Pub Date : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4095
A. Mariano, R. Abraham, P. Kozak, S. Khanna, R. Almeida, M. Ruebhausen, K. Muhammad
Introduction: Anticoagulation in COVID-19 induced hypercoagulable state remains to be balanced with bleeding complications. Spontaneous muscle hematomas (SMH) often occur in the rectus sheath or gluteal muscles. Risk factors include trauma, increased abdominal pressure, anticoagulation, and hypertension. We describe two cases of non-iatrogenic SMH in therapeutically anticoagulated COVID-19 patients. Case Report: 1. 64 year old Caucasian male with ARDS due to COVID-19 was treated with mechanical ventilation, proning, methylprednisolone, tocilizumab (TOZ), and azithromycin/hydroxychloroquine. Right popliteal-posterior tibial vein DVT led to full anticoagulation (FA) with enoxaparin. Later the hemoglobin dropped (12.2 to 6.1 g/dl). Imaging showed SMH in the left posterolateral chest wall and gluteus minimus requiring blood transfusions and cessation of FA. D-dimer was 1.2 μ g/ml. A week later, imaging showed increased hematoma size in the left chest wall and right gluteal area. After hemoglobin stabilized, he was started on DVT prophylaxis. He required tracheostomy/PEG tube and placement in a long term acute care (LTAC) facility where he had decannulation and PEG tube removal. Patient recovered fully and is home with normal function. 2. 27 year old Caucasian female with sepsis due to COVID-19 was treated with mechanical ventilation, dexamethasone, TOZ, convalescent plasma, colchicine, and remdesivir. D-dimer was 1.6 μ g/ml and FA was started with enoxaparin. After intubation, hemoglobin dropped (11-6.9 g/dl). Imaging showed SMH in left biceps and pectoralis. Decreased radial pulse and increased capillary refill time with enlarging forearm hematoma prompted arterial US and CT angiogram. No flow was seen in the distal left upper extremity. Fasciotomy of the left forearm and carpal tunnel was performed with adequate perfusion of radial and ulnar arteries. Debridement was required for the non-viable flexor carpi radialis, flexor digitorum superficialis and flexor digitorum profundus. Patient was extubated and did well thereafter. Discussion: Thrombosis contributes much to the morbidity and mortality in COVID-19 patients. In a recent Veterans Health Administration study, deep vein thrombosis, pulmonary embolism, and cerebral ischemia/infarction comprised 9.3% of these patients. Despite the study's limitations, HESACOVID has shown that therapeutic enoxaparin is associated with fewer days on the ventilator and large reductions in D-dimer levels. Monitoring for SMH should be routinely performed on these patients. Research on optimal anticoagulation is necessary to assess the risk/benefit in this population. The bleeding risks are however less likely to cause mortality or disability as compared to the coagulation problems.
{"title":"Intramuscular Hematomas and Compartment Syndrome - an Inevitable Consequence in the COVID-19 Saga","authors":"A. Mariano, R. Abraham, P. Kozak, S. Khanna, R. Almeida, M. Ruebhausen, K. Muhammad","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4095","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4095","url":null,"abstract":"Introduction: Anticoagulation in COVID-19 induced hypercoagulable state remains to be balanced with bleeding complications. Spontaneous muscle hematomas (SMH) often occur in the rectus sheath or gluteal muscles. Risk factors include trauma, increased abdominal pressure, anticoagulation, and hypertension. We describe two cases of non-iatrogenic SMH in therapeutically anticoagulated COVID-19 patients. Case Report: 1. 64 year old Caucasian male with ARDS due to COVID-19 was treated with mechanical ventilation, proning, methylprednisolone, tocilizumab (TOZ), and azithromycin/hydroxychloroquine. Right popliteal-posterior tibial vein DVT led to full anticoagulation (FA) with enoxaparin. Later the hemoglobin dropped (12.2 to 6.1 g/dl). Imaging showed SMH in the left posterolateral chest wall and gluteus minimus requiring blood transfusions and cessation of FA. D-dimer was 1.2 μ g/ml. A week later, imaging showed increased hematoma size in the left chest wall and right gluteal area. After hemoglobin stabilized, he was started on DVT prophylaxis. He required tracheostomy/PEG tube and placement in a long term acute care (LTAC) facility where he had decannulation and PEG tube removal. Patient recovered fully and is home with normal function. 2. 27 year old Caucasian female with sepsis due to COVID-19 was treated with mechanical ventilation, dexamethasone, TOZ, convalescent plasma, colchicine, and remdesivir. D-dimer was 1.6 μ g/ml and FA was started with enoxaparin. After intubation, hemoglobin dropped (11-6.9 g/dl). Imaging showed SMH in left biceps and pectoralis. Decreased radial pulse and increased capillary refill time with enlarging forearm hematoma prompted arterial US and CT angiogram. No flow was seen in the distal left upper extremity. Fasciotomy of the left forearm and carpal tunnel was performed with adequate perfusion of radial and ulnar arteries. Debridement was required for the non-viable flexor carpi radialis, flexor digitorum superficialis and flexor digitorum profundus. Patient was extubated and did well thereafter. Discussion: Thrombosis contributes much to the morbidity and mortality in COVID-19 patients. In a recent Veterans Health Administration study, deep vein thrombosis, pulmonary embolism, and cerebral ischemia/infarction comprised 9.3% of these patients. Despite the study's limitations, HESACOVID has shown that therapeutic enoxaparin is associated with fewer days on the ventilator and large reductions in D-dimer levels. Monitoring for SMH should be routinely performed on these patients. Research on optimal anticoagulation is necessary to assess the risk/benefit in this population. The bleeding risks are however less likely to cause mortality or disability as compared to the coagulation problems.","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":"85131934","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.A4083
H. Desai, J. Selickman, K. Pendleton
Introduction: Invasive pulmonary aspergillosis (IPA) is a rare, severe fungal infection with a poor prognosis and high mortality rate. IPA is mainly noted in patients with immunosuppressed status, hematological malignancies and stem cell transplants. Diagnosis is challenging and requires a high index of suspicion. Current literature supports treating patients with severe covid-19 pneumonia with high dose dexamethasone therapy for a prolonged period of time which may cause significant immune suppression. Here, we present a case of a patient with covid-19 pneumonia who developed IPA after dexamethasone and tocilizumab therapy. Case report: Patient is a 75-year-old male who was admitted to the medical ICU with severe hypoxemic respiratory failure secondary to covid-19 pneumonia requiring mechanical ventilation immediately on presentation to the emergency room. The patient had a past history of cavitary lung disease secondary to tuberculosis in 2018 and had completed treatment with 4-drug therapy. During this hospitalization, three sputum samples were negative for acid fast bacillus. He was started on dexamethasone therapy of 6mg daily for 10 days and received a single dose of tocilizumab. The patient initially improved but started to worsen again on the ninth day requiring increased ventilatory support and pronation therapy. His sputum culture grew Aspergillus FLavus. CT chest showed increased parenchymal infiltrates around prior cavitary lung disease. Serum aspergillus galactomannan antigen returned positive. Patient was started on intravenous Voriconazole. After initial improvement, the patient developed hemoptysis and worsening oxygenation. As per the family's wishes, patient was transitioned to comfort care and he passed away after compassionate extubation. Discussion:Treatment of COVID-19 pneumonia with high dose dexamethasone therapy may inadvertently cause an immunosuppressed state. These immunosuppressive effects may be further compounded by concurrent use of tocilizumab. Relative immunosuppression combined with possible epithelial damage due to viral infection may be a mechanism for development of IPA. A case series from France reported possible IPA in 9 of 27 (33.3%) ICU patients with COVID-19 with an expectedly high observed mortality rate. Conclusion: Clinicians should carry a high index of suspicion and pursue early investigations for other infections in COVID-19 patients who are not recovering or have worsened after initial improvement. Careful use of steroids in patients with prior structural lung disease is also warranted as they may be at high risk of developing IPA due to pre-existing aspergillus colonization.
