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Pneumopericardium is a rare medical condition that occurs following trauma, surgery, or other medical interventions. The presence of pneumopericardium after COVID-19 pneumonia has been reported in some cases, and it has been explained that most cases could be self-limited. Here, we describe a 51-year-old man afflicted by pneumopericardium with COVID-19 infection. The patient had pneumopericardium and massive pericardial effusions, necessitating surgical strategies such as pericardial windows. This case highlights the potential severity of COVID-19. We also suggest that cardiologists pay attention to the possibility of pneumopericardium in cases with COVID-19 infection. © 2023, Iranian Heart Association. All rights reserved.
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Case Report: Respiratory distress is one of the most common complaints evaluated by pediatric providers in the office and emergency department setting. While primary cardiopulmonary processes represent the majority of cases of respiratory distress, pleural effusions of extravascular origin remain a rare but important differential. In this case, we present a previously healthy adolescent female who presented to our institution with respiratory distress and was subsequently found to have a pancreatic pleural effusion in the setting of a pancreaticopleural fistula. A 13 year old female with no chronic past medical history presented to the emergency department for three weeks of progressively worsening shortness of breath. History was notable for SARS-CoV-2 infection 6 months prior and intermittent night sweats and fevers for previous 4 weeks. She denied trauma, abdominal pain, nausea, vomiting, diarrhea, or anorexia. Her exam was notable for tachycardia, tachypnea, tripod positioning and absent breath sounds on her left. Chest computed tomography (CT) revealed left pleural effusion of entire left hemithorax with midline shift in addition to right sided pulmonary thromboembolism, small right sided pleural effusion and venous thromboses of the left internal jugular, subclavian, and proximal innominate veins. A left thoracentesis was performed, and patient was admitted to the PICU on a heparin infusion with subsequent left chest tube placement. Follow-up CT imaging revealed bilateral renal infarcts, iliac vein thrombosis, and a pancreatic fluid collection extending into the mediastinum with pancreatic ductal dilation. Magnetic resonance cholangiopancreatography further characterized the pancreatic lesion as a cystic tract traversing from the inferior mediastinum into the retroperitoneum and replacing the majority of the pancreatic gland suggesting a pancreaticopleural fistula as the source of a pancreatic pleural effusion. Serum amylase was 256 U/L and serum lipase was 575 U/L. Pleural fluid amylase was 1702 U/L and pleural fluid lipase was >2400 U/L, exceeding detection limit of this institution's lab. An extensive diagnostic work-up included infectious, hematologic, oncologic, autoimmune and rheumatologic etiologies and was largely unremarkable. Given concern for pancreaticopleural fistula, patient underwent an endoscopic retrograde cholangiopancreatography (ERCP) which was diagnostic for pancreatic divisum. A pancreatic duct stent was placed with normalization of serumpancreatic enzymes prior to discharge and resolution of pleural effusion at one month post ERCP Although an initial episode of acute pancreatitis usually resolves with supportive care, this case is a reminder that pancreatitis can present with local and systemic complications including pulmonary effusion or venous thromboses and keeping a high index of suspicionfor it is crucial toavoid delaying diagnosis and care. Copyright © 2023 Southern Society for Clinical Investigation.
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Case Report: Protein losing enteropathy (PLE) occurs when proteins leak from the gastrointestinal (GI) system more rapidly than they are produced. Inflammation of the GI tract facilitates increased membrane permeability of gastric mucosa, leading to excess protein leakage. 1 PLE in children has been associated with CMV, rotavirus, COVID-19, HIV, C. difficile, and autoimmune diseases like Crohn's Disease. 2-6 Norovirus is a known cause of PLE in immunocompromised pediatric patients. 7-8 However, to our knowledge, there are no case reports about PLE precipitated by norovirus in immunocompetent pediatric patients. The purpose of this case report is to present a case of PLE precipitated by a norovirus infection in a 4- year-old previously healthy child. While the above gastrointestinal viruses have been proposed as precipitators for this disease, PLE precipitated by norovirus infection has not been well described. This case also highlights the importance of early diagnosis and management to avoid complications. Method(s): Our patient initially presented with two days of abdominal pain, diarrhea, emesis, reduced urine output, and swelling of the lower extremities. He was exposed to several sick family members-his sister had upper respiratory symptoms and his grandmother had gastrointestinal symptoms. Physical exam was notable for diminished breath sounds in the right lower lobe, abdominal distension with diffuse tenderness and dullness to percussion, significant scrotal and penile edema, and bilateral lower extremity pitting edema. Laboratory results revealed leukocytosis, hypoalbuminemia, hyponatremia, elevated aspartate aminotransferase (AST), and elevated serum alpha-1-antitrypsin, as well as low Immunoglobulins G and M. CD3 and CD4 levels were low reflecting cellular immune dysregulation seen in patients with PLE. IgA and Tissue Transglutaminase (TTF) were within normal limits. Ebstein Barr Virus and cytomegalovirus IgM antibodies were negative. COVID IgG was negative as well. His Polymerase chain reaction (PCR) gastrointestinal panel was positive for norovirus. A chest X-ray showed a large right pleural effusion. Abdominal CT revealed large ascites slightly more predominant in the upper abdomen, mesenteric lymphadenitis, and bilateral pleural effusions. Echocardiogram showed small anterior and apical pericardial effusions. Result(s): Based on the patient's elevated serum alpha-1 antitrypsin levels, hypoalbuminemia, low levels of immunoglobulins and lymphocytes, and clinical manifestations of ascites, bilateral pleural effusions, pericardial effusion, and dependent edema, along with a positive PCR for norovirus, the diagnosis of PLE secondary to Norovirus was made. Conclusion(s): This case demonstrates the importance of recognizing viruses like Norovirus as potential causes of PLE to avoid a delay in diagnosis and initiation of therapy, and to avoid unnecessary additional testing. Copyright © 2023 Southern Society for Clinical Investigation.
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Objective. To validate risk factors for mortality in patients treated for COVID-19 in a hospital emergency department during the sixth wave of the pandemic. Method. Prospective observational noninterventional study. We included patients over the age of 18 years with a confirmed diagnosis of COVID-19 between December 1, 2021, and February 28, 2022. For each patient we calculated a risk score based on age 50 years or older (2 points) plus 1 point each for the presence of the following predictors: Barthel index less than 90 points, altered level of consciousness, ratio of arterial oxygen saturation to fraction of inspired oxygen less than 400, abnormal breath sounds, platelet concentration less than 100 x 109/L, C-reactive protein level of 5 mg/dL or more, and glomerular filtration rate less than 45 mL/min. The model was assessed with the area under the receiver operating characteristic curve (AUC). Results. Of the 1156 patients included, 790 (68%) had received at least 2 vaccine doses. The probability of 30-day survival was 96%. A risk score was calculated for 609 patients. Four hundred seventeen patients were at low risk of death, 180 were at intermediate risk, and 10 were at high risk. The probability of death within 30 days was 1%, 13%, and 50% for patients in the 3 risk groups, respectively. The sensitivity, specificity, and positive and negative predictive values of a risk score of 3 points or less were 88%, 72%, 19%, 99%, respectively.The AUC for the model was 0.87. Conclusion. The risk model identified low risk of mortality and allowed us to safely discharge patients treated for COVID-19 in our tertiary-care hospital emergency department. Copyright © 2023, Saned. All rights reserved.
