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PubMedDate not supplied

A double-blind study of the effect on hemostasis of nabumetone (Relafen) compared to placebo.

A double-blind, placebo-controlled clinical trial comparing the effect on hemostasis of nabumetone (Relafen) to placebo in patients who were about to undergo forefoot surgery was performed. Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) are reported to inhibit platelet cyclooxygenase activity, resulting in altered platelet function and thus potentially enhanced bleeding. Nabumetone has been reported to have no effect on platelet aggregation and bleeding time in normal volunteers and in patients who have undergone knee arthroscopy. After fulfilling the inclusion criteria and after a 1-week washout period (acetaminophen controlled), 15 patients were enrolled in the nabumetone group and 15 patients were randomized in the placebo group. Hemostatic parameters [prothrombin time (PT), partial thromboplastin time (PTT), and Ivy bleeding time (IBT)] were assessed at baseline, visit 2, visit 3, and final visit. No meaningful differences were observed between treatment groups in any of the measured hemostatic parameters. No significant adverse events were reported. There was no significant change from baseline for PT, PTT, and IBT in the nabumetone group (PT, p < .06; PTT, p < .64; IBT, p < .17) versus the placebo group (PT, p < .61; PTT, p < .63; IBT, p < .25). The lack of bleeding diathesis and significant prolongation of PT, PTT, or IBT in this study suggests that nabumetone in dosages up to 1000 mg/day can be administered safely in the immediate preoperative period to patients undergoing forefoot surgery.

Adult↗
PubMedDate not supplied

Surgical hemostasis by pneumatic ankle tourniquet during 3027 podiatric operations.

A retrospective study was performed at the Denver Doctors Hospitals in which 3818 surgical cases on the foot and/or ankle were reviewed over a 4-year period from July 1986 through May 1990. From the 3027 ankle tourniquet cases reviewed, it was determined that pneumatic ankle tourniquets are safe and effective in providing hemostasis during foot surgery. There were five postoperative complications noted with ankle cuffs, with post-tourniquet syndrome being the most common (three cases). Over the 4-year period, ankle tourniquets failed a total of 50 times, a 1.8% failure rate (0.25% failure rate in the last 17 months). The most common pressure setting used for ankle cuffs was 325 mm. Hg (400 mm. Hg for thigh cuffs). Tourniquet ischemia lasted from 4 to 139 min.; the most common duration of ischemia noted for ankle tourniquets was 30 to 60 min. (60 to 90 min. for thigh tourniquets). A review of the potential complications associated with tourniquets, as well as safeguards, recommendations, and contraindications are presented.

Adolescent↗
PubMed1995

Suture placement for hemostasis during laparoscopy using the Stamey needle.

Bleeding at cannula insertion sites during laparoscopic procedures often is difficult to manage. The few published techniques for controlling abdominal wall bleeding include suturing under direct observation, electrocoagulation, and placement of a Foley catheter. These methods may provide less than adequate hemostasis, however. We developed a technique of direct suture placement under laparoscopic guidance using an absorbable monofilament suture and the Stamey needle as a ligature carrier.

Abdominal Muscles↗
PubMedDate not supplied

Liver resection using total vascular exclusion, scalpel division of the parenchyma, and a simple compression technique for hemostasis and biliary control.

Recent improvements in perioperative morbidity and long-term outcome following liver surgery have led surgeons to attempt larger and more technically challenging liver resections. Total vascular exclusion (TVE) of the liver during resection has been proposed as a technique that will facilitate these difficult resections while minimizing blood loss. Total vascular exclusion is performed by obtaining complete isolation of the vascular pedicle of the liver. Once the hepatic vein is clamped, rapid resections may be performed with a loss of only the blood volume contained within the liver itself. Safe performance of total vascular exclusion of the liver requires a thorough understanding of hepatic anatomy, patient selection criteria, and the physiologic changes incurred by hepatic exclusion and subsequent ischemia and reperfusion. The following report discusses these issues, gives a detailed description of the steps involved in obtaining safe total vascular exclusion, and presents a technique using rapid parenchymal excision with a scalpel and capsular compression to obtain hemostasis and prevent bile leaks. We briefly discuss our experience with 144 consecutive resections in which this technique was used.

