DOCSLIB.ORG

COVID-19 Pneumonia: the Great Radiological Mimicker

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
COVID-19 Pneumonia: the Great Radiological Mimicker Duzgun et al. Insights Imaging (2020) 11:118 https://doi.org/10.1186/s13244-020-00933-z Insights into Imaging EDUCATIONAL REVIEW Open Access COVID-19 pneumonia: the great radiological mimicker Selin Ardali Duzgun* , Gamze Durhan, Figen Basaran Demirkazik, Meltem Gulsun Akpinar and Orhan Macit Ariyurek Abstract Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly spread worldwide since December 2019. Although the reference diagnostic test is a real-time reverse transcription-polymerase chain reaction (RT-PCR), chest-computed tomography (CT) has been frequently used in diagnosis because of the low sensitivity rates of RT-PCR. CT fndings of COVID-19 are well described in the literature and include predominantly peripheral, bilateral ground-glass opacities (GGOs), combination of GGOs with consolida- tions, and/or septal thickening creating a “crazy-paving” pattern. Longitudinal changes of typical CT fndings and less reported fndings (air bronchograms, CT halo sign, and reverse halo sign) may mimic a wide range of lung patholo- gies radiologically. Moreover, accompanying and underlying lung abnormalities may interfere with the CT fndings of COVID-19 pneumonia. The diseases that COVID-19 pneumonia may mimic can be broadly classifed as infectious or non-infectious diseases (pulmonary edema, hemorrhage, neoplasms, organizing pneumonia, pulmonary alveolar proteinosis, sarcoidosis, pulmonary infarction, interstitial lung diseases, and aspiration pneumonia). We summarize the imaging fndings of COVID-19 and the aforementioned lung pathologies that COVID-19 pneumonia may mimic. We also discuss the features that may aid in the diferential diagnosis, as the disease continues to spread and will be one of our main diferential diagnoses some time more. Keywords: COVID-19, Pneumonia, Mimicker, Chest CT, Diferential diagnoses Introduction sampling and transportation limitations [4–6]. Because Severe acute respiratory syndrome coronavirus 2 (SARS- of these low sensitivity rates and the need for rapid diag- CoV-2), a novel coronavirus, was found to be associated nosis, non-contrast chest-computed tomography (CT) with a pneumonia outbreak frstly reported in Wuhan, has been frequently used in the current pandemic con- China, in December 2019 [1, 2]. Te disease subsequently dition. Also, several cases with initial negative RT-PCR called Coronavirus Disease 2019 (COVID-19) has caused results are reported to have positive chest CT fndings a lot of cases worldwide and was declared as a pandemic [4]. Although recent studies have reported the high sen- by the World Health Organization (WHO) on March 11, sitivity of chest CT for diagnosis with RT-PCR as a ref- 2020 [3]. erence, the specifcity of CT is relatively low. In a recent Te reference diagnostic test for COVID-19 pneumo- meta-analysis, chest CT had a pooled sensitivity of 94% nia is real-time reverse transcription-polymerase chain and a specifcity of 37% [4, 5, 7]. Tis may be explained by reaction (RT-PCR). Te specifcity of RT-PCR is approxi- the fact that besides previously reported typical appear- mately 95%, but the sensitivity of RT-PCR at the ini- ance, COVID-19 has various CT fndings, and some tial presentation is 60–71% because of kit performance, chest CT fndings of COVID-19 may closely resemble the imaging fndings of some other pathologies presenting *Correspondence: [email protected] with airspace disease. Department of Radiology, School of Medicine, Tıp Fakültesi Hastanesi, In this pictorial review, CT fndings of COVID- Hacettepe University, 06100 Sıhhiye, Ankara, Turkey 19 pneumonia and imaging features of COVID-19 © The Author(s) 2020. