Thromboembolism clinical presentation

A third variety, so-called delayed-onset heparin-induced thrombocytopenia has also been described in several reports. In 12 patients, recruited from secondary and tertiary care hospitals, thrombocytopenia and associated thrombosis occurred at a mean of 9.2 (range 5-19) days after the withdrawal of heparin nine received additional heparin, with further falls in platelet counts (32). In a retrospective case series, 14 patients, seen over a 3-year period, developed thromboembolic complications a median of 14 days after treatment with heparin (33). The emboli were venous (n — 10), or arterial (n — 2), or both (n — 2) of the 12 patients with venous embolism, 7 had pulmonary embolism. Platelet counts were mildly reduced in all but two patients at the time of the second presentation. On readmission, 11 patients received therapeutic heparin, which worsened their clinical condition and further reduced the platelet count. 

Heparin has been used clinically for decades to prevent and treat thromboembolic disease and is isolated on an industrial scale from animal tissues, in particular pig intestinal mucosa. The conesponding physiological blood anticoagulant is presumably not heparin, but an HS species that is located on the surface of vascular endothelial cells. Both heparin and HS contain a specific pentasaccharide sequence that binds and activates the plasma proteinase inhibitor AT. This pentasaccharide sequence (4) is present only in a subfraction of heparin and HS preparations. It displays a characteristic structural feature, namely a 3-0-sulfated GlcN residue, that is only rarely seen in other portions of heparin/HS chains. 

A variety of clinical states are associated with thrombosis. The present discussion is limited to a few of the more prominent thromboembolic diseases further Information on this subject may be found in several reviews.3,7-9 The most common clinical states which Involve clot-like, venous thrombi are deep vein thrombosis, particularly as a postsurgical complication, and pulmonary embolism. Anticoagulants such as heparin and the coumarins have been known for years to be effective in the prevention of these types of thrombi and more recent experience has demonstrated the efficacy of fibrinolytic agents such as streptokinase for their dissolution.3,9 Platelet aggregation Inhibitors have only recently been evaluated clinically in the prevention of venous thrombosis. These studies are crucial to the resolution of the controversy as to whether platelets play a vital role in the initiation of venous thrombi.10 There is persistent histological evidence that indicates venous thrombi begin as platelet aggregates.H Myocardial infarction and stroke are... 

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