MISTAKING CRYPTOGENIC-ORGANIZING PNEUMONIA (COP) FOR COMMUNITY-ACQUIRED PNEUMONIA (CAP) IN A CENTENARIAN

SESSION TITLE: Critical Diffuse Lung Disease Cases 2 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Recurrent episodes of community acquired pneumonia (CAP) have been shown to be common in elderly patients. Cryptogenic organizing pneumonia (COP) is an interstitial lung disease that is often mistaken for pneumonia, especially in the older population. Here, we present a 100-year-old woman diagnosed with COP after multiple failed courses of antibiotics for CAP. CASE PRESENTATION: A 100-year-old female with a history of cardiomyopathy, pulmonary hypertension, and autoimmune hemolytic anemia previously on prednisone, who presented with shortness of breath and non-productive cough. CT of the chest showed dense left upper and lower lobe consolidations. She was admitted 2 months prior with similar symptoms and found to have extensive right sided consolidations with concerns of CAP. She was treated with antibiotics without resolution of her symptoms. CXR from two years prior revealed right upper and right lower lobe consolidations. This admission, she was started on antibiotics with no improvement and required supplemental oxygen. She had no leukocytosis. COVID-19 testing was negative and she was unable to produce any sputum for culture. The patient declined bronchoscopy. She was seen by speech and swallow with no concern for aspiration. Prednisone was started empirically for COP and the patient experienced rapid improvement in symptoms and oxygenation. Ultimately, she was discharged on 20 mg of prednisone daily as well as Bactrim for PCP prophylaxis. She continued a slow taper as an outpatient with overall improvement in her clinical symptoms. Serial CT scans demonstrate complete resolution of the infiltrates with no recurrence or new infiltrates. DISCUSSION: Cryptogenic organizing pneumonia is a rare interstitial lung disease known to affect bronchioles and alveoli. Its etiology is unclear and symptoms often mimic other types of infectious pneumonia leading to frequent mis-diagnosis. The average age of onset is typically 50-60. Establishing this diagnosis can be difficult due to the non-specific symptomatology of dry cough and dyspnea. Bronchoscopy with lavage and transbronchial biopsies can be performed to rule out infectious and non-infectious etiologies but is not necessary for diagnosis. The most common radiographic pattern is multifocal asymmetrical parenchymal consolidations with air bronchograms that tend to migrate and appear in different sites over time. Less common presentations include ground glass opacities, nodular densities, and progressive fibrotic patterns. Steroids with a slow taper as outpatient are mainstay of therapy and the majority of patients respond with symptom and radiographic improvement. CONCLUSIONS: While elderly patients are particularly susceptible to recurrent CAP, the diagnosis of COP should be considered part of the differential diagnosis in those with recurrent unexplained consolidations on chest radiography without an infectious etiology. Reference #1: Hedlund J, Kalin M, Ortqvist A. Recurrence of pneumonia in middle-aged and elderly adults after hospital-treated pneumonia: aetiology and predisposing conditions. Scand J Infect Dis. 1997;29(4):387-92. doi: 10.3109/00365549709011836. PMID: 9360255. Reference #2: Tiralongo F, Palermo M, Distefano G, et al. Cryptogenic Organizing Pneumonia: Evolution of Morphological Patterns Assessed by HRCT. Diagnostics (Basel). 2020;10(5):262. Published 2020 Apr 29. doi:10.3390/diagnostics10050262 Reference #3: Lee JW, Lee KS, Lee HY, Chung MP, Yi CA, Kim TS, Chung MJ. Cryptogenic organizing pneumonia: serial high-resolution CT findings in 22 patients. AJR Am J Roentgenol. 2010 Oct;195(4):916-22. doi: 10.2214/AJR.09.3940. PMID: 20858818. DISCLOSURES: No relevant relationships by Vincent Chan No relevant relationships by Mackenzie Kramer No relevant relationships by John Madara No relevant relationships by Stephanie Tzarnas No relevant relationships by Laura Walters