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creat iveco mmons .org/licen ses/by/4.0/. Duzgun et al. Insights Imaging (2020) 11:118 Page 2 of 15 pneumonia that may mimic other infectious and non- been previously described in fungal infections and tuber- infectious diseases will be summarized. culosis [15–17]. Te diagnostic association of CT fndings for diferent CT fndings of COVID‑19 pneumonia infectious diseases is summarized in Table 1. Typical CT fndings of COVID-19 pneumonia are pre- dominantly peripheral, bilateral ground-glass opacities (GGOs), consolidations, combination of GGOs with con- Viral pneumonia solidations, and GGOs superimposed with interlobular/ Chest CT fndings of a wide range of viruses have been intralobular septal thickening creating a “crazy-paving” previously described, such as infuenza virus, parain- pattern and subpleural linear opacities. Air broncho- fuenza virus, adenovirus, respiratory syncytial virus grams, vascular enlargement, CT halo sign, and reverse (RSV), cytomegalovirus (CMV), human metapneumovi- halo sign are also reported. Cavitation, pleural or pericar- rus (HMPV), and other coronaviruses. Viral pneumonia dial efusion, and lymphadenopathy are rarely observed commonly manifests as interstitial pneumonia with non- [8–11]. specifc imaging fndings, such as GGOs, patchy consoli- Findings vary and usually progress during the course of dations, peribronchovascular thickening, centrilobular the disease. In the early phase, the predominant fnding nodular opacities, a “tree-in-bud” pattern, and interlobu- is unilateral or bilateral small peripheral GGOs. While lar septal thickening [18, 19] (Fig. 2). Unlike in other viral the size and number of GGOs and the number of afected pneumonia, centrilobular nodular opacities are not com- lobes increase, crazy-paving pattern and consolidations mon in COVID-19 pneumonia. appear as the disease progresses. Consolidations become Some typical fndings of COVID-19 pneumonia, such denser at the peak stage (Fig. 1). Approximately after as the subpleural distribution of opacities and a crazy- 2 weeks, opacities start to resolve gradually, and residual paving pattern, were also described for pneumonia subpleural curvilinear lines, fbrous stripes, and GGOs caused by other coronaviruses, severe acute respiratory may be seen [9, 12, 13]. syndrome virus (SARS), and middle east respiratory syn- drome virus (MERS), that caused outbreaks previously Infectious causes [20–22]. Te absence of cavitation, pleural efusion, and Diferentiation of COVID-19 pneumonia from other lymphadenopathy are common in both COVID-19 pneu- causes of infection is sometimes challenging, especially monia and SARS [20]. when it comes to viral pneumonia and other atypical pneumonia. Bai et al. reported some fndings in favor of COVID-19 pneumonia rather than non-COVID pneu- Bacterial pneumonia monia, such as the presence of GGOs, peripheral dis- Although viral and bacterial pneumonia have overlap- tribution, reverse halo sign, and vascular enlargement. ping imaging fndings, the latter generally causes lobar/ Pleural efusion and thickening, lymphadenopathy, and segmental pneumonia or bronchopneumonia and focal central distribution are less likely to be seen in COVID- or multifocal consolidations. Less commonly, GGOs may 19 pneumonia [14]. By contrast, some typical fndings be seen. Peribronchial thickening, centrilobular nodular described for COVID-19 pneumonia can be seen in non- opacities, and pleural efusion are much more frequent in COVID pneumonia or other pathologies. For example, bacterial pneumonia than in COVID-19 pneumonia [18, both the reverse halo sign and CT halo sign have also 23] (Fig. 2). Fig. 1 CT fndings of COVID-19 pneumonia. a The frst CT scan obtained on illness day 4 revealed patchy GGOs in both the lungs. b On day 8, the number and size of GGOs increased. c Consolidations were the dominant CT fnding on day 14 Duzgun et al. Insights Imaging (2020) 11:118 Page 3 of 15 Table 1 CT fndings of COVID‑19 pneumonia and other infectious diseases CT fnding COVID-19 Non-COVID viral Bacterial pneumonia PJP Fungal pneumonia pneumonia pneumonia GGO +++ ++ + +++ + Consolidation 0 ++ ++ +++ + Centrilobular nodular opacities −−− ++ ++ − + Crazy-paving ++ ++ + ++ − Lesion distribution Peripheral 0 +++ ++ + + Lower zone 0 +++ ++ + + Rounded morphology +++ + + −− ++ Cavitation −−− − + − ++ Pleural efusion 0 −− + ++ + Lymphadenopathy 0 −− + ++ + The most common fndings of aforementioned disease groups are presented. Signs indicate the strength of relation between the CT fnding and diagnosis; in a range of ( ) and ( ); ( ) indicating the strongest association +++ −−− +++ Fig. 2 Other infectious diseases that COVID-19 pneumonia may mimic. a Axial CT image shows a consolidation with rounded morphology in the right lower lobe. Hemophilus infuenza was detected in the respiratory panel. b Similar round consolidation is observed in the right upper lobe. The patient was tested positive on RT-PCR for COVID-19 pneumonia. The respiratory panel was negative for other causes. c Axial CT image shows GGOs with associated
