Coagulation disorders in pregnancy

Hematological Changes During Pregnancy: 1-Expansion of plasma volume and hemodilution. 2-Hb level increases, but there is physiological anemia. 3-RBC count decreases. 4- S. iron decreases, iron binding capacity increases. 5. Increase iron absorption from the gut. 6. Increase coagulation factors, so there is hypercoagulable state, except factors XI, XIII, and antithrombin III. 7. Decrease in fibrinolytic activity. 8. Decrease platelet count

Normal hemostasis: requires 3 main factors: Vascular constriction Platelet aggregation and formation of platelet plug Fibrin formation.

Fibrin formation

Coagulation system during pregnancy: Pregnancy represent a hypercoagulable state. This include the following: Plasma fibrinogen concentration rises during pregnancy by about 50%. Increase in factors V, VII, VIII, IX, X, XI I.

Hemostatic problems associated with pregnancy: Thromboembolism. Hemorrhage with or without coagulopathy.

Basic definition Venous thromboembolism (VTE ),any thrombo embolic event in the venous system. Deep venous thrombosis (DVD) radiologically confirmed occlusion of the deep venous system of the leg sufficient to produce symptoms of pain or swelling. Pulmonary embolism (PE) radiologically confirmed occlusion of pulmonary arteries sufficient to cause symptoms of breathlessness,chest pain or both

Thromboembolism (TE) is the most common cause of maternal death during pregnancy.

The most dangerous period for fatal pulmonary thromboembolism (PE) is the 1st week postpartum, then the 2nd week. Most cases occurs after CS. Most maternal deaths after CS are due to PE. 90% of death occurs in the 1st 24 h after delivery.

Risk factors: 1- Hypercoagulable state of pregnancy. 2- Decrease activity of naturally occurring anticoagulant. 3- Decrease fibrinolytic activity. 4- Increase tendency to venous stasis during pregnancy.

5. Other factors pregnancy related: Operative delivery. Age and parity. Obesity over 76 kg Restricted activity Estrogen for suppression of lactation. Endothelial injury

6. Other factors not pregnancy related: Previous TE. Lupus anticoagulants, anticardiolipin antibodies, and antiphospholipid syndrome. The thrombosis could be venous or arterial and could occur at any site. Inherited thrombophilia. smoking

Clinical Features of Venous TE: 1- Superficial thrombophlebitis: This means inflammation of a superficial vein which if extended to a deep vein it carries a risk of PE.

2. DVT: The classical signs of DVT are leg edema, calf tenderness, and positive Homans sign, which is calf pain on dorsiflexion of the foot, it could be asymptomatic.

3 -PE a. Massive PE: cyanosis, shortness of breath, chest pain, hemoptysis. b. Small PE: transient dyspnea, tinge of cyanosis, some pleuritic chest pain, unproductive cough, unexplained pyrexia, tachycardia, leukocytosis.

Diagnosis of DVT: Clinical features usually affects left femoral vein. Impedance plethysmography (IPG), little value in 3rd trimester. Dopplar US, same as IPG. Duplex US, used in pregnancy. Contrast venography, gold standard. Iodine 125 fibrinogen scan D –dimer level

Diagnosis of PE:...CXR...ECG...perfusion / ventilation lung scan...arterial blood gas analysis....pulmonary angiography....CT scan

Management of venous TE during pregnancy: Acute phase treatment. Chronic phase treatment.

Acute phase treatment: 1. Thrombolytic therapy: by streptokinase, and tissue plasminogen activaters. It can not be recommended during pregnancy except as a life saving procedure as in case of:..... shocked patient with massive PE iliofemoral venous thrombosis

2. Anticoagulants: unfractionated heparin 40,000 IU daily continuous intravenous infusion.Monitoring of the drug by APTT. If you want to stop the effect of heparin you should stop the drug and give protamin sulfate 1 mg for every 100 IU. Heparin is given for 3-7 days. 3. Surgery.

Chronic phase treatment: Warfarin which crosses the placenta. If this drug is given during pregnancy it should be stopped at 36 weeks. The action of warfarin is monitored by prothrombin time (PT).

DIC (Disseminated intravascular coagulation): trigger mechanism of DIC during pregnancy: 1- Endothelial injury: preeclampsia. Hypovolemia. septicemia

2. Release of thromboplastin as in: Abruptio placentae. Amniotic fluid embolism. Retained dead fetus. Intrauterine sepsis Hydatidiform mole Placenta accreta

3. Release of phospholipid as in: Intravascular hemolysis Incompatible blood transfusion Large fetomaternal bleed septicemia

Clinical manifestation of DIC: 1-Asymptomatic: compensated state. There is lab evidence of increased production and breakdown of coagulation factors, as in PET and in retained dead fetus. 2. Variable degrees of thrombocytopenia 3. Massive uncontrollable hemorrhage.

Diagnostic tests: 1.Thrombin time: 2. Increase in APTT. 3. Increase in PT 4. Decrease in fibrinogen level 5. Decrease in platelet count.

Management: Fluid replacement to avoid renal shut down usually by simple crystalloid eg Hartmanns solution FFP which contains all coagulation factors Fresh blood transfusion

Thrombophilia and adverse pregnancy outcome Severe PET Recurrent early pregnancy loss IUGR Late fetal loss Venous TE during pregnancy