Obstetrics Simplified - Diaa
Coagulation Defects in Pregnancy
Factors involved in the arrest of haemorrhage
- After injury to any blood vessel haemostasis is achieved by:
- Vascular responses: obliteration of the injured vessel by;
- vasoconstrictors released from platelets,
- external pressure by either haematoma formation, contraction
of the surrounding muscles (as in uterine and placental
blood vessels) or by artificially applied pressure.
- Platelets aggregation.
- Stage I: (few minutes)
- Intrinsic mechanism: Activation of factors XII, XI and IX
respectively by vessel wall damage + Ca++ and factor VIII
activation of factor X.
- Extrinsic mechanism: Tissue damage leads to release of factor
III and VII → activation of factor X.
- Stage II: (10-15 seconds)
- In which activated factor X (Xa) + factor V+ Ca++ lead to
conversion of prothrombin (factor II) → thrombin.
- Stage III: (1-2 seconds)
- Thrombin converts fibrinogen (factor I)
→ fibrin monomer
→ fibrin polymers ® fibrin.
Changes in pregnancy and labour
- Coagulation system:
- Fibrinogen (FI): increases from 2-4 gm/L
(normal level) to
- Factors VII, VIII and X: increase by 20-100%.
- Fibrinolytic system:
- Although plasminogen increases by about 100%, fibrinolytic activity
decreases due to;
- increase inhibitory activity,
- high oestrogen and progesterone level reduces fibrinolysis,
- placenta contains inhibitors.
- Uterine vasculature:
- The elastic lamina and smooth muscles of the terminal spiral
arteries are replaced by fibrin matrix . This facilitates increase
blood flow during pregnancy and closure of the sinuses postpartum
by myometrial contraction.
Coagulation Disorders in Pregnancy
- Disseminated intravascular coagulation:
- Von Willebrand’s disease: Inability to synthesise factor
VIII related antigen.
- Haemophilia A = inability to synthesise factor VIII.
- Haemophilia B = inability to synthesise factor IX.
- Thrombocytopenia: due to decreased production or increased
- Immunologic (idiopathic) thrombocytopenic purpura.
Disseminated Intravascular Coagulation (DIC)
Extensive vessels and tissues damage → release
of thromboplastins → utilisation of the fibrinogen
and other clotting factors in an aimless coagulation process
→ fibrin .→ stimulates
fibrinolytic system → breaks fibrin and fibrinogen
into FDP which have an anticoagulant effect →
aggravates haemorrhage and shock → ischaemia
→ more tissue damage →
N.B. The anticoagulant effect of FDP is due to:
- Inhibition of platelet function.
- Interference with thrombin/ fibrinogen reaction.
- Interference with fibrin polymerisation.
- Interference with myometrial contraction.
- Abruptio placentae.
- Amniotic fluid embolism.
- Endotoxic shock.
- Eclampsia and pre-eclampsia.
- Hydatidiform mole.
- IUFD and missed abortion.
- Intra amniotic hypertonic saline or urea for induction of abortion.
- Incompatible blood transfusion or transfusion of massive banked
blood which is deficient in factor V and VIII.
- Prolonged shock of whatever the cause.
- Placenta accreta.
- Rupture uterus.
Unexplained spontaneous bleeding from any site e.g.
- oozing of blood,
- haematoma formation especially at wound and venepuncture site,
- postpartum haemorrhage.
- Bed -side tests:
- Clot observation test:
- 5-10 C.C. of blood in a test tube will be clotted normally
within 10 minutes. In case of DIC no clot will be formed or
a clot is formed but it undergoes dissolution within one hour
- Fibrindex test:
- 0.5 C.C. of fibrindex which contains thrombin is added to
0.5 C.C. of plasma in a test tube. Normally, a visible clot
will be formed within 5-10 seconds. In DIC, clot formation is
delayed up to 30 seconds (hypofibrinogenaemia) or it will not
form at all (afibrinogenaemia).
- Schneider test:
- Thrombin is added to serial dilutions of the patient’s plasma
1:2, 1: 4, 1:8,......1:128.
- Clot formation in all tubes: Normal.
- No clot in all tubes: Afibrinogenaemia.
- No clot in dilutions 1: 16 onwards: Hypofibrinoginaemia.
- Laboratory tests:
- Plasma fibrinogen level:
- During pregnancy the normal level is 4-6 gm/L. Failure of
coagulation occurs when its level drops to 1 gm/L.
- Fibrinogen degradation products FDP: increased.
- Platelet count: decreased.
- Elimination of the underlying cause.
- Fresh blood transfusion: contains clotting factors particularly
F II, V and VIII.
- Fresh frozen plasma: contains 3 gm fibrinogen/L in addition to FV
- Fibrinogen: 4-6 gm IV may be given if there is no fresh frozen plasma.
However, it is not recommended as it may aggravate the coagulation process
(fuel on fire) and cause hepatitis B.
