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PubMed2004

Does hemodilution enhance coagulability?

UNLABELLED: Recent publications reported enhanced coagulability in hemodilution determined by TEG. In contrast, earlier reports have shown prolongation of in-vivo bleeding time in anemia. In order to take a closer look at this discrepancy undiluted and diluted anticoagulated blood samples (20 % with saline solution, hydroxyl-ethyl starch 6 % (HES), autologous platelet poor plasma (PPP)) were investigated by TEG (n = 10), ball (n = 10), and hook coagulometer (n = 15) as well as tests simulating primary hemostasis ex vivo (Platelet Function Analyzer PFA-100, n = 10). RESULTS: Dilution with plasma changed TEG parameters in a way, when started by recalcification of the blood sample, which is characteristic of enhanced coagulability (r decreased in all and k in 8 of 10 samples, maximal amplitude increased in 9 out of 10). With HES, changes in TEG parameters mainly indicated reduced coagulability (k increased in 7 out of 10, MA decreased in 10 out of 10). When the coagulation was additionally activated by PTT reagent (InTEG) the TEG parameters also mainly showed hypocoagulation with the three dilution solutions. Coagulation times with ball and hook coagulometers were significantly prolonged by dilution especially with saline (+ 25 % and + 17 %, p < 0.001). Dilution always significantly (often abnormally) prolonged closure time in PFA-100 (saline + 41 +/- 18 %, PPP + 37 +/- 20 %, HES + 69 +/- 24 %) demonstrating disturbance of primary hemostasis, particularly with HES. CONCLUSIONS: From the results obtained it can be concluded that the changes in the classical TEG (without addition of PTT-reagent), suggesting an enhanced coagulability, may be caused methodically as they are also found with autologous PPP. On the other hand, a disturbance of the primary hemostasis in hemodilution has to be taken into account from the results seen with the PFA-100 and a number of published data.

Blood Coagulation↗
PubMed2005

Perioperative monitoring of primary and secondary hemostasis in coronary artery bypass grafting.

On-pump cardiac surgery is accompanied by complex alterations of hemostasis. The excessive postoperative bleeding has been attributed to acquired platelet dysfunction, impaired plasmatic coagulation, and increased fibrinolysis. The characterization of the hemostatic defects responsible for bleeding is crucial for specific treatment and optimal clinical management of the patient. For rapid determination of platelet-dependent primary hemostatic capacity (PHC), the Platelet Function Analyzer PFA-100 system is available. To evaluate the PFA performance in perioperative monitoring, a study was performed in 49 patients selected for low bleeding risk undergoing selective primary coronary artery bypass grafting (CABG). We compared PHC with Simplate bleeding time (BT) and platelet aggregometry. Furthermore, we analyzed global hemostasis by thromboelastography (TEG) and plasmatic coagulation by standard clotting tests prothrombin time (PT, Quick), activated partial thromboplastin time (aPTT), thrombin time (TT) and clotting factors and fibrinolysis by batroxobin (reptilase) time (RT). In all patients BT was postoperatively increased by 1.5- to 2-fold irrespective of perioperative complications and decreased to mildly prolonged values on the first postoperative day (1st day). In patients without complications, PHC in both collagen-adenosine diphosphate closure time (CADP-CT: 83 seconds preop, 78 seconds postop, and 74 seconds 1st day) and collagen-epinephrine closure time (CEPI-CT: 98 seconds preop, 95 seconds postop, 85 seconds 1st day) remained nearly stable. Apart from a patient with postoperative moderate thrombocytopenia, in bleeding patients no other significant defect of postoperative platelet hemostatic capacity was observed. However, on 1st day, the PHC of those patients was significantly reduced compared with non-bleeding patients. In patients with postoperative myocardial ischemia, increased PHC was identified by significantly shorter postoperative CADP-CT (66 seconds vs. 83 seconds) than in uncomplicated patients. By aggregometry, partial platelet dysfunction was observed in some patients without correlation to bleeding complications. In seven of 9 patients the postoperative bleeding complication was attributed to prolonged heparin anticoagulation and/or mildly enhanced fibrinogenolysis/fibrinolysis by TEG and standard plasmatic coagulation tests (TEG: k time 18 minutes vs. 8 minutes; aPTT: 47 seconds vs. 32 seconds; TT: 18.0 seconds vs. 12.3 seconds) and (RT: 19.5 seconds vs. 17.7 seconds). The impairment of PHC, platelet aggregation, and clotting factors observed on the 1st day in bleeding and in intra-aortic balloon pump (IABP) patients are most likely secondary effects, for example, loss of active platelets and clotting factors, to the primary postoperative bleeding or implantation of the IABP. In conclusion, our data indicate that in standard CABG procedures highly variable alterations of the hemostatic system occur after cardiopulmonary bypass (CPB) even in patients with assumed low operative risks. For identification of post-CPB bleeding complications, thromboelastography, aPTT, and TT and heparin and batroxobin (reptilase) time as fibrinolysis-sensitive assays are useful. Platelet function appears to be rapidly restored in uncomplicated CABG. PHC determination by PFA-100 demonstrates a high specificity for adequate platelet function and, therefore, could be beneficial in improved transfusion of platelet concentrates. PHC testing by PFA-100 may help identify postoperative platelet hyper-reactivity associated with myocardial lesion.

