Coagulopathic Postpartum Haemorrhage

Coagulopathic postpartum haemorrhage is bleeding after birth in which the blood fails to clot because of a congenital or acquired clotting disorder. Causes include disseminated intravascular coagulation (from abruption, amniotic fluid embolism, sepsis, preeclampsia and HELLP syndrome, retained dead fetus), dilution from massive transfusion, von Willebrand disease, haemophilia carriers, low platelets and anticoagulants. It causes 1 percent of cases but is highly lethal.

• Risk factors: placental abruption, severe preeclampsia, sepsis, fetal death, previous bleeding disorder, anticoagulant use, massive haemorrhage.
• Fibrinogen below 2 g/L predicts severe bleeding.
• Treatment of the trigger is as important as replacing clotting factors.

Women have bleeding that does not clot, oozing from wounds, IV sites and gums, bruising and petechiae, in addition to features of the trigger (abruption, sepsis, hypertension).

• Blood in the pad or tray that does not clot.
• Bleeding from multiple sites.
• Differential diagnosis: uterine atony with dilutional coagulopathy, retained tissue, genital tract tear, thrombocytopenia, von Willebrand disease, liver failure, anticoagulant effect.
• Complications: massive haemorrhage, shock, acute kidney injury, acute respiratory distress syndrome, hysterectomy, Sheehan syndrome, maternal death.

The approach is point of care and laboratory clotting tests with a search for the cause.

• Bedside clotting test (2 mL blood in a glass tube; no clot at 7 to 10 minutes is abnormal).
• Platelets, fibrinogen (below 2 g/L abnormal), prothrombin time, activated partial thromboplastin time, D-dimer, blood film for fragments, haemoglobin, creatinine, liver enzymes, lactate, calcium.
• Group and cross-match 4 to 6 units; blood culture; malaria test.
• Von Willebrand screen, anti-Xa level or heparin history if indicated.

The principle is to replace clotting factors early based on tests, treat the trigger and stop uterine bleeding.

• Supportive: two large-bore cannulae; Ringer's lactate 1 to 2 litres rapidly; warm all fluids; oxygen; treat acidosis and hypocalcaemia; high dependency care; treat sepsis and abruption; deliver a dead fetus.
• Pharmacological: tranexamic acid 1 g IV over 10 minutes (repeat once after 30 minutes); fresh frozen plasma 15 mL/kg; cryoprecipitate 10 units or fibrinogen concentrate 2 to 4 g for fibrinogen below 2 g/L; platelets one adult dose for counts below 50 x 10^9/L; packed red cells for haemoglobin below 7 g/dL or instability; calcium gluconate 1 g IV after every 4 units of blood; vitamin K 10 mg IV for warfarin effect; protamine sulphate 1 mg per 100 IU of unfractionated heparin (1 mg per 1 mg of enoxaparin given in the last 8 hours) by slow IV injection; desmopressin 0.3 micrograms/kg IV over 30 minutes for von Willebrand disease or mild haemophilia carriers; oxytocin 10 IU IM then infusion of 40 IU in 1 litre Ringer's lactate at 250 mL per hour.
• Procedures: uterine massage and balloon tamponade (300 to 500 mL sodium chloride 0.9 percent); evacuation of retained tissue; surgery for uncontrolled bleeding with packing (damage control) rather than prolonged dissection; hysterectomy as a last resort.
• Special groups: von Willebrand disease and haemophilia carriers need factor replacement under haematology advice and tranexamic acid 1 g oral 8-hourly for 10 to 14 days; anticoagulated women have the reversal agent matched to the drug.
• Red flags: no clot at 10 minutes, fibrinogen below 1.5 g/L, platelets below 50 x 10^9/L, oliguria, bleeding from many sites.
• Follow-up: clotting profile every 4 to 6 hours until normal; haemoglobin daily; thrombophilia and bleeding tests at 6 weeks; counselling for later pregnancy.