Figure Core mechanisms examiners expect in CICM/FFICM/EDIC answers. Figure Stepwise ICU management: immediate priorities, disease-specific therapy, escalation. Figure Classification and decision thresholds used in exam answers. Figure Treat the cause first — an ISTH score of five or more is overt DIC; transfuse only for bleeding or high risk. DIC = systemic coagulation activation → microvascular THROMBOSIS + consumption → BLEEDING simultaneously. ISTH overt-DIC score (platelets, fibrinogen, D-dimer, PT — ≥5 = overt DIC). Management : (1) TREAT UNDERLYING CAUSE (#1 priority — antibiotics, delivery, treat malignancy). (2) Transfuse platelets (<50 bleeding), FFP (INR >1.5), cryoprecipitate (fibrinogen <1.5-2) — if BLEEDING or HIGH RISK (not prophylactically). (3) Anticoagulation controversial — for thrombotic DIC (heparin). (4) Recombinant thrombomodulin (ART-123) — emerging. Mortality 40-80% .
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Exam practice — SAQs
SAQ — Sepsis-associated DIC with purpura fulminans 10 minutes · 10 marks
Reveal all A 48-year-old man is admitted with fever, rigors, and a rapidly progressive purpuric rash. On examination: T 39.2 degrees C, HR 135, BP 72/40 on noradrenaline 0.4 mcg/kg/min, RR 32, SpO2 92 percent on 15 L, GCS 12. He has widespread purpura and necrotic black lesions on the fingertips and earlobes. Labs: platelets 18 x 10⁹/L, INR 2.8, aPTT 62 s, fibrinogen 0.8 g/L, D-dimer markedly elevated. Blood film shows schistocytes. Petechial rash on the palate.
a Calculate the ISTH overt-DIC score for this patient, interpret it, and outline the management prioritising the definitive treatment.
b Explain the pathophysiology of DIC — why does it cause BOTH bleeding and thrombosis simultaneously?
c Distinguish DIC from TTP using the coagulation profile, and explain why the distinction matters.
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SAQ — Acute promyelocytic leukaemia presenting with catastrophic DIC 10 minutes · 10 marks
Reveal all A 32-year-old woman presents with 1 week of gum bleeding, easy bruising, and fatigue. Today she developed a severe headache and confusion. Labs: Hb 58 g/L, platelets 12 x 10⁹/L, WCC 3.2 x 10⁹/L with 30 per cent abnormal promyelocytes (Auer rods visible), INR 2.2, aPTT 58 s, fibrinogen 0.9 g/L, D-dimer markedly elevated. CT brain shows a 20 mL intracerebral haemorrhage.
a Make the diagnosis, explain why DIC is the classic complication, and outline the immediate management including the disease-specific treatment.
b Describe the transfusion targets and monitoring in bleeding-predominant DIC, and explain why antifibrinolytics are contraindicated.
c What is the mortality of APL-related DIC and what has changed the prognosis?
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Clinical pearls
High-yield DIC points for CICM/FFICM exam
DIC = bleeding + thrombosis simultaneously (the paradox). (1) THE PATHOPHYSIOLOGY: (a) Systemic activation of COAGULATION (tissue factor released from underlying cause — sepsis, malignancy, etc. -> activates extrinsic pathway -> thrombin generated systemically -> fibrin formed throughout microvasculature). (b) MICROVASCULAR THROMBOSIS: fibrin clots in small vessels -> occludes -> ischaemia (AKI, ARDS, digital, purpura fulminans). (c) CONSUMPTION: clotting factors + platelets CONSUMED (used up making the microthrombi) -> DEPLETED -> BLEEDING (from lack of factors/platelets). (d) FIBRINOLYSIS: body tries to break down microthrombi -> plasmin generated -> D-dimer + FDP elevated -> fibrin degradation products interfere with fibrin polymerisation -> further impair clotting -> more bleeding. (2) THE PARADOX: the patient is both THROMBOSING (microvascular clots) and BLEEDING (consumed factors) AT THE SAME TIME. (3) CLINICAL: (a) BLEEDING: oozing from IV sites, petechiae, ecchymoses, GI/GU bleed, intracranial (devastating). (b) THROMBOSIS: purpura fulminans (skin necrosis), digital ischaemia (fingers/toes blue), AKI (renal microvascular), ARDS (pulmonary), MOF. (4) MANAGEMENT CHALLENGE: treating bleeding (transfusion) may 'fuel' thrombosis; treating thrombosis (anticoagulation) may worsen bleeding. Balance: treat the cause + supportive.