{"title":"Covid-19 Pneumonia and Invasive Pulmonary Aspergillosis","authors":"H. Desai, J. Selickman, K. Pendleton","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4083","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4083","url":null,"abstract":"Introduction: Invasive pulmonary aspergillosis (IPA) is a rare, severe fungal infection with a poor prognosis and high mortality rate. IPA is mainly noted in patients with immunosuppressed status, hematological malignancies and stem cell transplants. Diagnosis is challenging and requires a high index of suspicion. Current literature supports treating patients with severe covid-19 pneumonia with high dose dexamethasone therapy for a prolonged period of time which may cause significant immune suppression. Here, we present a case of a patient with covid-19 pneumonia who developed IPA after dexamethasone and tocilizumab therapy. Case report: Patient is a 75-year-old male who was admitted to the medical ICU with severe hypoxemic respiratory failure secondary to covid-19 pneumonia requiring mechanical ventilation immediately on presentation to the emergency room. The patient had a past history of cavitary lung disease secondary to tuberculosis in 2018 and had completed treatment with 4-drug therapy. During this hospitalization, three sputum samples were negative for acid fast bacillus. He was started on dexamethasone therapy of 6mg daily for 10 days and received a single dose of tocilizumab. The patient initially improved but started to worsen again on the ninth day requiring increased ventilatory support and pronation therapy. His sputum culture grew Aspergillus FLavus. CT chest showed increased parenchymal infiltrates around prior cavitary lung disease. Serum aspergillus galactomannan antigen returned positive. Patient was started on intravenous Voriconazole. After initial improvement, the patient developed hemoptysis and worsening oxygenation. As per the family's wishes, patient was transitioned to comfort care and he passed away after compassionate extubation. Discussion:Treatment of COVID-19 pneumonia with high dose dexamethasone therapy may inadvertently cause an immunosuppressed state. These immunosuppressive effects may be further compounded by concurrent use of tocilizumab. Relative immunosuppression combined with possible epithelial damage due to viral infection may be a mechanism for development of IPA. A case series from France reported possible IPA in 9 of 27 (33.3%) ICU patients with COVID-19 with an expectedly high observed mortality rate. Conclusion: Clinicians should carry a high index of suspicion and pursue early investigations for other infections in COVID-19 patients who are not recovering or have worsened after initial improvement. Careful use of steroids in patients with prior structural lung disease is also warranted as they may be at high risk of developing IPA due to pre-existing aspergillus colonization.","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":"90483962","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.A4101
A. Sunny, Varun B. Shah, T. Topacio, V. Voin
Birt Hogg Dube (BHD) syndrome is an autosomal dominant disease characterized by pulmonary cysts, spontaneous pneumothorax, skin hamartomas of the head/neck, and renal malignancies. We present a case of complications secondary to COVID 19 in a patient with BHD syndrome. A 55 year old male presented with fevers, chills and left sided pleuritic chest discomfort for 1 day. He was recently hospitalized for bacterial pneumonia and had COVID Pneumonia about 5 weeks ago. The patient was diagnosed with a lung bulla several months ago and is awaiting elective surgical resection. Vitals showed blood pressure 135/91 mmHg, temperature 36.5 Celsius, heart rate 74 and respiratory rate 18. Physical exam significant for decreased breath sounds of the left lower lobe. Labs showed white cell count 10.7 K/mcL, D-dimer 0.81 mcg/mL, lactic acid 0.7 mmol/L. SARS COV 2 PCR positive. Chest Xray showed left lower lobe multilobulated cavitary mass. CT Angiography Chest showed air-fluid level development within pre-existing large multiseptated bulla in the left lower lobe and dependently layering left pleural effusion (Figure 1). The patient was initiated on Vancomycin and Piperacillin-Tazobactam on admission. Thoracentesis was unable to be done due to low amount of pleural fluid. Patient stabilized with antibiotic treatment and supportive care, with subsequent discharge on a 2 week course of Piperacillin-Tazobactam. Diagnosis of BHD involves one or more of the following: greater than 2 or more fibrofolliculomas or trichodiscomas, multiple bilateral pulmonary cysts in the basilar lung regions, bilateral multifocal renal carcinomas or oncocytic renal tumors, pathogenic FLCN gene variant or family history of the disease [4]. Initial presentation of these patients is often via spontaneous pneumothorax. 70%-80% of BHD patients develop numerous, bilateral pulmonary cysts with majority having normal pulmonary function or mild obstructive disease [3,4]. On imaging, these thin-walled, irregularly shaped cysts are seen in the medial basilar lung regions. This is in contrast to the apical region air blebs seen in those patients with pneumothorax due to COPD or primary spontaneous pneumothorax. Our patient is unique in that he had recently developed COVID 19 Pneumonia with a superimposed bacterial pneumonia. The patient's previously known bullae became infected with subsequent abscess formation. To our knowledge, this is the first known case of Birt Hogg Dube Syndrome complicated by pulmonary cyst infection and abscess formation.
