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1 2 days Improvement in the platelet count may lag as much as 1 week behind control of the coagulopathy In replacement therapy, platelet transfusion should be used to maintain a platelet count greater than 30,000/mcL, and 50,000/mcL if possible Fibrinogen is replaced with cryoprecipitate, and the aim is for a plasma fibrinogen level of 150 mg/dL One unit of cryoprecipitate usually raises the fibrinogen level by 6 8 mg/dL, so that 15 units of cryoprecipitate will raise the level from 50 to 150 mg/dL Coagulation factor deficiency may require replacement with fresh-frozen plasma In some cases, when DIC is complicated by excessive fibrinolysis, even the combination of heparin and replacement therapy may not be adequate to control bleeding In these cases, EACA, 1 g intravenously per hour, may be added to decrease the rate of fibrinolysis, raise the fibrinogen level, and control bleeding EACA should not be used without heparin in DIC because of the risk of thrombosis Although infusions of large doses of antithrombin III have not reduced the mortality rate of severe sepsis complicated by DIC, one large trial has shown benefit for the use of activated protein C



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by the liver and thus may be elevated in hepatic dysfunction Hypofibrinogenemia is another important diagnostic laboratory feature, because only a few other disorders (congenital hypofibrinogenemia, severe liver disease) will lower the fibrinogen level In some cases of DIC, when the patient s baseline fibrinogen level is markedly elevated, the initial fibrinogen level may be normal However, since the half-life of fibrinogen is approximately 4 days, a declining fibrinogen level will confirm the diagnosis of DIC The PTT may or may not be prolonged In approximately 25% of cases, a microangiopathic hemolytic anemia is present, and fragmented red blood cells are seen on the peripheral smear Antithrombin III levels may be markedly depleted When fibrinolysis is activated, levels of plasminogen and 2-antiplasmin may be low Subacute DIC produces a very different laboratory picture Thrombocytopenia and elevated d-dimer are usually the only abnormalities Fibrinogen levels are normal, and the PTT may be normal





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Liver disease may prolong both the PT and PTT, but fibrinogen levels are usually normal, and the platelet count is usually normal or only slightly reduced However, severe liver disease may be difficult to distinguish from DIC Vitamin K deficiency will not affect the fibrinogen level or platelet count and will be completely corrected by vitamin K replacement Sepsis may produce thrombocytopenia and digital ischemia, and coagulopathy may be present because of vitamin K deficiency However, in these cases, the fibrinogen level should be normal TTP may produce fever and microangiopathic hemolytic anemia However, fibrinogen levels and other coagulation studies should be normal

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Franchini M et al Update on the treatment of disseminated intravascular coagulation Hematology 2004 Apr;9(2):81 5 [PMID: 15203862] Hoffmann JN et al Effect of long-term and high-dose antithrombin supplementation on coagulation and fibrinolysis in patients with severe sepsis Crit Care Med 2004 Sep;32(9): 1851 9 [PMID: 15343012]

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The CompTIA Network+ certification exam expects you to know how to 46 Given a scenario, implement [an appropriate] network troubleshooting methodology 51 Given a scenario, select the appropriate command line interface tool and interpret the output to verify functionality 52 Explain the purpose of network scanners 53 Given a scenario, utilize the appropriate hardware tools To achieve these goals, you must be able to Describe appropriate troubleshooting tools and their functions Analyze and discuss the troubleshooting process Tackle a variety of troubleshooting scenarios

Most cases of thromboembolism likely result from a convergence of an underlying genetic predisposition and acquired precipitating events such as immobilization, pregnancy, or surgery (Table 13 24)

The primary focus should be the diagnosis and treatment of the underlying disorder that has given rise to DIC DIC will often produce laboratory abnormalities with only mild clinical manifestations, and in these cases no specific therapy is required When the underlying cause of DIC is rapidly reversible (such as in obstetric cases), replacement therapy alone may be indicated The role of heparin in the treatment of DIC is controversial In some cases, when any increase in bleeding is unacceptable (neurosurgical procedures), heparin therapy is contraindicated However, when DIC is producing serious clinical consequences and the underlying cause is not rapidly reversible, heparin may be helpful One clear indication for heparin therapy is the presence of thrombosis or fibrin deposition leading to acral cyanosis In using heparin, a dose of 500 750 units per hour is usually sufficient Heparin cannot be effective if antithrombin III levels are markedly depleted Antithrombin III levels should be measured, and fresh-frozen plasma or concentrates of antithrombin III used to raise levels to greater than 50% In using heparin, it is not necessary to prolong the PTT Successful therapy is indicated by a rising fibrinogen level Fibrin degradation products will decline over

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