Pub Date : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1989
G. Palmer, D. Buus, P. Kasznica, F. Jamous
Introduction: Post-extubation stridor, or inspiratory noise following extubation, is frequently observed in patients post-extubation, due to laryngeal edema secondary to airway manipulation. Post-extubation stridor is of increasing concern during the COVID-19 pandemic, as risk for re-intubation and consequent poor outcome is high. We present a case of post-extubation stridor due to tracheal mucus plugging in the setting of COVID-19 pneumonia. Case Presentation: A 61-year-old female diagnosed with COVID-19 pneumonia, right lower lobe pulmonary embolus, and left lung pneumothorax with chest tube experienced a nontraumatic intubation and 13 days of ventilatory support due to respiratory failure. Four days following extubation patient developed stridor and increased oxygen requirement. Patient was given racemic epinephrine 0.5mL x two doses and IV solumedrol 40mg BID x four doses, maintaining oxygen saturation >91% on BiPAP. Direct visualization under flexible laryngoscopy showed small granulation tissue in posterior commissure and concretions and dried mucus in the trachea. The following day, patient displayed worsening stridor, hoarseness, and respiratory difficulty. Bronchoscopy versus tracheoscopy was considered. CT chest displayed moderate debris within the proximal trachea. Due to concern for airway compromise with bronchoscopy, patient underwent laryngoscopy and tracheoscopy with tracheal plug removal by airway forceps. Stridor and hoarseness improved following procedure;oxygen requirements declined in following two-three days leading to discharge. Discussion: Post-extubation stridor can occur in nearly 10% of intensive care unit patients, frequently due to laryngeal edema. In the present case, our patient underwent steroid and racemic epinephrine therapy to address this possible cause with no clinical improvement. Chest CT was performed for further characterization, which discovered moderate debris within the proximal trachea. We hypothesize the tracheal debris accumulation was due to illness with COVID-19, prolonged intubation, and a weak cough unable to clear airway secretions. Previous studies have shown that COVID-19 pneumonia causes bilateral diffuse alveolar damage with fibromyxoid exudates leading to excessive airway mucus. This excess mucus leads to increased airway resistance and decreased alveolar gas exchange. Weakness after critical illness and prolonged intubation likely contributed to our patient's inability to clear these secretions, leading to tracheal accumulation, increased oxygen requirement, and stridor. Bronchoscopy and/or intubation in patients with tracheal debris may be detrimental due to endotracheal tube obstruction or mucus plug mobilization into distal bronchi and subsequent respiratory failure. Therefore, it is important to maintain a broad differential diagnosis while assessing stridor after extubation, particularly in patients with COVID-19 pneumonia.
简介:拔管后喘鸣，或拔管后吸气噪声，在拔管后患者中经常观察到，由于气道操作继发的喉部水肿。在2019冠状病毒病大流行期间，拔管后喘鸣日益引起人们的关注，因为再次插管和由此导致的不良后果的风险很高。我们报告一例在COVID-19肺炎背景下因气管粘液堵塞而引起的拔管后喘鸣。病例介绍:一名61岁女性，诊断为COVID-19肺炎，右下叶肺栓塞，左肺气胸伴胸管，因呼吸衰竭接受非创伤性插管和13天的通气支持。拔管后4天患者出现喘鸣，需氧量增加。患者给予外消旋肾上腺素0.5mL x 2次剂量，静脉注射固美醇40mg BID x 4次剂量，BiPAP维持血氧饱和度91%。软性喉镜下直接观察可见后连合处小肉芽组织，气管内有结块和干燥粘液。第二天，患者表现出更严重的喘鸣、声音嘶哑和呼吸困难。考虑支气管镜检查与气管镜检查。胸部CT显示近端气管内有中度碎片。由于担心支气管镜检查对气道的损害，患者行喉镜检查和气管镜检查，并用气道钳取出气管塞。手术后患者的喘鸣和声音嘶哑得到改善，在出院前的2 - 3天内氧气需求下降。讨论:拔管后喘鸣可发生在近10%的重症监护病房患者，通常是由于喉水肿。在本病例中，我们的患者接受了类固醇和外消旋肾上腺素治疗来解决这个可能的原因，但没有临床改善。胸部CT进一步表征，发现近端气管内有中度碎片。我们假设气管碎片堆积是由于COVID-19疾病、长时间插管和无力咳嗽无法清除气道分泌物所致。既往研究表明，COVID-19肺炎可引起双侧弥漫性肺泡损伤，纤维黏液样渗出导致气道粘液过多。这种多余的粘液导致气道阻力增加和肺泡气体交换减少。危重疾病后的虚弱和长时间插管可能导致患者无法清除这些分泌物，导致气管积聚，氧气需求增加和喘鸣。气管碎片患者的支气管镜检查和/或插管可能是有害的，因为气管内管阻塞或粘液塞移动到远端支气管和随后的呼吸衰竭。因此，在评估拔管后的喘鸣时保持广泛的鉴别诊断非常重要，特别是在COVID-19肺炎患者中。
{"title":"Post-Extubation Stridor in COVID-19 Pneumonia: A Case for Rigid Tracheoscopy Over Bronchoscopy to Avert Airway Compromise","authors":"G. Palmer, D. Buus, P. Kasznica, F. Jamous","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1989","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1989","url":null,"abstract":"Introduction: Post-extubation stridor, or inspiratory noise following extubation, is frequently observed in patients post-extubation, due to laryngeal edema secondary to airway manipulation. Post-extubation stridor is of increasing concern during the COVID-19 pandemic, as risk for re-intubation and consequent poor outcome is high. We present a case of post-extubation stridor due to tracheal mucus plugging in the setting of COVID-19 pneumonia. Case Presentation: A 61-year-old female diagnosed with COVID-19 pneumonia, right lower lobe pulmonary embolus, and left lung pneumothorax with chest tube experienced a nontraumatic intubation and 13 days of ventilatory support due to respiratory failure. Four days following extubation patient developed stridor and increased oxygen requirement. Patient was given racemic epinephrine 0.5mL x two doses and IV solumedrol 40mg BID x four doses, maintaining oxygen saturation >91% on BiPAP. Direct visualization