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Chest ; 162(4):A1806-A1807, 2022.
Article in English | EMBASE | ID: covidwho-2060867


SESSION TITLE: Critical Diffuse Lung Disease Cases 1 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 12:45 pm INTRODUCTION: Acute exacerbations (AE) of idiopathic pulmonary fibrosis (IPF) are well recognized in the progression of this uniformly fatal disease. Here we describe a case of AE of undiagnosed IPF after ankle surgery. Our aim is to discuss the role of non-pulmonary surgery as a precipitating factor and its outcome. CASE PRESENTATION: The patient is a 61-year-old male with a medical history of chronic smoking, recent open reduction internal fixation of left ankle 5 days before the presentation, comes to the emergency room with acute onset, gradually worsening shortness of breath along with non-productive cough and pleuritic chest pain. He denied any sick contacts, COVID exposure, travel history, inhalation of toxic fumes, or any chemical/pets/bird exposure. He was saturating around 85% on room air, was switched to a nasal cannula with improvement in saturation. Computed tomography (CT) of the chest showed no evidence of pulmonary embolism but diffuse ground-glass opacities (GGO) were noted bilaterally with no effusion or emphysematous changes, which were new compared to CT chest 10 days prior (that is 5 days before ankle surgery) which showed only mild reticular opacity along anterior convexity of the lungs bilaterally. He was started on intravenous steroids with gradual improvement in clinical status. Bronchoscopy biopsies revealed no malignant cells, bronchoalveolar lavage with no infections, and a negative serum autoimmune panel. He was discharged with outpatient follow-up for a repeat CT chest 6 weeks later which showed improvement in GGO (not back to baseline) and he was still requiring oxygen support. DISCUSSION: The most common triggers for IPF are smoking, environmental toxins, viral (COVID infection) or bacterial infections, medications like antidepressants, beta-blockers, NSAIDs. There is increasing evidence that surgery can cause acute respiratory worsening in IPF, presumably through increased mechanical stress to the lungs. Prolonged mechanical ventilation, high tidal volume, and high concentration of supplemental oxygen during surgery have been proposed as potential causes(1). As per the results from the retrospective study, the incidence of postoperative AE of IPF in patients undergoing non-pulmonary surgery is slightly lower than in patients undergoing pulmonary surgery (2,3). As in our case, non-pulmonary surgery procedures can pose risk for IPF exacerbation, but at this time we have limited research evidence to conclude if this exacerbation can alter the course of the disease. Some studies showed preoperative elevated C-reactive protein as a possible risk factor for AE of IPF after a non-pulmonary surgery but a multicenter study is needed to clarify the preoperative risk factors for AE of IPF after non-pulmonary surgery. CONCLUSIONS: We need further studies to check risk factors and disease course alteration, to have better guidance to classify preoperative risk in our IPF patients. Reference #1: Acute Exacerbation of Idiopathic Pulmonary Fibrosis: A Proposal, PMID: 2441663 Reference #2: Exacerbations in idiopathic pulmonary fibrosis triggered by pulmonary and non-pulmonary surgery: a case series and comprehensive review of the literature, PMID: 22543997 Reference #3: Postoperative acute exacerbation of interstitial pneumonia in pulmonary and non-pulmonary surgery: a retrospective study DISCLOSURES: No relevant relationships by Arundhati Chandini Arjun No relevant relationships by Harshil Fichadiya no disclosure submitted for Boning Li;No relevant relationships by Gaurav Mohan No relevant relationships by Rana Prathap Padappayil No relevant relationships by Raghu Tiperneni

Chest ; 162(4):A1804, 2022.
Article in English | EMBASE | ID: covidwho-2060865


SESSION TITLE: Lung Cancer Imaging Case Report Posters 1 SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Pulmonary alveolar proteinosis (PAP) is a lung condition that is caused by a build-up of proteins, fats, and other substances (collectively called surfactants) in the alveoli of the lungs. Here we describe a case of a 47-year-old female diagnosed with PAP, with radiologic features conflicting with Coronavirus Disease 19 (COVID-19) pneumonia. CASE PRESENTATION: The patient is a 47-year-old female with no significant medical history who presents to the outpatient pulmonology clinic for shortness of breath evaluation. She reported that for the past 3-4 months she has been having progressively worsening shortness of breath (SOB) associated with dry cough, and nasal congestion. She reports no recent illness, no history of COVID or COVID exposure, no second-hand smoke exposure, no toxin/chemical exposure, no pets/birds at home. Her SOB has been impacting her lifestyle. Pulmonary function tests showed no obstruction, moderate restriction, mildly decreased diffusion capacity. Computed tomography (CT) of the chest showed multiple ground-glass opacities with septal wall thickening (appears crazy paving pattern) - suggestive of infection or inflammatory process. Infectious/inflammatory work up with HIV, COVID-19, hypersensitivity pneumonitis (HP) panel, autoimmune panel, immunoglobulins, QuantiFERON gold, IgM mycoplasma antibodies was negative. Repeat CT chest in 6 weeks as per patient request, was unchanged from prior. A bronchoscopy was done, bronchoalveolar lavage (BAL) negative for infection - fungal, acid-fast bacilli, Mycobacterium tuberculosis;GMS (Grocott's methenamine silver) stain negative for fungus;negative PCP (Pneumocystis pneumonia);left upper lobe and left lung biopsy showed lung parenchyma with scant amorphous eosinophilic material in alveolar sacs, Periodic Acid-Schiff stain (PAS) stain was positive confirming PAP diagnosis. DISCUSSION: PAP is a rare disease, affecting about 1 person in 100,000 people worldwide, with fewer than 10,000 of them in the United States. The "crazy paving pattern" is characteristic of PAP but recently it has appeared in the list of radiologic findings for COVID 19 pneumonia1,2,3. In these COVID times, these kinds of interactions might make the decision tougher, often leading to misdiagnosis. The decision of diagnosis/treatment should be based on symptoms and their duration, medical history, previous tests, response to treatment. Given our patient never had a COVID infection in the past or current infection, CT chest was typical for PAP with a crazy-paving pattern, no significant subjective/radiological improvement lead us to the diagnosis of PAP with eventual work up with bronchoscopy. CONCLUSIONS: A high index of suspicion is needed for the diagnosis of such rare diseases as PAP, which can be misdiagnosed as COVID-19 pneumonia, given radiological similarities. Early diagnosis and treatment can improve morbidity and mortality of PAP. Reference #1: PAP with COVID-19 Radiology - Differential Diagnosis Discussion, PMID: 33646114 Reference #2: Proteinaceous Lung With COVID-19: The Mimicker, PMID: 34703683 Reference #3: COVID-19 pneumonia: the great radiological mimicker - DISCLOSURES: No relevant relationships by Ahmad Al-Alwan No relevant relationships by Arundhati Chandini Arjun No relevant relationships by Farhan Khalid no disclosure submitted for Boning Li;No relevant relationships by Rana Prathap Padappayil No relevant relationships by Raghu Tiperneni