Disseminated Intravascular Coagulation

DIC is never a primary diagnosis but always secondary to an underlying condition. It is characterized by the simultaneous occurrence of thrombosis and haemorrhage. Triggers include sepsis (most common), trauma, malignancy (especially APML), and obstetric catastrophes (e.g., placental abruption). The massive release of tissue factor into the circulation triggers the coagulation cascade, leading to the formation of fibrin clots throughout the microvasculature. These clots cause organ ischaemia. Simultaneously, the compensatory activation of fibrinolysis and the consumption of platelets and clotting factors (I, II, V, VIII) lead to a systemic bleeding diathesis. DIC can be acute (decompensated, high mortality) or chronic (compensated, often seen in malignancy). Management focuses on treating the underlying cause and supportive replacement of blood components in the presence of bleeding.

The primary event in DIC is the systemic expression of tissue factor (TF), typically due to cytokine release (TNF-α, IL-6) or direct entry of TF (trauma/amniotic fluid) into the blood. TF binds with Factor VIIa to activate the coagulation cascade. This generates excessive thrombin. Under normal conditions, natural anticoagulants like Protein C and Antithrombin III would check this process, but in DIC, these are depleted. Extensive fibrin deposition in small vessels leads to microangiopathic haemolytic anaemia (MAHA), as RBCs are sheared when passing through fibrin webs. Plasmin is generated to break down these clots, producing high levels of Fibrin Degradation Products (FDPs) and D-dimers, which themselves have anticoagulant properties, further worsening the bleeding risk.

The presentation is dominated by the underlying cause (e.g., septic shock). DIC manifestations: 1) Bleeding: Oozing from venepuncture sites, surgical wounds, mucosal surfaces, or gastrointestinal tract. Petechiae and ecchymoses are common. 2) Thrombosis/Organ Dysfunction: Skin necrosis (Purpura Fulminans), acute kidney injury, respiratory failure (ARDS), and neurological deficit/coma. In chronic DIC (e.g., Trousseau's syndrome in malignancy), the thrombotic features predominate (recurrent VTE), while laboratory markers might be only mildly abnormal.

Bloods: FBC (thrombocytopenia), Blood film (Schistocytes). Clotting: Prolonged PT, Prolonged APTT, and Prolonged Thrombin Time. Biochemical: Low Fibrinogen (classic in acute DIC, though it is an acute phase reactant so 'normal' levels may be inappropriately low), Elevated D-dimer (very sensitive, reflecting fibrinolysis). ISTH Scoring System: Uses Platelets, D-dimer, PT prolongation, and Fibrinogen level to diagnose overt DIC.

1) Treat the underlying cause: Antibiotics for sepsis, obstetric delivery, or ATRA for APML. This is the most crucial step. 2) Supportive replacement (only if bleeding or high risk): Platelets (target >50 x 10^9/L). Fresh Frozen Plasma (FFP) to correct prolonged PT/APTT. Cryoprecipitate (to replace Fibrinogen if <1.5g/L). 3) Thrombosis: In rare cases of predominant thrombosis without severe bleeding, therapeutic heparin may be considered (controversial). 4) Monitoring: Serial clotting and FBC measurements (e.g., 4-6 hourly).