Pulmonary infarction mimicking a lung mass: a case report.

Pulmonary infarction usually appears as a wedge-shaped opacity with its base placed laterally. Rarely, pulmonary infarctions may appear as a well-defined rounded opacity mimicking lung cancer and surgical lung biopsy may often be required for definitive diagnosis. We report a patient who was admitted with submassive pulmonary embolism who had an incidental finding of a well-defined opacity in computed tomography (CT) scan. The lesion was avid on positron emission tomography (PET) scan and the patient was a smoker. So, we investigated him further with a percutaneous and later a thoracoscopic lung biopsy. Tumour-like pulmonary infarction is often a challenge for the clinicians.

Pulmonary infarction caused by sarcoidosis vascular involvement: A case report.

Sarcoidosis is a systemic granulomatous disease. In pulmonary sarcoidosis, granulomatous vascular involvement is a common feature that occurs in all types of vessels, including large elastic arteries to venules, but sarcoidosis complicated with pulmonary infarction has not been reported. We report a case of a 60 years old female, who was operated on a clinical diagnosis of lung cancer, and histological examination revealed a pulmonary infarction and sarcoidosis. In the pulmonary elastic arteries, granulomas infiltrated the adventitia and media, and caused elastic fiber collapse and destruction. Arterial occlusion by granulomas was observed in the edge of the infarcted area. It was considered that the arterial sarcoidosis granuloma involvement was the cause of pulmonary infarction. Sarcoidosis is a significant risk factor for cardiovascular events. However, pulmonary infarction is an extremely rare complication of sarcoidosis. Our case suggests that sarcoidosis may cause vascular events in the lungs.

Infarct-Like Spindle Cell Carcinoma of the Lung: Clinicopathologic, Immunohistochemical, and Molecular Analysis of 4 Cases.

Pulmonary spindle cell carcinoma is a rare and aggressive malignancy that often mimics benign conditions. We report 4 cases that simulate a pulmonary infarction, 2 of which were misdiagnosed. Patients were 3 men and 1 woman, smokers, presenting chest pain. All cases appeared as pleural-based, solitary, and rounded nodules. Patients underwent wedge resections followed by adjuvant chemotherapy (3/4) but died of disease. At histology, lesions consisted of widely necrotic nodules surrounded by organizing fibrosis and pleuritis. Examination and immunostains with pan-cytokeratins and epithelial membrane antigen (EMA) revealed atypical spindle cells encircling necrotic tissue and involving the vascular wall. Positive staining with PD-L1 was noted. Molecular analysis showed KRAS (2/4) and TP53 (1/4) mutations, whereas EGFR, ALK, and ROS1 alterations were not detected. Although in a limited series, these cases further evidence the treacherous appearance of spindle cell carcinomas and the need for careful attention when examining pulmonary infarcted tissue, thus requiring extensive sampling, meticulous examination of vascular structures, and immunostaining with cytokeratins.

Postmortem lung biopsies from four patients with COVID-19 at a tertiary hospital in Cape Town, South Africa.

