Lung infarction

Abstract: The aim of the present report is to describe abnormal 18F-fluorodeoxyglucose (FDG) accumulation patterns in the pleura and lung parenchyma in a group of lung cancer patients in whom lung infarction was present at the time of positron emission tomography (PET). Between November 2002 and December 2003, a total of 145 patients (102 males, 43 females; age range 38–85 years) were subjected to whole-body FDG PET for initial staging (n=117) or restaging (n=11) of lung cancer or for evaluation of solitary pulmonary nodules (n=17). Of these patients, 24 displayed abnormal FDG accumulation in the lung parenchyma that was not consistent with the primary lesion under investigation (ipsilateral n=12, contralateral n=9 or bilateral n=3). Without correlative imaging, this additional FDG uptake would have been considered indeterminate in differential diagnosis. Of the 24 patients who were identified as having such lesions, six harboured secondary tumour nodules diagnosed as metastases, while in three the diagnosis of a synchronous second primary lung tumour was established. Additionally, nine patients were identified as having post-stenotic pneumonia and/or atelectasis (n=6) or granulomatous lung disease (n=3). In the remaining six (4% of all patients), a diagnosis of recent pulmonary embolism that topographically matched the additional FDG accumulation (SUVmax range 1.4–8.6, mean 3.9) was made. Four of these six patients were known to have pulmonary embolism, and hence false positive interpretation was avoided by correlating the PET findings with those of the pre-existing diagnostic work-up. The remaining two patients were harbouring small occult infarctions that mimicked satellite nodules in the lung periphery. Based on histopathological results, the abnormal FDG accumulation in these two patients was attributed to the inflammatory reaction and tissue repair associated with the pathological cascade of pulmonary embolism. In patients with pulmonary malignancies, synchronous lung infarction may induce pathological FDG accumulation that can mimic active tumour manifestations. Identifying this potential pitfall may allow avoidance of false positive FDG PET interpretation.

Abstract: OBJECTIVES: Current knowledge of the pulmonary pathology of coronavirus disease 2019 (COVID-19) is based largely on postmortem studies. In most, the interval between disease onset and death is relatively short (<1 month). Information regarding lung pathology in patients who survive for longer periods is scant. We describe the pathology in three patients with severe COVID-19 who underwent antemortem examination of lung tissue at least 8 weeks after initial diagnosis. METHODS: We conducted a retrospective case series. RESULTS: The first patient developed acute respiratory failure and was started on extracorporeal membrane oxygenation (ECMO) on day 21, with subsequent hemothorax. Debridement (day 38) showed extensive lung infarction with diffuse alveolar damage and Candida overgrowth. The second patient developed acute respiratory failure requiring mechanical ventilation that did not improve despite ECMO. Surgical lung biopsy on day 74 showed diffuse interstitial fibrosis with focal microscopic honeycomb change. The third patient also required ECMO and underwent bilateral lung transplantation on day 126. The explanted lungs showed diffuse interstitial fibrosis with focal microscopic honeycomb change. CONCLUSIONS: This series provides histologic confirmation that complications of COVID-19 after 8 weeks to 4 months of severe disease include lung infarction and diffuse interstitial fibrosis.

Abstract: The value of ultrasound examination of the pleura and lungs remains highly underestimated to this day. While the ventilated lungs and the osseous skeleton of the thorax represent potent obstacles for ultrasound, a multitude of pathological processes of the chest wall, pleura, and lungs results in altered tissue composition, providing markedly increased access and visibility for sonographic examination. These conditions support the sonographic diagnosis of pleural and pulmonary disorders. However, the main value of pleura and lung ultrasonography is not the primary diagnosis of chest lesions but the follow up, differential diagnosis, detection of complications, such as abscesses and post embolic lung infarction, and guidance of diagnostic and therapeutic interventions in patients with pathological pleural and pulmonary findings. Punctures and drainages of fluids, e. g., haematothorax, empyema, chylothorax as well as biopsies of solid lesions can safely be performed under ultrasound-guidance. It is of special importance that pleura and lung ultrasonography, as a non-invasive method, can be repeated without discomfort or radiation exposure for the patient and is therefore valuable in the follow-up of pathological findings. Adequate interpretation of sonographic pleura and lung findings has to consider the patient's history, physical examination, chest X-ray and other results obtained by complementary imaging technologies (e. g. thoracic computed tomography).

Abstract: Purpose: The aim of this study was to identify factors predisposing to lung infarction in patients with pulmonary embolism (PE). Materials and Methods: We performed a retrospective analysis on 154 patients with the final diagnosis of PE being examined between January 2009 and December 2012 by means of a Toshiba Aquilion 64 CT scanner. The severity of clinical symptoms was defined by means of a clinical index with 4 classes. The pulmonary clot load was quantified using a modified severity index of PE as proposed by Miller. We correlated several potential predictors of pulmonary infarction such as demographic data, pulmonary clot burden, distance of total vascular obstruction and pleura, the presence of cardiac congestion, signs of chronic bronchitis or emphysema with the occurrence of pulmonary infarction. Results: Computed tomography revealed 78 areas of pulmonary infarction in 45/154 (29.2 %) patients. The presence of infarction was significantly higher in the right lung than in the left lung (p Conclusion: Neither cardiac congestion nor the degree of pulmonary vascular obstruction are main factors predisposing to pulmonary infarction in patients with PE. It seems that a peripheral total vascular obstruction more often results in infarction than even massive central clot burden. Key points: • A peripheral location of vascular occlusion is the main factor predisposing to pulmonary infarction. Citation Format: • Kirchner J, Obermann A, Stuckradt S et al. Lung Infarction Following Pulmonary Embolism: A Comparative Study on Clinical Conditions and CT Findings to Identify Predisposing Factors. Fortschr Rontgenstr 2015; 187: 440 – 444