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PubMed1997

Hemostasis in newborns of smoking and nonsmoking mothers.

OBJECTIVE: Our purpose was to determine the effect of smoking during pregnancy on neonatal hemostasis. STUDY DESIGN: Venous blood samples of 26 newborns of smoking and 25 newborns of nonsmoking mothers were obtained from the clamped umbilical cord immediately after birth. Prothrombin fragment 1+2, thrombin-antithrombin III complex, plasmin-alpha2-antiplasmin complex, and D-dimer levels were determined to assess activation of coagulation and fibrinolysis. Cotinine was measured in all neonates to objectify cigarette smoke exposure. The Mann-Whitney U test was used to compare the differences between the values of the parameters of coagulation and fibrinolysis in the two groups at the p < 0.05 level. RESULTS: The median values of prothrombin fragment 1+2 and thrombin-antithrombin III complex in newborns exposed to tobacco smoke in utero did not differ from values of newborns who were not exposed. Nor were the markers of fibrinolysis, plasmin-alpha2-antiplasmin complex and D-dimer levels, influenced by tobacco smoke exposure. CONCLUSION: The balance between the components of coagulation and fibrinolytic pathways in neonates is not disturbed by maternal smoking.

Antifibrinolytic Agents↗
PubMed1998

Hemostasis in the uteroplacental and peripheral circulations in normotensive and pre-eclamptic pregnancies.

OBJECTIVE: Our purpose was to determine the hemostatic changes in the uteroplacental and peripheral circulations in normotensive and pre-eclamptic pregnancies. STUDY DESIGN: This prospective, observational study involved 2 patient groups. Group 1 consisted of 30 normotensive women and 22 women with pre-eclampsia who were followed up longitudinally through pregnancy and post partum. Group 2 consisted of 20 women with established pre-eclampsia and 19 normotensive control subjects, all undergoing cesarean section. Plasma levels of thrombin-antithrombin III complex, soluble fibrin, plasmin-alpha2-antiplasmin complex, and fibrin-degradation product (D-dimer) were measured in blood drawn from the antecubital vein (group 1) and from both the antecubital and uterine veins (group 2). Data were analyzed by analysis of variance. RESULTS: In group 1 levels of thrombin-antithrombin III complex, soluble fibrin, and fibrin-degradation product were significantly higher during normal pregnancy than at 6 weeks post partum. Plasmin-alpha2-antiplasmin complex levels did not change. No differences between the pre-eclamptic and normotensive pregnancy groups were found for any of the hemostatic markers. In group 2 normotensive women undergoing cesarean section, thrombin-antithrombin III complex and soluble fibrin levels were significantly higher in the uterine vein than in the antecubital vein. In group 2 women with pre-eclampsia, thrombin-antithrombin III complex and fibrin-degradation product levels were significantly higher in the uterine vein than in the antecubital vein. In addition, plasmin-alpha2-antiplasmin complex and fibrin-degradation product levels were higher and soluble fibrin levels were lower in the uterine vein in the pre-eclamptic group than in the normotensive group. CONCLUSION: Both the coagulation and fibrinolytic systems are activated during normal pregnancy. Activation of these systems is more marked in the uteroplacental circulation than in the systemic circulation in both normotensive and pre-eclamptic pregnancies. An abnormal pattern of hemostasis occurs in the uteroplacental circulation in pre-eclampsia.

Adult↗
PubMed1988

Impaired hemostasis caused by beta-lactam antibiotics.

Beta-lactam antibiotics can directly impair hemostasis by two separate nonimmune mechanisms. First, the NMTT-substituted cephalosporin drugs may cause hypoprothrombinemia by interfering with the hepatic activation of clotting factors II, VII, IX, and X. Second, the antipseudomonal penicillins may cause the bleeding time to be prolonged by interfering with platelet aggregation to physiologic agonists. In surgical patients who are malnourished, have impaired gastrointestinal function, or have renal failure, the potential for these adverse effects is increased. Serious bleeding requires treatment with fresh frozen plasma when hypoprothrombinemia is caused by NMTT-containing cephalosporins, since the prothrombin time returns to baseline relatively slowly after therapy with vitamin K. Hemorrhage caused by beta-lactam-induced platelet dysfunction must be treated with platelet concentrates, since new platelets sufficient to correct the defect do not enter the circulation for several days after treatment with the offending drug is discontinued. The more desirable approach is to prevent hypoprothrombinemia by giving vitamin K prophylaxis and to avoid beta-lactams that impair platelet function in seriously ill patients at increased risk for bleeding.

