Overview
Disseminated Intravascular Coagulation (DIC)
Topic Overview
Summary
Disseminated intravascular coagulation (DIC) is a systemic activation of coagulation, leading to widespread microthrombi formation and consumption of clotting factors and platelets. This results in paradoxical bleeding and thrombosis. DIC is always secondary to an underlying condition (sepsis, trauma, malignancy, obstetric emergencies). The hallmark is simultaneous bleeding and clotting. Treatment focuses on the underlying cause plus supportive blood product replacement.
Key Facts
- Always secondary: Sepsis, trauma, malignancy, obstetric emergencies
- Pathology: Systemic activation of coagulation → microthrombi + consumption of factors
- Presentation: Bleeding AND thrombosis (paradox)
- Labs: Low platelets, elevated PT/APTT, low fibrinogen, high D-dimer, schistocytes
- Treatment: Treat underlying cause + blood products ± anticoagulation (if thrombosis predominant)
Clinical Pearls
DIC is never a primary diagnosis — always look for the underlying cause
"Consumptive coagulopathy" = using up clotting factors and platelets → bleeding
Fibrinogen under 1.0 g/L in DIC is critically low — replace with cryoprecipitate
Why This Matters Clinically
DIC is a haematological emergency that complicates many critical illnesses. Recognising and treating the underlying cause while supporting coagulation is life-saving.
Visual Summary
Visual assets to be added:
- DIC pathophysiology diagram
- Blood film showing schistocytes
- ISTH DIC scoring system
- DIC management algorithm
Epidemiology
Incidence
- Common in critically ill patients
- 30-50% of patients with severe sepsis have DIC
- High mortality (30-80% depending on cause)
Demographics
- All ages
- Critically ill patients
Causes
| Category | Examples |
|---|---|
| Sepsis | Most common cause; gram-negative and gram-positive |
| Trauma | Major trauma, burns, head injury |
| Malignancy | Acute promyelocytic leukaemia (APL), solid tumours (pancreas, prostate) |
| Obstetric | Placental abruption, amniotic fluid embolism, eclampsia, HELLP |
| Transfusion | Massive transfusion, ABO incompatibility |
| Vascular | Aortic aneurysm, giant haemangioma |
| Toxic/Immunologic | Snake bites, drug reactions |
Pathophysiology
Mechanism
- Underlying trigger activates coagulation
- Widespread thrombin generation
- Microthrombi form in small vessels → organ ischaemia
- Consumption of clotting factors (especially fibrinogen) and platelets
- Secondary fibrinolysis → elevated D-dimer
- Bleeding tendency due to depleted factors/platelets
Key Features
| Process | Effect |
|---|---|
| Microthrombi | Organ ischaemia (kidney, liver, lung) |
| Factor consumption | Bleeding |
| Fibrinolysis | Elevated D-dimer |
| Platelet consumption | Thrombocytopenia |
Why Bleeding AND Thrombosis
- Initial hypercoagulable state → microthrombi
- Consumption of factors/platelets → bleeding
- Both occur simultaneously
Clinical Presentation
Symptoms
Signs of Bleeding
Signs of Thrombosis
Red Flags
| Finding | Significance |
|---|---|
| Bleeding from multiple sites | Consumptive coagulopathy |
| Purpura fulminans | Severe DIC, often meningococcal |
| Multi-organ failure | Microthrombi |
| Low fibrinogen | Critical — replace urgently |
Bleeding (skin, mucous membranes, lines, wounds)
Common presentation.
Signs of underlying disease (sepsis, trauma)
Common presentation.
Organ dysfunction (renal, respiratory, hepatic)
Common presentation.
