Disseminated Intravascular

Coagulation (DIC)
 Essential of Diagnosis
Comsumptive thrombocytopenia
Underlying serious illness
Macrioangiopathic hemolytic
anemia may be present
Hypofibrinogenemia,
thrombocytopenia, fibrin
degradation products and prolonged
prothrombin time
Disseminated Intravascular
Coagulation (DIC) Causes
 Infection/septicemia
 Any microorganism – bacterial, viral, parasitic, rickettsial,
mycotic
 Triggered by membrane components of microorganism, i.e.
endotoxin, exotoxin, LPS
 Trauma & Burns
 Soft tissue injury, fat embolism, head injury
 Combination of triggers: fat, phospholipids, hemolysis,
endothelial injury, activation of cytokines
 Malignancy
 Solid tumors, especially metastatic tumors and hematologic
 Tissue factor involved in mechanism
 Vascular disorders
 Hemangioma (Kasabach-Merritt syndrome), aortic aneurysm
 Local activation of coagulation leads to systemic depletion of factors;
activated factors reach systemic circulation, causing DIC
 Organ destruction
 Pancreatitis, hepatic failure
 Toxins
 Snake bite, drugs
 Immunologic mediators
 Transfusion reaction, transplant rejection
 Obstetrical complications
 Abruptio placentae, amniotic fluid embolism, retained deceased fetus, 2 nd
trimester abortion
 Due to leakage of thromboplastin-like material
 Degree of placental separation correlates with severity of DIC
 Usually short-lived and self-limited

Levi, Marcel MD and Cate, Hugo MD. NEJM “Disseminated Intravascular Coagulation” Aug 19, 1999. Vol
341:586-592.
Toh, Cheng Hock. BMJ. “Disseminated Intravascular Coagulation: Old disease, new hope” 2003:327:974-77.
DIC
 Overwhelming production of Thrombin and
Fibrin
 Deposition of Fibrin in vasculature
 Inadequate Fibrinolysis
 Thrombotic or microangiopathic vasculopathy
 Organ damage(clot -ischemia)
 Exhausting the Bone marrow and liver
synthetic capability
 Thrombocytopenia and decreased coag.factors
 Mucosal bleeding(GI), oozing from IV puncture
sites
 D.I.C.
DIFFUSEFIBRIN
DIFFUSE FIBRINDEPOSITION
DEPOSITIONWIHIN
WIHIN
ARTERIOLESAND
ARTERIOLES ANDCAPILLARIES
CAPILLARIES

WIDESPREAD CLOTTING
WIDESPREAD CLOTTING

DEPLETION OF
DEPLETION OF CLOTTING
CLOTTING FACTORS
FACTORS
Disseminated Intravascular Coagulation
(D.I.C.) Mechanism
Systemic activation
of coagulation

Intravascular Depletion of platelets

deposition of fibrin and coagulation factors

Thrombosis of small Bleeding

and midsize vessels
with organ failure
Common clinical conditions
associated with D.I.C.
 Sepsis  Vascular disorders

 Trauma  Reaction to toxin (e.g.

 Head injury snake venom, drugs)
 Fat embolism  Immunologic disorders
 Severe allergic reaction
 Malignancy  Transplant rejection

 Obstetrical complications
 Amniotic fluid embolism
 Abruptio placentae
D.I.C. Laboratory
 Hypofibrinogenemia
 Elevated fibrin degradation products, D-
dimer
 Thrombocytopenia
 Prolonged PT and possible PTT
 Fragmented RBCs in slide
D.I.C. Diff.DX
 Liver disease-abn. PT/PTT, Fibrinogen
level may be normal or only sl.reduced
 Vitamin K deficiency: will not affect
Fibrinogen or Plt.count, will correct with
vitamin K therapy
 Sepsis: fibrinogen level is normal
 TTP: fibrinogen level is normal
 D.I.C.
Medical Treatment approaches
 Treatment of underlying disorder
 Anticoagulation with heparin
 Platelet transfusion
 Fresh frozen plasma
Treatment
 TREAT THE UNDERLYING DISEASE!!
 Replacement therapy
 Fresh frozen plasma **preferred
 Platelets, fibrinogen concentrates, cryoprecipitates
 Anticoagulants
 Heparin or LMWH– contradictory results
○ Safety in patients prone to bleeding?
○ Low dose 300-500U/hr
○ Likely of benefit in patients with extensive thromboemboli and fibrin
deposition
 Danaproid sodium, recombinant hirudin
 TFPI
○ Blocks tissue factor activity in endotoxin-induced DIC
 Recombinant nematode anticoagulant protein c2 (NaPc2) –
inhibits complex between TF/VIIa and Xa
  Restore anticoagulation pathway
 Antithrombin III
○ Might be of benefit in sepsis with improvement of DIC and organ function
 Recombinant tissue plasminogen activator
 Activated protein C
○ Also has anti-inflammatory and anti-apoptotic properties
○ Only anti-coagulant shown to be efficacious in trials with sepsis-triggered
DIC
○ Given as 96 hr infusion
○ Must use caution with thrombocytopenia  increased risk of intracerebral
hemorrhage

Frachini, Massimo. Thrombosis Journal “Recent acquisitions in the pathophysiology, diagnosis and
treatment of disseminated intravascular coagulation” Feb 2006, 4:4.
Davis-Jackson, Rachel. Thrombosis Journal “Antithrombin III and R-TPA used singly and in combination vs.
supportive care for treatment of endotoxin-induce DIC in the neonatal pig” May 18, 2006, 4:7.