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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Always secondary to an underlying trigger: sepsis (most common), malignancy (especially APML), obstetric emergencies (abruption, amniotic fluid embolism), major trauma, burns, snake bites
- Pathophysiology: widespread activation of coagulation → microvascular thrombosis → consumption of platelets AND clotting factors → paradoxical BLEEDING
- Lab hallmarks: prolonged PT and APTT, LOW fibrinogen (<1 g/L), RAISED D-dimer, LOW platelets, schistocytes on film
- Key distinction from TTP: in DIC the coagulation screen IS abnormal (prolonged PT/APTT, low fibrinogen). In TTP, coagulation is NORMAL
- Management: treat the UNDERLYING CAUSE (this is the most important step). Replace blood products: FFP, cryoprecipitate (for fibrinogen), platelets
Overview
Disseminated intravascular coagulation (DIC) is an acquired syndrome of pathological, widespread activation of coagulation leading to microvascular fibrin deposition throughout the body. This causes end-organ damage from microvascular thrombosis, while simultaneously consuming clotting factors and platelets, leading to a severe bleeding tendency. DIC is always secondary to an underlying condition and is not a primary diagnosis. It may present acutely (haemorrhagic — sepsis, obstetric emergency) or chronically (thrombotic — malignancy).
Epidemiology
DIC complicates up to 1% of hospital admissions. Sepsis is the most common cause, accounting for approximately 35% of cases. Obstetric complications (placental abruption, amniotic fluid embolism, HELLP syndrome) and malignancy (especially APML) are other major causes. DIC carries a high mortality rate (40-80%), primarily related to the severity of the underlying cause.
Clinical Features
Symptoms
Bleeding from multiple sites: venepuncture sites, surgical wounds, mucous membranes
Petechiae, purpura, ecchymoses
Haematuria, GI bleeding, pulmonary haemorrhage
Symptoms of end-organ ischaemia: confusion (cerebral), dyspnoea (pulmonary), oliguria (renal)
Acral ischaemia/gangrene in severe cases (microvascular thrombosis)
Signs
Oozing from venepuncture sites and wounds — classic sign of consumptive coagulopathy
Widespread petechiae and purpura
Signs of underlying cause: septic shock, placental abruption, etc.
Acral cyanosis and gangrene (purpura fulminans — especially meningococcal sepsis)
Signs of multi-organ dysfunction
Investigations
First-line
Coagulation screenProlonged PT and APTT (consumption of clotting factors). In chronic DIC, may be only mildly deranged
FibrinogenLOW (<1 g/L in acute DIC) — key finding. Fibrinogen is consumed. Note: fibrinogen is an acute phase reactant and may be "normal" in early/chronic DIC
D-dimer / FDPsMarkedly RAISED (fibrin degradation products from widespread clot breakdown). Very sensitive but non-specific
PlateletsLow (consumed in microvascular thrombosis). Progressive fall is concerning
Second-line
Blood filmSchistocytes (fragmented red cells from MAHA) + reduced platelets
ISTH DIC scoreInternational Society on Thrombosis and Haemostasis scoring system: platelet count, D-dimer, PT prolongation, fibrinogen level. Score ≥5 = overt DIC
Specialist
Identify underlying causeBlood cultures (sepsis), imaging (malignancy), obstetric assessment — treatment depends on the trigger
1
Treat the underlying cause — the MOST IMPORTANT step
- Sepsis: antibiotics, source control
- APML: ATRA immediately (DIC resolves as leukaemia responds)
- Obstetric: deliver the baby/remove the placenta
- Without treating the trigger, blood product replacement is futile
2
Blood product replacement
- FFP 15 mL/kg: if PT/APTT prolonged (>1.5× normal) with active bleeding or planned procedure
- Cryoprecipitate: 2 pools (10 units) if fibrinogen <1.5 g/L — target fibrinogen >1.5 g/L
- Platelets: if <50 × 10⁹/L with active bleeding or <20 × 10⁹/L prophylactically
- Packed red cells for symptomatic anaemia
3
Anticoagulation (chronic DIC)
- In chronic DIC (malignancy) where thrombosis predominates over bleeding, consider LMWH
- NOT appropriate in acute haemorrhagic DIC
4
Adjunctive
- Tranexamic acid: consider if hyperfibrinolysis predominates (controversial — avoid if thrombosis is the major feature)
- Maintain fibrinogen >1.5 g/L in obstetric haemorrhage (critical threshold)
Complications
- Multi-organ failure: Renal failure, hepatic failure, ARDS from microvascular thrombosis
- Haemorrhagic shock: From uncontrolled consumption coagulopathy
- Purpura fulminans: Symmetrical peripheral gangrene (meningococcal sepsis, protein C deficiency) — devastating complication
- Death: Mortality 40-80% depending on underlying cause and severity
UKMLA Exam Tips
- 1DIC = prolonged PT/APTT + low fibrinogen + raised D-dimer + low platelets. TTP = NORMAL PT/APTT. This is the key distinction
- 2Always identify the underlying CAUSE — DIC is never a primary diagnosis
- 3APML (AML with t(15;17)) is the classic haematological cause of DIC — start ATRA immediately
- 4Schistocytes on film are seen in BOTH DIC and TTP — the coagulation screen separates them
- 5Cryoprecipitate is the specific product for low fibrinogen — it contains concentrated fibrinogen, factor VIII, VWF, factor XIII
- 6ISTH DIC score ≥5 = overt DIC — serial scoring is more useful than a single snapshot
practicetest your knowledge on dicApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — haematology and beyond.
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