Pub Date : 2021-01-01DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2136
T. Chokshi, J. Celenza-Salvatore, K. Santana, E. Botti, R. Bodawala
Finely ground hydrous magnesium silicate, or talcum powder, finds significant utilization in the cosmetic industry for its absorbency. Long-term inhalation exposure to talc is associated with an interstitial lung disease termed talcosis, commonly seen in miners, industry workers, and IV drug users. However, it may unfortunately manifest in the general public secondary to chronic inhalation of talc-containing products. Here, we present a unique case of talcum powder pica induced pulmonary talcosis. 31-year-old female from Jamaica presented for evaluation of mild hemoptysis, subjective fevers, cough, weight loss, and dyspnea of three months duration. Vital signs were unremarkable. Physical examination was notable for bilateral costochondral tenderness. Labs were significant for elevated ESR and CRP. CT chest revealed bilateral apical predominant dense, consolidative airspace opacities with adjacent branching nodular densities and diffuse ground-glass opacification with innumerable miliary nodules. The patient was admitted for tuberculosis rule out. QuantiFERON-TB Gold and four sputum AFB smears and cultures resulted negative. Further questioning revealed history of intentional oral talcum powder ingestion from childhood until age 27. She underwent hemoptysis work-up in Jamaica including lung biopsy for confirmation of suspected sarcoidosis. However, results of pathology confirmed a diagnosis of pulmonary talcosis consistent with her history. Given CT findings, SARS-CoV-2 testing was repeated and resulted positive. However, pharmacologic therapy was not indicated given lack of oxygen requirement. She was discharged with outpatient Pulmonary follow-up. Pulmonary talcosis develops with chronic inhalation or intravenous exposure. Talco-silicosis and talco-asbestosis are seen in miners and industrial workers exposed to high levels of inhaled impure talc. Chronic exposure to cosmetic talc also has the potential to cause talcosis. Lung parenchymal changes are not always acutely evident and may manifest up to four decades after inciting events. Pathologic changes occur in the following three major patterns: diffuse interstitial fibrosis, nodular fibrosis, and foreign body granulomatosis. Pica is defined as the persistent consumption of nonnutritive substances that is not socially acceptable and occurs in the context of mental or medical disorders. As a result of an underlying psychiatric diagnosis, pica behavior was the driving force behind our patient's consumption of talc, resulting in chronic, repetitive inhalation exposure, and ultimately led to the development of pulmonary talcosis. Although our patient reported cessation of consumption four years prior, her exposure over time was significant enough for talcosis to develop. If pica was recognized and intervened upon in childhood, she may have been spared permanent lung injury.
{"title":"A Rare Case of Talcum Powder Pica Induced Pulmonary Talcosis","authors":"T. Chokshi, J. Celenza-Salvatore, K. Santana, E. Botti, R. Bodawala","doi":"10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2136","DOIUrl":"https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2136","url":null,"abstract":"Finely ground hydrous magnesium silicate, or talcum powder, finds significant utilization in the cosmetic industry for its absorbency. Long-term inhalation exposure to talc is associated with an interstitial lung disease termed talcosis, commonly seen in miners, industry workers, and IV drug users. However, it may unfortunately manifest in the general public secondary to chronic inhalation of talc-containing products. Here, we present a unique case of talcum powder pica induced pulmonary talcosis. 31-year-old female from Jamaica presented for evaluation of mild hemoptysis, subjective fevers, cough, weight loss, and dyspnea of three months duration. Vital signs were unremarkable. Physical examination was notable for bilateral costochondral tenderness. Labs were significant for elevated ESR and CRP. CT chest revealed bilateral apical predominant dense, consolidative airspace opacities with adjacent branching nodular densities and diffuse ground-glass opacification with innumerable miliary nodules. The patient was admitted for tuberculosis rule out. QuantiFERON-TB Gold and four sputum AFB smears and cultures resulted negative. Further questioning revealed history of intentional oral talcum powder ingestion from childhood until age 27. She underwent hemoptysis work-up in Jamaica including lung biopsy for confirmation of suspected sarcoidosis. However, results of pathology confirmed a diagnosis of pulmonary talcosis consistent with her history. Given CT findings, SARS-CoV-2 testing was repeated and resulted positive. However, pharmacologic therapy was not indicated given lack of oxygen requirement. She was discharged with outpatient Pulmonary follow-up. Pulmonary talcosis develops with chronic inhalation or intravenous exposure. Talco-silicosis and talco-asbestosis are seen in miners and industrial workers exposed to high levels of inhaled impure talc. Chronic exposure to cosmetic talc also has the potential to cause talcosis. Lung parenchymal changes are not always acutely evident and may manifest up to four decades after inciting events. Pathologic changes occur in the following three major patterns: diffuse interstitial fibrosis, nodular fibrosis, and foreign body granulomatosis. Pica is defined as the persistent consumption of nonnutritive substances that is not socially acceptable and occurs in the context of mental or medical disorders. As a result of an underlying psychiatric diagnosis, pica behavior was the driving force behind our patient's consumption of talc, resulting in chronic, repetitive inhalation exposure, and ultimately led to the development of pulmonary talcosis. Although our patient reported cessation of consumption four years prior, her exposure over time was significant enough for talcosis to develop. If pica was recognized and intervened upon in childhood, she may have been spared permanent lung injury.","PeriodicalId":23339,"journal":{"name":"TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE","volume":"42 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87426394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2146
Z. Muzaffarr
Introduction: Amiodarone is one of the most commonly prescribed antiarrhythmic medications in the United States. Adverse effects have been shown to affect multiple organ systems including cardiac, thyroid, hepatic, ocular and pulmonary. Pulmonary toxicity can vary in presentation from interstitial pneumonitis, eosinophilic pneumonia, organizing pneumonia and acute respiratory distress syndrome (ARDS)1. This is a case of ARDS caused by Amiodarone. Case Presentation: This is a case of an 81 yo male with a history of atrial fibrillation (on Amiodarone 200 mg daily), mechanical aortic valve replacement and diabetes who presented to the hospital with a four week history of dry cough and one week of dyspnea on exertion. He was treated for community acquired pneumonia prior to admission with steroids, Azithromycin, Ceftriaxone and Levofloxacin. On arrival he was afebrile, but hypoxic requiring oxygen support with nasal cannula. Physical exam was concerning for an ill appearing, lethargic elderly gentleman with extensive crackles throughout both lung fields more concentrated in the upper lobes. Laboratory was significant for negative SARS Coronavirus RNA PCR and Leukocytosis 14.7. Computed-tomography revealed extensive bilateral consolidations with air bronchograms worse in the upper lobes. As his clinical status worsened requiring use of non-invasive ventilation and transfer to the intensive care unit, it became clear that this was not an infectious process;work up thus far had been negative. Amiodarone was discontinued and the patient was started on Diltiazem and pulse dose steroids. Within four days, his respiratory and mental status improved. Discussion: Amiodarone pulmonary toxicity has been associated with higher doses of 400 mg, but 1.6% of cases are reported with less, making this case unique. The pathology appears to be related to direct cytotoxic effect and indirect immunological reaction. Patients will usually present with a nonproductive cough and shortness of breath. Imaging is key for diagnosis, demonstrating diffuse patchy infiltrates;with a preference to the right lung and upper lobes. Treatment centers on discontinuation of the drug and 40-60 mg of Prednisone per day tapered over the period of a few months2.
