Anti-emetic dexamethasone and postoperative infection risk: a retrospective cohort study.

Nausea and vomiting are common complications of anaesthesia. Dexamethasone is an effective prophylaxis but is immunosuppressive and may increase postoperative infection risk. This retrospective cohort study examined the association between the administration of a single intraoperative anti-emetic dose of dexamethasone (4 to 8 mg) and postoperative infection in 439 patients undergoing single procedure, non-emergency surgery in a university trauma centre. Exclusion criteria included comorbidities, immunosuppressive medications or procedures that confer an increased infection risk. In the 10-week study period and three-month follow-up period, there were 98 documented infections (22.3% of the cohort), of which 43 were detected only on post-discharge follow-up. Anti-emetic dexamethasone was given to 108 patients (24.6%). Stepwise, multivariate logistic regression modelling identified significant associations between female gender, symptomatic reflux, respiratory disease and the risk of infection. The adjusted odds ratio for dexamethasone was 0.88 (0.5 to 1.5, P = 0.656). We did not demonstrate an association between anti-emetic doses of dexamethasone and postoperative infection.

Prospective, randomized comparison of deep or superficial cervical plexus block for carotid endarterectomy surgery.

BACKGROUND: Carotid endarterectomy may be performed under cervical plexus block with local anesthetic supplementation by the surgeon as necessary during surgery. It is unclear, however, whether deep or superficial cervical plexus block offers the best operating conditions or patient satisfaction. Therefore, the authors compared the two in patients undergoing carotid endarterectomy. METHODS: Forty patients undergoing carotid endarterectomy were randomized to receive either a superficial or a deep cervical plexus block with 20 ml bupivacaine, 0.375%. Outcomes subjected to statistical analysis included supplemental anesthetic supplementation with lidocaine, 1%, by the surgeon, dermatomes affected by the block, paresthesia during block placement, postoperative pain scores, and analgesic requirements. RESULTS: Median supplemental lidocaine requirements were 6 ml (range, 0.5 to 20 ml) in the deep block group and 6 ml (range, 0 to 20 ml) in the superficial block group (P = 0.7323). Patients in the deep block group who reported paresthesia during block placement required less lidocaine supplementation (median, 2; range, 0.5 to 20 ml) than the 9.5 ml (range, 6 to 15.5 ml) required by those who did not experience paresthesia (P = 0.0113). Compared with patients in the superficial block group, those in the deep block group were less likely to need analgesia in the first 24 h after operation (P = 0.047), and those who required analgesia received it later (6.6 +/- 4.1 vs. 3.9 +/- 1.4 h after operation; Student's t test, P = 0.02). One patient in each group expressed dissatisfaction with the technique. CONCLUSIONS: Carotid endarterectomy may be performed satisfactorily during superficial or deep cervical plexus block placement with no differences in terms of supplemental local anesthetic requirements, although this is influenced by whether paresthesia is elicited during placement of the deep block. Therefore, the clinician's decision to use one block rather than another need not be based on any assumed superiority of one block based on intraoperative conditions or patient satisfaction.

Remifentanil and pulmonary extraction during and after cardiac anesthesia.

We measured the apparent blood clearance and pulmonary extraction ratio of remifentanil in 10 adult patients undergoing elective myocardial revascularization for the first time with hypothermic cardiopulmonary bypass (CPB). Patients received continuous infusions of remifentanil 1.0, 1.5 or 2.0 microg x kg(-1) x min(-1). After surgery, remifentanil was infused at 1.0 microg x kg(-1) x min(-1) in all patients. Remifentanil concentrations were measured in pulmonary and radial artery blood by gas chromatography with high resolution mass spectrometry before and after CPB and 165 min (60 SD) after surgery. Cardiac output was measured by thermodilution at the time of blood sampling. The mean pulmonary extraction ratio of remifentanil was 5.7% (13.1% SD), which was not significantly different from zero. However, pulmonary extraction ratio was related inversely to the pulmonary artery hydrogen ion concentration and directly to the percent of nonionized form of the base in the pulmonary artery. Remifentanil concentrations in pulmonary and radial artery blood were related directly to infusion rate, but not to duration of infusion. There was no evidence of accumulation or sequestration. Mean apparent blood remifentanil clearance was 2.03 L/min (0.35 SD) and, in contrast to remifentanil pulmonary extraction ratio, was related directly to cardiac index and oxygen delivery. Increased tissue perfusion increased blood remifentanil clearance. We found predictable blood remifentanil levels with no evidence of accumulation or pulmonary extraction.

