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PubMed1996

Haemostatic changes caused by i.v. regional anaesthesia with lignocaine.

The various components of i.v. regional anaesthesia (IVRA), that is ischaemia, tourniquet compression and the presence of high concentrations of local anaesthetics in the blood vessels of the extremity, may affect haemostatic mechanisms. We performed a cross-over study in 10 healthy male volunteers to examine the role of lignocaine in IVRA on several haemostatic variables, and those indicating fibrinolysis and platelet function in particular. Venous blood samples were obtained from the test arm and the opposite arm before IVRA, at the time of tourniquet cuff deflation and 30 min thereafter. Metal needle punctures were used, and for the sample from the test arm at the time of cuff deflation, cuff pressure was reduced from 300 mm Hg to individual mean arterial pressure. The IVRA technique included exsanguination by arm elevation and axillary artery compression, inflation of the tourniquet cuff for 20 min and deflation of the cuff in one step (after obtaining the venous sample). Each subject received, in random order, either 0.5% lignocaine 3 mg kg-1 or the corresponding volume of saline i.v. All fibrinolysis markers, that is, D-dimer, tissue plasminogen activator antigen (t-PA antigen), tissue plasminogen activator activity (t-PA activity), plasminogen activator inhibitor activity (PAI) and protein C indicated enhanced fibrinolysis by IVRA, but only t-PA antigen and PAI showed greater changes in the lignocaine compared with the saline group in the exposed arm at the time of cuff deflation. Platelet function tests (ADP-induced platelet aggregation, beta-thromboglobulin and thrombelastogram (TEG)) indicated no differences between the lignocaine and saline groups. Although IVRA appeared to induce some platelet dysfunction, there was a small increase in TEG amplitude indicative of improved fibrin-platelet interaction in the lignocaine-exposed arm at the time of cuff deflation. We conclude that the presence of high i.v. lignocaine concentrations (median 144.4 micrograms ml-1 in cubital veins at the end of the tourniquet time) potentiated ischaemia-induced fibrinolysis activation during IVRA. Concomitant platelet dysfunction was not aggravated by lignocaine.

Adult↗
PubMed2005

Prevalence of aspirin resistance measured by PFA-100.

BACKGROUND: Aspirin protects from cardiovascular events. However, a number of patients who take this drug suffer events, probably due to aspirin resistance. Our objective was to determine the prevalence of aspirin resistance in patients taking this drug and to test if resistance is related to different variables. METHODS: Platelet function was studied in 113 patients (90 men) aged 63+/-9 (80 with stable ischaemic heart disease) who took aspirin (100 to 300 mg/day). By a platelet function analyzer, called PFA-100, the epinephrine closure time was studied. We also analysed the possible relationship between epinephrine closure time and the following variables: total cholesterol, LDL, HDL cholesterol, total/HDL cholesterol, triglycerides, lipoprotein(a), and C reactive protein. The possible association between aspirin resistance (epinephrine closure time <161 s) and different variables was also analyzed with the SPSS statistical package. Results are expressed in median (interquartile range). RESULTS: Aspirin resistance was found in 32% of cases. Ischaemic heart disease, smoking habit, and treatment with statins were associated with a significantly greater percent of resistance (p=0.049, 0.009, and 0.043, respectively). Patients with aspirin resistance had higher levels of total/HDL cholesterol: 4.46 (3.76-5.55) vs. 3.97 (3.20-4.75) (p = 0.023); and lipoprotein(a): 57.2 (24.8-85.0) mg/dl vs. 13.1 (3.7-38.0) mg/dl (p = 0.007). CONCLUSIONS: Aspirin resistance is frequent and easily detected by PFA-100. It occurs more frequently in smokers. A mild association is found with ischaemic heart disease, some lipids, and treatment with statins. Our results support the applicability of this method to clinical practice.

Aged↗
PubMed1992

Perioperative blood and blood component therapy.

This overview examines blood, blood components, their indications and contra-indications, from an anaesthetist's viewpoint. The dangers of any blood transfusion, including infection transmission and immune suppression, as well as the risks of massive and rapid transfusions, are discussed. Autologous predonation, intraoperative haemodilution and salvage are described to help prevent some of the risks of homologous blood transfusion. Preoperatively an acceptable individualised haemoglobin concentration should be calculated for each patient and a history for potential bleeding problems taken. In most patients perioperative anaemia does not adversely influence patient morbidity and mortality. However, if blood is required, 4 ml.kg-1 body weight of packed red blood cells will raise the patient's haemoglobin concentration by 1 g.dl-1. The bleeding time as a test of platelet function does not predict perioperative blood loss. However, it remains a useful test in patients with a known bleeding problem or in operations where even small amounts of bleeding increase the surgical difficulty and patient morbidity. If bleeding is due to thrombocytopaenia it is usually slow enough to allow time to check platelet number and function before ordering and transfusing them. Fresh plasma is a much overused product which should mainly be used for coagulation factor replacement, in adequate volumes (4-8 packs in dilutional coagulopathy). The well-informed anaesthetist should be better able to use blood products which, while they may be life saving, are neither innocuous nor inexpensive.