Clinical Examination
Skin
- Petechiae, purpura
- Ecchymoses
- Necrotic lesions (purpura fulminans)
Mucosal
- Gum bleeding
- GI bleeding
Other
- Evidence of underlying cause (sepsis, trauma)
- Signs of organ failure
Investigations
Coagulation Studies
| Test | Finding |
|---|---|
| Platelet count | Low (often under 50) |
| PT/INR | Prolonged |
| APTT | Prolonged |
| Fibrinogen | Low (under 1.0 g/L is critical) |
| D-dimer | Elevated (often massively) |
Blood Film
- Schistocytes (fragmented RBCs — microangiopathic haemolysis)
- Low platelets
Other
| Test | Purpose |
|---|---|
| FBC | Anaemia, thrombocytopenia |
| LDH | Elevated (haemolysis) |
| U&E, creatinine | Renal function |
| LFTs | Liver function |
| Blood cultures | If sepsis suspected |
ISTH DIC Score
- Platelet count
- PT prolongation
- Fibrinogen
- D-dimer
- Score 5 or more = overt DIC
Classification & Staging
By Presentation
| Type | Features |
|---|---|
| Overt DIC | Decompensated; bleeding predominant |
| Non-overt (compensated) | Laboratory abnormalities only |
By Predominant Feature
- Bleeding-predominant (consumption)
- Thrombosis-predominant (microthrombi)
By Cause
- Septic DIC
- Traumatic DIC
- Obstetric DIC
- Malignancy-associated DIC
Management
Treat the Underlying Cause — Most Important
- Sepsis: Antibiotics, source control
- Trauma: Surgery, damage control
- Obstetric: Deliver baby, manage haemorrhage
- Malignancy: Chemotherapy (especially APL)
Supportive Blood Product Replacement
| Product | Indication | Target |
|---|---|---|
| Platelets | Platelet count under 50 with bleeding; under 20 if no bleeding | Over 50 if bleeding |
| FFP | PT/APTT over 1.5x normal with bleeding | Normalise coagulation |
| Cryoprecipitate | Fibrinogen under 1.0 g/L | Fibrinogen over 1.5 g/L |
| RBCs | Anaemia | Hb over 70-80 g/L |
Anticoagulation
- Consider if thrombosis predominant (e.g., purpura fulminans)
- Low-dose heparin (controversial — discuss with haematology)
- Tranexamic acid generally avoided (may worsen thrombosis)
Monitoring
- Serial coagulation studies
- Platelet count
- Fibrinogen
- Clinical response
Complications
Of DIC
- Multi-organ failure
- Haemorrhage (including intracranial)
- Limb ischaemia
- Death
Of Treatment
- Transfusion reactions
- Volume overload
- TRALI
Prognosis & Outcomes
Mortality
- 30-80% depending on underlying cause
- Highest in septic DIC and trauma
Factors Affecting Outcome
- Underlying cause (reversibility)
- Severity of DIC
- Speed of treatment
- Multi-organ dysfunction
Evidence & Guidelines
Key Guidelines
- ISTH Guidance on Diagnosis and Management of DIC
- BCSH Guideline on DIC
Key Evidence
- Treating underlying cause is most effective intervention
- Blood product replacement is supportive but essential
Patient & Family Information
What is DIC?
DIC is a condition where the blood clotting system becomes overactive, forming tiny clots throughout the body. This uses up clotting factors and platelets, leading to both clotting and bleeding at the same time.
Why Does It Happen?
DIC is always caused by another serious condition such as severe infection, major injury, or problems during pregnancy.
Treatment
- Treating the underlying condition
- Blood transfusions to replace clotting factors and platelets
- Intensive care monitoring
Resources
References
Primary Guidelines
- Wada H, et al. Guidance for diagnosis and treatment of DIC from harmonization of the recommendations from three guidelines (ISTH/BCSH/SISET). J Thromb Haemost. 2013;11(4):761-767. PMID: 23379279
Key Reviews
- Levi M, Scully M. How I treat disseminated intravascular coagulation. Blood. 2018;131(8):845-854. PMID: 29255070
- Gando S, et al. Disseminated intravascular coagulation. Nat Rev Dis Primers. 2016;2:16037. PMID: 27250996