From: Elizabeth M. Van Cott, M.D., and Michael Laposata, M.D., Ph.D., "Coagulation." In: Jacobs DS et al, ed. The Laboratory Test Handbook, 5th Edition. Lexi-Comp, Cleveland, 2001; 327-358.
Index of Tests
Disseminated Intravascular Coagulation Screen [CO003200]
Synonyms Consumptive Coagulopathy Screen; DIC Screen; Screen
for Disseminated Intravascular Coagulation
Applies to Fibrinolysis; Schistocytes
Abstract The most useful panel of tests to screen for disseminated
intravascular coagulation (DIC) includes D-dimer or fibrin degradation
products (FDP), prothrombin time (PT), activated partial thromboplastin
time (PTT), platelet count, and fibrinogen. These tests are not,
however, specific for DIC.
Specimen Plasma (and whole blood for platelet count and peripheral
Container Blue top (sodium citrate) tube; lavender top (EDTA)
tube for platelet count and peripheral blood smear
Collection Routine venipuncture. Draw blue top before lavender
top (EDTA) tube. If a red top is drawn, draw red top tube before
blue top tube. Immediately invert tube gently at least 4 times to
mix. Blue top tubes must be appropriately filled. Deliver tubes
immediately to the laboratory.
Storage Instructions Blue top tube: separate plasma from
cells as soon as possible; plasma may be stored on ice for up to
4 hours; otherwise store frozen
Causes for Rejection Blue top tube received more than 4 hours
after collection, blue top tube not filled, clotted specimens
Turnaround Time 1-2 hours (often less than 1 hour if requested
Reference Interval See individual tests.
Use Diagnose DIC in patients with an underlying disorder
known to cause DIC and/or with clinical suspicion of DIC
Limitations D-dimer and FDP are positive with physiologic
clot formation and lysis, and they may be positive in liver disease
because they are normally cleared by the liver. Therefore, DIC can
be difficult to diagnose in the presence of liver disease in some
cases. Results should be reviewed in relation to the clinical situation.
Methodology See individual tests.
Additional Information DIC is a common acquired coagulation
disorder resulting from excessive activation of the coagulation
system, usually due to massive tissue injury, sepsis, or certain
pregnancy complications. The normal anticoagulant and fibrinolytic
systems are overwhelmed and cannot contain the coagulation activation,
which becomes systemic, resulting in disseminated microvascular
thrombi. Thrombosis consumes platelets, coagulation factors, and
the natural anticoagulants, which consequently become depleted.
The decrease in coagulation factors causes PT and PTT prolongations,
and may lead to bleeding. Depletion of platelets also contributes
to the bleeding risk. The fibrinolytic system is activated to dissolve
the fibrin thrombi, resulting in consumption of plasminogen as it
is converted into plasmin, and the formation of fibrin degradation
products (FDP) including D-dimers as plasmin degrades fibrin clots.
FDP can contribute to bleeding, because they impair fibrin clot
formation and interfere with platelet function. In acute DIC, the
most obvious clinical symptom is bleeding, although the insidious
underlying disseminated microvascular thrombosis may lead to tissue
ischemia and consequently multiorgan failure. The key laboratory
findings are elevated D-dimers or FDP, prolonged PT and/or PTT,
and decreased or decreasing platelets and fibrinogen. Repeat testing
may be needed to show that fibrinogen and/or platelets are decreasing
over time. Fibrinogen is decreased in ~50% of acute DIC cases; the
PT is prolonged in ~70%; and the PTT is prolonged in ~50% of acute
DIC cases. Thus, it is important to note that these tests can
be normal in a substantial percentage of DIC cases.1,2 D-dimer or FDP should be positive in DIC. See D-Dimers
and Fibrin Degradation Products.
Chronic DIC may develop when the activation of the coagulation
system is low-grade and prolonged, as occurs with malignancy, retained
dead fetus, aneurysm,3 or hemangioma. The clinical features
and laboratory findings in chronic DIC can be much more subtle than
with acute DIC. Fibrinogen and platelet levels are commonly elevated,
because they can increase during acute phase reactions in response
to illness (including malignancy), injury, or other conditions.