Load more

Recommended publications
  • Rapid and Precise Diagnosis of Pneumonia Coinfected By
    Rapid and precise diagnosis of pneumonia coinfected by Pneumocystis jirovecii and Aspergillus fumigatus assisted by next-generation sequencing in a patient with systemic lupus erythematosus: a case report Yili Chen Sun Yat-Sen University Lu Ai Sun Yat-Sen University Yingqun Zhou First Peoples Hospital of Nanning Yating Zhao Sun Yat-Sen University Jianyu Huang Sun Yat-Sen University Wen Tang Sun Yat-Sen University Yujian Liang ( [email protected] ) Sun Yat-Sen University Case report Keywords: Pneumocystis jirovecii, Aspergillus fumigatus, Next generation sequencing, Case report Posted Date: March 19th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-154016/v2 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/12 Abstract Background: Pneumocystis jirovecii and Aspergillus fumigatus, are opportunistic pathogenic fungus that has a major impact on mortality in patients with systemic lupus erythematosus. With the potential to invade multiple organs, early and accurate diagnosis is essential to the survival of SLE patients, establishing an early diagnosis of the infection, especially coinfection by Pneumocystis jirovecii and Aspergillus fumigatus, still remains a great challenge. Case presentation: In this case, we reported that the application of next -generation sequencing in diagnosing Pneumocystis jirovecii and Aspergillus fumigatus coinfection in a Chinese girl with systemic lupus erythematosus (SLE). Voriconazole was used to treat pulmonary aspergillosis, besides sulfamethoxazole and trimethoprim (SMZ-TMP), and caspofungin acetate to treat Pneumocystis jirovecii infection for 6 days. On Day 10 of admission, her chest radiograph displayed obvious absorption of bilateral lung inammation though the circumstance of repeated fever had not improved.
    [Show full text]
  • Hypersensitivity Pneumonitis: Challenges in Diagnosis and Management, Avoiding Surgical Lung Biopsy
    395 Hypersensitivity Pneumonitis: Challenges in Diagnosis and Management, Avoiding Surgical Lung Biopsy Ferran Morell, MD1,2 Ana Villar, MD2,3 Iñigo Ojanguren, MD2,3 Xavier Muñoz, MD2,3 María-Jesús Cruz, PhD2,3 1 Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Catalonia, Spain Address for correspondence Ferran Morell, MD, Vall d’Hebron Institut 2 Ciber de Enfermedades Respiratorias (CIBERES), Barcelona, Spain de Recerca (VHIR), PasseigValld’Hebron, 119-129, 08035 Barcelona, 3 Servei de Pneumologia, Hospital Universitari Vall d’Hebron, Catalonia, Spain (e-mail: [email protected]). Barcelona, Spain Semin Respir Crit Care Med 2016;37:395–405. Abstract This review presents an update of the currently available information related to Keywords hypersensitivity pneumonitis, with a particular focus on the contribution of several ► hypersensitivity techniques in the diagnosis of this condition. The methods discussed include proper pneumonitis elaboration of a complete medical history, targeted auscultation, detection of specific ► bronchoalveolar immunoglobulin G antibodies against the most common antigens causing this disease, lavage skin tests, antigen-specific lymphocyte activation assays, bronchoalveolar lavage, and ► fi speci c inhalation cryobiopsy. Special emphasis is placed on the relevant contribution of specificinhalation challenge challenge (bronchial challenge test). Surgical lung biopsy is presented as the ultimate ► bronchial challenge recourse, to be used when the diagnosis cannot be reached through the other methods test covered.
