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Table5

Odds ratio of 30 day all-cause mortality, according to time of admission

Patient characteristics: type of fracture, fracture positioning, type of operation, age, sex, body-mass index, Charlson comorbidity index, marital status, housing, domicile region, native country, level of income and year of admission. Hospital characteristics: hospital region, type of unit and unit volume.

Adjusted for clustering by unit.

Adjusted for clustering by unit and patient characteristics.

Adjusted for clustering by unit, patient characteristics and hospital characteristics.

Adjusted for clustering by unit, patient characteristics and delay >48 h.

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Table5

Odds ratio of 30 day all-cause mortality, according to time of admission

Patient characteristics: type of fracture, fracture positioning, type of operation, age, sex, body-mass index, Charlson comorbidity index, marital status, housing, domicile region, native country, level of income and year of admission. Hospital characteristics: hospital region, type of unit and unit volume.

Adjusted for clustering by unit.

Adjusted for clustering by unit and patient characteristics.

Adjusted for clustering by unit, patient characteristics and hospital characteristics.

Adjusted for clustering by unit, patient characteristics and delay >48 h.

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We found that patients admitted with hip fractures during on-hours and off-hours were comparable. Furthermore, the admission time had no influence on compliance with performance measures for hip fracture care. However, the risk of surgical delay was lower for patients admitted off-hours compared with patients admitted on-hours. Additional analyses showed that this effect was driven by observations for patients admitted on weekdays during evening and night shifts; indeed the risk of delay was higher for patients admitted during weekends. We found no influence of the time of admission on the 30-day mortality risk in the primary pooled analyses, but additional analyses did reveal an increased mortality risk related to weekend admission.

The strengths included the study size, the nationwide design, the detailed prospective data collection, the complete follow-up and the extensive control for confounding. Only patients without contraindications for the specific performance measure were included in the analyses of the quality of care. This approach reduced the risk of confounding, e.g. by disease severity or by indication, and have also been used in similar studies in other patient groups [ 33 ]. Detailed registration of the exact time of admission enabled the definition of off-hours to reflect the work flow in every day clinical practice.

A variety of terms are used that generally do not match the definitions in this document closely enough to be used as synonyms of the defined terms. For example, a ‘faint’ approximately conforms to syncope but emphasizes vasovagal syncope (VVS) over other forms. A glossary of uncertain terms is shown in section 1 of the Easy Go Shopping Mens Fabric Mesh Vamp Fashion Sneaker Flat Heel Lace up Solid Color Shoes up Cricket Shoes Red get authentic ebay cheap price perfect sale online low price fee shipping vilMNdrP7t
.

Table 3 provides a classification of the principal causes of syncope, emphasizing groups of disorders with common pathophysiology, presentation, and risk. Clinical features, epidemiology, prognosis, impact on quality of life, and economic issues are shown in section 2 of the Web Practical Instructions .

Table 3

Classification of syncope

BP = blood pressure; OH = orthostatic hypotension; POTS = postural orthostatic tachycardia syndrome; VVS = vasovagal syncope.

Table 3

Classification of syncope

BP = blood pressure; OH = orthostatic hypotension; POTS = postural orthostatic tachycardia syndrome; VVS = vasovagal syncope.

The pathophysiological classification centres on a fall in systemic blood pressure (BP) with a decrease in global cerebral blood flow as the defining characteristic of syncope. Figure 3 shows low BP and global cerebral hypoperfusion as the central final common pathway of syncope. A sudden cessation of cerebral blood flow for as short as 6–8 s can cause complete LOC. A systolic BP of 50–60 mmHg at heart level, i.e. 30–45 mmHg at brain level in the upright position, will cause LOC. 8 , 9

Systemic BP is the product of cardiac output and total peripheral resistance; a fall in either can cause syncope. However, in syncope, both mechanisms often act together to a varying degree.

There are three primary causes of a low total peripheral resistance. The first is decreased reflex activity causing vasodilatation through withdrawal of sympathetic vasoconstriction: this is the ‘vasodepressive type’ of reflex syncope, seen in the outer ring in Figure 3 . The second is a functional impairment, and the third a structural impairment of the autonomic nervous system, with drug-induced, primary, and secondary autonomic failure in the outer ring. In autonomic failure, there is insufficient sympathetic vasoconstriction in response to the upright position.