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Case Description: 54-year-old man presented to the Emergency Department (ED) three weeks after Covid-19 infection for progressively worsening dyspnea and hypoxemia. Dexamethasone and prophylactic apixaban (2.5mg twice a day) were initiated and he was discharged 48 hours later. A week after discharge he re-presented to the ED requiring 6L of oxygen (O ) despite uninterrupted dexamethasone and apixaban therapy. His past medical history was significant for quiescent IgG4 disease on Rituximab and Type 1 Diabetes. He was afebrile, tachycardic and tachypneic with decreased right lower lobe breath sounds. He had an elevated erythrocyte sedimentation rate and C-reactive protein, no leukocytosis and no pulmonary embolism of CT. He was admitted and vancomycin and cefepime antibiotic therapy for a superimposed bacterial pneumonia was begun. On day 12 of the hospital stay, he experienced new onset chest pain. Evaluation showed an elevated troponin and submillimeter ST segment elevation concerning for an evolving STEMI. Coronary angiography demonstrated an 90% diffuse mid LAD stenosis and two large coronary aneurysms of the left circumflex artery (LCx). The mid-LAD was stented using a 3.0 x 38 mm and 2.75 x 26 mm Onyx drug eluting stents with resolution of his chest pain. IgG4 serum level was normal and imaging did not demonstrate active IgG4 disease. He was discharged on aspirin and clopidogrel. Due to concern for a hypercoagulable state in the setting of Covid 19 infection, IgG4 disease and the large coronary aneurysms for thrombus formation, warfarin anticoagulation was also initiated. On review of his coronary imaging, the largest LCx aneurysm was 9mm on admission and 12mm three weeks later with evidence of diffuse coronary inflammation. CT Fractional Flow Reserve (abnormal <= 0.80) demonstrated decreased flow at the distal aneurysm with no focal stenosis to account for flow reduction. Conclusion(s): 54-year-old man with IgG4 disease presenting with prolonged Covid-19 infection and acute NSTEMI. He was found to have large, flow limiting coronary aneurysms and inflamed coronary arteries all consistent with his IgG4 disease. Management of these aneurysms will be discussed.
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BACKGROUND: Small percentage of catheter-related bloodstream infection may present atypically with persistent low-grade fever without chills and rigor and in some of these cases blood culture can be negative. These may lead to diagnostic confusion and delay in detection of the common entity of catheter-related blood stream infections. AIM OF THE STUDY: Case discussion with learning points METHODS: We report a case with multiple pictorial images and discuss differential diagnosis with few learning points. RESULT(S): 42-year-old male patient, a known case of end-stage chronic kidney disease on maintenance hemodialysis through a tunneled catheter, presented with a history of intermittent, low-to-moderate fever for 3 weeks. The fever associated with generalized weakness, night sweats but was not associated with chill and rigor. His past medical history included endstage chronic kidney disease due to chronic glomerulonephritis and was on maintenance hemodialysis thrice weekly for last 6 months through tunneled catheter in right IJV. On physical examination, the patient had tachycardia, normotension with a blood pressure of 120/70.mmHg, normal saturation at room air with respiratory rate of 20 /minute. On auscultation, there was reduced breath sounds on left side and normal heart sounds. The catheter site showed no heat, erythema, swelling, tenderness. Chest radiograph revealed left hydropneumothorax with multiple focal pulmonary nodular opacities. CECT chest showed left loculated hydropneumothorax with multiple cavitary nodules with reverse halo sign (Figures 1 and 2). Lab investigations showed significant leukocytosis with neurophilia, random serum glucose of 250.mg/dL, and D-dimer of 3624.ng/mL. Blood cultures from hemodialysis catheter and contralateral peripheral vein were negative for pathogenic bacteria, mycobacteria, and fungal etiology. Urine analysis was sterile and did not have pus cells. On day 4 of admission, patient had left axillary pain. On clinical examination, there was focal tenderness on examination in the left axilla. On ultrasonography, there was a small collection which was aspirated under ultrasound guidance and showed gram-positive bacteria on microscopy. Trans esophageal echocardiography revealed multiple tiny vegetations on right side of interatrial septum on tricuspid valve (Figure 3). Subsequent culture results showed methicillin resistant staphylococcus sensitive to clindamyin, vancomycin, linezolid, ciprofloxacin (Figure 4 and 5). The patient was started on vancomycin and ceftazidine on empirical basis for microscopic findings, and after subsequent culture revealed methicillin-resistant Staphylococcus aureus, he was treated with vancomycin. Permanent catheter was removed. Hemodialysis was continued through temporary right IJV catheter. Blood cultures were cleared from MRSA on hospital day ten. She got discharged home on intravenous Vancomycin for 6-8 weeks and was reported doing well on follow-up. CONCLUSION(S): The learning points are- 1. MRSA infection is common in chronic kidney disease patient on hemodialysis. 2. Clinical presentation of metastatic MRSA infection with infective endocarditis may be indolent with cardiovascular and respiratory stability with absence of fever spikes, chill, and rigor. 3. Common infective causes of cavitary nodules in lung are typical and atypical mycobacterial infection, fungal infection, and pyogenic septic emboli. 4. Uncommon infective causes of reverse halo sign on CT chest need to be remembered and include bacterial pneumonia, septic embolism, mycobacterial infection, invasive aspergillosis, in addition to common infective etiology of reverse halo sign like mucormycosis infection and COVID19 infection.
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Introduction: Cefepime is a commonly used parenteral antibiotic for severe infections.85% of the drug is excreted renally and crosses the blood-brain barrier. Cefepime-induced neurotoxicity (CIN) manifests as encephalopathy, myoclonus and seizures. It is reported in patients with renal impairment if administered in high dosage. CIN is reversible after drug discontinuation and faster clinical recovery is achieved by intermittent hemodialysis (IHD). Case Description: A 53-year-old female with a history of sleep apnea, obesity, recent COVID pneumonia presented with worsening dyspnea on exertion for 5 days. Physical examination revealed tachycardia, tachypnea, diminished breath sounds at lung bases. Admission laboratory results were a creatinine (Cr), 0.96 mg/dl;BUN, 18 mg/dl. Chest x-ray showed bilateral ground glass pulmonary opacities. Patient was started on Vancomycin 2 g IV every 12 hours and Cefepime 2 g IV every 8 hours. On day 2 she was in septic shock due to E.Coli bacteremia, intubated and started on pressors. Vancomycin was discontinued. On day 8 Cr increased to 1.49 mg/dl. Patient remained on Cefepime without dosage change for six more days despite glomerular filtration rate decreased to 20 ml/min/1.73 m2. On day 18 patient was noted to have altered mental status and jerking movements of upper extremities and head. Cefepime was stopped, Cr peaked at 3.95 mg/dl, BUN was 130 mg/dl at that time. CT scan of head was negative for acute findings. EEG showed focal cortical hyperexcitability, no seizure activity. Cr increased to 4.41 mg/dl, IHD was started. After two IHD sessions jerking movements disappeared, and consciousness improved. Work up for acute kidney injury (AKI) revealed negative Hepatitis B,C, HIV serology. ANA, ANCA serology was negative. Patient regained renal function within 1 week after six IHD sessions. Discussion(s): CIN is a known complication in patients with renal dysfunction but remains challenging to recognize in critically ill patients. Our patient had various causes of altered mental status: shock, hypoxemia, uremia. Despite decline in renal function cefepime dose was not adjusted and patient developed CIN which required emergent hemodialysis initiation. A high index of suspicion for CIN is critical when evaluating a patient with AKI. Discontinuation of cefepime and emergent IHD initiation leads to resolution of neurological symptoms within 48 hours.