Anti-Bacterial Agents↗
PubMed1985

New applications of the laser in pulmonary surgery: hemostasis and sealing of air leaks.

In thoracic surgery, the laser has been used primarily as a destructive instrument (e.g., for extirpation of endobronchial lesions and for skin incisions). Previously, the carbon dioxide laser was used for its scalpel-like action but not for sealing. The neodymium:yttrium aluminum garnet (Nd:YAG) laser not only cuts but also seals blood vessels and bronchi. We have modified the CO2 laser technique to seal vessels and bronchi up to 3 mm on a cut surface by using low power in a defocused mode, and have evaluated the method in 12 dogs. Matched lesions in the lingula were sealed with each type of laser and compared with lesions closed by suture technique. These lesions were then evaluated at biweekly intervals up to 6 weeks following operation. All lesions demonstrated substantial air leak and bleeding prior to sealing. There was no bleeding or air leak (40 cm H2O of pressure) at any time after sealing (laser or suture). The CO2 laser sealing consistently produced the least damage both macroscopically and microscopically. However, this technique requires a relatively bloodless field. The Nd:YAG laser produced the deepest tissue destruction but functioned well under conditions of poor hemostasis. Suture closure produced large early injuries, which subsided gradually to approach the amount of damage seen with the CO2 laser. These studies demonstrate that the laser may be a useful adjunct to maximally preserve normal lung tissue and to seal bleeding, leaking, raw lung surfaces. Results of early clinical trials are also detailed.

Aged↗
PubMed1977

Control of heparinization by activated clotting time during bypass with improved postoperative hemostasis.

Heparin and protamine dosages monitored during open-heart operations by activated clotting time (ACT) have been reported to be superior to dosage schedules based on body weight or body surface area. To evaluate the automated ACT, 114 consecutive open-heart operations performed between October, 1974, and December, 1975, were studied. Fifty-eight operations prior to April, 1975, using a standard heparin-protamine protocol (Group I) were compared with 56 operations from April to December, 1975, monitored with an automated ACT (Group II). The two groups were similar with respect to surgical procedures, pump time, and perfusion techniques. The protamine/heparin ratio was 25% less in Group II compared with Group I, and the 12-hour postoperative blood loss was 48% less in Group II. The automated ACT is a reliable, rapid, and simple test that has resulted in improved hemostasis following cardiac operation.

Blood Coagulation Tests↗
PubMed1997

"Low-dose" aprotinin modifies hemostasis but not proinflammatory cytokine release.

BACKGROUND: Cytokines are implicated in the pathogenesis of the "whole-body inflammatory response" that may complicate the period after cardiopulmonary bypass (CPB). Low-Dose aprotinin in the pump during CPB has been shown to improve postoperative hemostasis and platelet preservation. We tested the hypothesis that low-dose aprotinin influences the inflammatory reaction (in terms of cytokine release) after CPB. METHODS: In a prospective, randomized study, 36 patients undergoing elective coronary artery bypass grafting were investigated. Nineteen patients received low-dose aprotinin (2 x 10(6) KIU (280 mg] in the pump), and a control group of 19 did not. Complement activation, cytokine production, leukocyte elastase release. D-dimer level, full blood count, postoperative blood loss, and transfusion requirements were analyzed before, during, and after after CPB. RESULTS: Interleukin-1 beta was not detected in either group, whereas traces of tumor necrosis factor-alpha were infrequently observed. Plasma elastase, interleukin-6, interleukin-8, and neutrophil count increased (p < 0.001) during and after CPB compared with the baseline levels, reaching a peak at 2 hours after protamine administration in both groups before returning toward baseline at 24 hours. Proinflammatory cytokine markers did not differ significantly (p > 0.1) between the groups throughout the study period. The C5b-9 level increased (p < 0.001) in both groups perioperatively, reaching its peak 15 minutes after protamine. Twenty-four-hour postoperative blood loss was significantly (p < 0.001) reduced in the aprotinin group in association with markedly reduced D-dimer levels (p < 0.001). Patients in the aprotinin group also received significantly less banked blood postoperatively than the control group (p < 0.01). CONCLUSIONS: Low-dose aprotinin fails to modify proinflammatory cytokine release, yet confers hemostatic improvement through reduced fibrinolysis in patients undergoing routine coronary artery bypass grafting.

