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1.
Chest ; 162(4):A911-A912, 2022.
Article in English | EMBASE | ID: covidwho-2060726

ABSTRACT

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

2.
American Journal of Respiratory and Critical Care Medicine ; 205(1), 2022.
Article in English | EMBASE | ID: covidwho-1927840

ABSTRACT

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.

3.
Critical Care Medicine ; 50(1 SUPPL):316, 2022.
Article in English | EMBASE | ID: covidwho-1691869

ABSTRACT

INTRODUCTION: HLH is a rare syndrome with an incidence of 1.2 cases per 1,000,000 individuals per year. Diagnosis of HLH is challenging given its varied presentation and strict diagnostic criteria. DESCRIPTION: A 40 year-old female with no medical history presented with two weeks of shortness of breath and cervical lymphadenopathy. She was evaluated in the ED on two separate occasions with workup significant for CT chest findings of mediastinal and axillary lymphadenopathy, pulmonary nodules and a left pleural effusion. Within one week, she presented a third time with worsening shortness of breath, fatigue and fevers. She was febrile, tachycardic, hypoxemic, leukopenic and thrombocytopenic. A repeat CT chest revealed increased lymphadenopathy and pleural effusion. She was started on empiric broad spectrum antibiotics and admitted to the hospital. Infectious workup, pleural fluid cytology and peripheral blood flow cytometry were negative. Bone marrow biopsy had markedly increased histiocytes and hemophagocytosis, but no evidence of malignancy. She developed progressive hypoxemia requiring intubation, shock requiring vasopressors and multiorgan failure. Fevers persisted with worsening pancytopenia, DIC, and markedly elevated inflammatory markers, notably a ferritin >33000. Further workup revealed positive Covid antibodies, elevated parvovirus IgG, elevated fungal markers and Candida in respiratory cultures. Secondary HLH due to sepsis or following COVID infection in the setting of malignancy was suspected. A course of antifungals and high dose steroids was given without improvement. Etoposide was considered, but avoided given possible sepsis, multiorgan failure and pancytopenia. A lymph node biopsy was performed with evidence of hemophagocytosis and ALK-positive anaplastic large cell lymphoma. Despite aggressive treatment, she developed progressive multiorgan failure resulting in death. Autopsy confirmed anaplastic large cell lymphoma with metastasis to the lymph nodes, lungs, epicardium and stomach. DISCUSSION: Malignancy is a known etiology of HLH in adults, however, few cases of ALK-positive anaplastic large cell lymphoma presenting as HLH have been reported. The rapid progression of HLH in this case stresses the importance of early diagnosis and treatment of HLH while pursuing an aggressive malignancy workup.

4.
American Journal of Respiratory and Critical Care Medicine ; 203(9):1, 2021.
Article in English | Web of Science | ID: covidwho-1407299
5.
American Journal of Respiratory and Critical Care Medicine ; 203(9), 2021.
Article in English | EMBASE | ID: covidwho-1277413

ABSTRACT

INTRODUCTION Airway Pressure Release Ventilation (APRV) is a pressure controlled intermittent mandatory mode of ventilation characterized by inverse ratio ventilation and high mean airway pressure. Several studies have showed that APRV can improve oxygenation and lung recruitment in patients with ARDS. Although most patients with COVID-19 meet the Berlin criteria, hypoxic respiratory failure due to COVID-19 may differ from traditional ARDS as patients often present with severe, refractory hypoxemia and significant variation in respiratory system compliance. To date, no studies investigating APRV in this population have been published.The aim of this study was to evaluate the effectiveness of APRV as a rescue mode of ventilation in critically ill patients diagnosed with COVID-19 and refractory hypoxemia.METHODS We conducted a retrospective analysis of patients admitted with COVID-19 who developed refractory hypoxemia (PaO2/FIO2 ratio (P/F ratio) <200) while on mechanical ventilation and were treated with a trial of APRV for at least 8 hours. P/F ratio, ventilatory ratio and ventilation outputs before and during APRV were compared.Student's t-test and Wilcoxon signed-rank test were used to compare parametric and nonparametric data, respectively.RESULTS There were 60 patients who met the inclusion criteria. Mean age was 65, 36.6% of the patients were female and in-hospital mortality was 80%. We found that APRV significantly improved the P/F ratio (103 [75-154.23] vs 131.75 [94.15-221, p 0.0001]) and decreased the FiO2 requirements (80[60-100] vs 100[75-100], p 0.0034). PaCO2 (45.8 [41-56.75]mmHg vs 54[42-73]mmHg p 0.0051), and Ventilatory ratio (2.32 [1.92-3.15] vs 2.85 [2.07-3.85], p 0.0054) were also improved during the APRV trial. There was an increase in tidal volume per predicted body weight during APRV (7.86 [7.06-9.85] mL/Kg vs 6.58 [5.69-7.86] mL/Kg, p< 0.0001]) and a decrease in total minute ventilation (10.87±3.11 L/min vs 12.39±2.99 L/min, p 0.0005). On multivariate analysis, higher I:E and airway pressure were associated with greater improvement of P/F ratio.CONCLUSION Patients with COVID-19 and severe hypoxemia have a high in-hospital mortality.APRV may benefit these patients as it maximizes alveolar recruitment resulting in improved oxygenation, alveolar ventilation and CO2 clearance.These effects are more pronounced for higher airway pressure and I:E ratio. APRV was associated with an increase in tidal volume.However, tidal volumes remained within the recommended limits of lung protective ventilation.This study contributes to the growing evidence on the positive effects of APRV on oxygenation and ventilation.Prospective studies are urgently needed to evaluate the potential benefits of APRV on clinical outcomes in patients with COVID-19 and severe hypoxemia.

