Limits of agreement between measures obtained from standard laboratory and the point-of-care device Hemochron Signature Elite(R) during acute haemorrhage.

BACKGROUND: Rapid diagnosis of coagulopathy in the bleeding patient using point-of-care (POC) devices would be ideal. The Hemochron Signature Elite(®) (HC(®)) is a POC device that determines international normalized ratio (INR) and activated partial thromboplastin time (aPTT). The aim of the study was to evaluate the agreement for INR and aPTT between the HC(®) and standard laboratory values in acute haemorrhage. METHODS: This was a single-centre observational prospective study including patients with acute haemorrhage. Laboratory INR and aPTT were compared with simultaneous measurements performed with the HC(®). The diagnostic performance of HC(®) was determined; bias and limits of agreement were calculated according to the method of Bland and Altman. RESULTS: Seventy-two pairs of measurements from 39 patients were analysed. The bias between the INR-HC(®) and aPTT-HC(®) measurements and the central laboratory were 0.02 and -1.13, respectively. The Spearman's correlation coefficients for the INR-HC(®)/INR-lab and the aPTT-HC(®)/aPTT-lab were 0.68 and -0.29, respectively. Twenty-seven per cent of INR-HC(®) values and 89% of the aPTT-HC(®) values exceeded the predefined limits of agreement. The INR-HC(®) measurement identified patients with a central laboratory INR >1.5 with a sensitivity, specificity, and positive and negative predictive values of 83%, 70%, 76%, and 77%, respectively. CONCLUSIONS: The results showed a lack of agreement between the INR-HC(®) and the aPTT-HC(®) measurements and the standard laboratory in the context of acute haemorrhage. The INR-HC(®) showed moderate performance as a decision-making tool to detect coagulopathy in the context of acute haemorrhage.

Pregnancy in women with portal vein thrombosis: results of a multicentric European study on maternal and fetal management and outcome.

BACKGROUND & AIMS: Women of childbearing age account for approximately 25% of patients with non-cirrhotic portal vein thrombosis (PVT). We aimed at assessing maternal and fetal outcome in pregnant women with known PVT. METHODS: We performed a retrospective analysis of the files of women with chronic PVT in three European referral centers between 1986 and 2010. RESULTS: Forty-five pregnancies, 28 (62%) treated with low molecular weight heparin, occurred in 24 women. Nine (20%) were lost before gestation week 20. Preterm birth occurred in 38% of deliveries: there were 3 births at week 24-25, 7 at week 32-36, and 26 after week 37. A term birth with a healthy infant occurred in 58% of pregnancies. Cesarean section was used in 53% of deliveries. Two women developed HELLP syndrome. A favorable outcome happened in 64% of pregnancies. Pregnancies with an unfavorable outcome were associated with a higher platelet count at diagnosis. Bleeding from esophageal varices occurred in 3 patients during pregnancy, all without adequate primary prophylaxis. Genital or parietal bleeding occurred postpartum in 4 patients, only one being on anticoagulation therapy. Thrombotic events occurred in 2 patients, none related to lower limbs or mesenteric veins. There were no maternal deaths. CONCLUSIONS: In pregnant PVT patients treated with anticoagulation on an individual basis, the rate of miscarriage and preterm birth appears to be increased. However, fetal and maternal outcomes are favorable for most pregnancies reaching gestation week 20. High platelet counts appear to increase the risk for unfavorable outcome. Pregnancy should not be contraindicated in stable PVT patients.

[Rapid centrifugation for routine coagulation testing]. / Intérêt de la centrifugation rapide pour la réalisation des tests d'hémostase.

Routine coagulation assays are performed with platelet-poor plasma obtained after centrifugation of whole citrated blood. Usually clinical laboratories centrifuge blood from 2,000 to 2,500 g for 15-30 minutes. Thirty two blood samples routinely submitted to coagulation tests, were assayed for the prothrombin time, activated partial thromboplastin time, and fibrinogen level, in order to compare results obtained using 2 types of centrifugation : centrifugation at 2,500 g for 15 minutes and rapid centrifugation on StatSpin Express 2 at 4,440 g for 2 minutes. A good correlation was observed for the prothrombin time, activated partial thromboplastin time, and fibrinogen levels being respectively 1,009, 0,908 and 1. We concluded that rapid centrifugation at 4,440 g for 2 minutes does not modify results and contributes, by decreasing duration of the pre-analytical variable to reduce the completion time of these tests.

Association of idiopathic hepatic sinusoidal dilatation with the immunological features of the antiphospholipid syndrome.

BACKGROUND: Isolated sinusoidal dilatation is an uncommon hepatic lesion and the cause is largely unknown. OBJECTIVE: To investigate whether prothrombotic disorders or perisinusoidal cell changes could be involved in pure idiopathic hepatic sinusoidal dilatation (HSD). METHODS: Evaluation for associated conditions, prothrombotic disorders, and studies of hepatic perisinusoidal cell activation in consecutive patients, seen between 1993 and 2002, with isolated sinusoidal dilatation unrelated to outflow block, sinusoidal infiltration, or hepatic granulomas. RESULTS: Among 11 patients, associated conditions were prothrombotic disorders (n = 5) and oral contraceptive use (n = 3). Prothrombotic disorders were polycythemia vera (n = 1) and anticardiolipin antibodies combined with lupus anticoagulant (n = 4). No genetic thrombophilia factor was found. Of four patients with lupus anticoagulant, three had antinuclear factors and high serum levels of anticardiolipin antibodies at repeated testing. There was no evidence of intrahepatic or extrahepatic thrombosis in any of the patients. Sinusoidal dilatation was marked in six of 11 patients (54%), including two patients with antiphospholipid antibodies. Activated perisinusoidal cells were only found around markedly dilated sinusoids. CONCLUSION: Idiopathic pure HSD is frequently associated with the immunological features of the antiphospholipid syndrome. Therefore, finding pure HSD in a liver biopsy specimen should prompt the search for antiphospholipid antibodies.