Bile↗
PubMed2001

[Value of pelvic tamponade in persistent hemorrhage afer hemostasis hysterectomy].

Obstetrical hemorrhage is a severe complication with vital prognosis at stake. Treatment depends on aetiology: a surgical procedure may be indicated initially or after failure of medical management. Radical treatment with hemostasis hysterectomy is generally successful. However, in case of persistent hemorrhage after hysterectomy, other means are available such as pelvic tamponade.

Adult↗
PubMed2002

Genetic mechanisms of hereditary hemostasis disorders.

This review summarizes known human genes whose mutations are associated with inherited hemostasis defects. These genes are divided into three groups. The genes of the first group are responsible for platelet adhesion, activation, and aggregation. The genes of the second group control the biosynthesis of blood-clotting factors and cofactors. The genes of the third group are required for the functioning of proteins involved in the anticoagulant system and fibrinolysis.

Blood Platelets↗
PubMed2002

Trophoblastic beta1-glycoprotein and hemostasis system in pregnant women with antiphospholipid syndrome.

Clinical and laboratory studies were carried out in 38 pregnant women with antiphospholipid syndrome. Increased functional activity of platelets and decreased protein-producing function of the placenta were observed starting from the early terms of gestation. These disorders were followed by the development of hypercoagulation in the plasma component of hemostasis, appearance of intravascular blood clotting markers, and inhibition of AT III and protein C. This led to the progress of disorders in the microcirculatory bed, fetoplacental insufficiency, decrease in trophoblastic beta1-glycoprotein level, chronic hypoxia, and fetal death. Infection accelerated this process. Measurements of trophoblastic beta1-glycoprotein every 2 weeks help to diagnose fetoplacental disorders, predict the course of pregnancy, and evaluate the efficiency of drug therapy.

Abortion, Habitual↗
PubMedDate not supplied

Mice deficient in heparan sulfate 3-O-sulfotransferase-1: normal hemostasis with unexpected perinatal phenotypes.

Heparan sulfate that contains antithrombin binding sites is designated as anticoagulant heparan sulfate (HS(act)) since, in vitro, it dramatically enhances the neutralization of coagulation proteases by antithrombin. Endothelial cell production of HS(act) is controlled by the Hs3st1 gene, which encodes the rate limiting enzyme-heparan sulfate 3-O-sulfotransferase-1 (Hs3st1). It has long been proposed that levels of endothelial HS(act) may tightly regulate hemostatic tone. This potential in vivo role of HS(act) was assessed by generating Hs3st1(-/-) knockout mice. Hs3st1(-/-) and Hs3st1(+/+) mice were evaluated with a variety of methods, capable of detecting altered hemostatic tone. However, both genotypes were indistinguishable. Instead, Hs3st1(-/-) mice exhibited lethality on a specific genetic background and also showed intrauterine growth retardation. Neither phenotypes result from a gross coagulopathy. So although this enzyme produces the majority of tissue HS(act), Hs3st1(-/-) mice do not show an obvious procoagulant phenotype. These results suggest that the bulk of HS(act) is not essential for normal hemostasis and that hemostatic tone is not tightly regulated by total levels of HS(act). Moreover, the unanticipated non-thrombotic phenotypes suggest structure(s) derived from this enzyme might serve additional/alternative biologic roles.

Animals↗
PubMed2003

[Interpretation of screening tests of hemostasis].

