CTPA of patient with PE Pulmonary Embolism
The patient's diagnosis was made based on the CT pulmonary angiogram (CTPA) of the chest, which revealed multiple thrombi extending into the lobar and segmental/ subsegmental branches of the right and left pulmonary arteries. Venous Doppler ultrasonography of both lower extremities was negative for deep vein thrombosis. A CT scan of the abdomen and pelvis with contrast did not reveal any thrombi in the pelvic veins. Venous Doppler ultrasonography of the upper extremities was not performed, as upper extremity thrombi are less common than lower extremity deep venous thrombi.
Pulmonary embolism is a serious and potentially fatal complication of thrombus formation within the deep venous circulation. Pulmonary embolism is the third leading cause of death in the United States, with approximately 650,000 patients developing pulmonary embolism each year. Most cases are not recognized antemortem; up to 80% of cases are diagnosed at autopsy.
The pathophysiology of pulmonary embolus is thought to result from obstructed pulmonary blood flow. Air, amniotic fluid, foreign bodies, parasite eggs, septic emboli, and tumor cells can all embolize in the pulmonary vasculature. The most common embolus is a thrombus, which can form anywhere in the venous system. The most common site for thrombus formation is in the deep veins of the lower extremities. The risk factors for thrombus formation are venous stasis, hypercoagulable state, and vessel wall (endothelial) damage (known as the Virchow triad). Several factors predispose individuals to an increased risk of pulmonary embolism, including an age of over 40 years, obesity, congenital thrombophilia, smoking, cancer, and pregnancy. The risk is also increased by use of oral contraceptives.
Although the presentation of pulmonary embolus can be extremely variable, the typical presentation includes dyspnea, cough, fever, leg pain and swelling, and chest pain. As the thrombus progresses, patients may develop apprehension, diaphoresis, palpitations, nausea, vomiting, chills, and syncope. If patients remain untreated, they may develop syncope, cyanosis, diaphoresis, tachycardia, hypotension, and shock. Less common signs include hemoptysis, atelectasis, wheezing, pleural friction rub, rales, accentuated S2 or S3, tricuspid regurgitation, jugular venous distension, and acute right ventricular strain. Signs of acute right ventricular strain that may be seen on an electrocardiogram include an S-wave in lead I, a Q-wave in lead III, and a T-wave in lead III. Right axis deviation and partial or complete right bundle branch block may also be noted.
The differential diagnosis of pulmonary embolism includes dissecting aortic aneurysm, pneumonia, acute bronchitis, bronchial carcinoma, pericardial or pleural disease, heart failure, costochondritis, pleurisy, pneumothorax, mucus plug, and myocardial ischemia.
Routine laboratory tests have limited value in the diagnosis of pulmonary embolism. Arterial blood gas may reveal hypoxemia, hypocapnia, and respiratory alkalosis with an elevated A-a gradient. A positive D-dimer is not specific for pulmonary embolism, but a negative D-dimer has a 95% negative predictive value; therefore, it is useful in ruling out pulmonary embolism in those with a low pretest probability of disease. Coagulation studies and coagulopathy workup are not useful in the diagnosis of pulmonary embolism, but they may be necessary once the diagnosis has been established to rule out an underlying hypercoagulable condition.
The gold standard for diagnosing pulmonary embolism has been pulmonary angiography; however, CTPA is rapidly gaining in popularity for diagnosing pulmonary embolism, with a sensitivity of 85-94%, and it is likely to become the new gold standard. Spiral CT scanning is less invasive and more available than pulmonary angiography. A ventilation-perfusion scan can be useful in ruling out pulmonary embolism, but it may be less useful in diagnosing pulmonary embolism because many clinical conditions can lead to defects in the perfusion scan as a result of decreased blood flow. A ventilation-perfusion scan is now generally done only when CT angiography is contraindicated. Chest radiography is usually performed, but it is rarely diagnostic and is often completely normal. An ECG is typically obtained to rule out alternative causes of chest pain/dyspnea, but it is also not of much diagnostic value in pulmonary embolism itself. The most common ECG abnormalities in pulmonary embolus include sinus tachycardia and nonspecific T-wave changes. Although the classic S1Q3T3 pattern was noted in hindsight in this patient, especially with return visits, it is not frequently seen.
The treatment for pulmonary embolism falls into 2 categories. The first category includes patients who are hemodynamically stable. For these patients, anticoagulation and prevention of recurrent pulmonary embolism are vital. Anticoagulation is initially obtained with the use of heparin, fondaparinux, or low molecular weight heparin (LMWH). After initial anticoagulation is started, warfarin may be commenced. Bridging with heparin or LMWH for the first 5 days of warfarin therapy, until a therapeutic international normalized ratio (INR; therapeutic range, 2-3) is achieved is necessary. To prevent recurrent pulmonary embolisms, inferior vena cava or other intravenous filters can be placed.
The second category of treatment addresses hemodynamically unstable patients. For these patients, there are 2 major treatment options. The first is direct removal of the clot, through surgical embolectomy or catheter-based extraction by an interventional radiologist. Surgical embolectomy should only be used in patients with contraindications to thrombolytics or failed thrombolytics, or in whom surgery may be the only chance for survival. The second form of treatment is thrombolysis. Although thrombolysis has not been shown to improve mortality, it is often readily available in EDs. Indications for thrombolytic therapy include patients with shock, right heart failure, underlying cardiopulmonary disease, recent pulmonary emboli, or severe pulmonary hypertension. Thrombolytics may cause significant bleeding, including central nervous system bleeding, and they should only be used in appropriate circumstances where the risk/benefit ratio is favorable.
Contraindications of thrombolysis include recent or suspected cerebrovascular accident, intracranial trauma or surgery within the past 2 months, active intracranial disease, major internal bleeding within the past 6 months, uncontrolled hypertension, bleeding diathesis/coagulopathy, recent major surgery within 10 days, recent trauma, infective endocarditis/pericarditis, pregnancy, aortic aneurysm or hemorrhagic retinopathy.
The patient (CT above) was admitted to the intensive care unit and started on LMWH and warfarin. Given the subacute nature of his symptoms and his apparent stability, thrombolytics were not initially administered. The patient's oxygen saturation and symptoms continued to improve during his hospitalization and further laboratory studies, including antinuclear antibody (ANA) , protein C and S, prothrombin mutation, factor V Leiden, lupus anticoagulant, and phosphatidyl antibody, were initiated. He was discharged once his INR was therapeutic at a range of 2-3 and followed up in an anticoagulation clinic to maintain a therapeutic INR. All coagulation panel labs were negative, and he has not had a recurrence of the pulmonary embolism. A CT scan of his chest, abdomen, and pelvis done 1 month after initiation of therapy revealed an approximate 95% decrease in the size of the emboli seen in the left pulmonary artery and an almost 80% decrease in the pulmonary emboli seen in the right pulmonary artery. The embolic source was never identified.
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