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1.
Chest ; 162(4):A1990-A1991, 2022.
Article in English | EMBASE | ID: covidwho-2060882

ABSTRACT

SESSION TITLE: Dirty Jobs: Occupational Lung Diseases SESSION TYPE: Case Reports PRESENTED ON: 10/18/2022 11:15 am - 12:15 pm INTRODUCTION: Hypersensitivity Pneumonitis (HP) is a group of immunologically mediated lung diseases. It develops in susceptible individuals with exposure to provoking antigens along with influence from genetic and environmental factors. There remains no standardized approach for assessing the various forms of HP and the diverse nature of the disease makes it difficult and often underdiagnosed. Cystic disease is not uncommon in HP, but the advanced cystic disease seen in our young patient was unique and likely compounded by her pregnancy as well as a previous illness with COVID-19. CASE PRESENTATION: A 26-year-old female construction worker at 12 weeks gestation, with a past medical history of polysubstance abuse and previous COVID-19 infection ten months prior, presented with progressively worsening dyspnea of 9 months. She was admitted with acute hypoxic respiratory failure due to recurrent right pneumothorax requiring multiple thoracenteses and eventually chest tube placement. CT Chest demonstrated severe cystic interstitial fibrosis with emphysematous changes. Initial lung biopsy showed interstitial fibrosis as a possible sequela of COVID-19. Due to her pregnancy and medical complications, she was transferred to a transplant center where she continued to have recurrent pneumothoraces requiring video-assisted thoracoscopic surgery. Autoimmune workup, HP panel, and extended myositis panel were negative. However, a repeat lung biopsy pointed to subacute HP. Despite steroid and immunosuppressant initiation, her hospital course was complicated by cardiac arrest and brain death. She went on to become an organ donor. DISCUSSION: Diffuse cystic lung diseases are characterized by parenchymal destruction of the airway walls leading to expansion of the distal airspaces forming multi-lobular cysts. A broad differential diagnosis for this exists including infection, Langerhans histiocytosis, lymphangioleiomyomatosis, interstitial pneumonia, and HP. The first step to evaluate HP is a detailed history of potential exposures. Our patient worked in construction and was exposed to commonly demonstrated antigens used in paint, plastic, and wood manufacture. Pregnancy appears to trigger symptoms in some patients, seen in prior case reports. Our patient's symptoms began after her COVID infection. Though not clearly studied, some studies have proposed that dysregulation of COVID - 19 immune response triggers interstitial fibrosis as a long-term sequela. Early diagnosis and treatment with steroids are vital to the treatment and prevention of complications such as recurrent pneumothorax. CONCLUSIONS: Covid-19 is an emerging risk factor for the propagation of various immune-mediated diseases. Progression of disease may occur even after the infection has been cured and limited data is available regarding its relation. Early recognition and treatment can be effective life-saving measures in these patients. Reference #1: Baldi BG, Carvalho CRR, Dias OM, Marchiori E, Hochhegger B. Diffuse cystic lung diseases: differential diagnosis. J Bras Pneumol. 2017;43(2):140-149. Reference #2: Densem C, Niven R, Barber P, Bishop P. Development of cryptogenic fibrosing alveolitis during pregnancy. J R Soc Med. 1998;91(11):591-593. Reference #3: Ambardar SR, Hightower SL, Huprikar NA, Chung KK, Singhal A, Collen JF. Post-COVID-19 Pulmonary Fibrosis: Novel Sequelae of the Current Pandemic. J Clin Med. 2021;10(11):2452. Published 2021 Jun 1 DISCLOSURES: No relevant relationships by Anastasia Brit No relevant relationships by Steven Colby No relevant relationships by Patrick Koo No relevant relationships by Vishruth Vyata No relevant relationships by Harika Yadav

2.
Chest ; 162(4):A1029, 2022.
Article in English | EMBASE | ID: covidwho-2060756

ABSTRACT

SESSION TITLE: Drug-Induced Critical Care SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Intravenous magnesium sulfate (MgSo4) is commonly used for inpatient magnesium repletion. However, it is infrequently shown to be associated with the development of pulmonary edema. We present a case of acute hypoxic respiratory failure due to pulmonary edema after starting magnesium infusion in a patient recovering from COVID-19. CASE PRESENTATION: 60 year old female with a history of metastatic breast cancer presented with hypoxic respiratory failure due to COVID-19. CT angiogram of her chest showed diffuse bilateral ground-glass opacities with no evidence of pulmonary embolism. She had prolonged weaning from high flow nasal cannula and was treated with antibiotics, remedesivir, and dexamethasone. Following treatment, her inflammatory markers significantly improved. On day thirty, she was on 25 L at 45% FiO2 on high flow nasal cannula. Her magnesium level was low at 1.5 mg/dl, and 2 grams of intravenous MgSo4 was given for replacement. A few minutes after starting the infusion, the patient complained of metallic taste, severe shortness of breath, and tachypnea with a drop in oxygen saturation to 67%, which improved with increasing oxygen. CXR showed worsening perihilar infiltrates compared to prior, suggesting acute pulmonary edema. An echocardiogram showed normal function without evidence of structural abnormalities. Thyroid function was normal. She did not receive any blood products or opioids prior to this event. She responded very well to diuresis, was weaned to 5L nasal cannula in three days, and was eventually discharged on 2L supplemental oxygen. DISCUSSION: Pulmonary edema is due to the movement of excess fluid into the alveoli. It can be due to cardiogenic and noncardiogenic causes. Noncardiogenic pulmonary edema is due to a rise in transcapillary filtration, causing an increase in capillary permeability due to several factors, most importantly direct endothelial damage due to inflammation. Mechanisms for MgSo4 induced pulmonary edema are unknown, but theories include direct capillary damage or transient cardiac depression. It is seen in studies to be an independent risk factor for the development of pulmonary edema in pregnancy. Higher risk is associated with faster MgSo4 infusion, less concentrated MgSo4, and infection[1]. She was on abemaciclib for breast cancer before her admission, known to cause pneumonitis but was thought unlikely to cause her acute decompensation. The lack of other etiologies explaining sudden respiratory failure, her rapid improvement on stopping magnesium, and her response to diuretics supported our diagnosis. CONCLUSIONS: Treatment of noncardiogenic pulmonary edema involves addressing the underlying cause of the event and is mainly supportive. Given how commonly Mgso4 is used for repletion in the inpatient setting, MgSo4 induced pulmonary edema should be in the differential for acute hypoxic respiratory failure and promptly addressed. Reference #1: Samol JM, Lambers DS. Magnesium sulfate tocolysis and pulmonary edema: the drug or the vehicle? Am J Obstet Gynecol. 2005 May;192(5):1430-2. doi: 10.1016/j.ajog.2005.02.093. PMID: 15902128. DISCLOSURES: No relevant relationships by Nasir Alhamdan No relevant relationships by Harshitha Mergey Devender No relevant relationships by Abira Usman No relevant relationships by Vishruth Vyata No relevant relationships by Harika Yadav

