Disseminated Intravascular Coagulation

Tutik Harjianti,SpPD,K-HOM
SubDiv.of Hematology & Medical Oncology
Dept.of Internal Medicine, Medical Faculty
Hasanuddin University
Sub Topics :

I. Introducton of D.I.C.
II. Trigger Mechanism of D.I.C.
III. Etiology of D.I.C.
IV. Clinical pictures of D.I.C.
V. Diagnosis of D.I.C.
VI. Management of D.I.C.
VII. Prognosis of D.I.C.
I. Introduction :

DIC
Disseminated : widespread
Intravascular : inside the bloodline
Coagulation : blood clot production
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Physiology of blood circulation :

 Blood always in a liquid form

 Vascular disruption  initiate coagulation
( as a part of normal hemostasis )
 Coagulation is limited in area of lesion
by the effect of :
- blood streaming / blood flow
- coagulation inhibitor inside the circulation
(esp. Anti Thrombin III / AT III)
PHYSIOLOGY of COAGULATION

Vasculature rupture / lesion 

A Vasoconstriction
B Primary hemostasis reaction
C Coagulation
D Fibrinolysis
( A,B,C & D = hemostasis mechanism)
Why DIC can be occured ?

 Overstimulation of coagulation
 suppresion of control mechanism
 DIC.
 Important Clue :

 The presence of thrombin circulating in

bloodline.
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Normally : thrombin can only be found in
area of lesion (where the coagulation
process is still running)
Result of excess of thrombin

 1. Decreased of fibrinogen
 2. Decreased of platelet
 3. Decreased of coagulation factors
 4. Exaggerated of fibrinolysis
 II. TRIGGER MECHANISM OF D.I.C :

1 TUMOR RELEASE OF
Tissue TRAUMA “TISSUE FACTOR” DIC
TissueNECROSIS INTO CIRCULATION

2 ENDOTOXIN ACTIVATION of
GRAM NEGATIVE BACT. COAGULATION DIC
CASCADE

(F XII)
EXPRESSION OF
TISSUE FACTOR
in MONOCYTE & ACCELERATION of COAG RX
ENDOTHELIAL
cells
III. ETIOLOGY of D.I.C.

DIC is not a stand alone disease entity

As a result of severe disease or condition
- Sepsis : gram +, gram -, & fungal infection
Tissue necrosis : (trauma & combustio/burn)
Obstetric : (abortus, emboli of liquor amnion,
fetal death)
Malignancy : (leukemia: Ca)
Other cause of DIC :

 Major hemolytic reaction as a result

of blood transfusion error.
DIC

- Oftenly undiagnosed
- Unexplained bleeding usually lead the
clinician to think about D.I.C.
IV. Clinical pictures of DIC :

 1. Abnormal coagulation
 2. Bleeding (more often)
- can be found at any place
- spontaneous bleeding
- at the site of wound, ooze, cath etc.
Coagulation disorders in DIC .

 Thrombosis can be occurred if the abnormality

of coagulation more prominent than fibrinolysis
- digital ischaemia
- gangrene (necrosis)
- Necrosis of cortex of kidney
- Adrenal gland necrosis & bleeding
Trousseau Syndrome

 Subacute DIC
 Oftenly found in cancer patients
 Thrombosis in superficial & profundal
veins (DVT), commonly recurrent
V. Diagnosis of D.I.C.

1. Clinical pictures (severe disease,

bleeding, thrombosis)
2. Laboratory : fibrinogen <
FDP >
platelet <
Prothrombin Time >
actvated Partial Thromboplastin
Time (aPTT) >
Differential Diagnosis of DIC :

 1. Liver Diseases (normal fibrinogen )

 2. Vit K defc (normal fibrinogen & platelet)
VI. Management of DIC :

 Treat the underlying disease/condition.

 Replacement Tx
1. Platelet concentrate transfusion
(maintain the platelet > 50.000 / mm3)
2. Cryoprecipitate transfusion
(maintain the fibrinogen > 150.000 mg/dL)
Management….

3. Fresh Frozen Plasma transfusion

(to increase coagulation factors)

4. Heparin : still controversial

Should be given with Replacement Tx
Dose : 500 – 750 u / hour
TERIMA KASIH
VII. Prognosis of DIC

Depends on :
1. severity of coagulation reaction
2. amount of bleeding
3. etiology of DIC (malignancy etc)
Action of Plasmin :

- fibrin degradation product (FDP) formed

- inactivation of f V & f VIII
- fibrin degradation
Thrombin :

 Fibrinogen conversion  fibrin monomer

 Stimulation of platelet aggregation
 Activation of f V & f VIII
 Release of plasminogen activator  plasmin
formation.