Association between perioperative fluid management and patient outcomes: a multicentre retrospective study.

BACKGROUND: Postoperative complications increase hospital length of stay and patient mortality. Optimal perioperative fluid management should decrease patient complications. This study examined associations between fluid volume and noncardiac surgery patient outcomes within a large multicentre US surgical cohort. METHODS: Adults undergoing noncardiac procedures from January 1, 2012 to December 31, 2017, with a postoperative length of stay ≥24 h, were extracted from a large US electronic health record database. Patients were segmented into quintiles based on recorded perioperative fluid volumes with Quintile 3 (Q3) serving as the reference. The primary outcome was defined as a composite of any complications during the surgical admission and a postoperative length of stay ≥7 days. Secondary outcomes included in-hospital mortality, respiratory complications, and acute kidney injury. RESULTS: A total of 35 736 patients met the study criteria. There was a U-shaped pattern with highest (Q5) and lowest (Q1) quintiles of fluid volumes having increased odds of complications and a postoperative length of stay ≥7 days (Q5: odds ratio [OR] 1.51 [95% confidence interval {CI}: 1.30-1.74], P<0.001; Q1: OR 1.20 [95% CI: 1.04-1.38], P=0.011) compared with Q3. Patients in Q5 had greater odds of more severe acute kidney injury compared with Q3 (OR 1.52 [95% CI: 1.22-1.90]; P<0.001) and respiratory complications (OR 1.44 [95% CI: 1.17-1.77]; P<0.001). CONCLUSIONS: Both very high and very low perioperative fluid volumes were associated with an increase in complications after noncardiac surgery.

Comparison of Lurasidone Versus Quetiapine for the Treatment of Delirium in Critically Ill Patients.

OBJECTIVE: To evaluate the efficacy and safety of lurasidone compared with quetiapine for treatment of delirium in critically ill patients. DESIGN: Prospective, observational cohort study. SETTING: Single-center community teaching hospital. PATIENTS: Forty adult intensive care unit (ICU) patients with delirium (Confusion Assessment Method in the ICU positive), tolerating enteral nutrition, and without active alcohol withdrawal or prior use of atypical antipsychotics. INTERVENTIONS: Patients were treated at the discretion of the prescriber with either lurasidone or quetiapine for delirium. Dose escalation and/or discontinuation were determined at the discretion of individual providers. RESULTS: Baseline characteristics differed with a higher severity of illness in patients in the quetiapine group (n = 20) and a higher baseline QTc interval in the lurasidone group (n = 20). No significant difference was seen in the time to delirium resolution (3.2 vs 3.4 days), average daily haloperidol requirements (5.7 vs 6.9 mg), hospital length of stay (LOS; 23.6 vs 27.9 days), or ICU LOS (12.1 vs 14.2 days). Lurasidone was associated with fewer ventilator support days (4.0 [interquartile range, IQR: 2.3-6.8] days vs 7 [IQR: 4.0-9.8; P = .0295] days) but also a fewer number of delirium-free days (0 [IQR: 0-1.0] days vs 2 [IQR: 0-3.0; P = .0231] days). Additionally, no difference was seen for ICU mortality (20% vs 20%), percentage of time oversedated (2.8% vs 2.7%), or incidence of QTc prolongation (10.0% vs 10.0%). CONCLUSIONS: Lurasidone for the treatment of delirium in critically ill patients did not differ in the time to delirium resolution when compared to quetiapine. Additionally, the incidence of QTc prolongation between agents does not appear to be different. Future randomized trials should evaluate dose escalation schemes and a larger proportion of patients to evaluate differences in mortality, efficacy, and life-threatening arrhythmias associated with atypical antipsychotic use.

Performance comparison of ventricular and arterial dP/dtmax for assessing left ventricular systolic function during different experimental loading and contractile conditions.

