eMedicine Specialties > Emergency Medicine > Hematology & Oncology

Disseminated Intravascular Coagulation: Differential Diagnoses & Workup

Author: Joseph U Becker, MD, Fellow, Global Health and International Emergency Medicine, Stanford University
Coauthor(s): Charles R Wira, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale School of Medicine
Contributor Information and Disclosures

Updated: Sep 10, 2009

Differential Diagnoses

Acute or chronic liver failure
Hemolytic Uremic Syndrome
Heparin-induced thrombocytopenia
Other consumptive coagulopathy
Thrombocytopenic Purpura

Other Problems to Be Considered

The differential diagnosis of disseminated intravascular coagulation (DIC) is broad and can include other consumptive coagulopathies such as trauma and major surgery. Also, severe liver disease can result in markedly reduced production of coagulation factors and inhibitors. Thrombocytopenia may occur in this setting as well secondary to splenic sequestration, resulting in an overall clinical picture quite similar to DIC. 

Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) is a thrombotic microangiopathy, similar to DIC; however, contrary to DIC, the mechanism of coagulation is not via the tissue factor-VIIa pathway. Rather, in TTP-HUS, activation of coagulation stems from direct platelet activation usually from widespread endothelial damage or via an inherited or acquired impairment of ADAMTS13, a protease that normally cleaves von Willebrand factor. However, TTP-HUS and DIC are usually distinguished by their occurrence in different clinical settings (trauma or sepsis in DIC and fever and neurologic symptoms in TTP-HUS). Furthermore, TTP-HUS does not demonstrate the laboratory abnormalities frequently encountered in DIC (see Lab Studies below).21  

Idiopathic thrombocytopenic purpura (ITP) additionally, while also distinct mechanistically, can have clinical components similar to DIC, that is thrombocytopenia and thrombus formation. Heparin-induced thrombocytopenia (HIT) is another clinical entity similar in presentation to DIC. A subpopulation of patients who have received heparin will develop antibodies against platelet antigens and can result in diminution of platelet number. Although thrombosis may be observed, HIT does not typically produce the consumptive coagulopathy of DIC.

Workup

Laboratory Studies

No one test is sensitive and specific enough to diagnose disseminated intravascular coagulation (DIC). Rather, the diagnosis is made based on the clinical picture in combination with laboratory studies, best evaluated serially. Most individual laboratory tests demonstrate high sensitivity but very low specificity for DIC.22 Furthermore, while acute DIC typically overwhelms compensatory anticoagulation mechanisms resulting in depletion of factors and laboratory derangements, chronic or localized DIC may produce only minimal abnormalities in laboratory tests.23  

Given that acute DIC entails massive thrombin activation and fibrin deposition with consumption of coagulation factors, many laboratory abnormalities are manifest. Because fibrin activation is a central component of DIC, evidence suggests that if soluble fibrin is elevated, the diagnosis of DIC can be made with confidence.24 However, soluble fibrin levels are not available to most clinicians in a relevant time frame. Likewise, laboratory assays aimed at differentiating between cross-linked fibrin, fibrinogen, and soluble fibrin have been developed but are not routinely available to the clinician. However, other commonly available laboratory tests often are frequently deranged in DIC. Typically, moderate-to-severe thrombocytopenia is present in DIC. Furthermore, the peripheral blood smear can demonstrate evidence of microangiopathic pathology (schistocytes). 

Fibrinolysis is an important component of DIC. As such, there is evidence of fibrin breakdown such as elevated D-dimer and fibrin degradation products (FDPs).

However, both of these assays may be elevated in other conditions such as venous thromboembolism, trauma, or recent surgery, limiting the specificity of these tests.8,25 Given the massive fibrin deposition in DIC, fibrinogen levels would seem to be decreased. However, this is not the case. Fibrinogen, as a positive acute-phase reactant is increased in inflammation, and while values may decrease as the illness progresses, they are rarely low.8,26 Given ongoing consumption of coagulation factors and impaired hepatic synthesis secondary to hypoperfusion or organ damage, typically global clotting times (aPTT and PT) are elevated. Antithrombin levels as well as other individual factors (V and VII) may also be diminished in acute DIC.

The diagnosis of DIC relies on multiple clinical and laboratory determinations. The International Society on Thrombosis and Haemostasis developed a simple scoring system for the diagnosis of overt DIC (see Table 2). A score of 5 or greater indicates overt DIC, whereas a score of less than 5 does not rule out DIC but may indicate non-overt DIC.1 Studies have demonstrated the DIC score to be 93% sensitive and 98% specific for DIC.27   
 