under flexible laryngoscopy showed small granulation tissue in posterior commissure and concretions and dried mucus in the trachea. The following day, patient displayed worsening stridor, hoarseness, and respiratory difficulty. Bronchoscopy versus tracheoscopy was considered. CT chest displayed moderate debris within the proximal trachea. Due to concern for airway compromise with bronchoscopy, patient underwent laryngoscopy and tracheoscopy with tracheal plug removal by airway forceps. Stridor and hoarseness improved following procedure;oxygen requirements declined in following two-three days leading to discharge. Discussion: Post-extubation stridor can occur in nearly 10% of intensive care unit patients, frequently due to laryngeal edema. In the present case, our patient underwent steroid and racemic epinephrine therapy to address this possible cause with no clinical improvement. Chest CT was performed for further characterization, which discovered moderate debris within the proximal trachea. We hypothesize the tracheal debris accumulation was due to illness with COVID-19, prolonged intubation, and a weak cough unable to clear airway secretions. Previous studies have shown that COVID-19 pneumonia causes bilateral diffuse alveolar damage with fibromyxoid exudates leading to excessive airway mucus. This excess mucus leads to increased airway resistance and decreased alveolar gas exchange. Weakness after critical illness and prolonged intubation likely contributed to our patient's inability to clear these secretions, leading to tracheal accumulation, increased oxygen requirement, and stridor. Bronchoscopy and/or intubation in patients with tracheal debris may be detrimental due to endotracheal tube obstruction or mucus plug mobilization into distal bronchi and subsequent respiratory failure. Therefore, it is important to maintain a broad differential diagnosis while assessing stridor after extubation, particularly in patients with COVID-19 pneumonia.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"03 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80083465","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 : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2003
D. Ford, R. Holladay, T. Sartawi, P. Charoenpong, J. D. Packer, K. K. Goddard
A myriad of acute clinicopathological effects of novel SARS Coronavirus 2 (SARS-Cov-2) infection are being described. Here, we present a case report which illustrates a biopsy proven distinct chronic complication of Covid-19 disease which afflicts some survivors: Post Covid-19 Organizing Pneumonia (PCOP). A 30 year old African-American female with known Human Immunodeficiency Virus (HIV) infection on anti-retroviral therapy (ART) and recently diagnosed nodular marginal zone lymphoma, on chemotherapy, became infected with SARS-Cov-2 in early August, 2020. She presented with fever, increased cough, and shortness of breath worsening over two weeks. In the emergency room, she had temperature 102o F, heart rate of 110 with oxygen saturation 88% on room air. Lab work was significant for Leukocytosis of 17.62 k/uL and recent absolute CD4 of 590/mm3. SARSCoV-2 Polymerase Chain Reaction (PCR) test was positive. Admission Chest Roentgenogram (X-ray) revealed bilateral basal opacities consistent with Covid-19 Pneumonia. Our patient was admitted and received Dexamethasone and a course of empiric antibiotics for community acquired pneumonia. She was discharged on brief oral prednisone taper with home oxygen 2L/min;However, she would be readmitted to hospital twice more over the next eight weeks with similar complaints of cough, recurrent fever, and dyspnea with new focal opacities on serial chest imaging (Figure 1). Her symptoms persisted despite broadened empiric antibiotics including antifungal therapy. Extensive lab work-up for secondary infection and autoimmune disease was unrevealing. Bronchoscopy was finally done with Transbronchial Cryobiopsy (TBC) revealing acute and chronic inflammation with interstitial fibrosis. Bronchoalveolar lavage (BAL) cultures were negative. As evidenced by serial imaging (Figure 1), our patient consistently improved with empiric steroids for organizing pneumonia. Her clinical findings recurred with attempts to taper steroids even at five months post initial positive SARS-CoV-2 PCR. This case illustrates Post Covid-19 Organizing Pneumonia (PCOP). It is a Clinicopathologic syndrome characterized by rapid resolution with corticosteroids, but frequent relapses when treatment is tapered or stopped.1 It also illustrates several salient issues in caring for patients who survive acute SARS-CoV-2 infection: i) Delayed viral clearance related to chronic immunosuppression,2 ii) Delayed Bronchoscopy in an effort to mitigate infection risk to care providers, iii) The impact of ongoing therapy on consequent delayed pathology findings,3 iv) Increased morbidity associated with both late disease recognition and our attempts to taper chronic steroid therapy in the setting of an Organizing Pneumonia4 and v) The possibility that earlier biopsy, diagnosis and uninterrupted therapy may prevent pulmonary fibrosis.