Aged↗
PubMed1999

Vascular clamp for hemostasis and stabilization during minimally invasive direct coronary artery bypass.

A soft vascular clamp was used for hemostasis and stabilization of the operative field during minimally invasive direct coronary artery bypass (MIDCAB). The instrument was gently applied so that it clamps the coronary artery by grasping the adjacent myocardium. The method offered dry and stable operative field without a special instrument or technique. The surgical results have been satisfactory. We found application of the vascular clamp to be very helpful for MIDCAB.

Arteries↗
PubMed1996

The effects of reformulated 2-rod Norplant implant on hemostasis after three years.

Prolonged use of reformulated and the original 2-rod Norplant implants showed similar changes in most hemostatic parameters studied. Raised hemoglobin concentration and hematocrit values with not enhanced platelet activation or significant changes in platelet numbers were seen. Factor VII showed an increase from 18 months compared to the first 12 months of original Norplant implant use, while with reformulated Norplant implant, the level at 36 months was significantly higher than the first 24 months of implant use. Fibrinogen levels were significantly elevated by 36 months of both implant use. No evidence of enhanced activation of coagulation, fibrinolysis/inhibitor were observed during prolonged implant use. Overall, no significant changes in tissue plasminogen activator (t-PA) levels were observed but urokinase-like plasminogen activator (u-PA) levels were significantly reduced, indicating no enhancement of tissue breakdown. Plasminogen activation inhibitor (PAI-1) antigen levels were significantly reduced from 12 to 36 months with original Norplant implant use compared to the pre-insertion levels, while a nonsignificant decreased trend was seen with prolonged reformulated Norplant implant use. The increased levels of fibrinogen and FVII at the end of 36 months of implant use require further observation as these factors are known markers of hypercoagulation and associated with increased arteriosclerotic and cardiovascular risks. This study is on-going to evaluate the effects of levonorgestrel-containing subdermal reformulated Norplant implants on hemostasis after five years of use.

Adult↗
PubMed1997

T-686, a novel inhibitor of plasminogen activator inhibitor-1, inhibits thrombosis without impairment of hemostasis in rats.

The aim of this study was to evaluate the antithrombotic potential of T-686 ((3E,4E)-3-benzylidene-4-(3,4,5-trimethoxy-benzylidene)-pyrr olidine-2,5-dione), a novel inhibitor of plasminogen activator inhibitor-1 (PAI-1), in rat thrombosis models. T-686 (0.1-100 mg/kg per day, p.o.) dose dependently decreased the weight of venous thrombi induced by a combination of stasis and hypercoagulability. The antithrombotic effect was enhanced by repeated administration of T-686. Warfarin (0.1 mg/kg per day for 3 days) also prevented thrombus formation. The antithrombotic action by warfarin was accompanied by prolongation of coagulation time, while no effect on coagulation time was observed in T-686-treated rats. T-686 lowered the activity of PAI-1 in plasma. In the arterio-venous shunt model, pretreatment with T-686 (10 mg/kg per day) or ticlopidine (100 mg/kg per day) for 8 days inhibited thrombus formation by 33% and 44%, respectively. T-686 had no effect on collagen-induced platelet aggregation ex vivo, while ticlopidine inhibited platelet aggregation. T-686 did not affect bleeding time at 10-100 times the antithrombotic dose, while warfarin dose dependently prolonged bleeding time at and around the antithrombotic dose. These results suggest that T-686 prevents thrombus formation in rats without impairment of hemostasis.

Animals↗
PubMed1995

Prospective validation of the Baylor bleeding score for predicting the likelihood of rebleeding after endoscopic hemostasis of peptic ulcers.