{"title":"Complications of COVID 19 in a Patient with Birt Hogg Dube Syndrome","authors":"A. Sunny, Varun B. Shah, T. Topacio, V. Voin","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4101","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4101","url":null,"abstract":"Birt Hogg Dube (BHD) syndrome is an autosomal dominant disease characterized by pulmonary cysts, spontaneous pneumothorax, skin hamartomas of the head/neck, and renal malignancies. We present a case of complications secondary to COVID 19 in a patient with BHD syndrome. A 55 year old male presented with fevers, chills and left sided pleuritic chest discomfort for 1 day. He was recently hospitalized for bacterial pneumonia and had COVID Pneumonia about 5 weeks ago. The patient was diagnosed with a lung bulla several months ago and is awaiting elective surgical resection. Vitals showed blood pressure 135/91 mmHg, temperature 36.5 Celsius, heart rate 74 and respiratory rate 18. Physical exam significant for decreased breath sounds of the left lower lobe. Labs showed white cell count 10.7 K/mcL, D-dimer 0.81 mcg/mL, lactic acid 0.7 mmol/L. SARS COV 2 PCR positive. Chest Xray showed left lower lobe multilobulated cavitary mass. CT Angiography Chest showed air-fluid level development within pre-existing large multiseptated bulla in the left lower lobe and dependently layering left pleural effusion (Figure 1). The patient was initiated on Vancomycin and Piperacillin-Tazobactam on admission. Thoracentesis was unable to be done due to low amount of pleural fluid. Patient stabilized with antibiotic treatment and supportive care, with subsequent discharge on a 2 week course of Piperacillin-Tazobactam. Diagnosis of BHD involves one or more of the following: greater than 2 or more fibrofolliculomas or trichodiscomas, multiple bilateral pulmonary cysts in the basilar lung regions, bilateral multifocal renal carcinomas or oncocytic renal tumors, pathogenic FLCN gene variant or family history of the disease [4]. Initial presentation of these patients is often via spontaneous pneumothorax. 70%-80% of BHD patients develop numerous, bilateral pulmonary cysts with majority having normal pulmonary function or mild obstructive disease [3,4]. On imaging, these thin-walled, irregularly shaped cysts are seen in the medial basilar lung regions. This is in contrast to the apical region air blebs seen in those patients with pneumothorax due to COPD or primary spontaneous pneumothorax. Our patient is unique in that he had recently developed COVID 19 Pneumonia with a superimposed bacterial pneumonia. The patient's previously known bullae became infected with subsequent abscess formation. To our knowledge, this is the first known case of Birt Hogg Dube Syndrome complicated by pulmonary cyst infection and abscess formation.","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":"90795768","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.A4078
S. Chandna, M. Shah, G. Aftab, A. Agrawal, D. Frenia
IntroductionSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces an immune response but the degree and duration for which it provides protective immunity is still unknown. Herein we report a case of reinfection where the patient was tested positive again after being tested negative two subsequent times. Case DescriptionA 31-year-old Hispanic female with a past medical history of asthma, gastric sleeve surgery, and pulmonary embolism during pregnancy presented in March 2020 with subjective fever, dry cough, headache, and fatigue for 5 days. Vitals were significant for oxygen saturation of 96% on room air and BMI 44.4 kg/m2. Physical examination was normal. Labs and chest radiograph were normal. SARS-CoV-2 RT-PCR was positive. The patient was discharged and was advised to quarantine herself and monitor her oxygen saturation. She was re-tested again in July 2020 and September 2020 and SARS-CoV-2 RT-PCR was negative both times. The patient came to the hospital again in November 2020 with subjective fevers, chills, shortness of breath, body ache, and malaise for 1 week. Vitals were significant for a heart rate of 112/min, temperature 99.6 °F, respiratory rate of 20/min, hypoxia requiring 5L nasal cannula to maintain an oxygen saturation of 95%, and BMI 44.7 kg/m2. Physical exam revealed decreased air entry in the lungs bilaterally. Complete blood count and basic metabolic profile were within normal limits. Inflammatory markers were elevated. Computed tomography (CT) thorax showed bilateral, predominantly peripheral, and subpleural ill-defined ground-glass opacities consistent with pneumonia. SARS-CoV-2 RT-PCR was positive. The patient was treated with intravenous remdesivir for 5 days and oral dexamethasone 6mg for 10 days. She improved clinically and was discharged on home oxygen. DiscussionAlthough the risk of COVID reinfection is low, cases of possible reinfection have been reported. Our patient was not immunocompromised, tested negative after 4 months and 6 months but presented again after 8 months with severe symptoms as compared to the first time. There have been case reports where the reinfection was more severe, however, there is not sufficient data to support that. There is not enough data demonstrating degree and duration of protection after the primary infection either. Reinfection could be due to infection with a more virulent strain or evolution of the previous viral strain in the body. The absence of genomic sequencing limits our ability to diagnose that. More research in this field and genomic sequencing can help us with an accurate diagnosis.
