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Objective. To assess the impact of obesity and overweight on the course of COVID-19. Patients and methods. This prospective study included 218 patients with SARS-CoV-2 infection aged 18 to 94 years hospitalized between June 2020 and March 2021. We evaluated their clinical and laboratory parameters and their association with body weight. All patients were divided into 3 groups depending on their body mass index (BMI). Group 1 included 81 patients with grade 1-3 obesity (BMI >=30);group 2 comprised 71 overweight patients (BMI >=25 and <30);group 3 included 66 patients with normal body weight (BMI >=18.5 and <25). We analyzed clinical symptoms (including shortness of breath, fever, myalgia, headache, fatigue, changes in the oropharynx, cough, rhinorrhea, sore throat, anosmia, and diarrhea), prevalence of concomitant disorders and complications, findings of computed tomography and pulse oximetry, and findings of instrumental and laboratory examinations (complete blood count, urine test, electrocardiography, echo cardiography, biochemical assays, including C-reactive protein, procalcitonin, alanine aminotransferase, aspartate aminotransferase, lactate, lactate dehydrogenase, activated partial thromboplastin time, prothrombin index, D-dimer, ferritin). Data analysis was performed using the Statistica 6.0 software. Results. We found that overweight and obese patients were more likely to have the main COVID-19 symptoms and comorbidities than those with normal weight. Overweight and obese patients also required respiratory support more frequently than patients with normal weight. Obese and overweight patients had more severe systemic inflammation (CRP, procalcitonin), cytolysis (ALT, AST), and thrombosis (D-dimer). Conclusion. Our findings suggest that obesity and overweight are the factors associated with a more severe SARS-CoV-2 infection, which should be considered when planning their treatment and developing resource strategies.Copyright © 2022, Dynasty Publishing House. All rights reserved.
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Objective: assessment of the efficacy and safety of the use of anticoagulant, glucocorticosteroid, metabolic therapy in patients with COVID-19 at the inpatient stage of treatment. Material and methods. In February 2021, a prospective, randomized, single-center, continuous comparative study was organized on the basis of the Gomel City Clinical Hospital No. 3, which included 827 patients with moderate and severe clinical course of COVID-19. Results. Stratification of the risks of an unfavorable outcome in patients with moderate and severe clinical course of COVID-19 made it possible to optimize treatment, with the selection of optimal doses of anticoagulant and glucocorticosteroid therapy, which led to an increase in patient survival. A high level of blood lactate reflects the degree of damage to the lung tissue, the severity of the course of the disease and requires an increase in the dose of anticoagulant therapy. The use of thiotriazoline effectively reduces the level of lactate, which makes it possible to restore the energy balance of the cell. Conclusion. The use of therapeutic (intermediate) doses of anticoagulant and optimal glucorticosteroid therapy in patients at high risk of poor outcomes with moderate and severe clinical course of COVID-19, can increase the survival rate from 82.1 to 96.8%, p<0.0001. The appointment of anticoagulant therapy was complicated by "minor" bleeding in 2.13% in the main group, in 2.11% in the control group, p>0.05, and the use of glucocorticosteroids was complicated by newly diagnosed diabetes mellitus (2.13% in the main group, 1.81% in the control group, p>0.05), which allows us to consider the therapy used is safe. The use of the metabolic, antioxidant agent thiotriazoline in patients with an LDH level of more than 800 U/L and with a high risk of an unfavorable outcome led to a decrease in LDH within five days of treatment by 447.9 U/L in the main group compared with the control group by 124.0 U/L (p=0.0001), which was accompanied by an improvement in the general condition, increased physical activity, and an earlier start of rehabilitation.Copyright © 2022 by the authors.