{"title":"A Rare Case of ARDS Caused by Amiodarone","authors":"Z. Muzaffarr","doi":"10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2146","DOIUrl":"https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2146","url":null,"abstract":"Introduction: Amiodarone is one of the most commonly prescribed antiarrhythmic medications in the United States. Adverse effects have been shown to affect multiple organ systems including cardiac, thyroid, hepatic, ocular and pulmonary. Pulmonary toxicity can vary in presentation from interstitial pneumonitis, eosinophilic pneumonia, organizing pneumonia and acute respiratory distress syndrome (ARDS)1. This is a case of ARDS caused by Amiodarone. Case Presentation: This is a case of an 81 yo male with a history of atrial fibrillation (on Amiodarone 200 mg daily), mechanical aortic valve replacement and diabetes who presented to the hospital with a four week history of dry cough and one week of dyspnea on exertion. He was treated for community acquired pneumonia prior to admission with steroids, Azithromycin, Ceftriaxone and Levofloxacin. On arrival he was afebrile, but hypoxic requiring oxygen support with nasal cannula. Physical exam was concerning for an ill appearing, lethargic elderly gentleman with extensive crackles throughout both lung fields more concentrated in the upper lobes. Laboratory was significant for negative SARS Coronavirus RNA PCR and Leukocytosis 14.7. Computed-tomography revealed extensive bilateral consolidations with air bronchograms worse in the upper lobes. As his clinical status worsened requiring use of non-invasive ventilation and transfer to the intensive care unit, it became clear that this was not an infectious process;work up thus far had been negative. Amiodarone was discontinued and the patient was started on Diltiazem and pulse dose steroids. Within four days, his respiratory and mental status improved. Discussion: Amiodarone pulmonary toxicity has been associated with higher doses of 400 mg, but 1.6% of cases are reported with less, making this case unique. The pathology appears to be related to direct cytotoxic effect and indirect immunological reaction. Patients will usually present with a nonproductive cough and shortness of breath. Imaging is key for diagnosis, demonstrating diffuse patchy infiltrates;with a preference to the right lung and upper lobes. Treatment centers on discontinuation of the drug and 40-60 mg of Prednisone per day tapered over the period of a few months2.","PeriodicalId":23339,"journal":{"name":"TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE","volume":"36 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78026023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2114
A. Manfra, J. Sharma, J. Kilburn, M. Chang, N. Noureddin
Hydrogen peroxide is a chemical commonly used as a household antiseptic for cleaning and disinfecting. Chronic inhalation of hydrogen peroxide is described in case reports as causing interstitial lung disease with radiographic images demonstrating septal line thickening, honeycombing, and traction bronchiectasis with associated ground glass opacification. In a literature review, no cases of acute hydrogen peroxide inhalation induced lung injury have been previously described. This is a case of acute hydrogen peroxide induced pneumonitis initially masquerading as Covid-19 pneumonia. An 82-year-old male with a pertinent history of diastolic heart failure, obstructive sleep apnea, and chronic obstructive pulmonary disease presented with worsening dyspnea and morning hemoptysis. He endorsed a COVID-19 exposure two weeks previously. Upon initial evaluation, he was afebrile and hemodynamically normal, with tachypnea and requiring 6 liters of supplemental oxygen to maintain spo2> 88%. Pulmonary auscultation revealed clear breath sounds and no signs of fluid overload were evident on the remainder of the physical exam. The initial chest x-ray and CT imaging demonstrated multifocal, bilateral, hazy consolidations with increased interstitial markings concerning for COVID-19 pneumonia. Pertinent lab results revealed negative COVID-19 and viral respiratory PCR results, and respiratory cultures with no growth of pathogenic bacteria. An echocardiogram revealed new systolic dysfunction with a reduced ejection fraction of 35-40%. The patient continued to have severe dyspnea and hypoxemia despite treatment for heart failure, COPD, and bacterial pneumonia consisting of diuretics, bronchodilators, and antibiotics. On further interview the patient recounted mixing hydrogen peroxide in his CPAP humidifier for the previous week before admission, based on a friend's advice in preventing COVID-19. The patient was subsequently initiated on systemic glucocorticoid therapy and had significant improvement in hypoxemia and dyspnea and oxygen requirements decreased from 6L to 2L nasal cannula at time of discharge. In light of the recent influential media attention and fear, cleaning products such as bleach have received disproportionate attention in the killing of the COVID-19 virus. Similarly, hydrogen peroxide is used as a disinfectant, which was intentionally inhaled in large amounts and over a one-week duration in this case. Prior case reports describe environmental and occupational exposure over 3-5 years developing into a non-specific interstitial pneumonia pattern. This case demonstrates a rare acute pneumonitis after the recent use of hydrogen peroxide in a CPAP humidifier. Inhalation of hydrogen peroxide may produce an acute pneumonitis distinct from what has been described previously with chronic inhalation.
