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5 курс / Пульмонология и фтизиатрия / Principles_of_Pulmonary_Medicine_S_E_Weinberger.pdf

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angiography is now rarely performed for this indication (Fig. 13.3). In this technique, direct evaluation of the pulmonary arterial system to identify intraluminal thrombus is accomplished invasively by advancing a catheter through a jugular or femoral vein through the right heart and injecting radiographic contrast material directly into the pulmonary arteries. Compared with CTA, pulmonary angiography is invasive, more expensive, and requires higher doses of radiation; therefore, it is not recommended in a standard evaluation.

FIGURE 13.3 Positive results of pulmonary angiogram show occlusion of the

vessel supplying the left lower lobe. The area of density left mid-lung probably

represents pulmonary infarction. Source: (Courtesy Dr. Morris Simon.)

Although echocardiography is not useful for diagnosis of pulmonary embolism, it is commonly performed as a supplementary test to assess the impact of documented embolic disease on pulmonary artery pressure and right ventricular function. In addition, in a patient with suspected pulmonary embolism who is hemodynamically unstable, evidence of right ventricular failure on echocardiography serves as presumptive evidence that the hemodynamic instability is due to acute pulmonary thromboembolism unless another cause is implicated.

Treatment

In addition to supporting oxygenation and circulation as needed, the standard treatment of a pulmonary embolus involves prompt initiation of anticoagulant therapy, usually beginning with subcutaneous low- molecular-weight heparin (LMWH) or intravenous unfractionated heparin, followed by an oral agent administered for at least 3 to 6 months. LMWH has a number of potential advantages over unfractionated heparin, including a lower risk of heparin-induced thrombocytopenia and more reliable pharmacokinetics.

Consequently, in most cases, LMWH does not require frequent laboratory monitoring of coagulation tests

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to guide dosage adjustment, and it can be given subcutaneously in one or two daily doses, avoiding the need for continuous intravenous infusion. For many years, the only oral agents used to complete therapy were coumarin-derived vitamin K antagonists, such as warfarin, which required frequent laboratory monitoring and dose adjustments. However, many newer oral anticoagulants that do not require routine laboratory monitoring are now available. These newer agents include direct thrombin inhibitors (e.g., dabigatran) and factor Xa inhibitors (e.g., apixaban and rivaroxaban).

Therapeutic options for pulmonary embolism:

1.Anticoagulation (heparin, warfarin, direct thrombin inhibitors, factor Xa inhibitors)

2.Thrombolysis (tPA, streptokinase, urokinase)

3.Inferior vena caval filter

4.Catheter-based or surgical removal of the clot (embolectomy)

By far the most important aspect of treating pulmonary embolism is achieving prompt, adequate anticoagulation. For the most part, after a patient with an embolus that has already entered the pulmonary circulation has sought medical attention, the biggest danger derives from a recurrent embolus that leads to hemodynamic instability. Therefore, treatment in high-risk patients is frequently started before the diagnosis is confirmed.

The rationale for the use of anticoagulants is to prevent the formation of new thrombi or the propagation of existing thrombi (in the legs), not to dissolve clots that have already embolized to the lungs. In the setting of massive pulmonary embolism and hemodynamic compromise, pharmacologic and/or catheterbased mechanical options are available to dissolve, break up, or remove clots and decrease their hemodynamic impact. Thrombolytic agents, particularly recombinant tissue plasminogen activator (rtPA), can lyse recent blood clots; they are ideally given within the first hours after the embolic event but may have some effect even up to 2 weeks after the embolism. Catheter-based options to decrease clot burden include both local delivery of a thrombolytic agent and mechanical fragmentation or removal of the clot. Use of a thrombolytic agent or catheter-based intervention is then followed by standard anticoagulant therapy.

In some circumstances, the treatment of pulmonary embolism involves placement of a filtering device into the inferior vena cava (IVC), with the goal of trapping thrombi from the lower extremities en route to the pulmonary circulation. This type of device, often called an IVC filter, is used most frequently (1) if there are contraindications to anticoagulant therapy (e.g., bleeding problems), (2) if thromboemboli have recurred despite adequate anticoagulation, or (3) if the patient already has such limited pulmonary vascular reserve that an additional clot to the lungs likely would be fatal. If there is no contraindication, anticoagulation is continued after the device is in place to decrease the risk of clotting in the veins distal to the filter. Once in place, some filters can be removed once the need for the filter has resolved.

No discussion of the treatment of pulmonary embolism is complete without considering prophylactic methods to prevent deep venous thrombosis in the high-risk patient. For low-risk patients, external compression of the lower extremities with an intermittently inflating pneumatic device is considered. For higher risk patients, pharmacologic prophylaxis is used. Options include LMWH, unfractionated heparin, or fondaparinux administered subcutaneously in low dosage. Prophylaxis is generally used in patients following thoracic, abdominal, or orthopedic surgery and in a variety of other at-risk patients who are relatively immobile in the hospital. In situations such as high-risk orthopedic surgeries when prophylaxis needs to be continued beyond the inpatient setting, generally an oral agent is used.

Treatment

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