Disseminated Intravascular

Coagulation

Dr. RUDY AFRIANT, SpPD-KHOM

 Definition of DIC
• DIC is a clinicopathologic syndrome in which
widespread intravascular coagulation is
induced by procoagulant that are introduce or
produce in circulation and overcome the natural
anticoagulant mechanisms.

• DIC may cause tissue ischemia from occlusive

microthrombi as well as bleeding from both
consumption of platelet and coagulation factor
and anticoagulation effect of product of
secondary fibrinolysis.
Disseminated Intravascular Coagulation
(DIC) Mechanism
Systemic activation
of coagulation

Intravascular
deposition of fibrin Depletion of platelets
and coagulation factors

Thrombosis of small
and midsize vessels
Bleeding
with organ failure
 DIC may be initiated by

Exposure of blood to tissue factor (eg after trauma).

Endothelial cell damage (eg by endotoxin or cytokines).

Release of proteolytic enzymes into the blood .

( eg pancreas , snake venom )

Infusion or release of activated clotting factor.

(eg Factor IX concentrate )

Massive thrombosis.

Severe hypoxia and acidosis.

Pathogenesis of DIC

Bachelor of Chinese Medicine

 Disseminated Intravascular Coagulation

• Primarily a thrombotic process

– Also called

consumption
coagulopathy

1. Schafer, A., I., Cecil Textbook of Medicine, Saunders, 2004, chapter 179,
HEMORRHAGIC DISORDERS: DISSEMINATED INTRAVASCULAR COAGULATION, LIVER FAILURE, AND VITAMIN K DEFICIENCY
2. Uptodote, 2005, www.utdol.com, Clinical feadures, diagnosis and teratment of disseminated intravascular coagulation
Disseminated Intravascular Coagulation
(DIC) Mechanism
Systemic activation
of coagulation

Intravascular
deposition of fibrin Depletion of platelets
and coagulation factors

Thrombosis of small
and midsize vessels
Bleeding
with organ failure
Stein B, Fuster V, Israel DH, et al. Platelet inhibitor agents in cardiovascular disease: an update. J Am Coll Cardiol. 1989;14:813–836.
 Disseminated Intravascular Coagulation
• Laboratory manifestations
– Prolonged prothrombin time (PT)
– Prolonged Activated partial thromboplastin time (aPTT)
– Thrombocytopenia.
– Increased fibrin formation
• Stimulates compensatory process of secondary
fibrinolysis,
• Plasminogen activators generate plasmin to digest
fibrin (and fibrinogen) into fibrin(ogen) degradation
products (FDPs).
– FDPs are potent circulating anticoagulants that
contribute further to the bleeding manifestations of
DIC.

Schafer, A., I., Cecil Textbook of Medicine, Saunders, 2004, chapter 179,
HEMORRHAGIC DISORDERS: DISSEMINATED INTRAVASCULAR COAGULATION, LIVER FAILURE, AND VITAMIN K DEFICIENCY
 DIC Score
• Platelet count : >100.000 = 0 , 50.000-
100.000 = 1, <50.000 =2
• D- Dimer : <500= 0, 500-1000 = 2, >1.000
=3
• Prothrombin : 3 s or less = 0, >3s & <6s =
1, >6s = 2
• Fibrinogen : >1 = 0, <1 = 1

• DIC = Score 5
 Disseminated Intravascular Coagulation

• DIC always has an underlying etiology

– Must be identified and eliminated to treat the
coagulopathy successfully.
– The development of DIC in many of these disorders
is associated with an unfavorable outcome1.
• Occurs in 1% of hospitalized patients2
• Mortality rate approaches 40-80%

1. Schafer, A., I., Cecil Textbook of Medicine, Saunders, 2004, chapter 179,
HEMORRHAGIC DISORDERS: DISSEMINATED INTRAVASCULAR COAGULATION, LIVER FAILURE, AND VITAMIN K DEFICIENCY
2. Uptodote, 2005, www.utdol.com, Clinical feadures, diagnosis and teratment of disseminated intravascular coagulation
Acute DIC

Acute DIC develops when blood is exposed to large

amounts of tissue factor over a brief period of time .

- Bleeding

- Acute renal failure

- Hepatic dysfunction

- Pulmonary disease
- Central nervous system dysfunction
- Malignancy
Chronic DIC:

chronic DIC develops when blood is

continuously or intermittently exposed
to small amounts of tissue factor and
compensatory mechanisms in the liver
and BM are largely able to replenish
the depleted coagulation proteins and
platelets .
Chronic DIC:
*Malignancy, particularly solid tumors, ( is
the most common cause of chronic DIC).

*Venous thromboses commonly present as

deep venous thrombosis in the extremities
or superficial migratory thrombophlebitis
(Trousseau's syndrome),
*Arterial thromboses can produce digital
ischemia, renal infarction, or stroke.
DIAGNOSIS of DIC
Acute DIC:
Fibrin degradation product or D-dimer levels.
Prothrombin time.
Activated partial thromboplastin time.
deficiencies of factors XII, XI, IX and VIII.
Plasma fibrinogen concentration .

Chronic DIC:

platelet count moderately reduced.

plasma fibrinogen is often normal or slightly elevated.
PT and PTT may be within normal limits.
 Disseminated Intravascular Coagulation

• Treatment
– Identify underlying cause and treat
– All other therapies are temporizing

Schafer, A., I., Cecil Textbook of Medicine, Saunders, 2004, chapter 179,
HEMORRHAGIC DISORDERS: DISSEMINATED INTRAVASCULAR COAGULATION, LIVER FAILURE, AND VITAMIN K DEFICIENCY
 Disseminated Intravascular Coagulation

• Asymptomatic patients with self-limited

DIC
– Have only laboratory manifestations of the
coagulopathy
– No treatment may be necessary.

Schafer, A., I., Cecil Textbook of Medicine, Saunders, 2004, chapter 179,
HEMORRHAGIC DISORDERS: DISSEMINATED INTRAVASCULAR COAGULATION, LIVER FAILURE, AND VITAMIN K DEFICIENCY
 Disseminated Intravascular Coagulation

• Actively bleeding or who are at high risk of

bleeding,
– Blood component treatments of choice
• Transfusions of platelets
– Improve the thrombocytopenia
• Fresh-frozen plasma (FFP)
– Replace all consumed coagulation factors and correct the
prolonged PT and aPTT.
– The theoretical concern that these blood products may
"fuel the fire" and exacerbate the DIC has not been
supported by clinical experience

Schafer, A., I., Cecil Textbook of Medicine, Saunders, 2004, chapter 179,
HEMORRHAGIC DISORDERS: DISSEMINATED INTRAVASCULAR COAGULATION, LIVER FAILURE, AND VITAMIN K DEFICIENCY
TREATMENT 0f DIC

Platelet transfusion

Fresh frozen plasma

Heparin ?

Treatment of the underlying disease

 Disseminated Intravascular Coagulation

• Pharmacologic inhibitors of coagulation and

fibrinolysis
– Heparin
– Theoretical benefit
• It blocks thrombin and the secondary fibrinolysis.
• Might exacerbate the bleeding tendency
THANK YOU