BACKGROUND: An outbreak of a novel coronavirus in China in late 2019 has resulted in a global pandemic. The virus (SARS-CoV-2) causes a severe acute respiratory syndrome and had been responsible for >14 000 deaths in South Africa (SA) at the time of writing, 30 August 2020. Autopsies in our setting have not been prioritised owing to the infective risks for staff, resulting in a lack of information on the histopathology of the disease in the SA setting. Postmortem biopsies are relatively quick and easy to perform and reduce the infective risk posed by full autopsies. OBJECTIVES: To determine whether postmortem biopsies of lung tissue could be used to determine cause of death in lieu of full autopsies in patients dying from COVID-19. METHODS: We performed postmortem biopsies of lung tissue on 4 patients with SARS-CoV-2 confirmed by reverse transcriptase polymerase chain reaction who died in the Tygerberg Hospital (Cape Town, SA) intensive care unit (ICU) in June - July 2020, in order to determine their cause of death. The biopsies were performed in the ICU with the necessary personal protective equipment within 2 hours after death. Clinical information was obtained from the hospital records and the histopathology was reviewed by two consultant histopathologists. Microbiology and electron microscopy were also performed on this tissue. RESULTS: All 4 patients were aged >50 years and had multiple comorbidities. Pulmonary pathology was present in only 3 cases, and the findings were surprisingly heterogeneous. One case demonstrated several findings including diffuse alveolar damage, extensive fibrin thrombi in pulmonary arteries with pulmonary infarction, organising pneumonia and bronchopneumonia. Other findings included type 2 pneumocyte hyperplasia, intra-alveolar macrophages and squamous metaplasia. An organising pneumonia was present in 2 other cases, although these findings were not deemed to be severe enough to be the cause of death. Fibrin thrombi were present in pulmonary arteries of 3 cases. One case showed no significant acute pulmonary pathology. The cause of death could only be determined in 1 case. CONCLUSIONS: The pulmonary findings we observed are in keeping with those described in the international literature. However, the pathology was surprisingly heterogeneous between cases, and was only deemed severe enough to be the cause of death in 1 of 4 cases. While lung-targeted, standardised postmortem biopsies may be safe, easy to perform and provide useful insights into the disease, they are not suitable to replace full autopsies in determining cause of death.

Incidence and morphological characteristics of the reversed halo sign in patients with acute pulmonary embolism and pulmonary infarction undergoing computed tomography angiography of the pulmonary arteries.

OBJECTIVE: To determine the incidence of the reversed halo sign (RHS) in patients with pulmonary infarction (PI) due to acute pulmonary embolism (PE), detected by computed tomography angiography (CTA) of the pulmonary arteries, and to describe the main morphological features of the RHS. METHODS: We evaluated 993 CTA scans, stratified by the risk of PE, performed between January of 2010 and December of 2014. Although PE was detected in 164 scans (16.5%), three of those scans were excluded because of respiratory motion artifacts. Of the remaining 161 scans, 75 (46.6%) showed lesions consistent with PI, totaling 86 lesions. Among those lesions, the RHS was seen in 33 (38.4%, in 29 patients). RESULTS: Among the 29 patients with scans showing lesions characteristic of PI with the RHS, 25 (86.2%) had a single lesion and 4 (13.8%) had two, totaling 33 lesions. In all cases, the RHS was in a subpleural location. To standardize the analysis, all images were interpreted in the axial plane. Among those 33 lesions, the RHS was in the right lower lobe in 17 (51.5%), in the left lower lobe in 10 (30.3%), in the lingula in 5 (15.2%), and in the right upper lobe in 1 (3.0%). Among those same 33 lesions, areas of low attenuation were seen in 29 (87.9%). The RHS was oval in 24 (72.7%) of the cases and round in 9 (27.3%). Pleural effusion was seen in 21 (72.4%) of the 29 patients with PI and the RHS. CONCLUSIONS: A diagnosis of PE should be considered when there are findings such as those described here, even in patients with nonspecific clinical symptoms.

Incidence and morphological characteristics of the reversed halo sign in patients with acute pulmonary embolism and pulmonary infarction undergoing computed tomography angiography of the pulmonary arteries / Incidência e características morfológicas do sinal do halo invertido em pacientes com tromboembolismo pulmonar agudo e infarto pulmonar submetidos a angiotomografia de artérias pulmonares