[1] }ISTH overt-DIC score — the diagnostic standard. (1) THE SCORE (International Society on Thrombosis and Haemostasis): (a) PLATELET COUNT: >100 = 0 points; <100 = 1; <50 = 2. (b) D-DIMER (or FDP): no increase = 0; moderate increase = 2; strong increase = 3. (c) PT PROLONGATION (vs normal): <3 sec = 0; 3-6 sec = 1; >6 sec = 2. (d) FIBRINOGEN: >1 g/L = 0; <1 g/L = 1. (2) INTERPRETATION: (a) Score ≥5 = OVERT DIC (compatible with DIC — in appropriate clinical setting). (b) Score <5 = suggest repeating in 1-2 days (may be early/evolving DIC). (3) REPEAT DAILY (trend — falling score = improving; rising = worsening). (4) PREREQUISITE: must have an UNDERLYING CONDITION known to cause DIC (sepsis, malignancy, obstetric, trauma, etc.) — the score alone doesn't diagnose (other conditions cause low platelets/fibrinogen). (5) EXCLUDE OTHER CAUSES: (a) Severe LIVER DISEASE (low factors from impaired synthesis — but normal D-dimer, no schistocytes). (b) THROMBOTIC MICROANGIOPATHY (TTP/HUS — schistocytes, low platelets, normal PT/fibrinogen — ADAMTS13 low in TTP). (c) Massive transfusion (dilutional — low everything but no D-dimer). (6) ALTERNATIVE SCORES: JAAM (Japanese), CDSS (Chinese) — ISTH most internationally used.[2] }Sepsis is the most common cause (50%). (1) SEPSIS -> DIC mechanism: (a) Endothelial injury (from cytokines, endotoxin) -> tissue factor expression on endothelium + monocytes -> activates coagulation. (b) IMPAIRED ANTICOAGULATION: sepsis reduces antithrombin, protein C, tissue factor pathway inhibitor (TFPI) -> less brake on coagulation. (c) IMPAIRED FIBRINOLYSIS: sepsis raises PAI-1 (plasminogen activator inhibitor) -> blocks fibrinolysis -> microthrombi persist. (2) OTHER CAUSES: (a) TRAUMA (tissue damage -> tissue factor release -> DIC — especially brain injury, crush, burns). (b) MALIGNANCY: (i) HAEMATOLOGICAL — APL (acute promyelocytic leukaemia — classic DIC — Auer rods, t(15;17)), other leukaemias. (ii) SOLID TUMOURS — mucin-producing (pancreatic, gastric, prostate, lung) — tissue factor + mucin activate coagulation. (c) OBSTETRIC: amniotic fluid embolus (catastrophic — amniotic fluid enters circulation -> massive DIC), placental abruption, severe pre-eclampsia/HELLP, retained dead fetus, septic abortion. (d) TRANSFUSION REACTION (acute haemolytic — ABO mismatch -> DIC). (e) SNAKE BITE (venom — activates/inhibits coagulation — species-dependent). (f) SEVERE LIVER DISEASE (impaired clearance of activated factors -> DIC-like — but actually a separate entity). (g) VASCULAR MALFORMATIONS (Kasabach-Merritt — giant haemangioma -> platelet trapping + localised DIC). (3) CLINICAL: ALWAYS look for + treat the cause (the #1 management step).