{"title":"Humidified Hydrogen Peroxide Associated Pneumonitis: A Cautionary Tale","authors":"A. Manfra, J. Sharma, J. Kilburn, M. Chang, N. Noureddin","doi":"10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2114","DOIUrl":"https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2114","url":null,"abstract":"Hydrogen peroxide is a chemical commonly used as a household antiseptic for cleaning and disinfecting. Chronic inhalation of hydrogen peroxide is described in case reports as causing interstitial lung disease with radiographic images demonstrating septal line thickening, honeycombing, and traction bronchiectasis with associated ground glass opacification. In a literature review, no cases of acute hydrogen peroxide inhalation induced lung injury have been previously described. This is a case of acute hydrogen peroxide induced pneumonitis initially masquerading as Covid-19 pneumonia. An 82-year-old male with a pertinent history of diastolic heart failure, obstructive sleep apnea, and chronic obstructive pulmonary disease presented with worsening dyspnea and morning hemoptysis. He endorsed a COVID-19 exposure two weeks previously. Upon initial evaluation, he was afebrile and hemodynamically normal, with tachypnea and requiring 6 liters of supplemental oxygen to maintain spo2> 88%. Pulmonary auscultation revealed clear breath sounds and no signs of fluid overload were evident on the remainder of the physical exam. The initial chest x-ray and CT imaging demonstrated multifocal, bilateral, hazy consolidations with increased interstitial markings concerning for COVID-19 pneumonia. Pertinent lab results revealed negative COVID-19 and viral respiratory PCR results, and respiratory cultures with no growth of pathogenic bacteria. An echocardiogram revealed new systolic dysfunction with a reduced ejection fraction of 35-40%. The patient continued to have severe dyspnea and hypoxemia despite treatment for heart failure, COPD, and bacterial pneumonia consisting of diuretics, bronchodilators, and antibiotics. On further interview the patient recounted mixing hydrogen peroxide in his CPAP humidifier for the previous week before admission, based on a friend's advice in preventing COVID-19. The patient was subsequently initiated on systemic glucocorticoid therapy and had significant improvement in hypoxemia and dyspnea and oxygen requirements decreased from 6L to 2L nasal cannula at time of discharge. In light of the recent influential media attention and fear, cleaning products such as bleach have received disproportionate attention in the killing of the COVID-19 virus. Similarly, hydrogen peroxide is used as a disinfectant, which was intentionally inhaled in large amounts and over a one-week duration in this case. Prior case reports describe environmental and occupational exposure over 3-5 years developing into a non-specific interstitial pneumonia pattern. This case demonstrates a rare acute pneumonitis after the recent use of hydrogen peroxide in a CPAP humidifier. Inhalation of hydrogen peroxide may produce an acute pneumonitis distinct from what has been described previously with chronic inhalation.","PeriodicalId":23339,"journal":{"name":"TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87411804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2124
C. Uhland, J. Siordia, B. Ainapurapu
Multiple chemotherapy medications are known to cause acute lung injury. One medication that causes injury to the lungs and can present with hypoxia is pomalidomide, a medication used for multiple myeloma. Chemotherapy-induced lung injury is commonly mistaken for infectious pneumonia. The diagnosis becomes difficult since patients are immunosuppressed and prone to infection. The presentation is complicated further during pandemics. Coronavirus Disease 19 (COVID19) has become a very common diagnosis during the pandemic in 2020. Multiple diagnostic tests are required to rule out infectious processes including that of less common organism. To ultimately deem the injury to be caused by medication side-effect is a diagnosis of exclusion. The following case illustrates the complexity of the diagnosis. Multiple case reports show a potential association between pomalidomide and acute lung injury. Lung injury arises about 120 to 480 days after continuous use. Pomalidomide promotes T-cell proliferation and secretion of IL-2 and INF-y. IL-2 causes increased vascular permeability leading to pulmonary edema and acute lung injury. INF-y further promotes hyperoxia-induced lung injury. Treatment is with pomalidomide cessation and corticosteroids. In some cases, the medication can be reintroduced but there have been reports of recurrence.
{"title":"Pomalidomide-Induced Lung Injury Mimicking COVID19 Pneumonia","authors":"C. Uhland, J. Siordia, B. Ainapurapu","doi":"10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2124","DOIUrl":"https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2124","url":null,"abstract":"Multiple chemotherapy medications are known to cause acute lung injury. One medication that causes injury to the lungs and can present with hypoxia is pomalidomide, a medication used for multiple myeloma. Chemotherapy-induced lung injury is commonly mistaken for infectious pneumonia. The diagnosis becomes difficult since patients are immunosuppressed and prone to infection. The presentation is complicated further during pandemics. Coronavirus Disease 19 (COVID19) has become a very common diagnosis during the pandemic in 2020. Multiple diagnostic tests are required to rule out infectious processes including that of less common organism. To ultimately deem the injury to be caused by medication side-effect is a diagnosis of exclusion. The following case illustrates the complexity of the diagnosis. Multiple case reports show a potential association between pomalidomide and acute lung injury. Lung injury arises about 120 to 480 days after continuous use. Pomalidomide promotes T-cell proliferation and secretion of IL-2 and INF-y. IL-2 causes increased vascular permeability leading to pulmonary edema and acute lung injury. INF-y further promotes hyperoxia-induced lung injury. Treatment is with pomalidomide cessation and corticosteroids. In some cases, the medication can be reintroduced but there have been reports of recurrence.","PeriodicalId":23339,"journal":{"name":"TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE","volume":"194 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81071139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2149
D. Chinn
A 74-year-old man with hypertension, chronic kidney disease, coronary artery disease, chronic systolic heart failure and prior cardiac arrest due to ventricular tachycardia status-post implantable cardioverter-defibrillator placement presented to the emergency department with worsening dyspnea. He reported shortness of breath with exertion and dry nonproductive cough which had gradually progressed over the past several months. He reported compliance with home medications although could not specify which medications he was taking. He previously worked as a plumber, without known environmental exposures, sick contact, travel or extensive tobacco use. Physical exam revealed diffuse crackles in the bilateral posterior lung fields, jugular venous distension and pitting bilateral lower extremity edema. Due to suspicion for community acquired pneumonia and acute on chronic heart failure exacerbation, he was admitted to the hospital for intravenous (IV) antibiotics and diuresis. Transthoracic echocardiogram showed a reduced left ventricular ejection fraction and elevated pulmonary artery pressures, otherwise no valvulopathy, shunting or right ventricular dysfunction. His fluid status improved, although his oxygen requirements continued to rise. He was escalated from high flow nasal cannula to bilevel positive airway pressure ventilation, and transferred to the medical intensive care unit. Computed tomography pulmonary angiogram revealed no evidence of pulmonary embolism, although was significant for bilateral diffuse ground glass opacities with septal thickening, honeycombing and traction bronchiectasis. Respiratory viral panel, COVID-19 testing, fungal serologies and autoimmune/vasculitis workup were negative. Outside records consisted of recent diagnostic bronchoscopy which yielded unremarkable cytology and cultures, pulmonary function tests demonstrating restrictive lung pattern and severely reduced diffusion capacity of carbon monoxide, and normal ventilation-perfusion scan. Calls were placed to outside providers who confirmed that the patient had been on high-dose amiodarone (400 mg twice daily) for over the past decade, as previous attempts transition down or off amiodarone had led to his prior cardiac arrest. After discussion in multidisciplinary conferences, the patient was started on high-dose IV steroids due to suspicion for amiodarone-induced pulmonary toxicity (AIPT). Unfortunately, he decompensated further, and his family ultimately pursued hospice care. While the incidence of AIPT is less than 10-15%, this case serves a reminder of the potentially fatal pulmonary adverse events associated with amiodarone use, and emphasizes upon the essential need for close multiorgan monitoring while on the medication. There remains a strong demand for further research to elucidate dose-dependent and duration-dependent relationships between amiodarone use and associated pulmonary toxicity, as well as identifying predisposing risk factors.