ABSTRACT Objective: To determine the incidence of the reversed halo sign (RHS) in patients with pulmonary infarction (PI) due to acute pulmonary embolism (PE), detected by computed tomography angiography (CTA) of the pulmonary arteries, and to describe the main morphological features of the RHS. Methods: We evaluated 993 CTA scans, stratified by the risk of PE, performed between January of 2010 and December of 2014. Although PE was detected in 164 scans (16.5%), three of those scans were excluded because of respiratory motion artifacts. Of the remaining 161 scans, 75 (46.6%) showed lesions consistent with PI, totaling 86 lesions. Among those lesions, the RHS was seen in 33 (38.4%, in 29 patients). Results: Among the 29 patients with scans showing lesions characteristic of PI with the RHS, 25 (86.2%) had a single lesion and 4 (13.8%) had two, totaling 33 lesions. In all cases, the RHS was in a subpleural location. To standardize the analysis, all images were interpreted in the axial plane. Among those 33 lesions, the RHS was in the right lower lobe in 17 (51.5%), in the left lower lobe in 10 (30.3%), in the lingula in 5 (15.2%), and in the right upper lobe in 1 (3.0%). Among those same 33 lesions, areas of low attenuation were seen in 29 (87.9%). The RHS was oval in 24 (72.7%) of the cases and round in 9 (27.3%). Pleural effusion was seen in 21 (72.4%) of the 29 patients with PI and the RHS. Conclusions: A diagnosis of PE should be considered when there are findings such as those described here, even in patients with nonspecific clinical symptoms.

RESUMO Objetivo: Verificar a incidência do sinal do halo invertido (SHI) associado a infartos pulmonares (IP) relacionados ao tromboembolismo pulmonar (TEP) agudo, identificado por angiotomografia (angio-TC) de artérias pulmonares, e demonstrar as principais características morfológicas do SHI. Métodos: Foram avaliadas 993 angio-TCs, após estratificação de risco clínico para TEP entre janeiro de 2010 e dezembro de 2014. TEP foi encontrado em 164 pacientes (16,5%), sendo que três exames foram descartados devido a artefatos de movimentação respiratória. Dos 161 exames restantes, em 75 (46,6%) foram identificadas imagens compatíveis com IP, totalizando 86 lesões; o SHI foi observado em 33 (38,4% dos pacientes) dessas lesões. Resultados: Dos 29 pacientes com lesões características de IP com o SHI, 25 pacientes (86,2%) apresentavam lesão única e 4 (13,8%), lesão dupla. Todas as imagens compatíveis com SHI eram de localização subpleural. Para padronizar a análise, todas as imagens foram interpretadas no plano axial. Em relação à distribuição lobar das 33 lesões, o SHI estava localizado no lobo inferior direito, em 17 (51,5%); no lobo inferior esquerdo, em 10 (30,3%); na língula, em 5 (15,2%) e no lobo superior direito, em 1 (3,0%). Áreas de baixa atenuação no interior dos IPs com o SHI foram observadas em 29 das 33 lesões (87,9%). O SHI apresentava formato ovalado em 24 (72,7%) dos casos e formato arredondado, em 9 (27,3%). Derrame pleural foi encontrado associado aos IP com o SHI em 21 pacientes (72,4%). Conclusões: O achado de imagens com essas características, mesmo em pacientes com sintomatologia inespecífica, deve alertar para a possibilidade do diagnóstico de TEP.

Pulmonary Infarction: An Often Unrecognized Clinical Entity.

Pulmonary infarction occurs in nearly one-third of the patients with acute pulmonary embolism. Infarcts are still often mistaken for pneumonia or lung cancer because of the deeply rooted belief that they ought to be triangular in shape. In reality, the apical portion of an embolized region is spared from infarction thanks to sufficient collateral blood flow. Infarcts are always arranged peripherally along the surface of the visceral pleura (costal, diaphragmatic, mediastinal, or interlobar). Their free margin is sharp and convex toward the hilum, casting a semicircular or cushion-like density on chest radiography or computed tomography (CT). Focal areas of hyperlucency within the infarction are often seen on CT. Clinical presentation is nonspecific. Pleuritic chest pain, either isolated or in combination with abrupt dyspnea, is the most frequent presenting symptom, whereas hemoptysis is much rarer. Recent data indicate that younger age, increasing body height, and active cigarette smoking are independent predictors of infarction in the setting of acute pulmonary embolism. Correct recognition of pulmonary infarction is fundamental because pleural-based consolidations suggestive of infarction may be the first manifestation of pulmonary embolism.