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Introduction. Acute myocarditis is a potential life-threatening disease and left ventricular thrombus could be a complication. Nowadays, myocarditis has been observed after SARS-CoV-2 vaccination. We report the case of a young adult female with left ventricular thrombus secondary to COVID19 mRNA vaccine-related acute myocarditis. Case report A 33-year-old afro-descendant female was admitted to the ED with dyspnea, heart-pounding and chest pain. The EKG showed sinus tachycardia with diffuse changes in repolarization. The lab tests showed: TnHS 8437 ng/mL, C-reactive protein 3,8 mg/dL, normal white blood cell count, NTproBNP 3800 pg/mL, GOT 171 UI/l, GPT 57 UI/l. She received the first dose of mRNA SARS-CoV-2 vaccine 21 days earlier. The PCR swab test for SARS-CoV-2 was negative. Clinical examination revealed HR 110 bpm, BP 105/75 mmHg, normal lung sounds, tachycardic heart sounds. Transthoracic echocardiogram showed EF 25%, massive apical adherent thrombus and mild diffuse pericardial effusion. Serological analysis for viral and bacterial infection were negative. Coronary angiography, cardiac- MRI, myocardial biopsy were not performed because of patient refuse and claustrophobia. LMWH 8000 UI bid, Ibuprofen 600 mg tid and Colchicine 0,5 mg/die were administered. The patient was discharged after 14 days with no symptoms, no residual thrombus and total EF recovery. The alleged adverse event was reported to the National Pharmacovigilance Network. Conclusions Myocarditis is a potential consequence of both COVID-19 and its mRNA vaccines. Post-vaccine myocarditis is usually self-limiting with a low rate of consequences.
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Background: Palytoxin poisoning is an uncommon exposure in the US, and is most frequently encountered amongst hobbiests and professionals in the aquarium industry. The toxin is produced by the microalgae Ostreopsis as well as the coral Palythoa toxica. Discovered in Hawaii, the name limu-make-o-Hana translates to "seaweed of death from Hana." Palytoxin interrupts Na+/ K+ ATPase pump, resulting in widespread cellular dysfunction. Persons are at highest risk when cleaning a fish tank housing the coral that produces palytoxin, resulting in cutaneous or inhalational exposure. We present a case of palytoxin inhalational exposure with computed tomography (CT) imaging. Case report: A 41-year-old male presented to the emergency department (ED) with dyspnea, cough, and wheezing after cleaning his saltwater fish tank. He reported that he maintains Zoanthid corals in his home saltwater fish tank and typically wears personal protective equipment when cleaning the tank. He had taken off his mask directly after using hot water to clean the tank, and quickly developed shortness of breath. He contacted Poison Control and was instructed to take loratadine with initial improvement in his symptoms. He then developed decreased appetite, nausea, and chills. The following day, in addition to these symptoms, he developed a fever of 102.5 degreeF and an oxygen saturation of 88% measured with an at-home pulse oximeter. He then proceeded to the ED where he was found to be hypoxic to 91% on room air, tachycardic to 120 bpm, hypotensive to 93/ 70mmHg, febrile to 100.9 degreeF and tachypneic at a respiratory rate of 30. Physical exam revealed clear lung sounds. Application of supplemental oxygen at 2 L resulted in improvement in his oxygen saturation and his hypotension and tachycardia responded to intravenous fluids. Significant laboratory results included WBC count of 20.4 with bands of 14%, elevated lactate of 2.4mmol/L, elevated D-dimer of 0.48 mug/mL and a negative COVID PCR test. CTA thorax revealed patchy ground-glass opacities in the bilateral upper and lower lobes with mosaicism. The patient received doxycycline in addition to broad spectrum antibiotics due to concern for inhalational marine toxicity. He was also started on 60mg prednisone, inhaled steroids, and bronchodilators for symptomatic treatment, with improvement in his symptoms. During his hospitalization, a respiratory viral panel was negative for common viruses associated with atypical pneumonia including influenza, coronavirus, metapneumovirus, rhinovirus, enterovirus, adenovirus, parainfluenza, bocavirus, Chlamydophila pneumoniae, and Mycoplasma pneumonia. His dyspnea gradually improved and he was weaned off supplemental oxygen prior to discharge home on hospital day 2. Discussion(s): It is unclear what changes are expected on thoracic imaging in patients with inhalational palytoxin exposure. Chest radiographs in two previous cases displayed scattered infiltrates, and a chest CT in another case showed pleural based consolidations. The ground-glass mosaicism suggests that a more diffuse reactive airway process after an inhalational palytoxin insult. Conclusion(s): Patients with inhalational palytoxin exposure may be found to have reactive airway symptoms along with ground glass opacities with mosaicism on CT imaging.
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SESSION TITLE: Challenging Cases of Hemophagocytic Lymphohistiocytosis SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Worsening respiratory disease is the most common complication of severe COVID-19. However, when patients develop multi-organ dysfunction, clinicians must have a high index of suspicion for rare syndromes such as hemophagocytic lymphohistiocytosis (HLH). CASE PRESENTATION: A 39-year-old male smoker presented with 1 week of shortness of breath and malaise. Initial physical examination revealed T 37.3 C, pulse 85 min-1, respiratory rate 18 breaths min-1, SPO2 96% and clear breath sounds without labored respirations. Chest X-ray showed bilateral patchy airspace opacities in the mid and lower lung fields. A SARS-COV2 PCR test was positive. The patient was prescribed antibiotics and discharged home. Subsequently, the patient's symptoms worsened and he presented 1 week later with SPO2 90% (O2 10 L/min via nasal cannula). He was admitted to the hospital with COVID-19 pneumonia and began remdesivir, barcitinib, systemic steroids, albuterol and IV antibiotics. On admission his complete blood count and complete metabolic panel were unremarkable. After 3 weeks of hospitalization, he developed multi-organ failure with acute liver injury, acute kidney injury, shock, pancytopenia and worsening hypoxemia leading to endotracheal intubation and mechanical ventilation. CT chest imaging showed bilateral ground glass opacities in the lungs with superimposed consolidation (figure 1). Blood cultures remained sterile, HIV, hepatitis B and C viral serologies were negative. Serum viral polymerase chain reaction detected Herpes Simplex Virus-1 (HSV-1) and Epstein Barr Virus (EBV) infections. Trans-jugular liver biopsy confirmed HSV-1 hepatitis and showed sub-massive hemorrhagic necrosis of the liver (figure 2). Bone marrow biopsy demonstrated phagocytic histiocytes engulfing red blood cells and platelets consistent with HLH (figure 3). The patient began HLH targeted therapy with anakinra and high dose steroids. Despite this, the patient continued to deteriorate, developed refractory shock and subsequently expired. DISCUSSION: HLH is a rare disease of the immune system in which a genetic or infectious trigger causes uncontrolled T cell activation. T cell activation triggers macrophage activation, cytokine storm and macrophage phagocytosis of erythrocytes, leukocytes, platelets and precursors in the bone marrow and other tissues. If the syndrome is unrecognized, it can quickly lead to multi-organ failure and death. EBV is the most common infectious trigger of HLH;however, infection with HSV-1 and SARS-COV-2 viruses have been identified as rare and independent causes. CONCLUSIONS: This case illustrates the high index of suspicion providers should have for HLH in patients with severe COVID-19 who develop multi-organ injuries. Once HLH is suspected, prompt initiation of HLH-94 protocol with etoposide and dexamethasone may be lifesaving. For those patients with liver failure, other agents (e.g. anakinra) may be provided. Reference #1: Ramos-Casals M, Brito-Zerón P, López-Guillermo A, et al.: Adult haemophagocytic syndrome. Lancet 2014;383:1503–1516 Reference #2: Risma K, Jordan MB: Hemophagocytic lymphohistiocytosis: updates and evolving concepts. Curr Opin Pediatr 2012;24:9–15 Reference #3: Trottestam H, Horne A, Aricò M, et al.: Chemoimmunotherapy for hemophagocytic lymphohistiocytosis: long-term results of the HLH-94 treatment protocol. Blood 2011;118:4577–4584 DISCLOSURES: No relevant relationships by Erin Biringen No relevant relationships by Christine Brennan No relevant relationships by Joann Hutto No relevant relationships by Daniel Puebla Neira
