Disseminated Intravascular Coagulation (DIC): Pathogenesis and clinical findings
Authors: Emily Wildman Mehul Gupta Sean Spence Yan Yu* Reviewers: Kiera Pajunen Wendy Yao Tristan Jones Man-Chiu Poon* Lynn Savoie* * MD at time of publication
Sepsis
Microorganisms express pathogen- associated molecular patterns (PAMPs)
Severe Trauma
Damaged endothelial cells release damage- associated molecular patterns (DAMPs)
Solid and Hematologic Malignancies
Cancer cells express tissue factor and release procoagulants
Immune cells recognize DAMPs and PAMPs and begin expressing tissue factor and releasing procoagulants
Systemic activation of coagulation cascade
Activation of coagulation cascade results in the factor X mediated conversion of large quantities of prothrombin (factor II) to its active form, thrombin (factor IIa)
Thrombin cleaves fibrinogen (factor I) circulating in blood to an activate form known as fibrin (factor 1a)
↓ Serum fibrinogen
Diffuse coagulation causes imbalances between coagulation and anticoagulation pathways
Consumption of coagulation factors (including platelets, fibrinogen, prothrombin, factor V, factor VIII) exceeds rate of production
Fibrin, in conjunction with platelets, form widespread thrombi within vasculature
Fibrin thrombi accumulate in the microvasculature and shear transiting red blood cells
Microangiopathic hemolytic anemia (MAHA)
↑ thrombi formation ↑ fibrinolysis, a parallel process that naturally degrades fibrin thrombi
Relative deficiency of coagulation factors leads to a bleeding diathesis (tendency to bleed) despite widespread clots
↑ Prothrombin time (PT)
↑ Partial thromboplastin time (PTT)
↑ D-dimer Fibrin thrombi
↑ Fibrin degradation products
Platelets are used up forming thrombià less free platelets in circulation
↓ Platelets on Complete Blood Count
accumulate in microvasculature of major organs
Deposition of thrombi occlude blood flow resulting in ischemia of organ parenchyma
Lack of coagulation factors can predispose spontaneous hemorrhage in various organs
Multiple organ dysfunction syndrome (MODS) – (renal failure, hepatic dysfunction, stroke, pulmonary disease)
Clinical manifestations of bleeding, including petechiae (pinpoint red spots on skin), ecchymoses (bruising), weeping wound sites, bleeding mucous membranes
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
First published Aug 7, 2012, updated July 27, 2019 & Aug 29, 2021 on www.thecalgaryguide.com