A Case Report: Cavitary Infarction Caused by Pulmonary Tumor Thrombotic Microangiopathy in a Patient with Pancreatic Intraductal Papillary Mucinous Neoplasm.

Pulmonary tumor embolism is commonly discovered at autopsy, but is rarely suspected ante-mortem. Microangiopathy is an uncommon and distinct form of simple tumor pulmonary embolism. Here, we present a 52-year-old male with tumor thrombotic microangiopathy and pulmonary infarction, which might have originated from intraductal papillary mucinous tumor of the pancreas. Multiple wedge-shaped consolidations were found initially and aggravated with cavitation. These CT features of pulmonary infarction were pathologically confirmed to result from pulmonary tumor thrombotic microangiopathy.

Lung Infarction due to Pulmonary Vein Stenosis after Ablation Therapy for Atrial Fibrillation Misdiagnosed as Organizing Pneumonia: Sequential Changes on CT in Two Cases.

Pulmonary vein (PV) stenosis is a complication of ablation therapy for arrhythmias. We report two cases with chronic lung parenchymal abnormalities showing no improvement and waxing and waning features, which were initially diagnosed as nonspecific pneumonias, and finally confirmed as PV stenosis. When a patient presents for nonspecific respiratory symptoms without evidence of infection after ablation therapy and image findings show chronic and repetitive parenchymal abnormalities confined in localized portion, the possibility of PV stenosis should be considered.

Case of round pneumonia: pulmonary infarct and a rare situation that is similar with the lung cancer.

BACKGROUND AND AIMS: Round pneumonia (RP) is a rare radiological presentation of a subtype of lobar pneumonia that arises because of a developmental defect in connective tissues (pores of Köhn and channels of Lambert). The round appearance on chest X-ray (CXR) is thought to occur from an infectious process that spreads from small peripheral alveoli centrifugally through interalveolar channels via the pores of Kohn and the canals of Lambert. This explains the nonsegmental distribution and shape of RP. The pathogenesis of RP is unknown. An alternative theory holds that RP in children occurs because of underdeveloped pores of Kohn and the absence of canals of Lambert, limiting the spread of the organism and resulting in a focal, round mass seen on radiographs. As a result of this developmental defect, dissemination of infection remains in a limited area. While this is a well-known entity in childhood, it has been described infrequently in adults. Lesions of RP are not necessarily round; oval lesions can also be seen. It is a radiological subtype of the pneumonia subtype and presents as a solitary nodule or a mass lesion in CXR. METHODS: We presented two cases of RP. One mimicked and was mistaken for pulmonary infarction because of triangular pleural-based density and the other mimicked pulmonary malignancy because of a homogeneous triangular opacity based on the pleura on the posteroanterior radiography and computed tomography. CONCLUSION: These cases were presented because of RP's importance, and RP should be considered a part of differential diagnosis of pulmonary infarct and lung tumor.

Reversed halo sign in pulmonary infarction with tumor emboli: a case report.

We describe the case of a 79-year-old woman with pulmonary infarction due to tumor emboli whose high-resolution CT (HRCT) scan demonstrated the reversed halo sign. The patient had gastric cancer and died because of cancer-related cerebral infarction. On autopsy, the central ground-glass area of the reversed halo sign on HRCT corresponded to pulmonary edema associated with alveolar septal capillary metastasis, whereas the peripheral ring-like consolidation consisted of a hemorrhagic infarct with tumor emboli. The present case is important because a detailed pathologic correlation with this unique HRCT appearance was revealed.

[Cavitating pulmonary infarcts revealing thromboembolic pulmonary hypertension]. / Infarctus pulmonaires excavés révélant une hypertension pulmonaire post-embolique.

