COAGULATION

DISORDERS

NORMAL
COAGULTION
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 Normal intravascular blood coagulation is
linked with three different interrelated
systems.
These are: • Coagulation system •
Coagulation inhibitory system • Fibrinolytic
system
Pathological disturbance of one or more of
the systems lead to intravascular coagulation
or a tendency to bleed.

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COAGULATION MECHANISM

 The complex system of blood coagulation,

“Enzyme cascade theory” involves two
different pathways, viz. intrinsic and
extrinsic. Both are initiated by different
stimuli and ultimately they culminate into a
common pathway for final conversion of inert
prothrombin to thrombin

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COAGULATION INHIBITORY
SYSTEM
 There are number of naturally occurring
anticoagulants in blood, to counter balance
the hypercoagulable state in pregnancy.
Antithrombin III (AT III) is a main physiological
inhibitor of thrombin and factor Xa. Protein C
combined with protein S and thrombomodulin
inactivates factors V and VIII. Their deficiency
is associated with recurrent
thromboembolism.

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PLASMA FIBRINOLYTIC
SYSTEM
 Fibrinolytic enzyme plasmin which operates
to dissolve the fibrin and other products is
usually not found in the blood as it is rapidly
inactivated by the circulatory antiplasmin.
However, marked production of activators
can activate the plasminogen to plasmin
overwhelming the antiplasmin activity

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Coagulation disorders in OBS/GYN
Pregnancy is a state of marked physiological changes
regarding haemostasis
1. Altered platelet function (numbers, adhesion and
aggregation)
2. Increased blood coagulation factors (II,VII,VII, IX and X)
3. Increased fibrinogen
4. Increased antithrombin III (heparin co-factor)
5. Activity of antithrombin III (heparin co-factor) and Protein C is
unchanged, while protein S activity is decreased.
 Antithrombin III balances action of thrombin and factor Xa, while
protein C and S balance activity of factors V and VIII.

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Role of obstetric physiological
changes
 Aim is to reduce risk of haemorrhage during
pregnancy, labour and puerperium
 With uterine contractility, ensure haemostasis
after the third stage of labour
 There is marked coagulability with reduced
fibrinolysis

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Haemostatic disorders associated with
pregnancy
The physiological changes carry the risk of
rapid, enhanced and sustained response to
coagulant stimuli.
This manifests as:
 Haemorrhage with or without coagulopathy
 Tendency towards increased coagulability of
blood leads to thromboembolism
 Disseminated intravascular coagulopathy

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Definition

 Disseminated intravascular coagulation (DIC)

is a syndrome of abnormal coagulation and
fibrinolysis. Consumption coagulopathy is a
disorder marked by reductions in blood
concentrations of platelets due to exhaustion
of the coagulation factors in the peripheral
blood as a result of DIC. It occurs in response
to certain obstetric complications that are
listed below.

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Steps of DIC
1. Trigger (local or extrinsic)
2. Local activation of coagulation (may end in
eventual recovery)
3. Intravascular coagulation
4. Consumption of clotting factors and
platelets and fibrin deposition

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Steps of DIC (cont’d)
5. Fibrinolysis and FDP formation
6. Organ dysfunction from FDPs or
thrombosed small vessels
7. Haemorrhage with local activation of
coagulation, with FDPs and platelets as the
trigger

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MECHANISM OF DIC

TRIGGER

LOCAL ACTIVATION

RECOVERY Intravascular coagulation

CONSUMPTION OF FACTORS AND PLATELETS Fibrin deposition

Haaemorrhage FIBRINOLYSIS thrombosis

FDPs Organ dysfunction

haemorrage Organ dysfunction

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Obstetric Conditions associated with DIC

 Intrauterine death (retained dead foetus)

 Abruptio placenta
 Severe pre-eclampsia and eclampsia
 Ruptured uterus
 Amniotic fluid embolism
 Irreversible hypovolaemic shock
 Excessive fluid (crystalloid) administration

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Gynaecological disorders associated
with DIC
 Septic abortion
 Missed abortion
 Induction of abortion with hypertonic fluids
 Hydatidiform mole
 Prolonged shock of any cause

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Pathogenesis of DIC
1 Vascular endothelial injury
 Septicaemia
 Pre-eclampsia
 Hypovolaemia
Act thru damage to collagen, leading to
release of platelet thromboplastin,
The intrinsic system of coagulation is
activated thru activation of factor XII

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Pathogenesis of DIC (cont’d)
2 Release of tissue thromboplastin into circulation
 Abruptio placenta
 Amniotic fluid embolism
 Retained dead foetus
 Intrauterine sepsis
 Hydatidiform mole
 Abortion induced with hypertonic fluids
Thromboplastin combines with factor VII to activate
factor X and thereby initiate the extrinsic pathway

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Pathogenesis of DIC (cont’d)
3 Tissue phospholipids
 Intravascular haemolysis
 Incompatible blood transfusion
 Feto-maternal haemorrahge
 Septicaemia
These activate factor V.
Together with Activated factor X and factor Va, they
acceleration of conversion of prothrombin to thrombin

