Marker Of In-hospital Mortality Research Articles

Importance of qSOFA Score in Terms of Prognosis and Mortality in Critical Care Patients.

Recent studies have analyzed the qSOFA (quick sequential organ failure assessment) score as a prognostic indicator in many diseases, particularly sepsis. However, the effect of qSOFA score on prognosis and mortality in critical care patients has not been sufficiently analyzed. There is not enough data, especially regarding its use as critical care mortality and prognosis scoring. In this study, we aimed to analyze the effect of qSOFA score on mortality and prognosis in critical care unit (CCU) patients. This study was conducted retrospectively using the chart review method. The APACHE II (Acute Physiology and Chronic Health Evaluation II) and SOFA (Sequential Organ Failure Assessment) scores of patients admitted to our CCU were compared with the qSOFA score. In addition, the need for intubation and mechanical ventilation, short- and long term mortality rates, the relationship between blood gas lactate values and qSOFA score were analyzed. A total of 1816 patients were included in the study. During critical care follow-up, 374 (20.6%) of our patients died, and at the end of 6 months, 796 (43.8%) of our patients died. A statistically significant association was found between in-hospital mortality and qSOFA, SOFA scores and lactate levels (P = 0.001, P = 0.001, P = 0.01 respectively). A statistically significant association was found between 6-month mortality and SOFA score only. (P = 0.001) The SOFA score appeared to be the most successful predictor of mortality. The cut-off for mortality using the ROC curve was ≥ 7 [sensitivity 78.1%; specificity 85.9%; AUC 0.91; 95% confidence interval (CI), 0.89 to 0.92; P = 0.001]. qSOFA scoring also performed well. The cut-off value for mortality using the ROC curve was ≥ 2 (sensitivity 42.5%; specificity 93.9%; AUC 0.83;95% CI, 0.80-0.85; P = 0.001). We believe that the qSOFA score can be used as a marker for in-hospital mortality and prognosis in critical care patients. Especially in cases where the qSOFA score is ≥ 2, it provides valuable information regarding mortality and prognosis.

Hemogram as marker of in-hospital mortality in COVID-19

The clinical impact of COVID-19 disease calls for the identification of routine variables to identify patients at increased risk of death. Current understanding of moderate-to-severe COVID-19 pathophysiology points toward an...

Eosinopenia and neutrophil-to-lymphocyte count ratio as prognostic factors in exacerbation of COPD

Exacerbations of Chronic Obstructive Pulmonary Disease (AECOPDs) are one of the most important clinical aspects of the disease, and when requiring hospital admission, they significantly contribute to mortality among COPD patients. Our aim was to assess the role of eosinopenia and neutrophil-to-lymphocyte count (NLR) as markers of in-hospital mortality and length of hospitalization (LoH) among patients with ECOPD requiring hospitalization. We included 275 patients. Eosinopenia was associated with in-hospital deaths only when coexisted with lymphocytopenia, with the specificity of 84.4% (95% CI 79.6–88.6%) and the sensitivity of 100% (95% CI 35.9–100%). Also, survivors presented longer LoH (P < 0.0001). NLR ≥ 13.2 predicted in-hospital death with the sensitivity of 100% (95% CI 35.9–100%) and specificity of 92.6% (95% CI 88.8–95.4%), however, comparison of LoH among survivors did not reach statistical significance (P = 0.05). Additionally, when we assessed the presence of coexistence of eosinopenia and lymphocytopenia first, and then apply NLR, sensitivity and specificity in prediction of in-hospital death was 100% (95% CI 35.9–100) and 93.7% (95% CI 90.1–96.3), respectively. Moreover, among survivors, the occurrence of such pattern was associated with significantly longer LoH: 11 (7–14) vs 7 (5–10) days (P = 0.01). The best profile of sensitivity and specificity in the prediction of in-hospital mortality in ECOPD can be obtained by combined analysis of coexistence of eosinopenia and lymphocytopenia with elevated NLR. The occurrence of a such pattern is also associated with significantly longer LoH among survivors.

Abstract 17073: In Hospital Outcomes in Patients With Infective Endocarditis With and Without Liver Cirrhosis - Insight From National Inpatient Sample