Several etiologies are involved in the pathogenesis of cavitating pulmonary disease including neoplastic, infectious or inflammatory processes. Another is pulmonary infarction associated with venous thromboembolism. The lung cavities tend to be located peripherally and are the result of pulmonary embolism. We report the case of a woman with chronic thromboembolic pulmonary hypertension (CTEPH), associated with familial thrombophilia, revealed by cavitating pulmonary infarcts. CTEPH is sometimes diagnosed during an episode of recurrent pulmonary embolism following previously unnoticed lesions. Thrombophilias such as isolated elevated factor VIII are risk factors for CTEPH.

Fatal thromboembolism following physical restraint in a patient with schizophrenia.

Fatal thromboembolism during physical restraint in patients suffering from psychotic disorders is a very rare occurrence. In the case we present here, the criteria used in forensic pathology for the age determination of venous thrombi are applied to a case of pulmonary embolism in a patient suffering from schizophrenia who died after physical restraint. The possible association between conventional antipsychotic drugs and deep venous thrombosis, followed by pulmonary embolism, in a man with no predisposing risk factors, as well as the question concerning the appropriateness of medical care, are discussed.

Pulmonary cavitation in a patient presenting with nonspecific complaints.

Most commonly, patients with pulmonary embolism present with dyspnea, chest pain, and/or tachypnea to the emergency department (ED). The presence of multiple suggestive symptoms, especially when severe, significantly reduces delay in diagnosis. We report a case of an 86-year-old patient presenting to the ED with nonspecific complaints: she claimed to feel lethargic and "reluctant to prepare meals." She did not complain of either dyspnea or chest pain. As underlying cause, an intrapulmonary cavitation with pulmonary embolism was found. The combination of absence of specific symptoms regarding pulmonary embolism and radiologic findings of an obstructed pulmonary artery supplying the cavitary lung segment is rare. Common etiologies of cavitary lung processes are discussed, and risk factors of pulmonary infarction are highlighted.

Laser-targeted photosensitizer-induced lung injury: noninvasive rat model of pulmonary infarction.

Pulmonary infarction is a life-threatening lung injury that requires rapid and accurate diagnosis for proper treatment. Targetable and reproducible small-animal models that would allow experimental development and preclinical evaluation of diagnostic methods for detecting pulmonary infarction are critically missing. The authors report here a novel procedure to selectively induce pulmonary infarction by photodestructive laser-light irradiation in a targeted location within a specific lung compartment after administration of a photosensitizer. Histopathological analysis of the illuminated lung tissue revealed massive hemorrhage and vascular occlusion after acute injury localized to the site of irradiation. Collapse of alveolar structure, neutrophil influx, and necrosis were subsequently observed. Computed tomography (CT) scans showed evidence of abnormal density and airspace consolidation in the irradiated area of the lung, but not elsewhere in the lung compartment. Perfusion imaging using 99mTc-labeled macroaggregated albumin by single-photon emission computed tomography revealed diminished scintigraphic signal in the opaque area of infarcted lung tissue. The histological changes, CT findings, and perfusion characteristics of pulmonary infarction are mimicked using laser-irradiated, photosensitizer-mediated photodestruction to selectively induce chronic lung injury in a localized area. This small-animal model can be easily and readily used for targeted induction of pulmonary infarction in a designated area of lung compartment and offers the potential for use in evaluating novel diagnostic and therapeutic methods.

Anabolic androgenic steroids abuse and cardiac death in athletes: morphological and toxicological findings in four fatal cases.