{"title":"Post-Covid Organizing Pneumonia","authors":"D. Ford, R. Holladay, T. Sartawi, P. Charoenpong, J. D. Packer, K. K. Goddard","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2003","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2003","url":null,"abstract":"A myriad of acute clinicopathological effects of novel SARS Coronavirus 2 (SARS-Cov-2) infection are being described. Here, we present a case report which illustrates a biopsy proven distinct chronic complication of Covid-19 disease which afflicts some survivors: Post Covid-19 Organizing Pneumonia (PCOP). A 30 year old African-American female with known Human Immunodeficiency Virus (HIV) infection on anti-retroviral therapy (ART) and recently diagnosed nodular marginal zone lymphoma, on chemotherapy, became infected with SARS-Cov-2 in early August, 2020. She presented with fever, increased cough, and shortness of breath worsening over two weeks. In the emergency room, she had temperature 102o F, heart rate of 110 with oxygen saturation 88% on room air. Lab work was significant for Leukocytosis of 17.62 k/uL and recent absolute CD4 of 590/mm3. SARSCoV-2 Polymerase Chain Reaction (PCR) test was positive. Admission Chest Roentgenogram (X-ray) revealed bilateral basal opacities consistent with Covid-19 Pneumonia. Our patient was admitted and received Dexamethasone and a course of empiric antibiotics for community acquired pneumonia. She was discharged on brief oral prednisone taper with home oxygen 2L/min;However, she would be readmitted to hospital twice more over the next eight weeks with similar complaints of cough, recurrent fever, and dyspnea with new focal opacities on serial chest imaging (Figure 1). Her symptoms persisted despite broadened empiric antibiotics including antifungal therapy. Extensive lab work-up for secondary infection and autoimmune disease was unrevealing. Bronchoscopy was finally done with Transbronchial Cryobiopsy (TBC) revealing acute and chronic inflammation with interstitial fibrosis. Bronchoalveolar lavage (BAL) cultures were negative. As evidenced by serial imaging (Figure 1), our patient consistently improved with empiric steroids for organizing pneumonia. Her clinical findings recurred with attempts to taper steroids even at five months post initial positive SARS-CoV-2 PCR. This case illustrates Post Covid-19 Organizing Pneumonia (PCOP). It is a Clinicopathologic syndrome characterized by rapid resolution with corticosteroids, but frequent relapses when treatment is tapered or stopped.1 It also illustrates several salient issues in caring for patients who survive acute SARS-CoV-2 infection: i) Delayed viral clearance related to chronic immunosuppression,2 ii) Delayed Bronchoscopy in an effort to mitigate infection risk to care providers, iii) The impact of ongoing therapy on consequent delayed pathology findings,3 iv) Increased morbidity associated with both late disease recognition and our attempts to taper chronic steroid therapy in the setting of an Organizing Pneumonia4 and v) The possibility that earlier biopsy, diagnosis and uninterrupted therapy may prevent pulmonary fibrosis.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"63 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80505286","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 : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1999
E. Stuewe, S. Kher
Introduction: About 30% of patients with severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) had persisting lung abnormalities after acute illness. However, little is known whether SARS coronavirus 2 (SARS-CoV-2) infection will cause long-term pulmonary complications. We present our experience with a patient with a new diagnosis of interstitial lung disease (ILD) during the pandemic. Case: A 61-year-old man with history of hypertension and obstructive sleep apnea developed acute onset cough and dyspnea in March 2020. The patient was not initially tested for COVID-19 because of the local department of public health's stay-at-home advisory. Cough resolved but dyspnea persisted. Two months later, polymerase chain reaction for SARS-CoV-2 was checked and was negative. Due to ongoing dyspnea, a CT chest was performed 5 months after symptom onset and showed diffuse, mild sub-pleural reticulonodular opacities in upper and lower lungs, concerning for ILD (Figure 1). Pulmonary function testing (PFT) showed normal spirometry and lung volumes, and mild impairment in gas exchange. Work up for causes of ILD, including assessment for exposures and serologies for rheumatologic disease, was unremarkable. IgG antibody for SARS-CoV-2 was detected (25.9 AU/ml;normal<1.00 AU/ml);IgM was undetectable. Work up for other causes of dyspnea included an echocardiogram, CT pulmonary angiogram, and ventilation-perfusion scan that revealed no evidence of structural heart disease or thromboembolic disease. Discussion: Given no other etiology of ILD was identified, it is most plausible that our patient had acute COVID-19 infection in March and developed secondary ILD over the ensuing months. Previous studies of patients with SARS and MERS have found occurrences of pulmonary fibrosis and PFT abnormalities persisting many months after onset of infection. Thus, it is prudent to be vigilant for symptoms of lung disease in patients with a known history of COVID-19 infection. An additional diagnostic challenge, as with the case above, lies with patients who present with new onset ILD but without a confirmation of COVID-19, particularly given the limited access to testing in the early stages of the pandemic. In these patients, we suggest a thorough history that includes screening for symptoms suggestive of prior viral syndromes, particularly with associated anosmia or dysgeusia, that can point to a history of COVID-19 infection. Another option is consideration of serologic testing, although such tests must be interpreted with caution in view of the paucity of supporting evidence and the possibility of both false-positives and false-negatives.
{"title":"Importance of Eliciting History of Prior SARS-CoV-2 Infection in Evaluation of New Diagnosis of Interstitial Lung Disease","authors":"E. Stuewe, S. Kher","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1999","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1999","url":null,"abstract":"Introduction: About 30% of patients with severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) had persisting lung abnormalities after acute illness. However, little is known whether SARS coronavirus 2 (SARS-CoV-2) infection will cause long-term pulmonary complications. We present our experience with a patient with a new diagnosis of interstitial lung disease (ILD) during the pandemic. Case: A 61-year-old man with history of hypertension and obstructive sleep apnea developed acute onset cough and dyspnea in March 2020. The patient was not initially tested for COVID-19 because of the local department of public health's stay-at-home advisory. Cough resolved but dyspnea persisted. Two months later, polymerase chain reaction for SARS-CoV-2 was checked and was negative. Due to ongoing dyspnea, a CT chest was performed 5 months after symptom onset and showed diffuse, mild sub-pleural reticulonodular opacities in upper and lower lungs, concerning for ILD (Figure 1). Pulmonary function testing (PFT) showed normal spirometry and lung volumes, and mild impairment in gas exchange. Work up for causes of ILD, including assessment for exposures and serologies for rheumatologic disease, was unremarkable. IgG antibody for SARS-CoV-2 was detected (25.9 AU/ml;normal<1.00 AU/ml);IgM was undetectable. Work up for other causes of dyspnea included an echocardiogram, CT pulmonary angiogram, and ventilation-perfusion scan that revealed no evidence of structural heart disease or thromboembolic disease. Discussion: Given no other etiology of ILD was identified, it is most plausible that our patient had acute COVID-19 infection in March and developed secondary ILD over the ensuing months. Previous studies of patients with SARS and MERS have found occurrences of pulmonary fibrosis and PFT abnormalities persisting many months after onset of infection. Thus, it is prudent to be vigilant for symptoms of lung disease in patients with a known history of COVID-19 infection. An additional diagnostic challenge, as with the case above, lies with patients who present with new onset ILD but without a confirmation of COVID-19, particularly given the limited access to testing in the early stages of the pandemic. In these patients, we suggest a thorough history that includes screening for symptoms suggestive of prior viral syndromes, particularly with associated anosmia or dysgeusia, that can point to a history of COVID-19 infection. Another option is consideration of serologic testing, although such tests must be interpreted with caution in view of the paucity of supporting evidence and the possibility of both false-positives and false-negatives.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"42 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82692551","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 : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1990
