Systemic activation of coagulation with simultaneous thrombosis and bleeding — always secondary to an underlying trigger.
Also known as: DIC, consumptive coagulopathy, disseminated intravascular coagulation
Overview
Acquired syndrome characterized by widespread intravascular activation of coagulation, leading to thrombin generation, microvascular fibrin deposition, consumption of platelets and clotting factors, and secondary fibrinolysis. Results in simultaneous thrombotic and hemorrhagic manifestations. Always secondary to an underlying disorder.
Epidemiology
Common complication of sepsis (especially gram-negative), trauma, obstetric emergencies, malignancy. Identified in ~10% of ICU patients. Associated with high mortality (40-80%) driven by the underlying illness.
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Question 1HematologyMedium
A 69-year-old man is admitted with gram-negative sepsis from a urinary source. Over 24 hours he develops oozing from IV sites, petechiae, and blood in his urine. Blood pressure is 88/50 mm Hg and he is febrile. Labs show a low platelet count, prolonged PT and aPTT, a low fibrinogen level, and markedly elevated D-dimer; the peripheral smear shows schistocytes. Which of the following is the most likely diagnosis?
ADisseminated intravascular coagulation
BImmune thrombocytopenic purpura
CThrombotic thrombocytopenic purpura
DVitamin K deficiency coagulopathy
Reveal answer & full explanation
Correct answer: A — Disseminated intravascular coagulation
ADisseminated intravascular coagulation✓
BImmune thrombocytopenic purpura
CThrombotic thrombocytopenic purpura
DVitamin K deficiency coagulopathy
Why Disseminated intravascular coagulation is correct
This patient has disseminated intravascular coagulation (DIC).
The core concept is systemic activation of the coagulation cascade that consumes platelets and clotting factors while simultaneously activating fibrinolysis, producing both bleeding and microthrombosis.
Sepsis, especially gram-negative endotoxemia, is among the most common triggers (others include trauma, malignancy, and obstetric catastrophes).
The combination of thrombocytopenia, prolonged PT and aPTT, LOW fibrinogen, high D-dimer, and schistocytes is the classic laboratory signature.
Why the others are wrong
Immune thrombocytopenic purpura — isolated thrombocytopenia with NORMAL PT/aPTT and normal fibrinogen; it does not cause consumptive coagulopathy or schistocytes.
Thrombotic thrombocytopenic purpura — a microangiopathy with thrombocytopenia and schistocytes, but coagulation times and fibrinogen are typically NORMAL, and it features neurologic changes and renal injury rather than consumption of clotting factors.
Vitamin K deficiency coagulopathy — prolongs PT (then aPTT) by reducing factors II, VII, IX, X, but platelets, fibrinogen, and D-dimer are normal and there are no schistocytes.
The consumptive profile with low fibrinogen and high D-dimer in sepsis makes DIC the answer.
Question 2HematologyMedium
A 64-year-old man is admitted to the ICU with fever, hypotension, and confusion. He has diffuse oozing from his peripheral IV sites and new petechiae over his trunk. Labs show platelets of 38,000/uL, prolonged PT and PTT, fibrinogen of 90 mg/dL, and a markedly elevated D-dimer; the peripheral smear shows schistocytes. Blood cultures are pending. Among his history, which of the following is the strongest risk factor for the syndrome he has developed?
AChronic immune thrombocytopenia in remission
BGram-negative bacteremia from a urinary source
CLong-standing well-controlled type 2 diabetes
DChronic stable atrial fibrillation on warfarin
Reveal answer & full explanation
Correct answer: B — Gram-negative bacteremia from a urinary source
AChronic immune thrombocytopenia in remission
BGram-negative bacteremia from a urinary source✓
CLong-standing well-controlled type 2 diabetes
DChronic stable atrial fibrillation on warfarin
Why Gram-negative bacteremia from a urinary source is correct
The vignette describes disseminated intravascular coagulation (DIC): thrombocytopenia, prolonged PT/PTT, low fibrinogen, high D-dimer, and schistocytes in a critically ill patient with simultaneous bleeding and microvascular thrombosis.
DIC is always secondary to an underlying trigger, and sepsis—especially gram-negative bacteremia and meningococcemia—is the single most common and strongest cause. Endotoxin drives massive tissue-factor expression, systemic thrombin generation, and consumption of platelets and clotting factors.
Recognizing the trigger matters because the definitive treatment of DIC is source control plus treatment of the underlying illness (here, empiric antibiotics and resuscitation).
Why the others are wrong
Long-standing well-controlled type 2 diabetes — a risk factor for atherosclerotic and microvascular disease, but it does not acutely activate systemic coagulation and is not a recognized trigger of DIC.
Chronic stable atrial fibrillation on warfarin — warfarin prolongs the PT and can cause bleeding, but it does not consume platelets or fibrinogen or produce schistocytes; it is a mimic to exclude, not a cause of DIC.
Chronic immune thrombocytopenia in remission — antibody-mediated peripheral platelet destruction produces an isolated thrombocytopenia with a normal PT/PTT, normal fibrinogen, and no schistocytes even when active; a quiescent ITP history does not activate systemic coagulation and cannot explain the low fibrinogen, prolonged clotting times, or elevated D-dimer.
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Snake envenomation, severe hepatic failure, hyperthermia/heat stroke
Giant hemangioma (Kasabach-Merritt syndrome)
Vascular: aortic aneurysm, large vascular malformation
Pathophysiology
Trigger releases tissue factor or other procoagulants into circulation, activating the extrinsic coagulation pathway. Widespread thrombin generation produces microvascular fibrin deposition (causing organ ischemia and microangiopathic hemolysis with schistocytes) and consumes platelets and clotting factors (factors V, VIII, fibrinogen). Secondary fibrinolysis releases fibrin degradation products and D-dimers. Imbalance of coagulation activation and inhibitor depletion (antithrombin, protein C) sustains the process.
