|
1
|
Kubiak K, Bazylewicz-Zakrzewska K, Poncyljusz W. Hampton's Hump-A Rare Radiological Feature in Patients with Pulmonary Embolism in a Single-Center Study. J Clin Med 2025; 14:1900. [PMID: 40142708 PMCID: PMC11942958 DOI: 10.3390/jcm14061900] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/10/2025] [Revised: 03/07/2025] [Accepted: 03/09/2025] [Indexed: 03/28/2025] Open
Abstract
Background: Pulmonary embolism is a potentially life-threatening condition caused by the sudden occlusion of pulmonary arteries. Its non-specific and highly variable clinical presentation often leads to undiagnosed cases, making computed tomography pulmonary angiography (CTPA) essential for diagnosis. Hampton's hump is a rare radiological finding associated with pulmonary embolism, characterized by a wedge-shaped, pleural-based opacification due to pulmonary infarction. Methods: This study examines the correlation between pulmonary embolism severity and the presence of Hampton's hump in CTPA based on a database of 428 patients. Results: We observed a correlation between the presence of Hampton's hump and an increased likelihood of rider-type embolism, pleural effusion, and dilation of the pulmonary trunk and left pulmonary artery. The data indicate that patients with at least one risk factor for severe pulmonary embolism are more likely to present with Hampton's hump. Furthermore, the presence of this sign in patients diagnosed with pulmonary embolism and pleural effusion substantially increases the risk of in-hospital death. Conclusions: This study underscores the significance of Hampton's hump as a rare but clinically relevant radiological finding in patients with pulmonary embolism. Given the limited number of studies on this topic, our findings provide valuable insights into the role of Hampton's hump in the context of pulmonary embolism.
Collapse
Affiliation(s)
- Kinga Kubiak
- Department of Diagnostic Imaging and Interventional Radiology, Pomeranian Medical University in Szczecin, 71-252 Szczecin, Poland
| | | | | |
Collapse
|
|
2
|
Boccatonda A, Andreetto L, Vicari S, Campello E, Simioni P, Ageno W. The Diagnostic Role of Lung Ultrasound and Contrast-Enhanced Ultrasound in Pulmonary Embolism. Semin Thromb Hemost 2024; 50:842-850. [PMID: 37832584 DOI: 10.1055/s-0043-1776006] [Citation(s) in RCA: 7] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/15/2023]
Abstract
The diagnosis of pulmonary embolism (PE) relies essentially on a probabilistic approach that requires careful clinical assessments, targeted laboratory tests, and the use of appropriate imaging tools. Nowadays, the diagnostic gold standard is computed tomographic pulmonary angiography. Lung ultrasound (LUS) can play a role in the diagnosis of PE mainly by allowing the visualization of peripheral lung infarctions. Hypoechoic, pleural-based parenchymal consolidation is the most typical and common finding of pulmonary infarction. More than 85% of infarct lesions are wedge-shaped, extending to the pleural surface and are localized to where the patient complains of pleuritic chest pain. Contrast-enhanced ultrasound can be performed in addition to basic ultrasound examination to ascertain nonvascularization of the consolidation, thus confirming that the lesion is an infarct. The aim of this narrative review is to summarize the latest evidence on the application of LUS to the diagnosis of PE, focusing purely on thoracic/lung signs.
Collapse
Affiliation(s)
- Andrea Boccatonda
- Internal Medicine, Bentivoglio Hospital, AUSL Bologna, Bentivoglio (BO), Italy
| | - Lorenzo Andreetto
- Internal Medicine, IRCCS Azienda Ospedaliero-Universitaria Policlinico di Sant'Orsola, Bologna, Italy
| | - Susanna Vicari
- Internal Medicine, Bentivoglio Hospital, AUSL Bologna, Bentivoglio (BO), Italy
| | - Elena Campello
- General Medicine and Thrombotic and Hemorrhagic Diseases Unit, Department of Medicine, University Hospital of Padova, Padova, Italy
| | - Paolo Simioni
- General Medicine and Thrombotic and Hemorrhagic Diseases Unit, Department of Medicine, University Hospital of Padova, Padova, Italy
| | - Walter Ageno
- Research Center on Thromboembolic Diseases and Antithrombotic Therapies, Department of Medicine and Surgery, University of Insubria, Varese, Italy
| |
Collapse
|
|
3
|
Kaptein FHJ, Stöger JL, van Dam LF, Ninaber MK, Mertens BJA, Huisman MV, Klok FA, Kroft LJM. Computed tomography diagnosis of pulmonary infarction in acute pulmonary embolism. Thromb Res 2024; 241:109071. [PMID: 38972272 DOI: 10.1016/j.thromres.2024.109071] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/19/2023] [Revised: 05/25/2024] [Accepted: 06/20/2024] [Indexed: 07/09/2024]
Abstract
INTRODUCTION Pulmonary infarction is a common sequela of pulmonary embolism (PE) but lacks a diagnostic reference standard. CTPA in the setting of acute PE does not reliably differentiate infarction from other consolidations, such as reversible alveolar hemorrhage or atelectasis. We aimed to assess the diagnostic accuracy for recognizing pulmonary infarction on CT in the acute phase of PE, with follow-up CT as reference. MATERIALS AND METHODS Initial and follow-up CT scans of 33 patients with acute PE were retrospectively assessed. Two radiologists independently evaluated the presence and size of suspected pulmonary infarction on the initial CT. Confirmation of infarction was established by detection of residual densities on follow-up CT. Sensitivity, specificity and interobserver variability were calculated. RESULTS In total, 60 presumed infarctions were found in 32 patients, of which 34 infarctions in 21 patients could be confirmed at follow-up. On patient-level, observers' sensitivity/specificity were 91 %/9 %, and 73 %/46 %, respectively, with interobserver agreement by Kappa's coefficient of 0.17. Confirmed infarctions were usually larger than false positive lesions (median approximate volume of 6.6 mL [IQR 0.84-21.3] vs. 1.3 mL [IQR 0.57-6.5], p = 0.040), but still small. An occluding thrombus in a supplying vessel was predictive for confirmed infarction (OR 11, 95%CI 2.1-55), but was not discriminative. CONCLUSIONS Pulmonary infarction is a common finding in acute PE, and generally small. Radiological identification of infarction was challenging, with considerable interobserver variability. Complete obstruction of the supplying (sub)segmental pulmonary artery was found as the strongest predictor for pulmonary infarction but was not demonstrated to be discriminative.
Collapse
Affiliation(s)
- Fleur H J Kaptein
- Department of Medicine - Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, the Netherlands.
| | - J Lauran Stöger
- Department of Radiology, Leiden University Medical Center, Leiden, the Netherlands
| | - Lisette F van Dam
- Department of Emergency Medicine, Franciscus Hospital, Rotterdam, the Netherlands
| | - Maarten K Ninaber
- Department of Pulmonology, Leiden University Medical Center, Leiden, the Netherlands
| | - Bart J A Mertens
- Department of Biomedical Data Science, Leiden University Medical Center, Leiden, the Netherlands
| | - Menno V Huisman
- Department of Medicine - Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, the Netherlands
| | - Frederikus A Klok
- Department of Medicine - Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, the Netherlands
| | - Lucia J M Kroft
- Department of Radiology, Leiden University Medical Center, Leiden, the Netherlands
| |
Collapse
|
|
4
|
Tsuchiya N, Xu YY, Ito J, Yamashiro T, Ikemiyagi H, Mummy D, Schiebler ML, Yonemoto K, Murayama S, Nishie A. Chronic thromboembolic pulmonary hypertension is associated with a loss of total lung volume on computed tomography. World J Radiol 2023; 15:146-156. [PMID: 37275304 PMCID: PMC10236971 DOI: 10.4329/wjr.v15.i5.146] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/26/2022] [Revised: 04/04/2023] [Accepted: 04/24/2023] [Indexed: 05/23/2023] Open
Abstract
BACKGROUND Although lung volumes are usually normal in individuals with chronic thromboembolic pulmonary hypertension (CTEPH), approximately 20%-29% of patients exhibit a restrictive pattern on pulmonary function testing.
AIM To quantify longitudinal changes in lung volume and cardiac cross-sectional area (CSA) in patients with CTEPH.
METHODS In a retrospective cohort study of patients seen in our hospital between January 2012 and December 2019, we evaluated 15 patients with CTEPH who had chest computed tomography (CT) performed at baseline and after at least 6 mo of therapy. We matched the CTEPH cohort with 45 control patients by age, sex, and observation period. CT-based lung volumes and maximum cardiac CSAs were measured and compared using the Wilcoxon signed-rank test and the Mann-Whitney u test.
RESULTS Total, right lung, and right lower lobe volumes were significantly reduced in the CTEPH cohort at follow-up vs baseline (total, P = 0.004; right lung, P = 0.003; right lower lobe; P = 0.01). In the CTEPH group, the reduction in lung volume and cardiac CSA was significantly greater than the corresponding changes in the control group (total, P = 0.01; right lung, P = 0.007; right lower lobe, P = 0.01; CSA, P = 0.0002). There was a negative correlation between lung volume change and cardiac CSA change in the control group but not in the CTEPH cohort.
