Transcript Coagulation failure in pregnancy

Dr : Hashmi Hajrai
MBBCh, DGO, M’MAS, MRCOG
Consultant Obstetrician & Gynaecologist
 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
 Understanding
the pathogenesis of DIC
syndrome, diagnosis, complications &
management outlines
 Brief knowledge on some other important
causes of coagulation failure in pregnancy
 Bleeding
during labour is dealt with
effectively by
- increased production of coagulation
factors during pregnancy
- increased blood volume
- myometrial contraction

this hypercoagulable state with local
activation of clotting system is associated
with increased risk of not only VTE but also
DIC
 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
 Primary

Hemostasis
Platelet Plug Formation:dependent on normal platelet
number & function
 Secondary

Activation of Clotting Cascade  Deposition &
Stabilization of Fibrin
 Tertiary

Hemostasis
Hemostasis
Dissolution of Fibrin Clot:dependent on Plasminogen
Activation
Normal Artery
Endothelium
Smooth
Muscle
Adventitia
Vascular Damage
Hemostasis
Overview of blood
coagulation
Vasoconstriction
Platelet
Activation
Vessel
Injury
Platelet
Plug
Platelet
Aggregation
Clot
Thrombin
Tissue
Factor
Coagulation
Cascade
Three phases
1.
2.
3.
Intrinsic pathway
Extrinsic pathway
Common pathway
Intrinsic pathway
XII
XI
APTT
Extrinsic pathway
VII
IX
VIII
Prothrombin
(II)
X
PT
thrombin
V, Ca, P/L
fibrinogen
fibrin
XIII
STABILISED FIBRIN
Congenital coagulation failure disorders
these are uncommon.....examples:
i.
ii.
Von Willebrand’s disease...will be discussed
Haemophilia A & B
are far more commonly seen
a.
b.
c.
Thrombocytopenic coagulopathies
Disseminated intravascular coagulation
..DIC
Anticoagulant therapy
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
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)
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
Other coagulation factor deficiencies
•
Factor VIII ( hemophilia A)
• Factor IX ( hemophilia B)
Autoimmune Thrombocytopenic Purpura
• Idiopathic thrombocytopenic purpura
• Immunoglobulin G (IgG)
•
Diagnosis
Platelet count < 100,000/mm3
• Increased numbers of megakaryocytes
• Increased platelet volume
• Diameter
•
•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
 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
 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
DEATH
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 - preeclampsia & eclampsia
 Conditions
having non-specific or indirect
action
- amniotic fluid embolism
- gram negative septicaemia
- saline abortion
Mechanism of DIC
Bick et al., 2002
 Those
of the underlying cause
 Those
due to Complications of DIC
Involving skin & mucus membranes
 Ecchymosis
 Petechiae
 Bleeding from the gum
 Haematuria
 GIT bleeding
 Venepunctur oozing
 Intracranial or intracerebral haemorrhage
 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
 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
 Fragments
 Schistocytes
 Paucity
of platelets
Fragmented RBC
T. TATU
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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
 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
 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
 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
 Use
of heparin is controversial .
Haematologist opinion should be sought
before it’s use