{"title":"When Antibiotics, Diuresis and Steroids Are Not Enough - A Fatal Case of Amiodarone-Induced Pulmonary Toxicity","authors":"D. Chinn","doi":"10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2149","DOIUrl":"https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2149","url":null,"abstract":"A 74-year-old man with hypertension, chronic kidney disease, coronary artery disease, chronic systolic heart failure and prior cardiac arrest due to ventricular tachycardia status-post implantable cardioverter-defibrillator placement presented to the emergency department with worsening dyspnea. He reported shortness of breath with exertion and dry nonproductive cough which had gradually progressed over the past several months. He reported compliance with home medications although could not specify which medications he was taking. He previously worked as a plumber, without known environmental exposures, sick contact, travel or extensive tobacco use. Physical exam revealed diffuse crackles in the bilateral posterior lung fields, jugular venous distension and pitting bilateral lower extremity edema. Due to suspicion for community acquired pneumonia and acute on chronic heart failure exacerbation, he was admitted to the hospital for intravenous (IV) antibiotics and diuresis. Transthoracic echocardiogram showed a reduced left ventricular ejection fraction and elevated pulmonary artery pressures, otherwise no valvulopathy, shunting or right ventricular dysfunction. His fluid status improved, although his oxygen requirements continued to rise. He was escalated from high flow nasal cannula to bilevel positive airway pressure ventilation, and transferred to the medical intensive care unit. Computed tomography pulmonary angiogram revealed no evidence of pulmonary embolism, although was significant for bilateral diffuse ground glass opacities with septal thickening, honeycombing and traction bronchiectasis. Respiratory viral panel, COVID-19 testing, fungal serologies and autoimmune/vasculitis workup were negative. Outside records consisted of recent diagnostic bronchoscopy which yielded unremarkable cytology and cultures, pulmonary function tests demonstrating restrictive lung pattern and severely reduced diffusion capacity of carbon monoxide, and normal ventilation-perfusion scan. Calls were placed to outside providers who confirmed that the patient had been on high-dose amiodarone (400 mg twice daily) for over the past decade, as previous attempts transition down or off amiodarone had led to his prior cardiac arrest. After discussion in multidisciplinary conferences, the patient was started on high-dose IV steroids due to suspicion for amiodarone-induced pulmonary toxicity (AIPT). Unfortunately, he decompensated further, and his family ultimately pursued hospice care. While the incidence of AIPT is less than 10-15%, this case serves a reminder of the potentially fatal pulmonary adverse events associated with amiodarone use, and emphasizes upon the essential need for close multiorgan monitoring while on the medication. There remains a strong demand for further research to elucidate dose-dependent and duration-dependent relationships between amiodarone use and associated pulmonary toxicity, as well as identifying predisposing risk factors.","PeriodicalId":23339,"journal":{"name":"TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE","volume":"43 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80777776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2147
K. Omar, R. Anees, A. Burza
INTRODUCTION-Amiodarone pulmonary toxicity risk is estimated to be around 1 to 5 percent, depending on risk factors like daily dose exceeding 400mg/day, intake of drug for more than two months, age above 60 years, duration of treatment of 6 to 12 months and prior history of lung disease. CASE -A 70-year-old white male with diabetes, chronic kidney disease, hypertension and obstructive sleep apnea, presented with atrial fibrillation with rapid ventricular response and acute hypoxic respiratory failure. SARS-CoV-2 RNA test was negative and pulmonary embolism was ruled out by CT Angiogram of chest. He underwent Transesophageal Echocardiogram guided cardioversion showing low normal left ventricular function and absence of left atrial appendage or thrombus. He was discharged on a anticoagulant and a diuretic. 2 weeks later he was readmitted with recurrent atrial fibrillation with rapid ventricular response. He was loaded with amiodarone intravenously and then transitioned to oral Amiodarone 400 mg orally twice daily. After 5 days he deteriorated requiring intubation for respiratory failure. CT Chest on day 5 of amiodarone administration showed new changes in form of bilateral ground glass attenuation, septal thickening and bilateral airspace consolidation when compared to previous admission. Laboratory findings included: white blood count 14000/uL, procalcitonin 0.28ng/ml, CRP 90 mg/L, BNP and negative respiratory viral panel. Flexible Bronchoscopy was performed which showed edematous airways and thin secretions. RESULT-Bronchoscopic alveolar lavage showed normal cell count, foamy macrophages, no malignant cells, and no growth on any culture. Biopsy was held given the acuity of his condition. His blood cultures, infectious work up and autoimmune workup was negative. Amiodarone was stopped and 60 mg oral prednisone was started for possible amiodarone induced acute interstitial pneumonitis and he responded well. He was extubated by day 10 and was on tapering oral steroid schedule for 6 months. CONCLUSION-Amiodarone pulmonary toxicity is usually recognized after 2-3 months of treatment, especially in patients taking dosages higher than 400 mg/day. This case is unique given the acute onset. The major hypothesis suggested include cytotoxic injury due to drug phospholipid complexes, alteration of phospholipid bilayer and free radical induced cellular injury and indirect Immunologic reaction. Currently there are no guidelines to prevent it. Acute pneumonitis although presents rarely, needs high index of suspicion for early diagnosis and immediate treatment with high dose intravenous steroids because of increased risk of mortality.