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Clinical presentation of DIC
 All triggers act by release of procoagulant
substances into maternal circulation
 Presentation is influenced by the triggering
condition
 Manifestation is markedly varied
 May be sub-clinical and asymptomatic in the
well compensated state, though laboratory
evidence of the condition exists

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Clinical presentation of DIC (cont’d)
Signs of Severe DIC
 Massive uncontrollable haemorrhage
 Very low fibrinogen and platelet levels
 High levels of Fibrinogen degradation
products (FDPs)

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Inestigations
 Clotting bedside tests
 Clotting time is prolonged if it takes greater
than 7–8 minutes for a clot to form.
Clot consolidation and retraction: The clot
should be able to withstand inversion of the
tube after 30 minutes and should not lyse or
breakdown within 1 hour. The clot should
occupy at least half of the total blood sample.

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Investigations
 Platelet count
 Activated PTT (tests intrinsic system)
 Prothrombin time (tests extrinsic system)
 Fibrinogen estimation
 Estimation of FDPs
 Thrombin time
(FDPs only provide an indirect test for DIC, and specimens
should be analyzed after management of the emergency )

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Investiations
 Platelet levels (platelet count) may be low or
progressively fall.
Partial thromboplastin time (PTT) is variable
and may only be prolonged later in the process
when the clotting factors are severely depleted.
Prothrombin time (PT) or International
Normalized Ratio (INR) will become prolonged.
Thrombin time (TT) is usually prolonged

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 Fibrinogen levels (fibrinogen assay) are
normally increased in pregnancy to 400-
650mg/dl. In DIC, the level falls but may be in
the normal non-pregnant range. With severe
DIC, the fibrinogen levels usually fall below
150mg/dl.
FDP: Levels of 80 /ml confirm a DIC diagnosis.
However, these elevated levels will remain for
24–48 hoursafter the DIC has been controlled.

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 A blood film or blood smear may show
abnormally shaped (―helmet‖ or ―tear‖
shaped) and fragmented red blood cells
(schistocytes). These are formed by the
alteration of normal red blood cells as they
are forced through the fibrin mesh in the
obstructed capillary bed.

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Treatment
 Adjuvant therapies (Vitamin K)—The
vitamin K dependent factors II, VII, IX, X are
consumed in DIC. 5-10 mg of Inj Vit K given
(IM), can help to replenish these
procoagulants.

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 CURATIVE : The management goal is to
identify and to correct the underlying
pathology. In most cases, delivery of the fetus
brings the resolution of coagulopathy. The
other part of the management is to achieve a
platelet count > 50,000/µL and a fibrinogen
level > 100 mg/dL.

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 Administer oxygen by face mask or by
endotracheal intubation and intermittent positive
pressure ventilation, if
necessary, to achieve satisfactory arterial
oxygenation.
Monitor the above by a central venous pressure
line if possible.
Monitor the urinary output. Aim to keep the urinary
output at least 30–60ml/hour.
Monitor the complete blood count. Aim to keep the
hematocrit >30%.
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Fluid replacement therapy
 Crystalloids (Saline, Hartmans, Ringers etc)
 Colloid solutions (e.g. Haemacel and NOT dextran)
 Whole blood (avoid old stored blood- devoid of factors V and VII)
 Fresh frozen plasma (contains all coagulation factors if obtained
within 6 hrs of donation; lacks platelets; storable for 1 year)
 Packed red blood cells
 Cryoprecipitate (richer in fibrinogen than FFP but lacks antithrombin III )
 Platelet concentrate transfusion

2929Transfuse 2 units of FFP for every 4 units of stored blood

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 Fresh frozen plasma replaces most clotting
factors and has the least risk of transmitting
hepatitis. As a working rule, give 1 unit after
the initial 4 to 6 units of whole blood and
thereafter 1 unit for every 2 units of whole
blood
required.

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 Cryoprecipitates may be necessary if
fibrinogen levels are low.
Platelets can be transfused in severe cases
of thrombocytopenia. One unit of platelets
can raise the number of platelets to about
5,000 to 10,000.

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 Heparin: It should be used when the vascular
compartment remains intact. In acute
condition such as amniotic fluid
embolism, intravenous heparin 5000 units
repeated 4-6 hours intervals is useful to stop
DIC and may be life saving.

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 Fibrinolytic inhibitors are mainly indicated in
postpartum hemorrhage following abruptio
placentae inspite of a firm and contracted
uterus and when blood fibrinogen level is 200
mg% or more.
Commonly available antifibrinolytic agents
are—(1) EACA—inhibits plasminogen and
plasmin (2) Trasylol—inhibits plasmin (3)
Aprotinin—nonspecific enzyme inhibitor.

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Management of coagulation failure

 The best mngt is to anticipate the disorder

and prevent it
 The second line mngt is early detection and
correction of the disorder
Mngt involves team work of doctors, nurses,
laboratory staff and anaethesiologists

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 END

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