BRASH SYNDROME: A DOWNWARD SPIRAL

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: BRASH Syndrome is a phenomenon characterized by bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia. Literature on this syndrome is limited given its under-recognition. CASE PRESENTATION: A 77-year-old female with a past medical history of atrial fibrillation, coronary artery disease, diastolic heart failure, and chronic kidney disease (CKD) III presented with dyspnea. Her home medications included furosemide, metoprolol, spironolactone, warfarin, and rosuvastatin. Comprehensive metabolic panel was significant for an elevated creatinine from baseline. Cardiac BNP was elevated, chest X-ray demonstrated cardiomegaly, and physical exam was significant for jugular venous distention. Electrocardiogram (EKG) revealed atrial fibrillation with rapid ventricular response (Image 1). Diltiazem was added for rate control however the patient was ultimately electrically cardioverted. Post procedure EKG revealed a junctional rhythm (Image 2). Hypotension persisted however. The patient soon developed oliguric renal failure and hyperkalemia, prompting upgrade to the medical intensive care unit (ICU) for shock. The patient had persistent bradycardia with heart rates as low as 32 beats per minute (bpm). Hemodialysis was initiated the following morning and the patient's shock, bradycardia, and hyperkalemia resolved. DISCUSSION: Transient abnormal rhythms have been reported post cardioversion, however the persistence of bradycardia with our patient's other abnormal lab findings raised concerns for different etiologies. BRASH syndrome is an under recognized pathophysiological phenomenon. Patients with congestive heart failure and CKD are at risk when in an inpatient setting. Different triggers are noted in recent reports, including medications such as Ranolazine and Bactrim, anaphylaxis, and even COVID-19. These cases varied in clinical severity, ranging from asymptomatic bradycardia to multiorgan failure. The hallmark mechanism of BRASH syndrome is a synergistic effect of AV nodal blocking medications and hyperkalemia promoting bradycardia. This, in conjunction with renal injury, produces the cycle of objective findings that define BRASH syndrome. Acute kidney injury caused by renal hypoperfusion can exacerbate the effects of AV nodal blocking medications as well as worsen hyperkalemia. Profound hyperkalemia and AV nodal blockade will in turn synergistically promote and prolong bradycardia. Bradycardia can depress cardiac output and further worsen renal hypoperfusion, continuing this viscous cycle. CONCLUSIONS: We believe electrical cardioversion into a junctional rhythm caused BRASH syndrome in our patient. Treatment is tailored to correcting the individual abnormalities. Many of these case reports had favorable outcomes. This case suggests that BRASH syndrome can often go undiagnosed yet still successfully be managed with supportive care. REFERENCE #1: Farkas, J., Long, B., Koyfman, A., et al. BRASH SYNDROME: BRADYCARDIA, RENAL FAILURE, AV BLOCKADE, SHOCK, AND HYPERKALEMIA. The Journal of Emergency Medicine, 59(2):216-223, pp. 1–8, 2020. DOI: 10.1016/j.jemermed.2020.05.001 REFERENCE #2: Cakulev, I., Efimov, I., Waldo, A., et al. Cardioversion: Past, Present, and Future. Circulation. Oct 20;120(16):1623-32. 2009. DOI:10.1161/circulationaha.109.865535 REFERENCE #3: Flores, S., Anaphylaxis induced bradycardia, renal failure, AV-nodal blockade, shock, and hyperkalemia: A-BRASH in the emergency department, American Journal of Emergency Medicine 38(9), P1987.E1-1987.E3. 2020. DOI: 10.1016/j.ajem.2020.05.033 DISCLOSURES: No relevant relationships by John Madara, source=Web Response No relevant relationships by Nathaniel Rosal, source=Web Response No relevant relationships by Franklin Thelmo, source=Web Response No relevant relationships by Stephanie Tzarnas, source=Web Response

Ventricular ectopy with remdesivir use in COVID-19

INTRODUCTION: Remdesivir is an antiviral medication that has demonstrated improvement in time to symptom resolution in Covid-19. The side effect profile documented in literature is still developing. To date, there have been no wide scale demonstrated cardiac toxicities noted. We present a case of COVID-19 who developed ventricular ectopy suspected to be due to Remdesivir. METHODS: A 70-year-old male with a past medical history of coronary artery disease, hypertension, and recurrent aspiration events presented from a nursing home in respiratory distress. The patient initially presented with findings consistent with aspiration pneumonia, however was also found to be positive for Covid-19. Vital signs were positive for fever, tachycardia, tachypnea, and an oxygen saturation of 90% on Non-Rebreather, requiring intubation. Metabolic panel on admission showed a slightly elevated ALT, but no electrolyte abnormalities or altered renal function. A leukocytosis and mild anemia were noted on complete blood count. Admission electrocardiogram was negative for ectopy. Remdesivir therapy for COVID-19 was planned. During infusion of the first dose, the patient had multiple premature ventricular complexes (PVCs) that developed into a short run of non-sustained ventricular tachycardia. During the second dose, PVCs again were noted, and Remdesivir was stopped. After infusion was held, ectopy resolved. Echocardiogram showed an ejection fraction of 60 - 65%, mild tricuspid and mitral regurgitation, and no evidence of wall motion abnormalities. After 48 hours, ectopy was no longer observed. RESULTS: A preliminary report of the Adaptive COVID-19 Treatment Trial evaluated Remdesivir's efficacy and safety. Of the patients receiving it, 29% had grade 3 or 4 adverse reactions, though none were cardiac in nature. In our patient, the onset of ectopy was noted immediately upon infusion and resolved upon abortion of infusion. Postulated mechanisms were drug interactions (carvedilol, atorvastatin, and sertraline were considered), CAD, or underlying disease of the conduction system. Further studies investigating the association of underlying conditions and medications with Remdesivir may shed light on this occurrence.