[5] }Transfusion strategy — if bleeding or high risk (not prophylactic). (1) THE CONTROVERSY: transfusing factors/platelets in DIC may 'FUEL' the consumption (factors transfused get used up by ongoing coagulation) — so: only transfuse if BLEEDING or HIGH RISK (not routine). (2) PLATELETS: (a) IF BLEEDING + platelets <50 x10^9/L -> transfuse. Target: >50. (b) IF NOT bleeding + platelets <20-30 -> transfuse (prophylactic — high bleeding risk, especially if sepsis/leukaemia). (c) Dose: 1 adult dose (apheresis or ~4 pooled units). (d) Check platelet count after (response — may be poor if ongoing consumption — repeat). (3) FRESH FROZEN PLASMA (FFP): (a) IF BLEEDING + PT/APTT prolonged (>1.5x normal) -> transfuse. (b) Provides clotting factors (all — II, V, VII, VIII, IX, X, XI, XII, XIII). (c) Dose: 15 mL/kg (4-6 units). (d) Check PT/APTT after (response). (e) VOLUME: FFP is volume — may cause overload (especially in elderly/heart failure) — balance. (4) CRYOPRECIPITATE: (a) IF fibrinogen <1.5-2 g/L (bleeding or high risk) -> transfuse. (b) Provides fibrinogen + factor VIII + von Willebrand factor + factor XIII. (c) Dose: 10 units (each raises fibrinogen ~0.5 g/L). (d) Target fibrinogen >1.5 g/L. (e) Check fibrinogen after (response). (5) PROTHROMBIN COMPLEX CONCENTRATE (PCC): (a) Alternative to FFP (more concentrated — less volume). (b) Contains II, VII, IX, X (not V, VIII, XI — so not complete for DIC). (c) Faster, less volume — but doesn't replace all factors. (d) Use if FFP not tolerated (volume) or rapid correction needed. (6) RED CELLS: if anaemic (bleeding) -> transfuse (oxygen-carrying capacity). Target Hb >70-80. (7) RECHECK labs after transfusion (platelets, fibrinogen, PT — response).[4] }Anticoagulation — for thrombotic-predominant DIC. (1) INDICATION: THROMBOTIC-predominant DIC (purpura fulminans, digital ischaemia, extensive microvascular thrombosis causing organ failure). (2) RATIONALE: the microvascular THROMBI are causing harm (ischaemia, organ failure) -> anticoagulate to prevent further thrombosis. (3) HEPARIN: (a) UNFRACTIONATED (preferred ICU — titratable, reversible): low-dose infusion (5-10 IU/kg/hr — not full therapeutic — balance bleeding risk). (b) LMWH (prophylactic dose — enoxaparin 40 mg SC daily — less titratable but simpler). (c) MONITOR: APTT (if UFH — keep 1.5-2x — but DIC APTT already prolonged — difficult to interpret — clinical judgement). (4) EVIDENCE: CONFLICTING: (a) NO clear mortality benefit in sepsis-DIC (SCC BLEED trial — heparin vs placebo in sepsis — no difference). (b) SOME evidence in THROMBOTIC-predominant (purpura fulminans — heparin improves skin outcomes). (c) RISK: heparin worsens BLEEDING (the other side of DIC). (5) CURRENT: CONTROVERSIAL — (a) USE in thrombotic-predominant (purpura fulminans, digital ischaemia — discuss with haematology). (b) AVOID in bleeding-predominant (worsens bleeding). (c) DVT PROPHYLAXIS: give (unless active bleeding) — LMWH prophylactic dose — reduces VTE (DIC patients are prothrombotic). (6) ALTERNATIVES: (a) RECOMBINANT THROMBOMODULIN (ART-123 — recombinant soluble thrombomodulin): binds thrombin -> inactivates coagulation + activates protein C (anticoagulant). SCARLET trial (sepsis-DIC) — trend to benefit in subset. APPROVED in Japan; emerging elsewhere. (b) RECOMBINANT ACTIVATED PROTEIN C (drotrecogin alfa — Xigris): WITHDRAWN (PROWESS-SHOCK 2012 — no benefit + bleeding). NOT available. (c) ANTITHROMBIN CONCENTRATE: theoretical (replaces consumed antithrombin) — KyberSept trial — no benefit — not routine.