In disseminated intravascular coagulation (DIC) the coagulation process is activated, causing widespread thrombosis and vascular occlusion, and resulting in consumption of clotting factors and platelets with concomitant activation of the fibrinolytic pathway. Conventional treatment of this consumptive coagulopathy is removal of the underlying trigger and support of the patient with replacement of clotting factors and platelets. In many respects, DIC can be seen as the haematological manifestation of a multi-organ disease such as sepsis or pre-eclampsia.
Problems and special considerations
The common triggers for DIC in the obstetric population are listed in Table 108.1. Many of these conditions have their own particular implications for analgesia and anaesthesia. The coagulopathy usually precludes regional anaesthesia.
Diagnosis of DIC depends on clinical features and laboratory tests. Presentation may be of rapid collapse, with shock, respiratory failure, renal impairment, acidosis, hypoxaemia and bleeding from venepuncture sites and the respiratory, gastrointestinal and urogenital tracts (the last including the uteroplacental bed). Coagulation studies show prolonged coagulation times, decreased fibrinogen concentration and platelet count and raised titres of fibrin degradation products. Some authors favour thromboelastography/thromboelasto- metry because it demonstrates changes in both coagulation and thrombolysis.
In some cases there may be a more insidious progression; initially, increased circulation of activated clotting factors may even shorten coagulation times. It is important to remember that, owing to the procoagulant physiological changes of pregnancy, changes in the prothrombin time (PT) and activated partial thromboplastin time (APTT) in DIC may not be immediately apparent, and that mild prolongation of these tests or even prolongation within their normal range should be regarded as significant.
Table 108.1 Triggers of disseminated intravascular coagulation (DIC) in obstetrics
Placental abruption
Pre-eclampsia/eclampsia
HELLP (haemolysis, elevated liver enzymes and low platelet count) syndrome
Acute fatty liver of pregnancy
Intrauterine death (DIC may occur after 3-4 weeks)
Amniotic fluid embolism
Massive blood transfusion (produces a dilutional coagulopathy; however, tissue factors released)
Drug reactions
Placenta accreta
The platelet count may initially be normal or mildly reduced, although a progressive decrease may aid diagnosis.
Fibrin degradation products have an anticoagulant effect by interfering with platelet function and reducing the efficiency of myometrial contraction, exacerbating blood loss. Levels are increased in pregnancy and may confuse the picture; trends are therefore more informative than absolute values.
Management options
Management of DIC requires timely recognition and removal of the precipitating factor. This usually involves delivering the fetus if antepartum.
In fulminant DIC there may be no time to wait for laboratory results in the face of massive blood loss, haemostatic failure and multi-organ failure. Patients often require hysterectomy. The successful management of fulminant DIC requires input from senior obstetricians, obstetric anaesthetists, haematologists, laboratory staff and intensivists (see Chapter 78, Major obstetric haemorrhage).
Conventional treatment of DIC is to correct the consumptive coagulopathy by administering exogenous clotting factors: fresh frozen plasma to treat prolongation of the APTT or PT, cryoprecipitate or fibrinogen concentrate to treat a low fibrinogen concentration (< 1.5 g/dl), and platelet concentrates.
Some authors have attempted to break the cycle of thrombosis and fibrinolysis by giving heparin, antithrombin or antifibrinolytic drugs. However, giving such agents to a bleeding patient is fraught with danger.
Transfer to an intensive care unit may be necessary to treat the multisystem dysfunction.
Key points
• Coagulopathy may coexist with other organ failures.
• Treatment includes removing the cause of the coagulopathy.
• Aggressive treatment is required to treat fulminating disseminated intravascular coagulation.
• Management of massive obstetric haemorrhage requires coordinated care with haematologists, obstetricians, obstetric anaesthetists and intensivists.
Further reading
Erez O. Disseminated intravascular coagulation in pregnancy: clinical phenotypes and diagnostic scores. Thromb Res 2017; 151: S56-60.
Erez O, Mastrolia SA, Thachil J. Disseminated intravascular coagulation in pregnancy: insights in pathophysiology, diagnosis and management. Am J Obstet Gynecol 2015; 213: 452-63.
Marti-Carvajal AJ, Comunian-Carrasco G, Pena-Marti GE. Haematological interventions for treating disseminated intravascular coagulation during pregnancy and postpartum. Cochrane Database Syst Rev 2011; (3): CD008577.
Squizzato A, Hunt BJ, Kinasewitz GT, et al. Supportive management strategies for disseminated intravascular coagulation: an international consensus. Thromb Haemost 2016; 215: 896-904.