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DISSEMINATED INTRAVASCULAR

COAGUL ATION (DIC)

PRESENTER:DR THADEO MAINA NYAMSHA.


FACILITATOR:DR BENJAMIN MTINANGI

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OBJECTIVES
DIC
-Definition
-Causes
-Pathophsiology
-Clinical features
-Laboratory investigations
-Management.

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What is DIC
DIC is a thrombohaemorrhagic disorder which
is caused by systemic activation of coagulation
pathways leading to formation of thrombi
throughout the microcirculation.

As a consequence of the widespread of thromboses


there is a consumption of platelets and coagulation
factors and secondary activation of fibrinolysis which
then results into bleeding.
It is a paradox in haemostastic
sequence in which
coagulation, clot dissolution and
bleeding all take
place at the same time.

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CAUSES OF DIC
Obstetric Condition
Abruption placenta
Dead foetus syndrome i.e Intra Uterine Foetal
death ( IUFD)
Pre- eclampsia and eclampsia
Amniotic fluid embolism
Retained placenta.
Septic abortion.
Cancers
Metastatic cancer, lung, stomach,
prostate,Pancrease
Leukaemia
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Infections
Acute bacterial infections this is due to
the release of endotoxins and exotoxins
which stimulates the synthesis and
release of the tissue factors involed in the
coagulation pathway. e.g. meningococcal
meningitis,
Acute viral infections
Parasitic infections( e.g. severe malaria)

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Shock
-septic shock
-severe hypovolemic shock
Haematological Conditions-Incompatible
Blood transfusion leading to severe
reactions

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Surgery
Extensive burns
Massive trauma
Snake bite eg rattle snake envenomation.

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Pathophytsiology of DIC
DIC Is not a primary disorders
It occurs as a complication in various disease condition
activating both intrinsic and Extrinsic pathways

Main triggering mechanism is


Massive activation of coagulation that overwhelm the
control mechanism.
Clot formation consume all available coagulation
factors and platelets leading to severe haemorrhage

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Fibrinolytic system is markedly activated,
FDPs act as natural anticoagulants by
inhibition of thrombin, platelets
aggregation and fibrin polymerization this
leads to further bleeding

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Massive tissue Endothelial
Sepsis
destruction injury

Activation Release of the tissue


Of factors
Plasmin PLT
aggregation
Widespread microvascula
Fibrinolysis thromboses
Proteolysis
FDP Of clotting Vascular
factors occlusion

Consumption
Bleeding Of coagulation Ischaemia
factors Haemolytic anaemia 11
CLINICAL MANIFESTATION
OF DIC
Depends mainly on whether one system is
activated more than the other.
i.e. CLOTTING OR FIBRINOLYTIC
system
If the clotting is mainly activated
Clinical picture is associated more with
THROMBOSIS and
INFARCTION
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If Fibrinolytic System dominates
More Fibrin Degradation
Product (FDP)
Generalised haemorrhage will
dominate
-Shock
-petechia and ecchymosis

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In general the acute form of DIC
as occurs in obstetric complications
is dominated by bleeding, while the
chronic form as in cancer is
dominated by thrombosis.

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LABORATORY INVESTIGATIONS

FBP- Thrombocytopaenia
-Normocytic anaemia
PT, PPT, Bleeding time- all are increased

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MANAGEMENT OF DIC

Manage the primary cause

Replace the clotting components


(Fresh frozen plasma)

Packed RBCs for- anaemia

Platelets concetrates for


thrombocytopaenia 16
REFERENCES
1.Robinson Textbook of Basic Pathology 8th
Edition.
2.Davidsons Principle and Practice of
Medicine 8th Edition
3.Physiology Lecture Notes By Dr MTINANGI.
4.Medical Physiolgy-Guyton and Hall -11th
Edition.

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