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INTRODUCTION: COVID-19 is often associated with hyper-inflammatory state reported as cytokine storm. Various markers have been proposed for early identification of developing cytokine storm and prognostication. Specifically, high ferritin levels have been shown to be an independent predictor of severity and in-hospital mortality. This study explores the trend of inflammatory markers on COVID-19 patients in hopes to provide clinical correlation with patient outcomes. METHOD(S): An IRB-approved retrospective study was done on 141 patients admitted for COVID-19 from March to April 2020. CRP, ferritin, and lactate dehydrogenase (LDH) levels were obtained on initial presentation and trended during hospitalization. Time to peak using Wilcox Signed Rank Test and area under the curve (AUC) was calculated. A subgroup analysis was done on patients who received high versus standard dose steroids to analyze effects on inflammatory markers. This is defined by at least 6 mg dexamethasone, 32mg methylprednisolone, or 40 mg prednisone daily for at least 3 days. Primary outcome of this study is to assess the trend of inflammatory markers throughout admission and clinically correlate with outcomes. RESULT(S): Time to peak for ferritin was slightly later[3.46 days+/-1.69(pCRP-Ferritin:0.046,pLDH-Ferritin:0.038)] compared to CRP(3.15 +/- 1.49) and LDH(3.04 +/- 1.75). AUC for CRP was significantly decreased(coef.-581CI[- 1029to-133]p0.013) for patients who received high dose steroids compared to those who received standard doses. There was no significant difference between AUC for LDH and ferritin. Peak CRP,LDH, and ferritin for survivors was 245(158-301), 604(448 -776), 1216(654-2478) respectively;and for non-survivors was 272(207-331) p0.049, 872(624-1220)p< 0.001, 2326(1016-3710)p0.012 respectively. CONCLUSION(S): Inflammatory markers have been a central topic of study in finding predictors of outcomes for COVID-19. This study showed that ferritin peak occurred slightly later than CRP and LDH. We can anticipate ferritin to have a slightly longer course to peak. AUC is suggestive of persistence of inflammation over time. We showed that CRP was significantly lower for patients who received high dose steroids compared with standard dose. Non-survivors had significantly increased peak levels of ferritin, LDH, and CRP.
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SESSION TITLE: Critical Care Management of COVID-19 SESSION TYPE: Original Investigations PRESENTED ON: 10/17/2022 01:30 pm - 02:30 pm PURPOSE: Superimposed bacterial co-infection is common among patients with Coronavirus disease-19 (COVID-19) pneumonia. Incidence of any superimposed infection ranges from 0% to 40%. Up to 50% of COVID-19 patients who died, had concomitant bacterial or fungal infection. Steroids are recommended for the treatment of acute hypoxemic respiratory failure (AHRF) due to COVID-19 and are thought to mitigate inflammatory organ injury. This retrospective study explores a subset of COVID-19 patients receiving Epoprostenol (iEPO) for AHRF and compared two different steroid treatment strategies and the impact on patient outcomes. METHODS: This is a retrospective study of 101 COVID-19 patients with AHRF receiving iEPO and systemic steroids. Patients in the high dose steroid group (n=59) received a minimum of dexamethasone 20mg daily or solumedrol 100mg daily while the standard dose steroid group (n=52) were those who received any lower dose. Patients that were DNR/I were excluded from the study. The primary outcome of the study was the rate of bacterial co-infection defined by positive cultures. Secondary outcome was mortality. RESULTS: Results showed that patients treated with high dose steroids were older (66.77±11.17 vs 60.33±14.49, p0.006) and received a longer treatment course (18 days (12-25) vs 12.5 days (10-17), p 0.004). Univariate and Multivariate analysis showed that higher dose steroids were not associated with increased risk of superimposed bacterial infection (OR 0.96, CI (0.34-2.66), p0.93). The duration of steroids, regardless of the dose, was associated with increased risk of superimposed bacterial infection (OR 1.06, CI (1.01-1.13), p0.033). When adjusted for comorbidities and inflammatory state, there was no significant difference in mortality between patients treated with high dose compared to standard dose steroids (OR 3.60, CI (0.65-19.93), p0.14). A longer duration of