{"title":"COVID 19 Reinfection: First Case in New Jersey","authors":"S. Chandna, M. Shah, G. Aftab, A. Agrawal, D. Frenia","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4078","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4078","url":null,"abstract":"IntroductionSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces an immune response but the degree and duration for which it provides protective immunity is still unknown. Herein we report a case of reinfection where the patient was tested positive again after being tested negative two subsequent times. Case DescriptionA 31-year-old Hispanic female with a past medical history of asthma, gastric sleeve surgery, and pulmonary embolism during pregnancy presented in March 2020 with subjective fever, dry cough, headache, and fatigue for 5 days. Vitals were significant for oxygen saturation of 96% on room air and BMI 44.4 kg/m2. Physical examination was normal. Labs and chest radiograph were normal. SARS-CoV-2 RT-PCR was positive. The patient was discharged and was advised to quarantine herself and monitor her oxygen saturation. She was re-tested again in July 2020 and September 2020 and SARS-CoV-2 RT-PCR was negative both times. The patient came to the hospital again in November 2020 with subjective fevers, chills, shortness of breath, body ache, and malaise for 1 week. Vitals were significant for a heart rate of 112/min, temperature 99.6 °F, respiratory rate of 20/min, hypoxia requiring 5L nasal cannula to maintain an oxygen saturation of 95%, and BMI 44.7 kg/m2. Physical exam revealed decreased air entry in the lungs bilaterally. Complete blood count and basic metabolic profile were within normal limits. Inflammatory markers were elevated. Computed tomography (CT) thorax showed bilateral, predominantly peripheral, and subpleural ill-defined ground-glass opacities consistent with pneumonia. SARS-CoV-2 RT-PCR was positive. The patient was treated with intravenous remdesivir for 5 days and oral dexamethasone 6mg for 10 days. She improved clinically and was discharged on home oxygen. DiscussionAlthough the risk of COVID reinfection is low, cases of possible reinfection have been reported. Our patient was not immunocompromised, tested negative after 4 months and 6 months but presented again after 8 months with severe symptoms as compared to the first time. There have been case reports where the reinfection was more severe, however, there is not sufficient data to support that. There is not enough data demonstrating degree and duration of protection after the primary infection either. Reinfection could be due to infection with a more virulent strain or evolution of the previous viral strain in the body. The absence of genomic sequencing limits our ability to diagnose that. More research in this field and genomic sequencing can help us with an accurate diagnosis.","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":"85792447","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.A4096
M. Arbex, C. Porto, G.A.K. Pirolla, M. I. Dognani, I. D. Elía, B. C. Abreu
MRS, 32, male, homeless, illicit drug user, smoker, alcoholic, with no family bonds, was admitted to the Nestor Goulart Reis Hospital, a São Paulo State Health Secretary reference centre, to treat multi/extensively resistant tuberculosis, on April 6, 2020, upon diagnosis with bacterial pneumonia and pulmonary tuberculosis (TB). An outpatient rapid molecular sputum test (RMT) performed on March 20, 2020 revealed positivity for M. tuberculosis with rifampicin resistance (R). The therapy established at the time was capreomycin (CM), ethambutol (E), levofloxacin (Lvx), pyrazinamide (P), and terizidone (Tzd). After hospitalisation, his general condition progressively decreased. A reverse-transcriptase polymerase chain reaction (RT-PCR) on April 9, 2020 was positive for SARS-CoV-2. The patient developed viral bronchopneumonia, bacterial pneumonia, septic shock with pulmonary focus, and respiratory and renal failure. He required orotracheal intubation, tracheostomy, and mechanical ventilation in the prone position. Anti-tuberculosis and antimicrobial therapy was maintained. The patient remains hospitalised for tuberculosis treatment. TB is the largest cause of death due to a single infectious agent, accounting for 1.5 million deaths in 2018 and approximately 4,000 deaths per day. Similar to SARS-CoV-2, TB undergoes direct airborne transmission and is considered a social disease. Its incidence increases or decreases according to socioeconomic and/or social protection measures. Risk factors such as older age, malnutrition, diabetes, agglomeration, social vulnerability, and signs and symptoms such as cough, fever, asthenia, and myalgia are common to both pathologies and may confound and/or delay the diagnosis of COVID/TB co-infections, thus increasing virus and/or bacillus dissemination. The patient had risk factors for both infections, besides structural pulmonary parenchyma involvement (X-ray), which may explain the viral infection severity, progression to Severe Acute Respiratory Syndrome, and need for mechanical ventilation Brazil is the ninth largest economy in the world. Meanwhile, 20% of the population remains in poverty. It is estimated that 12 million people live agglomerated in communities (shanty towns) without basic sanitation. This combination of factors may facilitate COVID-19/TB co-infection and increase the number of TB cases and deaths. In summary, health services, including those that diagnose and treat TB and lung diseases, may receive patients with COVID-19, many of whom have not been previously diagnosed. The consequences of co-infection are remaining unexplored. Patients will need close follow-up to assess possible late respiratory and systemic repercussions. Furthermore, effective public power and health system actions will be necessary for the most vulnerable populations to avoid cases as serious as the one presented here.
{"title":"Co-Infection Tuberculosis/Covid 19. An Announced Tragedy?","authors":"M. Arbex, C. Porto, G.A.K. Pirolla, M. I. Dognani, I. D. Elía, B. C. Abreu","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4096","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4096","url":null,"abstract":"MRS, 32, male, homeless, illicit drug user, smoker, alcoholic, with no family bonds, was admitted to the Nestor Goulart Reis Hospital, a São Paulo State Health Secretary reference centre, to treat multi/extensively resistant tuberculosis, on April 6, 2020, upon diagnosis with bacterial pneumonia and pulmonary tuberculosis (TB). An outpatient rapid molecular sputum test (RMT) performed on March 20, 2020 revealed positivity for M. tuberculosis with rifampicin resistance (R). The therapy established at the time was capreomycin (CM), ethambutol (E), levofloxacin (Lvx), pyrazinamide (P), and terizidone (Tzd). After hospitalisation, his general condition progressively decreased. A reverse-transcriptase polymerase chain reaction (RT-PCR) on April 9, 2020 was positive for SARS-CoV-2. The patient developed viral bronchopneumonia, bacterial pneumonia, septic shock with pulmonary focus, and respiratory and renal failure. He required orotracheal intubation, tracheostomy, and mechanical ventilation in the prone position. Anti-tuberculosis and antimicrobial therapy was maintained. The patient remains hospitalised for tuberculosis treatment. TB is the largest cause of death due to a single infectious agent, accounting for 1.5 million deaths in 2018 and approximately 4,000 deaths per day. Similar to SARS-CoV-2, TB undergoes direct airborne transmission and is considered a social disease. Its incidence increases or decreases according to socioeconomic and/or social protection measures. Risk factors such as older age, malnutrition, diabetes, agglomeration, social vulnerability, and signs and symptoms such as cough, fever, asthenia, and myalgia are common to both pathologies and may confound and/or delay the diagnosis of COVID/TB co-infections, thus increasing virus and/or bacillus dissemination. The patient had risk factors for both infections, besides structural pulmonary parenchyma involvement (X-ray), which may explain the viral infection severity, progression to Severe Acute Respiratory Syndrome, and need for mechanical ventilation Brazil is the ninth largest economy in the world. Meanwhile, 20% of the population remains in poverty. It is estimated that 12 million people live agglomerated in communities (shanty towns) without basic sanitation. This combination of factors may facilitate COVID-19/TB co-infection and increase the number of TB cases and deaths. In summary, health services, including those that diagnose and treat TB and lung diseases, may receive patients with COVID-19, many of whom have not been previously diagnosed. The consequences of co-infection are remaining unexplored. Patients will need close follow-up to assess possible late respiratory and systemic repercussions. Furthermore, effective public power and health system actions will be necessary for the most vulnerable populations to avoid cases as serious as the one presented here.","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":"79991005","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.A4073
