Disseminated Intravascular Coagulation

The Paradox at its Heart

Disseminated intravascular coagulation (DIC) is inappropriate activation of clotting throughout the circulation. This creates the defining paradox: the widespread clotting consumes platelets and clotting factors faster than they can be replaced, so the patient clots and bleeds at the same time — microthrombi block small vessels and damage organs, while the exhausted clotting system bleeds from every wound and puncture site. It is never primary — always a complication of a serious illness.

Pathophysiology

The trigger is usually release of tissue factor (from damaged tissue, tumour, or activated monocytes in sepsis), which ignites the cascade, generating thrombin that lays down fibrin microthrombi and consumes platelets and factors. The body then activates fibrinolysis to break down this excess clot, releasing fibrin degradation products including D-dimer — which themselves further impair clotting.

Causes

Classic triggers by category: sepsis (especially Gram-negative), major trauma/burns, obstetric emergencies (abruption, amniotic fluid embolism, retained products), and malignancy (especially acute promyelocytic leukaemia).

Clinical & Laboratory Picture

There is bleeding (oozing from wounds/cannulae/mucosa) with thrombosis and organ dysfunction. Every lab value follows from consumption: factors used up → prolonged PT and aPTT; platelets consumed → low count; fibrinogen consumed → low fibrinogen; clot broken down everywhere → raised D-dimer/FDPs; the film may show schistocytes. It exists on a spectrum — acute (decompensated) DIC presents with bleeding (sepsis, abruption), while chronic (compensated) DIC may present with thrombosis (malignancy).

Management

Two arms: treat the underlying cause (essential — DIC will not settle while sepsis, retained products or the tumour persist), and supportive replacement of what is consumed — FFP, platelets and cryoprecipitate — for the actively bleeding patient. Heparin has only a limited, selective role where thrombosis predominates.

Differential Diagnosis

Several conditions mimic DIC. In liver failure, clotting factors are not made (prolonged PT) but the platelet-consumption and D-dimer picture is less marked, and factor VIII (made outside the liver) is normal. The thrombotic microangiopathies (TTP and HUS) cause thrombocytopenia and red-cell fragmentation but with normal PT/aPTT and fibrinogen, because they are platelet/endothelial disorders, not activation of the whole cascade. This contrast — deranged versus normal clotting times — is the key discriminator.

DIC in Specific Settings

In acute promyelocytic leukaemia, leukaemic cells drive severe DIC, and all-trans retinoic acid (ATRA) plus chemotherapy helps control it. In obstetric DIC (abruption, amniotic fluid embolism, retained products), emptying the uterus — removing the source — is definitive. In each case the DIC settles only when its trigger is removed.

WHY It Self-perpetuates, & Support

Part of why DIC becomes self-sustaining is that the body's own brakes on clotting — antithrombin, protein C and protein S — are consumed alongside the clotting factors, so thrombin generation continues unchecked throughout the circulation. For the bleeding patient, replacement is targeted to the deficits — FFP for factors, cryoprecipitate when fibrinogen is low (below ~1 g/L), and platelets for significant thrombocytopenia with bleeding — followed with serial platelet counts, PT/aPTT, fibrinogen and D-dimer. These measures only buy time; the disorder resolves only when the trigger is treated.

Thrombosis and bleeding coexist — that is the paradox of DIC.

• DIC = system-wide clotting that consumes platelets/factors → simultaneous thrombosis and bleeding; always secondary.
• Mechanism: tissue factor → thrombin → microthrombi + consumption → reactive fibrinolysis (D-dimer/FDPs).
• Causes: sepsis, trauma/burns, obstetric emergencies, malignancy.
• Labs (consumption): prolonged PT/aPTT, low platelets, low fibrinogen, high D-dimer/FDPs, schistocytes; acute (bleeding) vs chronic (thrombosis).
• Treat the cause + support with FFP/platelets/cryoprecipitate.