ABSTRACT
Teledermatology is one of the most important developments of digitalisation in dermatology. It has helped to ensure continuity of care during the COVID-19 pandemic. The combination of teledermatology with artificial intelligence can significantly improve medical decision-making. Among imaging modalities, dermoscopy is the most widely used, and its effectiveness can be significantly enhanced when combined with artificial intelligence. Novel techniques that have emerged in recent years include high-frequency ultrasound, optical coherence tomography or multispectral imaging. These are currently used in dermatological research but are expected to gradually become part of daily patient care. The knowledge of digital technologies and new imaging techniques is essential for the modern dermatologist. In the future, it is expected to be an essential part of modern and optimised patient care.
ABSTRACT
SESSION TITLE: Late Breaking Chest Infections Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/18/2022 01:30 pm - 02:30 pm PURPOSE: Initial reports of COVID-19 autopsies revealed significant evidence of micro and macrovascular thrombosis. Due to concern for increased thrombotic events, many institutions implemented anticoagulation (AC) protocols for hospitalized patients. The study’s objective is to evaluate disease progression in patients treated with therapeutic anticoagulation vs. prophylactic anticoagulation in noncritical COVID-19 hospitalized patients. METHODS: We performed a retrospective cohort study of adults hospitalized with COVID-19 pneumonia between March 1-May 1, 2020. Inclusion criteria was any adult patient directly admitted to non-intensive care setting for radiologically confirmed COVID-19 pneumonia. T-test was performed for the continuous variables with normal distribution. Wilcoxon-rank-sum test for non-parametric groups. Chi-squared test for categorical variables. P-value <0.05 was considered statistically significant. RESULTS: Overall, 81 (34%) received therapeutic AC, and 159 (66%) subjected received prophylactic AC. The clinical characteristics of the therapeutic group included: average age 57.8 (vs. 55.7), 77.78% male (vs. 72.92%), 40.74% obese (vs. 37.92%), 64.74% had hypertension (vs. 40.88%), 44.44% had Diabetes Mellitus (vs. 37.92%) and 11.11% had chronic kidney disease (vs. 13.84%). Initial inflammatory markers were higher in therapeutic group vs. prophylactic, including D-dimer (845 vs 361ng/dL), Ferritin (918.5 vs. 632ng/mL), and CRP (20 vs. 11.2mg/dL). The average length of stay (LOS) of the therapeutic group was 10 days (vs. 7 for prophylactic), and a higher number of patients required mechanical ventilation (36 vs. 23), and hemodialysis (18 vs. 6). A higher number of adverse events (bleeding) was noticed in the therapeutic group (13.58% vs. 2.52%) with a p-value of <0.001. Higher odds of In-Hospital mortality observed in therapeutic group subjects with Hypertension (OR=5.41), chronic kidney disease (OR= 4.08), and lung disease (OR= 2.87) with a p-value of <0.05. CONCLUSIONS: In noncritically ill patients with COVID-19, treatment with therapeutic AC was related to greater LOS, requiring mechanical ventilation, hemodialysis, and adverse effects compared to prophylactic AC. We also observed a significantly higher D-dimer, ferritin, and CRP in the therapeutic group. RCT performed by ACTIV-4a investigators demonstrated increased organ support-free days in the therapeutic group, contrary to our study, which showed increased dependence of respiratory support and hemodialysis. Our therapeutic group patients appear to have higher comorbidities and significantly elevated initial inflammatory markers compared to the prophylactic group, which may explain these differences. CLINICAL IMPLICATIONS: Finally, our study supports the use of therapeutic anticoagulation depending on the patient overall clinical scenario. DISCLOSURES: No relevant relationships by Adebola Adetiloye No relevant relationships by Jennifer Arzu No relevant relationships by Kuldeep Ghosh No relevant relationships by Gabriel Ibarra no disclosure on file for Armeen Poor;No relevant relationships by Ingrid Portillo No relevant relationships by Fernando Quesada Mata No relevant relationships by Natoushka Trenard No relevant relationships by Julio Valencia Manrique
ABSTRACT