    [Show full text]
  • Postviral Bronchial Hyperreactivity Syndrome: Recognizing Asthma's
    • Postviral bronchial hyperreactivity syndrome: Recognizing asthmas great mimic DAVID OSTRANSKY, DO FRANCIS X. BLAIS, DO Although there are no prospec- (Key words: Viral infections, asthma, tive studies regarding the frequency of respiratory tract infections, postviral postviral bronchial hyperreactivity syn- bronchial hyperreactivity syndrome) drome, it is a common complication of upper and lower respiratory tract viral Viral respiratory tract infections frequently infections. The respiratory symptoms cause wheezing and other asthmalike symp- closely resemble those of asthma, but they toms. Several investigators have demonstrated are present for only 3 weeks to 3 months pertinent features of this abbreviated form of following the acute infection phase. Defin- asthma, including early response phase, late ing the mechanisms of this syndrome may response phase, and bronchial hyperreac- provide insight into the pathogenesis of tivity. 1-5 Understanding the mechanisms by asthma. Postviral bronchial hyperreac- which viral respiratory tract infections precipi- tivity syndrome is frequently misdiag- tate the airway abnormalities of asthma may nosed and inappropriately managed be- be a potential key to the pathogenesis of cause many physicians are unfamiliar asthma, although whether viral respiratory with this illness. Because of its character- tract infections truly cause asthma is un- istic history, diagnosis is straightforward proved.6 when the physician knows what to look The symptom complex following viral up- for, and response to therapy is excellent. per or lower respiratory tract infections (or This report presents a case history fol- both) has not been formally identified. It is fre- lowed by a review of the proposed mecha- quently misdiagnosed by physicians who then nisms of bronchial hyperreactivity follow- institute inappropriate diagnostic studies and ing viral respiratory infections.
    [Show full text]
  • Outcome and Prognostic Factors of Pneumocystis Jirovecii Pneumonia
    Gaborit et al. Ann. Intensive Care (2019) 9:131 https://doi.org/10.1186/s13613-019-0604-x RESEARCH Open Access Outcome and prognostic factors of Pneumocystis jirovecii pneumonia in immunocompromised adults: a prospective observational study Benjamin Jean Gaborit1,6* , Benoit Tessoulin2, Rose‑Anne Lavergne3, Florent Morio3, Christine Sagan4, Emmanuel Canet5, Raphael Lecomte1, Paul Leturnier1, Colin Deschanvres1, Lydie Khatchatourian1, Nathalie Asseray1, Charlotte Garret5, Michael Vourch5, Delphine Marest5, François Raf1, David Boutoille1,6 and Jean Reignier5 Abstract Background: Pneumocystis jirovecii pneumonia (PJP) remains a severe disease associated with high rates of invasive mechanical ventilation (MV) and mortality. The objectives of this study were to assess early risk factors for severe PJP and 90‑day mortality, including the broncho‑alveolar lavage fuid cytology profles at diagnosis. Methods: We prospectively enrolled all patients meeting pre‑defned diagnostic criteria for PJP admitted at Nantes university hospital, France, from January 2012 to January 2017. Diagnostic criteria for PJP were typical clinical features with microbiological confrmation of P. jirovecii cysts by direct examination or a positive specifc quantitative real‑time polymerase chain reaction (PCR) assay. Severe PJP was defned as hypoxemic acute respiratory failure requiring high‑ fow nasal oxygen with at least 50% FiO2, non‑invasive ventilation, or MV. Results: Of 2446 respiratory samples investigated during the study period, 514 from 430 patients were positive for P. jirovecii. Of these 430 patients, 107 met criteria for PJP and were included in the study, 53 (49.5%) patients had severe PJP, including 30 who required MV. All patients were immunocompromised with haematological malignancy ranking frst (n 37, 35%), followed by solid organ transplantation (n 27, 25%), HIV‑infection (n 21, 20%), systemic diseases (n 13,= 12%), solid tumors (n 12, 11%) and primary immunodefciency= (n 6, 8%).
    [Show full text]
  • Pneumocystis Pneumonia: Immunity, Vaccines, and Treatments
    pathogens Review Pneumocystis Pneumonia: Immunity, Vaccines, and Treatments Aaron D. Gingerich 1,2, Karen A. Norris 1,2 and Jarrod J. Mousa 1,2,* 1 Center for Vaccines and Immunology, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, USA; [email protected] (A.D.G.); [email protected] (K.A.N.) 2 Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, USA * Correspondence: [email protected] Abstract: For individuals who are immunocompromised, the opportunistic fungal pathogen Pneumocystis jirovecii is capable of causing life-threatening pneumonia as the causative agent of Pneumocystis pneumonia (PCP). PCP remains an acquired immunodeficiency disease (AIDS)-defining illness in the era of antiretroviral therapy. In addition, a rise in non-human immunodeficiency virus (HIV)-associated PCP has been observed due to increased usage of immunosuppressive and im- munomodulating therapies. With the persistence of HIV-related PCP cases and associated morbidity and mortality, as well as difficult to diagnose non-HIV-related PCP cases, an improvement over current treatment and prevention standards is warranted. Current therapeutic strategies have pri- marily focused on the administration of trimethoprim-sulfamethoxazole, which is effective at disease prevention. However, current treatments are inadequate for treatment of PCP and prevention of PCP-related death, as evidenced by consistently high mortality rates for those hospitalized with PCP. There are no vaccines in clinical trials for the prevention of PCP, and significant obstacles exist that have slowed development, including host range specificity, and the inability to culture Pneumocystis spp. in vitro. In this review, we overview the immune response to Pneumocystis spp., and discuss current progress on novel vaccines and therapies currently in the preclinical and clinical pipeline.
