Search

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 chloride110 mEq/L) and whether this electrolyte disturbance is associated with an increase in length of hospital stay, morbidity, or 30-day postoperative mortality.Data were retrospectively collected on consecutive adult patients (18 years of age) who underwent inpatient, noncardiac, nontransplant surgery between January 1, 2003 and December 31, 2008. The impact of postoperative hyperchloremia on patient morbidity and length of hospital stay was examined using propensity-matched and logistic multivariable analysis.The dataset consisted of 22,851 surgical patients with normal preoperative serum chloride concentration and renal function. Acute postoperative hyperchloremia (serum chloride110 mmol/L) is quite common, with an incidence of 22%. Patients were propensity-matched based on their likelihood to develop acute postoperative hyperchloremia. Of the 4955 patients with hyperchloremia after surgery, 4266 (85%) patients were matched to patients who had normal serum chloride levels after surgery. These 2 groups were well balanced with respect to all variables collected. The hyperchloremic group was at increased risk of mortality at 30 days postoperatively (3.0% vs 1.9%; odds ratio = 1.58; 95% confidence interval, 1.25-1.98) (relative risk 1.6 or risk increase of 1.1%) and had a longer hospital stay (7.0 days [interquartile range 4.1-12.3] compared with 6.3 [interquartile range 4.0-11.3]) than patients with normal postoperative serum chloride levels. Patients with postoperative hyperchloremia were more likely to have postoperative renal dysfunction. Using all preoperative variables and measured outcome variables in a logistic regression analysis, hyperchloremia remained an independent predictor of 30-day mortality with an odds ratio of 2.05 (95% confidence interval, 1.62-2.59).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.

BACKGROUND Acute β-blockade has been associated with a dose-dependent increase in adverse outcomes, including stroke and mortality. Acute blood loss contributes to the incidence of these adverse events. In an attempt to link the risks of acute blood loss and β-blockade, animal studies have demonstrated that acute β-blockade impairs cerebral perfusion after hemodilution. We expanded on these findings by testing the hypothesis that acute β-blockade with a highly β(1)-specific antagonist (nebivolol) causes dose-dependent cerebral hypoxia during hemodilution. METHODS Anesthetized rats and mice were randomized to receive vehicle or nebivolol (1.25 or 2.5 mg/kg) IV before hemodilution to a hemoglobin concentration near 60 g/L. Drug levels, heart rate (HR), cardiac output (CO), regional cerebral blood flow (rCBF, laser Doppler), and microvascular brain Po(2) (P(Br)O(2), G2 Oxyphor) were measured before and after hemodilution. Endothelial nitric oxide synthase (NOS), neuronal NOS (nNOS), inducible NOS, and hypoxia inducible factor (HIF)-1α were assessed by Western blot. HIF-α expression was also assessed using an HIF-(ODD)-luciferase mouse model. Data were analyzed using analysis of variance with significance assigned at P < 0.05, and corrected P values are reported for all post hoc analyses. RESULTS Nebivolol treatment resulted in dose-specific plasma drug levels. In vehicle-treated rats, hemodilution increased CO and rCBF (P < 0.010) whereas P(Br)O(2) decreased to 45.8 ± 18.7 mm Hg (corrected P < 0.001; 95% CI 29.4-69.7). Both nebivolol doses comparably reduced HR and attenuated the CO response to hemodilution (P < 0.012). Low-dose nebivolol did not impair rCBF or further reduce P(Br)O(2) after hemodilution. High-dose nebivolol attenuated the rCBF response to hemodilution and caused a further reduction in P(Br)O(2) to 28.4 ± 9.6 mm Hg (corrected P = 0.019; 95% CI 17.4-42.7). Both nebivolol doses increased brain endothelial NOS protein levels. Brain HIF-1α, inducible NOS, and nNOS protein levels and brain HIF-luciferase activity were increased in the high-dose nebivolol group after hemodilution (P < 0.032). CONCLUSIONS Our data demonstrate that nebivolol resulted in a dose-dependent decrease in cerebral oxygen delivery after hemodilution as reflected by a decrease in brain tissue Po(2) and an increase in hypoxic protein responses (HIF-1α and nNOS). Low-dose nebivolol treatment did not result in worsened tissue hypoxia after hemodilution, despite comparable effects on HR and CO. These data support the hypothesis that acute β-blockade with a highly β(1)-specific antagonist causes a dose-dependent impairment in cerebral perfusion during hemodilution.

Although β blockers have been found to decrease perioperative myocardial infarction (MI), β-blocker-mediated hypotension is associated with postoperative stroke and mortality. In this systematic review we assessed the safety and efficacy of the β1-specific, adrenergic receptor antagonist esmolol in noncardiac surgery. Safety was assessed by analyzing the incidence of postoperative hypotension and bradycardia, and efficacy was assessed by analyzing the incidence of myocardial ischemia.We searched electronic databases for randomized placebo-controlled trials of the perioperative use of esmolol in noncardiac surgery. We abstracted data on design, demographics, hemodynamic changes (planned or unplanned), myocardial ischemia, and MI. Heterogeneity was assessed via meta-regression.Our search identified 67 trials, which were well matched for study characteristics. The quality of the studies was limited by small sample size and poorly defined allocation concealment. Overall, the analysis demonstrates an increased incidence of unplanned hypotension (OR 2.13; 95% confidence interval [CI], 1.48 to 3.04), which was found to be dose related (R(2) = 0.408). An increased incidence of significant bradycardia was not demonstrated (OR 1.18; 95% CI, 0.69 to 2.02). Dose titration was shown to influence both the change in arterial blood pressure and heart rate. In comparison with placebo, esmolol decreased the frequency of myocardial ischemia in the 7 evaluating studies (OR 0.17; 95% CI, 0.02 to 0.45). We did not assess the effects of esmolol on the incidence of MI or stroke because the incidence of these events was too infrequent in the retrieved studies.This review suggests that titration of esmolol to a hemodynamic end point can be safe and effective. Safety data from studies in higher-risk patients are needed to establish a perioperative safety and efficacy profile of esmolol.