{"title":"Acute Interstitial Pneumonitis Secondary to Amiodarone","authors":"K. Omar, R. Anees, A. Burza","doi":"10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2147","DOIUrl":"https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2147","url":null,"abstract":"INTRODUCTION-Amiodarone pulmonary toxicity risk is estimated to be around 1 to 5 percent, depending on risk factors like daily dose exceeding 400mg/day, intake of drug for more than two months, age above 60 years, duration of treatment of 6 to 12 months and prior history of lung disease. CASE -A 70-year-old white male with diabetes, chronic kidney disease, hypertension and obstructive sleep apnea, presented with atrial fibrillation with rapid ventricular response and acute hypoxic respiratory failure. SARS-CoV-2 RNA test was negative and pulmonary embolism was ruled out by CT Angiogram of chest. He underwent Transesophageal Echocardiogram guided cardioversion showing low normal left ventricular function and absence of left atrial appendage or thrombus. He was discharged on a anticoagulant and a diuretic. 2 weeks later he was readmitted with recurrent atrial fibrillation with rapid ventricular response. He was loaded with amiodarone intravenously and then transitioned to oral Amiodarone 400 mg orally twice daily. After 5 days he deteriorated requiring intubation for respiratory failure. CT Chest on day 5 of amiodarone administration showed new changes in form of bilateral ground glass attenuation, septal thickening and bilateral airspace consolidation when compared to previous admission. Laboratory findings included: white blood count 14000/uL, procalcitonin 0.28ng/ml, CRP 90 mg/L, BNP and negative respiratory viral panel. Flexible Bronchoscopy was performed which showed edematous airways and thin secretions. RESULT-Bronchoscopic alveolar lavage showed normal cell count, foamy macrophages, no malignant cells, and no growth on any culture. Biopsy was held given the acuity of his condition. His blood cultures, infectious work up and autoimmune workup was negative. Amiodarone was stopped and 60 mg oral prednisone was started for possible amiodarone induced acute interstitial pneumonitis and he responded well. He was extubated by day 10 and was on tapering oral steroid schedule for 6 months. CONCLUSION-Amiodarone pulmonary toxicity is usually recognized after 2-3 months of treatment, especially in patients taking dosages higher than 400 mg/day. This case is unique given the acute onset. The major hypothesis suggested include cytotoxic injury due to drug phospholipid complexes, alteration of phospholipid bilayer and free radical induced cellular injury and indirect Immunologic reaction. Currently there are no guidelines to prevent it. Acute pneumonitis although presents rarely, needs high index of suspicion for early diagnosis and immediate treatment with high dose intravenous steroids because of increased risk of mortality.","PeriodicalId":23339,"journal":{"name":"TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74777616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2138
A. Khan, Y. Zhou, K. Young, S. Bhele, J. Mueller, F. Alroumi
Introduction-We present the case of a young male with constitutional symptoms thought to be consistent with community-acquired or COVID-19 pneumonia, who was instead found to have a history of vaping tetrahydrocannabinol (THC) and was diagnosed with EVALI (E-cigarette, or Vaping, Product Use-Associated Lung Injury). Case Presentation-21-year-old male college student presented to the hospital in July 2020 with a 2-week history of abdominal pain, vomiting, diarrhea, headache and generalized myalgias. More recently, he had a fever and dry cough associated with worsening shortness of breath. In the hospital, the patient was initially requiring minimal oxygen and was febrile to 102°F. Physical exam was consistent with a young, diaphoretic male with tachypnea who had bilateral basilar crackles on auscultation of lungs. Bloodwork revealed a leukocytosis of 19.2k/mm3, ferritin of 1081ng/mL and a CRP of 64mg/dL. An initial chest x-ray was consistent with bilateral interstitial markings. 2 days later, he was admitted to the intensive care unit since he was requiring high-flow nasal cannula. A Computed Tomography (CT) of the chest (Figure 1A, 1B) showed extensive peribronchial groundglass opacity with subpleural sparing. Complete respiratory viral panel, COVID-19, Tuberculosis, HIV and tickborne illnesses testing were all negative. By this time, the patient had been treated with antibiotics for presumed community-acquired pneumonia. The pulmonary service was consulted, and detailed social history-taking revealed that the patient had started vaping THC obtained from a less well-known brand, shortly before the onset of his symptoms. A bronchoscopy was performed which revealed evidence of anthracotic pigment present in distal airways. Bronchoalveolar lavage (BAL) ultimately revealed no evidence of infection or malignancy and showed foamy macrophages. Based on his presentation, a diagnosis of EVALI was made and the patient was started on intravenous corticosteroids. During the next 3 days, the patient's fever defervesced and his inflammatory markers down-trended. He was discharged home on room air with a corticosteroid taper. Discussion-Targeted history taking which addressed the specifics of the 'off-brand' or counterfeit THC vaping brands was key in revealing the etiology of the patient's symptoms and allowed the initiation of the correct treatment in a timely manner. Vitamin-E acetate has emerged as a potential common exposure among affected patients who use a variety of counterfeit products. Clinicians should be well versed with asking specific questions focused on type, duration and brand of products when EVALI is suspected.
