Pub Date : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4071
D. Chaudhary, D. Norton
Guillain-Barre Syndrome (GBS) is an acute autoimmune disorder that is provoked by a preceding infection. It is characterized by progressive, ascending, symmetrical muscle weakness accompanied by hyporeflexia or areflexia. We describe two cases of GBS associated with COVID-19. 36-year-old Hispanic female presented ten days after diagnosis of COVID-19 with symptoms of headache, bilateral leg and facial weakness, and facial paresthesias for five days. Within 24 hours of admission, she developed areflexia and progressive bulbar and appendicular weakness. Nerve conduction study and electromyography were consistent with demyelinating form of GBS. Due to difficulty with clearing oral secretions, patient was intubated two times during the hospitalization. 79-year-old Caucasian female presented with progressive weakness, weight loss and fevers. She was diagnosed with COVID-19 on the day of admission. She had paralysis of all four extremities with dysphagia and required intubation. She was extubated and re-intubated two more times due to worsening hypoxia and stridor which led to placement of a tracheostomy tube. Both our patients developed features of dysautonomia, including hypotension and tachycardia. Severe respiratory muscle weakness and dysphagia led to recurrent intubations. Their CT head and MRI brains were negative for facial nerve enhancement. Lumbar punctures in both revealed albuminocytologic dissociation. Plasma exchange was initiated in both females immediately after first intubation for total duration of five days. Upon outpatient follow up, they had significant improvement in motor function. Common precipitants of GBS are Campylobacter jejuni, EBV, CMV, HIV and Zika virus. Clearly, GBS is an infrequent complication of COVID-19. It is possible that SARS-CoV-2 evokes an immune response against peripheral nerve components leading to acute polyneuropathy of heterogenous presentation. Typically, demyelinating and axonal forms of GBS have been described. However, in our cases, both had demyelinating features including symmetric weakness with predominant bulbar symptoms of dysphagia and dysphonia. These cases highlight that GBS is a potential neurological complication of COVID-19 that physicians must be aware of. Thorough daily neurological exam is critical, and early recognition of GBS symptoms may prompt regular evaluation of negative inspiratory force and vital capacity. This may lead to early initiation of intravenous immunoglobulin (IVIG) or plasma exchange leading to improvement in motor symptoms thus avoiding ventilatory support. Plasma exchange should be considered as a first line treatment in COVID-19 patients since high concentrations of IVIG can lead to increased blood viscosity in these patients who are already at increased risk for thrombotic complications.
{"title":"Guillain-Barre Syndrome Secondary to SARS-CoV-2","authors":"D. Chaudhary, D. Norton","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4071","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4071","url":null,"abstract":"Guillain-Barre Syndrome (GBS) is an acute autoimmune disorder that is provoked by a preceding infection. It is characterized by progressive, ascending, symmetrical muscle weakness accompanied by hyporeflexia or areflexia. We describe two cases of GBS associated with COVID-19. 36-year-old Hispanic female presented ten days after diagnosis of COVID-19 with symptoms of headache, bilateral leg and facial weakness, and facial paresthesias for five days. Within 24 hours of admission, she developed areflexia and progressive bulbar and appendicular weakness. Nerve conduction study and electromyography were consistent with demyelinating form of GBS. Due to difficulty with clearing oral secretions, patient was intubated two times during the hospitalization. 79-year-old Caucasian female presented with progressive weakness, weight loss and fevers. She was diagnosed with COVID-19 on the day of admission. She had paralysis of all four extremities with dysphagia and required intubation. She was extubated and re-intubated two more times due to worsening hypoxia and stridor which led to placement of a tracheostomy tube. Both our patients developed features of dysautonomia, including hypotension and tachycardia. Severe respiratory muscle weakness and dysphagia led to recurrent intubations. Their CT head and MRI brains were negative for facial nerve enhancement. Lumbar punctures in both revealed albuminocytologic dissociation. Plasma exchange was initiated in both females immediately after first intubation for total duration of five days. Upon outpatient follow up, they had significant improvement in motor function. Common precipitants of GBS are Campylobacter jejuni, EBV, CMV, HIV and Zika virus. Clearly, GBS is an infrequent complication of COVID-19. It is possible that SARS-CoV-2 evokes an immune response against peripheral nerve components leading to acute polyneuropathy of heterogenous presentation. Typically, demyelinating and axonal forms of GBS have been described. However, in our cases, both had demyelinating features including symmetric weakness with predominant bulbar symptoms of dysphagia and dysphonia. These cases highlight that GBS is a potential neurological complication of COVID-19 that physicians must be aware of. Thorough daily neurological exam is critical, and early recognition of GBS symptoms may prompt regular evaluation of negative inspiratory force and vital capacity. This may lead to early initiation of intravenous immunoglobulin (IVIG) or plasma exchange leading to improvement in motor symptoms thus avoiding ventilatory support. Plasma exchange should be considered as a first line treatment in COVID-19 patients since high concentrations of IVIG can lead to increased blood viscosity in these patients who are already at increased risk for thrombotic complications.","PeriodicalId":23169,"journal":{"name":"TP100. TP100 UNEXPECTED COVID-19 CASE REPORTS","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81593457","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.A4072
L. F. Jiménez, J. Pedraza, J. R. L. Peña, M. A. Izquierdo, J. Carrillo, V. Rivillas
Introduction Covid-19 is a recent outbreak of pneumonia caused by severe respiratory syndrome coronavirus (SARS-CoV2). It affects mainly the lungs causing pneumonia and complications like acute respiratory distress syndrome. Computed tomography (CT) plays a key role in diagnosis, the most common findings are bilateral, peripheral and basal ground-glass opacities. Pneumothorax secondary to SARS-CoV2 infection is rare and seems to develop later in the course of the disease, its mechanism is not completely understood. There are several reports about Covid-19 and pneumothorax, but few descriptions associated with pulmonary cysts. We describe seven cases of pneumothorax in patients with Covid-19, some of them with pulmonary cysts. Case descriptions We found a series of seven patients with Covid-19 pneumonia with pneumothorax, some as the initial presentation and some developing after the course of the disease, two to three weeks after initial symptoms. Patients were male, most of them in their fifties, two were former smokers and two had COPD. Only one patient had mechanical ventilation, two of them had pulmonary cysts in the CT scan which were not documented before. A Multifocal upper lobe consolidations. B. 29 days later. Left upper-lobe subpleural cystic lesions, ground-glass opacities, right pneumothorax. Discussion The course of Covid-19 depends on the damage caused by the virus and the host's immune response. CT scan is of great value in diagnosis and monitoring of progression and complications. The most common patterns are ground-glass opacification (88%), peripheral distribution (76%), bilateral (87.5%) and multilobe involvement (78.8%). Pneumothorax or cysts in Covid-19 have been described in few case reports. Pneumothorax seems to occur after two weeks of symptom onset, predominantly in male patients. Liu et al. described a series of two men with pneumothorax and peripheral pulmonary cysts after 26 and 40 days of symptom onset;cysts decreased in number and size in subsequent images. Other reports have described cysts or bullae. Pneumothorax seems to develop later in the course of the disease and they are most likely related to the reparation process. Mechanical ventilation with positive pressure is not associated with all cases. The pathogenesis of pulmonary cysts formation in Covid-19 is not well understood. Proposed mechanisms of cystic lung disease include necrosis due to ischemia, remodeling of interstitial matrix, and bronchial obstruction with distal overinflation phenomenon. Information regarding mechanism of pneumothorax in patients with lung infection secondary to Covid-19 is not yet completely understood, but cysts formation may play a role.
