 5.3% of the traditional group; no complications occurred in the device group. The device group also achieved hemostasis faster and had earlier ambulation (P < .001). Patients in the device group were discharged a mean of 5 hours sooner than patients in the traditional group (P < .05). No significant differences were found in patients' satisfaction. CONCLUSIONS: VasoSeal is a safe and effective method of achieving hemostasis after cardiac catheterization that can hasten time to hemostasis, ambulation, and discharge.
Adult↗
[Endoscopic hemostasis against hemorrhage from the upper gastrointestinal tract: its indication and limitation].
We reviewed endoscopic hemostasis that had been performed upon 353 acutely hemorrhagic peptic ulcer cases: Among them, 145 received thrombin spraying; 36, electrocoagulation; 145, topical injection of ethanol; and 27, topical injection of aetoxyscrelol. Hemostasis lasting for more than 24 hours after the treatment was defined as transient hemostasis, and hemostasis lasting for more than two weeks, as permanent hemostasis. The overall rate of transient hemostasis was 87.5%; 84.8% by thrombin spraying, 83.4% by electrocoagulation, 89.0% by injection of ethanol, 100% by injection of aetoxyscrelol, respectively. The overall rate of permanent hemostasis was 71.1%; 75.9% by thrombin spraying, 58.3% by electrocoagulation, 69.7% by injection of ethanol, 70.4% by injection of aetoxyscrelol, respectively. The rate of emergency operation for bleeding was reduced to 9.9% after the induction of endoscopic hemostasis from 64.0% before the induction. The mortality was also reduced to 3.1% from 8.9%. Particularly, over the last 4 years, the emergency operation and the mortality have been reduced, accounting from 7.2% and 2.2%, respectively. In conclusions, thrombin spraying is the first choice for mild and diffuse hemorrhage, and topical injection of ethanol is indicated for hemorrhage from exposed vessels and for localized hemorrhage.
Aged↗
Infection and hemostasis in decompensated cirrhosis: a prospective study using thrombelastography.
Bacterial infections are common complications in decompensated cirrhosis, but their relationship with hemostasis has not been studied. We prospectively assessed whether infection affects hemostasis in cirrhosis using routine hemostasis tests and thrombelastography (TEG), a global test of hemostatic function. Eighty-four cirrhotic patients (Child-Pugh B: 26; C: 58) without overt bleeding or blood-product transfusion were prospectively evaluated with routine hemostasis tests and TEG on admission and/or the first day with signs of infection and 5 days later. There were 30 patients with infection; 15 had infection on admission, and 15 developed infection in hospital. In the patients who developed infection in hospital, there was a significant deterioration in all routine hemostasis tests except platelet count (PLT) and in all TEG parameters, on the first day of infection compared with 7 +/- 3 days previously. The same parameters significantly improved from the first day of infection to day 5 and after (P <.02) only in the 22 patients whose infection resolved, while the r, k, and alpha TEG parameters significantly worsened in the 8 patients with persistent infection. In those who developed infection in hospital and were cured (n = 11), the 5-day parameters did not differ from their preinfection values. In conclusion, bacterial infections frequently impair hemostasis in decompensated cirrhotic patients. Successful treatment of infection usually restores hemostasis parameters to preinfection levels in 5 days. Thus, infection may have a role in the bleeding diathesis of cirrhosis.
Adult↗
From normal to pathological hemostasis.
PURPOSE: To review the evolution of knowledge on physiological hemostasis and the main abnormalities that may interfere with hemostasis in the perioperative period. METHODS: Narrative review of the literature, including relevant papers published in English. PRINCIPAL FINDINGS: Physiological hemostasis controls blood fluidity and rapidly induces hemostatic plug formation in order to stop or limit bleeding. The three distinct phases of the hemostatic process, primary hemostasis, coagulation and fibrinolysis are closely linked to each other and precisely regulated in order to efficiently close vessel wounds, promote vascular healing and maintain vessel patency. Primary hemostasis is the result of complex interactions between the vascular wall, platelets and adhesive proteins. Initiation of the coagulation pathway in vivo is secondary to the exposure of tissue factor (TF) and the formation of TF/VIIa complex which can activate both FIX and FX. This initiation phase is followed by a propagation phase with amplification of thrombin generation. Several control mechanisms exist for localizing fibrin formation to the site of injury including tissue factor pathway inhibitor, protein C system, antithrombin, and glycosaminoglycans on the vessel wall. Fibrinolysis is also a highly regulated system that controls fibrin dissolution. Both constitutive and acquired hemostasic defects exist. The consequences of these abnormalities are highly variable according to the type of defect, and to the genetic and environmental background. CONCLUSION: Hemostasis is one of the most complex physiological self-defence systems, not only involved in control of blood fluidity but also interfering in major physiopathological processes. The evolution of our knowledge of the physiology of hemostasis has numerous implications for therapy.
Animals↗
A multicenter randomized trial comparing a percutaneous collagen hemostasis device with conventional manual compression after diagnostic angiography and angioplasty.