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SESSION TITLE: Pathologies of the Post-COVID-19 World SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Since the start of the COVID-19 pandemic, COVID-19 Associated Pulmonary Aspergillosis (CAPA) has been on the rise. This superinfection, if not properly identified and treated, has shown to increase mortality up to 67% in COVID-19 patients. We are presenting a late presentation of CAPA after 4-month of COVID-19 infection and treated successfully. CASE PRESENTATION: A 57-year-old female patient with past medical history type 2 diabetes mellitus, hypertension and cardiomyopathy in addition to COVID-19 pneumonia treated for months ago with azithromycin, Bamlanivimab/Etesevimab, and Dexamethasone who presents to the hospital with massive hemoptysis and shortness of breath requiring intubation and mechanical ventilation. There was no reported history of recent travel, smoking, alcohol, or illicit drug use. Physical exam showed diminished lung sounds at the right lower lobe. Her labs showed mild leukocytosis, lactic acidosis and negative COVID-19 PCR. CT scan showed dense consolidation on right lower lobe consistent with lobar pneumonia and centrilobular ground glass opacities in the right upper lobe. Bronchoscopy showed complete obstruction of right bronchus intermedius and minimal blood clots in LLL. BAL respiratory culture, fungal smear, acid fast bacilli were non-diagnostic and negative for malignancy. Patient continued to have hemoptysis and bronchoscopy was repeated with negative cytology and cultures. The patient continued to have hemoptysis and she was transferred to tertiary center were bronchoscopy was repeated and confirmed right bronchus intermedius stenosis, blood clots, and suspicious right mainstem nodules with mucosal lesion. Biopsy results from bronchoscopy came back positive for the morphologic features of Aspergillus species. The patient was started on voriconazole with significant improvement in her symptoms. DISCUSSION: The recent literature of COVID-19 suggest association between COVID infection and invasive pulmonary Aspergillosis. COVID-19 virus causes damage in the airway epithelium and enable aspergillus to invade the pulmonary tract leading to serious infections with Aspergillus. It has also been known that Aspergillus infections are associated with diabetes mellitus and immune suppression which can be precipitated by steroid use and other treatments for COVID-19 infection like IL-6 inhibitors. Here in our patient with help of tissue biopsy we diagnosed CAPA, started treatment early and treated successfully. CONCLUSIONS: CAPA can be difficult to diagnose and needs high index of suspicion in the appropriate clinical scenario when dealing with post COVID respiratory complaints like hemoptysis. Bronchoalveolar lavage alone without tissue biopsy might miss the diagnosis in the context of invasive aspergillosis like the scenario we observed in our case. Doing tissue biopsy through bronchoscopy might add more clinical benefit when Aspergillus infections are suspected. Reference #1: Chih-Cheng Lai, Weng-Liang Yu, COVID-19 associated with pulmonary aspergillosis: A literature review, https://doi.org/10.1016/j.jmii.2020.09.004 DISCLOSURES: No relevant relationships by Haytham Adada No relevant relationships by Mahmoud Amarna No relevant relationships by Rishika Bajaj No relevant relationships by Camelia Chirculescu No relevant relationships by Sonia Dogra No relevant relationships by Azad Patel
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SESSION TITLE: Cardiovascular Complications in Patients with COVID-19 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Even though COVID-19 is the largest pandemic of the twenty-first century, little is known about the disease or its management. Remdesivir has demonstrated some activity against severe ARDS associated with COVID-19. There is a dearth of data on the adverse effects of Remdesivir. We report a case of a COVID-19 patient who developed bradycardia following the administration of Remdesivir. CASE PRESENTATION: A 64-year-old man, who tested positive for COVID-19, presented with shortness of breath (SOB) for a week. SOB was accompanied by a cough with tan-colored sputum. Past medical history included hypertension and benign prostatic hyperplasia. Physical examination showed regular rate and rhythm of the heart and diffusely decreased breath sounds. His blood pressure was 104/60 mmHg and his heart rate was 80 bpm. Oxygen saturation was 58% at room air. Significant lab results showed elevated CRP: 17.13 mg/dl, D-Dimer: 10.16 ug/mL FEU, Lactic acid: 2.5 mg/dl, Creatinine: 1.8 mg/dl, BUN: 60 mg/dl, and AST: 46 U/L. Chest x-ray showed bilateral patchy interstitial airspace opacities. Calculated Well's score of 3 indicated a moderate risk for pulmonary embolism. CT scan showed moderate bilateral diffuse areas of ground-glass lung consolidation concerning diffuse atypical infection. The patient was admitted to the ICU and started on CPAP with PEEP of 12 and FiO2 of 100%. The management included dexamethasone 6 mg oral for 10 days, Remdesivir for 5 days, and Tocilizumab given elevated CRP level. The patient was found to develop asymptomatic bradycardia with a heart rate as low as 40 bpm. An EKG obtained demonstrated sinus bradycardia without any heart block. Echocardiography showed mildly dilated right ventricle & mild aortic regurgitation. Bradycardia resolved after the last dose of Remdesivir. DISCUSSION: Remdesivir is frequently used in severe COVID-19 infections. The commonly reported adverse events affect the gastrointestinal and renal systems. The reported cardiovascular adverse events include hypotension, atrial fibrillation, and cardiac arrest. However, bradycardia is becoming increasingly encountered. Although corticosteroids are known to cause bradycardia, the patient we managed developed bradycardia following remdesivir therapy. The baseline EKG was normal and the history was non-contributory. Given the asymptomatic nature of the finding, cardiac monitoring alone sufficed. The heart rate picked up following the last dose of remdesivir further suggesting its causative role. CONCLUSIONS: Bradycardia is becoming more common with Remdesivir use. If the patient is not exhibiting any symptoms, cardiac monitoring alone should suffice;bradycardia is expected to resolve when the drug is stopped. Reference #1: Elsawah HK, Elsokary MA, Abdallah MS, ElShafie AH. Efficacy and safety of remdesivir in hospitalized Covid-19 patients: Systematic review and meta-analysis including network meta-analysis. Rev Med Virol. 2021;31(4):e2187. Reference #2: Taqi M, Gillani SFUHS, Tariq M, Raza ZA, Haider MZ. Current updates on clinical management of COVID-19 infectees: a narrative review. Rev Assoc Med Bras (1992). 2021 Aug;67(8):1198-1203. doi: 10.1590/1806-9282.20210582. PMID: 34669870. DISCLOSURES: No relevant relationships by AISHA ADIGUN No relevant relationships by Mobeen Haider No relevant relationships by Yousra Khalid No relevant relationships by Muhammad Hasib Khalil No relevant relationships by Aleena Naeem No relevant relationships by Zarlakhta Zamani
