Disseminated Intravascular Coagulation in Emergency Medicine Workup

  • Author: Joseph U Becker, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP   more...
 
Updated: Oct 26, 2011
 

Laboratory Studies

Patients with DIC present can present with a wide range of abnormalities in their laboratory values. Typically, elongated coagulation times, thrombocytopenia, high levels of fibrin split products, and microangiopathic pathology (schistocytes) on peripheral smears are suggestive findings.

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.[33] 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.[34]

Furthermore, it is important to note that laboratory values may represent only a momentary glimpse into a very rapidly changing systemic process, and therefore repeated tests may be necessary in order to make a more clinically certain diagnosis.[35]

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.[36] 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.[11, 37] 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.[11, 38] 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.

Additionally, it is important to note the role played by the loss of coagulation factors via hemorrhage and decreased production due to liver pathology.[39] Conversely, a normal or even attenuated PT and aPTT may be encountered in up to 50% of DIC patients, and therefore such values cannot be used to exclude DIC.[40] This phenomenon may be attributed to certain activated clotting factors present in the circulation, such as thrombin or Xa, which may in fact enhance thrombin formation.[41] It is also important to note that only PT, and not INR should be used in the DIC monitoring process, as INR has only been proscribed for monitoring oral anticoagulants.[30]

Antithrombin levels as well as other individual factors (V and VII) may also be diminished in acute DIC.

Typically, moderate-to-severe thrombocytopenia is present in DIC. Thrombocytopenia is seen in up to 98% of DIC patients, and, in 50% of the patients, the platelet count can dip below 50 X 109.[42] A decreasing trend in platelet counts or a grossly reduced absolute platelet count is a sensitive (although not specific) indicator of DIC.[30] Repeated platelet counts are often necessary, as a single platelet measurement may indicate a level within the normal range, whereas trend values might show a precipitous drop from previous levels.

The peripheral blood smear can demonstrate evidence of schistocytes, although these are rarely seen in excess of 10% of RBCs. The presence of schistocytes is neither sensitive nor specific for DIC, but in certain instances, they may help confirm a chronic DIC diagnosis when they are seen in concert with normal coagulation values and increased D-Dimers.[42]

One study demonstrated that in up to 57% of DIC patients, the levels of fibrinogen may in fact remain within normal limit.[42]

Protein C and antithrombin are 2 natural anticoagulants that are frequently decreased in DIC. These are also significant because some studies have shown that they may serve roles as prognostic indicators.[43, 44] Nonetheless, the practical application of measuring these anticoagulants may be limited for most practitioners, because of generalized limitations in their availability.[30]

DIC has been shown to have association with an unusual light transmission profile on the aPTT, known as a biphasic waveform. The degree of biphasic waveform abnormality on has been shown in an 1187-patient ICU study to have an increasing positive predictive value for DIC, and it occurs independently of clotting time prolongation. Additionally, the waveform abnormalities are often evident prior to more conventionally used laboratory value derangements,[45] making it a quick and robust test for DIC. The limitations of this approach lie in the current lack of widespread availability of the photo-optical analyzers necessary in clot formation analysis.

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.[46]

Table 2. DIC Score[1] (Open Table in a new window)

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.[47]

Table 3: Scoring System for DIC (Japanese Association for Acute Medicine)[47] (Open Table in a new window)

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 >38ºC or < 36ºC



Heart rate >90 beats per minute



Respiratory rate >20 breaths/min or PaCO2 < 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.[48]

Next

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.
Previous
Next

Other Tests

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

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.
Previous
Proceed to Treatment & Management
 
 
Contributor Information and Disclosures
Author

Joseph U Becker, MD  Fellow, Global Health and International Emergency Medicine, Stanford University School of Medicine

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)

Avishek Kumar, MD  Resident Physician, Department of Internal Medicine, St Michael's Medical Center, Seton Hall University School of Health and Medical Sciences

Avishek Kumar, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Hamid Salim Shaaban  MD, Fellow in Hematology/ Oncology, Department of Internal Medicine, Seton Hall University School of Health and Medical Sciences

Hamid Salim Shaaban is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

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.

Specialty Editor Board

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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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.

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, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

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.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Mary A Furlong, MD, and Brendan R Furlong, MD, to the development and writing of this article.

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Table 1. Main Features of DIC in a Series of 118 Patients[31]
Features Affected Patients, %
Bleeding64%
Renal dysfunction25%
Hepatic dysfunction19%
Respiratory dysfunction16%
Shock14%
Central nervous system dysfunction2%
Table 2. DIC Score[1]
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



Table 3: Scoring System for DIC (Japanese Association for Acute Medicine)[47]
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 >38ºC or < 36ºC



Heart rate >90 beats per minute



Respiratory rate >20 breaths/min or PaCO2 < 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
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