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Introduction: The clinical and laboratory characteristics of patients who died with COVID 19 yet to be elucidated. Aims and objectives: We were aiming at identifying potential contributory factors for the mortality in COVID 19. Method(s): Patients died with COVID 19 at the intensive care unit (ICU), National Hospital, Kandy, Sri Lanka from 01.01.2021 to 31.12.2021 were retrospectively studied. Result(s): 79 deaths were analyzed. Males (44/79);median age 63 years (19, 94). Mean hospital and ICU stay were11 days (interquartile range-IQR:7,14), 7days (IQR: 2.5,9) subsequently. Median of 2 comorbidities (0,5) were present;diabetes(n=43), hypertension(n=43), ischemic heart disease(n=21), chronic kidney disease(n=10), post kidney transplant recipients(n=10), other(n=10). 14/79 had none. Mean systolic blood pressure on admission:130 mmHg (IQR: 115,148), mean SpO2/FiO2 ratio was 147(IQR 95,163), mean serum lactate level was 1.9(IQR: 1.08,2.25). The average heart rate 95(IQR: 81,108);mean respiratory rate was 28(IQR: 22, 33);mean random blood sugar was 229(IQR: 156, 289). 15/79 documented to be vaccinated (one =4/11: two=6/15: three=5/15). C-Reactive protein was available in 72/79;mean=122(IQR: 38, 182). Procalcitonin (PCT) on admission was available in 32/79;median=3.70 (0.01, 96), PCT was >1 in 16/32. 8/18 blood culture samples, 4/12urine culture samples detected bacterial pathogens. 25/46 demonstrated either PCT>1 or blood and/or urine culture positivity. Conclusion(s): Higher proportion of patients were unvaccinated, with multiple comorbidities predominantly diabetes. Hyperinflammation was common and significant proportion had bacterial co-infection.
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The purpose of this study was to investigate fitness indicators through cardiac stress test in post-COVID-19 athletes, who were not hospitalized, vs healthy ones. Forty male professional Greek soccer players, were divided into two groups: previously infected with COVID-19 and non-hospitalized (n=20, Age: 25.2+/-4.1 yrs, BSA: 1.9+/-0.2 m2, body fat: 11.8+/-3.4 %) vs. control (n=20, Age: 25.1+/-4.4 yrs, BSA: 2.0+/-0.3 m2, body fat: 10.8+/-4.5 %). Inclusion criteria were: age >=20-to-<=30 yrs, training age >=6 yrs, without recent injury (>12 months) and asymptomatic infected with COVID-19 (<7 days). For each athlete, prior to assessment cardiopulmonary function (CPF) were recorded body composition, spirometry and lactate blood level. Differences between groups were assessed with the independent samples t-test (<0.05). Several differences were detected between the two groups (COVID-19 vs. non-COVID-19 athletes, Table 1) during CPF. Results didn't showed differences between groups in VO2max (55.7+/-4.4 vs. 55.4+/-4.6 ml/min/kg Table 1. Results between groups (*p<0.05, #p<0.001) Post-COVID-19 athletes characterized by increased respiratory work at both rest and maximum effort as well as hyperventilation during exercise, which may explain increased metabolic needs and mechanical stress.
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INTRODUCTION: Medical complications among pregnant peripartum patients are not common. However, certain disease such as obstetric hemorrhage or respiratory failure could be associated with poor outcome among obstetric patients whose biological systems are already stretched. When a peripartum patients encounter a severe medical condition, they are frequently transferred to a tertiary center for management of these patients' complex conditions. Our study investigated the outcomes of the peripartum patients who were transferred from other hospitals (Interhospital transfer [IHT]) to the Intensive Care Unit at an academic quaternary center. METHOD(S): We retrospectively analyzed all adult IHT peripartum patients to our institution's ICU between Jan. 2017 to Dec. 2021. We presented descriptive analysis for our patients and used multivariable ordinal regressions for association between demographic, clinical factors, and patients' length of stay (LOS) in the ICU (ICULOS), hospital (HLOS). RESULT(S): Among 1794 IHT peripartum patients, 59 patients were transferred directly to an ICU, 8 (13.6%) to Medical ICU, 2 (3.4%) Neuro ICU, 2 (3.4%) Surgical ICU and 47 (79.7%) to our Critical Care Resuscitation Unit. Patients' mean (Standard Deviation) age was 32 (6) years, SOFA score 3 (3), APACHE II 8 (4), median Respiratory Oxygenation (ROx) index was 13 [Interquartile Range 4-22], and serum lactate 11 [9-15] mmol/L. Respiratory failure occurred in 19 (32%), postpartum hemorrhage 9 (15%), sepsis 8 (14%) patients. 16 (27%) patients were infected with COVID-19. 24 (41%) needed intubation, 13 (22%) vasopressor, 4 (7%) Extracorporeal Membrane Oxygenation. Median ICULOS and HLOS was 5 [2-12], 8 [5-17] days. Only 1 (1.7%) died, while 45 (76.3%) were discharged home directly. Having COVID-19 infection was associated with both ICULOS (Correlation Coefficient -2,23, OR 0.06, 95%CI 0.02-0.65, P = 0.016) and HLOS (Corr. Coeff. -2.75, OR 0.06, 95%CI 0.01-0.37, P = 0.002). CONCLUSION(S): Although severe medical conditions were uncommon among interhospital transferred peripartum patients, they could be severe, especially during the COVID-19 pandemic. Fortunately, the mortality rate for peripartum patients in our study was very low. Further studies with larger sample sizes are needed to confirm our observation.
