DISSEMINATED

INTRAVASCULAR
COAGULATION
Dr.Varun T M
DEFINITION

DIC is an acute, subacute Or chronic

thrombohaemorrhagic disorder characterized by
excess activation of coagulation, which leads to
formation of thrombi in microvasculature of body.
ETIOLOGY

DIC is not a primary disease

It is a coagulopathy that occurs in course of
variety of clinical conditions
PATHOGENESIS

Central mechanism of DIC is uncontrolled generation of

thrombi by exposure of blood to pathological levels of
tissue factor
Simultaneous suppression of physiologic anticoagulant
mechanism and abnormal fibrinolysis further accelerate
the process
 TRIGGERS

Two major mechanism trigger DIC

1. Release of tissue factor or thromboplastin into the
circulation
Derived from placenta ,dead fetus in obs complications
and cytoplasmic granules of acute promyelocytic
leukaemia and mucus realeased from certain
adenocarcinomas
2. Widespread injury to endothelial cell

 Exposure of subendothelial matrix leading to activation of

platelets and both arms of coagulation pathway
 TNF , imp mediator of DIC in sepsis , induces endothelial cells
to express tissue factor on cell surface and to decrease the
expression of thrombomodulin shifting checks and balances
which govern hemostasis towards coagulation
CLINICAL FEATURES

Possible consequences of DIC are twofold

1. Widespread deposition of fibrin in microcirculation
leading to ischaemic, microangiopathic hemolytic
anaemia
2. Consumption of platelets, coagulation factors and
activation of plasminogen leading to haemorrhagic
diasthesis
CLINICAL FEATURES

In general, acute DIC associated with obstetric

complications, major trauma ,sepsis dominated by a
bleeding diathesis
Whereas chronic DIC which occurs in cancer pts tends to
present with thrombotic complications
Waterhouse Friederichsen syndrome – Occult thrombosis
of adrenal vein leading to adrenal haemorrhage
Kassabach – Merritt syndrome is the consumptive
coagulopathy which occurs with Giant hemangiomas.
Purpura fulminans – Severe form of DIC resulting from
thrombosis of extensive areas of skin, predominantly
young children following viral or bacterial infection mainly
affecting those with protein c pathway deficiency
LABORATORY INVESTIGATIONS
Presence of Schistocytes in peripheral smear
D-dimer test is more specific for detection of fibrin
FDP Level is most sensitive for DIC
Chronic DIC – Giant hemangioma, Metastatic carcinoma
FDP ,D-dimer are elevated , PT aPTT are within normal range
or elevated , Mild thrombocytopenia or normal platelet
counts are also possible
DIFFERENTIAL DIAGNOSIS

TTP- Acute clinical onset of illness accompanied by

thrombocytopenia, red cell fragmentation and
multiorgan failure but there is no consumption of
coagulation factors and hyperfibrinolysis
Severe Liver Disease – laboratory parameters do not
change rapidly. Presence of portal hypertension nd
features of underlying liver disease. Factor viii levels will be
normal
MANAGEMENT

The morbidity and mortality associated with DIC are

primarily related to underlying disease rather than
complications of DIC
Attempts to treat DIC without accompanying treatment
of causative disease are likely to fail
1. Control or elimination of underlying cause
2. Control of precipitating factors
3. Management of haemorrhagic symptoms
4. Replacement of coagulation factors or fibrinolysis
inhibitors
MANAGEMENT OF
HAEMORRHAGIC SYMPTOMS
Administration of FFP , platelet concentrates are
indicated in pts with active bleeding Or at high risk of
bleeding
1. Platelet concentrates- 1-2U /10 kg
One unit (50ml) raises platelet count by 7500/ml
2. FFP-- 15-20ml/kg
Provides both volume replacement and coagulation
factors
One unit (250ml) raises fibrinogen by 5-10mg/dl
Albumin, clotting factors, antithrombin
3. Cryoprecipitate- 1U/ 10 kg
Thawed FFP , not used for volume replacement
One unit (40ml) raises fibrinogen by 6-10mg/dl
Fibrinogen, factor viii, vwf
4 .Clotting factor concentrates are not recommended
because of the limited efficacy
REPLACEMENT OF
COAGULATION FACTORS OR
FIBRINOLYSIS INHIBITORS
Low dose of continuous infusion heparin (5-10U /kg/hr)
may be effective in pts with low grade DIC associated
with solid tumor or acute promyelocytic leukaemia
Heparin is also indicated during surgical resection of giant
hemangiomas and during removal of dead fetus
Heparin not used in acute DIC as it aggravates bleeding
Use of Heparin in severe DIC has no proven benifits
Use of antifibrinolytic drugs like EACA or Tranexamic acid
to prevent fibrin degradation by plasmin may reduce
bleeding episodes in pts with DIC and confirmed
hyperfibrinolysis
However these drugs can increase the risk of thrombosis
and concomitant use of Heparin is indicated
Thank You