Evaluation of daily environmental cleaning and disinfection practices in veterans affairs acute and long-term care facilities: A mixed methods study.

OBJECTIVES: To describe daily environmental cleaning and disinfection practices and their associations with cleaning rates while exploring contextual factors experienced by healthcare workers involved in the cleaning process. METHODS: A convergent mixed methods approach using quantitative observations (ie, direct observation of environmental service staff performing environmental cleaning using a standardized observation form) and qualitative interviews (ie, semistructured interviews of key healthcare workers) across 3 Veterans Affairs acute and long-term care facilities. RESULTS: Between December 2018 and May 2019 a total of sixty-two room observations (N = 3602 surfaces) were conducted. The average observed surface cleaning rate during daily cleaning in patient rooms was 33.6% for all environmental surfaces and 60.0% for high-touch surfaces (HTS). Higher cleaning rates were observed with bathroom surfaces (Odds Ratio OR = 3.23), HTSs (OR = 1.57), and reusable medical equipment (RME) (OR = 1.40). Lower cleaning rates were observed when cleaning semiprivate rooms (OR = 0.71) and rooms in AC (OR = 0.56). In analysis stratified by patient presence (ie, present, or absent) in the room during cleaning, patient absence was associated with higher cleaning rates for HTSs (OR = 1.71). In addition, the odds that bathroom surfaces being cleaned more frequently than bedroom surfaces decreased (OR = 1.97) as well as the odds that private rooms being cleaned more frequently than semi-private rooms also decreased (OR = 0.26; 0.07-0.93). Between January and June 2019 eighteen qualitative interviews were conducted and found key themes (ie, patient presence and semiprivate rooms) as potential barriers to cleaning; this supports findings from the quantitative analysis. CONCLUSION: Overall observed rates of daily cleaning of environmental surfaces in both acute and long-term care was low. Standardized environmental cleaning practices to address known barriers, specifically cleaning practices when patients are present in rooms and semi-private rooms are needed to achieve improvements in cleaning rates.

Seventeen-electron chromium(i)tricarbonyltris(phosphine) complexes supported by tris(phosphinomethyl)phenylborates.

The inaugural crystallographic characterization of chromium(i)tricarbonyltris(phosphine) radicals has been achieved. Oxidation of [PPN][Cr(CO)3(PhBP)] (PhBP = [PhB(CH2PPh2)3]-) and analogous Cr(0) complexes featuring 3,5-dimethylphenyl and 3,5-bis(trifluoromethyl)phenyl borate substituents affords charge-neutral Cr(CO)3(PhBP) zwitterions, containing the first fully characterized [Cr(CO)3P3]+ units. The stabilization affected by the intramolecular charge separation established by PhBP ligands dramatically increases the robustness of these seventeen-electron Cr(i) complexes. Previous attempts to isolate salts of mer/fac-[Cr(CO)3P3]+ were frustrated by the thermal instability of these cations. The EPR spectroscopic data of Cr(CO)3(PhBP) supports Rieger's hypothesized low temperature preparation of fac-[Cr(CO)3{CH3C(CH2PPh2)3}]+. The robust [Cr(CO)3P3]+ unit of Cr(CO)3(PhBP) motivated the preparation of structurally characterized Cr(0)/Cr(i) (Cr(CO)3{η6-(PhBP)Cr(CO)3}, Cr(CO)3{η6-(((3,5-CH3)C6H3)BP)Cr(CO)3}) and W(0)/Cr(i) (W(CO)3{η6-(((3,5-CH3)C6H3)BP)Cr(CO)3}) complexes. While these bimetallics feature classical κ3-phosphine and η6-arene metal-binding, they are noteworthy since all other reported mixed-valent Cr(0)/Cr(i) complexes exhibit (a) significant thermal instability that has precluded their isolation and (b) greater uncertainty regarding the presence of distinct Cr(i) and Cr(0) centers. This work illustrates the utility of tris(phosphino)borates for the stabilization of cationic metal fragments within zwitterions that are inaccessible or difficult to characterize independently.

Inductive modulation of tris(phosphinomethyl)phenylborate donation at group VI metals via borate phenyl substituent modification.