There are four primary causes of low cardiac output. The first is a reflex bradycardia, known as cardioinhibitory reflex syncope. The second concerns cardiovascular causes: arrhythmia, structural disease including pulmonary embolism, and pulmonary hypertension. The third is inadequate venous return due to volume depletion or venous pooling. Finally, chronotropic and inotropic incompetence through autonomic failure may impair cardiac output.

Note that these primary mechanisms may interact in different ways: firstly, venous pooling and inadequate venous return is also a factor that can trigger an inappropriate reflex in orthostatic reflex syncope; secondly, a low total peripheral resistance may cause venous pooling of blood below the diaphragm, in turn decreasing venous return and consequently cardiac output.

Statistical analysis

Study population and patient characteristics . During the 7.5-year study period, a total of 24,179 infections with 27,847 organisms were reported by participating hospitals. Of these, 3432 clinically significant episodes of BSI (15%) were identified in pediatric patients (⩽16 years of age). Patients had a mean age of 51 ± 26.5 years (range, 0–102 years). Forty-four percent of patients were female.

Study population and patient characteristics

Approximately 51% (50.5%) of hospital-acquired BSIs occurred in the ICU. The clinical services most commonly diagnosing and reporting BSIs were internal medicine (38%), general surgery (20%), and pediatrics (13.5%).

The most frequent underlying conditions (recorded as diagnoses at admission) were malignancy, in 4237 patients (17.5%); cardiac conditions, in 3626 patients (15%); and gastrointestinal conditions, in 3269 patients (13.5%). However, underlying conditions were not specified for 4356 patients (14%).

Among the potential factors predisposing patients to BSI, intravascular devices were the most frequent. Central venous catheters were in place in 17,484 patients (72%), peripheral intravenous catheters were in place in 8426 patients (35%), and arterial catheters were in place in 3821 patients (16%). Urinary catheters were in place in 11,101 patients (46%). A total of 5791 patients (24%) were receiving total parenteral nutrition, and 1896 patients (8%) needed dialysis at the onset of BSI. Most of these patients underwent hemodialysis (1769 patients vs. 127 who underwent peritoneal dialysis). Ventilator support was necessary for 7844 patients (32%). Overall, 6618 patients died during hospitalization, accounting for a crude mortality rate of 27%.

The system-wide incidence of BSI was 60 cases per 10,000 hospital admissions. When stratified by pathogen, system-wide incidence rates of BSI due to the most commonly isolated pathogens varied between 1 and 16 cases per 10,000 admissions, which were the incidence rates for BSI due to Acinetobacter baumannii and CoNS, respectively ( table 1 ). The median hospital incidence of BSI was 43 cases per 10,000 hospital admissions (range, 6–252). Incidences did not vary significantly over time (mean ± SD, 54 ± 40 cases per 10,000 admissions in 1996 vs. 52 ± 38 in 2001), and no trend could be observed.

Table 1
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Incidence rates and distribution of pathogens most commonly isolated from monomicrobial nosocomial bloodstream infections (BSIs) and associated crude mortality rates for all patients, patients in intensive care units (ICU), and patients in non-ICU wards.

Table 1
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Incidence rates and distribution of pathogens most commonly isolated from monomicrobial nosocomial bloodstream infections (BSIs) and associated crude mortality rates for all patients, patients in intensive care units (ICU), and patients in non-ICU wards.

Microbiological features . Thirteen percent of all episodes of BSI ( n = 3201) were polymicrobial. Of 20,978 monomicrobial episodes, a total of 13,665 episodes (65%) were caused by gram-positive organisms and 5278 (25%) by gram-negative organisms. Fungi, mainly Candida species, were isolated in a total of 2002 episodes (9.5%). Anaerobic bacteria accounted for 1.3% of BSIs. These proportions did not change significantly during the study period. The rank order of the major pathogens ( table 1 ) shows that CoNS accounted for nearly one-third of all nosocomial BSIs (31%), followed in rank by S. aureus (20%), enterococci (9%), and Candida species (9%). E. coli (6% of episodes) and Klebsiella species (5%), were the most common gram-negative organisms.

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