CONCLUSION After at least 6 mo of treatment, CT showed an unexpected loss of total lung volume in patients with CTEPH that may reflect continued parenchymal remodeling.
Collapse
Affiliation(s)
- Nanae Tsuchiya
- Department of Radiology, Graduate School of Medical Science, University of the Ryukyus, Nishihara 903-0125, Okinawa, Japan
| | - Yan-Yan Xu
- Department of Radiology, China-Japan Friendship Hospital, Beijing 100029, China
| | - Junji Ito
- Department of Radiology, Graduate School of Medical Science, University of the Ryukyus, Nishihara 903-0125, Okinawa, Japan
| | - Tsuneo Yamashiro
- Department of Radiology, Yokohama City University, Yokohama 2360027, Japan
| | - Hidekazu Ikemiyagi
- Department of Cardiovascular Medicine, Nephrology and Neurology, Graduate School of Medicine, University of the Ryukyus, Nishihara 9030125, Okinawa, Japan
| | - David Mummy
- Center for In Vivo Microscopy and Department of Radiology, Duke University, Durham, NC 27710, United States
| | - Mark L Schiebler
- Department of Radiology, University of Wisconsin-Madison, Madison, WI 53792, United States
| | - Koji Yonemoto
- Department of Biostatistics, School of Health Sciences, Faculty of Medicine, University of the Ryukyus, Nishihara 903-0215, Okinawa, Japan
| | - Sadayuki Murayama
- Department of Radiology, Graduate School of Medical Science, University of the Ryukyus, Nishihara 903-0125, Okinawa, Japan
| | - Akihiro Nishie
- Department of Radiology, Graduate School of Medical Science, University of the Ryukyus, Nishihara 903-0125, Okinawa, Japan
| |
Collapse
|
|
5
|
Lio KU, O'Corragain O, Bashir R, Brosnahan S, Cohen G, Lakhter V, Panaro J, Rivera-Lebron B, Rali P. Clinical outcomes and factors associated with pulmonary infarction following acute pulmonary embolism: a retrospective observational study at a US academic centre. BMJ Open 2022; 12:e067579. [PMID: 36581412 PMCID: PMC9806066 DOI: 10.1136/bmjopen-2022-067579] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/31/2022] Open
Abstract
OBJECTIVE Pulmonary infarction is a common clinical and radiographic finding in acute pulmonary embolism (PE), yet the clinical relevance and prognostic significance of pulmonary infarction remain unclear. The study aims to investigate the clinical features, radiographic characteristics, impact of reperfusion therapy and outcomes of patients with pulmonary infarction. DESIGN, SETTING AND PARTICIPANTS A retrospective cohort study of 496 adult patients (≥18 years of age) diagnosed with PE who were evaluated by the PE response team at a tertiary academic referral centre in the USA. We collected baseline characteristics, laboratory, radiographic and outcome data. Statistical analysis was performed by Student's t-test, Mann-Whitney U test, Fischer's exact or χ2 test where appropriate. Multivariate logistic regression was used to evaluate potential risk factors for pulmonary infarction. RESULTS We identified 143 (29%) cases of pulmonary infarction in 496 patients with PE. Patients with infarction were significantly younger (52±15.9 vs 61±16.6 years, p<0.001) and with fewer comorbidities. Most infarctions occurred in the lower lobes (60%) and involved a single lobe (64%). The presence of right ventricular (RV) strain on CT imaging was significantly more common in patients with infarction (21% vs 14%, p=0.031). There was no significant difference in advanced reperfusion therapy, in-hospital mortality, length of stay and readmissions between groups. In multivariate analysis, age and evidence of RV strain on CT and haemoptysis increased the risk of infarction. CONCLUSIONS Radiographic evidence of pulmonary infarction was demonstrated in nearly one-third of patients with acute PE. There was no difference in the rate of reperfusion therapies and the presence of infarction did not correlate with poorer outcomes.
Collapse
Affiliation(s)
- Ka U Lio
- Department of Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA
| | - Oisin O'Corragain
- Department of Thoracic Medicine and Surgery, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA
| | - Riyaz Bashir
- Department of Cardiology, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA
| | - Shari Brosnahan
- Department of Pulmonary, Critical Care and Sleep Medicine, NYU Langone Health, New York City, New York, USA
| | - Gary Cohen
- Department of Radiology, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA
| | - Vladimir Lakhter
- Department of Cardiology, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA
| | - Joseph Panaro
- Department of Radiology, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA
| | - Belinda Rivera-Lebron
- Department of Pulmonary and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
| | - Parth Rali
- Department of Thoracic Medicine and Surgery, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA
| |
Collapse
|
|
6
|
Kriegshäuser G, Braunsteiner A. Temporal Association between Hampton's Hump Pulmonary Embolism and First-Dose ChAdOx1 nCov-19 Vaccine in a Patient with Activated Protein C Resistance. Vaccines (Basel) 2022; 10:vaccines10101659. [PMID: 36298523 PMCID: PMC9609840 DOI: 10.3390/vaccines10101659] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/08/2022] [Revised: 09/18/2022] [Accepted: 09/28/2022] [Indexed: 11/07/2022] Open
Abstract
A 58-year-old man presented to his practitioner with right-sided pleuritic chest pain, dyspnea, and fatigue 18 days following the first dose of the ChAdOx1 nCov-19 vaccine. Chest radiography showed a basal wedge-shaped consolidation indicative of a Hampton’s hump in the right lower lobe, which was confirmed by subsequent computed tomography pulmonary angiography. The major laboratory abnormalities were a markedly elevated D-dimer level of 7.53 µg/mL (normal range < 0.5 µg/mL), a CRP level of 62.8 mg/L (normal range < 5 mg/L), and a previously unknown activated protein C resistance of 1.3 (normal range ≥ 1.8). Genetic analysis identified the patient to be heterozygous for the FVLeiden mutation. Neither other errors of hemostasis nor antibodies against platelet factor 4-polyanion complexes could be observed. Moreover, we failed to demonstrate Severe Acute Respiratory Syndrome Coronavirus-2 infection. The patient fully recovered with no sequelae but is being continued on long-term anticoagulation given his risk of recurrent venous thromboembolism. Here we report on the temporal association between the first dose of the ChAdOx1 nCov-19 vaccine and extensive pulmonary embolism in an otherwise healthy patient with activated protein C resistance, however, further investigation is needed to prove causality.
Collapse
Affiliation(s)
- Gernot Kriegshäuser
- IHR LABOR Medical Diagnostic Laboratories, Wagramer Straße 144, 1220 Vienna, Austria
- School of Management, University of Applied Sciences BFI, 1020 Vienna, Austria
- Correspondence: ; Tel.: +43-1-8906701; Fax: +43-1-8906701-85
| | | |
Collapse
|
|
7
|
Pulmonary Embolism Presenting with Pulmonary Infarction: Update and Practical Review of Literature Data. J Clin Med 2022; 11:jcm11164916. [PMID: 36013155 PMCID: PMC9409643 DOI: 10.3390/jcm11164916] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/18/2022] [Revised: 07/08/2022] [Accepted: 08/19/2022] [Indexed: 11/17/2022] Open
Abstract
Pulmonary infarction (PI) is a possible consequence of pulmonary embolism (PE). The real incidence of PI could be underestimated considering only non-fatal PE presentation. However, following postmortem examination, the prevalence of PI is considerably higher. This evidence suggests the necessity of proper diagnostic protocol for identifying PI. Unfortunately, PI diagnosis can sometimes be challenging, due to the overlapping of symptoms with other diseases. Nowadays, the diagnosis is mainly based on radiological evaluation, although the combination with emerging imaging techniques such as ultrasound and nuclear scanning might improve the diagnostic algorithm for PI. This review aims to summarize the available data on the prevalence of PI, the main predisposing factors for the development of PI among patients with PE, to resume the possible diagnostic tools, and finally the clinical and prognostic implications.