{"title":"Spontaneous Pneumothorax with or Without Pulmonary Cysts in Patients Diagnosed with Covid-19 Pneumonia","authors":"L. F. Jiménez, J. Pedraza, J. R. L. Peña, M. A. Izquierdo, J. Carrillo, V. Rivillas","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4072","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4072","url":null,"abstract":"Introduction Covid-19 is a recent outbreak of pneumonia caused by severe respiratory syndrome coronavirus (SARS-CoV2). It affects mainly the lungs causing pneumonia and complications like acute respiratory distress syndrome. Computed tomography (CT) plays a key role in diagnosis, the most common findings are bilateral, peripheral and basal ground-glass opacities. Pneumothorax secondary to SARS-CoV2 infection is rare and seems to develop later in the course of the disease, its mechanism is not completely understood. There are several reports about Covid-19 and pneumothorax, but few descriptions associated with pulmonary cysts. We describe seven cases of pneumothorax in patients with Covid-19, some of them with pulmonary cysts. Case descriptions We found a series of seven patients with Covid-19 pneumonia with pneumothorax, some as the initial presentation and some developing after the course of the disease, two to three weeks after initial symptoms. Patients were male, most of them in their fifties, two were former smokers and two had COPD. Only one patient had mechanical ventilation, two of them had pulmonary cysts in the CT scan which were not documented before. A Multifocal upper lobe consolidations. B. 29 days later. Left upper-lobe subpleural cystic lesions, ground-glass opacities, right pneumothorax. Discussion The course of Covid-19 depends on the damage caused by the virus and the host's immune response. CT scan is of great value in diagnosis and monitoring of progression and complications. The most common patterns are ground-glass opacification (88%), peripheral distribution (76%), bilateral (87.5%) and multilobe involvement (78.8%). Pneumothorax or cysts in Covid-19 have been described in few case reports. Pneumothorax seems to occur after two weeks of symptom onset, predominantly in male patients. Liu et al. described a series of two men with pneumothorax and peripheral pulmonary cysts after 26 and 40 days of symptom onset;cysts decreased in number and size in subsequent images. Other reports have described cysts or bullae. Pneumothorax seems to develop later in the course of the disease and they are most likely related to the reparation process. Mechanical ventilation with positive pressure is not associated with all cases. The pathogenesis of pulmonary cysts formation in Covid-19 is not well understood. Proposed mechanisms of cystic lung disease include necrosis due to ischemia, remodeling of interstitial matrix, and bronchial obstruction with distal overinflation phenomenon. Information regarding mechanism of pneumothorax in patients with lung infection secondary to Covid-19 is not yet completely understood, but cysts formation may play a role.","PeriodicalId":23169,"journal":{"name":"TP100. TP100 UNEXPECTED COVID-19 CASE REPORTS","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76124195","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.A4109
B. Gillespie, E. Solomon, A. Carpio
Clot in Transit in COVID-19 Introduction: Thromboembolism is a known complication of COVID-19, frequently occurring in patients receiving deep venous thrombosis (DVT) prophylaxis. This case report describes a patient with COVID-19 on DVT prophylaxis who had no other risk factors and developed a pulmonary embolism (PE) and subsequently was found to have a clot in transit in the right ventricular outflow tract on echocardiography. Case Report: 53-year-old male with no previous history of tobacco use, venous thromboembolism, malignancy, or clotting disorder was admitted with acute hypoxemic respiratory failure due to COVID-19. On initial examination, the patient was found to be hypoxic and tachycardic, requiring high flow nasal cannula. Chest x-ray showed multifocal airspace opacities consistent with COVID-19 pneumonia. CT pulmonary angiography was performed due to hypoxia and tachycardia, which revealed no evidence of PE. Laboratory results showed elevated inflammatory markers and a D-dimer of 1,700. The patient was admitted and started on dexamethasone, remdesivir, and subcutaneous heparin for DVT prophylaxis. The patient improved and oxygen was weaned down. On day 6 of hospitalization the patient developed acute dyspnea, worsening hypoxia, and tachycardia. Repeat CT pulmonary angiogram revealed multiple PE and therapeutic enoxaparin was started. An echocardiogram was performed and revealed an enlarged right ventricle and a large multi-lobulated hyperechoic mass in the right ventricular outflow tract, consist with a clot in transit. Interventional Radiology successfully performed aspiration thrombectomy, and the patient quickly improved and was discharged home on Apixaban. Discussion: As COVID-19 patients often present with hypoxemic respiratory failure and elevated D-dimer, it can be challenging for physicians to determine who should be screened for the presence of PE. Our case demonstrates the severity of hypercoagulability in COVID-19 and the importance of maintaining high suspicion for thromboembolism in COVID-19, even in patients receiving appropriate DVT prophylaxis and without risk factors. SARS-CoV-2 has been shown to bind to ACE2 on platelets and enhance thrombosis, indicating that infection itself can lead to DVT or PE. Even patient under guideline directed DVT prophylaxis frequently develop venous thromboembolism. Further investigation into how to prevent and catch pulmonary embolism in COVID-19 patients is needed. Methods such as daily D-dimer level trending, may be helpful in identifying patients at higher risk of developing PE or DVT but more research is needed to identify ideal cutoffs and DVT prophylaxis in these patients.