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SESSION TITLE: COVID-19 Case Report Posters 2 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Fusobacterium (FB) are anaerobic, Gram-negative bacilli found in the normal flora of the oral, gastrointestinal, vaginal and upper respiratory tract mucosa. It can cause soft tissue infections and rarely causes bacteremia, yet Fusobacterium bacteremia is associated with high rate of ICU admission, extended hospitalization and significant mortality. Pyogenic liver abscess is a rare indolent disease and is mostly secondary to bacterial infection. CASE PRESENTATION: A 39-year-old female with no comorbidities presented with nausea, vomiting, fatigue, diarrhea, fatigue, heavy menstrual bleed, and high-grade fever. Symptoms started four days before the presentation. She reported a positive COVID-test two weeks earlier and a new IUD placement five weeks before presentation. She is sexually active with one male partner and does not use a contact barrier. On presentation, she was hypotensive, tachycardic, ill-looking with rapid shallow breathing, and fever of 100.7. EKG showed sinus tachycardia, CXR showed no pulmonary disease. Blood tests were significant for leukocytosis, elevated serum lactic acid, and elevated D-dimer. CTA chest was remarkable for two 2x3 cm liver cysts. Patient was admitted to the MICU and started on IV fluids Boluses, Norepinephrine drip, Ceftriaxone and Azithromycin. Gynecology was consulted and recommended against removing the IUD as patient had no signs of IUD infection. Patient continued to be critically sick. Gynecology team was recontacted and removed the IUD and was uninfected on culture. Antibiotics were switched to Vancomycin and Piperacillin-Tazobactam. MRI liver with contrast confirmed the diagnosis liver abscess. Patient received bedside US-guided aspiration, it was remarkable for 16 cc of frank pus. Patient showed significant improvement after procedure and was transferred to the medical floor within 24 hours. Blood culture grew F. Necrophorum and antibiotics were switched to Clindamycin. DISCUSSION: FB is part of the vaginal flora. Mucosal disruption during IUD placement can precipitate disseminated infection with liver abscesses and/or sepsis. Absence of signs of GU tract infection or a non-infective IUD doesn't rule out FB sepsis. Patient Presented five weeks after IUD placement which fits the indolent nature of pyogenic liver abscess. Four cases of F. Nucleatum bacteremia were reported recently in Belgium in COVID patients. One of the cases was healthy young female. Our similar scenario raises a question about a potential association between COVID and risk of floral septicemia. Our patient has F. necrophorum. CONCLUSIONS: Patient presenting with sepsis and liver cyst should be evaluated for liver abscess as appropriate. Recent procedures and mucosal instrumentation can precipitate liver abscess and should be considered if the timing suggest an indolent course. Further studies are needed to evaluate a potential link between COVID infection and FB bacteremia. Reference #1: Goldberg EA, Venkat-Ramani T, Hewit M, Bonilla HF. Epidemiology and clinical outcomes of patients with Fusobacterium bacteraemia. Epidemiol Infect. 2013 Feb;141(2):325-9. doi: 10.1017/S0950268812000660. Epub 2012 Apr 17. PMID: 22717143. Reference #2: Garcia-Carretero R. Bacteraemia and multiple liver abscesses due to Fusobacterium nucleatum in a patient with oropharyngeal malignancy. BMJ Case Rep. 2019 Jan 29;12(1):e228237. doi: 10.1136/bcr-2018-228237. PMID: 30700472;PMCID: PMC6352811. Reference #3: Wolff L, Martiny D, Deyi VYM, Maillart E, Clevenbergh P, Dauby N. COVID-19-Associated Fusobacterium nucleatum Bacteremia, Belgium. Emerg Infect Dis. 2021 Mar;27(3):975-977. doi: 10.3201/eid2703.202284. Epub 2020 Dec 8. PMID: 33292922;PMCID: PMC7920680. DISCLOSURES: No relevant relationships by Zainab Abdulsada No relevant relationships by Ahmed Abomhya No relevant relationships by Richard Fremont
