Surgical Treatment of Acute and Chronic Pulmonary Embolism

Clinical Presentation

Acute PE usually manifests suddenly. Symptoms and signs vary with the extent of blockage, the magnitude of the humoral response, and the pre-embolus reserve of the cardiac and pulmonary systems of the patient. The acute disease is stratified into submassive or massive embolism on the basis of hemodynamic stability, arterial blood gases, and lung scan or angiographic assessment of the percentage of blocked pulmonary arteries.

With submassive embolism, patients present with sudden, unexplained anxiety, tachypnea or dyspnea, pleuritic chest pain, and occasionally streak hemoptysis. Examination can reveal tachycardia, rales, low-grade fever, and a pleural rub. Heart sounds are often normal, but sometimes the pulmonary second sound is increased.

Massive PE is truly life threatening and is defined as a PE that causes hemodynamic instability and low cardiac output (<1.8 L/m ² / min). It usually is associated with occlusion of more than 50% of the pulmonary vasculature. In addition to the above symptoms, patients might lose consciousness, and cardiac arrest can occur. Neck veins are distended, and central venous pressure is elevated. Room air blood gases show severe hypoxia and hypocarbia with acidosis. Urine output falls; peripheral pulses and perfusion are poor.

Diagnosis

The clinical diagnosis of acute PE is unreliable. Differentiation of major or massive PE from acute myocardial infarction, aortic dissection, septic shock, and other catastrophic states is difficult and uncertain. A plain chest x-ray, an electrocardiogram, and insertion of a bedside Swan–Ganz catheter can add confirmatory information but might not necessarily prove the diagnosis.

Ventilation/perfusion ( $\dot{\text{V}}/\dot{\text{Q}}$ ) scans provide confirmatory evidence, but they may be unreliable, because pneumonia, atelectasis, and previous pulmonary emboli can cause a mismatch in ventilation and perfusion and mimic positive results. $\dot{\text{V}}/\dot{\text{Q}}$ scans lack specificity but have high sensitivity, and thus a negative $\dot{\text{V}}/\dot{\text{Q}}$ scan essentially excludes the diagnosis of clinically significant PE.

Conventional pulmonary angiograms provide the most definitive diagnosis, but collapse of the circulation might not allow time for this procedure.

Computed tomography angiography is a better noninvasive method for diagnosing pulmonary emboli and provides specific information regarding flow within the pulmonary vasculature. Because of its current general availability, it has become the gold standard for diagnosing acute PE.

Transthoracic or transesophageal echocardiography can provide reliable information about the presence or absence of major thrombi obstructing right-sided chambers or the main pulmonary artery and allow detection of right ventricular volume or contractile abnormalities.

Right ventricular dysfunction as evidenced by elevated brain natriuretic peptide (BNP) and troponin levels or hyponatremia have all been found to predict increased mortality, as is the presence of a DVT and right ventricular or atrial clot.

Management of Acute Pulmonary Embolism

Submassive PE allows sufficient time to definitively establish the diagnosis and to attempt pharmacologic therapy and possibly removal of embolic material by catheter methods. The mainstay of treatment for these patients is anticoagulation and support of the cardiorespiratory system and should take place in an intensive care unit (ICU) setting. Heparin is started to prevent propagation and formation of new thromboembolic material, allowing the patient’s own fibrinolytic system to lyse fresh thrombi over a period of days or weeks. Systemic or, if possible, pulmonary artery catheter–directed lytic therapy (streptokinase or recombinant tissue plasminogen activator) increases the rate of lysis of fresh thrombi and is recommended in patients with a stable circulation and no contraindications, but it carries a higher risk of bleeding complications. Contraindications to the use of these agents include fresh surgical wounds, recent stroke, peptic ulcer, anemia, or bleeding disorders.

Management of Massive Pulmonary Embolism

Eleven percent of patients with fatal PE die within the first hour, up to 80% within 2 hours, and 85% within 6 hours, and thus time is of paramount importance. To a great extent, circumstances and the timely availability of necessary equipment and personnel determine therapeutic options. Factors such as advanced age, irreversible underlying health problems, and the likelihood of brain damage also enter into decision making. A decision to treat medically in an effort to stabilize the circulation at a survival level can preempt life-saving surgery, but it also might make surgery unnecessary. Sometimes surgical treatment is not available immediately; at other times, deteriorating patients are referred to surgery too late after failing medical therapy. The relative infrequency of treatment opportunities in massive PE, mitigating factors, and the lack of clear criteria for prescribing medical or surgical therapy leave the management of massive PE unsettled.

In otherwise healthy patients in whom surgery poses little risk or morbidity, emergency thromboembolectomy with preoperative confirmation of the diagnosis in the operating room by transesophageal echocardiography offers the best chance of survival. When surgery is not immediately available or in patients who might not be surgical candidates or in whom an alternative diagnosis seems more likely, emergency peripheral extracorporeal life support (ECLS) is an attractive alternative. ECLS compensates for acute right heart failure and hypoxia and sustains the circulation until the clot partially lyses, pulmonary vascular resistance falls, and pulmonary blood flow becomes adequate.