S. Podder, N. Donthi, E. Ekanem, M. Desai
RATIONALE Covid-19 has been associated with multi-organ complications, including pneumothoraces. Retrospective studies, which have primarily been case reports and small case series, suggest that pneumothoraces may occur in 1-2% of patients with Covid-19. This potentially lethal complication is thought to more likely occur in mechanically ventilated patients and those with underlying lung disease. Our aim is to characterize the risk factor in patients hospitalized for Covid-19 who developed pneumothoraces. METHODS We conducted a retrospective chart review of patients with COVID-19 admitted at 5 hospitals within the Inova Health System between March 1, 2020 and May 21, 2020. Out of the 1619 hospitalized patients with Covid-19, 22 patients (1.4%) developed pneumothorax. Data on demographic, comorbidities, inflammatory markers, ventilatory mode and treatment methods were collected. Findings are displayed in Table 1. RESULTS The median length of stay was 18.5 days with the diagnosis of pneumothorax made between days 1 and 30 of hospitalization. All pneumothoraces were diagnosed on chest x-ray, with the most common reason for obtaining chest imaging being respiratory distress and worsening hypoxia. 10 patients developed left-sided pneumothorax, 11 patients developed right-sided pneumothorax and 1 patient developed bilateral pneumothoraces. 8 out of the 22 patients (36%) died, whereas the crude mortality of all patients admitted with Covid-19 during this time span was 15.8%. The median age of our cohort was 60 years and 82% were male. Majority of the patients were Latino. The most common comorbidities in this cohort included hypertension (52%) and diabetes (32%). Notably, only 19% of the patients had underlying lung pathology such as chronic obstructive pulmonary disease (COPD) and asthma. Less than half of the patients who had pneumothoraces were ventilated. 16 (73%) patients had chest tubes placed for treatment. CONCLUSION The marked inflammatory response, fibrosis, and need for positive pressure ventilation in Covid-19 pneumonia are likely contributory to the development of pneumothorax. Unlike most cases of pneumothoraces, the etiology in patients with Covid-19 appears to be multifactorial and not directly associated with high vent settings. This is supported by the fact that many patients in our patients were on nasal cannula at time of diagnosis. Prompt diagnosis and treatment are crucial to mitigate morbidity and mortality in this population.
{"title":"Spontaneous Pneumothorax as a Complication of Covid-19","authors":"S. Podder, N. Donthi, E. Ekanem, M. Desai","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1990","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1990","url":null,"abstract":"RATIONALE Covid-19 has been associated with multi-organ complications, including pneumothoraces. Retrospective studies, which have primarily been case reports and small case series, suggest that pneumothoraces may occur in 1-2% of patients with Covid-19. This potentially lethal complication is thought to more likely occur in mechanically ventilated patients and those with underlying lung disease. Our aim is to characterize the risk factor in patients hospitalized for Covid-19 who developed pneumothoraces. METHODS We conducted a retrospective chart review of patients with COVID-19 admitted at 5 hospitals within the Inova Health System between March 1, 2020 and May 21, 2020. Out of the 1619 hospitalized patients with Covid-19, 22 patients (1.4%) developed pneumothorax. Data on demographic, comorbidities, inflammatory markers, ventilatory mode and treatment methods were collected. Findings are displayed in Table 1. RESULTS The median length of stay was 18.5 days with the diagnosis of pneumothorax made between days 1 and 30 of hospitalization. All pneumothoraces were diagnosed on chest x-ray, with the most common reason for obtaining chest imaging being respiratory distress and worsening hypoxia. 10 patients developed left-sided pneumothorax, 11 patients developed right-sided pneumothorax and 1 patient developed bilateral pneumothoraces. 8 out of the 22 patients (36%) died, whereas the crude mortality of all patients admitted with Covid-19 during this time span was 15.8%. The median age of our cohort was 60 years and 82% were male. Majority of the patients were Latino. The most common comorbidities in this cohort included hypertension (52%) and diabetes (32%). Notably, only 19% of the patients had underlying lung pathology such as chronic obstructive pulmonary disease (COPD) and asthma. Less than half of the patients who had pneumothoraces were ventilated. 16 (73%) patients had chest tubes placed for treatment. CONCLUSION The marked inflammatory response, fibrosis, and need for positive pressure ventilation in Covid-19 pneumonia are likely contributory to the development of pneumothorax. Unlike most cases of pneumothoraces, the etiology in patients with Covid-19 appears to be multifactorial and not directly associated with high vent settings. This is supported by the fact that many patients in our patients were on nasal cannula at time of diagnosis. Prompt diagnosis and treatment are crucial to mitigate morbidity and mortality in this population.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75641178","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 : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2008
J. Wang, A. Abburi, G. Molina-Pallete
Introduction: The novel coronavirus 2019 (COVID-19) infection is a worldwide pandemic. The clinical course is highly variable. Most patients recover with humoral and cell mediated immunities against reinfection. Previous studies showed immunocompetent patients with severe infections all became seropositive for immunoglobulins against COVID-19, while only a minority of patients with mild infections remained seronegative. However, immunocompromised patients can remain seronegative for up to two months with severe infections while shedding active virus. This case describes a patient on obinutuzumab who has persistently positive SARS-CoV-2 polymerase chain reaction (PCR) with persistently negative anti-SARS-CoV-2 serum immunoglobulin. Case: Our patient is a 74 year old male with follicular lymphoma on obinutuzumab. Past medical history includes obstructive sleep apnea, hypertension, and type 2 diabetes mellitus. He first incidentally tested positive for SARS-CoV-2 PCR but was asymptomatic. He presented to the hospital 3 weeks later for dyspnea, fevers, and cough. Computed tomography (CT) angiography of the chest was negative for pulmonary embolism but showed multifocal infiltrates and a nonocclusive thrombus in the inferior vena cava (IVC). Inflammatory markers were elevated. Patient was started on anticoagulation for his IVC thrombus. He did not require supplemental oxygen, and was discharged home after a short inpatient observation. The patient had 3 more hospitalizations over the next 30 days with acute hypoxic respiratory failure requiring supplemental oxygen. He had serial CT imaging of his chest that remained negative for pulmonary embolism but showed progressively worsening multifocal infiltrates. His inflammatory markers remained elevated (see figure 1). He tested negative for SARS-CoV-2 Immunoglobulin G (IgG) on day 27 and 36 from the initial COVID-19 diagnosis while repeat SARS-CoV-2 PCRs remained positive. Discussion: Immunocompromised patients with COVID 19 infection tend to have worse clinical outcomes. Our patient had persistently positive SARS-CoV-2 PCR and negative IgG beyond 30 days along with worsening respiratory symptoms. It is possible that the lack of IgG response may be related to the monoclonal antibody obinutuzumab against CD 20 cells. In the case of our patient, despite his persistent positivity of SARS-CoV-2 by rapid PCR test, we did not have confirmation of active infection by whole genome sequence or viral culture. However he had persistent clinical deterioration, elevated inflammatory markers, as well as worsening serial CT images suggesting a prolonged active infection. The findings in our patient may have significant implications in the isolation, management and prognosis of patients receiving immunosuppressive therapy, specifically anti CD 20 management.