Adult↗
PubMed1987

[Changes in blood coagulation, thrombocyte function and vascular prostacyclin synthesis caused by magnesium sulfate].

Magnesium deficiency, prostacyclin deficiency and reduced prostacyclin sensibility of the thrombocytes may possibly play an important pathophysiological role in gestosis/pre-eclampsia. For this reason, we studied the influence of magnesium sulphate (in vitro 2-16 mVal/l) on thromboelastogram, spontaneous and ADP-induced thrombocyte aggregation, prostacyclin sensitivity of the thrombocytes and prostacyclin liberation from umbilical cord vessel preparations. The thromboelastogram showed an inhibitory influence of magnesium sulphate on all measurement parameters. Spontaneous and ADP-induced thrombocyte aggregation were inhibited to a statistically significant extent. The prostacyclin sensibility of the thrombocytes was increased by magnesium-sulphate. Magnesium sulphate enhanced prostacyclin liberation from the vascular wall significantly by 20-36%. It is possible that in gestosis magnesium sulphate may exercise a favourable influence on the disturbed balance between prostacyclin production and prostacyclin sensibility of the thrombocytes by exercising an influence on coagulation, thrombocyte function and prostacyclin liberation, and that it can thus contribute towards stabilising coagulation disturbances.

Blood Coagulation↗
PubMed1984

[Heparin level and coagulation potential after subcutaneous injection of 7500 international units of heparin calcium].

A dosage of 7500 IU heparin calcium (Calciparin) was administered subcutaneously twice daily in 15 probands. Prior to and after the 1st and 7th injection heparin levels were determined in plasma and coagulation studies were done. The highest heparin levels were found around 4 hours after the injection. They were significantly higher after the 7th injection than after the 1st. Values decreased markedly after 8 hours. After 10-12 hours they approached the initial values, however remained significantly increased. The appropriate changes were seen in activated partial thromboplastin time, thrombin time and reaction- and clotting time in the thrombelastogram. Activity and concentration of antithrombin III decreased by about 10%. Fibrinogen and platelets remained largely unaffected. The results show that twice daily subcutaneous injections of 7500 IU heparin calcium are able to close the anticoagulation gap in plasma which occurs with administration of twice 5000 IU between two injections.

Adult↗
PubMed1982

[Effects of cimetidine and ranitidine on blood coagulation].