Collapse
|
|
8
|
Ji Y, Wang Y, Shao C, Cui Y, Su N, Shao G, Zheng J. A Frequently Missed Pulmonary Infarction: Clinical and 18F-FDG PET/CT Manifestation of Hilar Tumor-Induced Pulmonary Infarction. Clin Nucl Med 2022; 47:473-479. [PMID: 35426843 PMCID: PMC9071030 DOI: 10.1097/rlu.0000000000004180] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/22/2021] [Revised: 02/10/2022] [Indexed: 11/26/2022]
Abstract
PURPOSE This study aimed to summarize the clinical and 18F-FDG PET/CT manifestations of hilar tumor-induced pulmonary infarction. METHODS A retrospective analysis was performed on patients with hilar masses who underwent FDG PET/CT scans between July 2015 and January 2021 and had complete clinical data. Pulmonary infarction was confirmed by concurrent chest CT and imaging follow-up or pathology. RESULTS A total of 58 patients (mean age, 56 [SD, 13] years; 44 males) with 122 infarcts were included in the study. Hilar masses were mostly associated with small cell lung cancer (64%). The most common clinical manifestations were cough (64%) and hemoptysis (36%). Most patients (62%) had multiple pulmonary infarcts. The CT findings of pulmonary infarcts included the "Hampton hump" (48%) and patchy consolidation (52%). The density of infarcts included "bubbly consolidation" (61%) and "homogenous consolidation" (39%). The metabolic activity of 95 infarcts (78%) was higher than lung parenchyma, with the SUVmax of 3.3 (SD, 1.1). The metabolic patterns on PET/CT were "rim sign," "mismatch between PET and CT," and "no metabolism." Pulmonary vein involvement was found in 25 patients (43%), pleural effusion in 22 patients (38%), and the pleural curvilinear sign in 8 patients (14%). CONCLUSIONS The clinical manifestations of hilar tumor-induced pulmonary infarction are not specific, and 18F-FDG PET/CT could be an effective diagnostic tool.
Collapse
Affiliation(s)
- Yu Ji
- From the Departments of Radiology
| | | | - Chunchun Shao
- Hospital-Acquired Infection Control, The Second Hospital, Cheeloo College of Medicine, Shandong University
| | - Yong Cui
- From the Departments of Radiology
| | - Na Su
- Department of PET/CT, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China
| | | | - Jingsong Zheng
- Department of PET/CT, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China
| |
Collapse
|
|
9
|
Carvallo FR, Stevenson VB. Interstitial pneumonia and diffuse alveolar damage in domestic animals. Vet Pathol 2022; 59:586-601. [DOI: 10.1177/03009858221082228] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/17/2022]
Abstract
Classification of pneumonia in animals has been controversial, and the most problematic pattern is interstitial pneumonia. This is true from the gross and histologic perspectives, and also from a mechanistic point of view. Multiple infectious and noninfectious diseases are associated with interstitial pneumonia, all of them converging in the release of inflammatory mediators that generate local damage and attract inflammatory cells that inevitably trigger a second wave of damage. Diffuse alveolar damage is one of the more frequently identified histologic types of interstitial pneumonia and involves injury to alveolar epithelial and/or endothelial cells, with 3 distinct stages. The first is the “exudative” stage, with alveolar edema and hyaline membranes. The second is the “proliferative” stage, with hyperplasia and reactive atypia of type II pneumocytes, infiltration of lymphocytes, plasma cells, and macrophages in the interstitium and early proliferation of fibroblasts. These stages are reversible and often nonfatal. If damage persists, there is a third “fibrosing” stage, characterized by fibrosis of the interstitium due to proliferation of fibroblasts/myofibroblasts, persistence of type II pneumocytes, segments of squamous metaplasia of alveolar epithelium, plus inflammation. Understanding the lesion patterns associated with interstitial pneumonias, their causes, and the underlying mechanisms aid in accurate diagnosis that involves an interdisciplinary collaborative approach involving pathologists, clinicians, and radiologists.
Collapse
Affiliation(s)
- Francisco R. Carvallo
- Virginia-Maryland College of Veterinary Medicine, Blacksburg, VA
- Virginia Department of Agriculture and Consumer Services, Harrisonburg, VA
| | | |
Collapse
|
|
10
|
A Case of Pulmonary Infarction Resembling Pneumonia during Immunosuppressive Treatment for Rheumatoid Arthritis. Case Rep Rheumatol 2021; 2021:5983580. [PMID: 34457368 PMCID: PMC8390160 DOI: 10.1155/2021/5983580] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/21/2021] [Accepted: 08/11/2021] [Indexed: 11/17/2022] Open
Abstract
A 67-year-old woman with rheumatoid arthritis (RA) presented with fever and dyspnea. Chest radiography and computed tomography (CT) revealed pulmonary infiltrates with ground-glass opacities. We considered bacterial or pneumocystis pneumonia because she was immunocompromised due to RA treatment. However, she had tachycardia and elevated D-dimer levels. We performed contrast-enhanced CT and subsequently diagnosed her with pulmonary embolism (PE). Though PE is not usually accompanied by parenchymal pulmonary shadows, pulmonary infarction may cause pulmonary infiltrates that can be mistaken for pneumonia. As RA is a thrombophilic disease, clinicians should be aware of PE and pneumonia as differential diagnoses in such patients.
Collapse
|
|
11
|
McGonagle D, Bridgewood C, Meaney JFM. A tricompartmental model of lung oxygenation disruption to explain pulmonary and systemic pathology in severe COVID-19. THE LANCET RESPIRATORY MEDICINE 2021; 9:665-672. [PMID: 34000237 PMCID: PMC8121498 DOI: 10.1016/s2213-2600(21)00213-7] [Citation(s) in RCA: 32] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 02/25/2021] [Revised: 04/16/2021] [Accepted: 04/21/2021] [Indexed: 12/28/2022]
Abstract
The emergent 21st century betacoronaviruses, including SARS-CoV-2, lead to clinicopathological manifestations with unusual features, such as early-onset chest pain, pulmonary infarction, and pulmonary and systemic thromboembolism that is pathologically linked to extensive capillary, arteriolar, and venular thrombosis. Early ground glass opacities detected by CT, which are reminiscent of lung infarcts associated with pulmonary embolism, point to a novel vascular pathology in COVID-19. Under physiological conditions, normal parenchymal oxygenation is maintained by three sources: the alveolus itself and dual oxygen supply from the pulmonary and bronchial artery circulations. We propose a model in which these three components are disrupted in COVID-19 pneumonia, with severe viral alveolitis and concomitant immunothrombotic obstruction of the pulmonary and bronchiolar circulation. Tricompartmental disruption might have two main consequences: systemic clot embolisation from pulmonary vein territory immunothrombosis, and alveolar–capillary barrier disruption with systemic access of thrombogenic viral material. Our model encompasses the known pathological and clinical features of severe COVID-19, and has implications for understanding patient responses to immunomodulatory therapies, which might exert an anti-inflammatory effect within the vascular compartments.
Collapse
Affiliation(s)
- Dennis McGonagle
- Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK; National Institute for Health Research Leeds Biomedical Research Centre, Leeds Teaching Hospitals, Leeds, UK.
| | - Charlie Bridgewood
- Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK
| | - James F M Meaney
- Department of Radiology and Thomas Mitchell Centre for Advanced Medical Imaging, St James Hospital and Trinity College Dublin, Dublin, Ireland.
| |
Collapse
|
|
12
|
Kaptein FHJ, Kroft LJM, Hammerschlag G, Ninaber MK, Bauer MP, Huisman MV, Klok FA. Pulmonary infarction in acute pulmonary embolism. Thromb Res 2021; 202:162-169. [PMID: 33862471 DOI: 10.1016/j.thromres.2021.03.022] [Citation(s) in RCA: 46] [Impact Index Per Article: 11.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/27/2021] [Revised: 03/05/2021] [Accepted: 03/24/2021] [Indexed: 01/10/2023]
Abstract
Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and ultimately necrosis of the lung parenchyma. It is most commonly caused by acute pulmonary embolism (PE), with a reported incidence of around 30%. Following an occlusion of the pulmonary artery, the bronchial arteries are recruited as primary source of perfusion of the pulmonary capillaries. The relatively higher blood pressure in the bronchial circulation causes an increase in the capillary blood flow, leading to extravasation of erythrocytes (i.e. alveolar hemorrhage). If this hemorrhage cannot be resorbed, it results in tissue necrosis and infarction. Different definitions of pulmonary infarction are used in literature (clinical, radiological and histological), although the diagnosis is nowadays mostly based on radiological characteristics. Notably, the infarcted area is only replaced by a fibrotic scar over a period of months. Hence and formally, the diagnosis of pulmonary infarction cannot be confirmed upon diagnosis of acute PE. Little is known of the impact and relevance of pulmonary infarction in acute PE, and whether specific management strategies should be applied to prevent and/or treat complications such as pain, pneumonia or post-PE syndrome. In this review we will summarize current knowledge on the pathophysiology, epidemiology, diagnosis and prognosis of pulmonary infarction in the setting of acute PE. We highlight the need for dedicated studies to overcome the current knowledge gaps.