V. T. Gonuguntla, A. Bernstein, Y. Kupfer
Introduction: Severe acute respiratory syndrome from COVID 19 typically presents with cough, fever, myalgias and progresses to respiratory and multi-organ failure. However, neurological manifestations of COVID 19, namely Guillain-Barre syndrome are rare. We present a case of acute inflammatory demyelinating polyneuropathy (AIDP), a form of GBS in a patient with recent COVID infection. Case: 66 year old man with no significant medical history presented to the emergency department for progressive weakness of all extremities for 2 days. Patient was diagnosed with COVID 19 three weeks prior to onset of weakness. As per patient, he only had mild respiratory illness with cough, general weakness without respiratory symptoms. Two days prior to presentation, he felt weakness in his lower extremities, which then progressed to involve the upper extremities. On initial evaluation the patient's pupils were symmetric and 3mm, reactive to light, visual field were full to confrontation, cranial nerves intact, shoulder shrug symmetric with full strength. He had decreased motor tone with 2/5 strength in both upper and lower extremities and depressed or absent reflexes in all extremities. His labs were significant for positive COVID 19 PCR and antibodies. CT head was negative for acute stroke or intracranial pathology. The patient was admitted to MICU where he developed respiratory muscle weakness with diminished vital capacity of 12ml/kg and negative inspiratory force of 12mmHg and he was intubated. Cerebral spinal fluid showed elevated protein to 145mg/dL, WBC of 4/UL with 50% lymphocytes and glucose of 67. Other CSF studies were negative for oligoclonal bands, EBV, CMV, cryptococcus, syphilis, and sarcoidosis. Electromyography was consistent with moderate AIDP. He received 5 doses of IVIG with no significant improvement so he underwent tracheostomy and was initiated on plasmapheresis for AIDP. Discussion: GBS is an immune-mediated disease that typically affects the peripheral neurons and nerve roots after respiratory or gastrointestinal illness. Typical infections are Campylobacter jejuni, Zika virus, Influenza, and there are even reports of GBS after MERS and SARS COV-1. However, there has been increasing evidence of COVID 19 causing neurologic manifestations such as encephalitis, meningitis, stroke, and GBS [1]. Patients, such as the one presented in this report with GBS, usually have a long and protracted disease despite aggressive treatments with IVIG and plasmapheresis with reliance on mechanical ventilator. Understanding the full spectrum of diseases and systems affected by COVID 19 can help clinicians provide better care.
{"title":"Case of Acute Inflammatory Demyelinating Polyneuropathy in SARS COVID 19 Pneumonia","authors":"V. T. Gonuguntla, A. Bernstein, Y. Kupfer","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4073","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4073","url":null,"abstract":"Introduction: Severe acute respiratory syndrome from COVID 19 typically presents with cough, fever, myalgias and progresses to respiratory and multi-organ failure. However, neurological manifestations of COVID 19, namely Guillain-Barre syndrome are rare. We present a case of acute inflammatory demyelinating polyneuropathy (AIDP), a form of GBS in a patient with recent COVID infection. Case: 66 year old man with no significant medical history presented to the emergency department for progressive weakness of all extremities for 2 days. Patient was diagnosed with COVID 19 three weeks prior to onset of weakness. As per patient, he only had mild respiratory illness with cough, general weakness without respiratory symptoms. Two days prior to presentation, he felt weakness in his lower extremities, which then progressed to involve the upper extremities. On initial evaluation the patient's pupils were symmetric and 3mm, reactive to light, visual field were full to confrontation, cranial nerves intact, shoulder shrug symmetric with full strength. He had decreased motor tone with 2/5 strength in both upper and lower extremities and depressed or absent reflexes in all extremities. His labs were significant for positive COVID 19 PCR and antibodies. CT head was negative for acute stroke or intracranial pathology. The patient was admitted to MICU where he developed respiratory muscle weakness with diminished vital capacity of 12ml/kg and negative inspiratory force of 12mmHg and he was intubated. Cerebral spinal fluid showed elevated protein to 145mg/dL, WBC of 4/UL with 50% lymphocytes and glucose of 67. Other CSF studies were negative for oligoclonal bands, EBV, CMV, cryptococcus, syphilis, and sarcoidosis. Electromyography was consistent with moderate AIDP. He received 5 doses of IVIG with no significant improvement so he underwent tracheostomy and was initiated on plasmapheresis for AIDP. Discussion: GBS is an immune-mediated disease that typically affects the peripheral neurons and nerve roots after respiratory or gastrointestinal illness. Typical infections are Campylobacter jejuni, Zika virus, Influenza, and there are even reports of GBS after MERS and SARS COV-1. However, there has been increasing evidence of COVID 19 causing neurologic manifestations such as encephalitis, meningitis, stroke, and GBS [1]. Patients, such as the one presented in this report with GBS, usually have a long and protracted disease despite aggressive treatments with IVIG and plasmapheresis with reliance on mechanical ventilator. Understanding the full spectrum of diseases and systems affected by COVID 19 can help clinicians provide better care.","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":"87816936","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.A4086
M. A. Ahmed, C. Sun, A. Mohan, D. Djondo
Since the outbreak of the Coronavirus Disease 2019 (COVID-19) pandemic, over seventy million cases have been reported worldwide. Patients present with various symptoms, including extra-pulmonary manifestations. However, manifestations on adrenal glands have not been reported extensively. Here, we present a case of functional adrenal insufficiency in a COVID-19 patient. A 61-year-old male with a history of hyperlipidemia presented with fatigue, cough, and dyspnea, subsequently tested positive for COVID-19. His blood pressure (BP) on admission was 128/68 mmHg with 86% oxygen saturation on room air. Dexamethasone 6mg daily was started for ten days. Remdesivir was contra-indicated, considering the ALT of 246 and AST of 248. On day seven of hospitalization, he had progressively worsening respiratory symptoms and was transferred to the Intensive Care Unit with BP of 105/63 mmHg. Within 48 hours, he showed positive orthostatic vitals with BP of 85/54 mmHg. Despite intravenous hydration, his BP was consistently low on subsequent days with 88/53 mmHg and 99/66 mmHg. His serum total cortisol level was 9.2 μg/dL, and he showed a positive response to IV Hydrocortisone 50mg as well as oral prednisone 10 mg the following day. We did not obtain a cosyntropin stimulation test because of recent corticosteroid therapy. Midodrine 2.5mg three times daily (TID) was started, then increased to 10 mg to maintain BP and alleviate orthostatic symptoms. However, symptomatic positive orthostatic vitals were persistent. He was discharged on midodrine 7.5 mg TID and Fludrocortisone 0.1 mg daily for suspicion of functional adrenal insufficiency. Additionally, a HDL level of 22 mg/dL was recorded (vs 56 mg/dL six months ago). At three months follow-up, he was off fludrocortisone and midodrine with improved orthostatic symptoms. Hypotension and orthostatic symptoms in COVID-19 could be due to IL-1, IL-6, or tumor necrosis factor-mediated reduction in ACTH secretion. Acute illnesses, including COVID-19, may also increase cortisol demand, causing adrenal insufficiency. Decreased HDL noted in our patient could be another etiology. "Critical Illness-Related Corticosteroid Insufficiency" (CIRCI) is a functional adrenal insufficiency that is not strictly dependent on cortisol level for diagnosis but mostly on the inadequacy of cortisol for inflammation control or supplying the raised metabolic demand. Decreased cortisol complex cleavage, increased activity of an enzyme responsible for cortisol inactivation, and decreased numbers and affinity of cortisol receptors were postulated to play a role. Therefore, adrenal insufficiency as a cause of hypotension following COVID-19 infection should not be overlooked despite normal cortisol levels.
