1. Coagulation failure in pregnancy
Dr : Hashmi Hajrai
MBBCh, DGO, M’MAS, MRCOG
Consultant Obstetrician & Gynaecologist

2. Learning objectives
The student should understand the alterations in coagulations & fibrinolysis associated with pregnancy
Refresh his mind about the normal coagulation cascade mechanisms and its triggers
Broad line classification of coagulation failure in pregnancy

3. Understanding the pathogenesis of DIC syndrome, diagnosis, complications & management outlines
Brief knowledge on some other important causes of coagulation failure in pregnancy

4. Coagulations changes in pregnancy
Bleeding during labour is dealt with effectively by
- increased production of coagulation
factors during pregnancy
- increased blood volume
- myometrial contraction

5. this hypercoagulable state with local activation of clotting system is associated with increased risk of not only VTE but also DIC

6. The fibrinolytic system is responsible for disposing of fibrin after fulfilling its haemostatic function
Plasma proteases are responsible for controlling the speed and extent of coagulation & fibrinolysis

7. Hemostasis is a balancing act between clot formation and fibrinolysis or clot dissolution.

8. HEMOSTASIS Primary + Secondary + Tertiary
Primary Hemostasis
Platelet Plug Formation:dependent on normal platelet number & function
Secondary Hemostasis
Activation of Clotting Cascade  Deposition & Stabilization of Fibrin
Tertiary Hemostasis
Dissolution of Fibrin Clot:dependent on Plasminogen Activation

9. Normal Artery
Endothelium
Smooth
Muscle
Adventitia

10. Vascular Damage

11. Hemostasis

12. Overview of blood coagulation

14. Second step is activation of coagulation
Three phases
Intrinsic pathway
Extrinsic pathway
Common pathway

15. Coagulation cascade thrombin fibrin X Intrinsic pathway XII XI
Extrinsic pathway IX
APTT
VII
VIII X PT
thrombin
Prothrombin
(II)
V, Ca, P/L
fibrin
fibrinogen
XIII
STABILISED FIBRIN

16. Thrombin converts fibrinogen to fibrin monomer by initially cleaving fibrinopeptides A and B. After a loosely cross-linked fibrin clot is formed, FXIIIa is able to cross-link fibrin, leading to clot stabilization.

17. The process of fibrinolysis enables cross-linked clots to be degraded
The process of fibrinolysis enables cross-linked clots to be degraded. The fibrinolytic process involves the zymogen plasminogen, which is converted to plasmin by tPA or uPA. PAI-1 and 2-antiplasmin are the physiologic inhibitors of plasminogen activator and plasmin, respectively.

18. Classification of coagulation disorders
Congenital coagulation failure disorders
these are uncommon.....examples:
Von Willebrand’s disease...will be discussed
Haemophilia A & B

19. Acquired coagulation failure disorders
are far more commonly seen
Thrombocytopenic coagulopathies
Disseminated intravascular coagulation ..DIC
Anticoagulant therapy

20. 4. Congenital Coagulopathies
Von Willebrand disease
Factor synthesized by endothelial cells &
megakaryocytes
Forms a complex with factor VIII
Mediates platelet adhesion and collagen
Inherited as autosomal dominant trait

21. Congenital Coagulopathies
Von Willebrand disease
During pregnancy
Prophylactic treatment factor VIII level below 25%
DDAVP is administered as labor begins –
repeated every 12 hrs.
FFP or cryoprecipitate (500-1,500 units of
factor VIII activity)

22. Congenital Coagulopathies
Von Willebrand disease
During labor
Factor VIII levels should be maintained at 50%
of normal
CS – factor VIII level to 80%of normal
Check daily during the post partum period

23. Congenital Coagulopathies
Other coagulation factor deficiencies
Factor VIII ( hemophilia A)
Factor IX ( hemophilia B)

24. Thrombocytopenic Coagulopathies
Autoimmune Thrombocytopenic Purpura
Idiopathic thrombocytopenic purpura
Immunoglobulin G (IgG)

25. Thrombocytopenic Coagulopathies
Diagnosis
Platelet count < 100,000/mm3
Increased numbers of megakaryocytes
Increased platelet volume
Diameter

26. Thrombocytopenic Coagulopathies treatment
Conservative management
Corticosteriods – if platelet count <20,000/mm3 before the onset of labor or
< 50,000/mm3 at time of delivery
High dose IV immunoglobulin produces
increase in platelet count
Significant hemorrhage – immediate
postpartum period platelet transfusion

27. The theoretical risk of intracranial haemorrhage in the thrombocytopenic foetus has not been shown to be reduced by C/S therefore C/S should be performed for obstetric reasons

28. DIC
SYSTEMIC ACTIVATION OF COAGULATION
An acquired syndrome characterized by systemic intravascular coagulation
Coagulation is always the initial event
Intravascular deposition of fibrin
Depletion of platelets and coagulation factors
Thrombosis of small and midsize vessels
Bleeding
DEATH
Organ failure

29. Obstetric causes of DIC
Falls into three categories
conditions associated with release of tissue thromboplastin that activates extrinsic pathway
- placental abruption
- dead foetus
- molar pregnancy
Conditions associated with endothelial damage leading to activation of intrinsic & extrinsic pathways - pre- eclampsia & eclampsia

30. Conditions having non-specific or indirect action
- amniotic fluid embolism
- gram negative septicaemia
- saline abortion

31. Mechanism of DIC
Bick et al., 2002

32. Clinical manifestation of DIC
Those of the underlying cause
Those due to Complications of DIC

33. Haemorrhagic manifestations
Involving skin & mucus membranes
Ecchymosis
Petechiae
Bleeding from the gum
Haematuria
GIT bleeding
Venepunctur oozing
Intracranial or intracerebral haemorrhage

34. Thrombotic manifestations
Neurologic with multifocal lesions , delirium & coma
Dermatologic with focal ischaemia & superficial gangreen
Renal with cortical necrosis and ureamia
GIT acute ulceration with bleeding
Vascular occlusion causing pulmonary infarction or peripheral vascular gangreen

35. Lab results Markedly decreased platelet count
Markedly Increased fibrin degradation products FDP’s
Fragmented RBCs & microspherocytes in peripheral blood film
Low fibrinogen , factor II , V & VII
Prolonged PT, PTT & TT

36. Microscopic findings in DIC
Fragments
Schistocytes
Paucity of platelets

37. Fragmented RBC
T. TATU
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38. Treatment of DIC Remove underlying cause Replenish depleted factors
FFP Provides source of most factors
Cryoprecipitate provides fibrinogen
Platelet and blood support
Cautious use of heparin
Up to date, emedicine

39. conclusion
Blood coagulation is a major component of haemostasis. Increased Coagulation factors levels in pregnancy is meant to minimize blood loss at time of delivery
This haemostatic mechanism could fail risking patient’s life

40. Thrombocytopenic coagulation failure and DIC syndrome are the most commonly seen in obstetric practice
Congenital causes of coagulation failure are uncommon and usually already diagnosed prior to pregnancy
DIC syndrome is always secondary to an underlying pathology

41. If diagnosis of DIC is missed or appropriate action is delayed it can cause serious maternal morbidity or even death
Platelet transfusion and coagulation factor replacement or fresh blood transfusion are the main stay of treatment besides other supportive therapy

42. Use of heparin is controversial
Use of heparin is controversial . Haematologist opinion should be sought before it’s use