OBJECTIVES: A new percutaneous collagen hemostasis device was compared with conventional compression techniques after diagnostic catheterization and angioplasty. BACKGROUND: Peripheral vascular complications after diagnostic catheterization or more complex interventional procedures, as well as the discomfort of manual compression and prolonged bed rest, represent significant morbidity for invasive cardiac procedures. METHODS: A prospective, multicenter, randomized trial was designed to compare the hemostasis time in minutes and the incidence of vascular complications in patients receiving a vascular hemostasis device with those undergoing conventional compression techniques. RESULTS: After diagnostic catheterization, hemostasis time was significantly less with the vascular hemostasis device than with conventional manual compression (4.1 +/- 2.8 min [n = 90 patients] vs. 17.6 +/- 9.2 min [n = 75], p < 0.0001). This difference was greater in patients undergoing angioplasty and was unrelated to the anticoagulation status (4.3 +/- 3.7 min [n = 71 not receiving heparin], 7.6 +/- 11.6 min [n = 85 receiving heparin], 33.6 +/- 24.2 min [n = 134 control patients not receiving heparin], p < 0.0001 vs. control patients). The time from the start of the procedure to ambulation was slightly less after diagnostic catheterization in patients treated with the device (13.3 +/- 12.1 h vs. 19.2 +/- 17.8 h, p < 0.05). It was also less in patients who underwent angioplasty when the device was used after discontinuation of anticoagulation (23.0 +/- 11.1 h, without heparin), as compared with control compression techniques (32.7 +/- 18.8 h, p < 0.0001). Time to ambulation was even shorter (16.1 +/- 11.1 h, p < 0.0001) in patients in whom the device was placed immediately after angioplasty while they were still fully anticoagulated with a prolonged activated clotting time (336 +/- 85 s). There were no major complications (surgery or transfusion) after diagnostic catheterization and a low incidence of major complications in patients who underwent angioplasty (0.7% in control patients, 1.4% with the device without heparin, 1.2% with the device and heparin, p = NS). After angioplasty, there was a trend toward fewer hematomas when the device was used in the absence of heparin (4.2% vs. 9.7% in control patients, p = 0.14). CONCLUSIONS: A new vascular hemostasis device can significantly reduce the puncture site hemostasis time and the time to ambulation without significantly increasing the risk of peripheral vascular complications. The role of this technology in reducing complications, length of hospital stay and cost remains to be determined.
Aged↗
Hemodynamic effects of brief pulmonary hemostasis.
We determined the hemodynamic effects of brief hemostasis in isolated blood-perfused rat lungs held at constant inflation pressure. Three periods of hemostasis, each lasting 20 min, alternated with equal durations of perfusion. Pulmonary vascular resistance (PVR), calculated as the ratio of the pulmonary arterial- (Ppa) left atrial (Pla) pressure difference to flow, was determined at baseline and after the third hemostasis period. Hemostasis increased PVR by 127% above baseline at constant Ppa and Pla (n = 8; P < 0.05) and by 71% at constant Pla and constant flow (n = 16; P < 0.05). The PVR increases were significantly attenuated by platelet (n = 5) or red blood cell (n = 4) removal from the lung perfusion, mechanical ventilation (n = 5), indomethacin (2 X 10(-6) M; n = 5), papaverine (10(-5) M; n = 4), and the thromboxane blocker SQ-29548 (7.8 X 10(-5) M; n = 4). By micropuncture we determined that the posthemostasis increase of the total pressure drop was 66% due to an increase of the venous pressure drop (P < 0.05). Isogravimetric pressure and lung water were not significantly altered by hemostasis. We conclude that brief hemostasis in the rat lung induces platelet- and red blood cell-dependent increase of vascular resistance. This effect may be attributable to hemostasis-induced platelet activation leading to thromboxane release.
Animals↗
Influence of hematocrit on hemostasis in continuous venovenous hemofiltration during acute renal failure.
BACKGROUND: Hematocrit plays a major role in primary hemostasis by influencing blood viscosity and platelet adhesion. During continuous venovenous hemofiltration (CVVH), it is suspected that an increased hematocrit is accompanied by an activation of hemostasis and frequently leads to thromboses in the extracorporeal system. In order to examine this hypothesis, we studied the influence of hematocrit on hemostasis during CVVH. METHODS: Fourteen patients (8 men and 6 women, mean age 65+/-10 years) with acute renal failure undergoing CVVH were prospectively enrolled. Polysulfone hemofilters (AV 600; Fresenius, Oberursel, Germany) were used in all of the patients; blood flow rates were adjusted to 120 ml/min. No blood products and coagulation-related medication, except unfractionated heparin, were applied. Study exclusion criteria included a history of thromboembolism and artificial heart valves. Hemostasis activation markers (fibrinopeptide A, thrombin-antithrombin III complex, beta-thromboglobulin, platelet retention) and hematocrit values were determined before and at three-day intervals during the course of CVVH treatment. RESULTS: The mean hematocrit value (mean +/- SEM) was 29+/-1% (range, 22 to 35%). Patients with hematocrit values of less than 30% (N = 7) were compared with patients with higher hematocrit values (>30%, N = 7). The patients with a lower hematocrit (<30%) showed a stronger activation of hemostasis during CVVH when compared with those with a higher hematocrit (>30%), as indicated by a tendency toward higher values for fibrinopeptide A (25+/-8 vs. 14+/-5 ng/ml, P = 0.35), thrombin-antithrombin III complex (15+/-4 vs. 10+/-2 ng/ml, P = 0.66), and a higher beta-thromboglobulin/creatinine ratio (0.62+/-0.17 vs. 0.48+/-0.12, P = 0.8). CONCLUSION: Contrary to our hypothesis, hematocrit values of more than 30% are not accompanied by an increased hemostasis activation during CVVH. Concerning hemostasis activation, hematocrit values between 30 and 35% may be suitable for patients on CVVH.
Acute Kidney Injury↗