3.
Chest ; 162(4):A623-A624, 2022.
Article in English | EMBASE | ID: covidwho-2060649

ABSTRACT

SESSION TITLE: Unusual Pneumonias SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Invasive pulmonary aspergillosis (IPA) commonly occurs in the setting of immunosuppression. Underlying lung disease is a well-known risk factor for IPA;however, interstitial lung disease (ILD) has not been recognized as a risk factor for IPA[1]. CASE PRESENTATION: A 40-year-old male with a history of a failed kidney transplant now on hemodialysis (HD), Juvenile Rheumatoid Arthritis, Mixed Connective Tissue Disease, Aspergilloma led to right lower lobectomy a year ago, COVID-19 infection three months ago, chronic lung disease (CLD) thought to be due to Nonspecific interstitial pneumonia (NSIP) presented with dyspnea. He had several hospitalizations for respiratory failure needing intubation or NIPPV, broad-spectrum antibiotics, steroids, and HD with improved respiratory status, eventually discharged. Bronchoalveolar lavage fluid culture grew aspergillus terreus but was negative for Pneumocystis (PCP), bacteria, acid-fast bacilli, and Nocardia. The transbronchial biopsies showed mixed inflammatory type and fungal forms in one specimen. Additionally, the initially negative galactomannan converted into a serial rise in galactomannan (>3.75 Index) along with a rise in beta d-glucan (>500 pg/ml). Unfortunately, he had gaps in antifungals and was readmitted similarly. Micafungin was added for dual fungal coverage and was planned for surgical lung biopsy to characterize ILD further once his respiratory status allows. DISCUSSION: He has multiple risk factors for developing IPA, such as high-dose steroids for ILD and recent COVID infection. Initially, respiratory failure was thought to be due to exacerbation of ILD, and suspicion for IPA was low because of lack of neutropenia, negative fungal biomarkers, lack of classic findings on lung imaging, and in-hospital clinical improvement with steroids. However, the eventual course of recurrent respiratory failure while on high-dose steroids, along with gaps in antifungal therapy and continued growth of Aspergillus, made IPA the most likely diagnosis. For IPA, the mainstay of treatment is both adequate antifungal therapy and reduction in immunosuppression to the extent possible[2];however, it is unclear if his underlying ILD can tolerate steroid taper. He will need a lung transplant after adequately treating IPA. CONCLUSIONS: There are no current guidelines on simultaneously treating IPA and NSIP. It is challenging to balance reduction in immunosuppression as tolerated for ILD and concurrently maintain antifungal therapy. During this patient's hospitalization, there have been considerations of using a steroid-sparing agent for his suspected NSIP, however, in the setting of active infection, its benefit is debatable.[3] Reference #1: Matsuyama H, Miyoshi S, Sugino K, et al. Fatal Invasive Pulmonary Aspergillosis Associated with Nonspecific Interstitial Pneumonia: An Autopsy Case Report. Intern Med. 2018;57(24):3619-3624. doi:10.2169/internalmedicine.1144-18 Reference #2: Thomas F. Patterson, George R. Thompson, III, David W. Denning, Jay A. Fishman, Susan Hadley, Raoul Herbrecht, Dimitrios P. Kontoyiannis, Kieren A. Marr, Vicki A. Morrison, M. Hong Nguyen, Brahm H. Segal, William J. Steinbach, David A. Stevens, Thomas J. Walsh, John R. Wingard, Jo-Anne H. Young, John E. Bennett, Practice Guidelines for the Diagnosis and Management of Aspergillosis: 2016 Update by the Infectious Diseases Society of America, Clinical Infectious Diseases, Volume 63, Issue 4, 15 August 2016, Pages e1–e60, https://doi.org/10.1093/cid/ciw326 Reference #3: Mezger, M., Wozniok, I., Blockhaus, C., Kurzai, O., Hebart, H., Einsele, H., & Loeffler, J. (2008). Impact of mycophenolic acid on the functionality of human polymorphonuclear neutrophils and dendritic cells during interaction with Aspergillus fumigatus. Antimicrobial agents and chemotherapy, 52(7), 2644–2646. https://doi.org/10.1128/AAC.01618-07 DISCLOSURES: No relevant relationships by Nasir Alhamdan No relevant relati nships by Parth Jamindar No relevant relationships by Harshitha Mergey Devender No relevant relationships by Abira Usman No relevant relationships by Vishruth Vyata

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