2. 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. 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.
8. 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
18. Congenital coagulation failure disorders
these are uncommon.....examples:
i. Von Willebrand’s disease...will be discussed
ii. Haemophilia A & B
19. are far more commonly seen
a. Thrombocytopenic coagulopathies
b. Disseminated intravascular coagulation
..DIC
c. Anticoagulant therapy
20. 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. 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. 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
26. •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. An acquired
syndrome
characterized by
systemic
intravascular
coagulation
Coagulation is
always the initial
event
SYSTEMIC ACTIVATION
OF COAGULATION
Intravascul
ar
deposition
of fibrin
Depletion of
platelets and
coagulation
factors
Thrombosis of
small and
midsize
vessels
Bleeding
Organ failure DEATHDEATH
29. 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
38. Treatment of DIC
• Remove underlying cause
• Replenish depleted factors
• FFP Provides source of most
factors
• Cryoprecipitate provides
fibrinogen
• Platelet and blood support
Up to date, emedicine
39. 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 .
Haematologist opinion should be sought
before it’s use
Editor's Notes
Hemostasis is a balancing act between clot formation and fibrinolysis or clot dissolution.
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.
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.
