Page 15 of 25

PA20.2 | DIC & Vitamin K Deficiency — SDL Guide (Part 2)

Clinical Features of DIC

A four-panel medical diagram showing DIC as simultaneous bleeding from multiple sites and microvascular thrombosis causing organ injury, with a clinical rule for urgent screening. — **Panel A:** Critically ill patient; venepuncture site bleeding; IV cannula bleeding; surgical wound bleeding; mucosal bleeding; haematuria; ecchymoses; purpura; gastrointestinal bleeding indicator.. **Panel B:** Microvascular bed; fibrin-rich microthrombi; consumed platelets; consumed clotting factors; fragmented red cells; thrombosis plus haemorrhage.. **Panel C:** Kidney microthrombi causing acute tubular necrosis and oliguria/anuria; lung microthrombi causing ARDS; brain microthrombi causing encephalopathy and seizures.. **Panel D:** Bleeding from three unrelated sites; urgent DIC screen; treat underlying trigger; sepsis source control; delivery of placenta; acute DIC with dramatic haemorrhage; chronic DIC with DVT and mild laboratory abnormalities; purpura fulminans from dermal vessel thrombosis..

The clinical picture reflects the dual pathology of thrombosis and haemorrhage:

Haemorrhagic manifestations:
• Bleeding from multiple sites simultaneously — venepuncture sites, IV cannulas, surgical wounds, mucous membranes
• Ecchymoses and purpura
• Haematuria, haemoptysis, gastrointestinal bleeding in severe cases

Thrombotic manifestations (often subclinical):
• Microthrombi in kidneys → acute tubular necrosis, oliguria/anuria
• Microthrombi in lungs → ARDS
• Microthrombi in brain → encephalopathy, seizures
• Purpura fulminans: haemorrhagic necrosis of skin from dermal vessel thrombosis — a dramatic and grave sign

Key clinical rule: bleeding from at least three unrelated sites in a critically ill patient should prompt urgent DIC screen. The underlying trigger must be treated simultaneously — treating DIC without treating sepsis or delivering the placenta is futile.

Acute DIC presents with dramatic haemorrhage. Chronic DIC (e.g., from metastatic carcinoma or giant haemangioma — Kasabach-Merritt syndrome) may present insidiously with deep vein thrombosis and mild lab abnormalities.

Laboratory Findings in DIC — The Classic Panel

A four-panel medical diagram explains the classic acute DIC laboratory pattern: consumed platelets and clotting factors, prolonged PT and aPTT, low fibrinogen, and elevated D-dimer and FDPs. — **Panel A:** Systemic coagulation activation, fibrin microthrombi, consumed platelets, consumed clotting factors, bleeding points, red blood cells. **Panel B:** Platelet count ↓, PT ↑, aPTT ↑, fibrinogen ↓↓, D-dimer ↑↑, FDPs ↑, mechanisms of consumption and fibrinolysis. **Panel C:** Pattern recognition summary: thrombocytopenia, prolonged clotting times, hypofibrinogenemia, raised fibrin degradation markers. **Panel D:** Cross-linked fibrin, plasmin-mediated fibrinolysis, D-dimer fragments, fibrin degradation products, secondary fibrinolysis.

The DIC laboratory panel is one of the most important diagnostic panels in clinical pathology. Learn it as a complete pattern:

Test	Typical finding in acute DIC	Why
Platelet count	↓ (< 100 × 10⁹/L)	Consumed in microthrombi
PT	↑ (prolonged)	Factors II, V, VII, X consumed
aPTT	↑ (prolonged)	Factors V, VIII, fibrinogen depleted
Fibrinogen	↓↓ (< 1.0 g/L in severe DIC)	Consumed; fibrinogen is an acute-phase reactant so even a "normal" level may be low relative to expected baseline
D-dimer	↑↑ (markedly elevated)	Secondary fibrinolysis of cross-linked fibrin
FDPs	↑↑	Fibrinolysis products; inhibit further fibrin polymerisation
Peripheral blood film	Schistocytes (fragmented RBCs)	MAHA from fibrin-strand shearing

ISTH scoring system (simplified): Platelet count, PT prolongation, fibrinogen level, and D-dimer are scored 0-2 each. A score ≥ 5 is consistent with overt DIC. The score is also used to track treatment response.

