Pulmonary infarction due to pulmonary embolism

Abstract

A 76-year-old man whose history included abdominal aortic aneurysm repair, bilateral femoral artery bypass for popliteal artery aneurysm, hypertension, and peptic ulcer disease was admitted to a community hospital with pleuritic chest pain and shortness of breath. Two days earlier, he had undergone repair of a ventral hernia.At the time of that admission, he reported no fever, chills, night sweats, cough, or history of heart or lung disease. His vital signs were normal, and physical examination had revealed no apparent respiratory distress, no jugular venous distention, normal heart sounds, and no pedal edema; however, decreased air entry was noted in the right lung base. Initial serum levels of troponin and Nterminal pro-B-type natriuretic peptide were normal.At that time, computed tomographic angiography of the chest showed segmental pulmonary emboli in the left upper and right lower lobes of the lungs and right pleural effusion. Transthoracic echocardiography showed normal atrial and ventricular sizes with no right or left ventricular systolic dysfunction and a left ventricular ejection fraction of 59%.Treatment with intravenous heparin was started, and the patient was transferred to our hospital. ■ PLEURAL EFFUSION AND PULMONARY EMBOLISM1 Which of the following is true about pleural effusion? □ It is rarely, if ever, associated with pulmonary embolism □ Most patients with pleural effusion due to pulmonary embolism do not have pleuritic chest pain □ Pulmonary embolism should be excluded in all cases of pleural effusion without a clear cause Pulmonary embolism should be excluded in all cases of pleural effusion that do not have a clear cause. As for the other answer choices: • Pulmonary embolism is the fourth leading cause of pleural effusion in the United States, after heart failure, pneumonia, and malignancy. 1 • About 75% of patients who develop pleural effusion in the setting of pulmonary embolism complain of pleuritic chest pain on the side of the effusion. 2 Most effusions are unilateral, small, and usually exudative. 3 ■ EVALUATION BEGINS: RESULTS OF THORACENTESISOur patient continued to receive intravenous heparin. He underwent thoracentesis on hospital day 3, and 1,000 mL of turbid sanguineous pleural fl uid was removed. Analysis of the fl uid showed pH 7.27, white blood cell count 3.797 × 10 9 /L with 80% neutrophils, and lactate dehydrogenase (LDH) concentration 736 U/L (a ratio of pleural fl uid LDH to a concurrent serum LDH > 0.6 is suggestive of an exudate); the fl uid was also sent for culture and cytology. Thoracentesis was terminated early due to cough, and follow-

Pulmonary Embolism Presenting with Pulmonary Infarction: Update and Practical Review of Literature Data

“…Furthermore, PI can be complicated by lung infections that are difficult to control, leading to abscess formation and cavitation, which are related to various predisposing factors such as more extensive infarction, concomitant congestion, or atelectasis, and poor dental health [ 1 ]. For this reason, the initiation of empiric antibiotic therapy has been proposed as a reasonable therapeutic strategy in case of PI detection, to avoid further complications such as empyema or fistulae, which may require surgical therapy [ 48 ].…”

“…Based on the evaluation of some clinical cases available in the literature, PI still represents a diagnostic challenge with a negative impact on the survival rate in case of misdetection [ 48 , 50 ]. In this section, we summarize how diagnostic progress can translate into a management strategy for patients with PI.…”

“…Once PI is diagnosed, the therapeutic strategy should be aimed at treating the underlying cause and lowering the risk of its serious complications. In this regard, oxygen administration can be useful to prevent hypoxia [ 10 ] as well as antibiotic therapy should be considered to avoid infectious complications [ 48 ]. Whatever PE is the cause of PI, pharmacological treatment includes anticoagulant medication such as heparin followed by warfarin or other oral anticoagulants [ 10 , 16 ].…”

Pulmonary venous thrombosis of traumatic origin as cause of bilobar infarction

“…This relationship between pulmonary and bronchial circulation causes an overlap of vascular flow in the lung, in which oxygenation in central regions depends on both systems, but at the peripheral level it increases the dependence on pulmonary arterial circulation, making them more prone to heart attacks [2] , [3] . Pulmonary infarcts occur more frequently in the presence of pulmonary thromboembolism, with an approximate incidence of 10–30 % [4] , the clot causes a pulmonary arterial occlusion and generally in peripheral areas of the lung where the vessels are smaller than 3 mm, it can trigger a heart attack [5] , [6] .…”

Endotelial dysfunction in condition of neoplastic intoxication

“…Зважаючи на те, що тромбоз у онкологічних хворих трапляється частіше, частіше уражує великі судини та призводить до летальних наслідків, постає актуальне питання вивчення особливостей патогенезу тромбозу в цієї групи пацієнтів [6,11]. Причини різниці в кількості та якості тромбозів у онкохворих та інших груп пацієнтів описані недостатньо, але є перспективними для вивчення та запобігання даній патології [1,3,4,5,12,13,16,17].…”