Introduction: COVID-19 is an infection caused by severe-acute-respiratory syndrome coronavirus-2 (SARS-CoV-2).1 Many recent reports have shown an increased risk of venous thromboembolism (VTE)4-5. Despite therapeutic anticoagulation with elevated D-dimer is widely described7, data on post-discharge prophylactic anticoagulation is limited.Case report: A 52-year-old female presented with 1-day mid-sternal chest pain and difficulty breathing. Her medical history included type-2-Diabetes Mellitus, obesity, and a hospital admission 4 weeks prior for COVID-19. She received Ceftriaxone, Azithromycin, Hydroxychloroquine, and prophylactic anticoagulation. She remained stable, with no fever or oxygen requirements and was discharged home to selfquarantine. She returned to the hospital, describing pain as sharp, constant, mild, radiating to left chest and back, aggravating on lying down and alleviating on leaning forward. Physical exam was normal, with no tachycardia, tachypnea, or hypoxemia. D-dimer was elevated (6834ng/dL), with normal troponin-T and pro Btype natriuretic peptide. In light of the findings, a contrasted Chest-CT was performed, showing a saddle pulmonary embolus (PE) in left pulmonary artery and non-obstructing thrombus in right main pulmonary artery. Electrocardiogram showed sinus rhythm and right-bundle-branch block, but no “S1Q3T3 pattern”.Patient was admitted to ICU and received enoxaparin. COVID-19 was negative. She remained hemodynamically stable. Lower extremities venous duplex scan was negative for DVT, echocardiogram reported normal ventricular function and dilation of inferior vena cava, consistent with elevated right atrial pressure. Patient was discharged on apixaban.Discussion: Several COVID-19 case-studies have highlighted the association with VTE4-5. During SARSCoV-1 epidemic the reported incidence of DVT and PE was 20% and 11% respectively10. The underlying pathophysiology is probably related to excessive inflammatory response “cytokine storm” and microvascular thrombosis. It is known that infections, either viral, bacterial or fungal can activate immune-thrombotic pathways as initial inflammatory response. However, in COVID-19, such response is disproportioned. McGonagle6 described that the tropism for angiotensin-converting enzyme 2 expressed on type-II pneumocytes and the proximity of these cells to vasculature, combined with the aforementioned inflammation may play the main role. Is COVID-19 a risk factor for PE at the recovery phase of the disease? When are the patients at the highest risk for VTE? Should COVID-19 PE be treated as provoked? Can D-dimer be relied upon as indicator for anticoagulation initiation in these settings? and if so, at what levels? Should COVID-19 patients be discharged on prophylactic anticoagulation? As more patients are being treated, COVID-19's role as risk factor for VTE in the recovery is still unclear.
ABSTRACT
Introduction: SARS-CoV-2, the cause of COVID-19, was first identified in December 2019 and declared a pandemic by the WHO in March 2020. Knowledge about COVID-19 is growing exponentially, but long-term pulmonary outcomes and factors influencing the development of fibrosis, such as intubation status, remain uncertain. We present three patients with no previous underlying pulmonary disease who developed post-ARDS fibrosis secondary to COVID-19 and continue to be severely impaired six months after initial hospitalization. Case Series: Three patients developed post-ARDS pulmonary fibrosis secondary to COVID-19 within one month of acute infection. Two males and one female, aged 56 to 75, were admitted 4 to 7 days after symptom onset and required ICU admission. One patient required 12 days of mechanical ventilation and was managed with noninvasive pressure ventilation (NIPPV) for 15 days and one was managed with HFNC for 37 days. One patient receiving oxygenation via HFNC and oxymask developed pneumomediastinum on day 30 of admission and was managed conservatively. All patients demonstrated characteristic bilateral ground-glass opacities on CT chest and follow up scans showed traction-bronchiectasis with diffuse fibrotic changes. C-reactive protein level on admission ranged from 41.22 to 30.79, and all patients received systemic corticosteroids along with therapeutic anticoagulation. All patients met criteria for home oxygen on discharge. Discussion: Post-ARDS pulmonary fibrosis in COVID-19 appears to be multifactorial. Possible outcome predictors identified include: advanced age, illness severity, length of ICU stay, mechanical ventilation, smoking, and chronic alcoholism. While the mechanism remains uncertain, virus-induced cell injury and inflammatory mediators may be responsible for the accelerated lung damage observed. Management has evolved over the course of the pandemic from emphasis on early intubation to maximal use of non-invasive pressure ventilation, taking into consideration the potential harm associated with patient self-inflicted lung injury versus ventilator induced injury. Our case series demonstrates three patients with varying comorbidities and elevated inflammatory markers, who received steroids and therapeutic anticoagulation. All patients had similar clinical outcomes irrespective of intubation status. Conclusion: Intubation status did not appear to have an impact on progression to post-ARDS pulmonary fibrosis in our case series of three patients. All patients developed fibrosis and continued to experience severe dyspnea requiring home oxygen six months after acute infection. Long-term observational cohort studies are required to better establish if mechanical ventilation is a predictor of post-ARDS pulmonary fibrosis from COVID-19.