{"title":"\"HIS-STORY\": The Clinical Key Leading to a Diagnosis of EVALI","authors":"A. Khan, Y. Zhou, K. Young, S. Bhele, J. Mueller, F. Alroumi","doi":"10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2138","DOIUrl":"https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2138","url":null,"abstract":"Introduction-We present the case of a young male with constitutional symptoms thought to be consistent with community-acquired or COVID-19 pneumonia, who was instead found to have a history of vaping tetrahydrocannabinol (THC) and was diagnosed with EVALI (E-cigarette, or Vaping, Product Use-Associated Lung Injury). Case Presentation-21-year-old male college student presented to the hospital in July 2020 with a 2-week history of abdominal pain, vomiting, diarrhea, headache and generalized myalgias. More recently, he had a fever and dry cough associated with worsening shortness of breath. In the hospital, the patient was initially requiring minimal oxygen and was febrile to 102°F. Physical exam was consistent with a young, diaphoretic male with tachypnea who had bilateral basilar crackles on auscultation of lungs. Bloodwork revealed a leukocytosis of 19.2k/mm3, ferritin of 1081ng/mL and a CRP of 64mg/dL. An initial chest x-ray was consistent with bilateral interstitial markings. 2 days later, he was admitted to the intensive care unit since he was requiring high-flow nasal cannula. A Computed Tomography (CT) of the chest (Figure 1A, 1B) showed extensive peribronchial groundglass opacity with subpleural sparing. Complete respiratory viral panel, COVID-19, Tuberculosis, HIV and tickborne illnesses testing were all negative. By this time, the patient had been treated with antibiotics for presumed community-acquired pneumonia. The pulmonary service was consulted, and detailed social history-taking revealed that the patient had started vaping THC obtained from a less well-known brand, shortly before the onset of his symptoms. A bronchoscopy was performed which revealed evidence of anthracotic pigment present in distal airways. Bronchoalveolar lavage (BAL) ultimately revealed no evidence of infection or malignancy and showed foamy macrophages. Based on his presentation, a diagnosis of EVALI was made and the patient was started on intravenous corticosteroids. During the next 3 days, the patient's fever defervesced and his inflammatory markers down-trended. He was discharged home on room air with a corticosteroid taper. Discussion-Targeted history taking which addressed the specifics of the 'off-brand' or counterfeit THC vaping brands was key in revealing the etiology of the patient's symptoms and allowed the initiation of the correct treatment in a timely manner. Vitamin-E acetate has emerged as a potential common exposure among affected patients who use a variety of counterfeit products. Clinicians should be well versed with asking specific questions focused on type, duration and brand of products when EVALI is suspected.","PeriodicalId":23339,"journal":{"name":"TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90113715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2122
L. Jones, M. Beg, D. Kellogg, S. Adams
Introduction: Crizotinib is an anaplastic lymphoma kinase (ALK) inhibitor used for advanced ALK-positive nonsmall cell lung cancer. It can rarely cause interstitial lung disease with a wide range of presentations from asymptomatic pulmonary radiological findings to fatal pneumonitis. Here, we present a case of rapid, acute hypoxemic respiratory failure due to crizotinib-induced pneumonitis. Case presentation: A 63-year-old man with a medical history of head and neck squamous cell cancer with metastasis to pulmonary parenchyma, pleura and mediastinal lymph nodes presented with dyspnea, fever and non-massive hemoptysis four days after initiation of crizotinib therapy. The patient was febrile, tachycardic, tachypneic and hypoxemic upon presentation. Laboratory investigations were unremarkable. Respiratory viral panel and reverse transcription-polymerase chain reaction for severe acute respiratory syndrome coronavirus 2 were negative. Further investigations including sputum, blood and urine culture were unrevealing. Chest radiographs rapidly progressed from baseline imaging to scattered patchy multifocal infiltrates. One day later, computerized tomography of the chest revealed rapidly progressing diffuse bilateral ground glass opacities. Despite empiric anti-microbial therapy, the patient's respiratory status deteriorated, and he was transferred to medical intensive care unit. He was pulsed with IV methylprednisolone 500mg twice a day for 3 days, followed by a slow taper for presumed pneumonitis secondary to crizotinib which led to a rapid improvement in his respiratory status. Discussion: ALK inhibitors are a relatively novel therapy for several malignancies and the side effects are not well known. In clinical trials, crizotinib was associated with interstitial lung disease in 2.4% of cases and presented at a median time of 20 days to 2 months after initiation. Management is challenging because there are no guidelines currently available for diagnosis and treatment of ALK inhibitor associated pneumonitis. Diagnosis generally requires a recent history of drug exposure, abnormal thoracic radiography, and clinical and/or radiologic improvement after discontinuation of the offending agent. Given their increasing use to treat various malignancies, it is imperative for clinicians to have a high index of suspicion for crizotinib-induced pneumonitis. A multidisciplinary approach will lead to rapid diagnosis and early treatment of this serious adverse events associated with this novel drug.
