What is the test for intravascular coagulation?


  • Disseminated intravascular coagulation (DIC) is an acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes
  • It can originate from and cause damage to the microvasculature, which if sufficiently severe, can produce organ dysfunction


  • underlying disease process-> pro-inflammatory cytokines (activation of mononuclear and endothelial cells)-> intravascular fibrin formation-> microvascular thrombi and organ dysfunction-> consumptive intravascular coagulopathy and thrombocytopenia

    -> widespread haemorrhage



  • shock
  • sepsis
  • haemolysis
  • malignancy (e.g. promyelocytic leukaemia, other hematological malignancies, solid tumors)
  • trauma (e.g. multi-trauma, TBI, fat embolism syndrome)
  • pancreatitis
  • severe hepatic failure
  • burns
  • major surgery
  • PE
  • ECMO
  • transplant rejection
  • transfusion reactions
  • obstetric: pre-eclampsia, amniotic fluid embolism, intrauterine death, abruption
  • vascular disorders (e.g. Kasabach-Merrit syndrome, large aneurysms)


  • may be chronic with little overt clinical effects
  • can be an acute catastrophe
  • haemorrhage
  • microthrombosis leading to multiorgan failure


  • anaemia
  • prolonged APTT, INR and PT
  • thrombocytopaenia (or falling platelets)
  • low fibrinogen
  • fragmented RBCs on blood film
  • high fibrin degradation products (FDPs) / D-dimer
  • low levels of plasma coagulation factors and inhibitors (if tested)

DIC score (Taylor et al, 2001)

  • useful for diagnosis of DIC
  • simple scoring system based on platelet count, PT, D-dimer levels and fibrinogen
  • sensitivity 93% and specificity 98%
  • strong independent predictor of mortality in patients with severe sepsis


Other important causes of prolonged APTT, INR and PT and low fibrinogen include:

  • Primary fibrinolysis
  • ‘Dilutional coagulopathy’ from massive transfusion
  • Trauma-induced coagulopathy
  • Post thrombolysis
  • Venom-induced consumptive coagulopathy (VICC) from snake bite envenoming


  • treat cause!
  • FFP for APTT and INR
  • cryoprecipitate for fibrinogen (>1.0)
  • platelets for thrombocytopaenia (aim > 50)
  • consider FIIa
  • consider heparin if not bleeding (in chronic DIC)

References and Links

  • Levi M, Opal SM. Coagulation abnormalities in critically ill patients. Crit Care. 2006;10(4):222. PMC1750988.
  • Taylor FBJ, Toh CH, Hoots WK, Wada H, Levi M. Towards definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation. Thromb Haemost.2001;86:1327–1330. PMID: 11816725

What is the test for intravascular coagulation?

What is the test for intravascular coagulation?

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

Disseminated intravascular coagulation (DIC) is an acquired syndrome characterized by activation of coagulation pathways, resulting in formation of intravascular thrombi and depletion of platelets and coagulation factors.

Clinical history can include epistaxis, gingival bleeding, hematuria, oliguria, cough, dyspnea, fever, delirium, and coma. Physical exam may reveal petechiae, ecchymosis, gangrene, mental disorientation, hypoxia, hypotension, and gastrointestinal bleeding.

Diagnosis is based on presence of ≥1 known underlying conditions causing DIC plus abnormal global coagulation tests: decreased platelet count, increased prothrombin time, elevated fibrin-related marker (D-dimer/fibrin degradation products), and decreased fibrinogen level.

Aggressive treatment of the underlying disorder is indicated, as well as fresh frozen plasma, platelet concentrate, antithrombin III, tissue factor pathway inhibitor, heparin, and recombinant factor VII activated for refractory hemorrhagic episodes.

Complications include life-threatening hemorrhage, acute renal failure, and gangrene and loss of digits.

Disseminated intravascular coagulation (DIC) is an acquired syndrome characterized by activation of coagulation pathways, resulting in formation of intravascular thrombi and depletion of platelets and coagulation factors. Thrombi may lead to vascular obstruction/ischemia and multiorgan failure. Spontaneous bleeding may occur. Generalized bleeding, evidenced by at least three unrelated sites, is highly suggestive of DIC.

DIC can be triggered by major trauma, organ destruction, sepsis or severe infection (including severe coronavirus disease 2019 [COVID-19] infection), severe obstetric disorders, some malignancies, major vascular disorders, and severe toxic or immunologic reactions.[1]Levi M, De Jonge E, van der Poll T. New treatment strategies for disseminated intravascular coagulation based on current understanding of the pathophysiology. Ann Med. 2004;36(1):41-9. http://www.ncbi.nlm.nih.gov/pubmed/15000346?tool=bestpractice.com [2]Franchini M, Lippi G, Manzato F. Recent acquisitions in the pathophysiology, diagnosis and treatment of disseminated intravascular coagulation. Thromb J. 2006 Feb 21;4:4. http://www.thrombosisjournal.com/content/4/1/4 http://www.ncbi.nlm.nih.gov/pubmed/16504043?tool=bestpractice.com [3]Asakura H, Ogawa H. COVID-19-associated coagulopathy and disseminated intravascular coagulation. Int J Hematol. 2021 Jan;113(1):45-57. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7648664 http://www.ncbi.nlm.nih.gov/pubmed/33161508?tool=bestpractice.com

Objective: To study the clinician's ordering pattern in the diagnosis of disseminated intravascular coagulation (DIC) and to analyze the utility of selected tests by assessing their sensitivity, specificity, and overall efficiency.

Design: Retrospective, nonrandomized, clinical study.

Setting: University hospital intensive care units.

Patients: A total of 82 inpatients treated in our intensive care units were identified from the hospital computer system as having been tested for DIC in a 3-month period.

Intervention: Screening tests for DIC were ordered for the suspected patients.

Measurements and main results: Prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen/fibrin degradation products (FDP), and fibrinogen were used most frequently as DIC diagnostic tests. The FDP and D-dimer combination (n = 39) had the highest diagnostic efficiency of 95%, with sensitivity being 91% and specificity 94%. This is followed by FDP (n = 71), efficiency 87%, sensitivity 100%, and specificity 67%; PT/PTT and FDP combination (n = 71), efficiency 86%, sensitivity 91%, and specificity 71%; and D-dimer (n = 44), efficiency 80%, sensitivity 91%, and specificity 68%. The rest of the commonly used tests, such as PT, PTT, thrombin time, platelet count, fibrinogen, and the presence of schistocytes (n = 80), had individually either low specificity or low sensitivity and, therefore, low efficiency scores (57%, 57%, 70%, 67%, 65%, and 51%, respectively).

Conclusions: The D-dimer and FDP tests offered the best test panel in the diagnosis of DIC. We propose the use of D-dimer, FDP, and antithrombin as the DIC diagnostic test panel, with D-dimer and FDP providing a rapid and specific diagnosis, antithrombin providing insight to the severity and prognosis, and FDP (rapid and less expensive than D-dimer) to follow-up the progress of the condition once the diagnosis is established.