steroids was associated with a trend towards improved mortality (OR 0.93, CI (0.87-1.00), p0.072). CONCLUSIONS: Our study suggests that the duration of steroids, rather than dosage, had an effect on patient outcomes. There was no difference in bacterial co-infection rates between the two groups, but infection rates were increased among those who received a longer course of steroid treatment. There was a trend towards lower mortality with increased steroid duration, however, this did not reach statistical significance. Given this trend towards lower mortality, future prospective studies should investigate steroid duration to determine if a longer course of treatment leads to better outcomes in patients with COVID-19 pneumonia and refractory AHRF. CLINICAL IMPLICATIONS: Based on our study, patients should not receive a higher dose or longer duration of steroid treatment given the increased risk of bacterial infection with no definitive improvement in mortality. DISCLOSURES: No relevant relationships by Natasha Garg No relevant relationships by Abhinav Hoskote No relevant relationships by Raymonde Jean No relevant relationships by Arpanjeet Kaur No relevant relationships by Sara Luby No relevant relationships by Omar Mahmoud No relevant relationships by Maria Athena Riego No relevant relationships by Edith Robin No relevant relationships by James Salonia No relevant relationships by DISHANT SHAH No relevant relationships by Venus Sharma No relevant relationships by Elizabeth Zipf
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Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is well described as an etiology to severe acute respiratory distress syndrome (ARDS). However, rare immunologic and allergic manifestations may also occur from this infection. We report a novel case of angioedema occurring in the setting of COVID-19 infection in a fully vaccinated patient. Case Report: A 61-yearold COVID-19 vaccinated female with hypertension presented to the emergency department with tongue and lip swelling, odynophagia, dysphonia, and difficulty breathing. She denied personal or family history of allergies, anaphylaxis, or angioedema. Her home medications included Aspirin, methadone, Seroquel, and Klonopin, with no recent changes reported. Physical exam was notable for significant lip and tongue edema, audible dysphonia, and bilateral end-inspiratory wheezing. She was hypoxemic and placed on nasal cannula. Laboratory findings revealed lymphopenia, elevated inflammatory proteins, including C-reactive protein (57), Lactate dehydrogenase (LDH) (238), and D-dimer (11.52). Functional C1 esterase inhibitor levels (>91) were normal. Nasal PCR swab returned positive for SARS-CoV-2. Ear, nose, and throat specialist was consulted given concern for angioedema, and flexible nasolaryngoscopy was performed revealing uvular, epiglottic, and bilateral arytenoid edema concerning for impending airway compromise. The patient was initiated on intravenous methylprednisolone, epinephrine, antihistamines, tranexamic acid and admitted to the medical intensive care unit (ICU). She was monitored closely in the ICU with subsequent improvement of the angioedema and resolution of the hypoxemia. She was discharged with an oral steroid regimen and scheduled for a follow-up appointment with an allergist. Discussion: There exists only a handful of case reports describing angioedema in patients with COVID-19 infection. In those reports, patients also had normal C1 esterase inhibitor levels and no personal or family history of inherited angioedema. Interestingly, our patient was vaccinated six months prior to her presentation. The association between SARS-CoV-2 and angiotensinconverting enzyme 2 (ACE-2), the primary receptor for viral entry into the epithelial cells of the lungs, could be a potential explanation for the occurrence of angioedema. ACE-2 plays a pivotal role in inhibiting a potent ligand of bradykinin receptor 1, Arginine bradykinin. It has been postulated that SARS-CoV-2 downregulation of ACE-2 leads to elevated angiotensin II levels and subsequent activation of the bradykinin pathway. Excessive bradykinin production generates high levels of nitric oxide and prostaglandins, resulting in vasodilation, increased vascular permeability, and angioedema. This case highlights the importance of recognizing atypical and rare presentations of COVID-19 infection, especially angioedema, given its sudden onset and life-threatening complications.