    [Show full text]
  • Fungal Infection in the Lung
    CHAPTER Fungal Infection in the Lung 52 Udas Chandra Ghosh, Kaushik Hazra INTRODUCTION The following risk factors may predispose to develop Pneumonia is the leading infectious cause of death in fungal infections in the lungs 6 1, 2 developed countries . Though the fungal cause of 1. Acute leukemia or lymphoma during myeloablative pneumonia occupies a minor portion in the immune- chemotherapy competent patients, but it causes a major role in immune- deficient populations. 2. Bone marrow or peripheral blood stem cell transplantation Fungi may colonize body sites without producing disease or they may be a true pathogen, generating a broad variety 3. Solid organ transplantation on immunosuppressive of clinical syndromes. treatment Fungal infections of the lung are less common than 4. Prolonged corticosteroid therapy bacterial and viral infections and very difficult for 5. Acquired immunodeficiency syndrome diagnosis and treatment purposes. Their virulence varies from causing no symptoms to death. Out of more than 1 6. Prolonged neutropenia from various causes lakh species only few fungi cause human infection and 7. Congenital immune deficiency syndromes the most vulnerable organs are skin and lungs3, 4. 8. Postsplenectomy state RISK FACTORS 9. Genetic predisposition Workers or farmers with heavy exposure to bird, bat, or rodent droppings or other animal excreta in endemic EPIDEMIOLOGY OF FUNGAL PNEUMONIA areas are predisposed to any of the endemic fungal The incidences of invasive fungal infections have pneumonias, such as histoplasmosis, in which the increased during recent decades, largely because of the environmental exposure to avian or bat feces encourages increasing size of the population at risk. This population the growth of the organism.
    [Show full text]
  • ICD-10 Coordination and Maintenance Committee Meeting Diagnosis Agenda March 5-6, 2019 Part 2
    ICD-10 Coordination and Maintenance Committee Meeting Diagnosis Agenda March 5-6, 2019 Part 2 Welcome and announcements Donna Pickett, MPH, RHIA Co-Chair, ICD-10 Coordination and Maintenance Committee Diagnosis Topics: Contents Babesiosis ........................................................................................................................................... 10 David, Berglund, MD Mikhail Menis, PharmD, MS Epi, MS PHSR Epidemiologist Office of Biostatistics and Epidemiology CBER/FDA C3 Glomerulopathy .......................................................................................................................... 13 David Berglund, MD Richard J. Hamburger, M.D. Professor Emeritus of Medicine, Indiana University Renal Physicians Association Eosinophilic Gastrointestinal Diseases ............................................................................................ 18 David Berglund, MD Bruce Bochner, MD Samuel M. Feinberg Professor of Medicine Northwestern University Feinberg School of Medicine and President, International Eosinophil Society ICD-10 Coordination and Maintenance Committee Meeting March 5-6, 2019 Food Insecurity.................................................................................................................................. 20 Donna Pickett Glut1 Deficiency ................................................................................................................................ 23 David Berglund, MD Hepatic Fibrosis ...............................................................................................................................