A series of zerovalent group VI metal complexes of tris(diisopropylphosphinomethyl)phenylborate ([PhB(CH2PiPr2)3]-, PhBPiPr3), including [PPN][M(CO)3(PhBPiPr3)] (M = Cr, Mo, W) and the first bimetallics in which PhBPiPr3 serves as a bridging ligand via binding M(CO)3 units at the three phosphorus atoms and the borate phenyl substituent, have been synthesized and fully characterized. Two new tris(phosphinomethyl)borates featuring 3,5-dimethylphenyl and 3,5-bis(trifluoromethyl)phenyl borate substituents were prepared as crystallographically characterized thallium salts, and metallated giving their inaugural transition metal complexes [PPN][M(CO)3(((3,5-Me)C6H3)BPPh3)] and [PPN][M(CO)3(((3,5-CF3)C6H3)BPPh3)]. A comparative ν(CO) infrared spectroscopic analysis and examination of half wave potentials assessed by cyclic voltammetry supports a ligand donor ranking of Tp > PhBPiPr3 ≥ Cp > PhBPPh3 > triphos. For these anionic complexes, in which a lower electrostatic contribution to zerovalent metal-PhBPR3 binding is likely operative relative to that present in the zwitterionic complexes most commonly prepared with tris(phosphinomethyl)borates, PhBPR3 ligands do not function as strongly donating scorpionates. Nevertheless, PhBPPh3 is a substantially stronger donor than triphos towards zerovalent M(CO)3; the half wave potentials of [Et4N][M(CO)3(PhBPPh3)] are ∼340 mV lower than those of M(CO)3(triphos). The potentials of the ((3,5-Me)C6H3)BPPh3 group VI metal tricarbonyl anions are more negative than those of the corresponding ((3,5-CF3)C6H3)BPPh3 group VI metal tricarbonyl anions by ∼50 mV, suggesting a modest, yet rational, tuning of PhBPPh3 donation via inductive modulation of the borate anion charge.

Fluid regimens in the first week of life may increase risk of patent ductus arteriosus in extremely low birth weight infants.

BACKGROUND: High fluid volumes may increase neonatal morbidity. However, evidence supporting fluid restriction is inconclusive and restricting fluids may restrict caloric intake. OBJECTIVE: To determine if higher fluid intake was associated with increased risk of patent ductus arteriosus (PDA) or bronchopulmonary dysplasia (BPD) in extremely low birth weight (ELBW) infants. STUDY DESIGN: A total of 204 ELBW (170 ml kg(-1) day(-1)) in the first days of life is associated with increased risk of PDA.

Feasibility and tolerability of probiotics for prevention of antibiotic-associated diarrhoea in hospitalized US military veterans.

BACKGROUND: Probiotics may be efficacious for the prevention of antibiotic-associated diarrhoea. The tolerability and acceptability of probiotics in an elderly US veteran population has not been assessed. PURPOSE: To undertake a randomized trial to determine the tolerability and acceptability of a probiotic, Florajen in an elderly population with multiple comorbidities. METHODS: Pilot randomized double-blind trial comparing a probiotic, Florajen to placebo for the prevention of antibiotic-associated diarrhoea in elderly hospitalized patients receiving antibiotics. RESULTS: Forty patients were enrolled and randomized. Antibiotic-associated diarrhoea occurred in 6/16 (37%) in the placebo group and 4/23 (17%) patients in the Florajen group, (RR 1.63, 95% CI 0.73-3.65, P = 0.15). Florajen was well tolerated in the study population with no major side effects that necessitated discontinuation. CONCLUSIONS: In this pilot study, Florajen was well tolerated in an elderly population, all of whom were taking several other medications. A larger study is needed to determine the effect of Florajen on antibiotic-associated diarrhoea and Clostridium difficile infection.

Anti-tumor necrosis factor-alpha antibody treatment reduces pulmonary inflammation and methacholine hyper-responsiveness in a murine asthma model induced by house dust.