{"title":"A Case of Functional Adrenal Insufficiency Secondary to COVID-19 Infection","authors":"M. A. Ahmed, C. Sun, A. Mohan, D. Djondo","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4086","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4086","url":null,"abstract":"Since the outbreak of the Coronavirus Disease 2019 (COVID-19) pandemic, over seventy million cases have been reported worldwide. Patients present with various symptoms, including extra-pulmonary manifestations. However, manifestations on adrenal glands have not been reported extensively. Here, we present a case of functional adrenal insufficiency in a COVID-19 patient. A 61-year-old male with a history of hyperlipidemia presented with fatigue, cough, and dyspnea, subsequently tested positive for COVID-19. His blood pressure (BP) on admission was 128/68 mmHg with 86% oxygen saturation on room air. Dexamethasone 6mg daily was started for ten days. Remdesivir was contra-indicated, considering the ALT of 246 and AST of 248. On day seven of hospitalization, he had progressively worsening respiratory symptoms and was transferred to the Intensive Care Unit with BP of 105/63 mmHg. Within 48 hours, he showed positive orthostatic vitals with BP of 85/54 mmHg. Despite intravenous hydration, his BP was consistently low on subsequent days with 88/53 mmHg and 99/66 mmHg. His serum total cortisol level was 9.2 μg/dL, and he showed a positive response to IV Hydrocortisone 50mg as well as oral prednisone 10 mg the following day. We did not obtain a cosyntropin stimulation test because of recent corticosteroid therapy. Midodrine 2.5mg three times daily (TID) was started, then increased to 10 mg to maintain BP and alleviate orthostatic symptoms. However, symptomatic positive orthostatic vitals were persistent. He was discharged on midodrine 7.5 mg TID and Fludrocortisone 0.1 mg daily for suspicion of functional adrenal insufficiency. Additionally, a HDL level of 22 mg/dL was recorded (vs 56 mg/dL six months ago). At three months follow-up, he was off fludrocortisone and midodrine with improved orthostatic symptoms. Hypotension and orthostatic symptoms in COVID-19 could be due to IL-1, IL-6, or tumor necrosis factor-mediated reduction in ACTH secretion. Acute illnesses, including COVID-19, may also increase cortisol demand, causing adrenal insufficiency. Decreased HDL noted in our patient could be another etiology. \"Critical Illness-Related Corticosteroid Insufficiency\" (CIRCI) is a functional adrenal insufficiency that is not strictly dependent on cortisol level for diagnosis but mostly on the inadequacy of cortisol for inflammation control or supplying the raised metabolic demand. Decreased cortisol complex cleavage, increased activity of an enzyme responsible for cortisol inactivation, and decreased numbers and affinity of cortisol receptors were postulated to play a role. Therefore, adrenal insufficiency as a cause of hypotension following COVID-19 infection should not be overlooked despite normal cortisol levels.","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":"85686757","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.A4107
S. Ricker, E. Bradley, A. Astua
Introduction: As further studies elucidate the extent of organ systems affected by COVID-19, extra-pulmonary involvement is emerging as an important contributor to its morbidity and lethality. Beta-islet cells in the pancreas have been shown to be affected by COVID-19 via ACE2 and TMPRSS2 receptors. Accordingly, diabetes mellitus (DM) has not only been described as an independent risk factor for severe COVID-19, but there is also an association between new-onset DM (NODM) and diabetic ketoacidosis (DKA) with COVID-19. This case report discusses a patient with NODM presenting with DKA precipitated by COVID-19. Case Summary: A 45-year-old male with no past medical history who emigrated from India in March 2020 presented to the emergency department with five days of dyspnea, chills, fatigue, polyuria, and polydipsia. He was COVID-19 PCR-positive while his labs were remarkable for WBC 14, sodium 126, bicarbonate 2, glucose 350, anion gap 33, pH 6.95, pCO2 26, lactate 4.4, D-dimer 479, LDH 350, Ferritin 2381, Procalcitonin 1.13, HIV negative, and significant ketonuria. Chest x-ray revealed bilateral lower lobe patchy infiltrates consistent with COVID-19. He was started on an insulin drip, therapeutic Enoxaparin, and fluid resuscitation. He did not require supplemental oxygen and was not treated with steroids or antivirals. He was transitioned to subcutaneous insulin after one day. He was discharged after an uncomplicated five-day hospital stay. Discussion: There has been an increasing number of reports describing DKA precipitated by COVID-19 in patients with NODM, though our patient presentation is unique because he had a mild COVID-19 course that precipitated severe DKA. This case indicates a more direct role of COVID-19 damaging beta-cells in the pancreas as our patient remained on insulin and no other diabetic medications at discharge and after follow-up, indicating a complete reliance on exogenous insulin and failure of the pancreas to produce insulin seen with type-1 DM. The patient's HbA1c of 13.3 indicates a chronic state of DM, though COVID-19 certainly contributed to establishing NODM and DKA likely by wiping the remaining function of the Beta-cells in the pancreas. This uncommon case presentation demonstrates that even mild COVID-19 can induce DKA, so it is imperative that further research be conducted on its mechanism and prevention in the future.