The specialized hemostasis laboratory offers a huge amount of coagulation tests. However, the most important test for the general physician are the so-called coagulation screening tests. These tests include the prothrombin time, the activated partial thromboplastin time, the thrombin clotting time (often in combination with the reptilase time), fibrinogen concentration and the platelet count. Primary haemostasis is investigated by using the bleeding time or the platelet function analyzer (PFA-100). Depending on the results, in a second phase of investigation specific factor assays or other tests may be indicated. In the present work, we present the individual tests and discuss possible reasons for abnormal results.

Blood Coagulation Disorders↗
PubMed2002

The levels of five markers of hemostasis and endothelial status at different stages of normotensive pregnancy.

BACKGROUND: Urinary 11-dehydrothromboxane B(2)/creatinine (11-DTXB(2)/Cr) is a marker for in vivo platelet activation and vascular constriction, blood thrombomodulin (TM) for endothelial damage and associated thrombosis, thrombin-antithrombin complex (TAT) for thrombin formation, and beta-thromboglobulin (beta-TG) and platelet factor 4 (PF-4) for in vivo platelet activation and releasing reaction. Little is known about the quantitative relationship among them during pregnancy. The present study investigated levels of five markers at different stages of normotensive pregnancy. METHODS: Subjects were 17 healthy non-pregnant women (Group 1, control) and 67 women carrying single fetuses in normotensive pregnancy. Of the pregnant women, 17 were in the 20th week of gestation (Group 2), 20 were in their 30th week (Group 3), and 30 were in their 36th week (Group 4). Urinary and circulating blood levels of 11-DTXB(2)/Cr, TM, TAT, beta-TG, and PF-4 were measured simultaneously. RESULTS: The 11-DTXB(2)/Cr and TAT levels showed elevated values at the 20th and 30th weeks of gestation, and markedly elevated values at the 36th week, whereas the TM level remained constant throughout pregnancy. The beta-TG and PF-4 levels maintained stable values at the 20th week, but showed elevated values at the 30th and 36th weeks. CONCLUSIONS: Platelet aggregation, vascular constriction, and thrombin formation (detected by 11-DTXB(2)/Cr and TAT) appear to be enhanced as early as the 20th week of gestation, continuously enhanced by the 30th week, and markedly enhanced by the 36th week. Platelet activation and releasing reaction (determined by beta-TG and PF-4) gradually enhanced from the 30th to 36th weeks. In contrast, endothelial damage and associated thrombosis (detected by TM) were minimal throughout pregnancy. Investigating these markers of hemostasis and endothelial function in normotensive pregnancy may provide insights into related disease states.

Adult↗
PubMed2003

A randomized comparison of a percutaneous suture device versus manual compression for femoral artery hemostasis after PTCA.

BACKGROUND: The prolonged bed rest following femoral sheath removal after PTCA is a source of discomfort for the patient. We designed a randomized study to evaluate the efficacy and safety of an arterial suture device developed to percutaneously close the vascular access site after PTCA, allowing immediate sheath removal and early ambulation, compared to manual compression. METHODS: After successful PTCA, patients were randomized to manual compression or immediate femoral percutaneous closure. Exclusion criteria were arteritis, age > 80 years and > 3 previous femoral punctures on the same side. The two-needle device was used for the 6F sheath removal and the four-needle device for the 8F sheath. Ambulation was allowed 4 hours after the arterial suture. RESULTS: One hundred and sixty-seven patients (59 +/- 10 years, 81% males) were randomized to suture device (n = 91) or to manual compression (n = 76). The two groups were similar in terms of age, sex, size of sheath, number of patients with stent implantation (62 vs 61%), procedural anticoagulation. Procedural duration was 8 +/- 6 minutes with percutaneous suture versus 25 +/- 11 minutes with manual compression (P < 0.0001). Procedural success with percutaneous suture was 93% whereas six technical failures were treated with prolonged manual compression. Nonsurgical hematoma occurred in five patients (5%) with the suture device and in two (3%) with manual compression with no need for blood transfusion (P = NS). Uneventful blood oozing occurred in 11 patients (12%) with percutaneous suture and in only 2 (3%) with manual compression (P < 0.06). The tolerance of the hemostasis procedure and the length of post-procedure hospital stay (40 +/- 32 hours) were similar in the two groups. CONCLUSION: Percutaneous suture of the femoral artery, allows immediate closure of femoral puncture sites after PTCA, without increasing the incidence of vascular complications. The use of this device should allow earlier discharge and subsequent cost savings.