6.
Chest ; 158(4):A807, 2020.
Article in English | EMBASE | ID: covidwho-866562

ABSTRACT

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: The rapid and unprecedented spread of severe acute respiratory syndrome coronavirus disease 2019 (COVID-19) has significantly limited our understanding of this disease. As the pandemic continues to evolve, cardio-pulmonary symptoms predominate, however new atypical manifestation of COVID are increasingly recognized. CASE PRESENTATION: A previously healthy 70-year-old man presents with a witnessed episode of new-onset seizures. Per family accounts, the episode lasted three minutes with tonic-clonic movements of all extremities, followed by a period of confusion. He had endorsed worsening fatigue and headaches with a declining appetite over the preceding two weeks. There was no history of cough, respiratory symptoms, sick contacts or prior similar episodes. Travel history was significant for a trip to California two weeks prior. He denied any medication, health supplement or illicit substance use. Past medical, surgical and family histories were unremarkable. On examination, the patient was obtunded and afebrile (37.3°C). He appeared visibly dyspneic, with an SpO2 of 85% on room air and RR of 34 /minute, but remained hemodynamically stable. Lung auscultation revealed scattered bilateral crackles while the neurological exam was non-focal. Clinically the patient appeared euvolemic. Computed tomography of the brain was unrevealing with no additional explanation for his prolonged altered mentation. Chest-radiography revealed bilateral air-space opacities. Labs indicated mild leukocytopenia (3.2 x109/L) with lymphopenia (0.6 x109/L) and a profound hyponatremia of 104 mEq/L. Renal and liver parameters were normal. Workup of his hyponatremia revealed a serum and urine osmolality of 230 mOsm/kg and 693 mOsm/Kg respectively with a urine sodium of 58 mmol/L. TSH and Cortisol levels were normal. Inflammatory markers were significantly elevated as summarized in Table 1. Influenza PCR, respiratory viral PCR panel, legionella urine antigen and blood cultures were all negative;however, the COVID-19 PCR assay was subsequently found to be positive. Based on the patient’s clinical and biochemical data, he was diagnosed with severe symptomatic hyponatremia secondary to SIADH in the setting of COVID-19 pneumonia. DISCUSSION: SIADH in the setting of pneumonia has been extensively studied and reported. A number of potential mechanisms have been postulated including extensive cytokine release, hypoxemia, nausea and stress. Additionally, inflammation (IL-6 in particular) itself has been reported to directly impair osmoregulation leading to hyponatremia. We hypothesize that milder forms of hypercytokinemia and hyper-inflammation could result in a number of less dramatic atypical presentations including SIADH. CONCLUSIONS: A high index of suspicion and awareness of this association is essential to mitigate SIADH related complications as cases of COVID-19 continue to rise. Reference #1: Edmonds, Z. V. (2012). Hyponatremia in pneumonia. Journal of Hospital Medicine, 7(S4). doi: 10.1002/jhm.1933 Reference #2: Swart RM, Swart RM, Hoorn EJ, Betjes MG, Zietse R. Hyponatremia and Inflammation: The Emerging Role of Interleukin-6 in Osmoregulation. NEP. 2011;118(2):p45–51. DISCLOSURES: No relevant relationships by Yasmin Herrera, source=Web Response No relevant relationships by Kam Sing Ho, source=Web Response no disclosure on file for Bharat Narasimhan;No relevant relationships by Archana Pattupara, source=Web Response No relevant relationships by Joseph Poon, source=Web Response no disclosure on file for James Salonia;

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