Background: Fibrinogen (FIB) levels less than 150 mg/dL have been associated with increased rates of bleeding and lower survival in critically ill cirrhosis patients. Objective: We aimed to determine if treatment with cryoprecipitate (CRYO) for low FIB levels were associated with bleeding complications or survival. Patients / Methods: 237 cirrhosis patients admitted to an intensive care unit at a tertiary care liver transplant center with initial FIB levels less than 150 mg/dL were retrospectively assessed for CRYO transfusion, bleeding events, and survival outcomes. Results: The mean MELD score was 27.2 (95% CI 26.0 - 28.3) and CLIF-C Acute on Chronic Liver Failure (ACLF) score was 53.4 (51.9 - 54.8). Ninety-nine (41.8%) were admitted for acute bleeding and the remainder were admitted for non-bleeding illnesses. FIB level on admission correlated strongly with disease severity. After adjusting for disease severity, FIB on admission was not an independent predictor of 30-day survival (HR 0.99, 95% CI 0.99 - 1.01, p = 0.68). CRYO transfusion increased FIB levels but had no independent effect on mortality or bleeding complications (HR 1.10, 95% CI 0.72 - 1.70, p = 0.65). Conclusions: In cirrhosis patients with critical illness, low FIB levels on presentation reflect severity of illness but are not independently associated with 30-day mortality. Treatment of low FIB with CRYO also does not affect survival or bleeding complications suggesting FIB is an additional marker of severity of illness but is not itself a direct factor in the pathophysiology of bleeding in critically ill cirrhosis patients.
Objective: The ratio of the partial pressure of arterial oxygen to fraction of inspired oxygen is a key component of the sequential organ failure assessment score that operationally defines sepsis. But, it is calculated infrequently due to the need for the acquisition of an arterial blood gas. So, we sought to find an optimal imputation strategy for the estimation of sepsis-defining hypoxemic respiratory failure using oximetry instead of an arterial blood gas. Approach: We retrospectively studied a sample of non-intubated acute-care patients with oxygen saturation recorded ⩽10 min before arterial blood sampling (N = 492 from 2013–2017). We imputed ratios of the partial pressure of arterial oxygen to the fraction of inspired oxygen and sepsis criteria from existing imputation equations (Hill, Severinghaus–Ellis, Rice, and Pandharipande) and compared them with the ratios and sepsis criteria measured from arterial blood gases. We devised a modified model-based equation to eliminate the bias of the results. Main results: Hypoxemia severity estimates from the Severinghaus–Ellis equation were more accurate than those from other existing equations, but showed significant proportional bias towards under-estimation of hypoxemia severity, especially at oxygen saturations >96%. Our modified equation eliminated bias and surpassed others on all imputation quality metrics. Significance: Our modified imputation equation, is the first one that is free of bias at all oxygen saturations. It resulted in ratios of partial pressure of arterial oxygen to fraction of inspired oxygen and sepsis respiratory criteria closest to those obtained by arterial blood gas testing and is the optimal imputation strategy for non-intubated acute-care patients.
Background:Clostridiodes difficile is the leading healthcare-associated pathogen, with significant morbidity associated with acute C. difficile infection (CDI). However, polymerase chain reaction stool testing is unable to differentiate colonization from infection, leading to frequent overdiagnosis, unnecessary iatrogenesis, and additional costs. As a result, IDSA guidelines do not recommend C. difficile testing in patients with diarrheal symptoms attributed to other causes, including laxatives. Our group has previously investigated the use of a computerized clinical decision support (CCDS) tool to reduce inappropriate C. difficile testing in a single tertiary-care health system, with a subsequent 41% reduction in testing. We investigated the reduction in proportion of inappropriately completed tests with the randomized addition of a laxative alert to our existing CCDS. Methods: An existing electronic medical record-based CCDS tool was augmented by the addition of an automatic alert that notified the user if a patient received any of a set of identified laxative medications within 48 hours. During the 78-day pilot period, users encountered the existing CCDS or the CCDS with laxative alert (CCDS-LA), randomized by patient identification number. A proportional χ2 analysis was used to compare the proportion of aborted to completed tests among patients who met laxative criteria in the CCDS versus CCDS-LA groups. Results: In total, 187 test orders were attempted during the pilot period in 119 patients meeting the laxative alert criteria, with 43.3% order