    [Show full text]
  • Am I Missing Something? Blindness • Dan Simons and Chris Chabris: Video Studies Created During Experimental Psychology Course
    5/24/2018 Is This Normal Lung? Looking Beyond the Interstitium Kirk D. Jones, MD UCSF Dept of Pathology [email protected] Inattentional Blindness • Ulric Neisser: Selective looking • Arien Mack and Irvin Rock: Inattentional Am I Missing Something? blindness • Dan Simons and Chris Chabris: Video studies created during Experimental Psychology course 1 5/24/2018 Inattentional Blindness • “when our attention is focused on one thing, we fail to notice other, unexpected things around us—including those we might want to see.” • In pathology of the lung, there are often two things that focus our attention: – The tumor in neoplastic disease – The alveoli in non-neoplastic disease The Neglected Compartments • Bronchioles – Inflammatory bronchiolitis – Fibrotic bronchiolitis ALVEOLI • Vessels – Pulmonary arteriopathy – Pulmonary venopathy • Pleura – Pleural inflammation or neoplasm bronchioles vessels pleura • Absence of alveoli – Cystic disease 2 5/24/2018 Overview of Talk • Bronchioles – Bronchiolitis – Diffuse panbronchiolitis – Constrictive bronchiolitis • Vessels – Pulmonary arteriopathy – Pulmonary veno-occlusive disease • Lack of alveoli – cystic disease – Lymphangioleiomyomatosis Classification of Bronchiolitis • Cellular infiltrates (inflammatory) – Intraluminal • Neutrophils: Acute bronchiolitis, bronchopneumonia • Macrophages: Respiratory bronchiolitis – Mural • Lymphocytes: Chronic/cellular bronchiolitis • Lymphoid follicles: Follicular bronchiolitis – Peribronchiolar/Interstitial • Macrophages: Diffuse panbronchiolitis 3 5/24/2018
    [Show full text]
  • CT Findings of High-Attenuation Pulmonary Abnormalities
    Insights Imaging (2010) 1:287–292 DOI 10.1007/s13244-010-0039-2 PICTORIAL REVIEW CT findings of high-attenuation pulmonary abnormalities Naim Ceylan & Selen Bayraktaroglu & Recep Savaş & Hudaver Alper Received: 5 June 2010 /Revised: 10 July 2010 /Accepted: 16 August 2010 /Published online: 4 September 2010 # European Society of Radiology 2010 Abstract features and radiological findings can significantly improve Objectives To review the computed tomography (CT) diagnostic accuracy. findings of common and uncommon high-attenuation pulmonary lesions and to present a classification scheme Keywords Computed tomography. Pulmonary of the various entities that can result in high-attenuation abnormalities . High attenuation . Nodules . Reticular pulmonary abnormalities based on the pattern and distribu- pattern . Consolidation . Extraparenchymal lesions tion of findings on CT. Background High-attenuation pulmonary abnormalities can result from the deposition of calcium or, less commonly, Introduction other high-attenuation material such as talc, amiodarone, iron, tin, mercury and barium sulphate. CT is highly High-attenuation pulmonary abnormalities can result from a sensitive in the detection of areas of abnormally high variety of different conditions, including from the deposi- attenuation in the lung parenchyma, airways, mediastinum tion of calcium. Amiodarone pulmonary toxicity may cause and pleura. The cause of the calcifications and other high- high-attenuation pulmonary parenchymal opacities. Multi- attenuation conditions may be determined based on the ple dense nodular opacities are rarely seen in siderosis, location and pattern of the abnormalities within the lung stannosis, talcosis and baritosis, in which iron, tin, talc and parenchyma and knowledge of the associated clinical barium sulfate respectively are deposited in the lungs.
