Pulmonary Infarction Due to Pulmonary Embolism
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SYMPTOMS TO DIAGNOSIS GREGORY W. RUTECKI, MD, Section Editor MELDA SONMEZ, MD LOUTFI S. ABOUSSOUAN, MD CAROL FARVER, MD Medical Student, Koc University Department of Pulmonary, Allergy, and Critical Care Department of Pathology, Cleveland Clinic; Professor of School of Medicine, Istanbul, Turkey Medicine, Cleveland Clinic; Associate Professor of Medicine, Pathology, Cleveland Clinic Lerner College of Medicine Cleveland Clinic Lerner College of Medicine of Case Western of Case Western Reserve University, Cleveland, OH Reserve University, Cleveland, OH SUDISH C. MURTHY, MD, PhD ROOP KAW, MD Department of Thoracic and Cardiovascular Departments of Hospital Medicine and Outcomes Research Surgery, Cleveland Clinic; Professor of Surgery, Anesthesiology, Cleveland Clinic; Associate Professor of Cleveland Clinic Lerner College of Medicine of Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Case Western University, Cleveland, OH Pulmonary infarction due to pulmonary embolism 76-year-old man whose history included □ It is rarely, if ever, associated with A abdominal aortic aneurysm repair, bilat- pulmonary embolism eral femoral artery bypass for popliteal artery □ Most patients with pleural effusion due to aneurysm, hypertension, and peptic ulcer pulmonary embolism do not have disease was admitted to a community hospi- pleuritic chest pain tal with pleuritic chest pain and shortness of □ Pulmonary embolism should be excluded breath. Two days earlier, he had undergone in all cases of pleural effusion without a repair of a ventral hernia. clear cause At the time of that admission, he reported Pulmonary embolism should be excluded in no fever, chills, night sweats, cough, or his- all cases of pleural effusion that do not have tory of heart or lung disease. His vital signs were normal, and physical examination had a clear cause. As for the other answer choices: A 76-year-old revealed no apparent respiratory distress, • Pulmonary embolism is the fourth lead- no jugular venous distention, normal heart ing cause of pleural effusion in the United man is admitted States, after heart failure, pneumonia, and sounds, and no pedal edema; however, de- 1 with pleuritic creased air entry was noted in the right lung malignancy. • About 75% of patients who develop pleural chest pain base. Initial serum levels of troponin and N- terminal pro-B-type natriuretic peptide were effusion in the setting of pulmonary embo- and shortness normal. lism complain of pleuritic chest pain on the 2 At that time, computed tomographic an- side of the effusion. Most effusions are uni- of breath 3 giography of the chest showed segmental pul- lateral, small, and usually exudative. 48 hours monary emboli in the left upper and right low- ■ after surgery er lobes of the lungs and right pleural effusion. EVALUATION BEGINS: Transthoracic echocardiography showed nor- RESULTS OF THORACENTESIS mal atrial and ventricular sizes with no right Our patient continued to receive intravenous or left ventricular systolic dysfunction and a heparin. left ventricular ejection fraction of 59%. He underwent thoracentesis on hospital Treatment with intravenous heparin was day 3, and 1,000 mL of turbid sanguine- started, and the patient was transferred to our ous pleural fl uid was removed. Analysis of hospital. the fl uid showed pH 7.27, white blood cell count 3.797 × 109/L with 80% neutrophils, ■ PLEURAL EFFUSION and lactate dehydrogenase (LDH) concen- AND PULMONARY EMBOLISM tration 736 U/L (a ratio of pleural fl uid LDH to a concurrent serum LDH > 0.6 is sugges- Which of the following is true about pleu- tive of an exudate); the fl uid was also sent 1ral effusion? for culture and cytology. Thoracentesis was doi:10.3949/ccjm.85a.17132 terminated early due to cough, and follow- 848 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 85 • NUMBER 11 NOVEMBER 2018 Downloaded from www.ccjm.org on October 2, 2021. For personal use only. All other uses require permission. SONMEZ AND COLLEAGUES up chest radiography showed a moderate- sized pneumothorax. Computed tomography (CT) of the chest at this time showed a small wedge-shaped area of lung consolidation in the right lower lobe (also seen on CT done 1 day before admission to our hospital), with an intrinsic air-fl uid level suggesting a focal infarct or lung abscess, now obscured by adjacent consolidation and atelectasis. In the interval since the previous CT, the multiloculated right pleural effusion had increased in size (Figure 1). ■ THE NEXT STEP What is the most appropriate next step for 2this patient? □ Consult an interventional radiologist for Figure 1. Computed tomography shows a wedge-shaped chest tube placement area of low attenuation suggesting a focal infarction in the □ Start empiric antibiotic therapy and ask collapsed and consolidated right lower lobe. an interventional radiologist to place a chest tube guineous but not frankly bloody, and therefore □ Start empiric antibiotic therapy, withhold we judged that it was not necessary to stop his