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SESSION TITLE: COVID-19 Co-Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: SARS-CoV-2 has been associated with co-infecting pathogens, such as bacteria, viruses, and fungi. Little has been reported about community acquired atypical bacterial co-infections with SARS-CoV-2. We present a case of a patient with recent COVID-19 pneumonia and diagnosis of Legionella and Mycoplasma pneumonia, in addition of E. coli and C. perfringens bacteremia, that emphasizes SARS-CoV-2 impact in human immunity and the need to consider community acquired infections. CASE PRESENTATION: A 64-year-old male with history of hypertension, alcohol use disorder, iron deficiency anemia, and recent COVID-19 pneumonia presented to the ED with shortness of breath, dark urine, and increased confusion. The patient was admitted to the hospital a week prior with COVID-19 pneumonia and acute kidney injury. He received dexamethasone, remdesivir, and IV fluids. After 8 days, he was discharged home. Upon evaluation, he was afebrile and normotensive, but tachycardic, 129/min, on 4 L of nasal cannula sating 100%. On exam, the patient was oriented only to person and had decreased breath sounds bilaterally. Labs revealed an elevated WBC, 15.3 K/mcL, with left shift, low Hgb, 7.8 g/dL, with low MCV, 61 fL, increased BUN/Cr, 56 mg/dL and 2.8 mg/dL, and an abnormal hepatic panel, AST 121 U/L, ALT 45 U/L, alkaline phosphatase 153 U/L. Ammonia, GGT, CPK and lactic acid were within normal range;but the D-dimer and procalcitonin were elevated, 4618 ng/mL and 25.12 ng/mL, respectively. A urinalysis showed gross pyuria, positive leukocyte esterase and mild proteinuria. CT head showed no acute abnormalities, but the chest X-Ray revealed a hazy opacity in the left mid and lower lung, followed by a CT chest that demonstrated peripheral and lower lobe ground glass opacities and a CT abdomen that showed right sided perinephric and periureteral stranding. Given increased risk for thromboembolism, a VQ scan was done being negative for pulmonary embolism. The patient was admitted with acute metabolic encephalopathy, acute kidney injury, transaminitis, pyelonephritis and concern for hospital acquired pneumonia. Vancomycin, cefepime and metronidazole were ordered. HIV screen was negative. COVID-19 PCR, Legionella urine antigen and Mycoplasma IgG and IgM serologies were positive. Blood cultures grew E. coli and C. perfringens. Infectious Disease and Gastroenterology were consulted. The patient was started on azithromycin and a colonoscopy was done showing only diverticulosis. After an extended hospital course, the patient was cleared for discharge, without oxygen needs, to a nursing home with appropriate follow up. DISCUSSION: Co-infection with bacteria causing atypical pneumonia and bacteremia should be considered in patients with recent or current SARS-CoV-2. CONCLUSIONS: Prompt identification of co-existing pathogens can promote a safe and evidence-based approach to the treatment of patients with SARS-CoV-2. Reference #1: Alhuofie S. (2021). An Elderly COVID-19 Patient with Community-Acquired Legionella and Mycoplasma Coinfections: A Rare Case Report. Healthcare (Basel, Switzerland), 9(11), 1598. https://doi.org/10.3390/healthcare9111598 Reference #2: Hoque, M. N., Akter, S., Mishu, I. D., Islam, M. R., Rahman, M. S., Akhter, M., Islam, I., Hasan, M. M., Rahaman, M. M., Sultana, M., Islam, T., & Hossain, M. A. (2021). Microbial co-infections in COVID-19: Associated microbiota and underlying mechanisms of pathogenesis. Microbial pathogenesis, 156, 104941. https://doi.org/10.1016/j.micpath.2021.104941 Reference #3: Zhu, X., Ge, Y., Wu, T., Zhao, K., Chen, Y., Wu, B., Zhu, F., Zhu, B., & Cui, L. (2020). Co-infection with respiratory pathogens among COVID-2019 cases. Virus research, 285, 198005. https://doi.org/10.1016/j.virusres.2020.198005 DISCLOSURES: No relevant relationships by Albert Chang No relevant relationships by Eric Chang No relevant relationships by KOMAL KAUR No relevant relationships by Katiria Pintor Jime ez
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SESSION TITLE: Issues After COVID-19 Vaccination Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Since the onset of the COVID-19 pandemic, vaccines were introduced to mitigate the spread of the virus. Depending on the COVID-19 vaccine, regimens consist of one dose (ie, J&J) or two doses (ie, Pfizer and Moderna) and is followed by a third dose/booster (for immunocompromised/immunocompetent individuals). Here, we present a case of COVID-19 infection in a triple vaccinated patient with concurrent rheumatoid arthritis (RA) receiving disease modifying antirheumatic drugs (DMARDs) who was unable to mount an adequate immune response to the vaccine. CASE PRESENTATION: Patient is a 67 year old male with PMH of RA (on DMARDs) presented to the ED with complaints of shortness of breath. He was on treatment for RA with leflunomide, rituximab and prednisone. He was COVID-19 triple vaccinated. In ED, the patient was found to be hypoxic, saturating at 87% on room air with a respiratory rate of 18. Physical examination was significant for coarse breath sounds bilaterally and remaining vitals were unremarkable. Patient was initially placed on 3 L oxygen via NC but due to persistent hypoxia, was transitioned to high-flow nasal cannula. Further investigations revealed that the patient was COVID-19 positive. He was treated with remdesivir and dexamethasone. His oxygen requirements continued to escalate and he was ultimately intubated. While in the ICU, the patient's hypoxia continued to worsen despite optimal medical and ventilatory management and he subsequently died. DISCUSSION: DMARDs are a group of medications used to slow the progression of rheumatoid arthritis. They work by reducing the immune response of B cells, T cells and cytokines. Our patient was on two commonly prescribed medications for rheumatoid arthritis, leflunomide and rituximab. The former acts by inhibiting the pyrimidine synthesis pathway, thereby decreasing T lymphocyte production and the latter depletes CD-20 positive B cells. While there is limited data on COVID-19 vaccine, it has been established that patients on DMARDs have reduced antibody titres after immunization against influenza and pneumonia vaccinations [1, 2]. A study assessing the effectiveness of a third vaccine dose in patients taking rituximab vs placebo found a significant difference in seroconversion (78.8% vs 18.2%, p=<0.0001) and neutralizing activity (80.0% vs 21.9%, p=<0.0001) [3]. In our case, the patient was on two immunosuppressive drugs which suppressed both the humoral and cell mediated immunity, resulting in an inadequate immune response and subsequently developing COVID. CONCLUSIONS: This case highlights patients on immunosuppressant therapy failing to mount an adequate immune response to the COVID-19 vaccine, warranting more booster doses in patients on DMARDs. Reference #1: Adler S, Krivine A, Weix J et al. Protective effect of A/ H1N1 vaccination in immune-mediated disease–a prospectively controlled vaccination study. Rheumatology 2012;51:695–700. Reference #2: Franca ILA, Ribeiro ACM, Aikawa NE et al. TNF blockers show distinct patterns of immune response to the pandemic influenza A H1N1 vaccine in inflammatory arthritis patients. Rheumatology 2012;51:2091–8. Reference #3: David S, Koray T, Filippo F et al. Efficacy and safety of SARS-CoV-2 revaccination in non-responders with immune-mediated inflammatory disease. http://dx.doi.org/10.1136/annrheumdis-2021-221554 DISCLOSURES: No relevant relationships by Gursharan Kaur No relevant relationships by Aishwarya Krishnaiah No relevant relationships by sandeep mandal
