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Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Disseminated intravascular coagulation classification

Introduction

Overview

Overview

Disseminated intravascular coagulation may be classified according to the degree of fibrinolytic activation into suppressed-fibrinolytic-type DIC (DIC with suppressed fibrinolysis), enhanced-fibrinolytic-type DIC (DIC with enhanced fibrinolysis) and balanced-fibrinolytic-type DIC (DIC with balanced fibrinolysis). Each type differs in clinical features and laboratory findings.

Classification

Classification

Disseminated intravascular coagulation may be classified according to the degree of fibrinolytic activation into the following subtypes/groups[1]:

Suppressed-fibrinolytic-type DIC (DIC with suppressed fibrinolysis) [2][3][4][5]

  • Severe coagulation activation
  • Mild fibrinolytic activation
  • Seen in sepsis mostly
  • Mild bleeding complications
  • Elevated thrombin-antithrombin complex (TAT) , a coagulation activation marker
  • Mildy elevated plasmin-α2 plasmin inhibitor complex (PIC), a fibrinolysis activation marker
  • Mildly elevated Fibrin/fibrinogen degradation products (FDPs) and D-dimers
  • Normal or only slightly decreased α2 plasmin inhibitor (α2PI)

Enhanced-fibrinolytic-type DIC (DIC with enhanced fibrinolysis)[2][3][4][5]

  • Presents with marked fibrinolysis activation corresponding to coagulation activation
  • Strong activation of fibrinolysis
  • With hardly any elevation in PAI
  • Severe bleeding severe.
  • Elevation in both TAT and PIC
  • Elevated FDPs and D-dimer
  • FDP/D-dimer ratio tends to increase (decrease when expressed as the D-dimer/FDP ratio).
  • Associated with APL, abdominal aortic aneurysm, and prostate cancer

Balanced-fibrinolytic-type DIC (DIC with balanced fibrinolysis) [2][3][4][5]

References

References

  1. ↑ Asakura H (2014). “Classifying types of disseminated intravascular coagulation: clinical and animal models”. J Intensive Care. 2 (1): 20. doi:10.1186/2052-0492-2-20. PMC 4267600. PMID 25520834.
  2. ↑ 2.0 2.1 2.2 Asakura H, Ontachi Y, Mizutani T, Kato M, Saito M, Kumabashiri I, Morishita E, Yamazaki M, Aoshima K, Nakao S (June 2001). “An enhanced fibrinolysis prevents the development of multiple organ failure in disseminated intravascular coagulation in spite of much activation of blood coagulation”. Crit. Care Med. 29 (6): 1164–8. PMID 11395595.
  3. ↑ 3.0 3.1 3.2 Takahashi H, Tatewaki W, Wada K, Hanano M, Shibata A (February 1990). “Thrombin vs. plasmin generation in disseminated intravascular coagulation associated with various underlying disorders”. Am. J. Hematol. 33 (2): 90–5. PMID 1689102.
  4. ↑ 4.0 4.1 4.2 Asakura H, Jokaji H, Saito M, Uotani C, Kumabashiri I, Morishita E, Yamazaki M, Aoshima K, Matsuda T (October 1994). “Study of the balance between coagulation and fibrinolysis in disseminated intravascular coagulation using molecular markers”. Blood Coagul. Fibrinolysis. 5 (5): 829–32. PMID 7865691.
  5. ↑ 5.0 5.1 5.2 Asakura H, Jokaji H, Saito M, Uotani C, Kumabashiri I, Morishita E, Yamazaki M, Matsuda T (March 1991). “Changes in plasma levels of tissue-plasminogen activator/inhibitor complex and active plasminogen activator inhibitor in patients with disseminated intravascular coagulation”. Am. J. Hematol. 36 (3): 176–83. PMID 1899963.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]