Convalescent plasma therapy in a refractory case of COVID-19 in an immunocompromised patient

INTRODUCTION: Convalescent plasma therapy (CPT) is a relatively new treatment option offered for COVID 19 pneumonia. Both the side effects and disease course after treatment with CPT have not been thoroughly investigated. CPT is primarily reserved for those participating in FDA approved clinical trials, however this case highlights an immunocompromised patient who benefited from CPT although was excluded from the clinical trial. METHODS: A 60-year-old female with a past medical history of rheumatoid arthritis (RA) was admitted for COVID 19 pneumonia on 6/18/2020. Her current management of her RA included Rituximab infusions which she received most recently one week prior to admission. On presentation she was noted to be febrile and in hypoxic respiratory failure requiring HFNC for oxygen support. She was treated with a 5-day course of dexamethasone and Remdesivir during her hospitalization. She initially had a great clinical response and was afebrile and weaned off of supplemental oxygen by the time of discharge. Patient was re-admitted three weeks later with fevers and SOB. COVID swab remained positive and coronavirus antibodies were negative. Patient was admitted to the ICU for high oxygen O2 requirements and required intubation. Bronchoscipt with alveolar lavage was performed which revealed no bacterial or fungal source of infection. Due to continued elevation of inflammatory markers, oxygen requirement and clinical symptoms, the patient was started on a second course of Remdesivir which was extended to 10 days. The patient was approved for CPT and received transfusion two weeks after admission with no adverse effects. Patient was discharged on room air 4 days after treatment and inflammatory markers markedly trended down. Her repeat COVID swab prior to discharge was negative. RESULTS: Research surrounding CPT in immunocompromised patients infected with COVID-19 is limited. With no vaccine available, CPT has been shown to be beneficial with clearance of viral load. Our case demonstrated the successful use of CPT in an immunocompromised individual. Further research needs to be done to evaluate the effectiveness of CPT in immunocompromised patients infected with COVID 19.

PULMONARY EMBOLISM AND RIGHT HEART STRAIN PATTERN IN COVID-19: AN INCIDENTAL FINDING OR A PERSISTENT PATTERN?

SESSION TITLE: Medical Student/Resident Pulmonary Vascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Coronavirus disease 2019 (CVOD-19) is presumed to be a prothrombotic state however, there is no concrete evidence supporting therapeutic anticoagulation in this disease. Here, we present a case of a 67-year old male diagnosed with COVID-19 who developed an acute pulmonary embolism and right ventricular strain pattern during hospitalization and was treated with therapeutic Lovenox. CASE PRESENTATION: A 67-year-old male who had tested positive for COVID-19 one week ago presented to the hospital with shortness of breath, fever (T 102.8), and generalized body aches. His oxygen saturation worsened, and he was put on the nasal cannula, later transitioning to non-rebreather, and finally intubation for not maintaining saturation. Computerized tomography (CT) scan of the chest on admission revealed bilateral, bibasilar and sub-pleural ground-glass opacities. (Figure 1) One week later, he became hypotensive, tachycardiac, and hypoxic on the same ventilator settings. Bedside echocardiogram revealed right ventricular dilatation and akinesis of the mid free wall. (Figure 2) A provisional diagnosis of pulmonary embolism was made and he was treated with therapeutic Lovenox. CT scan of the chest with contrast confirmed the diagnosis of pulmonary embolism. (Figure 3) His hospital course was complicated by pneumonia treated which was treated with antibiotics. He was discharged to a nursing home with a tracheostomy tube and Eliquis on the third week of hospitalization. DISCUSSION: Emerging as a cluster of pneumonia cases in Wuhan, China in December 2019, COVID-19 has spread across the world. It attaches to angiotensin-converting enzyme 2 expressed in the lungs, heart, and gastrointestinal tract. [1] Widespread microvascular thrombi in the pulmonary circulation as evidenced by autopsy studies cause profound hypoxia by a ventilation-perfusion mismatch in the lungs. The proposed mechanism of COVID-19 thrombosis includes hypercoagulable state and cytokine-mediated damage. [2] It is believed that 50 % of these patients have elevated D-dimer levels that in combination with elevated prothrombin time and reduction in fibrinogen level have been associated with increased mortality.[3] Some enterprises are therapeutically anticoagulating these patients based on these coagulation parameters while others are not. CONCLUSIONS: COVID-19 increases the incidence of microvascular and microvascular thrombotic complications. Worsening respiratory status not explained by radiological changes in the lung fields, and especially in conjunction with high titers of D-dimers, should raise the suspicion for pulmonary embolism. More studies are needed to evaluate the need for therapeutic anticoagulation in these patients without objective evidence of thrombosis. Reference #1: Yang XL, Wang XG, Hu B, Zhang L, Zhang W, et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature. 2020. https://doi.org/10.1038/s41586-020-2012-7. Reference #2: Mei H., Hu Y. (2020) Characteristics, causes, diagnosis and treatment of coagulation dysfunction in patients with COVID-19. Zhonghua Xue Ye Xue Za Zhi 41:E002. Reference #3: ang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. Journal of Thrombosis and Haemostasis. 2020 Apr 1. DISCLOSURES: No relevant relationships by John Madara, source=Web Response No relevant relationships by Sohaib Roomi, source=Web Response