{"title":"Clot in Transit and Pulmonary Embolism in COVID-19","authors":"B. Gillespie, E. Solomon, A. Carpio","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4109","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4109","url":null,"abstract":"Clot in Transit in COVID-19 Introduction: Thromboembolism is a known complication of COVID-19, frequently occurring in patients receiving deep venous thrombosis (DVT) prophylaxis. This case report describes a patient with COVID-19 on DVT prophylaxis who had no other risk factors and developed a pulmonary embolism (PE) and subsequently was found to have a clot in transit in the right ventricular outflow tract on echocardiography. Case Report: 53-year-old male with no previous history of tobacco use, venous thromboembolism, malignancy, or clotting disorder was admitted with acute hypoxemic respiratory failure due to COVID-19. On initial examination, the patient was found to be hypoxic and tachycardic, requiring high flow nasal cannula. Chest x-ray showed multifocal airspace opacities consistent with COVID-19 pneumonia. CT pulmonary angiography was performed due to hypoxia and tachycardia, which revealed no evidence of PE. Laboratory results showed elevated inflammatory markers and a D-dimer of 1,700. The patient was admitted and started on dexamethasone, remdesivir, and subcutaneous heparin for DVT prophylaxis. The patient improved and oxygen was weaned down. On day 6 of hospitalization the patient developed acute dyspnea, worsening hypoxia, and tachycardia. Repeat CT pulmonary angiogram revealed multiple PE and therapeutic enoxaparin was started. An echocardiogram was performed and revealed an enlarged right ventricle and a large multi-lobulated hyperechoic mass in the right ventricular outflow tract, consist with a clot in transit. Interventional Radiology successfully performed aspiration thrombectomy, and the patient quickly improved and was discharged home on Apixaban. Discussion: As COVID-19 patients often present with hypoxemic respiratory failure and elevated D-dimer, it can be challenging for physicians to determine who should be screened for the presence of PE. Our case demonstrates the severity of hypercoagulability in COVID-19 and the importance of maintaining high suspicion for thromboembolism in COVID-19, even in patients receiving appropriate DVT prophylaxis and without risk factors. SARS-CoV-2 has been shown to bind to ACE2 on platelets and enhance thrombosis, indicating that infection itself can lead to DVT or PE. Even patient under guideline directed DVT prophylaxis frequently develop venous thromboembolism. Further investigation into how to prevent and catch pulmonary embolism in COVID-19 patients is needed. Methods such as daily D-dimer level trending, may be helpful in identifying patients at higher risk of developing PE or DVT but more research is needed to identify ideal cutoffs and DVT prophylaxis in these patients.","PeriodicalId":23169,"journal":{"name":"TP100. TP100 UNEXPECTED COVID-19 CASE REPORTS","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76460381","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.A4079
G. Lee, J. Stoll, I. El Husseini
Introduction For decades, tuberculosis (TB) remained the leading cause of mortality due to a single infectious agent globally. In 2020, mortality due to the coronavirus disease 2019 (COVID-19) pandemic exceeded annual rates of death from TB. The impact of active COVID-19 and TB co-infection remain unclear. We present one of the first documented cases of active TB in the setting of COVID-19 infection in the United States. Case Report A 49-year-old man with a past medical history of mediastinal gray zone lymphoma and hypertension presented to the emergency room with a four-day history of diarrhea and hematochezia. The patient immigrated from Vietnam in 1995. Computed tomography imaging revealed thickening of the sigmoid wall, and bilateral pulmonary ground glass opacities consistent with COVID-19 pneumonia, which was confirmed by polymerase chain reaction (PCR). He was also neutropenic from recent chemotherapy. On admission, he began experiencing worsening hypoxia with exertion, and was started on remdesivir and dexamethasone for COVID-19 infection. Serial chest radiographs revealed worsening bibasilar opacities. He continued to have higher oxygen requirements and maxed out on high-flow nasal cannula and non-rebreather with 88-90% oxygen saturation, requiring transfer to the intensive care unit. A complete infectious workup was performed at this point. Cytomegalovirus PCR was positive at 1486IU and was started on ganciclovir. A bronchoscopy was performed but all testing was negative, including that for acid-fast bacilli (AFB) smear. The patient continued to become increasingly hypoxic, acidotic, and septic, and eventually underwent tracheostomy. Twenty days post-bronchoscopy, cultures from the bronchoalveolar fluid came back positive for Mycobacterium tuberculosis (MTB). A new sputum sample was sent and was found to be smear positive (2+ AFB) and MTB PCR positive. The patient was initiated on rifampin, isoniazid, pyrazinamide, and ethambutol therapy. Unfortunately, the patient continued to decompensate and was unable to be weaned off the ventilator. Comfort care was initiated by the family and the patient passed away on hospital day 68. Discussion The patient had several risk factors for latent TB reactivation, including malignancy, long-term corticosteroid use, and COVID-19 infection. Early research has shown that risk of death and recovery time with COVID-19 may be higher in patients with previous or active TB compared to those without. In patients with severe COVID-19 pneumonia and multiple risk factors for immunosuppression, latent TB reactivation should be considered in addition to secondary superinfection.
