The Levels of Tissue Factor Pathway Inhibitor in Sepsis Patients Receiving Prophylactic Enoxaparin.

OBJECTIVE: Sepsis syndrome is usually accompanied by activation of blood coagulation mechanisms. Earlier studies found deficiencies of the 3 main natural anticoagulants, antithrombin, protein C, and protein S. However, none of these inhibitors block tissue factor, the prime trigger of coagulation during sepsis that is controlled specifically by the tissue factor pathway inhibitor (TFPI). The aim of this study was to characterize the fluctuations in the levels of natural anticoagulants, particularly TFPI, in the course of sepsis and to find out their association with the anticoagulant action of the low-molecular-weight heparin enoxaparin. MATERIALS AND METHODS: We studied 51 consecutive patients with sepsis. Blood samples were collected from patients at baseline (0 h) and at 4, 12, and 24 h after enoxaparin administration. The following assays were undertaken using commercial kits: activated partial thromboplastin time, prothrombin time, thrombin time, total and free TFPI, protein C and protein S, antithrombin, fibrinogen, and anti-factor Xa. RESULTS: Before enoxaparin administration, there was significant prolongation of the prothrombin time and activated partial thromboplastin time, and this remained the case in the 3 subsequent samples. There was marked reduction in the levels of antithrombin, protein C, and total and free protein S to below control values throughout the study. In contrast, plasma levels of both total and free TFPI were markedly elevated and increased after enoxaparin therapy. Anti-factor Xa levels were within the therapeutic range throughout. There was no difference in TFPI levels between those patients who died and those who survived. CONCLUSION: Sepsis triggered marked release of TFPI from endothelial cells. This persisted and was increased further following the administration of enoxaparin. In contrast, there was marked consumption of the natural coagulation inhibitors antithrombin, protein C, and protein S. These results go some way towards explaining why the therapeutic use of recombinant TFPI fails to correct sepsis-associated coagulopathy.

Outcome of pulmonary embolism and clinico-radiological predictors of mortality: Experience from a university hospital in Saudi Arabia.

OBJECTIVES: The objective of this study is to determine the outcome of pulmonary embolism (PE) and the clinico-radiological predictors of mortality in a university hospital setting. METHODS: A Prospective observational study conducted at King Khalid University Hospital, Riyadh Saudi Arabia between January 2009 and 2012. A total of 105 consecutive patients (49.9 ± 18.7 years) with PE diagnosed by computed tomography pulmonary angiography were followed until death or hospital discharge. RESULTS: Overall in hospital mortality rate was 8.6%, which is lower than other international reports. Two-thirds of patients developed PE during the hospitalization. The most common risk factors were surgery (35.2%), obesity (34.3%) and immobility (30.5%). The localization of the embolus was central in 32.4%, lobar in 19% and distal in 48.6%. A total of 26 patients (25%) had evidence of right ventricular strain and 14 (13.3%) were hypotensive. Multivariate analysis revealed that heart failure (Beta = -0.53, P < 0.001), palpitation (Beta = -0.24, P = 0.014) and high respiratory rate (Beta = -0.211, P < 0.036) were significant predictors of mortality. There was no significant difference in the localization of the embolus or obstruction score between survivors and non-survivors. CONCLUSION: The outcome of PE is improving; however, it remains an important risk factor for mortality in hospitalized patients. Congestive heart failure, tachypnea and tachycardia at presentation were associated with higher mortality. These factors need to be considered for risk stratification and management decisions of PE patients. Radiological quantification of clot burden was not a predictor of death.