Introduction: Chronic liver disease is known to be an important prognostic factor in determining morbidity and mortality in preoperative risk assessment and mortality in general. Data are limited on outcomes in patients with infective endocarditis (IE) and comorbid concurrent liver cirrhosis. Objective of our study is to evaluate the clinical outcomes of patient with IE with and without underlying liver cirrhosis and determining in-hospital mortality and outcomes of interest i.e. renal failure, cardiogenic shock, hematologic (coagulopathy/thrombocytopenia) and hepatic complications (hepatic encephalopathy/hepatitis). Hypothesis: Liver Cirrhosis worsen clinical outcomes in patients with IE. Methods: Patients with principle diagnosis of IE with and without liver cirrhosis were identified by querying the Healthcare Cost and Utilization (HCUP) database, specifically, National Inpatient Sample for year 2013 and 2014 based on ICD9 codes. Results: During 2013 and 2014, a total of 17, 952 patients were admitted with diagnosis of IE, out of whom 780 had concurrent liver cirrhosis. There was an increased in-hospital mortality [15.6% vs 10.2%, aOR 1.57(1.27-1.93)], acute kidney injury [41.4% vs 32.6%, aOR 1.45(1.24-1.69)], coagulopathy/thrombocytopenia [32.1 vs 14.7%, aOR 2.87(2.44-3.37)] in patients with IE with liver cirrhosis when compared to patients with IE without liver cirrhosis. IE without liver cirrhosis underwent increased number of interventions i.e. aortic (7.2 vs 3.7%, 0.51(0.34-0.76)] and mitral (4.9% vs 3.4%, aOR 0.39(0.23-0.69)] valvular replacements as compared to without liver cirrhosis. Conclusions: Liver cirrhosis is an important prognostic marker of in-hospital mortality in patients with concurrent IE. High risk surgical state with coagulopathy, bleeding complications, worsening hepatic complications and renal dysfunction lead to higher mortality.

Nondyspnogenic acute hypoxemic respiratory failure in COVID-19 pneumonia.

COVID-19 is a multifaceted disease and respiratory failure is a common manifestation. Interestingly, several reports are suggesting that many patients with COVID-19 pneumonia seem to present less respiratory effort and experience less dyspnea when exposed to acute respiratory failure and hypoxemia, a phenomenon called “silent,” “happy,” or even “apathetic” hypoxemia. We present a personal view exploring potential pathways associated with this intriguing clinical feature. We also suggest that “nondyspnogenic acute hypoxemic respiratory failure” is a more accurate terminology to describe this clinical finding in COVID-19, as hypoxemia may not be the only trigger for dyspnea in patients with pneumonia associated with respiratory failure. Acute hypoxemic respiratory failure is a common clinical manifestation in patients with pneumonia caused by the new severe acute respiratory coronavirus 2 (SARS-CoV-2) infection and is a marker of in-hospital mortality (1, 2). The autonomic nervous system orchestrates a complex respiratory and cardiovascular response during a hypoxemic stress. Besides the lung and cardiovascular manifestations documented in patients with the new coronavirus disease 2019 (COVID-19) (3), there is growing evidence suggesting that SARS-CoV-2 is a neurotropic virus and may invade the peripheral and central nervous system (CNS) by several routes, with widespread brain injury, including the respiratory and cardiovascular autonomic centers (4, 5). In clinical practice, acute hypoxemic respiratory syndromes, such as those caused by bacterial or viral pneumonia, are generally accompanied by dyspnea sensation (6–8). In a cohort of 395 patients with community-acquired pneumonia, 94% of those with severe pneumonia presented with dyspnea (7). Interestingly, several anecdotal reports are suggesting that patients with COVID-19 pneumonia have an atypical nondyspnogenic response to acute hypoxemic respiratory failure (9–11). Some argue that these patients present with less respiratory effort and experience less dyspnea even when exposed to critical hypoxemia, a phenomenon called “silent,” “happy,” or even “apathetic” hypoxemia (11–13). The term “silent hypoxemia” has been criticized because dyspnea is a complex and multifactorial symptom not only dependent on systemic hypoxemia (14). Previous studies in healthy humans suggest that hypoxemia per se is generally well tolerated and hypoxemia associated with acute respiratory failure may be only a marker of a more complex respiratory pathophysiology and not the determinant cause of dyspnea (15–17). Moreover, in controlled human experiments, respiratory effort is not necessarily associated with dyspnea sensation (18). Therefore, in this review, we prefer to use the term nondyspnogenic acute hypoxemic respiratory failure in COVID-19 pneumonia to describe the apparently comfortable status of patients with COVID-19, despite marked acute hypoxemic respiratory failure (9, 10). Nondyspnogenic acute hypoxemic respiratory failure is not an expected feature in clinical practice when assisting patients with pneumonia. Conversely, nondyspnogenic respiratory failure is more common in chronic conditions, such as chronic pulmonary obstructive disease and pulmonary fibrosis, and can also be seen in high altitude sickness (19). The limited understanding of the complex mechanisms involved in dyspnea sensation and of the neuropathology associated with SARS-CoV-2 infection is a barrier to explain why patients with severe hypoxemia may present to the emergency department without any physical discomfort and almost asymptomatic. Two initial hypotheses have been speculated to explain the installation of nondyspnogenic acute hypoxemic respiratory failure in these circumstances: the association of iso/hypocapnia, preventing the uncomfortable feelings of air hunger (19); and the maintenance of pulmonary mechanics (total dead space, lung compliance, and resistance) in near-normal range in the first stages of respiratory failure, thus not increasing significantly the respiratory effort (19, 20). Although both mechanisms are biologically plausible, they fail to address why acute respiratory failure in COVID-19 pneumonia seems to be peculiarly undersensed by these patients. To integrate the current knowledge regarding SARS-CoV-2 infection with the peculiar nondyspnogenic acute hypoxemic respiratory failure in COVID-19 pneumonia, we hypothesize a different mechanism related to an early and complex interaction between SARS-CoV-2 infection and the peripheral and central nervous system disturbing the activation of brain regions responsible for dyspnea sensation during acute hypoxemic respiratory failure.