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SESSION TITLE: Critical Care Presentations of TB SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: TNFα plays a pivotal role in inflammation and maintenance of immune response against tuberculosis. The use of TNF inhibitors (TNFi) is associated with a significant increase in the incidence of tuberculosis (TB). TNFi may cause drug-induced lupus (ATIL) presenting as constitutional symptoms, rashes, pericardial and pleural effusions with positive autoantibodies. We present a case of pleural TB masquerading as drug-induced lupus. CASE PRESENTATION: A 68y/o woman with a history of ulcerative colitis (on infliximab, mesalamine), hypertension, T2DM, CAD, complained of low-grade fever, rashes, left-sided chest pain, dyspnea, and arthralgias for two weeks. Chest pain- worse with inspiration and cough. She emigrated from India to the USA 40 years ago. Six months before infliximab therapy, Quantiferon gold was negative. Exam: faint hyperpigmentation over shins, minimal swelling of MCPs and ankles, dullness to percussion over the left chest with decreased breath sounds. Labs: CRP 101 mg/dL, Hb 10.8 iron deficient, rheumatoid factor and anti-CCP negative, ANA 1:40, dsDNA 1:640, a reminder of ENA negative, anti-histone negative, C3/C4 normal, UA bland, protein/Cr 0.4 mg/gm, negative blood cultures, SPEP and LDH normal. CXR: opacification of the left lung up to midfield. CT chest: moderate left and small right pleural effusions, enlarged mediastinal lymph nodes. COVID and Quantiferon: negative. Thoracentesis: 850 ml of exudative fluid (2 out of 3 Light's criteria), lymphocytic predominance (76% of 4148 nucleated cells), adenosine deaminase (ADA) 42 U/L, gram stain, culture, acid-fast and MTB PCR negative, cytology negative. Thoracoscopy with biopsy of the parietal pleura: necrotizing granulomatous pleuritis with acid-fast bacilli. Sensitivity: pan-sensitive M. tuberculosis. Sputum: negative for TB. She was discharged on RIPE treatment for reactivation of TB. DISCUSSION: The incidence of infliximab-induced lupus is approximately 0.19% and confirming the diagnosis is challenging. The immunogenicity of infliximab is high, 66% of patients develop positive ANA. Anti-histone antibodies are less commonly associated with ATIL as opposed to classic drug-induced lupus and dsDNA is positive in up to 90% of cases of ATIL. Renal involvement is rare. The diagnostic usefulness of ADA (over 40 U/L) in lymphocytic pleural effusions for the diagnosis of tuberculosis in an immunosuppressed individual is demonstrated here. In countries with low TB burden, such as the USA, the positive predictive value of ADA in pleural fluid declines but the negative predictive value remains high. CONCLUSIONS: Tuberculous pleuritis is not always easily diagnosed since AFB smears and sputum may remain negative. When ADA level in lymphocytic pleural fluid is not low thorough search for TB with thoracoscopy and biopsy is justified. Reference #1: Shovman O, Tamar S, Amital H, Watad A, Shoenfeld Y. Diverse patterns of anti-TNF-α-induced lupus: case series and review of the literature. Clin Rheumatol. 2018 Feb;37(2):563-568. Reference #2: Benucci, M., Gobbi, F. L., Fossi, F., Manfredi, M. & Del Rosso, A. (2005). Drug-Induced Lupus After Treatment With Infliximab in Rheumatoid Arthritis. JCR: Journal of Clinical Rheumatology, 11 (1), 47-49. Reference #3: Valdés L, San José ME, Pose A, Gude F, González-Barcala FJ, Alvarez-Dobaño JM, Sahn SA. Diagnosing tuberculous pleural effusion using clinical data and pleural fluid analysis A study of patients less than 40 years-old in an area with a high incidence of tuberculosis. Respir Med. 2010 Aug;104(8):1211-7. DISCLOSURES: No relevant relationships by Adam Adam No relevant relationships by Moses Bachan No relevant relationships by Chen Chao No relevant relationships by Zinobia Khan No relevant relationships by Milena Vukelic
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SESSION TITLE: Rare Cases with Masquerading Pulmonary Symptoms SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: COVID vaccinations have been encouraged by many healthcare providers but many adverse effects have also been reported. The adverse effects of the vaccine can vary based on each individual. Common adverse effects of the vaccine included fatigue, fever, chills, sore throat, muscle pain, headache, rash at injection site. Pleurodynia, also known as Devil's Grip, is a viral myalgia which causes sharp chest pain or the sensation of a grip around one's chest. Pleurodynia treatment is mostly supportive like anti-inflammatories (NSAIDS), pain management, and antibiotics (if bacterial inflammation is suspected). CASE PRESENTATION: We present a case report of a 63-year-old female who presented with complaints of pleuritic chest pain worse with inspiration. She had a history of atrial fibrillation and HTN. Patient had received the Pfizer COVID booster vaccine a few days prior to onset of the pleuritic chest pain. She was obese and had a 40 pack year smoking history. She was on room air saturating 92% with no increased work of breathing. Lung sounds were diminished due to body habitus but clear. Chest x-ray showed low lung volumes with no evidence of acute pulmonary disease. Computed Tomography Angiography (CTA) chest showed no pulmonary embolism and small left partially loculated pleural effusion with peripheral airspace opacities abutting the pleura. Acute coronary syndrome was ruled out and other cardiac workup was negative. COVID PCR was negative. Patient was treated empirically for bacterial infection with ceftriaxone and azithromycin. She was given NSAIDS to decrease inflammation and pain. Patient's symptoms improved significantly with treatment. She was discharged on NSAIDS and advised to follow up outpatient with her primary care and pulmonology. DISCUSSION: Research studies have indicated that the COVID vaccines (like Pfizer) can cause exacerbation of inflammatory or autoimmune conditions. Multiple mechanisms may be responsible for myocarditis, pericarditis, and other inflammatory conditions post vaccines. One mechanism describes that lipid particles of SARS mRNA vaccines can induce inflammation by activating the NLR pyrin domain containing 3 inflammasome of mRNA which are recognized by toll like receptors and cytosolic inflammasome components leading to inflammation. Another mechanism explains that viral proteins can cause immune cross reactivity with self-antigens expressed in the myocardium leading to an inflammatory process. CONCLUSIONS: As per current literature review there are no case reports about pleurodynia post COVID vaccination but pericarditis and myocarditis have been described. Further research studies are indicated to assess the cause and pathophysiology of pleurodynia post COVID vaccine. Physicians should have a high index of clinical suspicion for pleurodynia when assessing a patient with pleuritic chest pain with a recent history of COVID vaccination. Reference #1: 1. Analysis of COVID 19 Vaccine Type and Adverse Effects Following Vaccination. Beatthy, A;Peyser, N;Butcher, X. AMA Netw Open. 2021;4(12):e2140364. doi:10.1001/jamanetworkopen.2021.40364 Reference #2: 1. Association of Group B Coxsackieviruses with Cases of Pericarditis Myocarditis, or Pleurodynia by Demonstration of Immunoglobulin M Antibody. Schmidt, N;Magoffin, R;& Lennette, E. Infection and Immunty Journal. 1973 Sep;8(3): 341–348. PMCID: PMC422854 Reference #3: 3. Autoimmune phenomena following SARS-CoV-2 vaccination. Ishay, Y;Kenig, A;Toren, T;Amer, R;et. al. International Journal of Immuno-pharmacology. 2021 Oct;99: 107970. DISCLOSURES: No relevant relationships by Olufunmilola Ajala No relevant relationships by Arij Azhar No relevant relationships by Louis Gerolemou No relevant relationships by Wael Kalaji No relevant relationships by Steven Miller No relevant relationships by Kunal Nangrani No relevant relationships by Gaurav Parhar No relevant relationships by iran Zaman