Collapse
Affiliation(s)
- F H J Kaptein
- Department of Medicine - Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, the Netherlands
| | - L J M Kroft
- Department of Radiology, Leiden University Medical Center, Leiden, the Netherlands
| | - G Hammerschlag
- Department of Respiratory and Sleep Medicine, The Royal Melbourne Hospital, Melbourne, Australia
| | - M K Ninaber
- Department of Pulmonology, Leiden University Medical Center, Leiden, the Netherlands
| | - M P Bauer
- Department of Medicine - Acute Medicine, Leiden University Medical Center, Leiden, the Netherlands
| | - M V Huisman
- Department of Medicine - Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, the Netherlands
| | - F A Klok
- Department of Medicine - Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, the Netherlands.
| |
Collapse
|
|
13
|
Copetti R, Cominotto F, Meduri S, Orso D. The "Survived Lung:" An Ultrasound Sign of "Bubbly Consolidation" Pulmonary Infarction. ULTRASOUND IN MEDICINE & BIOLOGY 2020; 46:2546-2550. [PMID: 32507699 DOI: 10.1016/j.ultrasmedbio.2020.04.036] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 09/24/2019] [Revised: 04/28/2020] [Accepted: 04/30/2020] [Indexed: 06/11/2023]
Abstract
Since the presence of "bubbly consolidation" (central lucencies) on a multi-slice computed tomography pulmonary angiography (MCTPA) is one of the highly specific imaging appearances of infarct secondary to pulmonary embolism, we investigated the ultrasound characteristics of these infarctions. In this study, 118 patients with MCTPA diagnosis of acute pulmonary embolism were enrolled. Pulmonary infarctions were detected in 21 patients (17.7%), of which 10 (47.6%) showed the typical appearance of bubbly consolidation on MCTPA. Lung ultrasound (LUS) was performed to evaluate the characteristics of the infarcts highlighted by MCTPA. The bubbly consolidations showed a very peculiar echographic aspect represented by a triangular hypoechoic consolidation with sharp margins, the absence of air bronchograms and a mostly central roundish hyperechoic area. Air lucencies within a pulmonary infarct is hypothesized to represent the coexistence of aerated non-infarcted lung with the infarcted lung in the same lobule. The ultrasound appearance confirms this hypothesis, so we named the roundish hyperechoic area the "survived lung." This picture was found in all patients with a diagnosis of bubbly consolidation on MCTPA (100%). Χ2 between MCTPA and LUS regarding the bubbly consolidation diagnosis is 17.18 (df = 1; p value = 0.00003). Bubbly consolidations show a very typical appearance on LUS. Their detection suggests further investigations (MCTPA or point-of-care multi-organ ultrasonography).
Collapse
Affiliation(s)
- Roberto Copetti
- Department of Emergency Medicine, University Hospital of Cattinara, Trieste, Italy
| | - Franco Cominotto
- Department of Emergency Medicine, San Giovanni di Dio Hospital, Gorizia, Italy
| | - Stefano Meduri
- Radiology Department, Latisana/Palmanova Hospitals, Latisana (UD), Italy
| | - Daniele Orso
- Anesthesiology and Intensive Care Medicine Division, Department of Medicine, ASUIUD University Hospital of Udine, Udine, Italy.
| |
Collapse
|
|
14
|
Rossi G, Nosseir S, Jocollé G, Sartori G, Banchelli I, Busetti S, Baldovini C. Infarct-Like Spindle Cell Carcinoma of the Lung: Clinicopathologic, Immunohistochemical, and Molecular Analysis of 4 Cases. Int J Surg Pathol 2020; 28:616-623. [PMID: 32188318 DOI: 10.1177/1066896920912471] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022]
Abstract
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.
Collapse
Affiliation(s)
- Giulio Rossi
- Operative Unit of Pathologic Anatomy, AUSL della Romagna, "S. Maria delle Croci" Hospital, Ravenna, Italy
| | - Sofia Nosseir
- Operative Unit of Pathologic Anatomy, AUSL della Romagna, "S. Maria delle Croci" Hospital, Ravenna, Italy
| | - Genny Jocollé
- Operative Unit of Pathologic Anatomy, AUSL della Valle d'Aosta, "Parini" Regional Hospital, Aosta, Italy
| | - Giuliana Sartori
- Pathology Unit, AUSL/IRCSS di Reggio Emilia, "S. Maria Nuova" Hospital, Reggio Emilia, Italy
| | - Isabella Banchelli
- Operative Unit of Pathologic Anatomy, AUSL della Romagna, "S. Maria delle Croci" Hospital, Ravenna, Italy
| | | | - Chiara Baldovini
- Operative Unit of Pathologic Anatomy, AUSL della Romagna, "S. Maria delle Croci" Hospital, Ravenna, Italy
| |
Collapse
|
|
15
|
Palaparti R, Dandamudi S, Chowdary PSS, Kondru P, Palaparthi S, Koduru G, Ghanta S, Mannuva B. “Bubbly lung consolidation” - A highly specific imaging marker for pulmonary infarction. JOURNAL OF DR. NTR UNIVERSITY OF HEALTH SCIENCES 2020. [DOI: 10.4103/jdrntruhs.jdrntruhs_111_19] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/09/2023] Open
|
|
16
|
Na YS, Jang S, Hong S, Oh YM, Lee SD, Lee JS. Clinical Phenotype of a First Unprovoked Acute Pulmonary Embolism Associated with Antiphospholipid Antibody Syndrome. Tuberc Respir Dis (Seoul) 2019; 82:53-61. [PMID: 30574689 PMCID: PMC6304333 DOI: 10.4046/trd.2018.0045] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/10/2018] [Revised: 07/22/2018] [Accepted: 10/16/2018] [Indexed: 01/08/2023] Open
Abstract
BACKGROUND Antiphospholipid antibody syndrome (APS), an important cause of acquired thrombophilia, is diagnosed when vascular thrombosis or pregnancy morbidity occurs with persistently positive antiphospholipid antibodies (aPL). APS is a risk factor for unprovoked recurrence of pulmonary embolism (PE). Performing laboratory testing for aPL after a first unprovoked acute PE is controversial. We investigated if a specific phenotype existed in patients with unprovoked with acute PE, suggesting the need to evaluate them for APS. METHODS We retrospectively reviewed patients with PE and APS (n=24) and those with unprovoked PE with aPL negative (n=44), evaluated 2006-2016 at the Asan Medical Center. We compared patient demographics, clinical manifestations, laboratory findings, and radiological findings between the groups. RESULTS On multivariate logistic regression analysis, two models of independent risk factors for APS-PE were suggested. Model I included hemoptysis (odds ratio [OR], 12.897; 95% confidence interval [CI], 1.025-162.343), low PE severity index (OR, 0.948; 95% CI, 0.917-0.979), and activated partial thromboplastin time (aPTT; OR, 1.166; 95% CI, 1.040-1.307). Model II included age (OR, 0.930; 95% CI, 0.893-0.969) and aPTT (OR, 1.104; 95% CI, 1.000-1.217). CONCLUSION We conclude that patients with first unprovoked PE with hemoptysis and are age <40; have a low pulmonary embolism severity index, especially in risk class I-II; and/or prolonged aPTT (above 75th percentile of the reference interval), should be suspected of having APS, and undergo laboratory testing for aPL.
Collapse
Affiliation(s)
- Yong Sub Na
- Department of Pulmonary and Critical Care Medicine, Chosun University Hospital, Gwangju, Korea
| | - Seongsoo Jang
- Department of Laboratory Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Seokchan Hong
- Department of Rheumatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Yeon Mok Oh
- Department of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Sang Do Lee
- Department of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Jae Seung Lee
- Department of Pulmonary and Critical Care Medicine, Center for Pulmonary Hypertension and Venous Thrombosis, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
| |
Collapse
|
|
17
|
Chengsupanimit T, Sundaram B, Lau WB, Keith SW, Kane GC. Clinical characteristics of patients with pulmonary infarction - A retrospective review. Respir Med 2018; 139:13-18. [PMID: 29857996 DOI: 10.1016/j.rmed.2018.04.008] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/15/2018] [Revised: 04/09/2018] [Accepted: 04/16/2018] [Indexed: 12/15/2022]
Abstract
BACKGROUND Pulmonary infarction is an infrequent complication of pulmonary embolism. Traditionally, it has been regarded as a sign of worse outcome because ischemia can only occur by the simultaneous failure of all oxygenation sources to the area of infarct, but supporting evidence is limited. METHODS We identified 74 cases of pulmonary infarction over 5 years at a single academic center via review of radiographic reports. Contrast-enhanced chest CT scans were examined to confirm evidence of pulmonary infarction, and patient clinical characteristics and imaging results were studied. RESULTS Survival to discharge was high (97%). Patients most commonly presented with dyspnea (69%), chest pain (46%), and swelling or pain in the lower extremities (31%), while underlying risk factors included history of malignancy (41%) and surgery within 30 days (24%). Many patients had concurrent cardiovascular (59%) and pulmonary disease (22%). Infarction disproportionately affected the lower lobes. CONCLUSIONS Survival after diagnosis of pulmonary infarction is comparable to uncomplicated pulmonary embolism, suggesting that outcome is not worse. While emboli occurred in multiple lobar sites, pulmonary infarction occurred most commonly in the lower lobes, suggesting unique underlying physiological mechanisms in pulmonary infarction development.