Endoscopic therapy is effective in securing hemostasis for bleeding ulcers, but bleeding recurs in 10% to 30% of patients. Prospective identification of patients at increased risk for rebleeding is requisite to reducing rebleeding rates. We previously developed a three-component scoring system that identifies patients at increased risk for rebleeding. In the present study, we prospectively validated our scoring system. Forty-seven men ranging in age from 23 to 95 years in whom endoscopic therapy for bleeding ulcers was successful were studied. Patients with pre-endoscopy scores greater than 5 or postendoscopy scores greater than 10 were stratified as high-risk, and patients with pre-endoscopy scores of 5 or less and post-endoscopy scores of 10 or less as low-risk. Twenty-six patients were categorized as high-risk and 19 as low-risk. All patients were followed until discharged from the hospital. The rebleeding rate for high-risk patients was 31% (8 of 26), compared with 0 for low-risk patients (p < .05). We conclude that our scoring system accurately predicts patients at increased risk for rebleeding after successful endoscopic therapy of bleeding ulcers.

Adult↗
PubMed1981

Angiomatous lymphoid hamartoma: inhibitory effects on erythropoiesis, growth, and primary hemostasis.

An 11-year-old boy was noted to have microcytic anemia, growth retardation, polyclonal hypergammaglobulinemia, and abnormal platelet function. An angiomatous lymphoid hamartoma was removed from the retroperitoneal space. Postoperatively the child exhibited a dramatic growth spurt and complete resolution of the abnormal laboratory measurements. Studies were performed before and after tumor removal to investigate the nature of the associated anemia, growth retardation, and altered hemostasis. There was no evidence of iron deficiency, thalassemia, or an antierythropoietin factor. Prolonged bleeding time and impaired ristocetin-induced platelet aggregation normalized following tumor resection. Serum obtained before surgery inhibited lymphocyte proliferation in mixed lymphocyte culture as well as fibroblast growth in vitro. Detailed study of growth regulatory hormones failed to reveal significant alterations except for significantly reduced somatomedin which normalized after surgery. The factor(s) which inhibit in vitro cellular growth and lower in vivo plasma somatomedin concentration remain unknown.

Adolescent↗
PubMed1987

Hemostasis and thromboembolism in children with nephrotic syndrome: differences from adults.

Eleven of 204 children with nephrotic syndrome had thrombotic complications: arterial thrombosis in five, venous thrombosis in four, and pulmonary embolism in two. Fifty-one episodes of thromboembolism were recognized in 116 adult patients with nephrotic syndrome. Despite the lower incidence, thromboembolic complications tended to be more severe in children. In vitro indices of hemostasis and clinical evidence of thromboembolic complications were compared in children and adults. Antithrombin III concentrations and activities were abnormal in seven of 10 children, but in only two of 32 adults. In both groups, alpha 2-macroglobulin was elevated, but more markedly so in children. No evidence for circulating granulocyte-derived proteases (elastase/antielastase complexes) was noted in either group. Protein C was significantly elevated in children with nephrotic syndrome, but was normal in adults. Children also differed from adults with nephrotic syndrome in laboratory evidence of subthreshold disseminated intravascular coagulation (i.e., elevated soluble fibrinogen monomeric complexes and fibrin degradation products) and indicators of in vivo platelet activation (elevated beta-thromboglobulin). The more severe coagulation abnormalities in children may be linked to the more pronounced hypoalbuminemia.

Adolescent↗
PubMed1996

Low-dose and high-dose aprotinin improve hemostasis in coronary operations.

Prophylactic aprotinin therapy has become a popular method to reduce bleeding associated with cardiac operations. Today essentially two dose regimens are used, a high-dose regimen with administration throughout the complete operative procedure and a low-dose regimen with administration only during bypass. In unblinded studies both regimens were found to be equally effective. This double-blind placebo-controlled study in 115 patients undergoing elective coronary artery bypass grafting was done to confirm these results without potential investigator bias. Intraoperative hemoglobin loss was significantly reduced (p < 0.01) by 42% in the high-dose group and by 17% in the low-dose group compared with loss in control subjects. Blood loss 6 hours after operation was 377 ml in the low-dose and 266 ml in the high-dose group compared with 630 ml in the placebo group (p < 0.05 and p < 0.001, respectively). The average number of transfusions with packed red blood cells was reduced 31% in the low-dose group and 45% in the high-dose group, but the reductions were not significant. In a subgroup of patients, markers for coagulation and fibrinolysis were studied to investigate whether a different extent of activation existed. Fibrinolysis as measured by D-dimer levels was completely inhibited by the high-dose regimen, but was only partly suppressed in the low-dose group as compared with findings in the placebo group. Thrombin generation during cardiopulmonary bypass as reflected by F1 + 2 levels was lower in patients treated with aprotinin, but the difference was not significant. Concentrations of thrombin inactivated by antithrombin III were not different between the groups. The observation that low-dose aprotinin significantly improved hemostasis but did not inhibit hyperfibrinolysis supports our previous finding that low-dose aprotinin mainly protects platelet adhesive function. The better result obtained with high-dose aprotinin may indicate the contribution of hyperfibrinolysis to bleeding after cardiopulmonary bypass. Because high-dose aprotinin is administered outside the period of full heparinization and might therefore increase the risk of thromboembolic complications, we propose a modification of the low-dose schedule to increase aprotinin levels sufficient for plasmin inhibition before release of the aortic crossclamp.