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SESSION TITLE: Dyspne Mysteries SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Anti-synthetase (AS) syndrome is characterized by interstitial lung disease (ILD), arthritis, myositis, fever, or Raynaud's phenomenon in the presence of an AS autoantibody (1). At least 70% of patients with AS syndrome develop ILD (2), and it represents the major cause of mortality in these patients with a 10 year survival rate of 73%. In a small cohort study, the anti-PL-12 antibody subtype was found to be strongly associated with ILD (3). CASE PRESENTATION: A 35 year old female with a history of tobacco use disorder presented to the hospital with three months of recurrent subjective fevers, non-productive cough, and dyspnea on exertion. She denied arthralgias, muscle weakness and hemoptysis. She initially presented to her primary care physician with these symptoms and was prescribed amoxicillin for streptococcal pharyngitis. The patient continued to be symptomatic and was treated empirically for COVID-19 pneumonia twice despite two negative COVID-19 tests and without any significant clinical improvement in her respiratory status. On admission, she was febrile, tachycardic, and had a new oxygen requirement with bilateral coarse breath sounds on exam. She had no leukocytosis and her COVID-19 test was negative. CT angiography of the chest showed extensive mixed reticular and airspace opacities with peribronchial predilection and peripheral sparing (figure 1). A bronchial alveolar lavage was notable only for neutrophilia (19%) and eosinophilia (4%). Rheumatological workup revealed elevated rheumatoid factor, positive antinuclear antibody (1:40), weakly positive anti–Sjögren's-syndrome-related antigen A antibody (50 AU/ml), undetectable anti-Jo-1 antibody and positive anti-PL-12 antibody. Pulmonary function testing revealed a TLC of 40% and DLCO of 28%, consistent with a restrictive pattern. Considering the patient's organizing pneumonia, positive antibodies, and findings of "mechanic's hands,” the patient was diagnosed with anti-synthetase syndrome with ILD. She was started on oral prednisone and mycophenolate mofetil. On follow-up, she was noted to have symptomatic improvement and stable hypoxia without clinical signs of disease progression. DISCUSSION: During the coronavirus pandemic, the resemblance of COVID-19 pneumonia to other diseases, in the absence of conscious suspicion for other etiologies, can lead to anchoring and availability bias thereby delaying diagnosis and appropriate treatment. Additionally, anti-synthetase syndrome should be considered in the differential diagnosis of ILD even in the absence of arthritis and myositis, as respiratory symptoms are often the first presenting signs. CONCLUSIONS: Increased responsibility is required of diagnosticians to exercise due diligence and active recognition of COVID availability and anchor bias to avoid missing crucial diagnoses. Reference #1: Cojocaru, Manole, Inimioara Mihaela Cojocaru, and Bogdan Chicos. "New insights into antisynthetase syndrome.” Maedica 11.2 (2016): 130. Reference #2: Marco, Joanna L., and Bridget F. Collins. "Clinical manifestations and treatment of antisynthetase syndrome.” Best Practice & Research Clinical Rheumatology 34.4 (2020): 101503. Reference #3: Kalluri, Meena, et al. "Clinical profile of anti-PL-12 autoantibody: cohort study and review of the literature.” Chest 135.6 (2009): 1550-1556. DISCLOSURES: No relevant relationships by Mario Flores No relevant relationships by David Jackson No relevant relationships by Lisa Saa No relevant relationships by Abu Baker Sheikh
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SESSION TITLE: Variety in Risk Factors and Treatment of VTE SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: The year of 2020 will be a year never forgotten when the COVID-19 pandemic began. The healthcare system is going into a crisis facing a disease that is unknown and overwhelming. Companies were frantic to find a solution to help prevent so many unnecessary deaths. Pfizer mRNA COVID-19 vaccine was granted emergency use by the FDA after proving efficacy in early trials. Many side effects were unknown and discovered as time went on. Unprovoked isolated pulmonary embolisms are rare. CASE PRESENTATION: A 24 year old male with no significant past medical history presented to the emergency department due to shortness of breath, hemoptysis and chest pain. He denied any family history or personal history of clotting disorders. He received the mRNA COVID-19 Pfizer vaccine 5 days prior to symptom onset. He describes it as constant sharp pain with varying intensity that he rates a 6/10 and can reach a 10/10 pain exacerbated with lying flat and deep breathing. He also states he has been coughing up a teaspoon amount of blood with this chest pain. Physical examination revealed reduced breath sounds in the left lower lobe. Patient was hemodynamically stable. Labs were stable and hemoglobin was stable throughout the hospital course. Fibrinogen was elevated and hypercoagulable work-up was negative. CTA of chest was performed and revealed left-sided pulmonary emboli involving the left lower lobe with pulmonary infarction. Therefore, he was managed by Eliquis. DISCUSSION: Pfizer released a safety and efficacy report of the BNT162b2 mRNA Covid-19 Vaccine. Many of the common side effects reported were pain at the injection site, fatigue, headache, and fever [1]. Adverse events that were reported were shoulder injury, right axillary lymphadenopathy, paroxysmal ventricular arrhythmia, and right leg paresthesia [1]. Isolated PE in a young healthy patient was never reported as an adverse event from the Pfizer safety and efficacy report. Severe acute respiratory syndrome-coronavirus-2 has been proven to increase the risk of venous thromboembolism because it is a prothrombotic virus [2]. Vaccination reports of pulmonary embolism are increasing, however, isolated PE without a DVT is still very underreported and rare. The literature states that a lot of patients that are having PE after mRNA vaccine also have associated thrombocytopenia, however, this is not what this patient demonstrates [3]. A total of 43, 548 participants were observed for the safety and efficacy report of the Pfizer COVID-19 report and not a single patient demonstrated an isolated pulmonary embolism event [1]. CONCLUSIONS: This case is a demonstration of a rare occurrence of isolated PE with no evidence of DVT in such close proximity to receiving the mRNA COVID-19 Pfizer vaccination.There are few reports of pulmonary embolism in healthy patients with no history of clotting disorders and further data are needed to support this association. Reference #1: Polack FP, Thomas SJ, Kitchin N, et al. Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine. N Engl J Med. 2020;383(27):2603-2615. doi:10.1056/NEJMoa2034577 Reference #2: Hesam-Shariati S, Fatehi P, Abouzaripour M, Fathi F, Hesam-Shariati N, Hesam Shariati MB. Increased pulmonary embolism in patients with COVID-19: a case series and literature review. Trop Dis Travel Med Vaccines. 2021;7(1):16. Published 2021 Jun 12. doi:10.1186/s40794-021-00145-3 Reference #3: Muster V, Gary T, Raggam RB, Wölfler A, Brodmann M. Pulmonary embolism and thrombocytopenia following ChAdOx1 vaccination. Lancet. 2021;397(10287):1842. doi:10.1016/S0140-6736(21)00871-0 DISCLOSURES: No relevant relationships by Muhammad Azaz Cheema No relevant relationships by Morcos Fahmy No relevant relationships by Christina Gearges No relevant relationships by Asma Iftikhar