{"title":"A Rare Case of Latent Tuberculosis Reactivation in the Setting of COVID-19 Infection","authors":"G. Lee, J. Stoll, I. El Husseini","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4079","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4079","url":null,"abstract":"Introduction For decades, tuberculosis (TB) remained the leading cause of mortality due to a single infectious agent globally. In 2020, mortality due to the coronavirus disease 2019 (COVID-19) pandemic exceeded annual rates of death from TB. The impact of active COVID-19 and TB co-infection remain unclear. We present one of the first documented cases of active TB in the setting of COVID-19 infection in the United States. Case Report A 49-year-old man with a past medical history of mediastinal gray zone lymphoma and hypertension presented to the emergency room with a four-day history of diarrhea and hematochezia. The patient immigrated from Vietnam in 1995. Computed tomography imaging revealed thickening of the sigmoid wall, and bilateral pulmonary ground glass opacities consistent with COVID-19 pneumonia, which was confirmed by polymerase chain reaction (PCR). He was also neutropenic from recent chemotherapy. On admission, he began experiencing worsening hypoxia with exertion, and was started on remdesivir and dexamethasone for COVID-19 infection. Serial chest radiographs revealed worsening bibasilar opacities. He continued to have higher oxygen requirements and maxed out on high-flow nasal cannula and non-rebreather with 88-90% oxygen saturation, requiring transfer to the intensive care unit. A complete infectious workup was performed at this point. Cytomegalovirus PCR was positive at 1486IU and was started on ganciclovir. A bronchoscopy was performed but all testing was negative, including that for acid-fast bacilli (AFB) smear. The patient continued to become increasingly hypoxic, acidotic, and septic, and eventually underwent tracheostomy. Twenty days post-bronchoscopy, cultures from the bronchoalveolar fluid came back positive for Mycobacterium tuberculosis (MTB). A new sputum sample was sent and was found to be smear positive (2+ AFB) and MTB PCR positive. The patient was initiated on rifampin, isoniazid, pyrazinamide, and ethambutol therapy. Unfortunately, the patient continued to decompensate and was unable to be weaned off the ventilator. Comfort care was initiated by the family and the patient passed away on hospital day 68. Discussion The patient had several risk factors for latent TB reactivation, including malignancy, long-term corticosteroid use, and COVID-19 infection. Early research has shown that risk of death and recovery time with COVID-19 may be higher in patients with previous or active TB compared to those without. In patients with severe COVID-19 pneumonia and multiple risk factors for immunosuppression, latent TB reactivation should be considered in addition to secondary superinfection.","PeriodicalId":23169,"journal":{"name":"TP100. TP100 UNEXPECTED COVID-19 CASE REPORTS","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76611319","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.A4089
H. Waseem, F. Zafar, M. Anser, M. Zia
Introduction: Coronavirus disease is a multi-organ disease caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS- CoV-2). Although acute kidney injury, collapsing glomerulopathy and thrombotic micro-angiopathy have been frequently attributed to COVID-19, pauci-immune glomerulonephritis (GN) has rarely been described [1]. Here we report a case of pauci-immune GN associated with SARS-CoV-2. Case Presentation: A 53 years old female with hypertension, diabetes mellitus, hepatitis C (treated 6 years ago), and recent covid-19 pneumonia (3 months ago), presented with dysuria, nausea, and vomiting. She denied fever, flank pain, and hematuria. The laboratory workup showed elevated blood urea nitrogen BUN 82 mg/dl and creatinine Cr 9.8 mg/dl (baseline creatinine was 0.9 mg/dl three months ago). Urinalysis showed proteinuria >1000 mg/dl and urine protein creatinine ratio of 5.3 (normal < 0.1), concerning for glomerulonephritis. Serological evaluation for glomerular disease showed normal complements C3 and C4, normal titers of anti-neutrophil cytoplasmic antibodies including p-ANCA, c-ANCA, atypical ANCA, and cryoglobulins. Screening for Hepatitis B and Hepatitis C was negative. The remainder of the autoimmune workup was unremarkable including Rheumatoid factor, Anti CCP antibodies (Ab), Anti Ribo-nucleoprotein Ab, and Anti Glomerular basement membrane antibodies. Coronavirus PCR was negative and qualitative IgG was reactive. CT chest showed idiopathic pulmonary fibrosis (IPF) and resolving ground glass opacities from prior coronavirus infection. CT abdomen and pelvis was unremarkable for obstructive uropathy. The renal biopsy showed pauci-immune focal sclerosis with 20% fibro-cellular crescents diagnostic for pauci-immune glomerulonephritis. The patient was treated for pauci-immune glomerulonephritis with pulse-dose intravenous steroids (methylprednisolone) followed by oral prednisone and rituximab. The renal functions improved dramatically (on day 15, her creatinine down-trended to 4 mg/dl from 9mg/dl on admission). She did not require intermittent hemodialysis and was discharged on day 15 with outpatient follow up. Discussion: The mechanisms of acute kidney injury in COVID-19 include renal hypoperfusion, endothelial dysfunction, micro-thrombi, and cytopathic effects of SARS-CoV-2 towards renal tubules and glomeruli. Due to a lack of scientific evidence related to coronavirus disease, the management of glomerulopathy is challenging. The existing literature favors the use of anti-viral therapy with immunosuppressive agents without the concern of worsening infection [2].
{"title":"Pauci Immune Glomerulonephritis; A Late Complication of COVID-19 Infection","authors":"H. Waseem, F. Zafar, M. Anser, M. Zia","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4089","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4089","url":null,"abstract":"Introduction: Coronavirus disease is a multi-organ disease caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS- CoV-2). Although acute kidney injury, collapsing glomerulopathy and thrombotic micro-angiopathy have been frequently attributed to COVID-19, pauci-immune glomerulonephritis (GN) has rarely been described [1]. Here we report a case of pauci-immune GN associated with SARS-CoV-2. Case Presentation: A 53 years old female with hypertension, diabetes mellitus, hepatitis C (treated 6 years ago), and recent covid-19 pneumonia (3 months ago), presented with dysuria, nausea, and vomiting. She denied fever, flank pain, and hematuria. The laboratory workup showed elevated blood urea nitrogen BUN 82 mg/dl and creatinine Cr 9.8 mg/dl (baseline creatinine was 0.9 mg/dl three months ago). Urinalysis showed proteinuria >1000 mg/dl and urine protein creatinine ratio of 5.3 (normal < 0.1), concerning for glomerulonephritis. Serological evaluation for glomerular disease showed normal complements C3 and C4, normal titers of anti-neutrophil cytoplasmic antibodies including p-ANCA, c-ANCA, atypical ANCA, and cryoglobulins. Screening for Hepatitis B and Hepatitis C was negative. The remainder of the autoimmune workup was unremarkable including Rheumatoid factor, Anti CCP antibodies (Ab), Anti Ribo-nucleoprotein Ab, and Anti Glomerular basement membrane antibodies. Coronavirus PCR was negative and qualitative IgG was reactive. CT chest showed idiopathic pulmonary fibrosis (IPF) and resolving ground glass opacities from prior coronavirus infection. CT abdomen and pelvis was unremarkable for obstructive uropathy. The renal biopsy showed pauci-immune focal sclerosis with 20% fibro-cellular crescents diagnostic for pauci-immune glomerulonephritis. The patient was treated for pauci-immune glomerulonephritis with pulse-dose intravenous steroids (methylprednisolone) followed by oral prednisone and rituximab. The renal functions improved dramatically (on day 15, her creatinine down-trended to 4 mg/dl from 9mg/dl on admission). She did not require intermittent hemodialysis and was discharged on day 15 with outpatient follow up. Discussion: The mechanisms of acute kidney injury in COVID-19 include renal hypoperfusion, endothelial dysfunction, micro-thrombi, and cytopathic effects of SARS-CoV-2 towards renal tubules and glomeruli. Due to a lack of scientific evidence related to coronavirus disease, the management of glomerulopathy is challenging. The existing literature favors the use of anti-viral therapy with immunosuppressive agents without the concern of worsening infection [2].","PeriodicalId":23169,"journal":{"name":"TP100. TP100 UNEXPECTED COVID-19 CASE REPORTS","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82917366","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.A4102