Aged↗
PubMed1999

Targeted disruption of cd39/ATP diphosphohydrolase results in disordered hemostasis and thromboregulation.

CD39, or vascular adenosine triphosphate diphosphohydrolase, has been considered an important inhibitor of platelet activation. Unexpectedly, cd39-deficient mice had prolonged bleeding times with minimally perturbed coagulation parameters. Platelet interactions with injured mesenteric vasculature were considerably reduced in vivo and purified mutant platelets failed to aggregate to standard agonists in vitro. This platelet hypofunction was reversible and associated with purinergic type P2Y1 receptor desensitization. In keeping with deficient vascular protective mechanisms, fibrin deposition was found at multiple organ sites in cd39-deficient mice and in transplanted cardiac grafts. Our data indicate a dual role for adenosine triphosphate diphosphohydrolase in modulating hemostasis and thrombotic reactions.

Adenosine Triphosphatases↗
PubMed2001

Plasma fibronectin supports neuronal survival and reduces brain injury following transient focal cerebral ischemia but is not essential for skin-wound healing and hemostasis.

Fibronectin performs essential roles in embryonic development and is prominently expressed during tissue repair. Two forms of fibronectin have been identified: plasma fibronectin (pFn), which is expressed by hepatocytes and secreted in soluble form into plasma; and cellular fibronectin (cFn), an insoluble form expressed locally by fibroblasts and other cell types and deposited and assembled into the extracellular matrix. To investigate the role of pFn in vivo, we generated pFn-deficient adult mice using Cre-loxP conditional gene-knockout technology. Here we show that pFn-deficient mice show increased neuronal apoptosis and larger infarction areas following transient focal cerebral ischemia. However, pFn is dispensable for skin-wound healing and hemostasis.

Animals↗
PubMed1997

Hemostasis in patients with severe von Willebrand disease improves after normal platelet transfusion and normalizes with further correction of the plasma defect.

BACKGROUND: A defective hemostatic effect of plasma concentrate infusion in patients with severe von Willebrand disease (vWD) has been ascribed to the absence of platelet von Willebrand factor (vWF) STUDY DESIGN AND METHODS: The role of platelet vWF in hemostasis of severe vWD was investigated. A plateletpheresis unit (4-5 x 10(11) platelets) from a normal compatible donor was transfused before any cryoprecipitate infusion to three type 3 vWD patients and to one patient with severe type 1 vWD with low levels of platelet vWF who required replacement therapy for bleeding episodes. Autologous platelets were transfused to one of the patients with type 3 vWD. RESULTS: Partial corrections of bleeding times (14-17 min vs. baseline >30 min) were observed in all patients after the transfusion of normal platelets. During cryoprecipitate infusion, bleeding times were normalized (<6 min), and bleeding episodes stopped when plasma levels of vWF activity ranged from 14 to 18 U per dL. Platelet interactions with the subendothelium increased in parallel with the correction of bleeding times. These results indicate that if approximately 20 percent of the total number of platelets have normal vWF antigen and if plasma vWF levels are at least 14 U per dL, then bleeding times will normalize and mucosal hemorrhages will stop. Transfusion of autologous platelets in one patient with type 3 vWD did not modify bleeding times or platelet adhesion on the subendothelium. CONCLUSION: The hemostatic effect of normal platelets in type 3 vWD seems to be related to the platelet vWF in the transfused platelets.

Bleeding Time↗
PubMed2003

Hemostasis and irreducible complexity.