Clinical presentation
Symptoms
Bleeding: oozing from IV sites, mucosal bleeding, hematuria, GI bleeding, intracranial hemorrhage
Thrombosis: purpura fulminans (especially meningococcemia, post-infectious), digital ischemia, gangrene of extremities, venous thromboembolism, stroke
Symptoms of underlying disease: sepsis, trauma, obstetric crisis
Signs / physical exam
Petechiae, ecchymoses, oozing from venipuncture/surgical sites
Purpura fulminans — symmetric ecchymotic skin necrosis (classic with meningococcemia)
Acral cyanosis, digital gangrene
Hypotension, fever, multiorgan dysfunction from underlying illness
Septic patient with widespread oozing from IV sites plus thrombocytopenia, prolonged PT/PTT, low fibrinogen, and elevated D-dimer.
Differential diagnosis
Severe liver disease — Prolonged PT/PTT, low factor V; fibrinogen often preserved or only mildly low (synthesized but consumed less than DIC); LFTs abnormal
TTP/HUS — Schistocytes + thrombocytopenia but NORMAL PT/PTT and fibrinogen; ADAMTS13 low in TTP
HIT — Heparin exposure, thrombosis (not bleeding), 4T score, anti-PF4 antibody; coagulation studies normal
Vitamin K deficiency / warfarin — Prolonged PT > PTT, normal fibrinogen, platelets normal, no schistocytes
Dilutional coagulopathy — Massive transfusion or volume resuscitation, history clarifies
Primary hyperfibrinolysis — Elevated D-dimer with normal platelets; rare; prostate cancer, snake bite
Diagnostic workup
Diagnostic criteria
Clinical setting consistent with DIC + thrombocytopenia + prolonged PT/PTT + low or falling fibrinogen + elevated D-dimer. Formal scoring by ISTH overt DIC score.
Identify underlying cause: blood cultures, lactate, CT for trauma/source, evaluate for obstetric emergency, peripheral smear/marrow for APL
Imaging
Directed by suspected underlying cause (CT abdomen/pelvis for trauma or sepsis source, head CT for hemorrhage, obstetric ultrasound)
Diagnostic algorithm
Test
DIC
Liver Disease
Vitamin K Deficiency
TTP/HUS
Platelets
Low
Low (hypersplenism)
Normal
Low
PT
Prolonged
Prolonged
Prolonged
Normal
PTT
Prolonged
Prolonged
Normal or mild prolong
Normal
Fibrinogen
Low (or falling)
Normal or mildly low
Normal
Normal
D-dimer
Markedly high
Normal or mildly high
Normal
Elevated (hemolysis)
Factor VIII
Low (consumed)
Normal or high
Normal
Normal
Schistocytes
Yes
No (target cells)
No
Yes
Laboratory pattern of DIC compared to common mimics.
Treatment
First-line
TREAT THE UNDERLYING CAUSE — most important and definitive intervention (source control, empiric antibiotics, deliver fetus, treat APL with ATRA + arsenic, etc.)
Supportive care: hemodynamic resuscitation, ventilation, renal replacement as needed
Bleeding patient: fresh frozen plasma (FFP) for prolonged PT/PTT, cryoprecipitate if fibrinogen <100-150 mg/dL, platelet transfusion if <20-50K with bleeding or <10K asymptomatic
Thrombotic-predominant DIC (purpura fulminans, organ ischemia): therapeutic anticoagulation with heparin can be considered after replacement of antithrombin
Vitamin K and folate supplementation if depletion suspected
Second-line / adjunct
Antithrombin concentrate, protein C concentrate, thrombomodulin — used in some settings (especially Japan); not standard in US
Avoid antifibrinolytics (tranexamic acid, aminocaproic acid) in classic DIC — can promote thrombosis; exception is hyperfibrinolytic phenotype (APL pre-induction, prostate cancer)
DIC is ALWAYS secondary — diagnosing DIC obligates a hunt for the underlying trigger.
Lab pattern: thrombocytopenia + prolonged PT/PTT + LOW fibrinogen + HIGH D-dimer + schistocytes — all four supportive features.
Serial fibrinogen trends are more useful than absolute values — fibrinogen is an acute phase reactant and may start high.
Acute promyelocytic leukemia (APL/M3) presents with severe hemorrhagic DIC and hyperfibrinolysis — START ATRA EMPIRICALLY when suspected; do not wait for cytogenetic confirmation.
Heparin in DIC is controversial — generally reserved for thrombosis-predominant phenotypes and chronic DIC of malignancy (Trousseau syndrome).
Purpura fulminans = symmetric skin necrosis from severe protein C deficiency, most classically meningococcemia.
Distinguish DIC from severe liver disease: in DIC factor VIII is LOW (acute phase reactant but consumed); in liver disease factor VIII may be normal or HIGH (extrahepatic synthesis preserved).
References
ISTH 2018 — ISTH guidance for diagnosis and management of disseminated intravascular coagulation (Wada et al., J Thromb Haemost)
BSH 2009 — Guidelines for the diagnosis and management of disseminated intravascular coagulation (Levi et al., Br J Haematol)
Sanz et al. — Management of acute promyelocytic leukemia: updated recommendations from an expert panel (Blood 2019)
Levi & Scully — How I treat disseminated intravascular coagulation (Blood 2018)
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