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Introduction Over the last 20 months Sars-CoV-2 research revealed tremendous insights into the pathophysiology resulting in vaccines and first immunomodulatory therapies in an unprecedented short time [1]. However, the patient's individual clinical course is remarkably heterogenous and the effectivity of immunomo-dulatory therapies especially in critically ill patients is still very variable [2]. Therefore,a better understanding of the patients' individual immune response is needed [3]. Methods Unbiased machine learning grouped 323 Covid-19 patients treated at the Klinikum Rechts der Isar ICU into 3 different clusters. For this we queried the ICU electronic files and analyzed relevant clinical features (Fig. 1+2). To delineate biological differences within these clusters, we applied a 14 parameter flow cytometric panel to PBMCs from 27 of these CoV2 ICU patients. Flow data was analyzed using FlowJo and the FlowSOM package for unsupervised clustering (Fig. 3+4). Written informed consent was obtained from all patients and healthy controls. The study was approved by the local ethical review board (Az249/20 S-EB). Results Patients from cluster 1 had above ICU average respiratory function (Fig. 2), reduced liver function and received lower dose catecholamines. Immunologically these patients had significantly higher amount of CD3+CD4+ T helper cells (Fig. 5). Whilst B cell numbers were reduced, they were highly activated (HLA-DR-ordf). Activated monocytes produced high amounts of TNFa. Interestingly, proinflammatory CD14+ HLA-DRlow monocytes were not increased. Cluster 2 contains patients with renal impairment, an increased tendency for bacterial infection and elevated blood lactate levels. Cluster 3 is made up of long-term ICU patients with severely reduced respiratory function and high ECMO-dependency (Fig. 1). These patients had significantly increased ratios of activated innate immune cells. We have detected elevated levels of an interesting population of CD14+ HLA-DRlow monocytes, a well-established player of immune suppression [4], while cytotoxic T cells and B cells were found to be significantly reduced. Conclusion These data provided evidence that clinically defined endotypes of critically ill Covid-19 patients exhibit a distinct immune profile. The immunological differences support our theory that these endotypes might require personalized immunomodulatory therapies to restore the pro-regenerative cell function in ICU Covid-19 populations and improve patient outcome in the future.
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Introduction: Introduction: Euglycemic diabetic ketoacidosis (EuDKA) is a rare but increasingly reported serious adverse effect of SGLT2 inhibitors. There is not much published literature on the incidence of EuDKA and the factors associated with it. Though SGLT2 inhibitors were introduced as glucose lowering agents, recent trials have demonstrated their favourable cardiovascular outcome in heart failure and ability to retard progression of proteinuric kidney disease, including in non-diabetics. Hence use of this class of drugs is anticipated to increase exponentially, given the combined high global burden of diabetes, coronary artery disease and chronic kidney disease. As we embark to use the SGLT2 inhibitors in different clinical scenarios, it becomes imperative to report their adverse effects encountered in uncommon clinical conditions as well. Methods: Case history: A 42-year-old gentleman with history of type 2 diabetes mellitus for 15 years and coronary artery disease, presented with difficulty in climbing stairs and walking for 5 days with progressive difficulty in getting up from bed. He did not have past history of covid infection and had been immunised with 1 dose of covid vaccine. On examination, patient had normal hemodynamics. There was flaccid quadriparesis with areflexia and truncal muscle weakness. Nerve conduction study confirmed acute demyelinating polyradiculoneuropathy. His baseline laboratory investigations revealed normal renal parameters but metabolic acidosis was noted at the time of admission. Patient was started on iv immunoglobulin 2mg/kg and the motor weakness improved from grade 2/5 to 4/5. However, the high anion gap metabolic acidosis worsened over the next 4 days and patient developed acidotic breathing. His sugars were within normal limits and the patient was on metformin, glimeperide, vildagliptin, voglibose and dapagliflozin. As blood lactate levels were normal with urine acetone positivity, euglycemic diabetic ketoacidosis secondary to SGLT2 inhibitor was suspected and all the oral hypoglycemic agents were stopped. He was started on hydration and insulin infusion. After 48 