DR ADEJUBE FRANCIS

BAMIJOKO
CONSULTANT/LECTURER
ABUAD
 INTRODUCTION
 Physiological changes in coagulation during pregnancy

⚫ To prevent excessive bleeding at delivery, the body

undergoes series of changes that produce overall

procoagulation in pregnancy.

⚫ The concentrations of fibrinogen, factors V, VII, VIII, IX, X,

XII and von Willebrand Factor (vWF) are increased.

⚫ FXIII increases initially but decreases towards term.

INTRODUCTION
⚫ Fibrinolysis is suppressed due to rise endothelial

derived plasminogen activator inhibitor 1(PAI-1) &

placenta derived plasminogen activator inhibitor 2(PAI-2)

⚫ Markers of coagulation activation are increased-

thrombin antithrombin complexes (TAT),

prothrombin fragments PF1+2 and D-dimer.

⚫ Approximately 4weeks post delivery, these changes are

returned to pre-pregnancy state.

COAGULATION FAILURE.
⚫ Though pregnancy is hypercoagulability state,

complications of pregnancy or medical conditions

in pregnancy can put excessive demand on the

physiological changes leading to coagulation

failure.
COAGULATION FAILURE.
⚫ Causes of coagulation failure in pregnancy can be classified
into
⚫ Acquired causes and congenital causes or obstetrics and
non obstetrics causes
⚫ Acquired causes
 THROMBOCYTOPENIA: Gestational
thrombocytopenia, idiopathic thrombocytopenic
purpura, secondary autoimmune thrombocytopenia
(APS,SLE, HIV, drug induced thrombocytopenia), MAHA
(PET, HELLP Syndrome)
 CONSUMPTIVE COAGULOPATHY.
Congenital causes:

 Congenital platelet disorders

 von Willebrand dx,

 Haemophilias.
. Obstetric causes
 Disseminated intravascular coagulopathy
⚫ DIC due to placental abruption, placenta
praevia, massive obstetric haemorrhage,
amniotic fluid embolism
⚫ DIC due to any other causes including sepsis,
trauma, incompatible transfusion reaction
 Thrombocytopenia, e.g. HELLP syndrome,
Non-obstetric causes
⚫ Thrombotic thrombocytopenic purpura-TTP

⚫ Thrombocytopenia, e.g. ITP, sepsis, alcohol

⚫ Liver failure in pregnancy, Liver failure due to alcohol,

paracetamol overdose etc.

⚫ Bone marrow failure due to effects of shock.

⚫ Bone marrow failure or infiltration.

⚫ Pre-existing diseases e.g. haemophilias
⚫ Iatrogenic hypothermia
Obstetrics consumptive
coaglopathy
⚫ Obstetrics consumptive coaglopathy

⚫ Characterized by activation of coagulation system, with

resultant widespread of intravascular deposits of fibrin-rich

thrombi, bleeding diathesis and peripheral organ ischemia.

⚫ Causes are abruptio placeta, retained dead fetus, amniotic

fluid embolism, sepsis, severe preeclampsia

⚫ It can be acute in onset or chronic as seen in retained dead fetus.

Consumptive coagulopathy

⚫ Mechanism of consumptive coagulopathy in pregnancy

⚫ 1) Vascular endothelial damage: PET, hypovolemic

shock, septicemic shock

⚫ 2) Release of tissue factor: Amniotic fluid

embolism, placenta accreta, acute fatty liver

⚫ 3) Production of procoagulants: Phospholipids ,

fetomaternal haemorrhage, septicemia,

intravascular haemolysis, incompatible blood

transfusion.

⚫ These triggers lead to thrombin production.

Thrombin promotes platelet activation and

aggregation , occlusion of the microvasculation.

Haemolysis occurs

and leads to microangiopathic haemolytic anaemia.

⚫ Fibrin is formed, but fibrinolysis is suppressed leading

to thrombosis of the small and meddle-size vessels.

⚫ Passage of erythrocytes through partially

occluded vessels leads to red cell fragmentation

and microangiopathic haemolytic anaemia.

Abruptio placenta
⚫ Abruptio placenta is the commonest (60%) cause of

obstetrics consumptive coagulopathy. It causes release

of tissue factor into maternal circulation. Also

hypovolemic shock, large volume transfusion and

high levels of fibrin degradation products (FDPs) act

as anticoagulant thereby exacerbate severe abruptio.