Antithrombin III↗
PubMed1977

Hydraulic hemostasis in transurethral resection of the prostate using the Iglesias continuous suction resectoscope.

An intravesicoprostatic hydrostatic pressure less than 10 mm. Hg maintains normal anatomy and physiology of the muscular and vascular prostatic structures. An increase in hydrostatic intravesicoprostatic pressure to more than 10mm. Hg produces a distortion in the musculature of the prostate, especially at the true capsule, opening the cut vessels and making possible the absorption of the irrigant free of electrolytes (transurethral resection syndrome). A low hydrostatic intravesicoprostatic pressure permits the compression of cut vessels by the inflow hydraulic pressure of 90 cm. water, achieving hydraulic hemostasis during transurethral resection of the prostate. Less electrocoagulation is necessary, resulting in more rapid patient recovery.

Hemostasis, Surgical↗
PubMed1987

Preoperative evaluation of hemostasis in patients with congenital heart disease.

The incidence of abnormal results of coagulation tests and the risks for postoperative hemorrhage were assessed in 235 patients with congenital heart disease. Preoperatively, the prothrombin time, partial thromboplastin time, activated partial thromboplastin time, thrombin time, or platelet count was abnormal in 45 of the 235 patients (19%), a significantly higher incidence than that expected in a normal population (P less than 0.002). Prolonged values for the prothrombin time or the partial thromboplastin time or activated partial thromboplastin time were seen most frequently. Further evaluation in eight of the patients with prolonged prothrombin time or partial thromboplastin or activated partial thromboplastin time showed decreased levels of either factor VII or IX in six of them, suggesting that impaired vitamin K-dependent carboxylation is commonly present. Normal results of preoperative coagulation tests do not exclude the presence of a major bleeding diathesis (von Willebrand's disease was later diagnosed in a patient with such findings). The use of blood products during subsequent cardiac operations was not significantly different in patients with normal or abnormal test results. Two of the three patients who required reoperation and were found to have a nonsurgical cause of bleeding had abnormalities in two or more of the preoperative coagulation tests. This finding suggests that abnormal results of preoperative coagulation tests may be predictive of defective hemostasis in the postoperative period.

Adolescent↗
PubMed1993

Abnormalities of hemostasis in ischemic stroke.

Despite important new diagnostic laboratory and imaging technologies, the cause of brain infarction remains unexplained in 20% to 40% of subjects. Most stroke patients do not require extensive evaluations of coagulation, but hypercoagulability may account for a significant proportion of unexplained strokes. Hemostatic abnormalities associated with stroke may be broadly classified as familial or acquired. Principal among the familial thrombotic coagulopathies are deficiencies in concentration or function in protein-C, protein-S, and antithrombin III, but other hereditary abnormalities include sickle cell disease, homocystinuria, and dysfibrinogenemia. The acquired disorders of hemostasis associated with stroke probably constitute a larger proportion of the important stroke-related coagulopathies. In particular, the aPL antibody syndrome is now strongly associated with thrombotic events including stroke, although neither the mechanism of thrombosis nor effective therapies for this syndrome have been clearly elucidated. Many of the acquired hemostatic abnormalities exist within a special clinical setting such as with malignancy or with myeloproliferative diseases, nephrotic syndrome, and liver disease. Presumably many of these share common pathways of coagulation activation or dysfunction with the inherited disorders. Most of the hemostatic disorders in stroke are associated with dysfunction of vascular endothelium and abnormalities of or interference with the natural anticoagulant proteins: protein-C, protein-S, and antithrombin III. Improved understanding of these relationships should lead to better diagnosis and treatment for people at risk of stroke.

Antithrombin III Deficiency↗
PubMed2001

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.

Blood Coagulation↗