{"title":"Prolonged Novel Coronavirus 2019 Infection with Negative Immunoglobulins in a Patient on Obinutuzumab","authors":"J. Wang, A. Abburi, G. Molina-Pallete","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2008","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2008","url":null,"abstract":"Introduction: The novel coronavirus 2019 (COVID-19) infection is a worldwide pandemic. The clinical course is highly variable. Most patients recover with humoral and cell mediated immunities against reinfection. Previous studies showed immunocompetent patients with severe infections all became seropositive for immunoglobulins against COVID-19, while only a minority of patients with mild infections remained seronegative. However, immunocompromised patients can remain seronegative for up to two months with severe infections while shedding active virus. This case describes a patient on obinutuzumab who has persistently positive SARS-CoV-2 polymerase chain reaction (PCR) with persistently negative anti-SARS-CoV-2 serum immunoglobulin. Case: Our patient is a 74 year old male with follicular lymphoma on obinutuzumab. Past medical history includes obstructive sleep apnea, hypertension, and type 2 diabetes mellitus. He first incidentally tested positive for SARS-CoV-2 PCR but was asymptomatic. He presented to the hospital 3 weeks later for dyspnea, fevers, and cough. Computed tomography (CT) angiography of the chest was negative for pulmonary embolism but showed multifocal infiltrates and a nonocclusive thrombus in the inferior vena cava (IVC). Inflammatory markers were elevated. Patient was started on anticoagulation for his IVC thrombus. He did not require supplemental oxygen, and was discharged home after a short inpatient observation. The patient had 3 more hospitalizations over the next 30 days with acute hypoxic respiratory failure requiring supplemental oxygen. He had serial CT imaging of his chest that remained negative for pulmonary embolism but showed progressively worsening multifocal infiltrates. His inflammatory markers remained elevated (see figure 1). He tested negative for SARS-CoV-2 Immunoglobulin G (IgG) on day 27 and 36 from the initial COVID-19 diagnosis while repeat SARS-CoV-2 PCRs remained positive. Discussion: Immunocompromised patients with COVID 19 infection tend to have worse clinical outcomes. Our patient had persistently positive SARS-CoV-2 PCR and negative IgG beyond 30 days along with worsening respiratory symptoms. It is possible that the lack of IgG response may be related to the monoclonal antibody obinutuzumab against CD 20 cells. In the case of our patient, despite his persistent positivity of SARS-CoV-2 by rapid PCR test, we did not have confirmation of active infection by whole genome sequence or viral culture. However he had persistent clinical deterioration, elevated inflammatory markers, as well as worsening serial CT images suggesting a prolonged active infection. The findings in our patient may have significant implications in the isolation, management and prognosis of patients receiving immunosuppressive therapy, specifically anti CD 20 management.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86472458","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 : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2001
M. Patel, J. Willoughby, M. Kousha
A 49-year-old female presented due to sore throat, productive cough, fever, shortness of breath with a past medical history significant for COVID-19 infection in 04/20, nonsmoker, NSTEMI and diabetes mellitus type 2. On admission, labs revealed leukocytosis 16.33 K/mcL with left shift, D-dimer 9660 ngFEU/mL, elevated troponin x 3, lactic acid 2.4 mmol/L. Repeat COVID-19 test was negative on 05/20. Patient had an abnormal chest CT with diffuse ground glass opacities which is compatible with COVID-19 related post infectious inflammation. HIV panel and respiratory viral panel were negative. Due to elevated troponins with wall motion abnormalities patient underwent cardiac catheterization which revealed no obstructive coronary artery disease however right ventricular dysfunction was noted with elevated right ventricle (44 mmhg) and right atrium pressures (42 mmhg), normal pulmonary capillary wedge pressure. RV dysfunction was likely related to post COVID myocarditis/hypoxemic respiratory failure. Patient was discharged home on a course of prolonged steroid taper and 3-4 L oxygen. Four months later in 09/20 the patient again presented with similar complaints of shortness of breath and chest pain. Due to an elevated D-dimer and tachycardia, a CTA was obtained which was negative for pulmonary embolism however showed diffuse ground glass opacities which appeared to be persistent;distribution attenuation was also similar to previous study with worsening basilar regions concerning for consolidation. Laboratory studies in 09/2020 remarkable for leukocytosis with left shift, elevated troponin and total CK, urine toxicology was negative. Patient completed treatment for CAP on both admissions with no significant improvement. Routine immunology workup positive for ANA, speckled pattern with titer greater than 1:1280, serial rheumatoid factor 336.5 Lunits/ml, RNP antibody greater than 8 Al, SmRNP antibodies > 8.0 Al. All other immunologic workup were negative and the patient had no signs of rheumatologic conditions. Patient was started on a prolonged steroid course due to concern for superimposed mixed connective tissue disease (MCTD) pulmonary involvement with underlying CT manifestation of COVID 19, which drastically reduced her oxygen requirement. Chest CT images in patients with underlying COVID-19 infection can resemble and obscure new onset rheumatologic conditions with pulmonary involvement, such as mixed connective tissue disease, systemic lupus erythematosus, rheumatoid arthritis and hence it may delay the diagnosis of progressive pulmonary conditions which require prompt treatment. CTA on 09/20 (right) on admission showing bilateral diffuse ground glass opacities throughout the lung parenchyma with predominantly dense lower lobe opacities and mild air bronchogram (Left 05/20).