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SESSION TITLE: Occupational and Environmental Lung Disease Cases SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Chlorine gas is a pulmonary irritant with pungent odor that damages the respiratory tract. Chlorine gas exposure occurs in industrial or household exposures,Chlorine gas has two forms either a liquid or gas, toxicity of chlorine gas depends on the dose and duration of exposure. Chlorine gas used in manufacturing products like paper, insecticides, Chlorine is used to treat bottled and swiming pool water. CASE PRESENTATION: A 37 Y.O Male, no PMH presents with progressive dyspnea for three days worse with activity,decreases with rest, denied cough fever or chest pain he is vaccinated for COVID,no smoking history. The patient worked at a chlorine gas factory in the Dominican Republic for 15 years. Exam: Vitals: BP 124/72 mmHg. HR 100 BPM. RR 21 BPM. SpO2 84%. General: acute distress. Heart: normal S1, S2. RRR. Lung: wheeze bilaterally. Abdomen: Soft. Musculoskeletal: no pitting edema. he was placed on 6 LPM NC saturation improved to 90%. CBC and Chemistry were unremarkable, he was started on steroid, breathing treatment with antibiotics. ABG showed hypoxemia. he was placed on Venturi mask and his saturation improved to 95%.CTA was negative for PE. EKG, troponin were unremarkable. A proBNP normal. The antibiotics were discontinued because of a negative workup. A TTE study was normal. HRCT scan of the chest, showed atelectasis and infiltrates of lower lobes. No interstitial fibrosis.A PFT showed obstructive airway disease. He was discharged on oral and inhaled steroids.Hi new onset obstructive airway could be due to chlorine gas exposure. DISCUSSION: Chlorine gas causes cellular injury through oxidative damage but further damage results from activation and recruitment of inflammatory cells with subsequent release of oxidants and proteolytic enzymes. Humans can detect chlorine gas odor at a concentration between 0.1-0.3 ppm. At 1-3 ppm,it causes irritation of oral,eye mucosal membranes. At 30-40 ppm causes cough, chest pain, and SOB. At 40-60 ppm, toxic pneumonitis and pulmonary edema and can be fatal at 430 ppm concentration or higher within thirty minutes. Chronic exposure to chlorine gas lead to chest pain, cough, sore throat, hemoptysis, recurrent asthma. Physical exam findings include tachypnea cyanosis, wheezing, intercostal retractions, decreased breath sounds. Pulmonary function tests may reveal obstructive lung function disease. Chronic exposure to a low level was found to be associated with an increased risk of asthma in swimmers. CONCLUSIONS: Chlorine exposure results in direct chemical toxicity to the airways with acute airways obstruction or airways hyperreactivity, presentation varies from acute overwhelming intoxication with acute lung injury and or death, occupational exposure increase the likelihood of chronic bronchitis or isolated wheezing attacks. Treatment for chlorine exposure is largely supportive. Reference #1: 1- Center of disease control and prevention website/emergency preparedness and response/ https://emergency.cdc.gov/agent/chlorine/basics/facts.asp Reference #2: 2- C- Morim A, Guldner GT. Chlorine Gas Toxicity. [Updated 2021 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537213/. Reference #3: A- Gummin DD, Mowry JB, Beuhler MC, et al. 2020 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 38th Annual Report. Clin Toxicol (Phila). 2021;59(12):1282-1501. doi:10.1080/15563650.2021.1989785 DISCLOSURES: No relevant relationships by Abdallah Khashan No relevant relationships by Samer Talib no disclosure on file for Matthew Yotsuya;
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SESSION TITLE: Drug-Induced Lung Injury Pathology Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: The most dangerous complication of amiodarone use is amiodarone-induced pulmonary toxicity (AIPT) (1). AIPT has no pathognomonic findings & is therefore diagnosed based on clinical suspicion & exclusion of other possible pulmonary diseases (2) CASE PRESENTATION: A 91-year-old female with history of CHF & atrial fibrillation on amiodarone 200mg once daily for approximately 10 years, presented for worsening shortness of breath for 3 days. On admission vitals were stable & pulse oximetry revealed a SpO2 of 89% on room air which increased to 96% on 4 litres oxygen. Examination revealed decreased breath sounds at bases, bilateral rales right>left. No clinical signs of fluid overload. Chest x-ray (fig 1) showed increased bilateral airspace opacities and computed tomography (CT) of chest (fig 3) revealed diffuse airspace opacities, right > left. Initial lab work was within normal limits. She was admitted with a working diagnosis of acute hypoxemic respiratory failure due to community acquired pneumonia (CAP) versus COVID-19 pneumonia due to high suspicion based on her clinical picture. She received remdesvir, empiric antibiotics and amiodarone was discontinued. COVID-19 PCR was negative, patient did not spike fevers or had any leukocytosis & pneumonia workup was negative. Therefore we now considered AIPT. Gallium scan for AIPT revealed abnormal uptake involving lungs bilaterally consistent with AIPT. Patient was continued on dexamethasone, after which patient's oxygen requirement subsequently decreased & repeat chest x-ray (fig 2 ) showed a significant decrease in bilateral infiltrates on steroids. She was discharged home on 2 litres oxygen & prednisone taper for 4 months. DISCUSSION: The advent of the highly contagious SARS-CoV-2 has made it further essential to diagnose AIPT correctly & to differentiate between these two entities. They have similar & non-specific features which makes this an even a greater challenge. Our elderly patient on long-term amiodarone use represents an at-risk group for AIPT (1). Her clinical picture was non-specific, initially suggesting CAP versus COVID-19 pneumonia. In our case, the consistent gallium scan findings confirmed the diagnosis of AIPT & enabled prompt anti-inflammatory treatment along with cessation of amiodarone which resulted in improved prognosis & outcome. AIPT should be suspected in patients taking amiodarone who have new or worsening symptoms with an insidious onset &/or new infiltrates on chest x-ray. Greater parenchymal activity on gallium scintigraphy scanning & the presence of lung biopsy findings can help further confirm the diagnosis (1) CONCLUSIONS: In the era of the COVID-19 pandemic, it becomes even more challenging to diagnose and differentiate AIPT from SARS-CoV-2 pneumonia, which can have a similar presentation (3). Early recognition of AIPT is critical to prevent or minimize its potentially devastating pulmonary effects. Reference #1: Martin, W. J., & Howard, D. M. (1985). Amiodarone-induced lung toxicity: In vitro evidence for the direct toxicity of the drug. American Journal of Pathology, 120(3), 344–350. Reference #2: Benassi, F., Molardi, A., Righi, E. et al. ECMO for pulmonary rescue in an adult with amiodarone-induced toxicity. Heart Vessels 30, 410–415 (2015). Reference #3: Macera M, De Angelis G, Sagnelli C, Coppola N, Vanvitelli Covid-Group. Clinical Presentation of COVID-19: Case Series and Review of the Literature. Int J Environ Res Public Health. 2020 Jul 14;17(14):5062. DISCLOSURES: No relevant relationships by Nayaab Bakshi No relevant relationships by Navjot Kaur Grewal No relevant relationships by Talha Munir No relevant relationships by Anusha Singhania