[3] }APL (acute promyelocytic leukaemia) — the classic DIC malignancy. (1) APL: a subtype of acute myeloid leukaemia (AML-M3) — t(15;17) translocation -> PML-RARa fusion. (2) DIC: CLASSIC — the leukaemic promyelocytes release procoagulant substances (tissue factor + cancer procoagulant) -> severe DIC. (a) Often the PRESENTING feature (bleeding — especially INTRACRANIAL — catastrophic — early death). (b) HYPERGRANULAR promyelocytes (Auer rods) on blood film. (3) DIAGNOSIS: (a) FBC (pancytopenia — low platelets + low Hb + low WCC — OR high WCC with blasts). (b) Blood film (promyelocytes — Auer rods). (c) Bone marrow biopsy (confirmed APL). (d) Cytogenetics (t(15;17) — definitive). (e) Coagulation (DIC — low fibrinogen, high D-dimer, prolonged PT). (4) TREATMENT: (a) ALL-TRANS RETINOIC ACID (ATRA — differentiates leukaemic cells -> stops procoagulant release -> resolves DIC). START IMMEDIATELY (on suspicion — don't wait for cytogenetics — bleeding risk high). (b) ARSENIC TRIOXIDE (ATO — for high-risk or relapse). (c) CHEMOTHERAPY (anthracycline — idarubicin — for high WCC). (d) TRANSFUSE AGGRESSIVELY: platelets (target >30-50), fibrinogen (target >1.5), FFP (correct PT) — until DIC resolves (with ATRA — days). (e) DIFFERENTIATION SYNDROME (ATRA/ATO side effect — capillary leak, fever, dyspnoea, renal failure) -> dexamethasone. (5) PROGNOSIS: with ATRA — excellent (cure rate >80% — one of the most curable leukaemias). Without ATRA — death from DIC/bleeding. (6) KEY: ANY patient with leukaemia + severe bleeding -> suspect APL -> start ATRA IMMEDIATELY + transfuse aggressively.[5] }Amniotic fluid embolism — catastrophic obstetric DIC. (1) AMNIOTIC FLUID EMBOLUS (AFE): amniotic fluid (containing trophoblasts, debris) enters maternal circulation (via uterine veins — during labour/delivery/C-section) -> reaches pulmonary circulation -> (a) ANAPHYLACTOID reaction (complement, cytokines -> vasodilation, bronchospasm). (b) PULMONARY VASOOCCLUSION (debris -> acute pulmonary hypertension -> RV failure). (c) DIC (tissue factor in amniotic fluid -> massive coagulation activation -> consumption -> bleeding). (2) CLINICAL (during/shortly after labour/delivery): (a) Phase 1 (acute — minutes): hypoxaemia (pulmonary vasoocclusion + ARDS), hypotension (anaphylactoid + RV failure), CARDIAC ARREST (often). (b) Phase 2 (DIC — hours): severe bleeding (uterus, IV sites, surgical wounds), multi-organ failure. (3) DIAGNOSIS: CLINICAL (no specific test — exclusion — 'clinical diagnosis of exclusion'). (4) MANAGEMENT: (a) RESUSCITATE: oxygen (high-flow — or ventilate), vasopressors (noradrenaline — for shock), fluids (cautious — RV failure). (b) DELIVER (if viable — emergency C-section — if cardiac arrest in pregnant — 'resuscitative hysterotomy' at 4 min — perimortem C-section guidelines). (c) DIC: transfuse AGGRESSIVELY (massive transfusion protocol — RBC, plasma, platelets, cryoprecipitate for fibrinogen). (d) SUPPORTIVE: ICU, ventilation, RRT for AKI, inotropes. (e) NO specific antidote. (5) MORTALITY: 20-60% (high — catastrophic). (6) This is a CLASSIC cause of catastrophic obstetric DIC — know it.[5] }Purpura fulminans — thrombotic DIC in skin. (1) PURPURA FULMINANS: a SEVERE form of DIC characterised by SKIN NECROSIS (dermal microvascular thrombosis -> skin infarction -> purpuric/necrotic lesions). (2) CAUSES: (a) MENINGOCOCCAEMIA (Neisseria meningitidis — classic — Gram-negative sepsis with DIC + purpura fulminans + Waterhouse-Friderichsen syndrome — adrenal haemorrhage). (b) PNEUMOCOCCAL sepsis. (c) Other Gram-negative sepsis. (d) POST-INFECTIOUS (viral — varicella, streptococcal — anticoagulant deficiency — protein C/S). (e) INHERITED (protein C/S deficiency — neonatal purpura fulminans). (3) CLINICAL: (a) SEPSIS (fever, shock). (b) PURPURIC RASH (petechiae -> purpura -> necrotic black eschars — on extremities, trunk). (c) DIGITAL ISCHAEMIA (fingers/toes blue/black — microvascular thrombosis -> gangrene -> amputation). (d) Multi-organ failure (AKI, ARDS, liver). (4) MANAGEMENT: (a) ANTIBIOTICS (ceftriaxone — for meningococcus — within 1h — sepsis). (b) HEPARIN (controversial — may reduce skin necrosis progression — discuss with haematology). (c) TRANSFUSE (bleeding or very low platelets/fibrinogen). (d) PROTEIN C CONCENTRATE (for protein C deficiency — inherited; or severe acquired). (e) SUPPORTIVE: ICU, vasopressors, ventilation, RRT. (f) SURGICAL: debridement of necrotic skin, fasciotomy (if compartment syndrome), amputation (if gangrene — unavoidable). (5) MORTALITY: high (30-50% — from sepsis + multi-organ failure). Survivors: skin scarring, amputations.