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Disseminated Intravascular Coagulation (DIC)

Anesthesia Implications

Updated On: July 22, 2026

Anesthesia Implications

Treat the trigger - DIC is secondary; the priority is identifying and treating the precipitating cause (sepsis, hemorrhage, obstetric emergency) — support alone won't fix it.

Component replacement - Guided by labs and bleeding: platelets, fresh frozen plasma, and cryoprecipitate (fibrinogen); use viscoelastic testing where available to target the deficits.

Diffuse bleeding - Expect oozing from every site (lines, wounds, mucosa); secure large-bore access, transfuse to keep up, and warm everything.

Avoid neuraxial - Active coagulopathy contraindicates neuraxial techniques and complicates invasive procedures.

Organ support - Microthrombi cause organ dysfunction (renal, pulmonary); support perfusion and monitor organ function.

Pathophysiology

Disseminated intravascular coagulation is systemic activation of the clotting cascade — triggered by sepsis, trauma, obstetric catastrophe, or malignancy — that consumes platelets and clotting factors while depositing microthrombi.

The paradox is simultaneous thrombosis and bleeding: microvascular clots cause organ ischemia while consumption of factors and platelets, plus fibrinolysis, causes diffuse hemorrhage. It is always secondary to a precipitating illness, and treatment centers on that cause plus supportive replacement.


Suggested Reading

Hemmings HC Jr, Yao FF, Goldstein PA, et al, eds. Yao & Artusio's Anesthesiology: Problem-Oriented Patient Management. 10th ed. Wolters Kluwer; 2025.
Gropper MA, Eriksson LI, Fleisher LA, et al, eds. Miller's Anesthesia. 10th ed. Elsevier; 2024.
Hines RL, ed. Stoelting's Anesthesia and Co-Existing Disease. 8th ed. Elsevier; 2021.
Matsumoto H, Takeba J, Umakoshi K, et al. Successful treatment for disseminated intravascular coagulation (DIC) corresponding to phenotype changes in a heat stroke patient. J Intensive Care. 2019. PMID: 30675362.