A. Menon, M. Bachan, Z. Khan
Introduction: COVID-19 was declared a global pandemic by the WHO in March 2020. The gold standard for diagnosis relies heavily on clinical suspicion along with PCR based assays of respiratory swabs. This nucleic acid study is highly sensitive and specific, however, there are faults, especially during the incubation period, during which the virus is hard to detect. Here we present a case of a patient, presenting with signs and symptoms of pneumonia, with serial negative viral swabs spaced out over time, who was ultimately diagnosed with COVID-19 infection via more invasive means. Case: A 49-year-old female with no significant past medical history presented to the emergency department with cough and shortness of breath for 2 days which developed when she returned to New York from Florida. Her personal history was significant for her occupation as an ER nurse and a history of vaping for 5-6 years.After arrival to the emergency department, the patient was febrile to 103.3 F, tachycardic, and hypoxic, saturating 89% on room air. Her laboratory work was significant for a mildly elevated D-dimer level, elevated CRP (11.23), normal procalcitonin level, and two negative COVID-19 swabs over 2 days. Her initial chest X ray showed multifocal pneumonia and a CT chest showed ground glass opacities amid dense consolidation. The patient was empirically treated for community-acquired bacterial pneumonia with antibiotics. The patient's respiratory and hemodynamic status started to decline, despite treatment. Ultimately, the patient required further investigation - a bronchoalveolar lavage was ultimately found to be positive for the COVID-19 virus, and the patient was immediately started on Remdesivir. Discussion: In this day and age, countries are increasingly utilizing the COVID-19 reverse-transcriptase PCR and are pushing for widespread testing for case detection, but how sensitive and specific is this test, really? Serial testing with swabs performed at intervals should be the answer as the viral load of the COVID RNA steadily rises and peaks over 0-9 days after onset of symptoms. However, this may not be the case in a majority of patients and more invasive testing using bronchoscopy and bronchoalveolar lavage may be the only way to truly diagnose COVID-19 pneumonia. The delay in confirmation, however, could prove to be truly fatal, subjecting patients to painful measures like intubation. This case brings to light the realization that nasopharyngeal/oropharyngeal swabs may not be sufficient to detect the virus with full certainty.
{"title":"When COVID Goes Undetected","authors":"A. Menon, M. Bachan, Z. Khan","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4102","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4102","url":null,"abstract":"Introduction: COVID-19 was declared a global pandemic by the WHO in March 2020. The gold standard for diagnosis relies heavily on clinical suspicion along with PCR based assays of respiratory swabs. This nucleic acid study is highly sensitive and specific, however, there are faults, especially during the incubation period, during which the virus is hard to detect. Here we present a case of a patient, presenting with signs and symptoms of pneumonia, with serial negative viral swabs spaced out over time, who was ultimately diagnosed with COVID-19 infection via more invasive means. Case: A 49-year-old female with no significant past medical history presented to the emergency department with cough and shortness of breath for 2 days which developed when she returned to New York from Florida. Her personal history was significant for her occupation as an ER nurse and a history of vaping for 5-6 years.After arrival to the emergency department, the patient was febrile to 103.3 F, tachycardic, and hypoxic, saturating 89% on room air. Her laboratory work was significant for a mildly elevated D-dimer level, elevated CRP (11.23), normal procalcitonin level, and two negative COVID-19 swabs over 2 days. Her initial chest X ray showed multifocal pneumonia and a CT chest showed ground glass opacities amid dense consolidation. The patient was empirically treated for community-acquired bacterial pneumonia with antibiotics. The patient's respiratory and hemodynamic status started to decline, despite treatment. Ultimately, the patient required further investigation - a bronchoalveolar lavage was ultimately found to be positive for the COVID-19 virus, and the patient was immediately started on Remdesivir. Discussion: In this day and age, countries are increasingly utilizing the COVID-19 reverse-transcriptase PCR and are pushing for widespread testing for case detection, but how sensitive and specific is this test, really? Serial testing with swabs performed at intervals should be the answer as the viral load of the COVID RNA steadily rises and peaks over 0-9 days after onset of symptoms. However, this may not be the case in a majority of patients and more invasive testing using bronchoscopy and bronchoalveolar lavage may be the only way to truly diagnose COVID-19 pneumonia. The delay in confirmation, however, could prove to be truly fatal, subjecting patients to painful measures like intubation. This case brings to light the realization that nasopharyngeal/oropharyngeal swabs may not be sufficient to detect the virus with full certainty.","PeriodicalId":23169,"journal":{"name":"TP100. TP100 UNEXPECTED COVID-19 CASE REPORTS","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89589334","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.A4091
K. Ahmad, S. Srinivas, R. B. Century, E. Abu-Hamda, E. Libre
Introduction: Pulmonary fibrosis after pneumonia due to SARS-CoV-2 (COVID-19) is poorly understood. In patients who required transplantation, explant gene expression profiles are similar to those in patients with pulmonary fibrosis. Currently, two antifibrotic agents have been shown to reduce the rate of progression in other etiologies of lung fibrosis. Here, we describe our experience with antifibrotic therapy in COVID-19 patients. Case#1 A 45 year old male with metabolic syndrome presented with 4 days of worsening dyspnea. He failed initial therapy with high flow nasal cannula (HFNC) and noninvasive ventilation requiring intubation on hospital day 10. He received treatment with remdesivir, steroids and inhaled nitric oxide (iNO). He remained intubated for 21 days, complicated by pneumomediastinum. Total hospitalization was 75 days. Chest imaging throughout hospitalization had cystic changes and bronchiectasis. Pirfenidone was initiated at the time of discharge. On 6-month clinic follow up, he remained on oxygen. He denied any significant side effects to pirfenidone and had no lab abnormalities. Case#2 A 61 year old male with no past medical history (PMH) presented with week-long constitutional symptoms. HFNC for severe hypoxia was started but ultimately intubation was required. He was treated with remdesivir, steroids, iNO, an interleukin-6 inhibitor and convalescent plasma. Weaning from ventilatory support after tracheostomy tube placement was complicated by pneumomediastinum. He was discharged on nocturnal ventilation to long term acute care. He was started on pirfenidone during hospitalization and continued without incident. On subsequent clinic follow up, tracheostomy was decannulated and he could tolerate low flow nasal cannula. Case#3 A 64 year old male with no PMH was admitted with 10 days of worsening respiratory symptoms. The patient required HFNC. He received remdesivir, steroids, broad spectrum antibiotics and convalescent plasma. He was discharged after 13 days on supplemental oxygen. On one month follow up, chest imaging showed reticular and ground glass opacities and traction bronchiectasis. Nintedanib was initiated. One month later he was off supplemental oxygen. Follow up CT imaging showed resolution of ground glass and reticular opacities after 6 months. The patient denied any medication intolerance but abnormal liver function lead to dose reduction of nintedanib. Conclusion: COVID-19 pneumonia can lead to significant pulmonary fibrosis. Further analysis is needed to determine the long term incidence of persistent fibrosis and any risk factors predicting its development. Additionally, in those patients with established pulmonary fibrosis, the role of antifibrotic therapy should prospectively be investigated.