[1] }Differential — what's NOT DIC. (1) SEVERE LIVER DISEASE: (a) Low clotting factors (impaired synthesis) -> prolonged PT, low fibrinogen. (b) BUT: normal D-dimer (no fibrinolysis — liver can't clear, but not produced), normal platelets (usually — or low from hypersplenism, not consumption). (c) KEY: liver disease + low factors + normal D-dimer = liver (not DIC). Liver disease + DIC: possible (sepsis in cirrhosis -> DIC on top of liver disease — complex). (2) THROMBOTIC MICROANGIOPATHY (TTP/HUS): (a) Microvascular thrombosis (platelet-rich — not fibrin) -> schistocytes (fragmented RBCs), low platelets, AKI (HUS) / neuro (TTP). (b) BUT: NORMAL PT, normal fibrinogen (coagulation cascade NOT activated — it's primary haemostasis — platelet). (c) KEY: low platelets + schistocytes + normal PT/fibrinogen = TMA (not DIC). (d) TTP: ADAMTS13 low (<10%). HUS: complement, Shiga toxin. (e) MANAGEMENT: plasma exchange (TTP), eculizumab (aHUS) — different from DIC. (3) MASSIVE TRANSFUSION (dilutional): (a) Large volume transfusion (RBC + crystalloid) -> dilutes platelets + factors -> low everything. (b) BUT: no D-dimer (no fibrinolysis), no schistocytes. (c) KEY: post-transfusion + low everything + normal D-dimer = dilutional (treat with platelets/FFP). (4) ANTICOAGULANT OVERDOSE (warfarin, heparin, DOAC): (a) Prolonged PT (warfarin) or APTT (heparin) -> bleeding. (b) BUT: normal platelets (usually), normal fibrinogen, normal D-dimer. (c) KEY: specific antidote (vitamin K for warfarin, protamine for heparin, idarucizumab for dabigatran, andexanet for apixaban). (5) CLINICAL: distinguish carefully — management DIFFERS (DIC: treat cause + transfuse; TMA: plasma exchange; liver: supportive; dilutional: transfuse; anticoagulant: antidote).[2] }D-dimer — high in DIC (but non-specific). (1) D-DIMER (fibrin degradation product): (a) Elevated in DIC (massive fibrin formation -> breakdown -> D-dimer high). (b) STRONGLY elevated (often >10,000 — massive). (c) The MOST SENSITIVE marker of DIC (if normal -> DIC unlikely). (2) LIMITATION: (a) NON-SPECIFIC — elevated in ANY thrombosis/inflammation (PE, DVT, sepsis without DIC, malignancy, surgery, pregnancy, trauma). (b) So: elevated D-dimer DOESN'T diagnose DIC (other conditions elevate it). (c) But: NORMAL D-dimer EXCLUDES DIC (if no fibrinolysis -> no D-dimer -> not DIC). (3) FDP (fibrinogen degradation products): similar to D-dimer (both measure fibrin breakdown) — less specific than D-dimer. (4) TREND: rising D-dimer = worsening DIC; falling = improving. (5) USE in ISTH score (strong increase = 3 points — the highest single-category score — reflects importance).[2] }Organ failure — DIC affects all organs. (1) KIDNEY (AKI): (a) Microvascular thrombosis (glomerular capillaries) -> AKI. (b) May need RRT. (c) May progress to CKD (if severe). (2) LUNG (ARDS): (a) Pulmonary microvascular thrombosis + capillary leak -> ARDS. (b) Lung-protective ventilation. (c) High mortality. (3) LIVER: (a) Ischaemic hepatitis (microvascular thrombosis in liver). (b) May worsen coagulopathy (liver synthesises factors — if ischaemic -> low factors -> synergistic with DIC). (4) BRAIN: (a) Microvascular thrombosis -> altered mental