Nurses' job satisfaction: a proposed measure

Thirty-three items originally developed to measure three dimensions of nurses' job satisfaction were subjected to a series of checks designed to determine the number of dimensions being measured and the reliability and validity of the measures of these dimensions. Although the hypothesis of only three dimensions was not supported, the eight interpretable factors that did emerge could meaningfully be placed within these three dimensions. The eight factors were satisfaction with extrinsic rewards, scheduling, family/work balance, co-workers, interaction, professional opportunities, praise/recognition, and control/responsibility. Internal consistency and test-retest reliabilities are reported, as well as checks for criterion-related and construct validity.     

Time course of endothelial damage in septic shock: prediction of outcome

Introduction

Endothelial damage accounts greatly for the high mortality in septic shock. Higher expression of mediators (IL-6, IL-8, soluble intercellular adhesion molecule 1 [sICAM-1], soluble endothelial-linked adhesion molecule 1 [sELAM-1]) have been described for non-survivors in comparison with survivors. We investigated the predictive value of the mediators IL-6, IL-8, sELAM-1 and sICAM-1 and their time course in intensive care unit patients who developed septic shock with respect to outcome.

Materials and methods

We measured serum levels of IL-6, IL-8, sELAM-1 and sICAM-1 in 40 intensive care unit patients who developed septic shock. Measurements were performed until death or until resolution of septic shock. Clinical and laboratory data were also recorded.

Results

After 48 hours the levels of sELAM-1 and sICAM-1 increased in non-survivors and decreased in survivors. sELAM-1 was predictive for outcome on the third day (P = 0.02) and the fourth day (P = 0.02) after diagnosis of septic shock. This difference in the time course between survivors and non-survivors occurred 7 days before death of the patients (median, 10 days). sICAM-1 levels increased significantly in non-survivors over the study period (P < 0.001). sELAM-1 (P = 0.04), IL-6 (P = 0.04) and IL-8 (P = 0.008) were significantly higher in non-survivors over the whole study period. The age and norepinephrine dose >0.5 μg/kg/min were significantly different between the groups.

Conclusion

sELAM-1 showed a markedly opposing course after 48 hours of septic shock. This adhesion molecule may be a useful early predictor of disease severity in the course of septic shock after early initial treatment of the patients, and might suggest considering endothelial-restoring therapy.     

Dobutamine administration in septic shock: addition to a standard protocol

Dobutamine administration has been shown to increase oxygen delivery in various conditions, but there are little data to document its effects in septic shock. We investigated the effects of dobutamine infusion at a rate of 5 micrograms/kg.min in 18 patients (mean 60 +/- 16 yr) with septic shock initially characterized by hypotension, oliguria, and hyperlactatemia in the presence of a documented source of sepsis. Early resuscitation had consisted of fluid administration and vasopressors when required. When added to this standard regimen, dobutamine had no significant effect on mean arterial pressure (MAP) (from 71 +/- 12 to 73 +/- 13 mm Hg), but markedly increased cardiac index (from 3.0 +/- 0.7 to 3.9 +/- 1.0 L/min.m2, p less than .001), stroke index (from 32 +/- 8 to 37 +/- 9 ml/m2, p less than .001) and oxygen transport (from 410 +/- 105 to 530 +/- 146 ml/min.m2, p less than .001). Oxygen consumption (VO2) increased concurrently (from 137 +/- 42 to 162 +/- 66 ml/min.m2, p less than .002). MAP increased (from 68 +/- 9 to 76 +/- 11 mm Hg) in 12 patients and decreased moderately (from 76 +/- 18 to 69 +/- 17 mm Hg) in six patients. The two subgroups of patients had similar hemodynamic profiles before the dobutamine infusion, but vasopressor therapy was already used in one of the 12 patients in the first subgroup and in three of the six patients in the second subgroup (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Low-dose corticosteroids to treat septic shock: a critical literature review

