This is also referred to as consumption coagulopathy, which reflects the pathogenesis. Essentially, the process represents the inappropriate triggering of the coagulation cascade in flowing blood by specific disease processes. There is considerable variation in severity, ranging from the coagulopathy as the predominant clinical manifestation (with haemostatic failure) to merely a laboratory sign of the underlying disease with no clinical haemostatic lesion. Some possible causes are listed in Table 23.1.
The principal laboratory findings are produced by the consumption of platelets during intravascular coagulation with reduction of fibrinogen and elevation of FDP in the serum as secondary (physiological) fibrinolysis breaks down thrombus. Thrombocytopenia, hypofibrinogenaemia and elevation of serum FDP are thus the hallmarks of DIC. Scrutiny of the blood film may reveal red cell distortion or fragmentation if there is associated microangiopathy.
As the majority of clotting tests rely on the fibrinogen-fibrin reaction as the end-point, the PT, APTT and thrombin time are prolonged as a result of the anticoagulant effect of FDP and consumption of other coagulation factors (II, V, VIII). DIC that is associated with endotoxaemia and endothelial damage tends to
Tabic 23.1 Clinical associations of disseminated intravascular coagulation
Release tif tissue Kclampsia thromboplastin Placental abruption fetal death in utero Amniotic fluid embolism Disseminated malignancy inclining acute leukaemia Head injury Ru rns
Bacteria, especially Gram-negative Viruses
Extracorporeal circulation Antigen-antibody complexes Fat embolism Pulmonarv embolism Shock have more profound thrombocytopenia. There is some suggestion that in severe DIC, there is, in addition, an induced platelet function defect. DIC is inevitable to some degree where there is tissue damage (particularly the brain), hypotension, shock and poor organ perfusion.
Variants of the syndrome (with similar laboratory findings) may occur with localized extravascular consumption (e.g. placental abruption) and localized intravascular consumption (e.g. aortic aneurysm). Occasionally, primary pathological fibrinolysis (PF) occurs without the microthrombosis seen in DIC, e.g. in neoplasia. Laboratory tests are not dissimilar to those used in DIC but the platelet count tends to be higher. Differentiation of the commoner DIC from the less common PF rests on a careful clinical assessment and informed interpretation of additional laboratory tests, which may require haematological advice.
The management of DIC depends on clinical rather than laboratory severity. Whatever the degree of DIC, the first principle is an attempt to alleviate the underlying cause. In septicaemia, the infection should be treated vigorously along conventional lines, and in hypovolaemic shock with DIC, adequate blood volume expansion is required. Obstetric causes of DIC usually recover promptly after evacuation of the uterus. After successful treatment, most patients with DIC settle spontaneously and only in those with significant and continuing coagulation failure is there a need to repair the haemostatic mechanism with blood components. This includes the administration of FFP, cryoprecipitate (which is rich in fibrinogen) and platelets. As a rough guide, platelets should be maintained above 50 x 10 9 L_1, fibrinogen > lg L_1 and PT and APTT not greater than 1.5 times the control. Heparin may be required if thrombosis is the predominant feature. Clinical trials suggest that antithrombin and protein C concentrates may be of value for severe cases. Advice should be sought from the haematologist.
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