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thrombin is bypassed, the platelet count is normal unlike the platelet count in DIC. Yet all other parts of the DIC coagulation profile are abnormal. There is controversy as to whether primary fibrinolysis is a disease entity unto itself or rather just a continuum in the vicious DIC cycle.

Clinical Symptoms and Laboratory Results in Acute Disseminated Intravascular Coagulation

In hemorrhagic episodes, most patients have extensive skin and mucous membrane bleeding, including ecchy-mosis, epistaxis, and petechiae. Areas of entry such as surgical incisions, catheters, or venipuncture sites may also ooze and must be carefully observed. In thrombotic episodes, patients may exhibit acrocyanosis, hypotension, or shock. Microthrombi may occur in the nose, genitalia or digits, or major organs such as kidney, liver, or brain.

Acute DIC is a medical emergency. The entire basic DIC coagulation profile is abnormal (Table 18.3). PT and PTT are prolonged, fibrinogen and platelets are decreased, and FDPs and D-dimers are dramatically increased. D-dimer results are an essential piece of data in emerging DIC patients; however, other pathologies such an inflammation, renal disease, or local clot may elevate the result.10 For this reason, all laboratory data must be carefully reviewed in concert with clinical symptoms before reaching the diagnosis. It has been shown that not all patients in DIC have decreased fib-rinogen levels. Indeed, recent studies have shown that for those patients exhibiting DIC but near normal fibrinogen, clinical outcomes were much poorer, resulting in severe organ failure.11 Recovering patients should be monitored over time using the same initial profile for comparison and evaluation of their coagulation status. The patient will develop a microangiopathic hemolytic anemia due to microthrombi disposition in the small vessels. Schistocytes will be observed as a morphological marker for this process.

Table 18.3 O Disseminated Intravas cular Coagulation Laboratory Profile

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