attempts randomized to the existing CCDS and 56.7% to the CCDS-LA. Of order attempts via the CCDS-LA, 50.0% were completed, compared to 64.2% of orders completed via the existing CCDS (22.1% relative reduction in test completion; P = .0525). Conclusions: We demonstrated substantially fewer completed C. difficile tests among patients receiving laxatives who were randomized to modified laxative-alert CCDS. Although our result did not reach statistical significance, the trend toward reduced inappropriate testing prompted the CCDS-LA alert to be adopted hospital-wide following completion of the test period. Further analyses of the pre- and postintervention periods are required to determine whether this intervention significantly impacts testing rates over time, as well as to determine the durability and safety of the CCDS-LA. Additional analyses are also needed to assess the impacts on hospital-onset CDI rate and the associated costs.Funding: NoneDisclosures: None
Introduction: The usage of cytogenetics and next generation sequencing (NGS) has become more prominent in recent years for risk stratification of patients (pts) with myelodysplastic syndromes (MDS). Management of these patients is a multi-faceted endeavor which requires understanding of how MDS genetics interacts with a patient's lifestyle and co-morbidities. Obesity rates in the United States continue to rise; the current rate in Virginia is 30% (Centers for Disease Control and Prevention, CDC). This study analyzed whether body mass index (BMI) at diagnosis was correlated with the number or type of MDS mutations seen on initial NGS and whether obesity influenced outcomes stratified by individual mutations. Methods: Adult pts diagnosed with MDS at the University of Virginia from August 2012 to December 2019 who had cytogenetics and NGS panels done prior to initiation of MDS therapy were included. Any patient without the aforementioned initial diagnostic information was excluded. MDS disease characteristics, treatment type, comorbidities, and patient demographics were assessed including weight, height, and BMI (categories defined per CDC) at time of diagnosis. The primary aim of this analysis was to evaluate the association of BMI with the number and type of mutations on NGS panel at diagnosis. Wilcoxon-Mann-Whitney tests were used to explore the difference in BMI by presence of 13 mutations of interest: ASXL1, DNMT3A, FLT3, IDH1, IDH2, NPM1, NRAS, SETBP1, SF3B1, SRSF2, TET2, TP53, and U2AF1. The Spearman correlation coefficient was used to assess the relationship between BMI and total number of mutations. Kaplan-Meier estimates, log rank tests, and Cox proportional hazard models were used for time-to-event analyses. All analyses were performed using SAS 9.2 (SAS Institute, Cary, NC). Results: 143 MDS pts met inclusion criteria with a median age at diagnosis of 69 (range 39-87) and 60.7% (n=88) were male. The median weight was 81.3 kg and the median BMI at diagnosis was 27.7 kg (range 16.04-52.66). There were 29 pts in the normal BMI class (20%), 4 pts in the underweight class (3%), 38 pts in the obese class (26%), and 72 pts in the overweight class (50%). By IPPS-R risk scoring system, 64 pts were low or very low risk (44%), 39 pts intermediate risk (27%), and 41 pts high or very high risk (29%). There was no difference in the median number of mutations across BMI groups with a spearman correlation coefficient of 0.05 (Figure 1). However, the median BMI was significantly lower in patients with the NPM1 mutation versus those without (p=0.04), diagnosed prior to the WHO re-classification of these patients to acute myeloid leukemia (AML). Presence of the NPM1 mutation in MDS is also associated with worse PFS and an increased hazard ratio of 9.4 (p=0.0003), likely behaving similarly to AML. In comparison, presence of the SF3B1 mutation was found to be protective wherein patients who lacked the mutation had an increased hazard ratio of 6.0 (p=0.0133). BMI alone did not predict for progression free survival (PFS) or overall survival (OS); this was also true regardless of patient residency based on zip code. However, obese patients exhibiting the NPM1 and SF3B1 had better PFS (Figure 2). Moreover, the landmark analysis indicates among patients who are alive and free of progression at 20 months after MDS diagnosis, overweight patients exhibit better PFS than normal/underweight or obese patients (p=0.0192) (Figure 3). Conclusion: While BMI in pts with MDS does not appear to predict the gross number of NGS mutations, NPM1 mutations occurred more often in pts with low BMIs. Overweight pts who did not progress by 20 months have a better PFS. Prospective and larger retrospective studies are needed to expand on the findings that BMI may have an unexplored potential in stratifying pts with newly diagnosed MDS. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
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