The influence of cimetidine and ranitidine on blood coagulation and plasmatic fibrinolysis were assessed in vitro and in vivo. After an intravenous bolus of 200 mg cimetidine a marked prolongation of plasmatic thrombin time was observed, which however did not occur after 50 mg of ranitidine. In vitro addition of cimetidine (0.12 mg/ml) and ranitidine (0.06 mg/ml) again led to prolongation of plasmatic thrombin time only after cimetidine, reaching double the initial value. This requires application of cimetidine in acute intestinal haemorrhage not as a bolus, but only by drip infusion. Continuous application of 600 mg over 12 hours did not result in changes of coagulation values. In contrast, ranitidine may be administered as a bolus. Bolus injections of 50 to 100 mg did not result in any prolongation of plasmatic thrombin time. The antifibrinolytic effect of both H2-receptor antagonists was investigated in the streptokinase-induced fibrinolysis spindle of the thrombelastogram. Clear-cut antifibrinolytic properties were not demonstrable for either preparation with this method.

Blood Coagulation↗
PubMed2003

Low-dose oral contraceptive effects on thromboelastogram criteria and relationship to hypercoagulability.

OBJECTIVE: The study was undertaken to assess hypercoagulability, by using thromboelastography, in women who use low-dose oral contraceptives (OCs). STUDY DESIGN: Forty-three women using low-dose OCs (<or=35 microg ethinyl estradiol) underwent thromboelastography before starting OCs and again during the third month of OC use. Prior and 3-month mean values of four thromboelastogram parameters (maximum amplitude [MA], K time, alpha angle, and R time) were compared by using paired t tests. Comparison according to progestin type was also performed with unpaired t tests. RESULTS: Prior versus 3-month values for MA, alpha, and K were not significantly different (P values-K: 0.8; alpha:.34; MA: 0.49); power was adequate to detect small differences. The 3-month R time was decreased compared with pre-OC values (P =.025), although the magnitude of this change was not characteristic of hypercoagulability. Comparison according to progestin type demonstrated no difference. CONCLUSION: We found no significant trend toward hypercoagulability in women who used low-dose OCs and who otherwise had no known thromboembolic risks.

Adolescent↗
PubMed2006

Whole blood thrombelastographic coagulation profiles using minimal tissue factor activation can display hypercoagulation in thrombosis-prone patients.

OBJECTIVE: Recently, our laboratory devised a dynamic whole blood (WB) thrombelastographic coagulation model employing activation with minute amounts of tissue factor. A series of studies were conducted to validate the feasibility of the model to illustrate hypocoagulation in various bleeding disorders and its usefulness in detecting the haemostatic effect of pro-coagulants by ex vivo titration experiments. In this context, the present study hypothesized that the thrombelastographic model also can reveal hypercoagulation. Hence, the objective of the present study was to record dynamic WB coagulation profiles in a series of patients (n=76) who had previously suffered from a venous (n=34) or arterial (n=42) thrombo-embolic event and to compare the results with those of a group of healthy reference subjects (n=60). MATERIAL AND METHODS: Patients receiving vitamin K antagonist treatment were not enrolled in the study. Forty-four of the patients had no known thrombophilia risk factor and 32 patients had at least one thrombophilia risk factor. RESULTS: The most commonly found risk factors were mild hyperhomocysteinaemia and heterozygosity for the factor V Leiden polymorphism. The data showed that, as compared with the healthy controls, patients with a history of venous or arterial thromboembolism had a significantly greater hypercoagulant WB coagulation clot signature as defined by a shortened clotting time together with an accelerated maximum velocity of clot propagation. CONCLUSIONS: In future studies with ex vivo dose titration assessment of pro-coagulant components mixed with blood from a patient suffering from compromised haemostasis, observation of a significantly shortened clot initiation concomitant with a distinctly accelerated clot propagation is likely to indicate an increased risk of thrombosis.

Adolescent↗
PubMed2004

Effect of sodium valproate on esophageal motility in healthy subjects and patients with gastroesophageal reflux.