BACKGROUND/AIMS: Recent studies documented that sensitization and exposure to cockroach allergens significantly increase children's asthma morbidity as well as severity, especially among inner city children. TNF-alpha has been postulated to be a critical mediator directly contributing to the bronchopulmonary inflammation and airway hyper-responsiveness in asthma. This study investigated whether an anti-TNF-alpha antibody would inhibit pulmonary inflammation and methacholine (Mch) hyper-responsiveness in a mouse model of asthma induced by a house dust extract containing both endotoxin and cockroach allergens. METHODS: A house dust sample was extracted with phosphate-buffered saline and then used for immunization and two additional pulmonary challenges of BALB/c mice. Mice were treated with an intravenous injection of anti-TNF-alpha antibody or control antibody 1 h before each pulmonary challenge. RESULTS: In a kinetic study, TNF-alpha levels within the bronchoalveolar lavage (BAL) fluid increased quickly peaking at 2 h while BAL levels of IL-4, IL-5, and IL-13 peaked at later time-points. Mch hyper-responsiveness was measured 24 h after the last challenge, and mice were killed 24 h later. TNF inhibition resulted in an augmentation of these Th2 cytokines. However, the allergic pulmonary inflammation was significantly reduced by anti-TNF-alpha antibody treatment as demonstrated by a substantial reduction in the number of BAL eosinophils, lymphocytes, macrophages, and neutrophils compared with rat IgG-treated mice. Mch hyper-responsiveness was also significantly reduced in anti-TNF-alpha antibody-treated mice and the pulmonary histology was also significantly improved. Inhibition of TNF significantly reduced eotaxin levels within the lung, suggesting a potential mechanism for the beneficial effects. These data indicate that anti-TNF-alpha antibody can reduce the inflammation and pathophysiology of asthma in a murine model of asthma induced by a house dust extract.

Reproducibility of a novel model of murine asthma-like pulmonary inflammation.

Sensitization to cockroach allergens (CRA) has been implicated as a major cause of asthma, especially among inner-city populations. Endotoxin from Gram-negative bacteria has also been investigated for its role in attenuating or exacerbating the asthmatic response. We have created a novel model utilizing house dust extract (HDE) containing high levels of both CRA and endotoxin to induce pulmonary inflammation (PI) and airway hyperresponsiveness (AHR). A potential drawback of this model is that the HDE is in limited supply and preparation of new HDE will not contain the exact components of the HDE used to define our model system. The present study involved testing HDEs collected from various homes for their ability to cause PI and AHR. Dust collected from five homes was extracted in phosphate buffered saline overnight. The levels of CRA and endotoxin in the supernatants varied from 7.1 to 49.5 mg/ml of CRA and 1.7-6 micro g/ml of endotoxin in the HDEs. Following immunization and two pulmonary exposures to HDE all five HDEs induced AHR, PI and plasma IgE levels substantially higher than normal mice. This study shows that HDE containing high levels of cockroach allergens and endotoxin collected from different sources can induce an asthma-like response in our murine model.

Phase I study of the mitomycin C analogue BMS-181174.

BMS-181174 is an aminodisulphide derivative of Mitomycin C (MMC) with activity against a range of tumour cell lines and xenografts, including MMC-resistant tumours. In a phase I study of 82 patients with confirmed malignancy, we administered BMS-181174 at doses of 0.8-75 mg m(-2) by intravenous injection every 28 days. At least three patients were evaluated at each dose level, and 174 courses were administered. The pharmacokinetics were dose linear at BMS-181174 doses of 11.5-75 mg m(-2) and the drug appeared to undergo wide distribution. The maximum-tolerated dose was 65 mg m(-2) in previously treated patients and 75 mg m(-2) in chemotherapy-naive cases. The dose-limiting toxicity was myelosuppression, particularly thrombocytopenia, which was prolonged and cumulative. Three patients treated at 65-75 mg m(-2) died suddenly with evidence of pneumonia/pneumonitis, thought to be drug-related. Other toxicities included thrombophlebitis, possible cardiotoxicity (asymptomatic, reversible decline in left ventricular function) and renal impairment. The partial response rate was 5% (4 out of 82) overall, and 9% (3 out of 32) in patients treated at 65-75 mg m(-2). Responses occurred in treated and previously-untreated patients, including cases of colorectal cancer, non-small-cell lung cancer, ovarian cancer and adenocarcinoma of unknown primary site. BMS-181174 has anti-cancer activity but, because of its toxicity, particularly pneumonitis and thrombophlebitis, no phase II studies are planned.

Long-term L-arginine supplementation improves small-vessel coronary endothelial function in humans.