Accurate risk stratification may help reduce the burden of excessive blood loss after cardiac surgery. We measured the incremental value of thrombelastography to an existing risk prediction model for excessive blood loss in cardiac surgery.This observational study included 434 patients who underwent cardiac surgery with cardiopulmonary bypass (CPB) and had thrombelastographic measures before and during CPB, their risk of excessive blood loss could be calculated with an existing risk prediction model and they had not received clopidogrel or warfarin within 5 days of surgery. Excessive blood loss was defined as transfusion ofor = 5 U of red blood cells from termination of CPB to 1 day after surgery. Logistic regression models including an existing risk prediction model without and with thrombelastographic measures were constructed. Improvement in risk prediction was measured by the area under the curve and net reclassification improvement.Excessive blood loss occurred in 59 of 434 patients (13.6%). The only thrombelastographic measure that improved risk stratification was maximum amplitude during CPB, which reflects maximum clot strength. Although the addition of this variable to the existing prediction model did not have a material effect on the area under the curve (increased from 0.780 to 0.784; P = 0.8), it did improve the net reclassification improvement by 12% (P = 0.05), primarily by improving the detection of high-risk cases.Risk stratification for excessive blood loss after cardiac surgery is improved when on-CPB thrombelastography is added to an existing risk prediction model that incorporates readily available patient- and surgery-related variables, but large, multicenter trials are needed to verify this finding and create a new risk prediction model.

Isocapnic hyperpnoea (IH) reduces recovery time from isoflurane anesthesia in animals and humans. We studied the effect of IH on the emergence profile of sevoflurane-anesthetized patients by comparing postoperative recovery variables in patients administered IH (IH group) to those recovered in the customary fashion (control group).We enrolled 30 ASA I-III patients undergoing elective gynecological surgery. Induction and maintenance of anesthesia were standardized with a protocol consisting of fentanyl, propofol, rocuronium, and sevoflurane in air/O2. Patients were randomly assigned to control (C) or IH groups at the end of the surgery. We recorded time intervals from discontinuing sevoflurane to recovery milestones.Time to tracheal extubation was much shorter in the IH group compared with group C (6.2 +/- 2.1 vs 12.3 +/- 3.8 min, respectively, P0.01). The IH group also had shorter times to initiation of spontaneous ventilation (4.2 +/- 1.7 vs 6.5 +/- 3.8 min, P = 0.047), eye opening (5.5 +/- 1.4 vs 13.3 +/- 4.4 min, P0.01), bispectral index value75 (3.9 +/- 1.1 vs 8.8 +/- 3.7 min, P0.01), leaving operating room (7.7 +/- 2.0 vs 15.3 +/- 3.4 min, P0.01), and eligibility for postanesthetic care unit discharge (67.2 +/- 19.3 vs 90.6 +/- 20.0 min, P0.01).IH accelerates recovery from sevoflurane anesthesia and shortens operating room and postanesthetic care unit stay.

Nitrous oxide anesthesia causes increased postoperative plasma homocysteine levels. Acute increases in plasma homocysteine are associated with impaired endothelial function and procoagulant effects. This nitrous oxide-induced plasma homocysteine increase may therefore affect the risk of perioperative cardiovascular events. This prospective, randomized study was therefore designed to evaluate the effect of nitrous oxide anesthesia and postoperative plasma homocysteine levels on myocardial ischemia in patients undergoing carotid endarterectomy. After institutional review board approval and written informed consent, 90 ASA Class I-III patients presenting for elective carotid endarterectomy were randomized to receive general anesthesia with or without nitrous oxide. Prior to induction, on arrival in the postanesthesia care unit, and after 48 h, blood samples were obtained for homocysteine analysis. Three hours prior to induction and for 48 h postoperatively patients were monitored by a three-channel, seven-lead Holter monitor. Postoperatively in the postanesthesia care unit and at 48 h the nitrous oxide group had increased mean plasma homocysteine concentrations of 15.5 +/- 5.9 and 18.8 +/- 14.7 when compared with the nonnitrous group of 11.4 +/- 5.2 and 11.3 +/- 4.0 micromol/L, P:0.001. The nitrous oxide group had an increased incidence of ischemia (46% vs. 25%, P:0.05), significantly more ischemia (63 +/- 71 vs. 40 +/- 68 min, P:0.05), had more ischemic events (82 vs. 53, P:0.02), and had more ischemic events lasting 30 min (23 vs. 14, P:0.05) than the nonnitrous group. This study reconfirmed that intraoperative nitrous oxide is associated with postoperative increases in plasma homocysteine concentration. This was associated with an increase in postoperative myocardial ischemia.Use of nitrous oxide during carotid artery surgery induces increases in postoperative plasma homocysteine concentration and is associated with increases in postoperative myocardial ischemia.

IMPLICATIONS This report describes the appearance of CO2 on the capnograph during inspiration, which was linked to disconnection of the inner tube of a coaxial circuit extension piece. The increased use of coaxial breathing systems for adults makes inner tubes disconnections an important consideration when the CO2 appears during inspiration.