{"title":"Determining New Onset Pulmonary Involvement of Connective Tissue Disease in a Patient with Recently Diagnosed Coronavirus Disease 2019","authors":"M. Patel, J. Willoughby, M. Kousha","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2001","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2001","url":null,"abstract":"A 49-year-old female presented due to sore throat, productive cough, fever, shortness of breath with a past medical history significant for COVID-19 infection in 04/20, nonsmoker, NSTEMI and diabetes mellitus type 2. On admission, labs revealed leukocytosis 16.33 K/mcL with left shift, D-dimer 9660 ngFEU/mL, elevated troponin x 3, lactic acid 2.4 mmol/L. Repeat COVID-19 test was negative on 05/20. Patient had an abnormal chest CT with diffuse ground glass opacities which is compatible with COVID-19 related post infectious inflammation. HIV panel and respiratory viral panel were negative. Due to elevated troponins with wall motion abnormalities patient underwent cardiac catheterization which revealed no obstructive coronary artery disease however right ventricular dysfunction was noted with elevated right ventricle (44 mmhg) and right atrium pressures (42 mmhg), normal pulmonary capillary wedge pressure. RV dysfunction was likely related to post COVID myocarditis/hypoxemic respiratory failure. Patient was discharged home on a course of prolonged steroid taper and 3-4 L oxygen. Four months later in 09/20 the patient again presented with similar complaints of shortness of breath and chest pain. Due to an elevated D-dimer and tachycardia, a CTA was obtained which was negative for pulmonary embolism however showed diffuse ground glass opacities which appeared to be persistent;distribution attenuation was also similar to previous study with worsening basilar regions concerning for consolidation. Laboratory studies in 09/2020 remarkable for leukocytosis with left shift, elevated troponin and total CK, urine toxicology was negative. Patient completed treatment for CAP on both admissions with no significant improvement. Routine immunology workup positive for ANA, speckled pattern with titer greater than 1:1280, serial rheumatoid factor 336.5 Lunits/ml, RNP antibody greater than 8 Al, SmRNP antibodies > 8.0 Al. All other immunologic workup were negative and the patient had no signs of rheumatologic conditions. Patient was started on a prolonged steroid course due to concern for superimposed mixed connective tissue disease (MCTD) pulmonary involvement with underlying CT manifestation of COVID 19, which drastically reduced her oxygen requirement. Chest CT images in patients with underlying COVID-19 infection can resemble and obscure new onset rheumatologic conditions with pulmonary involvement, such as mixed connective tissue disease, systemic lupus erythematosus, rheumatoid arthritis and hence it may delay the diagnosis of progressive pulmonary conditions which require prompt treatment. CTA on 09/20 (right) on admission showing bilateral diffuse ground glass opacities throughout the lung parenchyma with predominantly dense lower lobe opacities and mild air bronchogram (Left 05/20).","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90018064","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 : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2002
L. Mcnamara, V. A. Brady
Introduction: Organizing pneumonia is a histologic subsect of interstitial lung disease (ILD). While a non-specific reaction to lung injury, it can be associated with infection, autoimmunity, or medication toxicity, or be characterized as idiopathic. Association with COVID-19 infection remains under active investigation. Beyond the initial viremia seen in COVID-19, the subsequent phase, characterized by an over-active host immune response, is less well understood. Anti-melanoma differentiation-associated gene 5 (MDA5) antibodies have been implicated in autoimmune pathology, including dermatomyositis and rapidly progressive ILD, and found to be positive in some patients with COVID-19. We describe a case of rapidly progressive organizing pneumonia with anti-MDA5 positivity, perhaps precipitated by earlier COVID-19 infection. Case: A 70-year-old gentleman with history of COVID-19 infection several months earlier presented with subacute dyspnea. He had not required hospitalization for COVID-19 infection, but subsequently developed slowly progressive dyspnea, wheezing, and inflammatory, migratory polyarthritis. Outpatient management with oral methylprednisolone 32mg daily, improved his arthritis, however, his respiratory symptoms did not improve despite additional inhaled corticosteroids and beta agonists. Admission imaging showed new bilateral upper lobe predominant ground glass opacities, reticulation of peripheral interstitium and bronchiectasis (Figure 1). Infectious workup, including SARS-CoV-2 testing, was negative. Rheumatologic workup revealed positive rheumatoid factor, anti-nuclear antibody (1:160, diffuse pattern) and anti-MDA5 antibody. The patient received broad spectrum antimicrobials and diuresis, but developed worsening acute hypoxemic/hypercarbic respiratory failure, requiring intubation and mechanical ventilation, proning, and neuromuscular blockade. Pulse dose steroids with intravenous methylprednisolone 250mg every six hours, were trialed for several days without improvements. Video assisted thorascopic surgery was performed and biopsy revealed bronchiolitis obliterans and organizing pneumonia with areas of fibrosis, without hyaline membrane formation or visible micro-organisms. The patient was not a candidate for extracorporeal membrane oxygenation and by the time the aforementioned biopsy resulted, he transitioned to comfort focused care, and died. Post-mortem examination revealed progression to diffuse alveolar damage with hyaline membrane formation, foci of early fibroplasia and squamous metaplasia and organizing parenchymal scars. Discussion: Anti-MDA5 antibody positivity has been implicated in rapidly progressive ILD often refractory to conventional treatments like steroids. While this patient's pathology showed organizing pneumonia, there was unfortunately no improvement with steroids. This case, of a patient with prior COVID-19 infection, who subsequently presented with rapidly progressive ILD in the setting of anti-MDA5 an