BACKGROUND: Coronary endothelial dysfunction is characterized by an imbalance between endothelium-derived vasodilating and vasoconstricting factors and coronary vasoconstriction in response to the endothelium-dependent vasodilator acetylcholine. Thus, the present double-blind, randomized study was designed to test the hypothesis that long-term, 6-month supplementation of L-arginine, the precursor of the endothelium-derived vasodilator NO, reverses coronary endothelial dysfunction to acetylcholine in humans with nonobstructive coronary artery disease. METHODS AND RESULTS: Twenty-six patients without significant coronary artery disease on coronary angiography and intravascular ultrasound were blindly randomized to either oral L-arginine or placebo, 3 g TID. Endothelium-dependent coronary blood flow reserve to acetylcholine (10(-6) to 10(-4) mol/L) was assessed at baseline and after 6 months of therapy. There was no difference between the two study groups in clinical characteristics or in the coronary blood flow in the response to acetylcholine at baseline. After 6 months, the coronary blood flow in response to acetylcholine in the subjects who were taking L-arginine increased compared with the placebo group (149 +/- 20% versus 6 +/- 9%, P < 0.05). This was associated with a decrease in plasma endothelin concentrations and an improvement in patients' symptoms scores in the L-arginine treatment group compared with the placebo group. CONCLUSIONS: Long-term oral L-arginine supplementation for 6 months in humans improves coronary small-vessel endothelial function in association with a significant improvement in symptoms and a decrease in plasma endothelin concentrations. This study proposes a role for L-arginine as a therapeutic option for patients with coronary endothelial dysfunction and nonobstructive coronary artery disease.

Cardiac secretion of adrenomedullin in human heart failure.

Adrenomedullin (ADM) is a newly discovered endogenous vasorelaxing and natriuretic peptide. Recently, we have reported that plasma ADM is increased in severe congestive heart failure (CHF) in humans and that increased immunohistochemical staining is observed in the failing human ventricular myocardium. The present study was designed to test the hypothesis that the failing human ventricle secretes ADM and that circulating ADM progressively increases with the severity of clinical CHF. Plasma ADM was significantly increased in human CHF (39.8 +/- 3.6 pg/ml, P < 0.001 vs. normal) as compared with normal subjects (14.4 +/- 2.7 pg/ml). Plasma ADM was increased in mild CHF (NYHA class II, 30.1 +/- 3.4 pg/ml, P < 0.01 vs. normal), moderate CHF (NYHA class III, 31.5 +/- 3.0 pg/ml, P < 0.01 vs. normal), and severe CHF (NYHA class IV, 66.1 +/- 9.4 pg/ml, P < 0.001 vs. normal). In 13 patients with CHF in whom plasma samples were obtained from aorta (AO), coronary sinus (CS) and anterior interventricular vein (AIV), there was a significant step-up in plasma ADM between AO and AIV (50.6 +/- 9.3 pg/ml and 62.1 +/- 11.1 pg/ml, respectively, P < 0.01) and between AO and CS (50.6 +/- 9.3 pg/ml and 58.6 +/- 11.4 pg/ml, respectively, P < 0.05). The current study demonstrates that the failing human heart secretes ADM in human CHF suggesting contribution to the increase in plasma ADM, and indicates for the first time an additional endocrine system of cardiac origin which is activated in human CHF and may function in cardiorenal regulation.

Elevation of circulating and ventricular adrenomedullin in human congestive heart failure.