Collapse
Affiliation(s)
- Tayoot Chengsupanimit
- Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, United States.
| | - Baskaran Sundaram
- The Division of Cardiothoracic Radiology, Department of Radiology, Thomas Jefferson University, Philadelphia, PA, United States
| | - Wayne Bond Lau
- The Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA, United States
| | - Scott W Keith
- The Division of Biostatistics, Department of Pharmacology and Experimental Therapeutics, Thomas Jefferson University, Philadelphia, PA, United States
| | - Gregory C Kane
- The Jefferson - National Jewish Jane and Leonard Korman Respiratory Institute, Division of Pulmonary, Allergy & Critical Care Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA, United States
| |
Collapse
|
|
18
|
Ocampo JM, Urrea-Zapata JK, Gutiérrez-Londoño H, Jurado-Delgado J, Uribe-Valencia MA. Tumor evanescente: un reto diagnóstico. REVISTA COLOMBIANA DE CARDIOLOGÍA 2018. [DOI: 10.1016/j.rccar.2017.08.023] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022] Open
|
|
19
|
Shinohara T, Naruse K, Hamada N, Yamasaki T, Hatakeyama N, Ogushi F. Fan-shaped ground-glass opacity (GGO) as a premonitory sign of pulmonary infarction: a case report. J Thorac Dis 2018; 10:E55-E58. [PMID: 29600105 DOI: 10.21037/jtd.2017.12.64] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/06/2022]
Abstract
Radiological findings of pulmonary infarction have been well characterized mainly in established infarction. However, the early course CT appearance of patients who develop pulmonary infarction has not yet been fully elucidated. A 50-year-old female with a history of postmenopausal hormone replacement therapy (HRT) presented with dry cough and high-resolution computed tomography (HRCT) findings of fan-shaped segmental ground-glass opacity (GGO) in the right lower lobe. As the parenchymal density in the GGO gradually enlarged over a period of 4 weeks in spite of antibiotic treatment, the patient was referred to our hospital on clinical suspicion of bronchioloalveolar cell carcinoma. However, the pathological findings of a transbronchial biopsy of the lesion were compatible with pulmonary infarction. After an endoscopic examination, the typical CT appearance of established pulmonary infarction was observed. Moreover, enhanced CT detected an intraluminal filling defect in the right lower lobe artery suggesting peripheral pulmonary emboli. Our case was a peripheral pulmonary infarction probably induced by HRT, and suggested that fan-shaped GGO may be a premonitory sign of pulmonary infarction.
Collapse
Affiliation(s)
- Tsutomu Shinohara
- Department of Clinical Investigation, National Hospital Organization Kochi Hospital, Kochi, Japan
| | - Keishi Naruse
- Division of Pathology, National Hospital Organization Kochi Hospital, Kochi, Japan
| | - Norihiko Hamada
- Division of Radiology, National Hospital Organization Kochi Hospital, Kochi, Japan
| | - Takashi Yamasaki
- Division of Cardiovascular Disease, National Hospital Organization Kochi Hospital, Kochi, Japan
| | - Nobuo Hatakeyama
- Division of Pulmonary Medicine, National Hospital Organization Kochi Hospital, Kochi, Japan
| | - Fumitaka Ogushi
- Division of Pulmonary Medicine, National Hospital Organization Kochi Hospital, Kochi, Japan
| |
Collapse
|
|
20
|
Wong CC, Ng AC, Lau JK, Chow V, Sindone AP, Kritharides L. The prognostic impact of chest pain in 1306 patients presenting with confirmed acute pulmonary embolism. Int J Cardiol 2016; 221:794-9. [DOI: 10.1016/j.ijcard.2016.07.129] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/21/2016] [Accepted: 07/08/2016] [Indexed: 11/24/2022]
|
|
21
|
Affiliation(s)
- WA Seed
- Department of Medicine, Charing Cross and Westminster Medical School, London, UK
| |
Collapse
|
|
22
|
Mangas-Moro A, Díaz-Pollán B. Masa cavitada en paciente con disnea súbita. Rev Clin Esp 2015; 215:423-4. [DOI: 10.1016/j.rce.2015.02.021] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/23/2015] [Accepted: 02/23/2015] [Indexed: 10/23/2022]
|
|
23
|
Bray T, Mortensen K, Gopalan D. Multimodality imaging of pulmonary infarction. Eur J Radiol 2014; 83:2240-2254. [DOI: 10.1016/j.ejrad.2014.07.016] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/20/2014] [Revised: 06/16/2014] [Accepted: 07/20/2014] [Indexed: 12/12/2022]
|
|
24
|
Tsang JYC, Hogg JC. Gas exchange and pulmonary hypertension following acute pulmonary thromboembolism: has the emperor got some new clothes yet? Pulm Circ 2014; 4:220-36. [PMID: 25006441 DOI: 10.1086/675985] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/25/2013] [Accepted: 02/17/2014] [Indexed: 01/09/2023] Open
Abstract
Patients present with a wide range of hypoxemia after acute pulmonary thromboembolism (APTE). Recent studies using fluorescent microspheres demonstrated that the scattering of regional blood flows after APTE, created by the embolic obstruction unique in each patient, significantly worsened regional ventilation/perfusion (V/Q) heterogeneity and explained the variability in gas exchange. Furthermore, earlier investigators suggested the roles of released vasoactive mediators in affecting pulmonary hypertension after APTE, but their quantification remained challenging. The latest study reported that mechanical obstruction by clots accounted for most of the increase in pulmonary vascular resistance, but that endothelin-mediated vasoconstriction also persisted at significant level during the early phase.
Collapse
Affiliation(s)
- John Y C Tsang
- Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
| | - James C Hogg
- Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada
| |
Collapse
|
|
25
|
Abstract
BACKGROUND The reversed halo sign, originally described in cryptogenic organizing pneumonia, has been observed in a variety of pulmonary diseases, including pulmonary embolism (PE). PURPOSE To describe the computed tomographic (CT) findings in patients with the reversed halo sign and acute PE at initial presentation and in subsequent scans. MATERIAL AND METHODS Contrast-enhanced CT examinations of 12 patients with the reversed halo sign and acute PE were analyzed retrospectively. The diagnosis of pulmonary embolism was made by CT angiography in 11 cases and by a routine contrast-enhanced scan of the chest in the other case. Follow-up scans of seven patients and follow-up radiographs of two patients were also examined retrospectively. The average age of the patients was 49 years (range, 21-80 years). Seven (58%) patients were women. Six patients had no significant medical history, and six patients had deep venous thrombosis initially. RESULTS The reversed halo sign was observed as a single lesion in 10 patients; in two patients, two lesions were found. The lesions, all pleural-based, occurred more frequently in the lower lobes and were associated with acute thromboemboli in segmental and subsegmental pulmonary arteries of the corresponding segment. Ten (10/14, 71%) lesions displayed an ellipsoid configuration, two (2/14, 14%) had a pyramidal shape, and two involved an almost entire pulmonary segment. The average largest dimension was 3.9 cm (range, 2.1-6.7 cm). All lesions subtended one or more bronchovascular bundles; three (3/14, 21%) showed air-bronchograms, and a thromboembolus was identified in the subtended arteries in nine (9/14, 64%) lesions. In succeeding CT scans (eight lesions) and follow-up radiographs (three lesions), the lesions became smaller, and the majority evolved into pleural-based linear scars by 7 months. CONCLUSION The reversed halo sign very likely corresponds to pulmonary infarction in patients with acute PE. Its recognition may have important clinical implications.
Collapse
Affiliation(s)
- Joseph Casullo
- Department of Diagnostic Radiology, Montreal General Hospital, McGill University Health Center, Montreal, Quebec, Canada
| | - Alexandre Semionov
- Department of Diagnostic Radiology, Montreal General Hospital, McGill University Health Center, Montreal, Quebec, Canada
| |
Collapse
|
|
26
|
Densmore JC, Jeziorczak PM, Clough AV, Pritchard KA, Cummens B, Medhora M, Rao A, Jacobs ER. Rattus model utilizing selective pulmonary ischemia induces bronchiolitis obliterans organizing pneumonia. Shock 2013; 39:271-7. [PMID: 23364425 PMCID: PMC3578046 DOI: 10.1097/shk.0b013e318281a58c] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/27/2022]
Abstract
Bronchiolitis obliterans organizing pneumonia (BOOP), a morbid condition when associated with lung transplant and chronic lung disease, is believed to be a complication of ischemia. Our goal was to develop a simple and reliable model of lung ischemia in the Sprague-Dawley rat that would produce BOOP. Unilateral ischemia without airway occlusion was produced by an occlusive slipknot placed around the left main pulmonary artery. Studies were performed 7 days later. Relative pulmonary and systemic flow to each lung was measured by injection of technetium Tc 99m macroaggregated albumin. Histological sections were examined for structure and necrosis and scored for BOOP. Apoptosis was detected by immunohistochemistry with an antibody against cleaved caspase 3. Pulmonary artery blood flow to left lungs was less than 0.1% of the cardiac output, and bronchial artery circulation was ∼2% of aortic artery flow. Histological sections from ischemic left lungs consistently showed Masson bodies, inflammation, and young fibroblasts filling the distal airways and alveoli, consistent with BOOP. In quantitative evaluation of BOOP using epithelial changes, inflammation and fibrosis were higher in ischemic left lungs than right or sham-operated left lungs. Apoptosis was increased in areas exhibiting histological BOOP, but there was no histological evidence of necrosis. Toll-like receptor 4 expression was increased in ischemic left lungs over right. An occlusive slipknot around the main left pulmonary artery in rats produces BOOP, providing direct evidence that ischemia without immunomodulation or coinfection is sufficient to initiate this injury. It also affords an excellent model to study signaling and genetic mechanisms underlying BOOP.