BACKGROUND: There is experimental evidence to show that upper gastrointestinal tract motility is influenced by a GABAergic mechanism. Sodium valproate acts as a GABA agonist, and has been proven to affect the human internal anal sphincter. The aim of this study was to evaluate any possible effect of sodium valproate on esophageal motility in healthy subjects and patients with gastroesophageal reflux disease (GERD). METHODS: Ten healthy volunteers (4 M, 6 F; age range: 20-61 years) and 12 patients (4 M, 8 F; age range: 25-70 years) with GERD were included in the study. Standard esophageal manometry and ambulatory 24-h esophageal pH monitoring were performed before and 5 days after oral administration of sodium valproate (400 mg four times per day). Main measurements included a) lower esophageal sphincter (LES) resting pressure and amplitude and duration of peristalsis at 5, 10 and 15 cm proximal to LES, and b) percentage of time with esophageal pH <4 and number of reflux episodes. RESULTS: Sodium valproate (i) significantly increased LES resting pressure in both groups (P<0.05), without affecting either the LES postdeglutition relaxation or any of the parameters of the esophageal peristaltic activity, (ii) significantly reduced the number of reflux episodes at the postprandial period in both healthy subjects (P=0.02) and reflux patients without hiatal hernia (P=0.04) and (iii) the time percentage with esophageal pH <4 at the postprandial period in reflux patients (P=0.01). CONCLUSIONS: Sodium valproate increases normal and reduced tonic activity of the human LES and reduces the number of reflux episodes in health and GERD. This action could be attributed to a central GABAergic mechanism.

Adult↗
PubMed2003

Influence of platelet count and activity on thromboelastography parameters.

It has been suggested that thromboelastography TEG) can help in limiting or directing the appropriate use of blood products during surgery. However, the contribution of platelets to the TEG profile has not been studied in detail. Blood was taken from eight healthy subjects and eight patients with peripheral arterial disease (PAD). Immunomagnetic separation was achieved by the addition of Dynabeads labeled with a CD41 murine antibody (to the GPIIb/IIIa receptor) to achieve 90-100% depletion of platelets from blood. This was then titrated with whole blood to achieve platelet counts of approximately 0, 25 and 50% of the original count to compare with whole blood using TEG. Platelet function was also assessed by spontaneous platelet aggregometry (SPA) at baseline and at the 50% dilution. SPA, maximum amplitude (MA) and K time were significantly different in PAD patients compared to controls (P < 0.05). In both controls and PAD patients there was a strong linear correlation between Log10 [platelet count] and MA (r = 0.97 for controls, r = 0.89 for PAD) and K time (r = -0.86 for controls, r = -0.68 for PAD). Correlation between Log10 [platelet count] and R time was poor in both groups. The MA and K TEG parameters may be most useful for assessing platelet transfusion requirements.

Aged↗
PubMed2006

Platelet-dependent coagulation assays for factor VIII efficacy measurement after substitution therapy in patients with haemophilia A.

FVIII therapy for haemophilia A is safe and effective, with the problem of individually sufficient efficacy unsettled. Routine one-stage clotting assays and tests employing chromogenic substrates poorly detect individual haemostatic effects of FVIII due to artificial test conditions. In particular, the use of cell-free and diluted plasma samples neglect the crucial role of platelets for thrombin and fibrin formation. To optimize FVIII substitution therapy, we measured in 40 patients with severe to mild haemophilia A before and after FVIII substitution the FVIII activity in cell-free plasma samples using a one-stage clotting assay as well a chromogenic substrate assay and compared the data with those obtained with cell-based coagulation tests, i.e. thrombin generation in platelet-rich plasma (PRP) and thromboelastography (TEG) in samples of citrated whole blood (WB). To determine the maximum ex vivo haemostatic effect we added 1 unit/ml of FVIII to samples of PRP and WB and measured the maximum thrombin generation in the thrombin generation test (TGT) and the maximum clot firmness (MCF) in TEG. After FVIII substitution we observed a nearly linear relation between the individual FVIII activities administered to the patients and the activities measured in the plasma samples. However, data obtained with TGT and TEG revealed a high inter-individual variation and a very poor correlation to the administered FVIII activity. Actually, it could be shown that FVIII substitution yielding in a FVIII plasma activity of about 30% is sufficient to get an ex vivo haemostatic effect of more that 90% as measured by maximum thrombin generation and MCF. FVIII substitution up to a plasma activity of more than 90% did not further enhance the haemostatic effect. Our data clearly demonstrate that the haemostatic effect of FVIII is not only dependent on the activity that is measured in plasma but also depends on the interplay between coagulation and blood cells, in particular with platelets. The use of cell-based coagulation tests such us TGT or TEG may help to optimize FVIII therapy by determining the individual FVIII dosage that produces a maximum haemostatic effect.

