Diagnosing Disseminated Intravascular Coagulopathy in Acute Promyelocytic Leukemia

Beth McCraw, ARNP, ACNS-BC, OCN; Debra E. Lyon, RN, PhD, FNP


Clin J Oncol Nurs. 2008;12(5):717-720. 

In This Article


Physical Assessment

Clinical manifestations of DIC are highly variable and complex. Vital signs may demonstrate a normal or increased temperature, tachycardia, hypotension, or tachypnea (Murphy-Ende & Chernecky, 2002). Initial signs and symptoms often are subtle and may go unnoticed until a catastrophic event occurs, such as a cerebral vascular accident, myocardial infarction, massive hemorrhage, or acute renal failure. The mortality rate in a patient with DIC is greater than 75% (Ferri, 2007). For this reason, a thorough assessment of the patient with APL is essential for early recognition of DIC. Generally, the initial sign of acute DIC presents in hemorrhagic form. Often, the DIC patient will have bleeding from three unrelated sites (McCance & Huether, 2006). Symptoms may present as hemorrhagic or embolic events, but microvascular and macrovascular clotting cause irreversible damage (Holmes-Gobel, 2002). Signs and symptoms of DIC are presented by system.

Integumentary. Patients may exhibit oozing from previous venipuncture sites, IV or arterial lines, or from surgical wounds. Bleeding mucous membranes, such as epistaxis may be noted, along with bleeding from the sclera and conjunctiva. Often ecchymotic lesions such as petechiae and purpura will occur. Microvascular thrombosis may be manifested by symmetrical cyanosis of the fingers and toes, which can lead to gangrene and subsequent amputation (Geiter, 2003; McCance & Huether, 2006). Jaundice also may occur because of hemorrhage related to excessive release of bilirubin (Holmes-Gobel, 2002).

Neurologic. Manifestations may include an altered level of consciousness and changes in behavior or mental status (Geiter, 2003). An excruciating headache, often described as the worst headache the patient has ever experienced, is sometimes reported (Murphy-Ende & Chernecky, 2002). Patients may exhibit onset of new seizure activity or confusion (McCance & Huether, 2006). Because of microembolisms, patients may experience a cerebral vascular accident, exhibiting signs and symptoms of a stroke such as aphasia, facial droop, or motor weakness.

Cardiovascular. Signs and symptoms of hemodynamic instability may ensue because of a decrease of intravascular volume related to hemorrhage. If the patient becomes acidotic, the shift in electrolytes may lead to cardiac arrhythmias (Teal, 2007). The patient may have tachycardia, hypotension, and hypoxia. Patients may complain of chest pain or experience myocardial infarction.

Pulmonary. Pulmonary embolus or acute respiratory distress syndrome may result from hypoxia (Geiter, 2003). Patients may exhibit dyspnea, tachypnea, and desaturation of oxygen levels, as well as extreme anxiety. Hemorrhagic signs of the pulmonary system such as cough and hemoptysis may occur.

Gastrointestinal. Gastrointestinal (GI) bleeding may occur, resulting in signs and symptoms of shock. Physical examination may reveal abdominal tenderness and rigidity, hematemesis, rectal bleeding, and melena (Murphy-Ende & Chernecky, 2002). GI signs and symptoms may include hypoactive or absent bowel sounds. If thrombosis occurs, the patient may develop ischemia to the bowels, exhibiting high-pitched or tinkling bowel sounds above the area of infarction (Teal, 2007).

Renal. Hemorrhage or thrombosis may result in oliguria (less than 0.5 ml/kg/hr) or hematuria. Acute tubular necrosis and proteinuria may lead to further development of electrolyte imbalances, resulting in acidosis (Teal, 2007).

Laboratory Data

No single blood test can definitively diagnose DIC. Multiple blood tests are examined, including platelet count, fibrin degradation products (FDP), D-dimer, fibrinogen, prothrombin time, activated partial prothrombin time, thrombin time, blood smear, factor VII, and antithrombin III (Teal, 2007). FDP and D-dimer levels are the most reliable tests for DIC, the D-dimer level is the most specific (Holmes-Gobel, 2002; McCance & Huether, 2006). Table 1 reviews laboratory results in the presence of DIC.

Fibrinogen degradation products: Although FDPs may be elevated in conditions other than DIC, 85%-100% of patients diagnosed with DIC demonstrate some degree of elevation in FDP levels (McCance & Huether, 2006). FDPs have anticoagulant properties. Exceptionally high levels of FDPs are found during acute DIC because of the rapid formation and breakdown of fibrin clots, producing an anticoagulant effect (Teal, 2007).

D-dimer: Along with the FDP assay, the D-dimer is the most reliable index for diagnosing DIC. Normally, the D-dimer level is low because the body maintains a homeostasis of clot formation and subsequent clot degradation. During DIC, the D-dimer is elevated, demonstrating an increased level of fibrin formation. Because of increased levels of fibrin, the body attempts to maintain a balance by increasing fibrin dissolution. D-dimer is produced by plasmin lysis of cross-linked fibrin clots only, not of the fibrinogen that is unclotted; therefore, the D-dimer is an indicator of fibrin formation rather than fibrin degradation (Holmes-Gobel, 2002; McCance & Huether, 2006).


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