    [Show full text]
  • Pediatric Ambulatory Community Acquired Pneumonia (CAP)
    ANMC Pediatric (≥3mo) Ambulatory Community Acquired Pneumonia (CAP) Treatment Guideline Criteria for Respiratory Distress Criteria For Outpatient Management Testing/Imaging for Outpatient Management Tachypnea, in breaths/min: Mild CAP: no signs of respiratory distress Vital Signs: Standard VS and Pulse Oximetry Age 0-2mo: >60 Able to tolerate PO Labs: No routine labs indicated Age 2-12mo: >50 No concerns for pathogen with increased virulence Influenza PCR during influenza season Age 1-5yo: >40 (ex. CA-MRSA) Blood cultures if not fully immunized OR fails to Age >5yo: >20 Family able to carefully observe child at home, comply improve/worsens after initiation of antibiotics Dyspnea with therapy plan, and attend follow up appointments Urinary antigen detection testing is not Retractions recommended in children; false-positive tests are common. Grunting If patient does not meet outpatient management criteria Radiography: No routine CXR indicated Nasal flaring refer to inpatient pneumonia guideline for initial workup Apnea and testing. AP and lateral CXR if fails initial antibiotic therapy Altered mental status AP and lateral CXR 4-6 weeks after diagnosis if Pulse oximetry <90% on room air recurrent pneumonia involving the same lobe Treatment Selection Suspected Viral Pneumonia Most Common Pathogens: Influenza A & B, Adenovirus, Respiratory Syncytial Virus, Parainfluenza No antimicrobial therapy is necessary. Most common in <5yo If influenza positive, see influenza guidelines for treatment algorithm. Suspected Bacterial
    [Show full text]
  • Pathology of Allergic Bronchopulmonary Aspergillosis
    [Frontiers in Bioscience 8, e110-114, January 1, 2003] PATHOLOGY OF ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS Anne Chetty Department of Pediatrics, Floating Hospital for Children, New England Medical Center, Boston, MA TABLE OF CONTENTS 1. Abstract 2. Introduction 3. Immunopathogenesis 4. Pathologic Findings 4.1. Plastic bronchitis 4.2. Allergic fungal sinusitis 4.3. ABPA in cystic fibrosis 5. Acknowledgement 6. References 1. ABSTRACT Allergic bronchopulmonary aspergillosis (ABPA) individuals with episodic obstructive lung diseases such as occurs in patients with asthma and cystic fibrosis when asthma and cystic fibrosis that produce thick, tenacious Aspergillus fumigatus spores are inhaled and grow in sputum. bronchial mucus as hyphae. Chronic colonization of Aspergillus fumigatus and host’s genetically determined Decomposing organic matter serves as a substrate immunological response lead to ABPA. In most cases, for the growth of Aspergillus species. Because biologic lung biopsy is not necessary because the diagnosis is made heating produces temperatures as high as 65° to 70° C, on clinical, serologic, and roentgenographic findings. Some Aspergillus spores will not be recovered in the latter stages patients who have had lung biopsies or partial resections of composting. Aspergillus species have been recovered for atelectasis or infiltrates will have histologic diagnoses. from potting soil, mulches, decaying vegetation, and A number of different histologic diagnoses can be found sewage treatment facilities, as well as in outdoor air and even in the same patient. In the early stages the bronchial Aspergillus spores grow in excreta from birds (1) wall is infiltrated with mononuclear cells and eosinophils. Mucoid impaction and eosinophilic pneumonia are seen Allergic fungal pulmonary disease is manifested subsequently.
    [Show full text]
  • Risk Factors of Daptomycin-Induced Eosinophilic Pneumonia in a Population with Osteoarticular Infection
    antibiotics Communication Risk Factors of Daptomycin-Induced Eosinophilic Pneumonia in a Population with Osteoarticular Infection Laura Soldevila-Boixader 1,2, Bernat Villanueva 1, Marta Ulldemolins 1 , Eva Benavent 1,2 , Ariadna Padulles 3, Alba Ribera 1,2, Irene Borras 1, Javier Ariza 1,2,4 and Oscar Murillo 1,2,4,* 1 Infectious Diseases Service, IDIBELL-Hospital Universitari Bellvitge, Feixa Llarga s/n, Hospitalet de Llobregat, 08907 Barcelona, Spain; [email protected] (L.S.-B.); [email protected] (B.V.); [email protected] (M.U.); [email protected] (E.B.); [email protected] (A.R.); [email protected] (I.B.); [email protected] (J.A.) 2 Bone and Joint Infection Study Group of the Spanish Society of Clinical Microbiology and Infectious Diseases (GEIO-SEIMC), 28003 Madrid, Spain 3 Pharmacy Department, IDIBELL-Hospital Universitari Bellvitge, Feixa Llarga s/n, Hospitalet de Llobregat, 08907 Barcelona, Spain; [email protected] 4 Spanish Network for Research in Infectious Diseases (REIPI RD16/0016/0003), Instituto de Salud Carlos III, 28029 Madrid, Spain * Correspondence: [email protected]; Tel.: +34-93-260-7625 Abstract: Background: Daptomycin-induced eosinophilic pneumonia (DEP) is a rare but severe adverse effect and the risk factors are unknown. The aim of this study was to determine risk factors for DEP. Methods: A retrospective cohort study was performed at the Bone and Joint Infection Citation: Soldevila-Boixader, L.; Unit of the Hospital Universitari Bellvitge (January 2014–December 2018). To identify risk factors Villanueva, B.; Ulldemolins, M.; for DEP, cases were divided into two groups: those who developed DEP and those without DEP.
    [Show full text]