Treatment of Disseminated Intravascular Coagulation

Primary Treatment Principle

The cornerstone of DIC management is aggressive treatment of the underlying disorder—sepsis requires source control and antibiotics, malignancy requires chemotherapy or surgery, obstetric complications require delivery, and trauma requires surgical intervention—with simultaneous supportive hemostatic therapy guided by bleeding status and specific laboratory thresholds rather than laboratory abnormalities alone. 1, 2

Step 1: Identify and Treat the Underlying Trigger

Sepsis-associated DIC: Implement source control and appropriate antibiotics immediately 1, 2
Cancer-associated DIC: Initiate cancer-directed therapy (chemotherapy, surgery, or radiation) as the primary intervention 2
- In acute promyelocytic leukemia specifically, early all-trans retinoic acid achieves excellent resolution of the coagulopathy 2
Obstetric complications: Deliver the fetus and manage eclampsia or other pregnancy-related triggers 1
Trauma: Surgical intervention for hemorrhage control 1

Step 2: Classify the DIC Phenotype

The International Society on Thrombosis and Haemostasis recognizes three distinct forms that dictate management strategy 1, 2:

Procoagulant (Thrombosis-Predominant) DIC

Common in pancreatic cancer and adenocarcinomas 2
Presents with arterial ischemia, venous thromboembolism, or microvascular thrombosis 2
Management: Therapeutic anticoagulation is the priority 1, 3

Hyperfibrinolytic (Bleeding-Predominant) DIC

Typical of acute promyelocytic leukemia and metastatic prostate cancer 2
Presents with widespread bleeding from multiple sites 2
Management: Aggressive transfusion support; heparin is contraindicated 1, 3

Subclinical DIC

Laboratory abnormalities without overt clinical manifestations 1
Monitor for progression with serial platelet counts (≥30% drop indicates progression) 1, 2

Step 3: Supportive Hemostatic Management for Bleeding Phenotype

Platelet Transfusion Thresholds

Active bleeding: Maintain platelets >50×10⁹/L 1, 3, 2
High bleeding risk without active hemorrhage:
- Acute promyelocytic leukemia: transfuse if <30×10⁹/L 3
- Other malignancies: transfuse if <20×10⁹/L 3

Fresh Frozen Plasma (FFP)

Administer 15-30 mL/kg for prolonged PT/aPTT in patients with active bleeding 1, 3, 2
Dose adjustments should be guided by clinical response rather than isolated laboratory values 3
When volume overload is a concern, prothrombin complex concentrates may replace plasma, though they provide only selected clotting factors 3

Fibrinogen Replacement

If fibrinogen remains <1.5 g/L despite FFP, administer two pools of cryoprecipitate or fibrinogen concentrate 1, 3, 2

Critical Caveat

Transfused platelets and clotting factors have a very short lifespan in DIC due to ongoing consumption, often necessitating repeated transfusions 1, 3
Do not transfuse based solely on laboratory abnormalities—clinical bleeding or procedural risk must drive transfusion decisions 3

Step 4: Anticoagulation Strategy for Thrombotic Phenotype

Indications for Therapeutic-Dose Anticoagulation

Therapeutic anticoagulation is indicated when any of the following occur 1, 2:

Arterial or venous thromboembolism
Severe purpura fulminans with acral ischemia
Vascular skin infarction
Cancer-associated DIC with documented thrombotic events

Prophylactic Anticoagulation

Initiate prophylactic heparin in all cancer-associated DIC patients except when 2:
- DIC phenotype is hyperfibrinolytic, OR
- Platelets <20×10⁹/L, OR
- Active bleeding is present
Low molecular weight heparin (LMWH) is the first-choice agent for most patients 2
In patients at high bleeding risk with renal impairment, unfractionated heparin is preferred because of its rapid reversibility 1, 3

Critical Decision Point: Thrombosis with Severe Thrombocytopenia (25-50×10⁹/L)

Three management options exist 2:

Platelet transfusion combined with therapeutic anticoagulation
Intermediate-dose or prophylactic anticoagulation without platelet transfusion
No anticoagulation unless thrombus location is critical (e.g., pulmonary embolism versus distal DVT)

Balance bleeding risk against thrombotic risk based on the specific anatomic site 2

Key Principle

Abnormal coagulation screens (prolonged PT/aPTT) alone should not preclude anticoagulation in the absence of bleeding, as DIC reflects a rebalanced hemostatic state with simultaneous loss of pro- and anticoagulant factors 3

Absolute Contraindication

Heparin must be avoided in hyperfibrinolytic DIC, where it can exacerbate bleeding 3

Step 5: Monitoring Strategy

Acute DIC: Monitor CBC, PT/aPTT, fibrinogen, and D-dimer daily 1, 2
Chronic stable DIC: Adjust monitoring frequency to monthly based on clinical stability 1, 2
Subclinical DIC progression: A 30% drop in platelet count may indicate progression, even if absolute count remains normal 1, 2

Agents to Avoid

Tranexamic Acid

Should not be used routinely in DIC as it may increase thrombotic events 1, 2
Reserved only for therapy-resistant bleeding in hyperfibrinolytic DIC phenotypes 1, 2

Recombinant Factor VIIa

Discouraged in DIC because its benefit is uncertain and it carries a definite risk of inducing thrombosis 1, 2

Inferior Vena Cava (IVC) Filters

Should be avoided except in highly selected patients who cannot receive anticoagulation and have proximal lower-limb thrombosis at high risk of embolization; in such cases, temporary filters may be considered 2

Corticosteroids and Antiplatelet Agents

Corticosteroids have no established benefit and are not recommended 3
Antiplatelet agents are not indicated and may increase bleeding risk 3

Common Pitfalls to Avoid

Do not withhold anticoagulation solely because of prolonged PT/aPTT in thrombotic DIC—the coagulation abnormalities reflect the disease process, not a contraindication to anticoagulation 3
Do not use heparin in bleeding-predominant or hyperfibrinolytic DIC—this will worsen hemorrhage 1, 3
Recognize that transfused blood products have reduced survival in active DIC, often requiring repeated administrations 3
Do not delay treatment of the underlying disorder—supportive measures alone will not resolve DIC 1, 2

Special Considerations for DNR Patients

Transfused platelets and fibrinogen have a very short lifespan in DIC with vigorous activation, often necessitating repeated transfusions that may not align with comfort-focused goals of care 1
Repeated blood-product transfusions provide only short-lived correction of laboratory abnormalities, making their routine use in DNR patients potentially futile 1

What is the recommended management of disseminated intravascular coagulation?

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