Disseminated Intravascular Coagulation (DIC)

Related Subjects: |Microangiopathic Haemolytic anaemia |Haemolytic anaemia |Immune (Idiopathic) Thrombocytopenic Purpura (ITP) |Thrombotic Thrombocytopenic purpura (TTP) |Haemolytic Uraemic syndrome (HUS) |Thrombocytopenia |Disseminated Intravascular Coagulation (DIC)

⚠️ Disseminated intravascular coagulation (DIC) is a life-threatening clinicopathological syndrome. It arises from widespread activation of coagulation, generating fibrin clots that cause organ dysfunction, while consuming platelets and clotting factors → paradoxical bleeding + thrombosis. 💀 Classic teaching: “DIC = Death Is Coming”.

📖 About

• Seen in ~1% of inpatients, usually in the context of severe underlying illness.
• Characterised by uncontrolled coagulation → consumption of clotting factors → bleeding.
• Results in massive haemorrhage, microthrombi, multi-organ failure; prognosis is poor.

🦠 Important Causes

• Sepsis – esp. Gram-negative, but also Gram-positive, viral (HIV, CMV, hepatitis), fungal (Histoplasma), parasitic (malaria).
• Trauma & tissue injury – burns, snake bites, crush injuries.
• Malignancy – Acute promyelocytic leukaemia (M3/APL), metastatic cancers.
• Obstetric catastrophes – amniotic fluid embolism, placental abruption, severe pre-eclampsia.
• Other: severe liver failure, transfusion reactions (ABO incompatibility), vasculitis, IBD, aneurysms, recreational drugs.

🧬 Pathophysiology

• Excess thrombin generation → fibrin clots in microvasculature.
• Consumption of fibrinogen & clotting factors.
• Platelet trapping within thrombi → thrombocytopenia.
• Secondary fibrinolysis → ↑ fibrin degradation products (FDPs).

🩺 Clinical Features

• Occurs in critically ill patients.
• Bleeding: IV line sites, surgical wounds, mouth, GI tract, haematuria, epistaxis, intracerebral haemorrhage.
• Microvascular thrombosis → digital ischaemia, organ failure (renal, hepatic, pulmonary, CNS).
• Respiratory failure: ARDS on CXR.

🔬 Investigations

• Platelets: ↓ <50 x10⁹/L.
• PT, APTT, bleeding time: prolonged ⏳.
• Fibrinogen: ↓ <1 g/L.
• Factor VIII, vWF: reduced.
• ↑ FDPs / D-dimer (fibrinolysis markers).
• Blood film: schistocytes (microangiopathic haemolysis).
• CXR: ARDS pattern in severe cases.

📊 Scoring System (Overt DIC – ISTH)

• Platelet count (<100 = 1; <50 = 2).
• Fibrin markers (none = 0; moderate = 2; strong = 3).
• PT prolongation (<3s = 0; 3–6s = 1;>6s = 2).
• Fibrinogen (>1 g/L = 0; <1 g/L = 1).
• Score ≥5 = compatible with overt DIC → repeat daily. <5 = non-overt → repeat every 1–2 days.

📌 Differentials

• Thrombotic thrombocytopenic purpura (TTP).
• Haemolytic uraemic syndrome (HUS).
• HELLP syndrome, pre-eclampsia.
• Severe malignant hypertension.

🩸 Blood Film: Schistocytes

💊 Management (always involve Haematology)

• 1. Treat the underlying cause – sepsis, malignancy, obstetric event, trauma.
• 2. Supportive measures:
  • Active bleeding → platelets (<50x10⁹/L) and FFP (15 mL/kg).
  • Low fibrinogen (<1 g/L) → cryoprecipitate or fibrinogen concentrate.
  • Monitor: platelet count, PT/APTT, fibrinogen after replacement.
• 3. Thrombosis-predominant DIC: therapeutic heparin may be indicated (e.g. purpura fulminans, acral ischaemia).
• 4. Non-bleeding critically ill patients: LMWH prophylaxis to prevent VTE.
• IV Pabrinex if risk of thiamine deficiency in alcoholics/sepsis (avoid precipitating Wernicke’s).

📚 Teaching Pearls

🔑 Think of DIC in any septic, bleeding, or rapidly deteriorating ICU patient. 💡 Labs: low platelets + prolonged PT/APTT + high D-dimer + low fibrinogen = classic pattern. 📉 Prognosis depends on reversing the underlying trigger – supportive therapy alone is insufficient.

📚 Reference

• British Society for Haematology: Guidelines for diagnosis & management of DIC

Cases — Disseminated Intravascular Coagulation (DIC)

• Case 1 — Obstetric Emergency: A 32-year-old woman presents with massive postpartum haemorrhage following placental abruption. She is hypotensive and oozing blood from venepuncture sites. Bloods show platelets 45 ×10⁹/L, PT and APTT prolonged, fibrinogen very low, D-dimer markedly elevated. Diagnosis: Acute DIC secondary to obstetric catastrophe.
• Case 2 — Sepsis-Associated DIC: A 70-year-old man with pneumonia becomes hypotensive and develops mottled skin and purpura fulminans. He has active bleeding from his nasogastric tube. FBC: platelets 30 ×10⁹/L, Hb 7.8 g/dL. Coagulation profile: prolonged PT/APTT, low fibrinogen, high fibrin degradation products. Diagnosis: Sepsis-induced DIC.
• Case 3 — Malignancy-Related Chronic DIC: A 65-year-old woman with known metastatic pancreatic cancer presents with bruising, mucosal bleeding, and recurrent venous thromboembolism despite anticoagulation. Platelets are 80 ×10⁹/L, fibrinogen borderline low, PT mildly prolonged, D-dimer persistently elevated. Diagnosis: Chronic DIC in the context of malignancy.

Teaching Commentary 🩸

DIC is a pathological activation of the coagulation cascade, leading to simultaneous thrombosis and bleeding. In the acute setting (e.g., sepsis, trauma, obstetrics), consumption of clotting factors and platelets causes life-threatening bleeding. In chronic forms (e.g., malignancy), the balance is subtler, with recurrent thrombosis alongside bleeding. Diagnosis is clinical plus labs: prolonged PT/APTT, thrombocytopenia, hypofibrinogenaemia, and raised D-dimer. Management focuses on treating the underlying cause, supportive transfusion (platelets, FFP, cryoprecipitate), and careful use of anticoagulation if thrombosis predominates.