Disseminated intravascular coagulation

Question 1

What is DIC?

Answer 1

Acquired syndrome characterised by activation of coagulation pathways resulting in intravascular thrombi and platelet/coagulation factor depletion. In other words, you have simultaneously too much and too little clotting.

Question 2

What are the two types of DIC?

Answer 2

ACUTE OVERT: bleeding and depletion of platelets and clotting factors; CHRONIC NON-OVERT: thromboembolism and generalised activation of coagulation system

Question 3

What is the aetiology of DIC? (x6)

Answer 3

• Sepsis esp. Gram negative.
• Obstetric complications (miscarriage, severe pre-eclampsia, placental abruption, amniotic emboli)
• Trauma
• Surgery
• Blood transfusion reaction
• Malignancy

Question 4

What is the aetiology of acute and chronic DIC?

Answer 4

Acute is more common in rapid-onset underlying conditions such as trauma, sepsis. Chronic DIC is more common with malignancies.

Question 5

What is the pathophysiology of acute DIC?

Answer 5

Activation of the coagulation is a consequence of endothelial damage and increased release of granulocyte/macrophage procoagulant substances such as TF (secondary to IL-6 and TNF-alpha). Subsequent thrombin generation depletes clotting factors and platelets, while simultaneously activating the fibrinolytic system. This leads to bleeding into subcutaneous tissues, skin and mucous membranes. Occlusion of blood vessels from fibrin in microcirculation leads to microangiopathic haemolytic anaemia (MAHA) and ischaemic organ damage.

Question 6

What is MAHA?

Answer 6

Destruction of RBCs by fibrin in the small blood vessels. RBCs are broken down into schistocytes.

Question 7

What is the pathophysiology of chronic DIC?

Answer 7

Process is identical to acute DIC but at a slower rate allowing for compensatory responses which diminish the likelihood of bleeding but give rise to hypercoagulable states and thromboses.

Question 8

What is the relationship between inflammatory and coagulation pathways?

Answer 8

IL-6 and TNF-a, produced in inflammatory pathways, activates coagulation pathways. Similarly, Factor Xa, thrombin and fibrin activate endothelial cells to release pro-inflammatory cytokines. Therefore, both coagulation and inflammatory pathways positively reinforce each other.

Question 9

What are the symptoms of DIC?

Answer 9

Severely unwell, confusion, SOB, evidence of bleeding.

Question 10

What are the signs of DIC? (x2, x7 and x4)

Answer 10

• Fever
• Shock
• ACUTE: petechiae, purpura, ecchymoses, epistaxis, mucosal bleed, signs of end organ damage, respiratory distress, oliguria (if renal failure or a sign of shock)
• CHRONIC: DVT, arterial thrombosis, emboli, superficial VT

Question 11

What is the different between petechiae, purpura and ecchymoses?

Answer 11

All occurs as a result of bleeding into the skin from broken blood vessels. Petechiae form tiny red dots. Purpura manifest in larger flat areas. Ecchymoses occur as a result of blunt trauma and result in large area of bruising.

Question 12

What are the investigations for DIC? (x2)

Answer 12

• BLOOD: low Hb (fibrin damages RBCs), high APTT/PT, low fibrinogen, very high fibrin degradation products (high d-dimers), low platelets
• PERIPHERAL BLOOD FLOW: schistocytes (fragmented RBCs; fibrin causes damage to RBCs)