Table 2. DIC Score1

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Table
Risk assessmentDoes the patient have an underlying disorder (eg, sepsis, trauma, obstetric emergency) compatible with DIC?
Laboratory coagulation testsPlatelet count
D-dimer and FDPs
Fibrinogen
PT and aPTT
ScoringPlatelet count: >100 = 0 points, <100 = 1 point, <50 = 2 points
Elevated fibrin marker: No elevation = 0 points, moderate increase = 2 points, strong increase = 3 points
Prolonged PT: <3 sec = 0 points, >3 <6 = 1 point, >6 = 2 points
Fibrinogen level: >1 g/L = 0 points, <1 = 1 point
Calculate scoreGreater than or equal to 5 = compatible with overt DIC, repeat scoring daily
Less than 5 suggestive of non-overt DIC
Risk assessmentDoes the patient have an underlying disorder (eg, sepsis, trauma, obstetric emergency) compatible with DIC?
Laboratory coagulation testsPlatelet count
D-dimer and FDPs
Fibrinogen
PT and aPTT
ScoringPlatelet count: >100 = 0 points, <100 = 1 point, <50 = 2 points
Elevated fibrin marker: No elevation = 0 points, moderate increase = 2 points, strong increase = 3 points
Prolonged PT: <3 sec = 0 points, >3 <6 = 1 point, >6 = 2 points
Fibrinogen level: >1 g/L = 0 points, <1 = 1 point
Calculate scoreGreater than or equal to 5 = compatible with overt DIC, repeat scoring daily
Less than 5 suggestive of non-overt DIC

Despite the utility of this scoring regimen for the diagnosis of DIC, there has been concern regarding the validity of this tool in identifying non-overt DIC. In response to these concerns, the Japanese Association for Acute Medicine (JAAM) developed the following diagnostic criteria for critically ill patients. This system has been prospectively validated and found to be able to diagnose DIC earlier than previous methods. Furthermore, evidence suggests that early identification of patients with DIC using this scoring system and as well early and aggressive treatment of DIC and the underlying disorder can lead to improvements in patient outcome and reduced mortality.28

Table 3: Scoring System for DIC (Japanese Association for Acute Medicine)28
 

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Table
Clinical conditions that should be ruled out
Thrombocytopenia
Dilution and abnormal distribution
Massive blood loss, massive infusion
Idiopathic thrombocytopenic purpura (ITP), TTP/HUS, HIT, HELLP
Disorders of hematopoiesis
Liver disease
Hypothermia
Spurious laboratory results
Diagnostic algorithm for systemic inflammatory response syndrome
Temperature >38 º C or <36 º C
Heart rate >90 beats per minute
Respiratory rate >20 breaths/min or PaCO 2 <32 torr (<4.3 kPa)
White blood cell >12,000 cells/mm3, <4000 cells/mm3, or 10% immature (band) forms
Diagnostic algorithm
Systemic inflammatory response system criteria 		Score

>31
0-20
Platelet count (109/L) 
<80 or >50 % decrease within 24 hours3
>80 and <120 or >30% decrease within 24 hours1
>1200
Prothrombin time (value of patient/normal value)
>1.21
<1.20
Fibrin/fibrinogen degradation products (mg/L) 
>253 
>10 and <251
<100
Diagnosis
4 points or more 		 DIC
Clinical conditions that should be ruled out
Thrombocytopenia
Dilution and abnormal distribution
Massive blood loss, massive infusion
Idiopathic thrombocytopenic purpura (ITP), TTP/HUS, HIT, HELLP
Disorders of hematopoiesis
Liver disease
Hypothermia
Spurious laboratory results
Diagnostic algorithm for systemic inflammatory response syndrome
Temperature >38 º C or <36 º C
Heart rate >90 beats per minute
Respiratory rate >20 breaths/min or PaCO 2 <32 torr (<4.3 kPa)
White blood cell >12,000 cells/mm3, <4000 cells/mm3, or 10% immature (band) forms
Diagnostic algorithm
Systemic inflammatory response system criteria 		Score

>31
0-20
Platelet count (109/L) 
<80 or >50 % decrease within 24 hours3
>80 and <120 or >30% decrease within 24 hours1
>1200
Prothrombin time (value of patient/normal value)
>1.21
<1.20
Fibrin/fibrinogen degradation products (mg/L) 
>253 
>10 and <251
<100
Diagnosis
4 points or more 		 DIC

Recent evidence also suggests that serum thrombomodulin levels correlate well with the clinical course of DIC, multiorgan system dysfunction, and mortality in septic patients. Thrombomodulin, a marker for endothelial cell damage, is elevated in DIC and correlates well with not only the severity of DIC but can also serve as a marker for the early identification as well as monitoring of DIC.29

Imaging Studies

  • Base diagnostic imaging on the underlying pathologic process as well as on areas suggestive of thrombosis and hemorrhage.
  • Perform a bilateral perihilar soft-density chest radiograph if pulmonary injury is present.

Other Tests

  • Base other tests on the underlying pathologic process as well as on areas suggestive of thrombosis and hemorrhage.

Procedures

  • Base procedures on the underlying pathologic process as well as on areas suggestive of thrombosis and hemorrhage.
  • Conduct invasive procedures with care because of bleeding complications. Procedures should follow the administration of clotting factor and platelet repletion.

More on Disseminated Intravascular Coagulation

Overview: Disseminated Intravascular Coagulation
Differential Diagnoses & Workup: Disseminated Intravascular Coagulation
Treatment & Medication: Disseminated Intravascular Coagulation
Follow-up: Disseminated Intravascular Coagulation
References
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Further Reading

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Contributor Information and Disclosures

Author

Joseph U Becker, MD, Fellow, Global Health and International Emergency Medicine, Stanford University
Joseph U Becker, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Charles R Wira, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale School of Medicine
Charles R Wira, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

Steven A Conrad, MD, PhD, Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center
Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Jeffrey L Arnold, MD, FACEP, Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center
Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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