{"title":"COVID-19: Too Sweet to Handle? A Case of New-Onset Diabetes Mellitus with Severe Diabetic Ketoacidosis Precipitated by Mild COVID-19 Pneumonia","authors":"S. Ricker, E. Bradley, A. Astua","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4107","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4107","url":null,"abstract":"Introduction: As further studies elucidate the extent of organ systems affected by COVID-19, extra-pulmonary involvement is emerging as an important contributor to its morbidity and lethality. Beta-islet cells in the pancreas have been shown to be affected by COVID-19 via ACE2 and TMPRSS2 receptors. Accordingly, diabetes mellitus (DM) has not only been described as an independent risk factor for severe COVID-19, but there is also an association between new-onset DM (NODM) and diabetic ketoacidosis (DKA) with COVID-19. This case report discusses a patient with NODM presenting with DKA precipitated by COVID-19. Case Summary: A 45-year-old male with no past medical history who emigrated from India in March 2020 presented to the emergency department with five days of dyspnea, chills, fatigue, polyuria, and polydipsia. He was COVID-19 PCR-positive while his labs were remarkable for WBC 14, sodium 126, bicarbonate 2, glucose 350, anion gap 33, pH 6.95, pCO2 26, lactate 4.4, D-dimer 479, LDH 350, Ferritin 2381, Procalcitonin 1.13, HIV negative, and significant ketonuria. Chest x-ray revealed bilateral lower lobe patchy infiltrates consistent with COVID-19. He was started on an insulin drip, therapeutic Enoxaparin, and fluid resuscitation. He did not require supplemental oxygen and was not treated with steroids or antivirals. He was transitioned to subcutaneous insulin after one day. He was discharged after an uncomplicated five-day hospital stay. Discussion: There has been an increasing number of reports describing DKA precipitated by COVID-19 in patients with NODM, though our patient presentation is unique because he had a mild COVID-19 course that precipitated severe DKA. This case indicates a more direct role of COVID-19 damaging beta-cells in the pancreas as our patient remained on insulin and no other diabetic medications at discharge and after follow-up, indicating a complete reliance on exogenous insulin and failure of the pancreas to produce insulin seen with type-1 DM. The patient's HbA1c of 13.3 indicates a chronic state of DM, though COVID-19 certainly contributed to establishing NODM and DKA likely by wiping the remaining function of the Beta-cells in the pancreas. This uncommon case presentation demonstrates that even mild COVID-19 can induce DKA, so it is imperative that further research be conducted on its mechanism and prevention in the future.","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":"76482210","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.A4099
S. Patel, V. Villgran, M. Young
Introduction Reverse-transcriptase polymerase chain reaction testing (RT-PCR) remains the mainstay in diagnosing SARS-CoV-2. Though a positive result is highly specific for the virus, the false negative rate of the test can vary from 20% to 100%. This can have implications including, but not limited to, delay in treatment, improper management, and more costly and invasive testing. We present a case of a 54 year old male who presented for hypoxic respiratory failure diagnosed with SARS-CoV-2 on bronchoalveolar lavage (BAL) after extensive workup including 5 negative nasopharyngeal RT-PCR SARS-CoV-2 tests (NP RT-PCR). Case The patient is a 54 year old male with a past medical history significant for morbid obesity and well controlled asthma who presented for dyspnea on exertion. Throughout the patient's hospitalization, his oxygen requirements rapidly increased leading to a short course of ventilator support. CT angiogram of the chest on presentation did not show evidence of pulmonary embolism however did show bilateral multi-lobar ground glass opacities. The patient admitted to recently removing an old carpet at work but denied any other significant inhalational exposures. Dozens of his co-workers recently tested positive for SARS-CoV-2. Extensive workup including respiratory virus panel, 5 NP RT-PCR tests one week apart, basic rheumatologic serologies, and hypersensitivity pneumonitis panel were all unremarkable. Treatment for community acquired pneumonia was completed without improvement. Empiric treatment with steroids was started. BAL and trans-bronchial biopsies were initially unremarkable (Table 1). Repeat imaging demonstrated multiple sub-segmental pulmonary emboli. RT-PCR of the BAL specimen and serum antibodies for SARS-CoV-2 were collected, both of which resulted positive. The patient was eventually discharged on oral anticoagulation, a short prednisone taper, and 2L oxygen via nasal cannula on exertion with scheduled outpatient follow-up. Conclusion NP RT-PCR has become the gold standard diagnostic test for SARS-CoV-2, but it does not come without imperfections. Timing of the test in relation to symptoms, assay limit of detection, and sample collection technique all affect the results. Our patient's clinical presentation, known recent exposure, and imaging findings increased his probability of having SARS-CoV-2. However, NP RT-PCR was negative on 5 separate occasions. Limitations of this test may therefore extend beyond our current understanding. After obtaining SARS-CoV-2 diagnosis from the BAL, this obviated the need for a thoracoscopic biopsy and treatment with prolonged steroids. BAL RT-PCR SARS-CoV-2 testing consequently may play a necessary role in such patients with negative NP RT-PCR testing.