A novel protamine variant reversal of heparin anticoagulation in human blood in vitro.

PURPOSE: Protamine reversal of heparin anticoagulation during cardiovascular surgery may cause severe hypotension and pulmonary hypertension. A novel protamine variant, [+18RGD], has been developed that effectively reverses heparin anticoagulation without toxicity in canine experiments. Heretofore, human studies have not been undertaken. This investigation hypothesized that [+18RGD] would effectively reverse heparin anticoagulation of human blood in vitro. METHODS: Fifty patients who underwent anticoagulation therapy during vascular surgery had blood sampled at baseline and 30 minutes after receiving heparin (150 IU/kg). Activated clotting times were used to define specific quantities of [+18RGD] or protamine necessary to completely reverse heparin anticoagulation in the blood sample of each patient. These defined amounts of [+18RGD] or protamine were then administered to the heparinized blood samples, and percent reversals of activated partial thromboplastin time, thrombin clotting time, and antifactor Xa/IIa levels were determined. In addition, platelet aggregation assays, as well as platelet and white blood cell counts were performed. RESULTS: [+18RGD] and protamine were equivalent in reversing heparin as assessed by thrombin clotting time, antifactor Xa, antifactor IIa levels, and white blood cell changes. [+18RGD], when compared with protamine, was superior in this regard, as assessed by activated partial thromboplastin time (94.5 +/- 1.0 vs 86.5 +/- 1.3% delta, respectively; p < 0.001) and platelet declines (-3.9 +/- 2.9 vs -12.8 +/- 3.4 per mm3, respectively; p = 0.048). Platelet aggregation was also decreased for [+18RGD] compared with protamine (23.6 +/- 1.5 vs 28.5 +/- 1.9%, respectively; p = 0.048). CONCLUSIONS: [+18RGD] was as effective as protamine for in vitro reversal of heparin anticoagulation by most coagulation assays, was statistically more effective at reversal than protamine by aPTT assay, and was associated with lesser platelet reductions than protamine. [+18RGD], if less toxic than protamine in human beings, would allow for effective clinical reversal of heparin anticoagulation.

Enoximone and warming after hypothermic cardiopulmonary bypass.

In a randomized, controlled study of 24 patients undergoing myocardial revascularization, we found that enoximone 0.5 mg kg-1 i.v., followed by 5 micrograms kg-1 min-1, when rewarming after hypothermic cardiopulmonary bypass, prevented subsequent cooling of the periphery after transfer to the intensive care unit. Skin surface temperatures on the foot increased by mean 0.33 (SD 0.5) degree C h-1 in the enoximone group, but decreased by 0.43 (0.4) degree C h-1 in the control group until core temperature had increased to 37 degrees C (P < 0.001); only then did peripheral temperatures begin to increase in the control group. Enoximone did not merely redistribute heat from the core to the periphery. The capacity to transfer heat by the circulation rather than the ability to generate heat in the core appeared to limit body warming in the ICU after hypothermic cardiopulmonary bypass.

Treatment of perioperative low cardiac output syndrome.

New approaches to the treatment of perioperative low cardiac output are considered. In particular, use of the phosphodiesterase III inhibitors and their cardiovascular actions are reviewed and contrasted with those of conventional inotropic agents. The increasing recognition of right-sided dysfunction is highlighted, and appropriate therapeutic strategies are considered. The increasing role of pulmonary-specific vasodilators such as inhaled nitric oxide is emphasized. Strategies to preserve right heart perfusion while producing pulmonary vasodilatation are discussed.