The PT and PTT may actually be short, possibly due to increased
circulating activated coagulation factors. Large-vessel thrombosis
can occur in chronic DIC of malignancy. The main laboratory abnormality
for acute or chronic DIC is positive D-dimers or FDP, neither of
which are specific for DIC.
Schistocytes are present on the peripheral blood smear in 50% or
more of acute DIC cases.4,5 Schistocytes are generated
by microangiopathic hemolysis of red blood cells severed by flowing
through fibrin strands. A large number of other coagulation tests
may be abnormal in acute or chronic DIC, but their clinical utility
for DIC diagnosis remains uncertain. These include decreases in
the natural anticoagulant proteins antithrombin, protein C, and
protein S; prolonged thrombin time; elevated markers of coagulation
activation (eg, prothrombin fragment 1.2, fibrinopeptide A, fibrinopeptide
B, fibrin monomers,6 thrombin-antithrombin complexes6),
and the appearance of markers of fibrinolysis (plasmin-antiplasmin
complexes,6 decreased plasminogen, and antiplasmin) (see Hypercoagulation Panel). The
thrombin time is often prolonged because of decreased fibrinogen
and/or elevated FDP. Elevated FDP interfere with fibrin polymerization,
prolonging the thrombin time. Plasma markers of platelet activation,
such as platelet factor 4 and beta-thromboglobulin, may also be
detected. None of these markers are specific for DIC.
Treatment of the underlying condition is the primary treatment
of DIC, along with supportive care including transfusions if needed
for bleeding. Heparin use is controversial. New strategies, such
as antithrombin concentrates or recombinant activated protein C,
are under investigation.7
1. Spero JA, Lewis JH, and Hasiba U, "Disseminated Intravascular
Coagulation: Findings in 346 Patients,"Thromb Haemost, 1980,
2. Siegal T, Seligsohn U, Aghai E, et al, "Clinical and Laboratory
Aspects of Disseminated Intravascular Coagulation (DIC): A Study
of 118 Cases,"Thromb Haemost, 1978, 39(1):122-34.
3. Sakakibara Y, Takeda T, Hori M, et al, "Disseminated Intravascular
Coagulation in Aortic Aneurysms: Assessment of Consumption Site
Using Labeled-Platelet Scintigraphy,"Thorac Cardiovasc Surg,
4. Chuansumrit A, Hotrakitya S, Sirinavin S, et al, "Disseminated
Intravascular Coagulation Findings in 100 Patients,"J Med Assoc
Thai, 1999, 82(Suppl 1):S63-8.
5. Gilbert JA and Scalzi RP, "Disseminated Intravascular Coagulation,"Emerg
Med Clin North Am, 1993, 11(2):465-80.
6. Wada H, Sakuragawa N, Mori Y, et al, "Hemostatic Molecular Markers
Before the Onset of Disseminated Intravascular Coagulation,"Am
J Hematol, 1999, 60(4):273-8.
7. Eisele B and Lamy M, "Clinical Experience With Antithrombin
III Concentrates in Critically Ill Patients With Sepsis and Multiple
Organ Failure,"Semin Thromb Hemost, 1998, 24(1):71-80.
Baglin T, "Disseminated Intravascular Coagulation: Diagnosis and
Treatment,"BMJ, 1996, 312(7032):683-7.
Levi M and ten Cate H, "Disseminated Intravascular Coagulation,"N
Engl J Med, 1999, 341(8):586-92.
Marder VJ, Feinstein DI, Francis CW, et al, "Consumptive Thrombohemorrhagic
Disorders,"Hemostasis and Thrombosis: Basic Principles and Clinical
Practice, 3rd ed, Chapter 52, Colman RW, Hirsh J, Marder VJ,
et al, eds, Philadelphia, PA: Churchill Livingstone, 1994, 1023-63.