{"title":"Rapid Onset of Acute Respiratory Failure Due to Crizotinib-Induced Pneumonitis","authors":"L. Jones, M. Beg, D. Kellogg, S. Adams","doi":"10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2122","DOIUrl":"https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2122","url":null,"abstract":"Introduction: Crizotinib is an anaplastic lymphoma kinase (ALK) inhibitor used for advanced ALK-positive nonsmall cell lung cancer. It can rarely cause interstitial lung disease with a wide range of presentations from asymptomatic pulmonary radiological findings to fatal pneumonitis. Here, we present a case of rapid, acute hypoxemic respiratory failure due to crizotinib-induced pneumonitis. Case presentation: A 63-year-old man with a medical history of head and neck squamous cell cancer with metastasis to pulmonary parenchyma, pleura and mediastinal lymph nodes presented with dyspnea, fever and non-massive hemoptysis four days after initiation of crizotinib therapy. The patient was febrile, tachycardic, tachypneic and hypoxemic upon presentation. Laboratory investigations were unremarkable. Respiratory viral panel and reverse transcription-polymerase chain reaction for severe acute respiratory syndrome coronavirus 2 were negative. Further investigations including sputum, blood and urine culture were unrevealing. Chest radiographs rapidly progressed from baseline imaging to scattered patchy multifocal infiltrates. One day later, computerized tomography of the chest revealed rapidly progressing diffuse bilateral ground glass opacities. Despite empiric anti-microbial therapy, the patient's respiratory status deteriorated, and he was transferred to medical intensive care unit. He was pulsed with IV methylprednisolone 500mg twice a day for 3 days, followed by a slow taper for presumed pneumonitis secondary to crizotinib which led to a rapid improvement in his respiratory status. Discussion: ALK inhibitors are a relatively novel therapy for several malignancies and the side effects are not well known. In clinical trials, crizotinib was associated with interstitial lung disease in 2.4% of cases and presented at a median time of 20 days to 2 months after initiation. Management is challenging because there are no guidelines currently available for diagnosis and treatment of ALK inhibitor associated pneumonitis. Diagnosis generally requires a recent history of drug exposure, abnormal thoracic radiography, and clinical and/or radiologic improvement after discontinuation of the offending agent. Given their increasing use to treat various malignancies, it is imperative for clinicians to have a high index of suspicion for crizotinib-induced pneumonitis. A multidisciplinary approach will lead to rapid diagnosis and early treatment of this serious adverse events associated with this novel drug.","PeriodicalId":23339,"journal":{"name":"TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE","volume":"63 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76249498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2126
J. Adunse, Y. Yoon, M. Taleb, C. Gatto-Weis, G. Chang, F. Safi
Introduction: Eosinophilic pneumonia is a condition defined by eosinophilic infiltration of the lung parenchyma. Eosinophilic pneumonia is a known side effect of Dupilumab, a monoclonal antibody targeting the alpha chain of interleukin-4 (IL-4) that is used to treat moderate to severe atopic dermatitis and asthma by its inhibition of IL-4 and IL-13, which are key drivers in the TH2 response. We present a case of a patient presenting with eosinophilic pneumonia ten weeks after being started on Dupilumab. Case report: A 55-year-old female with history of asthma, bullous pemphigoid and chronic dermatitis who was started on Dupilumab (Dupixant) by her rheumatologist for treatment of her dermatitis and bullous pemphigoid ten weeks prior to presentation. Patient presented to the pulmonary clinic with four weeks history of worsening cough, shortness of breath, generalized body aches, lowgrade fevers, chills, chest pains and non-drenching night sweats. She had been treated by primary physician with a course of antibiotics without improvement in her symptoms. Outpatient chest computed tomography (CT chest) showed extensive bilateral reticular nodular opacities and scattered ground glass opacities (Panel A) for which she was admitted to the hospital for further evaluation. Patient was hypoxic and required 4 liters/minute oxygen by nasal cannula. Her laboratory testing showed normal leucocyte count 9.57 X 103/uL with eosinophilia of 17% (total eosinophilic count 17,000). Her immunoglobulin E was 2096 U/mL. Covid testing was negative. Rheumatologic workup was negative. Patient underwent fiberoptic bronchoscopy with bronchoalveolar lavage (BAL) which showed 29% eosinophil count (Panel B) and was negative for bacterial and fungal cultures.Following BAL results, Dupilumab was discontinued and patient received single dose 60mg intravenous methylprednisone then oral prednisone 40 mg daily, resulting in rapid improvement in her symptoms, oxygen requirements and complete resolution of peripheral eosinophilia. She was discharged on oral prednisone taper. Discussion: Drug induced eosinophilic pneumonias are reported with medications such as non-steroidal anti-inflammatory drugs (NSAIDS), and antibiotics. There are very few described cases of Dupilumab-induced eosinophilic pneumonia in the medical literature. Eosinophilic pneumonia and eosinophilic conditions are listed side effects of Dupilumab which inhibits Th2 pathway by inhibiting IL-4 and IL-13 and should in theory decrease tissue eosinophilia, eosinophil degranulation, and reduce eosinophil survival. This case illustrates Dupilumab-induced eosinophilic pneumonia, suggesting that despite the drug's effect on Th2 cytokines, it can cause eosinophilic tissue infiltration and eosinophilia which if promptly identified and treated can lead to excellent outcomes. .
{"title":"A Case of Dupilumab-Induced Eosinophilic Pneumonia","authors":"J. Adunse, Y. Yoon, M. Taleb, C. Gatto-Weis, G. Chang, F. Safi","doi":"10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2126","DOIUrl":"https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2126","url":null,"abstract":"Introduction: Eosinophilic pneumonia is a condition defined by eosinophilic infiltration of the lung parenchyma. Eosinophilic pneumonia is a known side effect of Dupilumab, a monoclonal antibody targeting the alpha chain of interleukin-4 (IL-4) that is used to treat moderate to severe atopic dermatitis and asthma by its inhibition of IL-4 and IL-13, which are key drivers in the TH2 response. We present a case of a patient presenting with eosinophilic pneumonia ten weeks after being started on Dupilumab. Case report: A 55-year-old female with history of asthma, bullous pemphigoid and chronic dermatitis who was started on Dupilumab (Dupixant) by her rheumatologist for treatment of her dermatitis and bullous pemphigoid ten weeks prior to presentation. Patient presented to the pulmonary clinic with four weeks history of worsening cough, shortness of breath, generalized body aches, lowgrade fevers, chills, chest pains and non-drenching night sweats. She had been treated by primary physician with a course of antibiotics without improvement in her symptoms. Outpatient chest computed tomography (CT chest) showed extensive bilateral reticular nodular opacities and scattered ground glass opacities (Panel A) for which she was admitted to the hospital for further evaluation. Patient was hypoxic and required 4 liters/minute oxygen by nasal cannula. Her laboratory testing showed normal leucocyte count 