hours of stopping dapagliflozin, acidosis resolved completely and the patient was reintroduced back on the other 4 class drugs. At follow-up, there was no recurrence of acidosis and patient was able to walk with support and physiotherapy. [Formula presented] Results: Discussion: SGLT2 inhibitors cause glycosuria and directly induce glucagon release from pancreas. Combined with insulin deficiency, this results in lipolysis, fatty acid oxidation and ketogenesis. They also cause increased renal reabsorption of ketone bodies. The precipitating factors for EuDKA identified so far include abrupt reduction in insulin dosage, reduced oral intake, infections, surgery, excess alcohol use, volume depletion, type 1 diabetes and heavy physical exercise. This is the first reported case of SGLT2 inhibitor-induced EuDKA in a patient with Guillain-Barre syndrome. As symptoms of dehydration may not be significant due to lack of hyperglycemia in EuDKA, there may be a delay in the diagnosis of this complication. Conclusions: Conclusion: The possibility of EuDKA to be kept in mind while evaluating metabolic acidosis in a diabetic patient on SGLT2 inhibitors. Temporarily withholding the SGLT2 inhibitors during an intercurrent illness will prevent the occurrence of the above serious adverse effect. No conflict of interest
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Red Blood Cells from COVID-19 Patients Show Evidence of Increased Oxidative Stress and Increased Lactate Influx Corona Disease 19 (COVID-19) is caused by SARS-CoV-2, a novel, highly infectious, single stranded RNA virus. In severe cases, excess oxidative stress produced by a ‘cytokine storm’ may generate excess reactive oxygen species (ROS) and lead to tissue damage in the lungs and elsewhere. As the potential role of RBCs in the pathophysiology of COVID-19 remains controversial (1), we investigated for evidence of increased oxidative stress and increased thrombotic tendency in RBCs from patients with COVID-19 infection. Following ethical approval and written informed consent, we used flow cytometry (BD FACSCanto II) to measure baseline RBC ROS following incubation with 2‘-7‘-dichlorofluorescein diacetate (DCF). RBC ROS were also measured following pre-incubation with hydrogen peroxide (H2O2) (2mM) +/- antioxidant N-acetyl cysteine (NAC) (0.6mM). We also measured RBC surface expression of adhesion molecules CD44, CD47 and CD242, as well as CD147. Results were expressed as mean +/- standard deviation (SD). RBC ROS were measured in 22 COVID-19 positive patients and in 10 age matched healthy controls. One patient died from respiratory failure, whilst only 3 others required ITU admission for continuous positive airway pressure (CPAP) or intubation. There was no statistical difference in mean basal RBC DCF mean fluorescence intensity (MFI) levels between COVID-19 positive patients and controls. However, mean increase in RBC DCF MFI following H2O2 incubation was significantly higher in the COVID-19 positive group (1105.7+/-336.3) compared to the control group (843.4+/-256.7)( p= 0.042). The increase in RBC DCF MFI in the COVID-19 positive group correlated with CRP (p=0.014) but not with D-dimer, serum ferritin or any complete blood count (CBC) parameters. Incubation of RBC with 0.6 mM NAC for 30 minutes prior to H2O2 exposure caused a mean reduction in DCF MFI of 26.7% in the COVID-19 positive group. RBC expression of CD44, CD47, CD242 and CD147 were measured In a separate cohort of COVID-19 positive patients (n=32), and in 22 age matched controls. There were no statistically significant differences in mean expression levels of CD44, CD47 and CD242 between the 2 groups. However, mean RBC CD147 MFI expression was higher in the COVID-19 group (1319.64+/-374.76) compared to controls (1061.59+/-253.33) (p=0.018). There was no significant correlation between RBC CD147 MFI and D-dimer, CRP, serum ferritin or any CBC parameters in the COVID-19 positive group. However, 21 of the 32 COVID-19 positive patients had blood lactate levels measured and there was a positive correlation between CD147 MFI expression and blood lactate (R=0.56, p=0.0077). Induction of oxidative stress by H2O2 resulted in a greater increase in ROS in RBCs from COVID-19 patients compared to controls and with correlation to CRP, despite the fact that there were very few patients with severe disease in the study. This