ABSTRACT
BACKGROUND: The Centers for Disease Control (CDC) created a classification to help stratify surgical wounds based on contamination and risk of developing a surgical site infection. The classification includes four options (I to IV) depending on the level of contamination present. Although universally applied to a variety of surgical specialties, it is unknown whether the current system is reliable when considering orthopaedic surgeries. The purpose of this study was to compare the degree of interobserver reliability between orthopaedic surgeons using the current CDC wound class definitions. METHODS: A questionnaire containing 30 clinical vignettes was completed by 39 orthopaedic surgeons at our institution. After each vignette, respondents were asked to determine the appropriate wound class based on information provided in the vignette. The overall interobserver agreement among all participants was analyzed. In addition, respondents were queried about the adequacy of the current classification system in describing orthopaedic surgical wound class. RESULTS: Interobserver agreement was poor at 66%, with a coefficient of concordance of 0.48. Only six physicians (15.4%) thought that the current wound classification system adequately covered orthopaedic surgery. CONCLUSIONS: There is poor interobserver reliability using the CDC surgical wound class definitions for orthopaedic surgeries. Alternate definitions are needed to improve the validity of the system for subspecialty procedures.
Subject(s)
Orthopedic Surgeons , Surgical Wound , Centers for Disease Control and Prevention, U.S. , Humans , Reproducibility of Results , Surgical Wound Infection , United StatesABSTRACT
Previous studies showed that Src homology-2 tyrosine phosphatase (Shp2) is an important regulator of body weight. In this study, we examined the impact of Shp2 deficiency specifically in proopiomelanocortin (POMC) neurons on metabolic and cardiovascular function and on chronic blood pressure (BP) and metabolic responses to leptin. Mice with Shp2 deleted in POMC neurons (Shp2/Pomc-cre) and control mice (Shp2(flox/flox)) were implanted with telemetry probes and venous catheters for measurement of mean arterial pressure (MAP) and leptin infusion. After at least 5 days of stable control measurements, mice received leptin infusion (2 µg·kg(-1)·day(-1) iv) for 7 days. Compared with Shp2(flox/flox) controls, Shp2/Pomc-cre mice at 22 wk of age were slightly heavier (34 ± 1 vs. 31 ± 1 g) but consumed a similar amount of food (3.9 ± 0.3 vs. 3.8 ± 0.2 g/day). Leptin infusion reduced food intake in Shp2(flox/flox) mice (2.6 ± 0.5 g) and Shp2/Pomc-cre mice (3.2 ± 0.3 g). Despite decreasing food intake, leptin infusion increased MAP in control mice, whereas no significant change in MAP was observed in Shp2/Pomc-cre mice. Leptin infusion also decreased plasma glucose and insulin levels in controls (12 ± 1 to 6 ± 1 µU/ml and 142 ± 12 to 81 ± 8 mg/100 ml) but not in Shp2/Pomc-cre mice. Leptin increased VÌo2 by 16 ± 2% in controls and 7 ± 1% in Shp2/Pomc-cre mice. These results indicate that Shp2 signaling in POMC neurons contributes to the long-term BP and antidiabetic actions of leptin and may play a modest role in normal regulation of body weight.
Subject(s)
Arterial Pressure/drug effects , Blood Glucose/drug effects , Brain/drug effects , Energy Metabolism/drug effects , Leptin/administration & dosage , Neurons/drug effects , Pro-Opiomelanocortin/metabolism , Protein Tyrosine Phosphatase, Non-Receptor Type 11/metabolism , Signal Transduction/drug effects , Animals , Blood Glucose/metabolism , Body Weight/drug effects , Brain/enzymology , Eating/drug effects , Homeostasis , Infusions, Intravenous , Insulin/blood , Male , Mice, 129 Strain , Mice, Inbred C57BL , Mice, Knockout , Motor Activity/drug effects , Neurons/enzymology , Oxygen Consumption/drug effects , Protein Tyrosine Phosphatase, Non-Receptor Type 11/deficiency , Protein Tyrosine Phosphatase, Non-Receptor Type 11/genetics , Time FactorsABSTRACT
Obesity is recognized as a major worldwide health problem. Excess weight gain is the most common cause of elevated blood pressure (BP) and markedly increases the risk of metabolic, cardiovascular and renal diseases. Although the mechanisms linking obesity with hypertension have not been fully elucidated, increased sympathetic nervous system (SNS) activity contributes to elevated BP in obese subjects. Recent evidence indicates that leptin and the central nervous system (CNS) melanocortin system, including melanocortin 4 receptors (MC4R), play a key role in linking obesity with increased SNS activity and hypertension. Leptin, a peptide-hormone produced by adipose tissue, crosses the blood-brain barrier and activates brain centers that control multiple metabolic functions as well as SNS activity and BP via the CNS melanocortin system. The crosstalk between peripheral signals (e.g., leptin) and activation of CNS pathways (e.g., MC4R) that regulate energy balance, SNS activity and BP represents an important target for treating obesity and its metabolic and cardiovascular consequences.
