Personnel flux and workplace anxiety: Personal and interpersonal consequences of understaffing in UK ultrasound departments.

INTRODUCTION: By 2013, the UK government's Migration Advisory Committee had determined sonography to be a formal shortage speciality, and understaffing remains a key concern for research in the domain. This paper, emergent of a qualitative study funded by Health Education North West, explores unit managers' perspectives on the present state of UK ultrasound. The focus herein falls upon the personal and interpersonal consequences of this circumstance for individuals working in specific understaffed departments. METHODS: A thematic analysis informed by a Straussian model of Grounded Theory was utilised; N = 20 extended accounts provided by ultrasound department leads in public (n = 18) and private (n = 2) units were collected and analysed accordingly. RESULTS: The global themes addressed herein describe (a) how both inter-departmental movement of senior sonographers and early retirement, within a nationally understaffed picture, impacts upon local knowledge economies, and (b) how such staffing instabilities can undermine the day-to-day confidence of managerial staff and practicing sonographers alike. CONCLUSIONS: It is personnel flux, rather than simple short-staffing, that is reported to cause the greatest social-psychological problems for both managers and sonographers. The issues raised herein require further examination from the perspective of sonographers themselves, in order to corroborate the views of the managers interviewed.

Postoperative Serratia marcescens wound infections traced to an out-of-hospital source.

From 25 August to 28 September 1994, 7 cardiovascular surgery (CVS) patients at a California hospital acquired postoperative Serratia marcescens infections, and 1 died. To identify the outbreak source, a cohort study was done of all 55 adults who underwent CVS at the hospital during the outbreak. Specimens from the hospital environment and from hands of selected staff were cultured. S. marcescens isolates were compared using restriction-endonuclease analysis and pulsed-field gel electrophoresis. Several risk factors for S. marcescens infection were identified, but hospital and hand cultures were negative. In October, a patient exposed to scrub nurse A (who wore artificial fingernails) and to another nurse-but not to other identified risk factors-became infected with the outbreak strain. Subsequent cultures from nurse A's home identified the strain in a jar of exfoliant cream. Removal of the cream ended the outbreak. S. marcescens does not normally colonize human skin, but artificial nails may have facilitated transmission via nurse A's hands.

Differential alterations in plasma colony-stimulating factor concentrations in meningococcaemia.

To determine whether circulating levels of any of the colony-stimulating factors (CSF) might contribute to the host response in severe sepsis, plasma concentrations of granulocyte CSF (G-CSF), granulocyte-macrophage CSF (GM-CSF), and macrophage CSF (M-CSF) were measured by immunoassays in 20 subjects with meningococcaemia, a bloodstream infection caused by Neisseria meningitidis, that has proven to be a valuable model to study the responses of other inflammatory mediators during sepsis and septic shock in humans. Plasma G-CSF concentrations were transiently elevated in most subjects during the early phase of meningococcaemia, and were higher in subjects with septic shock (mean +/- s.d. = 165 +/- 142 ng/ml, n = 9) compared with those who remained normotensive (mean +/- s.d. = 7 +/- 2 ng/ml, n = 10) (P < 0.05). Peak plasma G-CSF concentrations > 10 ng/ml were associated with the development of septic shock (P < 0.01), disseminated intravascular coagulation (P < 0.01), fulminant infection (P < 0.05), and a fatal outcome (P < 0.01). Plasma GM-CSF concentrations > 1 ng/ml were briefly present in subjects with life-threatening septic shock (1-15 ng/ml, n = 5), and were strongly associated with fulminant meningococcaemia (P < 0.01). Plasma M-CSF concentrations were marginally elevated in all subjects, but were not associated with complications related to or arising from sepsis-induced organ injury. This study demonstrates that plasma levels of G-CSF, GM-CSF and M-CSF show very different responses during meningococcaemia, changes which presumably reflect the different roles played by these mediators in sepsis and, potentially, in septic shock.

Leukemia inhibitory factor protects against experimental lethal Escherichia coli septic shock in mice.

Leukemia inhibitory factor (LIF) has recently been associated with septic shock in humans. In this study we sought to determine, in mice, the role of LIF in septic shock. During sublethal endotoxemia, serum LIF levels, as determined by radio-receptor competition assay, peaked at 2 h and were low (3 ng/ml), whereas in lethal Escherichia coli septic shock serum LIF levels rose progressively (> 30 ng/ml) in the premorbid phase coincident with the development of tissue injury. Single i.v. injections of high doses (up to 50 micrograms per mouse) of recombinant murine LIF had no obvious acute detrimental effects, whereas continued i.p. administration (30 micrograms per mouse per day) for 3-4 days induced a fatal catabolic state without evidence of preceding hemodynamic collapse or shock. Simultaneous or subsequent administration of high doses of LIF had no effect on mortality from sublethal and lethal E. coli septic shock, whereas prior administration conferred significant protection against lethality (P << 0.001 by log-rank test), an effect that was dose and interval dependent. This protective effect resembled endotoxin tolerance and was characterized by suppression of E. coli-induced serum tumor necrosis factor concentration (P < 0.05), reduction in the number of viable bacteria (P < 0.05), and prevention of sepsis-induced tissue injury. These observations suggest that systemic LIF production is part of the host response to both endotoxin and sepsis-induced tissue injury.

Circulating leukemia inhibitory factor levels correlate with disease severity in meningococcemia.

Circulating concentrations of the proinflammatory cytokine leukemia inhibitory factor (LIF) were prospectively determined by radioreceptor competition assay (sensitivity, 1 ng/mL) in 33 subjects with meningococcemia. LIF was detected in the plasma of 13 subjects and was associated with development of septic shock (P < .01), disseminated intravascular coagulation (P < .05), multiorgan failure (P < .05), and death (P < .01). Plasma LIF concentrations were highest (1-1772 ng/mL) at hospital admission and became undetectable within 36 h, and the peak levels correlated inversely with systolic blood pressure (r, -.70, P < .001), peripheral blood leukocyte count (r, -.58, P < .01), and prodromal interval (r, -.60, P < .001). Plasma LIF concentrations > 400 ng/mL were present only in subjects with fatal fulminant infection. LIF concentrations in plasma collected within 12 h of hospital admission correlated with disease severity in patients with meningococcemia. It is likely that LIF participates in the host response to infection, and it may contribute to the pathogenesis of septic shock.

Oxidative metabolism of carbazeran in vitro by liver cytosol of baboon and man.

The metabolism of carbazeran has been investigated in vitro using liver cytosol from dog, baboon and man. Carbazeran was not metabolized in cytosol prepared from dog liver but was rapidly metabolized to a single product in baboon- and human-liver cytosol. The product was identified as 4-hydroxy carbazeran. The enzyme responsible for the 4-hydroxylation of carbazeran in vitro was shown by the use of inhibitors to be liver aldehyde oxidase. Species differences in the metabolism of carbazeran in vitro correlate well with studies in vivo; these showed that following an oral dose to man and baboon, the compound was almost completely cleared via pre-systemic 4-hydroxylation, whereas in the dog, this metabolic route appeared unimportant.