Blood Component Transfusion↗
PubMed2005

Evaluation of the platelet function analyzer (PFA-100) vs. the thromboelastogram (TEG) in the parturient.

BACKGROUND: The platelet function analyzer (PFA-100) is a bedside test of coagulation designed to evaluate platelet function. It measures the time required for whole blood to occlude a membrane impregnated with either epinephrine (EPI) or adenosine 5'diphosphate (ADP). The results are reported as closure time (CT-EPI or CT-ADP) in seconds. The thromboelastogram (TEG) measures whole blood clotting and the maximum amplitude (MA) correlates with platelet count and function. We wished to establish whether there is a correlation between the CT and platelet count, between the CT and MA, and between the MA and platelet count. METHODS: Platelet count, CT, and MA were measured in blood drawn from 172 healthy term parturients using the PFA-100. RESULTS: We were unable to detect a significant correlation between the CT-EPI and platelet count (r=-0.1, P=0.21), or the CT-ADP and platelet count (r=-0.02, P=0.83). We also did not find a correlation between the CT-EPI and MA (r=-0.13, P=0.12) or between the CT-ADP and MA (r=-0.11, P=0.19). However, we found a significant correlation between platelet count and MA (r=0.33, P<0.001). CONCLUSIONS: We conclude that the CT does not correlate with the platelet count or MA in the parturient, but the TEG does. Therefore the TEG may be a better tool to evaluate coagulation in the parturient with thrombocytopenia.

Adolescent↗
PubMed2003

Assessment of platelet activation in several different anticoagulants by the Advia 120 Hematology System, fluorescence flow cytometry, and electron microscopy.

In vivo platelet activation results are often confounded by activation induced in vitro during the preparative procedures. We measured ex vivo (basal) and in vitro (thrombin-induced) platelet activation in sodium citrate, ethylenediaminetetraacetic acid (EDTA), and Citrate Theophylline Dipyridamole Adenosine (CTAD) whole blood specimens. Determinations were made by measurements of platelet density (mean platelet component: MPC concentration) on the Advia 120 Hematology System. The MPC has been previously shown to correlate with a fluorescence flow cytometric method, also determined in this study, using the surface expression of CD62P. Moreover, platelet shape and structure changes in EDTA and CTAD anticoagulated whole blood specimens were characterized by transmission electron microscopy (TEM). Observations made using the Advia 120 Hematology System platelet density parameter, MPC, in the absence of thrombin were 25.7 +/- 0.9 g/dl, 27.9 +/- 0.9 g/dl and 24.8 +/- 1.2 g/dl in sodium citrate, EDTA and CTAD whole blood specimens, respectively. Addition of thrombin induced a significant change in platelet MPC for sodium citrate (21.9 +/- 1.9 g/dl; p<0.0001) and EDTA (23.2 +/- 0.9 g/dl; p<0.0001) whole blood specimens. In contrast, thrombin had no effect on MPC measured in whole blood taken into CTAD tubes. In vitro fluorescence flow cytometric platelet activation experiments measuring the percentage of platelets expressing anti-CD62P showed increase in sodium citrate specimens from 9.2 +/- 7.0 to 55.5 +/- 23.1 % (p<0.0001) and in EDTA specimens from 1.9 +/- 1.7 to 64.6 +/- 12.4 % (p<0.0001) after addition of thrombin. However, in blood taken into CTAD tubes, there was no significant change. Studies on platelets isolated from whole blood in CTAD showed activation by thrombin indicating that platelets in CTAD, while protected in its presence remained functional upon its removal. When observed by TEM over time, platelets in EDTA appear more activated and contain fewer granules than platelets in CTAD. We conclude that CTAD demonstrates in vitro platelet activation inhibition and may be useful in stabilizing ex vivo platelet activation. The novel platelet activation parameter, MPC, measured by an automated routine hematology system, using customized proprietary software, may be used in conjunction with CTAD, a stabilizing anticoagulant, to measure the ex vivo platelet activation state in whole blood specimens. TEM studies verify shape modifications and simultaneous retention of intracellular granules at early post-venipuncture time periods in CTAD specimens.

Anticoagulants↗
PubMed1975

Transient, spontaneous bruising with long bleeding time and normal platelet count.

Spontaneous, widespread bruising in apparently healthy individuals relatively common among Thai children. It is a transient problem, unaccompanied by any common bleeding disorder of childhood. The physical defect is limited to the painless cutaneous lesions. Screening tests for hemostasis as well as tests of platelet function were measured in 24 of these patients. The significant abnormal findings were eosinophilia, prolonged bleeding time, positive tourniquet test and platelet dysfunction--i.e., defective ADP release and adhesivity to glass beads. So far, the condition appears to 0e a self-limited diathesis of unknown etiology.

Adenosine Diphosphate↗