Amniotic fluid embolism
⚫ Amniotic fluid contains tissue factor, fetal squames.

Squames embolisation into the pulmonary vessels causes

severe pulmonary hypertension and maternal death.

⚫ If the mother survives, the tissue factor may cause

anaphylactoid reaction which is associated with

maternal cardiovascular collapse, pulmonary edema and

consumptive coagulopathy.
SEPSIS
⚫ Sepsis causes consumptive coagulopathy by release
of proimflamatory cytokines like tumor necrotic
factors a(TNF-a), IL-1, and IL-6.

⚫ These may trigger expression of tissue factor

by monocytes and endothelial cells.
Severe preeclampsia
⚫ Severe preeclampsia causes

severe vasopasm, ischemic endothelial injury

and therefore expression of tissue factor.

It can cause abruptio, HELLP syndrome

Clinical features of consumptive
coagulopathy
⚫ Clinical features include excessive bleeding from placenta

site, C/S wound, venepunture sites

⚫ Laboratory findings include low platelet count, prolonged

APPT and PT, low fibrinogen level- less than 1g/l , D-

dimer levels increase and exceed the normal value of

200ng/ml to above 2000ng/ml.

⚫ Blood film shows fragments of red cells in keeping with

microangiopathic haemolysis.
Principle of management
⚫ Removal of precipitating factors,

⚫ Correction of aggravating factors

⚫ Replacement of missing coagulation factors and platelets.

⚫ Correct associated/aggravating factors

⚫ Prevent and correct hypoxia: Oxygen and

blood transfusion.
Principle of management
 Sepsis: IV antibiotics

 Replacement of clotting factors: FFP

 Severe hypofibrinogenemia: Cryoprecipitate

 Heparin is contraindicated in obstetrics

consumptive coagulopathy except in retained dead

fetus.
Principle of management
⚫ Monitoring of replacement therapy in coagulation failure

is by

⚫ - aiming at achieving platelet count >50x10^9/l

⚫ - aiming at fibrinogen level >1.0g/l

⚫ -shortening of the APTT and PT to approach their

normal values.
Congenital causes of coagulation
failure
⚫ Congenital causes of coagulation failure include

⚫ Congenital platelet disorder - Bernard- soulier

syndrome: Spontaneous bleeding, epistaxis menorrhagia

, thrombocytopenia, poor platelet aggregation

⚫ von Willebrand disease

⚫ Haemophilias A and B
Congenital causes of coagulation
failure
⚫ Deficiencies of clotting factors like fibrinogen,

FVII, FX, FXI, FXIII

⚫ Combined deficiencies of the vitamin K-

dependent factors II, VII, IX and X.

Von Willebrand disease
⚫ Vwd is the commonest inherited bleeding disorder.
⚫ It is caused by deficiency in plasma levels or
structural deficiency of von Willebrand factor vWF .
⚫ vWF is a carrier protein in plasma for FVIII, is a bridge
between platelets and subendothelial collagen fibers
⚫ In pregnancy both factor VIII and vWf levels are
increased.
⚫ Antepartum haemorrhage is uncommon with vWF.
⚫ The disease often manifest after delivery causing secondary
postpatum haemorrhage especially 3-5days after delivery.
⚫ vWf concentrate and desmopressin (DDAVP) can be
used to correct bleeding disorder.
 HEAMOPHILIAS
⚫ Haemophilia A is due to deficiency of factor FVIII
and haemophilia B is due to deficiency of factor FIX.
⚫ Both conditions are X-linked therefore almost
a disease of the male.
⚫ Women carriers should be monitored regularly.
⚫ FVIII/IX levels should not be lower than 40%
for vaginal delivery and not less than 50% for
c/s
⚫ Treatment is by giving recombinant FVIII/IX
or DDAVP
⚫ Plasma –derived factor concentrates
Conclusion
⚫ Understanding of coagulation changes in pregnancy

helps is managing delivery and postpartum

complications.

⚫ Obstetric causes of cougulation failure are common

and preventive measures help to minimise morbidity

and mortality associated with this condition.