anticoagulation, and consult a thoracic heparin. surgeon □ Start empiric antibiotic therapy and ■ HOW DOES PULMONARY INFARCTION consult a thoracic surgeon while PRESENT CLINICALLY? On thoracentesis, continuing anticoagulation 1,000 mL The most appropriate next step is to start em- Which of the following statements about piric antibiotic therapy and consult a thoracic 3pulmonary infarction is incorrect? of turbid surgeon while continuing anticoagulation. □ Cavitation and infarction are more sanguineous In this patient, it is appropriate to initiate common with larger emboli pleural fl uid antibiotics empirically on the basis of his sig- □ Cavitation occurs in fewer than 10% nifi cant pleural loculations, a wedge-shaped of pulmonary infarctions was removed consolidation, and 80% neutrophils in the □ Lung abscess develops in more than 50% pleural fl uid, all of which suggest infection. of pulmonary infarctions The unmasking of a wedge-shaped consoli- □ Pulmonary thromboembolism is the most dation after thoracentesis, with a previously common cause of pulmonary infarction noted air-fl uid level and an interval increase in multiloculated pleural fl uid, raises suspicion Lung abscess develops in far fewer than 50% of a necrotic infection that may have ruptured of cases of pulmonary infarction. The rest of into the pleural space, a possible lung infarct, the statements are correct. or a malignancy. Hence, simply placing a chest Cavitation complicates about 4% to 7% tube may not be enough. of infarctions and is more common when Blood in the pleural fl uid does not neces- the infarction is 4 cm or greater in diam- sitate withholding anticoagulation unless the eter.4 These cavities are usually single and bleeding is heavy. A pleural fl uid hematocrit predominantly on the right side in the api- greater than 50% of the peripheral blood he- cal or posterior segment of the upper lobe or matocrit suggests hemothorax and is an in- the apical segment of the right lower lobe, dication to withhold anticoagulation.1 Our as in our patient.5–8 CT demonstrating scal- patient’s pleural fl uid was qualitatively san- loped inner margins and cross-cavity band CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 85 • NUMBER 11 NOVEMBER 2018 849 Downloaded from www.ccjm.org on October 2, 2021. For personal use only. All other uses require permission. PULMONARY INFARCTION ter decortication, resection of the lung abscess, and closure of the bronchopleural fi stula. No signifi cant air leak was noted after resection of this segment of lung. Pathologic study showed acute organizing pneumonia with abscess formation; no malig- nant cells or granulomas were seen (Figure 2). Pleural fl uid cultures grew Streptococcus inter- medius, while the tissue culture was negative for any growth, including acid-fast bacilli and fungi. On 3 different occasions, both chest tubes were shortened, backed out 2 cm, and rese- cured with sutures and pins, and Heimlich valves were applied before the patient was dis- charged. Intravenous piperacillin-tazobactam was Figure 2. Infarcted lung with alveoli, ischemic necrosis, and started on the fi fth hospital day. On discharge, a fi brinous exudate on pleural surface (arrow) (hematoxy- lin and eosin, x 12.5). the patient was advised to continue this treat- ment for 3 weeks at home. The patient was receiving enoxaparin sub- shadows suggests a cavitary pulmonary in- cutaneously in prophylactic doses; 72 hours farction.9,10 after the thorascopic procedure this was in- Infection and abscess in pulmonary in- creased to therapeutic doses, continuing after farction are poorly understood but have been discharge. Bridging to warfarin was not ad- linked to larger infarctions, coexistent conges- vised in view of his chest tubes. tion or atelectasis, and dental or oropharyn- Our patient appeared to have developed The abscess geal infection. In an early series of 550 cases of a right lower lobe infarction that cavitated was resected, pulmonary infarction, 23 patients (4.2%) de- and ruptured into the pleural space, caus- the fi stula veloped lung abscess and 6 (1.1%) developed ing a bronchopleural fi stula with empyema empyema.11 The mean time to cavitation for after a recent pulmonary embolism. Other was closed, an infected pulmonary infarction has been re- reported causes of pulmonary infarction in and chest tubes ported to be 18 days.12 pulmonary embolism are malignancy and A reversed halo sign, generally described heavy clot burden,6 but these have not been were placed as a focal, rounded area of ground-glass opac- confi rmed in subsequent studies.5 Malig- ity surrounded by a nearly complete ring of nancy was ruled out by biopsy of the resect- consolidation, has been reported to be more ed portion of the lung, and our patient did frequent with pulmonary infarction than with not have a history of heart failure. A clear other diseases, especially when in the lower cavity was not noted (because it ruptured lobes.13 into the pleura), but an air-fl uid level was described in a wedge-shaped consolidation, ■ CASE CONTINUED: THORACOSCOPY suggesting infarction.