BACKGROUND: Adrenomedullin (ADM) is a newly discovered vasodilating and natriuretic peptide that may play an important role in cardiorenal regulation. Although ADM was originally isolated from human pheochromocytoma, ADM-like immunoreactivity has also been widely detected in various tissues, including the cardiovascular system. METHODS AND RESULTS: In view of reports that ADM circulates in the body and that ADM gene and ADM-like immunoreactivity are present in the heart, the present study was designed to determine the plasma concentration of ADM in healthy subjects and in patients with congestive heart failure (CHF) and to investigate the immunohistochemical presence and localization of ADM in normal and failing human hearts. Plasma ADM concentration was 13.2 +/- 2.3 pg/mL in healthy subjects (n = 11) and increased to 47.3 +/- 6.7 pg/mL in patients with CHF (n = 11 P < .05 versus normal). Human cardiac tissues were obtained from five patients with end-stage CHF undergoing cardiac transplantation. Five normal donor hearts that were used for cardiac transplantation served as sources for normal atrial tissues. Normal ventricular myocardium was also obtained by endomyocardial biopsy from the right ventricles of these donor hearts immediately before cardiac transplantation. Positive immunostaining was detected within the myocardia in both atria and ventricles of healthy and severely failing human transplanted hearts and was more intense in the atria than in the ventricles. Although there were no significant differences in the intensity of immunoreactivity between normal and failing atria, ADM immunoreactivity was significantly more intense in the ventricular myocytes from failing hearts compared with normal hearts. CONCLUSIONS: The present study demonstrates that plasma concentration of ADM is increased in patients with CHF and that ADM is present in the human heart. ADM immunoreactivity is markedly increased in the failing human ventricle, suggesting that ventricular ADM expression may be influenced by the circumstances associated with CHF. This supports a potential role for this newly identified vasoactive and natriuretic peptide, ADM, in the neurohumoral activation that characterizes human CHF.

Circulating N-terminal atrial natriuretic peptide as a marker for symptomless left-ventricular dysfunction.

Early identification of patients with symptomless left-ventricular dysfunction and early pharmacologic intervention may have an impact on the outlook of patients with heart failure. Atrial natriuretic peptide (ANP) is a cardiac hormone that is released as a C-terminal (C-ANP) and an N-terminal peptide (N-ANP). Since N-ANP has reduced clearance rates compared with C-ANP, N-ANP circulates at higher concentrations. Based on the known increased concentration of C-ANP in symptomatic congestive heart failure, our study was designed to evaluate prospectively N-ANP profile and left-ventricular function in subjects with symptomless and symptomatic heart failure, and the role of plasma N-ANP as a marker for early identification of patients with heart failure. 180 patients who were referred for rest and exercise radionuclide angiography for evaluation of left-ventricular function were studied. Blood was taken for measurement of C-ANP and N-ANP before angiography. Patients were grouped according to New York Heart Association (NYHA) heart failure classification and left-ventricular function. Mean (SD) plasma N-ANP concentration in patients with symptomless left-ventricular dysfunction (NYHA class I, n = 70) was 243 (256) pmol/L (range 27-922 pmol/L), and was higher (p < 0.001) than in 25 control subjects (28 pmol/L). A plasma N-ANP concentration above 54 pmol/L (mean +/- 1.96SD of the control group) had a sensitivity of 90% and a specificity of 92% for detection of patients with symptomless left-ventricular dysfunction. We have shown that plasma N-ANP concentrations are significantly increased in patients with symptomless left-ventricular dysfunction and that this peptide can serve as a marker for diagnosis of such patients.

Are baseline prothrombin time/partial thromboplastin time values necessary before instituting anticoagulation?

STUDY OBJECTIVES: To determine whether baseline prothrombin time (PT) or partial thromboplastin time (PTT) values provide information that is useful to the clinician before initiating anticoagulation and whether emergency physicians elicit historical information about bleeding disorders before beginning anticoagulant therapy. DESIGN: A three-year retrospective review of the records of 199 patients admitted through the ED with an ICD-9-CM diagnosis of deep-vein thrombosis or pulmonary embolus using a predesigned study sheet that included historical questions, baseline PT and PTT values, treatment given, timing of treatment, and underlying medical problems. SETTING: University-affiliated tertiary-care hospital. MEASUREMENTS AND MAIN RESULTS: Deep-vein thrombosis was the primary diagnosis in 75% of patients. Pertinent historical items were not documented in 92% to 100% of patients. Baseline PT and PTT values were obtained in 94% of patients. An elevated baseline PT was found in 26 patients, all of whom were taking warfarin. An elevated baseline PTT was found in 21 patients. These results were attributed to laboratory error (one), warfarin use (nine), heparin therapy before baseline tests (five), anticardiolipin antibodies (five, one of whom was on warfarin therapy), and unknown causes (three). Heparin therapy was not altered for any patient. CONCLUSION: Emergency physicians rarely document pertinent questions about bleeding disorders before initiating anticoagulation therapy. Baseline PT and PTT values are almost routinely obtained despite the fact that they do not alter therapy or serve as sensitive or specific screening tests. Routine baseline PT and PTT values are rarely needed before initiating anticoagulation. Eliminating such routine testing would result in significant cost savings.

