Académique Documents
Professionnel Documents
Culture Documents
DIC
Clinicopathological syndrome in response to some pathologic condition in the human body Systemic activation of coagulation cascade process producing both thrombosis and hemorrhage Also called consumption coagulopathy and defibrination syndrome Its clinical manifestation may be widespread hemorrhage in acute, fulminant cases
Process in DIC
Underlying disorder associated with DIC Systemic activation of coagulation
Consumption of PLT & coagulation factors Thrombocytopenia & coagulation factor deficiency
Microvascular thrombosis
BLEEDING
Pathophysiology
Entry into the circulation of procoagulant substances
Trigger systemic activation of the coagulation system and platelets Lead to the disseminated deposition of fibrin-platelet thrombi.
.
Tissue factor triggers
Thrombin
Protease Induces fibrin formation and platelet activation
Other procoagulants
Cysteine protease Mucin Trypsin
Nonovert DIC
-Mild & clinically insignificant
Etiology
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.
Obstetrics
The placenta and uterine contents are rich sources of
Tissue factor Other procoagulants that normally are excluded from the maternal circulation
Clinical manifestations of DIC may accompany obstetric complications, especially in the third trimester.
These syndromes range from
Acute, fulminant, and often fatal DIC in amniotic fluid embolism Blood is exposed to large amounts of tissue factor in a short period of time creating large amounts of thrombin Multiorgan failure Chronic or subacute DIC with a retained dead fetus. Exposure to small amounts of tissue factor
Diagnosis
Diagnosis of severe, acute
Prolongation of PT, aPTT and Thrombin time
Due to consumption and inhibition of clotting factors
Diagnosis
Chronic or compensated forms of DIC
Highly variable patterns of abnormalities in "DIC screen" coagulation tests. Increased FDPs and prolonged PT are generally more sensitive measures than are abnormalities of the aPTT and platelet count. Overcompensated synthesis of consumed clotting factors and platelets in some chronic forms
Cause shortening of the PT and aPTT and/or thrombocytosis Though, elevated levels of FDPs indicate secondary fibrinolysis in such cases.
Fibrinogen level
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.
Intravascular fibrin deposition can cause fragmentation of red blood cells and lead to the appearance of schistocytes in blood smears Hemolytic anemia is unusual in DIC. Microvascular thrombosis in DIC can compromise the blood supply to some organs and lead to multiorgan failure
Treatment
Treatment
Identify underlying cause and treat All other therapies are temporizing
Clinical indicators for use Symptomatic bleeding with fibrinogen <100mg/dL PLT <20,000 or PLT <50,000 with bleeding Symptomatic bleeding with fibrinogen <80-100mg/dL
Fibrinogen concentrates
2-3 g
2. Anticoagulant
To be considered in DIC where thrombosis predominates, eg arterial or venous thromboembolism, severe purpura fulminans a/w acral ischaemia or vascular skin infarction Unfractionated heparin (UFH), short life & reversibility- 10g/kg/H In critically ill, non bleeding patients with DIC, prophylaxis for venous thromboembolism with Heparin or LMWH is recommended
4. Antifibrinolytic
Generally are contraindicated
May precipitate thrombosis
If DIC characterized by a primary hyperfibrinolytic state and who present with severe bleeding could be treated with lysine analogues such as tranexamic acid eg 1g every 8 H