{"title":"A Potential Role for Antifibrotic Use in Post-COVID-19 Pulmonary Fibrosis","authors":"K. Ahmad, S. Srinivas, R. B. Century, E. Abu-Hamda, E. Libre","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4091","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4091","url":null,"abstract":"Introduction: Pulmonary fibrosis after pneumonia due to SARS-CoV-2 (COVID-19) is poorly understood. In patients who required transplantation, explant gene expression profiles are similar to those in patients with pulmonary fibrosis. Currently, two antifibrotic agents have been shown to reduce the rate of progression in other etiologies of lung fibrosis. Here, we describe our experience with antifibrotic therapy in COVID-19 patients. Case#1 A 45 year old male with metabolic syndrome presented with 4 days of worsening dyspnea. He failed initial therapy with high flow nasal cannula (HFNC) and noninvasive ventilation requiring intubation on hospital day 10. He received treatment with remdesivir, steroids and inhaled nitric oxide (iNO). He remained intubated for 21 days, complicated by pneumomediastinum. Total hospitalization was 75 days. Chest imaging throughout hospitalization had cystic changes and bronchiectasis. Pirfenidone was initiated at the time of discharge. On 6-month clinic follow up, he remained on oxygen. He denied any significant side effects to pirfenidone and had no lab abnormalities. Case#2 A 61 year old male with no past medical history (PMH) presented with week-long constitutional symptoms. HFNC for severe hypoxia was started but ultimately intubation was required. He was treated with remdesivir, steroids, iNO, an interleukin-6 inhibitor and convalescent plasma. Weaning from ventilatory support after tracheostomy tube placement was complicated by pneumomediastinum. He was discharged on nocturnal ventilation to long term acute care. He was started on pirfenidone during hospitalization and continued without incident. On subsequent clinic follow up, tracheostomy was decannulated and he could tolerate low flow nasal cannula. Case#3 A 64 year old male with no PMH was admitted with 10 days of worsening respiratory symptoms. The patient required HFNC. He received remdesivir, steroids, broad spectrum antibiotics and convalescent plasma. He was discharged after 13 days on supplemental oxygen. On one month follow up, chest imaging showed reticular and ground glass opacities and traction bronchiectasis. Nintedanib was initiated. One month later he was off supplemental oxygen. Follow up CT imaging showed resolution of ground glass and reticular opacities after 6 months. The patient denied any medication intolerance but abnormal liver function lead to dose reduction of nintedanib. Conclusion: COVID-19 pneumonia can lead to significant pulmonary fibrosis. Further analysis is needed to determine the long term incidence of persistent fibrosis and any risk factors predicting its development. Additionally, in those patients with established pulmonary fibrosis, the role of antifibrotic therapy should prospectively be investigated.","PeriodicalId":23169,"journal":{"name":"TP100. TP100 UNEXPECTED COVID-19 CASE REPORTS","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83808558","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.A4076
M. Forson, D. Bajaj, V. Ramalingam
Introduction: Acute fibrinous and organizing pneumonia (AFOP) is a rare histological pattern of lung injury. Organizing Pneumonia (OP) may be occurring more frequently than realized in patients with lung injury from COVID-19. This case report reviews the presentation and disease course of AFOP in a patient with COVID-19. Case description:A 49-year-old male with a history of Diabetes Mellitus and Chronic Lymphocytic Lymphoma on Venetoclax and Obinutuzumab presented with fever, exertional dyspnea, and dry cough and was diagnosed with COVID-19. His CT scan showed extensive peripheral predominant patchy and heterogenous ground glass opacities with mediastinal lymphadenopathy (Image A). His serum aspergillus galactomannan index was 4.37 and he was started on voriconazole. He however remained febrile;so, he had a transbronchial cryobiopsy. His pathology revealed marked interstitial T-cell lymphocytic inflammatory infiltrate with fibrinous and organizing pneumonia. There was proliferative bronchiolitis and evidence of acute pulmonary hemorrhage, without features of vasculitis/capillaritis. No evidence of malignancy or organisms were identified. He was started on methylprednisolone daily and he initially improved, however, his fever returned and his oxygen requirements increased rapidly with steroid taper. His repeat chest CT scan showed a marked increase in bilateral patchy areas of consolidation with surrounding areas of ground glass opacity and intralobular septal thickening ("crazy paving") Image B. His infectious work up was extensive but negative. At this point, he required invasive mechanical ventilation;after which he received pulse dose steroids for three days followed by high dose maintenance. He improved and was extubated. However, he required high flow supplemental oxygen and was unable to be weaned past 100% fraction of inspired oxygen;as a result, Ruxolitinib was added. Unfortunately, his hypoxemia remained refractory and he developed sudden cardiovascular collapse which led to his demise. The patient died 40 days after admission. Discussion: Understanding the histopathology, disease course, and sequelae of COVID-19 is of paramount importance, because AFOP in COVID-19 adds complexity to management. Our patient's antemortem biopsy was performed prior to acute respiratory distress syndrome and mechanical ventilation as opposed to previous case reports with post mortem findings of AFOP after prolonged mechanical ventilation. Notably, 30% - 60% of intensive care patients with SARS CoV 1 had OP and AFOP. Additionally, the CT findings of COVID-19 are similar to OP and this lends support to the possibility that OP is an underlying pattern of lung injury in COVID-19.
