Despite a large body of evidence describing care processes known to reduce the incidence of surgical site infections, many are underutilized in practice.
Fifty-six hospitals volunteered to redesign ...their systems as part of the National Surgical Infection Prevention Collaborative, a 1-year demonstration project sponsored by the Centers for Medicare & Medicaid Services. Each facility selected quality improvement objectives for a select group of surgical procedures and reported monthly clinical process measure data.
Forty-four hospitals reported data on 35,543 surgical cases. Hospitals improved in measures related to appropriate antimicrobial agent selection, timing, and duration; normothermia; oxygenation; euglycemia; and appropriate hair removal. The infection rate decreased 27%, from 2.3% to 1.7% in the first versus last 3 months.
The Collaborative demonstrated improvement in processes known to be associated with reduced risk of surgical site infections. Quality improvement organizations can be effective resources for quality improvement in the surgical arena.
Collaborative infection control improvement: reply Dellinger, E. Patchen, M.D; Hausmann, Susan M., M.S; Bratzler, Dale W., D.O., M.P.H ...
The American journal of surgery,
2007, 2007-01-00, 20070101, Letnik:
193, Številka:
1
Journal Article
Recenzirano
...we measured the number of surgical operations between individual infections.
Mutations in glucokinase (GCK) cause a spectrum of glycemic disorders. Heterozygous loss-of-function mutations cause mild fasting hyperglycemia irrespective of mutation severity due to compensation ...from the unaffected allele. Conversely, homozygous loss-of-function mutations cause permanent neonatal diabetes requiring lifelong insulin treatment. This study aimed to determine the relationship between in vitro mutation severity and clinical phenotype in a large international case series of patients with homozygous GCK mutations. Clinical characteristics for 30 patients with diabetes due to homozygous GCK mutations (19 unique mutations, including 16 missense) were compiled and assigned a clinical severity grade (CSG) based on birth weight and age at diagnosis. The majority (28 of 30) of subjects were diagnosed before 9 months, with the remaining two at 9 and 15 years. These are the first two cases of a homozygous GCK mutation diagnosed outside infancy. Recombinant mutant GCK proteins were analyzed for kinetic and thermostability characteristics and assigned a relative activity index (RAI) or relative stability index (RSI) value. Six of 16 missense mutations exhibited severe kinetic defects (RAI ≤ 0.01). There was no correlation between CSG and RAI (r(2) = 0.05, P = 0.39), indicating that kinetics alone did not explain the phenotype. Eighty percent of the remaining mutations showed reduced thermostability, the exceptions being the two later-onset mutations which exhibited increased thermostability. Comparison of CSG with RSI detected a highly significant correlation (r(2) = 0.74, P = 0.002). We report the largest case series of homozygous GCK mutations to date and demonstrate that they can cause childhood-onset diabetes, with protein instability being the major determinant of mutation severity.
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