Contribution of D-Dimer determination in the exclusion of deep venous thrombosis in spinal cord injury patients.

UNLABELLED: Deep vein thrombosis (DVT) is a common complication of paraplegia despite prophylactic anticoagulant therapy. The diagnosis relies primarily on ultrasonography or phlebography; these investigations are difficult, expensive and can be time-consuming in paraplegic patients. STUDY DESIGN: To evaluate the usefulness of coagulation activation markers in excluding a diagnosis of DVT, D-Dimers, thrombin-antithrombin complexes, prothrombin fragments (F1+2) and activated factor VIIa. OBJECTIVES: To improve the diagnosis of deep venous thrombosis in paraplegic patients. SETTING: This collaborative work was done at Raymond Poincaré Hospital, Garches, France. METHODS: To evaluate the usefulness of coagulation activation markers in excluding a diagnosis of DVT, D-Dimers (D-Di), thrombin-antithrombin (TAT) complexes, prothrombin fragments (F1+2) and activated factor VIIa (FVIIa), were determined in a prospective study of 67 consecutive patients with paraplegia or tetraplegia. Doppler ultrasonography and/or phlebography of the lower limbs and D-Di, TAT, F1+2 level determination were systematically done in each patient at admission to our rehabilitation unit. RESULTS: Despite prophylactic low molecular weight heparin therapy, six of the 67 patients developed DVT diagnosed by radiologic explorations. D-Di levels measured by a reference ELISA (Asserachrom D-Di, Diagnostica Stago) or a new rapid automated turbidimetric test (STA-Liatest D-Di) were greater than 500 ng/ml in all DVT patients and in 40 non-DVT patients, of whom most had urinary tract infections, osteomas, or pressure sores. D-Di values were normal in only 21/67 patients (31%). The negative predictive value of D-Di in our study was 100% since all DVT patients had D-Di values greater than 500 ng/ml. TAT and F1+2 levels were not correlated with D-Di levels but also had a negative predictive value of 100%. Comparison of D-Di levels obtained using the two tests showed that results of the reference ELISA were closely correlated to those of the new rapid automated turbidimetric. TAT, F1+2, and factor VIIa are not useful for measuring hypercoagulability in paraplegic or tetraplegic patients since no rapid tests for determining these parameters are available. CONCLUSION: D-Di levels determined using an ELISA or a new rapid automated turbidimetric test have a good negative predictive value for DVT in paraplegic or tetraplegic patients and may reduce the need for Doppler ultrasonography and/or phlebography by 31%.

Endothelial fibrinolytic reactivity and the risk of deep venous thrombosis after spinal cord injury.

Deep vein thrombosis (DVT) is a frequent event in patients with spinal cord injury, even with prophylactic anticoagulant therapy. Lower limb paralysis is a known major risk factor for venous thrombosis, supposedly due to the venostasis in relation with total immobility. The main goal of this study was to evaluate the endothelial response to anoxia to determine whether recovery of fibrinolytic potential occurs in patients subjected to forced bedrest because of a spinal cord injury and whether this recovery is related to the incidence and/or evolution of DVT. We evaluated vascular endothelium reactivity in the lower limbs no longer submitted to the hydrostatic pressure of the erected position in 15 patients with paraplegia or tetraplegia and in 10 normal volunteers after venous occlusion produced by the application of 10 cm Hg pressure to the lower limb for 15 min comparatively to the upper limb used as reference. Among the 15 patients, 10 whose spinal cord injury had occurred 1 to 6 months earlier were still receiving prophylactic anticoagulant therapy, whereas the five other patients were not receiving prophylactic anticoagulants because the injury dated back 6 months or more. After venostasis, tissue plasminogen activator (tPA) increased significantly in both patients and controls in the upper limb (tPA levels twofold and threefold respectively in controls and patients) but showed no significant changes in the lower limb; prolonged immobility did not allow recovery in the lower limbs of a level of fibrinolytic responsiveness identical to that in the upper limbs. The plasminogen activator inhibitor (PAI1) remained unchanged after anoxia, although wide interindividual variations were seen. Natural coagulation inhibitors and circulating blood stigmates of hypercoagulability were measured. None of the patients had abnormally low levels of coagulation inhibitors (ie, antithrombin III, protein C and protein S levels were normal). Seventy-five per cent of patients (prophylactically anticoagulated or not) had very high levels of fibrin degradation products (D. Dimer levels sevenfold to eightfold those of the controls), but all patients had normal levels of thrombin-antithrombin complexes and prothrombin fragments 1 + 2. The permanence of the thrombotic process characterized by an increase in D. Dimer levels without recovery of fibrinolytic potential suggests a proposal for the patients an indefinite antithrombotic treatment at curative doses.