{"title":"The One-Two Punch: SARS-CoV-2 and Acute Fibrinous and Organizing Pneumonia","authors":"M. Forson, D. Bajaj, V. Ramalingam","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4076","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4076","url":null,"abstract":"Introduction: Acute fibrinous and organizing pneumonia (AFOP) is a rare histological pattern of lung injury. Organizing Pneumonia (OP) may be occurring more frequently than realized in patients with lung injury from COVID-19. This case report reviews the presentation and disease course of AFOP in a patient with COVID-19. Case description:A 49-year-old male with a history of Diabetes Mellitus and Chronic Lymphocytic Lymphoma on Venetoclax and Obinutuzumab presented with fever, exertional dyspnea, and dry cough and was diagnosed with COVID-19. His CT scan showed extensive peripheral predominant patchy and heterogenous ground glass opacities with mediastinal lymphadenopathy (Image A). His serum aspergillus galactomannan index was 4.37 and he was started on voriconazole. He however remained febrile;so, he had a transbronchial cryobiopsy. His pathology revealed marked interstitial T-cell lymphocytic inflammatory infiltrate with fibrinous and organizing pneumonia. There was proliferative bronchiolitis and evidence of acute pulmonary hemorrhage, without features of vasculitis/capillaritis. No evidence of malignancy or organisms were identified. He was started on methylprednisolone daily and he initially improved, however, his fever returned and his oxygen requirements increased rapidly with steroid taper. His repeat chest CT scan showed a marked increase in bilateral patchy areas of consolidation with surrounding areas of ground glass opacity and intralobular septal thickening (\"crazy paving\") Image B. His infectious work up was extensive but negative. At this point, he required invasive mechanical ventilation;after which he received pulse dose steroids for three days followed by high dose maintenance. He improved and was extubated. However, he required high flow supplemental oxygen and was unable to be weaned past 100% fraction of inspired oxygen;as a result, Ruxolitinib was added. Unfortunately, his hypoxemia remained refractory and he developed sudden cardiovascular collapse which led to his demise. The patient died 40 days after admission. Discussion: Understanding the histopathology, disease course, and sequelae of COVID-19 is of paramount importance, because AFOP in COVID-19 adds complexity to management. Our patient's antemortem biopsy was performed prior to acute respiratory distress syndrome and mechanical ventilation as opposed to previous case reports with post mortem findings of AFOP after prolonged mechanical ventilation. Notably, 30% - 60% of intensive care patients with SARS CoV 1 had OP and AFOP. Additionally, the CT findings of COVID-19 are similar to OP and this lends support to the possibility that OP is an underlying pattern of lung injury in COVID-19.","PeriodicalId":23169,"journal":{"name":"TP100. TP100 UNEXPECTED COVID-19 CASE REPORTS","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90703227","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.A4111
K. Syed, H. Chaudhary
Background: Spontaneous pneumomediastinum (SPM) is the presence of free air in the mediastinum which is not preceded by any trauma, instrumentation, or medical procedure. SPM is a recognized complication in various clinical settings, including infections. There have been several reports of pneumomediastinum secondary to invasive ventilation in the current pandemic. However, the occurrence of spontaneous pneumomediastinum has been infrequently described with the background of Covid-19 infection. Case Presentation: A 65-year-old gentleman presented with three days history of fever, cough, and exertional dyspnea to our hospital. He denied any trauma, emesis, chest or neck pain. Past medical history was significant for a remote history of 10-pack-year smoking. On presentation, he was in distress with a respiratory rate of 26, saturating 85% on ambient air and otherwise hemodynamically stable. His chest X-ray showed bilateral infiltrates and subcutaneous emphysema. Complete blood count and electrolyte panel was unremarkable. D-Dimer was 8.47ug/ml with a CRP of 10.8mg/dl. Nasopharyngeal RT-PCR was positive for SARS-COV-2. A CT-Chest showed multifocal ground glass opacities along with pneumomediastinum(fig.1). He was managed conservatively with oxygen supplementation, IV dexamethasone and remdesivir. He was discharged after 7 days of hospitalization with interval resolution of the SPM. Discussion:SPM is an uncommon phenomenon in a viral pneumonia. The development of SPM occurs due to increased intra-thoracic pressures that cause alveolar rupture and leakage of air. It travels along the pulmonary interstitium to reach the mediastinum. The mechanism in Covid-19 is poorly understood but is hypothesized as intense alveolar inflammation that predisposes these patients to such a complication, further precipitated by bouts of cough. Previous reports have described the presence of subpleural bullae or cysts on CT images caused by the infectious process that led to the development of SPM. However, this finding was not present in our patient denoting a different mechanism. Use of non-invasive or mechanical ventilation carries a potential to either cause or exacerbate SPM as well. Conclusion: SPM is an infrequent complication of viral pneumonia. We highlight the importance of this phenomenon in COVID-19 patients with an unknown mechanism. Development of SPM may warrant monitoring for the possibility of pneumomediastinum-related cardiovascular and respiratory complications, especially in those requiring ventilation.
