D.I.

C is not a disease, it is a
syndrome that can be caused
by many diseases

Although there are some similarities

but their pathogenesis, approaches
and treatments are different
 NEW CONCEPT OF DIC
 Not only a disorder of consumptive coagulopathy
that produce bleeding tendency:
PROCOAGULATION
 But also a disorder that produce multiple organ
damage : PROINFLAMMATION
Initiation of the D.I.C process

Rupture of Intact
Endothelium Endothelium

Obstetric accidents Sepsis

Prolonged operation Malignancy
Burn and trauma etc Shock etc
 Endo/Exotoxin
Coagulation activation
Fibrinolysis Inhibition
PAI-1
t-PA
Prot-C
Cell adherence TNF, IL-1
IL-6

Damage

Endothelium
 Endothelium Damage
or
Cytokines
(TNF, IL-1)

COAGULATION INFLAMMATION

Bleeding Organ damage

 Endo/Exotoxin

Coagulation activation
&
Platelet activation
TNF, IL-1
IL-6

platelet-fibrin plug Damage

Endothelium
 THROMBIN
The critical point
Once thrombin is generated, it is
irreversible
 THROMBIN

COAGULATION INFLAMMATION

LOCAL SYSTEMIC

localized organ damage

 THROMBIN
Endo/Exotoxin
Inflammation Fibrinolysis Coagulation
Rbc, neutro t-PA/PAI fibro&vitro
Selectin,PGI
complement

plt
TNF, IL-1
rbc
rolling

neutro Endothelium
 Balance In Perfect Harmony

“Wound Healing” “Closing of wound”

Inflammation THROMBIN Coagulation

rolling

neutro Endothelium
 D.I.C
happens when the balance is disturbed because
the compensatory mechanism fails to overcome

DOCUMENTED COMPENSATORY
MECHANISMS
1. Tissue factor pathway inhibitor (TFPI)
2. Activated Protein C (APC)
3. Anti-thrombin III (AT-III)
 Imbalance

“Organ Damage” “Bleeding”

Inflammation THROMBIN Coagulation

rolling

neutro Endothelium
D.I.C DUE TO ENDOTHELIAL
RUPTURE
USUALLY PRODUCES
BLEEDING !!!
Sudden and Life-threatening
 DIC NOT CAUSED BY
ENDOTHELIAL RUPTURE

Such as in sepsis usually does not

cause bleeding but
MULTI ORGAN FAILUURE
 One example is
PURPURA FULMINANS
 Due to Neisseria meningitidis; a Gram (-)ve
 Diplococcus
 More common in pediatrics than in adults
 INFLAMMATORY: tissue necrosis
 PURPURA FULMINANS
 Differentials:Henoch-Schonlëin purpura
 Microangiopathic picture
 Low FV:a FVIII:a, platelets
 Prolonged: PT, aPTT, TT, D-dimer, Hess test,
bleeding time
 “Low Protein-C”
 PURPURA FULMINANS
 >50% mortality
 Traditional treatment and control of DIC
(such as arresting of bleeding) does not
affect the progression of the necrosis and
rate of amputation
When P.T, A.P.T.T and T.T are
all prolonged
Think about possibility of D.I.C
(Disseminated Intravascular Coagulation)
Measure D-dimer
 D-dimer
 To detect action of fibrinolysis (plasmin digestion
of X-linked fibrin)
 To show that X-linked Fibrin has been generated.
 This all shows evidence of D.I.C (Disseminated
Intravasculkar Coagulation)
 FXIII FXIIIa

THROMBIN

Fibrinogen Fibrin Fibrin X-linked

Monomer Polymer Fibrin

PLASMINOGEN PLASMIN

t-PA
D-dimer test by ICT technique (qualitative)
D-dimer by chomogenic assay (quantitative) in ng/ml
 Diagnosis of D.I.C
 Clinicalgrounds
 Laboratory: prolonged PT, APTT, TT,
 Confirmatory test: increase of D-dimer > 500
ng/ml or > 1.000 ng/ml in operative case