Dr : Hashmi Hajrai

MBBCh, DGO, MMAS, 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 Hemostasis
Activation

of Clotting Cascade Deposition &

Stabilization of Fibrin

Tertiary Hemostasis
Dissolution

Activation

of Fibrin Clot:dependent on Plasminogen

Normal Artery
Endothelium
Smooth
Muscle
Adventitia

Vascular Damage

Hemostasis

Overview of blood
coagulation
Vasoconstriction
Platelet
Activation

Vessel
Injury

Platelet
Plug

Clot

Platelet
Aggregation
Tissue
Factor

Thrombin
Coagulation
Cascade

2D Medical Animation- Clot Formation and Clot Breakdown.flv

Three phases
1. Intrinsic

pathway
2. Extrinsic pathway
3. Common pathway

Intrinsic pathway
XII
XI
APTT

Extrinsic pathway
VII

IX
VIII
Prothrombin
(II)

X
V, Ca, P/L

PT

thrombin

fibrinogen

fibrin
XIII

STABILISED FIBRIN

Congenital coagulation failure disorders

these are uncommon.....examples:
Von Willebrands disease...will be discussed
ii. Haemophilia A & B
i.

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 FDPs
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

37

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 patients 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 its use