Augmentation index as an early marker of in-hospital mortality in patients with acute ischemic stroke.

Augmentation index as an early marker of in-hospital mortality in patients with acute ischemic stroke.

Sodium levels during hospitalization with acute myocardial infarction are markers of in-hospital mortality: Soroka acute myocardial infarction II (SAMI-II) project.

Abnormalities in sodium homeostasis are common in hospitalized patients. Hyponatremia upon admission is a poor prognostic marker in acute myocardial infarction (AMI) patients. However, little is known about the association between changes in sodium levels and in-hospital mortality. We delineated changes in sodium levels and studied the association of such changes with in-hospital mortality of AMI patients. Retrospective analysis of AMI patients hospitalized for > 6days. Sodium levels throughout the 6-day post-admission were divided into five equally sized groups (quintiles = Q) and thereafter categorized as follows: Q1 (< 135mEq/L), Q2-Q4 (135-140mEq/L, reference group), and Q5 (≥141mEq/L). in-hospital mortality. A total of 8306 patients (10,416 admissions) were included (mean age 67.8±14.0years, 33.4% women, 45.5% STEMI). In-hospital mortality was 6.6%. Q1 and Q5 upon admission were both related to higher risk for in-hospital mortality, compared with the reference group (OR 1.47 and OR 1.33, respectively, p < 0.001 each). Q1 was more frequent in non-survivors throughout the entire study period, while the prevalence of Q5 levels was similar in survivors and non-survivors upon admission carrying increasing mortality risk thereafter: for Q1 consistent OR 1.50, while for Q5 it, increased from OR 1.32 upon admission to OR 1.90 on the sixth day, p < 0.001. Low and high sodium levels are associated with increased risk for in-hospital mortality in patients with AMI. The risk is unchanged for hyponatremia, while it consistently increases for increased sodium levels.

The prognostic value of the relationship between right atrial and pulmonary capillary wedge pressure in diverse cardiovascular conditions

BackgroundPhysical examination of jugular venous pressure is used to estimate right atrial (RA) pressure and infer left-sided filling pressure to assist volume management. Previous studies in advanced heart failure patients showed about 75% concordance between RA and pulmonary capillary wedge (PCW) pressures. We sought to determine the relationship between mean RA and mean PCW pressure and assess the clinical significance in a broad population of patients undergoing invasive right heart catheterization (RHC). MethodsWe examined 4135 RHC cases at a single academic medical center from February 2007 to December 2014, analyzing baseline variables, hemodynamic data, and in-hospital mortality. ResultsThe overall Pearson correlation for mean RA and PCW pressures was 0.68 with 70% concordance between dichotomized pressures (RA ≥10 and PCW ≥22 mmHg). Results were similar in subgroups with heart failure (r=0.67, 72%), STEMI/NSTEMI (r=0.60, 69%), unstable angina (r=0.78, 69%), stable/no angina (r=0.72, 67%), and valvular disease (r=0.61, 72%; Chi-square P=.15). Mean RA pressure was independently associated with in-hospital mortality in multivariate analysis (OR 1.12 [95% CI 1.081-1.157] per 1 mmHg increase, P<.001). The RA/PCW ratio was not independently associated with in-hospital mortality. Mean RA pressure was also weakly associated with worse renal function (rho=−0.16, P<.001). ConclusionIn patients undergoing right catheterization for diverse indications, the mean RA and PCW pressures correlated moderately well, but there was discordance in a sizable minority, in whom assessment of left-sided filling pressures using estimated jugular venous pressure may be misleading. Elevated right atrial pressure is a marker for in-hospital mortality.

Validity of GRACE Risk Score as a Prognostic Marker of In-hospital Mortality after Acute Coronary Syndrome.