Anabolic androgenic steroids (AAS) are the main class of doping agents and their consumption produces adverse effects involving several organs and systems. Three cases of sudden cardiac death (SCD) and one of death due to congestive heart failure of previously healthy athletes who were AAS users are herein reported. Concentric cardiac hypertrophy with focal fibrosis (one case), dilated cardiomyopathy with patchy myocyte death (two cases) and eosinophilic myocarditis (one case) were observed and most probably relate to the final event. Molecular investigation for viral genomes was positive in one case (Ebstein virus). Our data confirm previous findings, showing that the most typical cardiac abnormality in AAS abusers is left ventricular hypertrophy, associated with fibrosis and myocytolysis. An exceptional cardiovascular substrate was represented by the case with drug induced eosinophilic myocarditis. These features are at risk of ventricular arrhythmias as well as congestive heart failure. The cause-effect relationship between AAS abuse and cardiac death can be established only by a rigorous methodology with the use of standardized protocols, including precise morphological studies of all target organs to search for chronic toxic effects. Laboratory investigations should focus on AAS searching on a wide range of biological matrices to demonstrate type, magnitude and time of exposure.

Chronic thromboembolic pulmonary hypertension with pulmonary infarction occuring in a hypertensive.

We present a 72-year-old man and a known hypertensive with poor drug compliance seen here on 22-03-06, with a 4-year history of progressive dyspnoea, associated with cough and a wheeze. On examination he was chronically ill looking with altered state of consciousness, pale, centrally cyanosed, febrile (T-38 degrees C), in respiratory distress (RR-33 pm). Significant chest radiological findings include marked aortic unfolding and cardiomegaly, with biventricular involvement. Numerous nodular opacities in both lung fields especially the Right side with right apical opacification/thickening. Treatment as appropriate was instituted but unfortunately the patient succumbed after thirty days on admission and an autopsy carried out revealed multiple pulmonary infarcts with pulmonary thrombo-embolism.

Chronic thromboembolic pulmonary hypertension with pulmonary infarction occuring in a hypertensive.

We present a 72-year-old man and a known hypertensive with poor drug compliance seen here on 22-03-06,with a 4-year history of progressive dyspnoea, associated with cough and a wheeze. On examination he was chronically ill looking with altered state of consciousness, pale, centrally cyanosed, febrile (T-38 degrees C), in respiratory distress (RR-33pm). Significant chest radiological findings include marked aortic unfolding and cardiomegaly, with biventricular involvement. Numerous nodular opacities in both lung fields especially the Right side with right apical opacification/thickening. Treatment as appropriate was instituted but unfortunately the patient succumbed after thirty days on admission and an autopsy carried out revealed multiple pulmonary infarcts with pulmonary thrombo-embolism.

A retrospective study of pulmonary infarction in patients with systemic lupus erythematosus from southern Taiwan.

Since large-scale reports of pulmonary infarction in systemic lupus erythematosus (SLE) are limited, a retrospective study was performed for this manifestation in 773 hospitalized patients in southern Taiwan from 1999 to 2009. Pulmonary infarction was defined as the presence of pulmonary embolism, persistent pulmonary infiltrates, and characteristic clinical symptoms. Demographic, clinical, laboratory, and radiological images data were analyzed. There were 12 patients with pulmonary embolism and 9 of them had antiphospholipid syndrome (APS). Six patients (19 to 53 years, average 38.2 ± 12.6) with 9 episodes of lung infarction were identified. All cases were APS and four episodes had coincidental venous thromboembolism. There were four episodes of bilateral infarction and seven episodes of larger central pulmonary artery embolism. Heparin therapy was routinely prescribed and thrombolytic agents were added in two episodes. Successful recovery was noted in all patients. In conclusion, there was a 0.8% incidence of pulmonary infarction in patients with SLE, all with the risk factor of APS. Differentiation between pulmonary infarction and pneumonia in lupus patients should be made; they have similar chest radiography with lung consolidation but require a different clinical approach in management. Although this report is a retrospective study with relatively small numbers of lupus patients with lung infarcts, our observation might provide beneficial information on the clinical features and radiological presentations during the disease evolution of pulmonary infarction in SLE with APS.