Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2013
Hyperchloremia after noncardiac surgery is independently associated with increased morbidity and mortality: a propensity-matched cohort study.
The use of normal saline is associated with hyperchloremic metabolic acidosis. In this study, we sought to determine the incidence of acute postoperative hyperchloremia (serum chloride >110 mEq/L) and whether this electrolyte disturbance is associated with an increase in length of hospital stay, morbidity, or 30-day postoperative mortality. ⋯ This retrospective cohort trial demonstrates an association between hyperchloremia and poor postoperative outcome. Additional studies are required to demonstrate a causal relationship between these variables.
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Anesthesia and analgesia · Aug 2013
Randomized Controlled Trial WebcastsPatient warming excess heat: the effects on orthopedic operating room ventilation performance.
Patient warming has become a standard of care for the prevention of unintentional hypothermia based on benefits established in general surgery. However, these benefits may not fully translate to contamination-sensitive surgery (i.e., implants), because patient warming devices release excess heat that may disrupt the intended ceiling-to-floor ventilation airflows and expose the surgical site to added contamination. Therefore, we studied the effects of 2 popular patient warming technologies, forced air and conductive fabric, versus control conditions on ventilation performance in an orthopedic operating room with a mannequin draped for total knee replacement. ⋯ Excess heat from forced air warming resulted in the disruption of ventilation airflows over the surgical site, whereas conductive patient warming devices had no noticeable effect on ventilation airflows. These findings warrant future research into the effects of forced air warming excess heat on clinical outcomes during contamination-sensitive surgery.
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Anesthesia and analgesia · Aug 2013
The surgical apgar score is strongly associated with intensive care unit admission after high-risk intraabdominal surgery.
Understanding intensive care unit (ICU) triage decisions for high-risk surgical patients may ultimately facilitate resource allocation and improve outcomes. The surgical Apgar score (SAS) is a simple score that uses intraoperative information on hemodynamics and blood loss to predict postoperative morbidity and mortality, with lower scores associated with worse outcomes. We hypothesized that the SAS would be associated with the decision to admit a patient to the ICU postoperatively. ⋯ The SAS is strongly associated with clinical decisions regarding immediate ICU admission after high-risk intraabdominal surgery. These results provide an initial step toward understanding whether intraoperative hemodynamics and blood loss influence ICU triage for postsurgical patients.
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Anesthesia and analgesia · Aug 2013
Propofol stimulates noradrenalin-inhibited neurons in the ventrolateral preoptic nucleus by reducing GABAergic inhibition.
The cellular mechanisms underlying the sedative effect of general anesthetics are not completely understood. Accumulating evidence indicates that the ventrolateral preoptic area (VLPO) of the hypothalamus plays a critical role. The VLPO contains 2 major types of neurons, the noradrenalin-inhibited GABAergic projecting neurons (NA(-) neurons) and the noradrenalin-excited interneurons (NA(+) neurons) which are probably also γ-aminobutyric acid (GABA)-containing neurons. Our previous work suggests that NA(-) neurons are normally under the inhibitory control of NA(+) neurons. Previous studies also show that GABAergic agents including propofol activate GABAergic projecting neurons in the VLPO, which is believed to lead to the inhibition of the arousal-producing nuclei in the tuberomammillary nucleus and sedation. However, how propofol activates VLPO neurons remains unclear. We explored the possibility that propofol activates NA(-) neurons indirectly, by inhibiting GABAergic transmission including those from VLPO NA(+) neurons. ⋯ Propofol excites VLPO NA(-) neurons by reducing GABAergic transmission, at least in part by inhibiting VLPO NA(+) neurons. This may be a critical mechanism contributing to propofol-induced sedation.