Disseminated Intravascular Coagulation

DR NORA AZURA DINTAN ANAESTHESIOLOGY DEPT HOSPITAL KUALA LUMPUR

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

Widespread fibrin deposition

Consumption of PLT & coagulation factors Thrombocytopenia & coagulation factor deficiency

Microvascular thrombosis

Tissue injury/ Organ failure

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.

– Procoagulant stimulus is tissue factor (most cases)
• Lipoprotein • Not normally exposed to blood.

– Tissue factor gains access to blood by
• Tissue injury, • Malignant cells, • Expression on the surfaces of monocytes and endothelial cells by inflammatory mediators.

.
• Tissue factor triggers
– Thrombin
• Protease • Induces fibrin formation and platelet activation

• Other procoagulants
– Cysteine protease – Mucin – Trypsin

Overt or Acute DIC
-Coagulation factors are consumed at a rate in excess of the capacity of the liver to synthesize them, -Platelets are consumed in excess of the capacity of bone marrow megakaryocytes to release them

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.

• Occurs in 1% of hospitalized patients • Mortality rate approaches 40-80%

• 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

– Other obstetric problems associated with DIC include
• Abruptio placentae • Toxemia • Septic abortion.

Diagnosis
• Diagnosis of severe, acute
– Prolongation of PT, aPTT and Thrombin time
• Due to consumption and inhibition of clotting factors

– Thrombocytopenia – Fibrin degradation products
• Increased due to secondary fibrinolysis
– Measured by latex agglutination or D-dimer assays.

– Schistocytes may be seen in the peripheral blood smear
• Neither sensitive nor specific for DIC.

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.

Scoring system for overt DIC
• International Society on Thrombosis and Hemostasis (ISTH) Scoring System • Risk assessment: Does the pt have an underlying disorder known to be associated with overt DIC? • If yes: proceed • If no: do not use this algorithm • Order global coagulation tests (PT, PLT count, fibrinogen, fibrin related marker • Calculate score
– 5 and above compatible with overt DIC, repeat score daily – <5 suggestive for non overt DIC, repeat next 1-2 days

ISTH Diagnostic Scoring System for DIC
Laboratory Test Platelet count (cells/L) Result >100,000 50,000 – 100,000 <50,000 No increase Moderate increase Strong increase <3 s 3-5.9 s >6 s >1g/dL <1g/dL Score 0 1 2 0 2 3 0 1 2 0 1

Increase in fibrinogen & fibrin related markers eg D –dimer, FDP Prolonged PT

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

• Asymptomatic patients with self-limited DIC
– Have only laboratory manifestations of the coagulopathy – treatment may be not necessary.

1. Plasma(FFP) and platelets
• Should not base on lab results alone • Actively bleeding or who are at high risk of bleeding eg post op patients or patients undergoing invasive procedure • Severe hypofibrinogenaemia (<1g/L) that persists despite FFP replacement may be treated with fibrinogen concentrate or cryoprecipitate • If FFP transfusion not possible eg fluid overload, consider using factor concentrates such as prothrombin complex concentrate

Replacement therapy Fresh frozen plasma (FFP) platelet concentrates cryoprecipitate

Suggested dosage 15-20ml/kg 1-2 U/10 kg 1 U/10 kg

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

Symptomatic bleeding with fibrinogen <100mg/dL

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- 10g/kg/H • In critically ill, non bleeding patients with DIC, prophylaxis for venous thromboembolism with Heparin or LMWH is recommended

3. Anticoagulant factor concentratesactivated protein C
• Consider treating patients with severe sepsis & DIC with recombinant human activated protein C, continuous infusion, 24/kg/H for 4 days • Contraindicated if
– High risk of bleeding – PLT <30,000 – If patients going for invasive procedures, discontinued shortly before intervention

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

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