Healthy pregnancy is accompanied by changes in the haemostatic system which
convert it into a hypercoagulable state vulnerable to a spectrum of disord
ers ranging from venous thromboembolism to disseminated intravascular coagu
lation (DIC). This latter is always a secondary phenomenon triggered by spe
cific disorders such as abruptio placentae and amniotic fluid embolism due
to release of thromboplastin intravascularly or endothelial damage resultin
g from pre-eclampsia and sepsis. In modern obstetric practice the most comm
on cause is haemorrhagic shock with delay in resuscitation leading to endot
helial damage. The initial management of massive obstetric haemorrhage is t
he same whether associated with coagulopathy initially or not. Low-grade DI
C, associated with pre-eclampsia, is monitored haematologically by serial p
latelet counts and serum fibrin degradation products (FDPs). Supportive mea
sures and removal of the triggering mechanism are the key to successful man
agement. Outcome depends primarily on our ability to deal with the trigger
and not on direct attempts to correct the coagulation deficit.