{"title":"Is COVID-19 the Culprit? A Case of Anti-MDA5 Antibody Positivity in a Rapidly Progressive Organizing Pneumonia","authors":"L. Mcnamara, V. A. Brady","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2002","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2002","url":null,"abstract":"Introduction: Organizing pneumonia is a histologic subsect of interstitial lung disease (ILD). While a non-specific reaction to lung injury, it can be associated with infection, autoimmunity, or medication toxicity, or be characterized as idiopathic. Association with COVID-19 infection remains under active investigation. Beyond the initial viremia seen in COVID-19, the subsequent phase, characterized by an over-active host immune response, is less well understood. Anti-melanoma differentiation-associated gene 5 (MDA5) antibodies have been implicated in autoimmune pathology, including dermatomyositis and rapidly progressive ILD, and found to be positive in some patients with COVID-19. We describe a case of rapidly progressive organizing pneumonia with anti-MDA5 positivity, perhaps precipitated by earlier COVID-19 infection. Case: A 70-year-old gentleman with history of COVID-19 infection several months earlier presented with subacute dyspnea. He had not required hospitalization for COVID-19 infection, but subsequently developed slowly progressive dyspnea, wheezing, and inflammatory, migratory polyarthritis. Outpatient management with oral methylprednisolone 32mg daily, improved his arthritis, however, his respiratory symptoms did not improve despite additional inhaled corticosteroids and beta agonists. Admission imaging showed new bilateral upper lobe predominant ground glass opacities, reticulation of peripheral interstitium and bronchiectasis (Figure 1). Infectious workup, including SARS-CoV-2 testing, was negative. Rheumatologic workup revealed positive rheumatoid factor, anti-nuclear antibody (1:160, diffuse pattern) and anti-MDA5 antibody. The patient received broad spectrum antimicrobials and diuresis, but developed worsening acute hypoxemic/hypercarbic respiratory failure, requiring intubation and mechanical ventilation, proning, and neuromuscular blockade. Pulse dose steroids with intravenous methylprednisolone 250mg every six hours, were trialed for several days without improvements. Video assisted thorascopic surgery was performed and biopsy revealed bronchiolitis obliterans and organizing pneumonia with areas of fibrosis, without hyaline membrane formation or visible micro-organisms. The patient was not a candidate for extracorporeal membrane oxygenation and by the time the aforementioned biopsy resulted, he transitioned to comfort focused care, and died. Post-mortem examination revealed progression to diffuse alveolar damage with hyaline membrane formation, foci of early fibroplasia and squamous metaplasia and organizing parenchymal scars. Discussion: Anti-MDA5 antibody positivity has been implicated in rapidly progressive ILD often refractory to conventional treatments like steroids. While this patient's pathology showed organizing pneumonia, there was unfortunately no improvement with steroids. This case, of a patient with prior COVID-19 infection, who subsequently presented with rapidly progressive ILD in the setting of anti-MDA5 an","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"98 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74498420","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 : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2006
S. Narvaneni, A. Samuel, S. Nanavati, R. Manickam, M. Azzam
Introduction: As the pandemic sweeps on, it is important to recognize some of the unique outcomes of the still very abstract SARS-COV2 viral pneumonia. In this case, we describe a patient that developed acute eosinophilic pneumonia secondary to COVID19 infection. Case Presentation: A 65-year-old Hispanic female with history of osteoporosis, fibromyalgia and depression presented to the ER with dyspnea and non-productive cough for two days. She was hypoxic at 91% on room air. Chest X-ray showed bilateral reticular infiltrates. COVID 19 PCR was positive. Lactate dehydrogenase, Ferritin, C-reactive protein were elevated. Initial treatment consisted of supplemental oxygen, ceftriaxone, azithromycin, hydroxychloroquine, therapeutic anticoagulation, tocilizumab and methylprednisolone, and convalescent plasma. However, she had worsening hypoxia despite maximizing noninvasive ventilation leading to Endo-Tracheal Intubation. She also developed septic shock requiring empiric coverage with meropenem, vancomycin and micafungin. Blood cultures grew MRSA. Urine culture grew E. coli. 2D Echo and Transesophageal Echo were negative for endocarditis. Gallium scan, and CT abdomen and pelvis were negative for other sources of infection. As her hypoxia worsened, CT thorax was done which revealed diffuse ground glass appearance, interstitial lung disease, fibrosis and bronchiectasis. Complete blood count with differential demonstrated new peripheral eosinophilia (2630/mm3). Serum antigens, sputum, and stool cultures for fungal agents, parasites, and Giemsa staining returned negative. Other triggers of peripheral eosinophilia such as smoking, parasitic infections, allergies, allergic interstitial nephritis, medications were ruled out. Broncho alveolar lavage, although planned, was not performed due to hemodynamic instability and severe hypoxemia. Based on acutely worsening respiratory status and significant peripheral eosinophilia, we considered the diagnosis of acute eosinophilic pneumonia and started her on high dose methylprednisolone. She had significant improvement in oxygen requirement, chest X-ray and subsequent thoracic CT scans. She then had a tracheostomy and was discharged to acute care facility. Discussion: The SARS-COV2 infection is thought to be a TH1 type response with IL-2 activation. However, in this case, TH2 mediated responses with IL-13/IL-5 activation and eosinophil release, which are the predominant mechanisms behind acute eosinophilic pneumonia, must be explored. There have been at least 2 reported cases of eosinophilic pneumonia in COVID19 infected patients. It is important to further our understanding of the pathophysiology behind SARS-COV2 related eosinophilic pneumonia to plan for efficacious treatment, and reduce excessive work up in search for other causes. It is also relevant to understand the role of high dose steroids in its treatment.