Angiotensin inhibition potentiates the renal responses to neutral endopeptidase inhibition in dogs with congestive heart failure.

The renal natriuretic actions of endogenous atrial natriuretic factor are enhanced by neutral endopeptidase inhibition (NEP-I). Recognizing that activation of the renin-angiotensin-aldosterone system in congestive heart failure (CHF) antagonizes the renal actions of atrial natriuretic factor, we hypothesized that angiotensin II antagonism with converting enzyme inhibition would potentiate the renal actions of NEP-I in CHF. To test this hypothesis, the renal responses to a specific NEP-I (SQ 28,603) were assessed in dogs with eight days of experimental CHF produced by rapid ventricular pacing. The renal natriuretic responses to NEP-I in experimental CHF were significant. In the same model of CHF, chronic angiotensin antagonism with converting enzyme inhibition potentiated both renal hemodynamic and excretory responses to NEP-I. The potentiated renal hemodynamic response included significant increases in glomerular filtration rate and filtration fraction. In the CHF group with angiotensin antagonism, an intrarenal infusion of low-dose angiotensin abolished the potentiated renal responses to NEP-I, supporting the concept that intrarenal angiotensin antagonism, rather than improved systemic hemodynamics or potentiation of other peptide systems, mediated the enhanced renal responses to NEP-I in the presence of converting enzyme inhibition.

Induction and prevention of radiocontrast-induced nephropathy in dogs with heart failure.

Radiocontrast-induced nephropathy (RCIN) is a clinically important cause of acute renal failure with no effective treatment. Recognizing the high incidence of RCIN in humans with severe congestive heart failure (CHF), this study was designed to test the hypotheses that dogs with experimental CHF are at increased risk for RCIN and that pharmacologic renal levels of atrial natriuretic factor (ANF) can prevent RCIN in this model. In chronic experiments, three groups of five conscious dogs received intravenous radiocontrast (7 ml/kg). One group consisted of normal controls, while the two other groups had experimental CHF induced by eight days of ventricular pacing at 250 beats per minute. One of the CHF groups received an infusion of ANF (30 ng/kg/min) into the suprarenal aorta for one hour before, during and after the infusion of radiocontrast to achieve pharmacologic renal plasma levels. Renal function remained stable in the normal controls in contrast to the consistent decreases in daily creatinine clearance during the five days following radiocontrast in experimental CHF. In addition, ANF prevented radiocontrast-induced reductions in creatinine clearance in dogs with experimental CHF. Additional studies performed in two groups of anesthetized dogs with experimental CHF demonstrated that, in this model of RCIN, the reduction in renal function appears biphasic, and the action of ANF may be to increase glomerular filtration rate prior to radiocontrast, thus allowing a maintenance of renal function during and after radiocontrast.

Effect of the Harrington compression system on the correction of the rib hump in spinal instrumentation for idiopathic scoliosis.

To analyze the effect of the Harrington compression system on the rib hump in thoracic idiopathic scoliosis, intraoperative measurements were made on 21 cases during correction with the distraction system and after addition of the compression system. The data show that the compression system makes a major contribution to the correction of total rib deformity in over two-thirds of the patients, and the correction of the rib valley is much more significant than correction of the rib hump. Analysis of postoperative spine roentgenograms seems to indicate that the extent of the rib correction does not correlate with spine derotation as measured by the system of Nash and Moe. The improvement in rib correction achieved by addition of the compression system appears to result from changes centered about the costovertebral joints.

Idiopathic and congenital scoliosis in twins.

This report contains a case presentation of monozygotic twins who had concordant right thoracic scoliosis of differing severities. One twin also had an associated congenital left lumbar scoliosis and urologic abnormalities. This report would suggest that the genetic basis of scoliosis may occur at multiple gene loci.

Occurrence of cold agglutinins in congenital scoliosis.

Eighty-seven patients undergoing spinal surgery for a variety of conditions were surveyed for the presence of cold agglutinins. Patients with congenital scoliosis or metastatic lesions of the spine were found to have a frequency of cold agglutinins that was 250 to 1000 times greater than that in the general population. This greater frequency was independent of ABO blood group, sex, or age. Pre-admission screening of congenital scoliosis patients is urged.