{"title":"An Air of Despair-Spontaneous Pneumomediastinum in Covid-19","authors":"K. Syed, H. Chaudhary","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4111","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4111","url":null,"abstract":"Background: Spontaneous pneumomediastinum (SPM) is the presence of free air in the mediastinum which is not preceded by any trauma, instrumentation, or medical procedure. SPM is a recognized complication in various clinical settings, including infections. There have been several reports of pneumomediastinum secondary to invasive ventilation in the current pandemic. However, the occurrence of spontaneous pneumomediastinum has been infrequently described with the background of Covid-19 infection. Case Presentation: A 65-year-old gentleman presented with three days history of fever, cough, and exertional dyspnea to our hospital. He denied any trauma, emesis, chest or neck pain. Past medical history was significant for a remote history of 10-pack-year smoking. On presentation, he was in distress with a respiratory rate of 26, saturating 85% on ambient air and otherwise hemodynamically stable. His chest X-ray showed bilateral infiltrates and subcutaneous emphysema. Complete blood count and electrolyte panel was unremarkable. D-Dimer was 8.47ug/ml with a CRP of 10.8mg/dl. Nasopharyngeal RT-PCR was positive for SARS-COV-2. A CT-Chest showed multifocal ground glass opacities along with pneumomediastinum(fig.1). He was managed conservatively with oxygen supplementation, IV dexamethasone and remdesivir. He was discharged after 7 days of hospitalization with interval resolution of the SPM. Discussion:SPM is an uncommon phenomenon in a viral pneumonia. The development of SPM occurs due to increased intra-thoracic pressures that cause alveolar rupture and leakage of air. It travels along the pulmonary interstitium to reach the mediastinum. The mechanism in Covid-19 is poorly understood but is hypothesized as intense alveolar inflammation that predisposes these patients to such a complication, further precipitated by bouts of cough. Previous reports have described the presence of subpleural bullae or cysts on CT images caused by the infectious process that led to the development of SPM. However, this finding was not present in our patient denoting a different mechanism. Use of non-invasive or mechanical ventilation carries a potential to either cause or exacerbate SPM as well. Conclusion: SPM is an infrequent complication of viral pneumonia. We highlight the importance of this phenomenon in COVID-19 patients with an unknown mechanism. Development of SPM may warrant monitoring for the possibility of pneumomediastinum-related cardiovascular and respiratory complications, especially in those requiring ventilation.","PeriodicalId":23169,"journal":{"name":"TP100. TP100 UNEXPECTED COVID-19 CASE REPORTS","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91419119","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.A4081
S. Katta, M. Khoshnevis
Aspergillus is a ubiquitous fungus that causes a variety of clinical syndromes in the lung. The type and severity of airway and parenchymal disease produced by Aspergillus are influenced by the patient's immunologic status and the presence of pre-existing lung disease. There is increasing concern that patients with coronavirus disease 2019 (COVID-19) might be at risk of developing invasive pulmonary aspergillosis co-infection particularly in the context of immunomodulatory monoclonal antibodies. We present a case report of pseudomembranous aspergillus tracheobronchitis complicated by COVID-19 pneumonia. A 59-year-old female with a medical history of drug-induced interstitial lung disease from methotrexate, rheumatoid arthritis, was admitted to the intensive care unit secondary to dyspnea and hypoxemic respiratory failure. She was diagnosed recently with COVID-19 pneumonia treated with remdesevir and high dose systemic corticosteroids for 14 days. one week after she is re-admitted with shortness of breath requiring high flow nasal cannula. she had a temperature of 38.2°, blood pressure of 110/80 mmHg, heart rate of 90 bpm, and respiratory rate of 30 breaths/min. Chest auscultation was significant for diffuse bilateral inspiratory coarse crackles. She was started on broad-spectrum antibiotics with vancomycin and meropenem. RT PCR COVID test remains positive since the last admission and Anti-SARS-CoV-2 IgG Antibodies are negative. Arterial blood gas values were pH 7.41, PaCO2 63 mmHg, PaO2 60 mmHg, and SaO2 91%. The complete blood count showed hemoglobin of 10.1 g/L and 16,800 leucocytes, with no growth in blood cultures. Initial CT chest reveals bilateral diffuse ground-glass opacities consistent with COVID pneumonia. Subsequently, she was intubated and mechanically ventilated for worsening respiratory failure, empiric micafungin was started. A bronchoscopy demonstrated extensive whitish exudative membranes covering the trachea and both mainstem bronchi. The endobronchial biopsy specimens and bronchial washing fluid revealed Aspergillus fumigatus. Serum Galactomannan and fungitel came back positive. Micafungin was changed to isavuconazole, two days later the patient developed refractory septic shock. Despite using isavuconazole and supportive care, acute deterioration followed with refractory hypoxemia and oliguria, resulting in a fatal cardiac arrest on the sixth day of the intensive care unit stay. Aspergillus tracheobronchitis is an unusual manifestation of IPA accounts for <10% of cases. diagnosis of this condition is extremely difficult and hence is delayed given its relatively nonspecific presentation and the lack of specific radiographic findings. This case illustrates a need for careful screening for opportunistic infections in patients treated with high-dose systemic steroids, immunomodulators with underlying COVID pneumonia.
{"title":"Fatal Invasive Pulmonary Aspergillosis Associated with Coronavirus Disease 2019 (COVID 19) Infection","authors":"S. Katta, M. Khoshnevis","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4081","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4081","url":null,"abstract":"Aspergillus is a ubiquitous fungus that causes a variety of clinical syndromes in the lung. The type and severity of airway and parenchymal disease produced by Aspergillus are influenced by the patient's immunologic status and the presence of pre-existing lung disease. There is increasing concern that patients with coronavirus disease 2019 (COVID-19) might be at risk of developing invasive pulmonary aspergillosis co-infection particularly in the context of immunomodulatory monoclonal antibodies. We present a case report of pseudomembranous aspergillus tracheobronchitis complicated by COVID-19 pneumonia. A 59-year-old female with a medical history of drug-induced interstitial lung disease from methotrexate, rheumatoid arthritis, was admitted to the intensive care unit secondary to dyspnea and hypoxemic respiratory failure. She was diagnosed recently with COVID-19 pneumonia treated with remdesevir and high dose systemic corticosteroids for 14 days. one week after she is re-admitted with shortness of breath requiring high flow nasal cannula. she had a temperature of 38.2°, blood pressure of 110/80 mmHg, heart rate of 90 bpm, and respiratory rate of 30 breaths/min. Chest auscultation was significant for diffuse bilateral inspiratory coarse crackles. She was started on broad-spectrum antibiotics with vancomycin and meropenem. RT PCR COVID test remains positive since the last admission and Anti-SARS-CoV-2 IgG Antibodies are negative. Arterial blood gas values were pH 7.41, PaCO2 63 mmHg, PaO2 60 mmHg, and SaO2 91%. The complete blood count showed hemoglobin of 10.1 g/L and 16,800 leucocytes, with no growth in blood cultures. Initial CT chest reveals bilateral diffuse ground-glass opacities consistent with COVID pneumonia. Subsequently, she was intubated and mechanically ventilated for worsening respiratory failure, empiric micafungin was started. A bronchoscopy demonstrated extensive whitish exudative membranes covering the trachea and both mainstem bronchi. The endobronchial biopsy specimens and bronchial washing fluid revealed Aspergillus fumigatus. Serum Galactomannan and fungitel came back positive. Micafungin was changed to isavuconazole, two days later the patient developed refractory septic shock. Despite using isavuconazole and supportive care, acute deterioration followed with refractory hypoxemia and oliguria, resulting in a fatal cardiac arrest on the sixth day of the intensive care unit stay. Aspergillus tracheobronchitis is an unusual manifestation of IPA accounts for <10% of cases. diagnosis of this condition is extremely difficult and hence is delayed given its relatively nonspecific presentation and the lack of specific radiographic findings. This case illustrates a need for careful screening for opportunistic infections in patients treated with high-dose systemic steroids, immunomodulators with underlying COVID pneumonia.","PeriodicalId":23169,"journal":{"name":"TP100. TP100 UNEXPECTED COVID-19 CASE REPORTS","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78426483","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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