Septic shock is the 13th leading cause of death in the United States. The rate of severe sepsis nearly doubled and mortality increased more than 60% during the 10-year period ending in 2003. Systemic inflammatory response syndrome has noninfectious and infectious causes. Noninfectious ones include burns, trauma, severe pancreatitis, and therapy with monoclonal antibodies or immunomodulatory drugs such as interleukin 2. Progression from sepsis syndrome to septic shock is caused by a series of immune responses. As an infectious injury progresses, host activation of the coagulation, immunological, and stress response systems ensues, resulting in tissue hypoperfusion and organ failure. Early studies with small numbers of patients suggest that treatment with low-dose corticosteroids has marked beneficial effects on shock reversal, the immune system, and the hemodynamic profile. Low-dose corticosteroids should only be administered to a subset of patients with septic shock who are unresponsive to fluid replacement and vasopressor therapy.     

Prehospital shock index to assess 28-day mortality for septic shock

ContextIn the prehospital setting, early identification of septic shock (SS) with high risk of mortality aims to initiate early treatments and to decide delivery unit (emergency department (ED) or intensive care unit (ICU)). In this context, there is a need for a prognostic measure of severity and death in order to early detect patients with a higher risk of pejorative evolution.In this study, we describe the association between prehospital shock index (SI) and mortality at day 28 of patients with SS initially cared for in the prehospital setting by a mobile intensive care unit (MICU).MethodsPatients with SS cared for by a MICU between January 2016 and May 2019 were retrospectively analyzed. Using propensity score, the association between SI and mortality was assessed by Odd Ratio (OR) with 95 percent confidence interval [95 CI].ResultsOne-hundred and fourteen patients among which 78 males (68%) were analysed. The mean age was 71 ± 14 years old. SS was mainly associated with pulmonary (55%), digestive (20%) or urinary (11%) infection. Overall mortality reached 33% (n = 38) at day 28.Median SI [interquartile range] differed between alive and deceased patients: 0.73 [0.61–1.00] vs 0.80 [0.66–1.10], p < 0.001*). After adjusting for confounding factors, the OR of SI > 0.9 was 1.17 [1.03–1.32].ConclusionIn this study, we report an association between prehospital SI and mortality of patients with prehospital SS. A SI > 0.9 is a readily available tool correlated with increased mortality of patients with SS initially cared for in the prehospital setting.     

Understanding sepsis: from SIRS to septic shock

Sepsis remains the leading cause of death in non-coronary ICU patients, despite improvements in supportive treatment modalities such as antimicrobial drugs and ventilation therapy. Further, the incidence of sepsis is projected to increase in years to come, related to factors including a rise in immunosuppressed patient populations and more widespread use of invasive lines and procedures. In this article, the authors seek to advance nurses' understanding of sepsis by reviewing the SIRS to septic shock paradigm and using a case study to illustrate how a patient progressed along the continuum. The role of the critical care nurse is an important aspect of the care of these patients. Early identification of patients at risk for, or who are developing, sepsis is crucial in order to improve patient outcomes.     

Therapy for septic shock.

To adequately appraoch the therapeutics of such a diffuse disorder as sepsis, a firm grasp of the multiple pathophysiologic subsets is imperative. With this as a basis, therapy comes as close to applied physiology as is possible in medicine today.     

Lactic acidosis: from sour milk to septic shock

Lactic acidosis is frequently encountered in the intensive care unit. It occurs when there is an imbalance between production and clearance of lactate. Although lactic acidosis is often associated with a high anion gap and is generally defined as a lactate level >5 mmol/L and a serum pH <7.35, the presence of hypoalbuminemia may mask the anion gap and concomitant alkalosis may raise the pH. The causes of lactic acidosis are traditionally divided into impaired tissue oxygenation (Type A) and disorders in which tissue oxygenation is maintained (Type B). Lactate level is often used as a prognostic indicator and may be predictive of a favorable outcome if it normalizes within 48 hours. The routine measurement of serum lactate, however, should not determine therapeutic interventions. Unfortunately, treatment options remain limited and should be aimed at discontinuation of any offending drugs, treatment of the underlying pathology, and maintenance of organ perfusion. The mainstay of therapy of lactic acidosis remains prevention.