Collapse
|
|
27
|
Kinoshita Y, Sakamoto A, Koga T, Hidaka K. Diffuse alveolar damage associated with pulmonary thromboembolism. Respir Med Case Rep 2013; 8:25-7. [PMID: 26029610 PMCID: PMC3920436 DOI: 10.1016/j.rmcr.2012.12.005] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/30/2012] [Revised: 10/18/2012] [Accepted: 12/14/2012] [Indexed: 12/01/2022] Open
Abstract
In contrast to other internal organs, pulmonary arterial hypoperfusion does not always show ischemic changes in the lung parenchyma. Pulmonary thromboembolism (PTE)-related lung injury is extremely rare except in the case of pulmonary infarctions, in which PTE occasionally causes necrosis of the parenchyma. We describe the case of an 86-year-old woman who presented with respiratory failure and bilateral ground-glass opacity predominantly the upper lobes. Autopsy revealed a saddle-shaped old organized thrombi in the main pulmonary artery, relatively fresh thrombi in both pulmonary arteries, and localized diffuse alveolar damage (DAD) in the bilateral upper lung fields. The hypoperfused regions resulting from the thromboembolism anatomically coincided with the pulmonary lesion where DAD was identified. Although PTE is not regarded as a causal factor of DAD, it might induce DAD as a result of hypoperfusion in limited cases.
Collapse
Affiliation(s)
- Yoshiaki Kinoshita
- Division of Respiratory Medicine, Department of Internal Medicine, National Hospital Organization, Kokura Medical Center, Fukuoka, Japan
| | - Atsuhiko Sakamoto
- Division of Respiratory Medicine, Department of Internal Medicine, National Hospital Organization, Kokura Medical Center, Fukuoka, Japan
| | - Takaomi Koga
- Division of Pathophysiological and Experimental Pathology, Department of Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
| | - Kouko Hidaka
- Division of Respiratory Medicine, Department of Internal Medicine, National Hospital Organization, Kokura Medical Center, Fukuoka, Japan
| |
Collapse
|
|
28
|
A 47-Year-Old Man With Progressive Shortness of Breath and Exercise Intolerance. Am J Med Sci 2012; 344:407-12. [DOI: 10.1097/maj.0b013e31825176ac] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022]
|
|
29
|
Abstract
Venous thromboembolism (VTE) originates in systemic venous thrombosis and has different etiological mechanisms and natural history from arterial thrombosis. VTE typically originates as deep venous thrombosis in a lower extremity, where it may give rise to acute symptoms “upstream” from the obstructed vein, result in pulmonary embolism, and/or cause chronic venous obstruction. Pulmonary embolism may result in acute respiratory symptoms, cardiovascular collapse and, uncommonly, may also cause chronic disease.
Collapse
Affiliation(s)
- Timothy A Morris
- Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California, San Diego School of Medicine, 200 West Arbor Drive, San Diego, CA 92103-8378, USA.
| |
Collapse
|
|
30
|
Cha SI, Shin KM, Lee J, Hwangbo Y, Yoo SS, Lee J, Lee SY, Kim CH, Park JY, Jung TH. Clinical relevance of pulmonary infarction in patients with pulmonary embolism. Thromb Res 2012; 130:e1-5. [PMID: 22482830 DOI: 10.1016/j.thromres.2012.03.012] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/13/2012] [Revised: 03/12/2012] [Accepted: 03/13/2012] [Indexed: 11/16/2022]
Abstract
INTRODUCTION Data regarding the clinical relevance of pulmonary infarction (PI) in patients with pulmonary embolism (PE) are lacking. The aim of this study was to investigate the clinical features of PE patients with PI and the prognostic role of PI for PE patients. MATERIALS AND METHODS Based on computed tomography scan, 509 patients with PE were divided into two groups, the infarction group (n=45) and the non-infarction group (n=464). A variety of clinical parameters were compared between the two groups. RESULTS In the infarction group, the largest pulmonary arteries involved by emboli were central rather than peripheral and more proximal as compared to the non-infarction group (p=0.01 and p<0.03, respectively). Thrombolytic agents tended to be more frequently administered in the infarction group (13.3% [n=6] versus 6.3% [n=29], p=0.07). In-hospital mortality, PE-related deaths, and the recurrence rate of PE did not differ between the two groups. CONCLUSIONS The present study did not demonstrate that PI is a prognostic indicator of recurrence and mortality in PE patients. We suggest the possibility that blood clot burden is greater in PE patients with PI, although PI by itself occurs in small pulmonary arteries.
Collapse
Affiliation(s)
- Seung-Ick Cha
- Department of Internal Medicine, Kyungpook National University School of Medicine, Daegu, Korea.
| | | | | | | | | | | | | | | | | | | |
Collapse
|
|
31
|
Messmer AS, Kubera KM, Buser PJ, Tamm M, Muenst S, Nickel CH, Bingisser R. Pulmonary cavitation in a patient presenting with nonspecific complaints. Am J Emerg Med 2011; 30:1662.e1-3. [PMID: 22100464 DOI: 10.1016/j.ajem.2011.09.004] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/26/2011] [Accepted: 09/01/2011] [Indexed: 11/20/2022] Open
Abstract
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.
Collapse
Affiliation(s)
- Anna Sarah Messmer
- Department of Emergency Medicine, University Hospital Basel, Switzerland
| | | | | | | | | | | | | |
Collapse
|
|
32
|
Weng CT, Chung TJ, Liu MF, Weng MY, Lee CH, Chen JY, Wu AB, Lin BW, Luo CY, Hsu SC, Lee BF, Tsai HM, Chao SC, Wang JY, Chen TY, Chen CW, Chang HY, Wang CR. A retrospective study of pulmonary infarction in patients with systemic lupus erythematosus from southern Taiwan. Lupus 2011; 20:876-85. [PMID: 21693494 DOI: 10.1177/0961203311401458] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022]
Abstract
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.
Collapse
Affiliation(s)
- CT Weng
- Section of Rheumatology and Immunology, Department of Internal Medicine, National Cheng Kung University Hospital and Dou-Liou Branch, Tainan, Taiwan–Republic of China
| | - TJ Chung
- Department of Radiology, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - MF Liu
- Section of Rheumatology and Immunology, Department of Internal Medicine, National Cheng Kung University Hospital and Dou-Liou Branch, Tainan, Taiwan–Republic of China
| | - MY Weng
- Section of Rheumatology and Immunology, Department of Internal Medicine, National Cheng Kung University Hospital and Dou-Liou Branch, Tainan, Taiwan–Republic of China
| | - CH Lee
- Section of Cardiology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - JY Chen
- Section of Cardiology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - AB Wu
- Section of Nephrology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - BW Lin
- Department of Surgery, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - CY Luo
- Department of Surgery, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - SC Hsu
- Department of Emergency Medicine, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - BF Lee
- Department of Nuclear Medicine, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - HM Tsai
- Department of Radiology, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - SC Chao
- Department of Dermatology, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - JY Wang
- Department of Pediatrics, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - TY Chen
- Section of Hemato-oncology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - CW Chen
- Section of Critical Care Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - HY Chang
- Section of Chest Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan–Republic of China
| | - CR Wang
- Section of Rheumatology and Immunology, Department of Internal Medicine, National Cheng Kung University Hospital and Dou-Liou Branch, Tainan, Taiwan–Republic of China
| |
Collapse
|
|
33
|
Guidelines for the diagnosis, treatment and prevention of pulmonary thromboembolism and deep vein thrombosis (JCS 2009). Circ J 2011; 75:1258-81. [PMID: 21441695 DOI: 10.1253/circj.cj-88-0010] [Citation(s) in RCA: 239] [Impact Index Per Article: 17.1] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
|
|
34
|
|
|
35
|
Gleeson TG, Cheyne I, English JC, Quadri SM, Leipsic JA. A 50-Year-Old Woman With a History of Atrial Fibrillation Presents With Acute Dyspnea and Pleuritic Chest Pain. Chest 2010; 137:1225-1230. [DOI: 10.1378/chest.09-1362] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 08/30/2023] Open
|
|
36
|
Cho JH, Kim JT, Kim L, Lee KH, Ryu JS, Kwak SM, Lee HL. A pulmonary nodule due to pulmonary infarction diagnosed by video-assisted thoracoscopy. Yonsei Med J 2009; 50:591-3. [PMID: 19718413 PMCID: PMC2730627 DOI: 10.3349/ymj.2009.50.4.591] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/13/2007] [Revised: 01/04/2008] [Accepted: 01/04/2008] [Indexed: 11/27/2022] Open
Abstract
We report a pulmonary infarction in 68-year-old man who was referred for an asymptomatic pulmonary nodule in chest radiography. Computed tomography (CT), positron emission tomography (PET), and transthoracic needle aspiration suggested suspicion for malignancy. Video-assisted thoracoscopic surgery (VATS) was performed for histologic diagnosis. Our case is a pulmonary nodule due to pulmonary infarction diagnosed by VATS in Korea.