BACKGROUND: Maximal left ventricular (LV) pressure rise (LV dP/dtmax), a classical marker of LV systolic function, requires LV catheterization, thus surrogate arterial pressure waveform measures have been proposed. We compared LV and arterial (femoral and radial) dP/dtmax to the slope of the LV end-systolic pressure-volume relationship (Ees), a load-independent measure of LV contractility, to determine the interactions between dP/dtmax and Ees as loading and LV contractility varied. METHODS: We measured LV pressure-volume data using a conductance catheter and femoral and radial arterial pressures using a fluid-filled catheter in 10 anesthetized pigs. Ees was calculated as the slope of the end-systolic pressure-volume relationship during a transient inferior vena cava occlusion. Afterload was assessed by the effective arterial elastance. The experimental protocol consisted of sequentially changing afterload (phenylephrine/nitroprusside), preload (bleeding/fluid bolus), and contractility (esmolol/dobutamine). A linear-mixed analysis was used to assess the contribution of cardiac (Ees, end-diastolic volume, effective arterial elastance, heart rate, preload-dependency) and arterial factors (total vascular resistance and arterial compliance) to LV and arterial dP/dtmax. RESULTS: Both LV and arterial dP/dtmax allowed the tracking of Ees changes, especially during afterload and contractility changes, although arterial dP/dtmax was lower compared to LV dP/dtmax (bias 732 ± 539 mmHg⋅s- 1 for femoral dP/dtmax, and 625 ± 501 mmHg⋅s- 1 for radial dP/dtmax). Changes in cardiac contractility (Ees) were the main determinant of LV and arterial dP/dtmax changes. CONCLUSION: Although arterial dP/dtmax is a complex function of central and peripheral arterial factors, radial and particularly femoral dP/dtmax allowed reasonably good tracking of LV contractility changes as loading and inotropic conditions varied.

Utilization of Medical Codes for Hypotension in Shock Patients: A Retrospective Analysis.

PURPOSE: To evaluate the utilization of hypotension diagnosis codes by shock type and year in known hypotensive patients. PATIENTS AND METHODS: Retrospective analysis of the Medicare fee-for-service claims database. Patients with a shock diagnosis code between 2011 and 2017 were identified using the International Classification of Diseases, Ninth and Tenth Revision, Clinical Modification (ICD-9-CM and ICD-10-CM). Based on specific ICD codes corresponding to each shock type, patients were classified into four mutually exclusive cohorts: cardiogenic shock, hypovolemic shock, septic shock, and other/unspecified shock. Annual proportion and counts of cases with at least one hypotension ICD code for each shock cohort were generated to produce 7-year medical code utilization trends. A Cochran-Armitage test for trend was performed to evaluate the statistical significance. RESULTS: A total of 2,200,275 shock patients were analyzed, 13.3% (n=292,192) of which received a hypotension code. Hypovolemic shock cases were the most likely to receive a hypotension code (18.02%, n=46,544), while septic shock cases had the lowest rate (11.48%, n=158,348). The proportion of patients with hypotension codes for other cohorts were 18.0% (n=46,544) for hypovolemic shock and 16.9% (n=32,024) for other/unspecified shock. The presence of hypotension codes decreased by 0.9% between 2011 and 2014, but significantly increased from 10.6% in 2014 to 17.9% in 2017 (p <0.0001, Z=-105.05). CONCLUSION: Hypotension codes are remarkably underutilized in known hypotensive patients. Patients, providers, and researchers are likely to benefit from improved hypotension coding practices.

A 1-minute blood test detects decreased immune function and increased clinical risk in COVID-19 patients.

Upon infection with SARS-CoV-2, the virus that causes COVID-19, most people will develop no or mild symptoms. However, a small percentage of the population will become severely ill, and some will succumb to death. The clinical severity of COVID-19 has a close connection to the dysregulation of the patient's immune functions. We previously developed a simple, nanoparticle-enabled blood test that can determine the humoral immune status in animals. In this study, we applied this new test to analyze the immune function in relation to disease severity in COVID-19 patients. From the testing of 153 COVID-19 patient samples and 142 negative controls, we detected a drastic decrease of humoral immunity in COVID-19 patients who developed moderate to severe symptoms, but not in patients with no or mild symptoms. The new test may be potentially used to monitor the immunity change and predict the clinical risk of patients with COVID-19.

Endothelial nitric oxide synthase is central to skeletal muscle metabolic regulation and enzymatic signaling during exercise in vivo.