Coagulation evolved as a means to stem the loss of blood and to defend against pathogens. The complexity of the clotting cascade has been cited as evidence for the existence of divine intervention. The objective of this review is to draw on the debate between creationists and evolutionary biologists to highlight important evolutionary principles that underlie the hemostatic mechanism. I propose the following: (a) as with all biological systems, the hemostatic mechanism displays non-linear complexity; (b) the cellular response represents primary hemostasis owing to its place in the evolutionary time scale and functional importance; and (c) the rapid evolution of the hemostatic mechanism in vertebrates is testimony to the power and versatility of gene duplications and exon shuffling.

Animals↗
PubMed2001

Influence of coconut water on hemostasis.

Coconut water (CNW) can be used as short-term intravenous hydration and resuscitation fluid. We investigated the influence of coconut water on plasma coagulation in vitro. Either CNW or physiological saline (PS) was added to citrated plasma of 8 healthy volunteers. Coagulation capability of diluted plasma was evaluated by thrombelastography (TEG). Replacement of up to 50 % of citrated plasma by CNW or PS did not influence initiation of coagulation as indicated by split point and reaction time, respectively. Strength of fibrin clot as expressed by maximum amplitude (MA) of TEG recording dose dependently declined in both groups. Replacing 50 % of citrated plasma by CNW or PS reduced MA by 39% and 32%, respectively. The influence of coconut water on hemostasis as assessed by TEG does not differ from the effect caused by an identical volume of PS.

Blood Coagulation↗
PubMed2004

Challenges for providing effective hemostasis in surgery and trauma.

Vascular injury, whether surgical or traumatic, triggers a complex series of regulatory events. The understanding of these events, their interdependence, and their effect on hemostasis and thrombosis, is slowly being unraveled. The current understanding of these processes is reviewed in this paper. The application of this knowledge to the operating theatre has been slow and is severely limited by the lack of effective tools to monitor the coagulopathic status of individual patients. Hence, the initial treatment of patients with severe hemorrhage relies on improving the patient's physiological status and on basic surgical techniques. Should these efforts fail, then a number of topical hemostatic agents, selective inhibitors of fibrinolysis, and procoagulant molecules, such as recombinant factor VIIa, may be utilized. However, many of these agents have not yet been tested in clinical trials and studies are urgently needed to determine efficacy, safety, optimal dosage and time of administration.

Anticoagulants↗
PubMed2003

The action of high-dose factor VIIa (FVIIa) in a cell-based model of hemostasis.

We have developed a cell-based model of hemostasis. This model suggests that the defect in hemophilia is specifically a failure of platelet-surface factor Xa (FXa) generation, leading to a failure of platelet surface thrombin generation. Activation of FX by FVIIa/tissue factor (TF) does not compensate for a lack of FXa activation on the platelet surface by the FVIIIa/FIXa complex. This is because plasma protease inhibitors prevent FXa from moving through the fluid phase from the TF-bearing cell to the platelet surface. We have previously proposed a platelet-dependent mechanism of action for high-dose factor VIIa (FVIIa; Novoseven, Novo Nordisk, Copenhagen, Denmark). Our data suggest that, when present at high levels, FVIIa binds to activated platelets and activates small amounts of FX independent of TF. This platelet-surface FXa can partially restore platelet-surface thrombin generation in hemophilia. Recently, van't Veer and colleagues reported results from an in vitro model in which coagulation reactions were initiated by relipidated TF. The authors concluded that high-dose FVIIa may exert a hemostatic effect in hemophilia by overcoming inhibition of FVIIa/TF activity by zymogen FVII. By contrast, we found that plasma levels of FVII did not slow thrombin generation in a model system initiated with cell-associated TF. This discrepancy highlights the potential differences between the studies of the coagulation reactions assembled on living cells compared to phospholipid vesicles. Our data suggest that in a cellular system high-dose FVIIa acts primarily by enhancing the rate of thrombin generation on platelet surfaces and not by overcoming inhibition by zymogen FVII of TF-dependent activation of FX.

Animals↗