Collapse
Affiliation(s)
- Jae Hwa Cho
- Department of Internal Medicine, School of Medicine, Inha University, Incheon, Korea.
| | | | | | | | | | | | | |
Collapse
|
|
37
|
The surgical pathology of pulmonary infarcts: diagnostic confusion with granulomatous disease, vasculitis, and neoplasia. Mod Pathol 2009; 22:679-85. [PMID: 19287460 DOI: 10.1038/modpathol.2009.20] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/09/2022]
Abstract
Twenty-three cases of surgically resected pulmonary infarcts sent in consultation were reviewed to evaluate their morphology and to assess reasons for consultation. The morphology of these infarcts demonstrated that only a minority had the classical triangular shape at low magnification (26%) whereas the majority were either spherical (17%) or had a geographic pattern of necrosis (35%). The margin of the infarcted tissue often had a pseudogranulomatous appearance due to palisaded histiocytes, foam cells, or perpendicularly oriented proliferations of fibroblasts and myofibroblasts (74%) and occasional cholesterol- and hemosiderin-laden giant cells. Basophilic granular karyorrhectic necrosis was seen focally (52%) as was vascular inflammation (56%) raising the differential diagnosis of Wegener's granulomatosis or infectious granulomas. These nonclassical features combined with a low incidence of clinical hemoptysis, chest pain and pleurisy, and a primary radiographic diagnosis of 'nodule r/o malignancy' highlight the need to consider thromboembolic pulmonary infarcts in the differential diagnosis of necrotic lung nodules with a histiocytic and fibroproliferative rim.
Collapse
|
|
38
|
|
|
39
|
Takahashi M, Murakami Y, Nitta N, Murata K, Tezuka N, Fujino S, Okabe H. Pulmonary infarction associated with bronchogenic carcinoma. ACTA ACUST UNITED AC 2008; 26:76-80. [DOI: 10.1007/s11604-007-0192-9] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/08/2007] [Accepted: 10/02/2007] [Indexed: 11/30/2022]
|
|
40
|
Ravnic DJ, Konerding MA, Pratt JP, Wolloscheck T, Huss HT, Mentzer SJ. The murine bronchopulmonary microcirculation in hapten-induced inflammation. J Thorac Cardiovasc Surg 2007; 133:97-103. [PMID: 17198790 DOI: 10.1016/j.jtcvs.2006.08.054] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/27/2006] [Revised: 07/12/2006] [Accepted: 08/07/2006] [Indexed: 11/21/2022]
Abstract
OBJECTIVE The clinical observation of central bronchial artery hypertrophy in chronic lung inflammation suggests the possibility that the bronchial circulation may also participate in adaptive responses in peripheral lung inflammation. METHODS To investigate the potential role of the bronchial microcirculation in peripheral lung inflammation, we developed a murine model of lung inflammation using the intratracheal instillation of the peptide-hapten trinitrophenol in presensitized mice. RESULTS Clinical parameters indicated a peak inflammatory response at 96 hours. Similarly, gross and microscopic evidence of inflammation was observed 96 hours after antigen instillation. Using a forced oscillation technique to probe peripheral lung mechanics at 96 hours, we detected no change in central airway resistance (P > .05), but a significant increase in peripheral tissue resistance (P < .05). The structure of the bronchial circulation was investigated by microsphere occlusion of the pulmonary circulation and corrosion casting of the bronchial circulation. SEM of the bronchial artery casts demonstrated (1) the presence of the peripheral bronchial circulation in mice, (2) interconnections of the two systems in the distal bronchial arteries and at the level of alveolar capillaries, and (3) functional evidence of increased bronchial perfusion of alveolar capillaries during mononuclear inflammation. CONCLUSION These results suggest an important adaptive role of the bronchial circulation in pulmonary inflammation.
Collapse
Affiliation(s)
- Dino J Ravnic
- Division of Thoracic Surgery, Brigham & Women's Hospital, Boston, Mass 02115, USA
| | | | | | | | | | | |
Collapse
|
|
41
|
He H, Stein MW, Zalta B, Haramati LB. Pulmonary infarction: spectrum of findings on multidetector helical CT. J Thorac Imaging 2006; 21:1-7. [PMID: 16538148 DOI: 10.1097/01.rti.0000187433.06762.fb] [Citation(s) in RCA: 62] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022]
Abstract
OBJECTIVE Despite the dual blood supply to the lung, acute pulmonary embolism (PE) can lead to a spectrum of ischemic injury to the lung resulting in infarction and hemorrhage. In this series we systematically describe the spectrum of CT findings and clinical correlates of pulmonary infarction in patients with PE. METHODS We retrospectively identified 24 consecutive adults with pulmonary infarction on multidetector CT between July 2002 and March 2004. There were 13 women and 11 men, with a mean age of 59 years. The cases were identified by review of 74 consecutive CTs demonstrating PE. Each CT was evaluated by 2 of 3 reviewers in consensus for presence and characteristics of peripheral parenchymal opacities and extent of PE. Peripheral opacities were evaluated for degree of enhancement, internal air lucencies, and contour. The presence of adjacent vessels and linear strands were noted. At the end of interpreting each case, the reviewers determined whether or not an infarct was present based on the constellation of previously described imaging features. The extent of pulmonary vascular obstruction was graded using the CT clot burden scoring system. Each chart was reviewed for predisposing factors for PE and infarction, presenting clinical symptoms/signs, and co-existing pulmonary or cardiac conditions. RESULTS Thirty-two percent (24/74) of patients with PE had pulmonary infarction. Thirty-three percent (8/24) of patients had more than 1 infarct. Seventy-three percent (27/37) of infarcts were in the lower lobes. The CT findings of pulmonary infarction included: focal decrease in parenchymal enhancement in 95% (35/37), broad pleural base in 65% (24/37), truncated apex in 57% (21/37), convex border in 46% (17/37), internal air lucencies in 32% (12/37), linear stranding from the apex toward the hilum in 24% (9/37), and a thickened vessel leading to the apex of the infarct in 14% (5/37). There was a trend toward a higher mean clot burden (12.3 vs. 10.5) between the patients with PE with and without infarction. Ninety-six percent (23/24) of patients with pulmonary infarction had predisposing factors for infarction, including PE involving more than 1 lobe (n = 21), malignancy (n = 5), and heart failure (n = 3). Pleuritic chest pain was significantly more frequent in patients with infarction (P = 0.0064). CONCLUSION Pulmonary infarction occurred in nearly 1/3 of patients with PE in this series. The infarcts were peripheral parenchymal opacities characterized by a distinctive complex of findings on CT reflecting ischemic injury in the setting of a dual blood supply to the lung. Pleuritic chest pain was significantly associated with infarction.
Collapse
Affiliation(s)
- Hongying He
- Department of Radiology, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY 10467, USA
| | | | | | | |
Collapse
|
|
42
|
Parambil JG, Savci CD, Tazelaar HD, Ryu JH. Causes and Presenting Features of Pulmonary Infarctions in 43 Cases Identified by Surgical Lung Biopsy. Chest 2005. [DOI: 10.1016/s0012-3692(15)34464-0] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/15/2023] Open
|
|
43
|
George CJ, Tazelaar HD, Swensen SJ, Ryu JH. Clinicoradiological features of pulmonary infarctions mimicking lung cancer. Mayo Clin Proc 2004; 79:895-8. [PMID: 15244386 DOI: 10.4065/79.7.895] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]
Abstract
OBJECTIVE To describe presenting features of pulmonary infarction that may simulate those of lung cancer. PATIENTS AND METHODS We reviewed the medical records of 43 patients with pulmonary infarction diagnosed by surgical lung biopsy at the Mayo Clinic in Rochester, Minn, from January 1, 1996, to December 31, 2002. Of 16 patients presenting with an undiagnosed solitary pulmonary nodule or mass, 6 had features suggestive of lung cancer on additional imaging, including abnormalities on contrast-enhancement computed tomography (CT), positron emission tomography (PET), or nonsurgical lung biopsy before surgical resection. We examined the presenting symptoms, epidemiological, clinical, and radiological features, and clinical course of these 6 patients. RESULTS All 6 patients, ranging in age from 41 to 85 years, had a history of smoking and underlying cardiopulmonary disease. In 5 of the 6 patients, CT showed a nodule in the subpleural region of the lung. Three patients had abnormalities on contrast-enhancement CT, 2 had abnormalities on PET, and 1 had abnormal cytologic findings on a transthoracic needle biopsy of the lung; all these studies showed abnormalities suggestive of lung cancer. Surgical resection of the nodule or mass revealed pulmonary infarction associated with organizing thrombi in all 6 patients. CONCLUSIONS Pulmonary infarctions can closely mimic the clinicoradiological characteristics of lung cancer, an association not reported previously. Furthermore, cytologic changes that occur in pulmonary infarctions may produce malignant-appearing cells on needle biopsy of the lung. The possibility of pulmonary infarction should be considered in the differential diagnosis of a solitary lung nodule or mass located in the subpleural region, even in the absence of clinically recognized venous thromboembolism.