9.57 X 103/uL with eosinophilia of 17% (total eosinophilic count 17,000). Her immunoglobulin E was 2096 U/mL. Covid testing was negative. Rheumatologic workup was negative. Patient underwent fiberoptic bronchoscopy with bronchoalveolar lavage (BAL) which showed 29% eosinophil count (Panel B) and was negative for bacterial and fungal cultures.Following BAL results, Dupilumab was discontinued and patient received single dose 60mg intravenous methylprednisone then oral prednisone 40 mg daily, resulting in rapid improvement in her symptoms, oxygen requirements and complete resolution of peripheral eosinophilia. She was discharged on oral prednisone taper. Discussion: Drug induced eosinophilic pneumonias are reported with medications such as non-steroidal anti-inflammatory drugs (NSAIDS), and antibiotics. There are very few described cases of Dupilumab-induced eosinophilic pneumonia in the medical literature. Eosinophilic pneumonia and eosinophilic conditions are listed side effects of Dupilumab which inhibits Th2 pathway by inhibiting IL-4 and IL-13 and should in theory decrease tissue eosinophilia, eosinophil degranulation, and reduce eosinophil survival. This case illustrates Dupilumab-induced eosinophilic pneumonia, suggesting that despite the drug's effect on Th2 cytokines, it can cause eosinophilic tissue infiltration and eosinophilia which if promptly identified and treated can lead to excellent outcomes. .","PeriodicalId":23339,"journal":{"name":"TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE","volume":"22 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75125328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2159
T. Rayburn, N. Ahmed, F. Surtie, K. Fagan
INTRODUCTION: Bleomycin is an antitumor agent most often used to treat Hodgkin lymphoma. The use of bleomycin is limited by potential for oxidative lung damage. Incidence correlates with cumulative dose, with most cases occurring with >400 international units (IU). Here we present an expository case of bleomycin-induced lung injury at an unusually low dose with additional important diagnostic considerations. CASE SUMMARY: A 37-year-old woman with a past medical history of HIV, Hodgkin's lymphoma, and renal failure requiring dialysis was evaluated for dyspnea and dry cough. The patient had completed three cycles of chemotherapy with ABVD (Doxorubicin, Bleomycin, Vinblastine, Dacarbazine). The cumulative dose of bleomycin was 32 IU. On examination, the patient was cachectic with mild bibasilar crackles noted on lung auscultation. The oxygen saturation was 97% while receiving supplemental oxygen at 2 liters per minute by nasal cannula. The CD4 count was 220. Chest radiography revealed patchy infiltrates scattered throughout both lungs not present on imaging five months prior. High-resolution CT showed widespread interstitial thickening and diffuse ground-glass opacities. Broad-spectrum antibiotics were started for suspected community acquired pneumonia to no effect. Further laboratory testing and bronchoalveolar lavage ruled out infectious etiology, including PCP and COVID19. Subsequent VATS and wedge resection was performed. Pathology demonstrated interstitial cellular infiltrate and fibrosis. A diagnosis of organizing pneumonia possibly related to bleomycin was made. Future treatment with bleomycin was discontinued. Systemic glucocorticoids were administered. Despite initial improvement, the patient's clinical course was complicated by hypoxemic respiratory failure, for which she underwent intubation and mechanical ventilation. She died on hospital day 30. No postmortem examination was performed. DISCUSSION: The diagnosis of bleomycin-induced lung injury is one of exclusion;often made within weeks of chemotherapy administration and rarely after six months. In this case, concurrent infection with HIV prolonged the time to diagnosis due to high clinical suspicion for atypical pneumonia. Moreover, the patient's limited renal function likely narrowed the chemotherapeutic safety window, given bleomycin is eliminated almost entirely by the kidney. Our case illustrates the importance of early consideration of this entity even at doses not routinely associated with toxicity. Upon diagnosis, treatment is immediate cessation of the causative agent followed by systemic glucocorticoids. The prognosis is grim, with most patients succumbing to respiratory failure within months of symptom onset.
{"title":"It's Not Always Pneumonia: Bleomycin-Induced Lung Injury in a Patient with HIV","authors":"T. Rayburn, N. Ahmed, F. Surtie, K. Fagan","doi":"10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2159","DOIUrl":"https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2159","url":null,"abstract":"INTRODUCTION: Bleomycin is an antitumor agent most often used to treat Hodgkin lymphoma. The use of bleomycin is limited by potential for oxidative lung damage. Incidence correlates with cumulative dose, with most cases occurring with >400 international units (IU). Here we present an expository case of bleomycin-induced lung injury at an unusually low dose with additional important diagnostic considerations. CASE SUMMARY: A 37-year-old woman with a past medical history of HIV, Hodgkin's lymphoma, and renal failure requiring dialysis was evaluated for dyspnea and dry cough. The patient had completed three cycles of chemotherapy with ABVD (Doxorubicin, Bleomycin, Vinblastine, Dacarbazine). The cumulative dose of bleomycin was 32 IU. On examination, the patient was cachectic with mild bibasilar crackles noted on lung auscultation. The oxygen saturation was 97% while receiving supplemental oxygen at 2 liters per minute by nasal cannula. The CD4 count was 220. Chest radiography revealed patchy infiltrates scattered throughout both lungs not present on imaging five months prior. High-resolution CT showed widespread interstitial thickening and diffuse ground-glass opacities. Broad-spectrum antibiotics were started for suspected community acquired pneumonia to no effect. Further laboratory testing and bronchoalveolar lavage ruled out infectious etiology, including PCP and COVID19. Subsequent VATS and wedge resection was performed. Pathology demonstrated interstitial cellular infiltrate and fibrosis. A diagnosis of organizing pneumonia possibly related to bleomycin was made. Future treatment with bleomycin was discontinued. Systemic glucocorticoids were administered. Despite initial improvement, the patient's clinical course was complicated by hypoxemic respiratory failure, for which she underwent intubation and mechanical ventilation. She died on hospital day 30. No postmortem examination was performed. DISCUSSION: The diagnosis of bleomycin-induced lung injury is one of exclusion;often made within weeks of chemotherapy administration and rarely after six months. In this case, concurrent infection with HIV prolonged the time to diagnosis due to high clinical suspicion for atypical pneumonia. Moreover, the patient's limited renal function likely narrowed the chemotherapeutic safety window, given bleomycin is eliminated almost entirely by the kidney. Our case illustrates the importance of early consideration of this entity even at doses not routinely associated with toxicity. Upon diagnosis, treatment is immediate cessation of the causative agent followed by systemic glucocorticoids. The prognosis is grim, with most patients succumbing to respiratory failure within months of symptom onset.","PeriodicalId":23339,"journal":{"name":"TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76055181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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