suggests a role for oxidative stress in disease pathogenesis. Pre-incubation with NAC attenuated this increase in ROS, suggesting a possible role for antioxidants in therapy. Increased RBC cell surface expression of adhesion molecules CD44, CD47 and CD242 can facilitate RBC interaction with platelets and/or endothelial cells, potentially contributing to thrombosis. We found no increase in their expression in COVID-19 patients compared to controls although RBCs may contribute to thrombosis in COVID-19 infection by other means (1). CD147 is tightly associated with and enables proper expression of monocarboxylate transporter 1, the lactate transporter for RBCs. We found increased surface expression of CD147 on RBCs of COVID-19 patients, whilst CD147 expression showed a moderate correlation with serum lactate levels, suggesting that RBCs in COVID-19 infection may be acting as a lactate sink to protect against lactic acidosis. In summary, our study suggests that COVID-19 infection causes increased oxidative stress and increased lactate influx i RBCs. Further studies are warranted into the role of RBCs in COVID-19 infection. Reference: (1) Murphy P, Glavey S, Quinn J. Anemia and red blood cell abnormalities in COVID-19. Leuk Lymphoma 2021;62:1539 Disclosures: Quinn: Takeda: Honoraria. Glavey: Abbvie: Research Funding;Celgene and BMS company: Research Funding;Janssen: Honoraria, Research Funding;Amgen: Honoraria, Research Funding.
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Introduction/Purpose: COVID19 can be associated with life-threatening organ dysfunction due to septic shock, frequently requiring ICU admission, respiratory and vasopressor support. Therefore, clear clinical criteria are pivotal to early recognition of patients more likely to have poor outcomes, needing prompt organ support. Although most patients with severe COVID19 meet the Sepsis-3.0 criteria for septic shock, it has been increasingly recognized that, in this population, hyperlactatemia is frequently absent, possibly leading to an underestimation of illness severity and mortality risk. Purpose: This study aimed to identify the proportion of patients with COVID19 with hypotension despite adequate volume resuscitation, needing vasopressors to have a MAP>65mmHg, with and without hyperlactatemia, in ICU, and describe its clinical outcomes and mortality rate. Methods: We performed a single-center retrospective cohort study. All adult patients admitted to ICU with COVID19 were eligible and were further divided in 3 groups according to hyperlactatemia (lactate >2mmol/L) and persistent hypotension with vasopressor therapy requirement: (1) sepsis group (without both criteria), (2) vasoplegic shock (with persistent hypotension with vasopressor therapy requirement without hyperlactatemia) and (3) septic shock 3.0 (with both criteria). COVID19 was diagnosed using clinical and radiologic criteria with a SARS-CoV-2 positive RT-PCR test. Qui-square test was used for categorical variables and Kruskal-Wallis and logistic regression were used on continuous variables for statistical assessment of outcomes between groups. Kaplan-Meier survival curve and logrank test were also obtained. Results: 103 patients (mean age 62 years, 71% males) were included in the analysis (N=45 sepsis, N=25 vasoplegic shock;N=33 septic shock 3.0). SOFA score at ICU admission and ICU length of stay were different between groups (p<0.001). Ventilator-free days and vasopressor-free days were also different between sepsis vs vasoplegic shock and septic shock 3.0 groups (both p<0.001 and p<0.001, respectively), and similar in vasoplegic vs septic shock 3.0 groups (p=0.387 and p=0.193, respectively). Mortality was significantly higher in vasoplegic shock and septic shock 3.0 when compared with sepsis group (p<0.001) without difference between the former two groups (p=0.595). Log rank test of Kaplan-Meier survival curves were also different (p=0.07). Logistic regression identified the maximum dose of vasopressor therapy used (OR 1.065;CI 95%: 1.023-1.108, p=0.02) and serum lactate level (OR 1.543;CI 95%: 1.069-2.23, p=0.02) as the major explanatory variables of mortality rates. Conclusions: In severe COVID19 patients, the Sepsis 3 criteria of septic shock may exclude patients with a similarly high risk of poor outcomes and mortality rate, that should be equally approached. (Table Presented).