status, seizures, stroke. (b) Intracranial BLEEDING (from thrombocytopenia + factor depletion — devastating). (5) HEART: (a) Microvascular thrombosis -> ischaemia, infarction (uncommon but possible). (6) SKIN (purpura fulminans — see above). (7) ADRENAL (Waterhouse-Friderichsen): meningococcaemia -> adrenal haemorrhage -> adrenal insufficiency (addisonian crisis) -> give steroids. (8) EXTREMITIES: digital ischaemia -> gangrene -> amputation. (9) MANAGEMENT: organ-specific support (ventilation, vasopressors, RRT) + TREAT DIC (cause + transfuse/anticoagulate).[1] }Recombinant thrombomodulin (ART-123) — emerging. (1) THROMBOMODULIN: a natural ANTICOAGULANT (on endothelial surface — binds thrombin -> thrombin-thrombomodulin complex activates PROTEIN C -> protein C inactivates factors Va + VIIIa -> anticoagulant). (2) IN DIC: (a) Endothelial injury -> thrombomodulin SHED (lost from surface -> less protein C activation -> procoagulant). (b) RECOMBINANT SOLUBLE THROMBOMODULIN (ART-123 — recombinant): replaces the lost thrombomodulin -> restores protein C activation -> anticoagulant -> reduces microvascular thrombosis. (3) EVIDENCE: (a) SCARLET trial (2019, Annals of Internal Medicine): ART-123 vs placebo in sepsis-associated DIC -> (i) NO significant difference in PRIMARY (28-day mortality in ITT). (ii) BUT: SUBGROUP with 'overt DIC' (ISTH ≥5) — ART-123 trend to benefit. (iii) SAFETY: no excess bleeding (unlike heparin). (b) JAPAN: approved for DIC (stronger evidence in Japanese trials — MALIGNANCY-DIC especially). (c) ELSEWHERE: emerging — not yet approved (more trials ongoing). (4) ADVANTAGE over heparin: (a) Less bleeding (thrombomodulin modulates — doesn't globally anticoagulate like heparin). (b) Targets the DIC mechanism (restores protein C). (5) PRACTICE: discuss with haematology — may be considered for sepsis-associated overt DIC (especially in Japan; emerging elsewhere).[6] }Mortality + prognosis. (1) MORTALITY: 40-80% (high — reflects underlying severity). (a) SEPSIS-DIC: mortality 35-45% (sepsis + DIC worse than sepsis alone). (b) TRAUMA-DIC: variable (depends on injury). (c) MALIGNANCY-DIC: poor (underlying cancer). (d) OBSTETRIC-DIC: 20-60% (depends on cause — AFE high; HELLP lower). (2) PREDICTORS of poor outcome: (a) HIGHER ISTH score (worse). (b) OLDER age. (c) UNDERLYING cause (sepsis worse than obstetric). (d) ORGAN FAILURE (AKI, ARDS — worse). (e) DELAY in treating cause. (3) RESOLUTION: if CAUSE treated, DIC resolves over DAYS (labs normalise — platelets rise, fibrinogen rises, PT normalises, D-dimer falls). Trend daily. (4) LONG-TERM: (a) May have residual ORGAN damage (AKI -> CKD; digital amputation; skin scarring; neurological deficit). (b) RECURRENCE: depends on cause (if trigger persists -> recurrent DIC). (5) SURVIVORSHIP: close follow-up (renal, skin, rehabilitation, psychological).[1] }Prevention — address the trigger. (1) PREVENT DIC by PREVENTING/TREATING the cause: (a) SEPSIS: early antibiotics, source control, vaccination (pneumococcal, meningococcal). (b) OBSTETRIC: good antenatal care (detect pre-eclampsia early), safe delivery (avoid prolonged labour, trauma). (c) MALIGNANCY: early detection + treatment (APL — ATRA early). (d) TRAUMA: prevention (seat belts, safety), early damage control resuscitation. (e) TRANSFUSION: careful group/crossmatch (avoid ABO mismatch). (2) EARLY RECOGNITION: in sepsis/obstetric/trauma — check coagulation (platelets, PT, fibrinogen, D-dimer) -> detect DIC EARLY (before catastrophic bleeding/thrombosis) -> intervene. (3) ISTH score DAILY in at-risk (sepsis in ICU) -> trend -> detect worsening early. (4) AVOID: unnecessary anticoagulants (in at-risk), prolonged severe hypotension (worsens endothelial injury). (5) PUBLIC HEALTH: sepsis awareness (early presentation), vaccination (infection prevention), safe obstetric care.[1] } Red flags
