Disseminated Intravascular Coagulation (DIC)
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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Risk factors
- Sepsis (most common cause, especially gram-negative bacteremia, meningococcemia, severe COVID-19)
- Trauma (severe injury, head trauma, burns, crush injury, fat embolism)
- Obstetric: amniotic fluid embolism, placental abruption, retained dead fetus, severe preeclampsia/HELLP, septic abortion
- Malignancy: acute promyelocytic leukemia (APL/M3) — classic; pancreatic adenocarcinoma, gastric, prostate (chronic compensated DIC)
- Severe transfusion reaction (ABO incompatibility)
- 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
- Confusion, jaundice (microangiopathic hemolysis), oliguria
Classic findings
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.
Labs
- CBC — thrombocytopenia
- Peripheral smear — schistocytes (microangiopathic hemolysis)
- PT prolonged, PTT prolonged (factor consumption)
- Fibrinogen LOW (or falling from a high baseline — acute phase reactant; serial measurements informative)
- D-dimer markedly elevated (fibrin degradation)
- Fibrin degradation products (FDPs) elevated
- Markers of hemolysis: LDH elevated, indirect hyperbilirubinemia, low haptoglobin
- Antithrombin and protein C levels reduced
- ISTH overt DIC score (5+ = overt DIC): platelets, D-dimer, PT prolongation, fibrinogen
- 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 |
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)
- Acute promyelocytic leukemia DIC: all-trans retinoic acid (ATRA) + arsenic trioxide reverses coagulopathy rapidly — start before confirmatory cytogenetics if APL strongly suspected
Complications
- Multiorgan failure (renal, hepatic, pulmonary)
- Major bleeding — intracranial, GI, surgical
- Limb ischemia and amputation from purpura fulminans
- Stroke, pulmonary embolism, deep vein thrombosis
- Death from underlying disease and DIC sequelae
- Long-term: post-amputation morbidity, chronic kidney disease, cognitive sequelae
PANCE pearls
- 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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