Collapse
Affiliation(s)
- C Joseph George
- Division of Pulmonary and Critical Care Medicine, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA
| | | | | | | |
Collapse
|
|
44
|
Frazier AA, Galvin JR, Franks TJ, Rosado-De-Christenson ML. From the archives of the AFIP: pulmonary vasculature: hypertension and infarction. Radiographics 2000; 20:491-524; quiz 530-1, 532. [PMID: 10715347 DOI: 10.1148/radiographics.20.2.g00mc17491] [Citation(s) in RCA: 132] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022]
Abstract
Pulmonary hypertension is the hemodynamic consequence of vascular changes within the precapillary (arterial) or postcapillary (venous) pulmonary circulation. These changes may be idiopathic, as in primary pulmonary hypertension or pulmonary veno-occlusive disease, but more commonly they represent a secondary response to alterations in pulmonary blood flow. The pulmonary and systemic bronchial circulations form broad anastomoses that largely prevent infarction except in settings of markedly elevated pulmonary venous pressure, underlying malignancy, or excessive embolic burden. Causes of precapillary pulmonary hypertension include long-standing cardiac left-to-right shunt, chronic thromboembolic disease, and widespread pulmonary embolism arising from intravascular malignant cells, parasites, or foreign materials. The classic radiologic features of precapillary pulmonary hypertension are central arterial enlargement, sharply pruned peripheral vascularity, and right-sided heart hypertrophy and chamber dilatation. Postcapillary pulmonary hypertension may develop secondary to focal venous constriction or to compromised pulmonary venous drainage due to left atrial neoplasia, mitral stenosis, or left ventricular failure. Radiologic manifestations of postcapillary pulmonary hypertension include prominent septal lines, small pleural effusions, and occasionally air-space opacities. In addition, radiologic evaluation of postcapillary pulmonary hypertension may demonstrate evidence of pulmonary arterial hypertension, secondary to the retrograde transmission of elevated pulmonary venous pressure across the capillary bed.
Collapse
Affiliation(s)
- A A Frazier
- Departments of Radiologic Pathology, Armed Forces Institute of Pathology, Washington, DC, 20306-6000, USA.
| | | | | | | |
Collapse
|
|
45
|
Abstract
Venous thromboembolic disease has emerged as a significant cause of morbidity and mortality in hospitalized patients. This article reviews the salient features of venous thromboembolism as they pertain to the critically ill. Emphasis is placed on identifying risk factors, diagnostic strategies, prophylaxis, and treatment of this disorder. Deep venous thrombosis and pulmonary embolism, both being manifestations of the same disease processes, are considered together in this discussion of venous thromboembolism.
Collapse
Affiliation(s)
- B M Legere
- Department of Pulmonary and Critical Care Medicine, Cleveland Clinic Foundation, Ohio, USA
| | | | | |
Collapse
|
|
46
|
Katsumura Y, Ohtsubo KI. Correlation between clinical and pathological features of pulmonary thromboemboli and the development of infarcts. Respirology 1998; 3:203-6. [PMID: 9767621 DOI: 10.1111/j.1440-1843.1998.tb00122.x] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/27/2022]
Abstract
Factors that predispose pulmonary thromboembolism to infarction have not been completely understood. The present autopsy study was carried out to evaluate these factors both clinically and pathologically. Between 36 subjects with pulmonary infarction and 33 individuals who had multiple pulmonary thromboembolism but no infarction, clinical and pathological features including congestive heart failure (CHF), shock, sepsis, neoplasm, emphysema, pneumonia, the amount of pleural effusion, diameter of occluded arteries, and segmental and dimensional location of thromboemboli were compared. Multiple regression analysis revealed that clinically CHF was significantly associated with the development of infarction. In pathological factors, thromboemboli located in the distal artery and in the lower lobe were significantly associated with infarction. The size of the infarcts was small and all the complete infarcts were in contact with the pleura. In addition to CHF, occlusion of small arteries in the lower lobe and near the pleura seems to be associated with the occurrence of infarction.
Collapse
Affiliation(s)
- Y Katsumura
- Department of Respiratory Medicine, Showa University Fujigaoka Hospital, 1-10 Fujigaoka, Aobaku, Yokohama City
| | | |
Collapse
|
|
47
|
Shibayama Y, Fukunshi K, Nariyama K, Ohsawa N. Interruption of pulmonary arterial flow with inadequate ventilation leads to pulmonary infection. Virchows Arch 1996; 427:607-12. [PMID: 8605572 DOI: 10.1007/bf00202892] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
We examined the effect of interruption of pulmonary arterial flow and inadequate ventilation on the development of pulmonary infarction in rats. Pulmonary arterial flow was blocked by the injection of agar into the inferior vena cava and inadequate ventilation was produced by obstructing the left main bronchus with a polypropylene tip. Histological and angiographic examination of the lung demonstrated that: pulmonary artery embolism alone does not induce pulmonary infarction; obstruction of a bronchus does not induce significant changes, but that pulmonary infarction develops when pulmonary artery embolism and obstruction of a bronchus occur simultaneously. It has been thought that pulmonary infarction is caused by acute obstruction of a pulmonary artery, however, the alveolar walls are supplied with oxygen by both the pulmonary circulation and by ventilation. Interruption of pulmonary arterial flow alone is probably not sufficient to induce pulmonary infarction, which is probably caused by deficiency of oxygen supply to the alveolar walls by a synergy between interruption of pulmonary arterial flow and inadequate ventilation.
Collapse
|
|
48
|
Manganelli D, Palla A, Donnamaria V, Giuntini C. Clinical features of pulmonary embolism. Doubts and certainties. Chest 1995; 107:25S-32S. [PMID: 7813325 DOI: 10.1378/chest.107.1_supplement.25s] [Citation(s) in RCA: 70] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/27/2023] Open
Abstract
The diagnosis of pulmonary embolism (PE) can be accurately made by perfusion lung scan and pulmonary angiography; however, when these diagnostic techniques are not promptly available, simple clinical procedures may be useful to identify patients with high probability PE. To this end, collection of clinical data through a standardized questionnaire and the use of findings from chest radiograph, ECG, and blood gas analysis may raise clinical suspicion and decide on therapeutic management. By reviewing published literature and our own experience, we found that unexplained dyspnea and chest pain are the most frequent symptoms, and sudden onset dyspnea and pleuritic chest pain are the most typical. Chest radiograph is abnormal in more than 80% of patients with PE, showing typical signs such as "sausage-like" descending pulmonary artery, Westermark sign, etc. The ECG may show findings characteristic of PE, such as tachycardia, T wave inversion in V1-V2, and PR displacement. Arterial blood gas data frequently demonstrate hypoxia and hypocapnia, being helpful in suspecting or excluding PE. Recent statistical techniques, such as discriminant or logistic analysis, may be applied to the above clinical assessment to refine and improve the noninvasive diagnosis of PE.
Collapse
Affiliation(s)
- D Manganelli
- Istituto di Fisiologia Clinica, CNR, Pisa, Italy
| | | | | | | |
Collapse
|
|
49
|
Abstract
Acute pulmonary thromboembolism produces a number of pathophysiologic derangements of pulmonary function. Foremost among these alterations is increased pulmonary vascular resistance. For patients without preexistent cardiopulmonary disease, increased pulmonary vascular resistance is directly related to the degree of vascular obstruction demonstrated on the pulmonary arteriogram. Vasoconstriction, either reflexly or biochemically mediated, may contribute to increased pulmonary vascular resistance. Acute pulmonary thromboembolism also disturbs matching of ventilation and blood flow. Consequently, some lung units are overventilated relative to perfusion (increased dead space), while other lung units are underventilated relative to perfusion (venous admixture). True right-to-left shunting of mixed venous blood can occur through the lungs (intrapulmonary shunt) or across the atrial septum (intracardiac shunt). In addition, abnormalities of pulmonary gas exchange (carbon monoxide transfer), pulmonary compliance and airway resistance, and ventilatory control may accompany pulmonary embolism. Thrombolytic therapy can reverse the hemodynamic derangements of acute pulmonary thromboembolism more rapidly than anticoagulant therapy. Limited data suggest a sustained benefit of thrombolytic treatment on the pathophysiologic alterations of pulmonary vascular resistance and pulmonary gas exchange produced by acute pulmonary emboli.
Collapse
Affiliation(s)
- C G Elliott
- Pulmonary Division, LDS Hospital, Salt Lake City, UT 84143
| |
Collapse
|
|
50
|
|