{"title":"Increasing Prevalence of Sars-cov2 Related Eosinophilic Pneumonia","authors":"S. Narvaneni, A. Samuel, S. Nanavati, R. Manickam, M. Azzam","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2006","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2006","url":null,"abstract":"Introduction: As the pandemic sweeps on, it is important to recognize some of the unique outcomes of the still very abstract SARS-COV2 viral pneumonia. In this case, we describe a patient that developed acute eosinophilic pneumonia secondary to COVID19 infection. Case Presentation: A 65-year-old Hispanic female with history of osteoporosis, fibromyalgia and depression presented to the ER with dyspnea and non-productive cough for two days. She was hypoxic at 91% on room air. Chest X-ray showed bilateral reticular infiltrates. COVID 19 PCR was positive. Lactate dehydrogenase, Ferritin, C-reactive protein were elevated. Initial treatment consisted of supplemental oxygen, ceftriaxone, azithromycin, hydroxychloroquine, therapeutic anticoagulation, tocilizumab and methylprednisolone, and convalescent plasma. However, she had worsening hypoxia despite maximizing noninvasive ventilation leading to Endo-Tracheal Intubation. She also developed septic shock requiring empiric coverage with meropenem, vancomycin and micafungin. Blood cultures grew MRSA. Urine culture grew E. coli. 2D Echo and Transesophageal Echo were negative for endocarditis. Gallium scan, and CT abdomen and pelvis were negative for other sources of infection. As her hypoxia worsened, CT thorax was done which revealed diffuse ground glass appearance, interstitial lung disease, fibrosis and bronchiectasis. Complete blood count with differential demonstrated new peripheral eosinophilia (2630/mm3). Serum antigens, sputum, and stool cultures for fungal agents, parasites, and Giemsa staining returned negative. Other triggers of peripheral eosinophilia such as smoking, parasitic infections, allergies, allergic interstitial nephritis, medications were ruled out. Broncho alveolar lavage, although planned, was not performed due to hemodynamic instability and severe hypoxemia. Based on acutely worsening respiratory status and significant peripheral eosinophilia, we considered the diagnosis of acute eosinophilic pneumonia and started her on high dose methylprednisolone. She had significant improvement in oxygen requirement, chest X-ray and subsequent thoracic CT scans. She then had a tracheostomy and was discharged to acute care facility. Discussion: The SARS-COV2 infection is thought to be a TH1 type response with IL-2 activation. However, in this case, TH2 mediated responses with IL-13/IL-5 activation and eosinophil release, which are the predominant mechanisms behind acute eosinophilic pneumonia, must be explored. There have been at least 2 reported cases of eosinophilic pneumonia in COVID19 infected patients. It is important to further our understanding of the pathophysiology behind SARS-COV2 related eosinophilic pneumonia to plan for efficacious treatment, and reduce excessive work up in search for other causes. It is also relevant to understand the role of high dose steroids in its treatment.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"123 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83517662","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 : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1996
J. Wieckowska, K. E. Fitton, O. Khorfan
Observational studies have suggested that respiratory failure in COVID-19 is not solely driven by the development of ARDS but also concomitant micro-and macrovascular thrombosis. Many patients with COVID-19 develop a hypercoagulable state that has been associated with an increased risk of death. Current treatment guidelines do not support the use for or against empiric anticoagulation. We present a case of a 57-year-old Caucasian male with COVID-19 who was started on full-dose anticoagulation empirically based on an elevated D-Dimer level and was later found to have bilateral pulmonary emboli with right heart strain and pulmonary infarction. Patient had a medical history significant for diabetes mellitus type II, hypertension, hyperlipidemia, and presented to the hospital on 4/18/20 with fever, fatigue, myalgias, weakness, productive cough, shortness of breath, non-bloody diarrhea, abdominal pain, after testing positive for COVID-19 outpatient on 4/1/20. His O2 saturation was 72% on pulse oximetry. He had no prior pulmonary history. In the ED, chest x-ray demonstrated no abnormality (image 1) and D-dimer was 5325 ng/mL. In light of significantly elevated D-dimer, the patient was started empirically on systemic anticoagulation with unfractionated heparin drip. Due to low pre-test probability and trying to limit further exposure to COVID-19, doppler ultrasound of bilateral lower extremities was chosen to rule out VTE. It was negative. Patient clinically improved over the next day and was subsequently transferred out of the ICU. Prior to discharge the patient underwent CTA to rule out PE on 4/21/20. Results demonstrated acute bilateral pulmonary emboli, including large saddle embolism left main pulmonary artery distally, with right heart strain and pulmonary infarction. Since the patient was hemodynamically stable, no systemic or catheter-based thrombolysis was indicated. Patient was started on a DOAC and discharged on 4/23/20 with oxygen only at night. Although the exact etiology of VTE associated with COVID-19 remains unclear, the available data has shown it to cause a prothrombotic state. Studies have shown the risk of VTE in COVID-19 patients admitted to the ICU to be around 2.5-5 times higher than the general ICU population. Our case serves to highlight the need for heightened vigilance for VTE as well as question the utility of common risk stratification tools such as the Well's score in COVID-19. Further studies are needed to identify when and how to anticoagulate patients with COVID-19 in addition to validating risk stratification tools that may aid clinicians in these situations.
{"title":"A Case of Submassive Pulmonary Embolism in COVID-19 Patient","authors":"J. Wieckowska, K. E. Fitton, O. Khorfan","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1996","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1996","url":null,"abstract":"Observational studies have suggested that respiratory failure in COVID-19 is not solely driven by the development of ARDS but also concomitant micro-and macrovascular thrombosis. Many patients with COVID-19 develop a hypercoagulable state that has been associated with an increased risk of death. Current treatment guidelines do not support the use for or against empiric anticoagulation. We present a case of a 57-year-old Caucasian male with COVID-19 who was started on full-dose anticoagulation empirically based on an elevated D-Dimer level and was later found to have bilateral pulmonary emboli with right heart strain and pulmonary infarction. Patient had a medical history significant for diabetes mellitus type II, hypertension, hyperlipidemia, and presented to the hospital on 4/18/20 with fever, fatigue, myalgias, weakness, productive cough, shortness of breath, non-bloody diarrhea, abdominal pain, after testing positive for COVID-19 outpatient on 4/1/20. His O2 saturation was 72% on pulse oximetry. He had no prior pulmonary history. In the ED, chest x-ray demonstrated no abnormality (image 1) and D-dimer was 5325 ng/mL. In light of significantly elevated D-dimer, the patient was started empirically on systemic anticoagulation with unfractionated heparin drip. Due to low pre-test probability and trying to limit further exposure to COVID-19, doppler ultrasound of bilateral lower extremities was chosen to rule out VTE. It was negative. Patient clinically improved over the next day and was subsequently transferred out of the ICU. Prior to discharge the patient underwent CTA to rule out PE on 4/21/20. Results demonstrated acute bilateral pulmonary emboli, including large saddle embolism left main pulmonary artery distally, with right heart strain and pulmonary infarction. Since the patient was hemodynamically stable, no systemic or catheter-based thrombolysis was indicated. Patient was started on a DOAC and discharged on 4/23/20 with oxygen only at night. Although the exact etiology of VTE associated with COVID-19 remains unclear, the available data has shown it to cause a prothrombotic state. Studies have shown the risk of VTE in COVID-19 patients admitted to the ICU to be around 2.5-5 times higher than the general ICU population. Our case serves to highlight the need for heightened vigilance for VTE as well as question the utility of common risk stratification tools such as the Well's score in COVID-19. Further studies are needed to identify when and how to anticoagulate patients with COVID-19 in addition to validating risk stratification tools that may aid clinicians in these situations.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"59 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75155662","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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