Adult↗
PubMed2000

A prospective study of thromboelastography (TEG) and filter life during continuous veno-venous hemofiltration.

Anticoagulants are commonly used to prolong circuit life during continuous hemofiltration. However, a clear correlation between routinely performed blood coagulability tests and circuit life has not been demonstrated. This lack of correlation may derive from the limited ability of such tests to describe the likelihood of in vivo clotting. We hypothesized that thromboelastography (TEG), which derives its variables from a closer reproduction of in vivo coagulation, would significantly correlate with filter life. Accordingly, we conducted a prospective pilot study of the correlation between filter life and TEG-derived variables in 21 hemofilters used in 6 critically ill patients admitted to a tertiary intensive care unit. It involved the performance of TEG during steady state anticoagulation, measurement of circuit life, and of routine coagulation variables. The results showed that the mean circuit life was 20.7+/-4.0 h despite an average aPTT of 67.7+/-12.8 s and a mean heparin dose of 472.5+/-96.2 IU/h. The mean INR was 1.4+/-1 and the mean platelet count was 118+/-16 x 10(3)/mm3. Although several TEG variables correlated with heparin dose (p < 0.03), no correlation was found between any of the routine coagulation variables or any of the TEG variables and circuit life. In conclusion, no significant correlation between TEG derived variables or routinely measured coagulation variables and circuit life could be demonstrated. These findings suggest that such tests are not useful indicators of circuit anticoagulation adequacy and that factors other than blood coagulability may play a role in circuit failure.

Anticoagulants↗
PubMed1978

Picotamide: effects on coagulation, fibrinolysis and platelet aggregation during prolonged administration in the aged.

Picotamide was administered in a daily dose of 1500 mg per os for 30 days to 30 aged, arteriosclerotic subjects and as single doses of 500 mg and 1000 mg to another group of 16 subjects. A reduction of platelet aggregation (methods of Born and Breddin) was observed within 24 hours of commencement of treatment and became more evident in the subsequent days. The reduction was both consistent and significant. A marked increase in fibrinolytic activity (fibrin plate method) was observed during the first 24 hours, particularly for euglobulins with activator. The reaction and clot formation times (r and k) were prolonged and the maximal amplitude (ma) in thrombelastogram was reduced by a definite, though small amount. After the administration of a single dose the maximal effect was observed after eight hours and was still evident after 48 and, to a lesser degree, after 72 hours. The drug was in all cases well tolerated, without any significant side-effects nor untoward reactions.

Administration, Oral↗
PubMed1995

Effect of ketorolac, bupivacaine and low-dose heparin on thrombelastographic variables in vitro.

We have studied the effects of ketorolac, bupivacaine and low-dose heparin on three thrombelastographic (TEG) variables (r, alpha, MA) in vitro. Blood samples were obtained from 12 healthy volunteers and 88 ASA I-II elective surgical patients. Clinically relevant concentrations of ketorolac (4.1 micrograms ml-1) and bupivacaine (2.7 micrograms ml-1) had little or no effect on the TEG variables. However, low concentrations of heparin (0.07-0.28 u. ml-1) had marked effects on all three TEG variables. Thus the interpretation of TEG abnormalities during anaesthesia and surgery may be confounded by the presence of heparin, but not by clinical concentrations of ketorolac or bupivacaine.

Adult↗