No abstract

Development of hyperglycemia after major operations is very common and is modulated by many factors. These factors include perioperative metabolic state, intraoperative management of the patient, and neuroendocrine stress response to surgery. Acute insulin resistance also develops perioperatively and contributes significantly to hyperglycemia. Hyperglycemia is associated with poor outcomes in critically ill and postsurgical patients. A majority of the investigations use the term "hyperglycemia" very loosely and use varying thresholds for initiating treatment. Initial studies demonstrated improved outcomes in critically ill, postsurgical patients who received intensive glycemic control (IGC) (target serum glucose <110 mg/dL). These results were quickly extrapolated to other clinical areas, and IGC was enthusiastically recommended in the perioperative period. However, there are few studies investigating the value of intraoperative glycemic control. Moreover, recent prospective trials have not been able to show the benefit of IGC; neither an appropriate therapeutic glycemic target nor the true efficacy of perioperative glycemic control has been fully determined. Practitioners should also appreciate technical nuances of various glucose measurement techniques. IGC increases the risk of hypoglycemia significantly, which is not inconsequential in critically ill patients. Until further specific data are accumulated, it is prudent to maintain glucose levels <180 mg/dL in the perioperative period, and glycemic control should always be accompanied by close glucose monitoring.

To identify and quantitate complications occurring in the postanesthesia care unit (PACU), a prospective study evaluated 18,473 consecutive patients entering a PACU at a university teaching hospital. Using a standardized collection form, the incidence of intraoperative and PACU complications was determined. The combined PACU and intraoperative complication rate was 26.7%. Data showed a PACU complication rate of 23.7%, with an overall intraoperative complication rate of 5.1%. Nausea and vomiting (9.8%), the need for upper airway support (6.9%), and hypotension requiring treatment (2.7%) were the most frequently encountered PACU complications. Patients in whom PACU complications developed were analyzed by ASA physical status. Of all patients experiencing nausea and vomiting (n = 1571), the highest percentage were ASA physical status II patients (n = 831). Likewise, in the group of 1450 patients who demonstrated a need for upper airway support, 792 were ASA physical status II. In patients experiencing a major cardiovascular complication, for example, variables associated with a greater risk of developing any PACU complications were ASA physical status (status II), duration of anesthesia (2-4 h), anesthetic technique, emergency procedures, and certain types of surgical procedures (orthopedic or abdominal). For patients admitted with a temperature of less than 35 degrees C the duration of the PACU stay was 152 +/- 46 min compared with 116 +/- 65 min for patients with a temperature greater than or equal to 36 degrees C (P less than 0.01). In conclusion, events occurring during the PACU period continue to be a source of patient morbidity.

Plasma cocaine levels were determined in 7 subjects after intranasal and oral cocaine. Intranasal doses of 0.19, 0.38, 0.75, 1.5, and 2.0 mg/kg were given as a 10% aqueous solution; 0.38 mg/kg was given as crystalline cocaine HCl. Oral cocaine was administered in doses of 2.0 and 3.0 mg/kg. Intranasal cocaine kinetics were described by a 1-compartment open model with 2 consecutive first-order input steps and first-order elimination. Oral cocaine disposition was described by a 1-compartment open model with a lag time followed by a single first-order input phase and first-order elimination. The mean elimination half-life (t 1/2) for cocaine by the intranasal route to 7 subjects was 75 +/- 5 min (mean +/- SE). The mean t 1/2 after oral administration to 4 subjects was 48 +/- 3 min. The relative bioavailability [as determined by the area under the concentration-time curve (AUC)] for the 2.0-mg/kg dose by the intranasal and oral routes was not different. There was a linear increase in AUC with increasing intranasal dose.