Bleeding + thrombosis simultaneously = DIC (microvascular clots + consumed factors).[1] }ISTH overt-DIC score ≥5 = overt DIC (platelets, fibrinogen, D-dimer, PT).[2] }TREAT UNDERLYING CAUSE is #1 priority (sepsis, malignancy, obstetric, trauma).[1] }Transfuse if BLEEDING or HIGH RISK (platelets <50, fibrinogen <1.5, PT >1.5x) — NOT prophylactically.[4] }Anticoagulation controversial — for thrombotic-predominant (purpura fulminans) — heparin.[3] }APL (leukaemia) : classic DIC — start ATRA IMMEDIATELY + transfuse aggressively.[5] }Amniotic fluid embolus : catastrophic obstetric DIC — deliver + massive transfusion.[5] }Purpura fulminans (meningococcaemia) : skin necrosis + digital ischaemia — antibiotics + heparin (controversial).[1] }Distinguish from TMA (TTP/HUS) — normal PT/fibrinogen in TMA (DIC has prolonged PT/low fibrinogen).[2] }Mortality 40-80% (reflects underlying severity).[1] } Prognosis
DIC evidence and outcomes [6]
Densification notes for fellowship revision
This leaf is densified to the ICU fellowship gate standard (CICM / FFICM / EDIC): embedded SAQ practice, multi-figure visual scaffolding, examiner map alignment, and MCQ coverage of definition, mechanism, first-hour management, evidence, and traps.
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Revision checkpoint 1 (1_definition): Systemic coagulation activation.
Revision checkpoint 2 (2_causes): Sepsis #1.
Revision checkpoint 3 (3_isth): Platelets, PT, fibrinogen, FDP/D-dimer.
Revision checkpoint 4 (4_labs): Low fibrinogen hallmark.
Revision checkpoint 5 (5_diff): TTP/HUS (normal PT/fib often).
Revision checkpoint 6 (6_treat_cause): Antibiotics source control.
Revision checkpoint 7 (7_transfuse): If bleeding or procedure risk.
Revision checkpoint 8 (8_anticoag): Heparin thrombotic DIC selected.
Revision checkpoint 9 (9_special): Purpura fulminans.
Revision checkpoint 10 (10_evidence): ISTH guidance.
Revision checkpoint 11 (11_traps): Transfuse numbers without bleed.
Revision checkpoint 12 (12_icu): Serial coag screen.
Revision checkpoint 13 (13_prognosis): Mortality 40–80% severity linked.
Revision checkpoint 14 (14_boards): Calculate ISTH score.
Revision checkpoint 15 (15_saq): Score this panel.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action for disseminated intravascular coagulation isth management.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
[1] References [1] Wada H, et al. Guidance for diagnosis and treatment of DIC from harmonization of the recommendations from three guidelines. Journal of thrombosis and haemostasis : JTH , 2013.PMID 23379279 [2] Taylor FB Jr, et al. Towards definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation. Thrombosis and haemostasis , 2001.PMID 11816725 [3] Iba T, et al. Diagnosis and management of sepsis-induced coagulopathy and disseminated intravascular coagulation. Journal of thrombosis and haemostasis : JTH , 2019.PMID 31410983 [4] Levi M, et al. Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology. British journal of haematology , 2009.PMID 19222477 [5] Papageorgiou C, et al. Disseminated Intravascular Coagulation: An Update on Pathogenesis, Diagnosis, and Therapeutic Strategies. Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis , 2018.PMID 30296833 [6] Vincent JL, et al. Effect of a Recombinant Human Soluble Thrombomodulin on Mortality in Patients With Sepsis-Associated Coagulopathy: The SCARLET Randomized Clinical Trial. JAMA , 2019.PMID 31104069 