{"title":"COVID-19: The Great Masquerader","authors":"S. Patel, V. Villgran, M. Young","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4099","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4099","url":null,"abstract":"Introduction Reverse-transcriptase polymerase chain reaction testing (RT-PCR) remains the mainstay in diagnosing SARS-CoV-2. Though a positive result is highly specific for the virus, the false negative rate of the test can vary from 20% to 100%. This can have implications including, but not limited to, delay in treatment, improper management, and more costly and invasive testing. We present a case of a 54 year old male who presented for hypoxic respiratory failure diagnosed with SARS-CoV-2 on bronchoalveolar lavage (BAL) after extensive workup including 5 negative nasopharyngeal RT-PCR SARS-CoV-2 tests (NP RT-PCR). Case The patient is a 54 year old male with a past medical history significant for morbid obesity and well controlled asthma who presented for dyspnea on exertion. Throughout the patient's hospitalization, his oxygen requirements rapidly increased leading to a short course of ventilator support. CT angiogram of the chest on presentation did not show evidence of pulmonary embolism however did show bilateral multi-lobar ground glass opacities. The patient admitted to recently removing an old carpet at work but denied any other significant inhalational exposures. Dozens of his co-workers recently tested positive for SARS-CoV-2. Extensive workup including respiratory virus panel, 5 NP RT-PCR tests one week apart, basic rheumatologic serologies, and hypersensitivity pneumonitis panel were all unremarkable. Treatment for community acquired pneumonia was completed without improvement. Empiric treatment with steroids was started. BAL and trans-bronchial biopsies were initially unremarkable (Table 1). Repeat imaging demonstrated multiple sub-segmental pulmonary emboli. RT-PCR of the BAL specimen and serum antibodies for SARS-CoV-2 were collected, both of which resulted positive. The patient was eventually discharged on oral anticoagulation, a short prednisone taper, and 2L oxygen via nasal cannula on exertion with scheduled outpatient follow-up. Conclusion NP RT-PCR has become the gold standard diagnostic test for SARS-CoV-2, but it does not come without imperfections. Timing of the test in relation to symptoms, assay limit of detection, and sample collection technique all affect the results. Our patient's clinical presentation, known recent exposure, and imaging findings increased his probability of having SARS-CoV-2. However, NP RT-PCR was negative on 5 separate occasions. Limitations of this test may therefore extend beyond our current understanding. After obtaining SARS-CoV-2 diagnosis from the BAL, this obviated the need for a thoracoscopic biopsy and treatment with prolonged steroids. BAL RT-PCR SARS-CoV-2 testing consequently may play a necessary role in such patients with negative NP RT-PCR testing.","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":"89625569","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.A4077
A. E. Martínez, L. F. Enciso, P. Torres, J. Piraquive, G. Diaz, E. Cortes, C. Rodriguez
INTRODUCTION: residual lung injury in patients recovering from COVID-19 information is scarce. Herein, we present a previous confirmed SARS-CoV2 infection case series including five patients, who underwent either open or transbronchial lung biopsy due to no clinical improvement. DESCRIPTION: Case 1: a 73-year-old male patient initially asymptomatic, with positive RT-PCR after transurethral resection of the prostate. Consulted for dyspnea and room air desaturation after 24 days during postoperative. Chest computed tomography reported findings compatible with organizing pneumonia, then a transbronchial biopsy was performed confirming diagnosis. Case 2: a 48-year-old male patient with COVID-19 pneumonia who required 14 days hospitalization. He was readmitted after 25 days since initial symptoms due to dyspnea and room air desaturation with a chest CT that revealed findings suggestive of pulmonary fibrosis. Therefore, an open lung biopsy was performed with a probable usual interstitial pneumonia pattern report. Case 3: a 86-year-old male patient, with initial mild COVID-19 infection who later progressed to severe pneumonia requiring high levels of supplemental oxygen. At 18 days of admission, due to persistent clinical compromise, a chest CT was performed with findings of organizing pneumonia. Therefore, he was taken to transbronchial lung biopsy that revealed non-specific interstitial pneumonia in the fibrosing phase. Case 4: a 61-year-old male patient with HIV/AIDS infection presented acute respiratory distress syndrome due to severe COVID-19 pneumonia with inability to withdraw invasive mechanical ventilation after one month. An open lung biopsy was performed with histopathology diagnosis of diffuse alveolar damage in the proliferative phase.Case 5: 41-year-old male patient with severe COVID-19 pneumonia requiring invasive mechanical ventilation, with persistent use of high levels of supplemental oxygen after 30 days since symptomatic. The chest CT suggested pulmonary fibrosis;therefore, an open lung biopsy was performed and confirmed Non-Specific Interstitial Pneumonia. DISCUSSION: to date, reports of interstitial lung disease due to COVID-19 refer to imaging findings or post-mortem histopathological studies which have been relatively limited given the strict guidelines and restrictions for performing bronchoscopies and lung surgery during the pandemic. The foregoing highlights the importance of tissue analysis under rigorous safety protocols in order to provide an early detection of interstitial lung involvement secondary to SARS-CoV-2 infection and then evaluate a prolonged steroid treatment recommendation.
{"title":"Histopathogical Lung Patterns of SARS CoV2 Infection","authors":"A. E. Martínez, L. F. Enciso, P. Torres, J. Piraquive, G. Diaz, E. Cortes, C. Rodriguez","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4077","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A4077","url":null,"abstract":"INTRODUCTION: residual lung injury in patients recovering from COVID-19 information is scarce. Herein, we present a previous confirmed SARS-CoV2 infection case series including five patients, who underwent either open or transbronchial lung biopsy due to no clinical improvement. DESCRIPTION: Case 1: a 73-year-old male patient initially asymptomatic, with positive RT-PCR after transurethral resection of the prostate. Consulted for dyspnea and room air desaturation after 24 days during postoperative. Chest computed tomography reported findings compatible with organizing pneumonia, then a transbronchial biopsy was performed confirming diagnosis. Case 2: a 48-year-old male patient with COVID-19 pneumonia who required 14 days hospitalization. He was readmitted after 25 days since initial symptoms due to dyspnea and room air desaturation with a chest CT that revealed findings suggestive of pulmonary fibrosis. Therefore, an open lung biopsy was performed with a probable usual interstitial pneumonia pattern report. Case 3: a 86-year-old male patient, with initial mild COVID-19 infection who later progressed to severe pneumonia requiring high levels of supplemental oxygen. At 18 days of admission, due to persistent clinical compromise, a chest CT was performed with findings of organizing pneumonia. Therefore, he was taken to transbronchial lung biopsy that revealed non-specific interstitial pneumonia in the fibrosing phase. Case 4: a 61-year-old male patient with HIV/AIDS infection presented acute respiratory distress syndrome due to severe COVID-19 pneumonia with inability to withdraw invasive mechanical ventilation after one month. An open lung biopsy was performed with histopathology diagnosis of diffuse alveolar damage in the proliferative phase.Case 5: 41-year-old male patient with severe COVID-19 pneumonia requiring invasive mechanical ventilation, with persistent use of high levels of supplemental oxygen after 30 days since symptomatic. The chest CT suggested pulmonary fibrosis;therefore, an open lung biopsy was performed and confirmed Non-Specific Interstitial Pneumonia. DISCUSSION: to date, reports of interstitial lung disease due to COVID-19 refer to imaging findings or post-mortem histopathological studies which have been relatively limited given the strict guidelines and restrictions for performing bronchoscopies and lung surgery during the pandemic. The foregoing highlights the importance of tissue analysis under rigorous safety protocols in order to provide an early detection of interstitial lung involvement secondary to SARS-CoV-2 infection and then evaluate a prolonged steroid treatment recommendation.","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":"90394900","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：