Chronic DIC: D-dimer and FDPs are elevated, fibrinogen may be normal or high (compensated), platelets may be low-normal.

DIC laboratory panel dashboard showing six key tests with directional changes, schistocytes on blood film, and D-dimer versus FDPs comparison flowchart. — **Panel A:** DIC laboratory dashboard showing platelet count (↓), PT (↑), aPTT (↑), fibrinogen (↓), D-dimer (↑), and peripheral film changes with mechanistic explanations. **Panel B:** Peripheral blood film showing schistocytes (helmet cells, fragmented RBCs) characteristic of microangiopathic hemolytic anemia in DIC. **Panel C:** Flowchart distinguishing D-dimer (fibrin-specific, elevated in DIC) from FDPs (less specific, elevated in both primary and secondary fibrinolysis).

CLINICAL PEARL

D-dimer vs FDPs — know the difference: D-dimer is a fibrin-specific degradation product (from cross-linked fibrin) and is the more specific DIC marker. FDPs include both fibrinogen and fibrin breakdown products — they are sensitive but less specific. A very high D-dimer with elevated FDPs strongly supports secondary fibrinolysis in DIC. In primary fibrinolysis (rare, e.g., thrombolytic overdose), FDPs are elevated but D-dimer is low-to-normal because cross-linked fibrin is not the primary substrate. This distinction matters in examinations.

Schistocytes and MAHA in DIC

Diagram showing how fibrin strands in DIC shear red cells into schistocytes, with a blood film view and a comparison chart distinguishing DIC from TTP and HUS. — **Panel A:** Microvascular lumen, fibrin strands, sheared erythrocyte, schistocyte fragment, platelet consumption. **Panel B:** Peripheral blood film at 100x showing normal RBCs, helmet cells, triangular schistocytes, fragmented red cells, and reduced platelet density. **Panel C:** Comparison of DIC, TTP, and HUS using schistocytes, platelet count, PT/aPTT, fibrinogen, D-dimer, and clinical clue.

Red cell fragmentation occurs when erythrocytes are mechanically sheared by fibrin strands stretched across microvascular lumens. The resulting fragments — schistocytes (also called helmet cells or fragmented red cells) — are visible on the peripheral blood film as irregular, helmet-shaped, or triangular red cell remnants.

In DIC, the combination of:
• Schistocytes on film
• Thrombocytopenia
• Elevated LDH and falling haemoglobin

…constitutes microangiopathic haemolytic anaemia (MAHA). MAHA is not unique to DIC — recall from H5 that TTP and HUS also produce MAHA. The distinguishing features are:
• DIC: PT and aPTT both prolonged, fibrinogen ↓, D-dimer ↑↑
• TTP: coagulation tests NORMAL (schistocytes + thrombocytopenia without PT/aPTT prolongation)
• HUS: predominantly renal failure, often follows diarrhoeal illness

Blood film showing fragmented red blood cells (schistocytes) in DIC with comparison chart of secondary versus primary fibrinolysis laboratory findings. — **Panel A:** Peripheral blood film at 100× showing labeled schistocytes (helmet cells and fragments), normal RBCs, and reduced platelet density. **Panel B:** Comparison chart differentiating secondary fibrinolysis (DIC) from primary fibrinolysis based on D-dimer, fibrinogen, FDPs, and schistocyte presence.

SELF-CHECK

A patient with DIC has a peripheral blood film showing fragmented red cells, a platelet count of 45 × 10⁹/L, and a markedly elevated D-dimer. Which finding most specifically confirms secondary fibrinolysis rather than primary fibrinolysis in this case?

A. Elevated FDPs

B. Prolonged aPTT

C. Markedly elevated D-dimer with low fibrinogen

D. Schistocytes on peripheral smear

Reveal Answer

Answer: C. Markedly elevated D-dimer with low fibrinogen

D-dimer is a fragment generated specifically from the plasmin degradation of cross-linked fibrin (i.e., fibrin that has already been incorporated into a clot and factor XIIIa-cross-linked). A markedly elevated D-dimer combined with low fibrinogen (consumed in clot formation) confirms that clotting occurred first (generating cross-linked fibrin) and fibrinolysis followed — this is secondary fibrinolysis as seen in DIC. In primary fibrinolysis (plasminogen activator excess), FDPs are high but D-dimer is NOT elevated because primary fibrinolysis degrades fibrinogen, not already cross-linked fibrin.