To determine validity of GRACE risk score as a determinant of immediate death during hospitalization for Acute Coronary Syndrome (ACS) and analyze the percentage of cardiac deaths among high, intermediate and low risk groups. Cross-sectional study. Coronary Care Unit of Mayo Hospital, Lahore, from April to July 2015. Patients with acute chest pain were selected according to inclusion and exclusion criteria. Online GRACE risk score calculator was used to determine the predicted risk of death following ACS according to the score. Data was analyzed on SPSS 20. Quantitative data was in the form of median (IQR). Discrimination of GRS was evaluated by using c-statistics, area under the ROC curve. Calibration of GRS was tested by Hosmer-Lameshow test. The correlation between GRACE risk score category and predicted risk of death was determined using Kendall's tau-b bivariate correlation test. Shapiro-Wilk test was applied to check normality of data. The various parameters of GRACE score were studied in patients using Mann-Whitney U-test. The statistically significant p-value was <0.05. There were 165 cases in the study. Overall median GRS was 139 (54). In-hospital deaths were 12.2%. Discrimination of GRS evaluated by area under the ROC curve was 0.913 (95% CI 0.843-0.982; p<0.0001). Application of Hosmer-Lameshow test revealed a p-value of 0.236. Kendall's tau-b bivariate correlation coefficient was 0.384 (p<0.001). GRS is an excellent tool to stratify patients of ACS into different risk categories according to various parameters noted at the time of presentation. The risk of predicted death according to the score was variable among different cases, especially those with higher scores. Even though GRS is an effective and valid tool, but it has some tendency of overestimating probability of death following ACS and may require a fine tuning in some cases.

Red cell distribution width: A marker of in-hospital mortality in ST-segment elevation myocardial infarction patients?

BackgroundRed cell distribution width (RDW) is the percentage of the erythrocyte volume variation and has been identified as a biological marker in patients with cardiovascular disease. Increased levels have been associated to worse clinical outcomes and it is suggested that it could be useful as a prognostic risk factor in this group of patients. MethodsThis was an observational, prospective, longitudinal and analytic study with the objective of determining the correlation between RDW and in-hospital mortality in ST elevation myocardial infarction (STEMI) patients. 61 patients were included. We analyzed the correlation between RDW and in-hospital mortality as well as that between RDW and the GRACE risk score at hospital admission. Pearson correlation was determined in both cases by using IBM SPSS statistics software. Results61 STEMI patients were included, 77% (47) male and 14% (14) female. Average age was 61.8±11.7 years. Average GRACE risk score was 154.9±40.3. Average RDW was 14.3±1.07. In-hospital mortality presented in 5 (8.1%) cases. It was found, as expected, a positive correlation between in-hospital mortality and the GRACE risk score (r=0.314, P=0.05). Regarding the primary end-point of the study, it was found a positive correlation between RDW and in-hospital mortality (r=0.343), however there was no statistical significance. Regarding the secondary end-point we observed a positive statistically significant correlation between RDW and the GRACE risk score at hospital admission (r=0.410, P=0.01). ConclusionsRDW is a biological marker of easy acquisition that does not generate additional cost to neither the patient nor the health institutions. High RDW levels could be useful to predict in-hospital mortality in STEMI patients, as well as to give additional value to established risk scores such as the GRACE.

Arterial carbon dioxide tension on admission as a marker of in-hospital mortality in community-acquired pneumonia

Respiratory failure is the leading cause of death among patients admitted with community-acquired pneumonia. We sought to determine the association between arterial carbon dioxide tension (P(a)CO(2)) and in-hospital mortality in patients admitted with pneumonia. We analyzed data from 2171 patients aged >or=17 years who had been admitted for community-acquired pneumonia to an acute care hospital in Edmonton, Alberta. We compared the risk of all-cause in-hospital mortality using a Cox proportional hazards model across categories of P(a)CO(2). Overall, in-hospital mortality was 10% (n = 218). Compared with patients with normal P(a)CO(2) values (40 to 44 mm Hg), in-hospital mortality was greater (adjusted odds ratio [OR] = 1.8; 95% confidence interval [CI]: 1.0 to 3.2) among patients with hypocapnia (P(a)CO(2) <32 mm Hg). In-hospital mortality was also greater (OR = 2.6; 95% CI: 1.5 to 4.5) in patients with hypercapnia (>or=45 mm Hg). In-hospital mortality was similar in patients with P(a)CO(2) values between 32 and 35 mm Hg (OR = 1.55; 95% CI: 0.89 to 2.79) and those with values between 36 and 39 mm Hg (OR = 1.42; 95% CI: 0.77 to 2.61). Among patients admitted with community-acquired pneumonia, in-hospital mortality was greater in those with hypocapnia or hypercapnia. These data suggest that measurement of P(a)CO(2) adds prognostic information to standard prediction rules and should be used for clinical and epidemiologic purposes to risk-stratify in-hospital patients with community-acquired pneumonia.

Right ventricular involvement in acute myocardial infarction.

The presence of right ventricular dysfunction in patients with acute myocardial infarction has important implications. It is a marker for in-hospital mortality and failure to recognize it may lead to inappropriate treatment with serious consequences for the patient. Patients surviving the acute event do, however, have a relatively good long-term prognosis.