We have investigated the effects of haemodilution with either saline or hydroxyethyl starch (200/0.5) (HES) on blood coagulation in healthy volunteers in vivo. Standard haematological tests (packed cell volume (PCV), platelets, prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, antithrombin III, bleeding time and platelet aggregation), and thrombelastography (TEG) were performed before and after administration of either 0.9% saline 1000 ml or HES 1000 ml i.v. over a 30-min period. Dilution of PCV and platelet concentrations as a result of volume load were 9% in the saline group and 19% in the HES group. Reductions in fibrinogen (18.6% and 28.8%) and antithrombin III (25.5% and 37.8%) were significantly greater than could be explained by haemodilution alone in both groups. Indices of platelet aggregation were significantly enhanced by saline haemodilution, but not by HES, which inhibited epinephrine-induced aggregation and prolonged bleeding time. TEG in the saline group showed significantly shortened r and k times (24% and 26%, respectively), and increased alpha angle (24%) and maximum amplitude (MA, 6%). HES haemodilution decreased MA (11%) but did not affect other TEG variables. We conclude that haemodilution of normal blood exerted a procoagulant effect, possibly by enhancement of thrombin formation. Circulating concentrations of antithrombin III were depleted more than could be explained by haemodilution alone, leading to a hypercoagulable state. This effect was offset by an antiplatelet action of HES, which was not seen with saline. The mechanism is unknown.
In our experience, severe pulmonary tuberculosis (PTB) is often complicated by deep venous thrombosis (DVT). Because of the association between inflammation and haemostatic changes that can result in a hypercoagulable state, we have prospectively examined such predisposing factors in representative patients. Sequential analyses in a control group with active PTB showed anaemia, thrombocytosis, elevations in plasma fibrinogen, fibrin(ogen) degradation products (FDP), tissue plasminogen activator (t-PA) and inhibitor (PAI-1) with depressed antithrombin III levels. Age, sex and disease matched individuals with venographically proven DVT had higher FDP (15.8 +/- 14.3 v 3.2 +/- 1.7 micrograms/ml:P < 0.01), t-PA (19.4 +/- 14.9 v 11.3 +/- 0.8 ng/ml:P < 0.01), and functional PAI-1 activity (11.6 +/- 6.3 v 4.2 +/- 4.1:P < 0.01) with lower platelet counts (347 +/- 110 v 563 +/- 230 x 10(9)/1:P < 0.01). Fibrinogen levels in all patients rose during the first 2 weeks of therapy and, together with related disturbances, corrected within 12 weeks. In conclusion, elevated plasma fibrinogen with impaired fibrinolysis coupled with a decrease in antithrombin III and reactive thrombocytosis would appear to favour the development of DVT in PTB.
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