- Heparin: to inhibit fibrin production and consumption of the clotting
factors but it is contraindicated if there is current bleeding.
- Antifibrinolytic agents: as EACA, trasylol or tranexamic acid may
be given to suppress the fibrinolytic process. However, this may enhance
DEEP VEIN THROMBOSIS (DVT)
- Venous stasis,
- increased blood coagulability,
- venous intimal damage.
These three factors meet with pregnancy and labour due to:
- increased clotting factors I, VII, VIII and X.
- reduced fibrinolytic activity.
- pressure of the gravid uterus on pelvic veins.
- antenatal rest, prolonged labour, dehydration, excessive blood loss,
pressure on calf muscles during delivery, delay in mobilisation, trauma
and pelvic infection.
- oestrogen for postpartum suppression of lactation.
- Superficial Thrombophlebitis:
- Common in varicose veins of the calf, thigh, inguinal region
- There is discomfort, localised superficial tenderness, and pain.
- A palpable lump.
- A low grade fever.
- Deep Vein Thrombosis:
- Pain and tenderness in calf muscles due to involvement of the
posterior tibial vein which may extend to popliteal, femoral and
- Oedema of the affected leg diagnosed by difference in girth
of the limbs of more than 1cm.
- Hotness and cyanosis of the leg.
- Positive Homan’s sign: calf pain on dorsiflexion of the foot
but neither its presence nor absence is reliable.
- Doppler ultrasound:
- The flow of blood as detected by reflection of the waves on
RBCs is absent in DVT.
- Ascending phlebography:
- 30-40 ml of contrast medium is injected into a vein of the dorsum
of the foot after obstructing superficial venous return with a sphygmomanometer
cuff at the ankle and thigh. Flow is monitored on a television screen.
- Isotope venography:
- using technetium - 99m albumin followed with a gamma camera.
- The rise of temperature of the affected limb is detected by
a thermovision infrared camera.
- Elastic bandage and elevation of the affected leg to improve the
venous return and reduce oedema. This is continued until acute swelling
subsides and gradual ambulation is allowed as soon as pain is improved.
- Start with 10.000-15.000 units IV, followed by continuous IV
infusion of 10.000 units/ 4-6 hours.
- The aim is to make the blood clotting time or partial thromboplastin
time 1.5-2 times their normal values.
- Subcutaneous heparin: can be given instead of IV infusion in
a dose of 10.000 units/ 12 hours.
- During labour: Dosage is reduced to 5000 units/ 12 hours.
- Postpartum: 5000 units/ 8 hours is recommended.
- Antidote: Protamine sulphate 1% solution; 10 mg (1ml) for every
1000 units heparin is given by slow IV injection.
- Heparin cannot cross the placenta because of its high molecular
weight (16.000-40.000 dalton).
- Oral anticoagulants as coumarin are teratogenic and excreted
in breast milk causing foetal haemorrhage and chondrodysplasia punctata
(nasal hypoplasia, saddle nose, frontal bossing, short stature,
mental retardation, cataract and optic atrophy).
- Warfarin can be given orally to the postpartum non-lactating
woman in an initial dose of 0.75mg/ kg body weight to a maximum
of 50 mg. Maintenance dose is 5-13 mg daily controlled by prothrombin
time which should be 2-4 times the normal value.
- Antidote: Vit. K1 10-20 mg slowly IV which can be
repeated every 3 hours to a maximum of 40 mg in 24 hours.
- It may occur with or without preceding deep vein thrombosis.
- DVT occurs either during delivery, surgery or in the first
24 hours following them.
- Clinical signs of pulmonary embolism appear within 4-14 days
after DVT formation.
- Range from minimal disturbance to sudden collapse and death
depending on the size, number and site of the emboli;
- chest pain,
- frothy blood stained sputum,
- nausea, vomiting and sudden desire to
- Mild pyrexia,
- raised jugular venous pressure,
- pleural friction rub,
- pleural effusion,
- right ventricular failure.
- ECG: inverted T waves and atrial arrythmia.
- triangular radio
- opaque shadow (infarction),
- pleural effusion,
- raised copula of the diaphragm.
- Subcutaneous heparin: 5000-7500 units/12 hours in puerperium
for women with past history of thrombo-embolism.
- Dextran 70: 500-1000 ml during surgery increases fibrinolysis.
- Heparin: start immediate IV therapy as discussed before.
- Defibrinating drugs: as streptokinase 600.000 IU over 30 minutes,
followed by 100.000 IU/hour by infusion for 72 hours. They are contraindicated
during pregnancy, labour and early puerperium for fear of haemorrhage.
- Analgesic: e.g. morphine sulphate 10 mg.
- Digoxin: as an inotropic.
- Aminophylline: 250-500 mg IV to relieve dyspnoea.
- Pulmonary embolectomy; partial or total occlusion of the inferior
vena cava by an umbrella filter or iliofemoral thrombectomy are
surgical procedures that may be used.
Print this page
Edited by Aldo Campana,