Endothelial nitric oxide synthase (eNOS) is associated with a number of physiological functions involved in the regulation of metabolism; however, the functional role of eNOS is poorly understood. We tested the hypothesis that eNOS is critical to muscle cell signaling and fuel usage during exercise in vivo, using 16-wk-old catheterized (carotid artery and jugular vein) C57BL/6J mice with wild-type (WT), partial (+/-), or no expression (-/-) of eNOS. Quantitative reductions in eNOS expression ( approximately 40%) elicited many of the phenotypic effects observed in enos(-/-) mice under fasted, sedentary conditions, with expression of oxidative phosphorylation complexes I to V and ATP levels being decreased, and total NOS activity and Ca(2+)/CaM kinase II Thr(286) phosphorylation being increased in skeletal muscle. Despite these alterations, exercise tolerance was markedly impaired in enos(-/-) mice during an acute 30-min bout of exercise. An eNOS-dependent effect was observed with regard to AMP-activated protein kinase signaling and muscle perfusion. Muscle glucose and long-chain fatty acid uptake, and hepatic and skeletal muscle glycogenolysis during the exercise bout was markedly accelerated in enos(-/-) mice compared with enos(+/-) and WT mice. Correspondingly, enos(-/-) mice exhibited hypoglycemia during exercise. Thus, the ablation of eNOS alters a number of physiological processes that result in impaired exercise capacity in vivo. The finding that a partial reduction in eNOS expression is sufficient to induce many of the changes associated with ablation of eNOS has implications for chronic metabolic diseases, such as obesity and insulin resistance, which are associated with reduced eNOS expression.

Abnormal shock index exposure and clinical outcomes among critically ill patients: A retrospective cohort analysis.

PURPOSE: To assess the predictive value of a single abnormal shock index reading (SI ≥0.9; heart rate/systolic blood pressure [SBP]) for mortality, and association between cumulative abnormal SI exposure and mortality/morbidity. MATERIALS AND METHODS: Cohort comprised of adult patients with an intensive care unit (ICU) stay ≥24-h (years 2010-2018). SI ≥0.9 exposure was evaluated via cumulative minutes or time-weighted average; SBP ≤100-mmHg was analyzed. Outcomes were in-hospital mortality, acute kidney injury (AKI), and myocardial injury. RESULTS: 18,197 patients from 82 hospitals were analyzed. Any single SI ≥0.9 within the ICU predicted mortality with 90.8% sensitivity and 36.8% specificity. Every 0.1-unit increase in maximum-SI during the first 24-h increased the odds of mortality by 4.8% [95%CI; 2.6-7.0%; p < .001]. Every 4-h exposure to SI ≥0.9 increased the odds of death by 5.8% [95%CI; 4.6-7.0%; p < .001], AKI by 4.3% [95%CI; 3.7-4.9%; p < .001] and myocardial injury by 2.1% [95%CI; 1.2-3.1%; p < .001]. ≥2-h exposure to SBP ≤100-mmHg was significantly associated with mortality. CONCLUSIONS: A single SI reading ≥0.9 is a poor predictor of mortality; cumulative SI exposure is associated with greater risk of mortality/morbidity. The associations with in-hospital mortality were comparable for SI ≥0.9 or SBP ≤100-mmHg exposure. Dynamic interactions between hemodynamic variables need further evaluation among critically ill patients.

Determinants of left ventricular ejection fraction and a novel method to improve its assessment of myocardial contractility.

BACKGROUND: The aim of this study was to quantify the impact of different cardiovascular factors on left ventricular ejection fraction (LVEF) and test a novel LVEF calculation considering these factors. RESULTS: 10 pigs were studied. The experimental protocol consisted of sequentially changing afterload, preload and contractility. LV pressure-volume (PV) loops and peripheral arterial pressure were obtained before and after each intervention. LVEF was calculated as stroke volume (SV)/end-diastolic volume (EDV). We studied global cardiac function variables: LV end-systolic elastance (Ees), effective arterial elastance (Ea), end-diastolic volume and heart rate. Diastolic function was evaluated by means of the ventricular relaxation time (τ) and ventricular stiffness constant (ß) obtained from the end-diastolic PV relationship. Ventriculo-arterial coupling (VAC), an index of cardiovascular performance, was calculated as Ea/Ees. LV mechanical efficiency (LVeff) was calculated as the ratio of stroke work to LV pressure-volume area. A linear mixed model was used to determine the impact of cardiac factors (Ees, Ea, EDV and heart rate), VAC and LVeff on LVEF during all experimental conditions. LVEF was mainly related to Ees and Ea. There was a strong relationship between LVEF and both VAC and LVeff (r2 = 0.69 and r2 = 0.94, respectively). The relationship between LVEF and Ees was good (r2 = 0.43). Adjusting LVEF to afterload ([Formula: see text]) performed better for estimating Ees (r2 = 0.75) and improved the tracking of LV contractility changes, even when a peripheral Ea was used as surrogate (Ea = radial MAP/SV; r2 = 0.73). CONCLUSIONS: LVEF was mainly affected by contractility and afterload changes and was strongly related to VAC and LVeff. An adjustment to LVEF that considers the impact of afterload provided a better assessment of LV contractility.