Curry, Timothy B.

Abstract Background: Surgical site infections (SSI) contribute to surgical patients' morbidity and costs. Operating room traffic may be a modifiable risk factor for SSI. We investigated the impact of additional operating room personnel on the risk of superficial SSI (sSSI). Patients and Methods: In this matched case-control study, cases included patients in whom sSSI developed in clean surgical incisions after elective, daytime operations. Control subjects were matched by age, gender, and procedure. Operating room personnel were classified as (1) surgical scrubbed, (2) surgical non-scrubbed, or (3) anesthesia. We used conditional logistic regression to test the extent to which additional personnel overall and from each work group were associated with infection. Results: In total, 474 patients and 803 control subjects were identified. Each additional person among total personnel and personnel from each work group was significantly associated with greater odds of infection (all personnel, odds ratio [OR] = 1.082, 95% confidence interval [CI] 1.031–1.134, p = 0.0013; surgical scrubbed OR = 1.132, 95% CI 1.029–1.245, p = 0.0105; surgical non-scrubbed OR = 1.123, 95% CI 1.008–1.251, p = 0.0357; anesthesia OR = 1.153, 95% CI 1.031–1.290, p = 0.0127). After adjusting for operative duration, body mass index, diabetes mellitus, and vascular disease, additional personnel and sSSI were no longer associated overall or for any work groups (total personnel OR = 1.033, 95% CI 0.974–1.095, p = 0.2746; surgical scrubbed OR = 1.060, 95% CI 0.952-1.179, p = 0.2893; surgical non-scrubbed OR = 1.023 95% CI 0.907–1.154, p = 0.7129; anesthesia OR = 1.051, 95% CI 0.926–1.193, p = 0.4442). Conclusion: The presence of additional operating room personnel was not independently associated with increased odds of sSSI. Efforts dedicated to sSSI reduction should focus on other modifiable risk factors.

New Findings What is the central question of this study? Is lower body negative pressure a useful surrogate to study white blood cell responses to haemorrhage in humans? What is the main finding and its importance? We found that lower body negative pressure appears to be a useful surrogate to study the early white blood cell mobilization response during blood loss. Hypovolaemia has been associated with an immune response that might be secondary to sympathoexcitation. We tested the hypothesis that simulated hypovolaemia using lower body negative pressure (LBNP) and real hypovolaemia induced via experimental blood loss (BL) cause similar increases in the white blood cell concentration ([WBC]). We measured [WBC] and catecholamine concentrations in 12 men who underwent an LBNP and a BL protocol in a randomized order. We compared 45 mmHg of LBNP with 1000 ml of BL; therefore, [WBC] and catecholamine concentrations were plotted against central venous pressure to obtain stimulus–response relationships using the linear regression line slopes for both protocols. Mean regression line slopes were similar for total [WBC] (LBNP 183 ± 4 μl−1 mmHg−1 versus BL 155 ± 109 μl−1 mmHg−1, P = 0.15), neutrophils (LBNP 110 ± 2 μl−1 mmHg−1 versus BL 96 ± 72 μl−1 mmHg−1, P = 0.15) and lymphocytes (LBNP 65 ± 21 μl−1 mmHg−1 versus BL 59 ± 38 μl−1 mmHg−1, P = 0.90). Mean regression line slopes for adrenaline were similar (LBNP 15 ± 5 pg ml−1 mmHg−1 versus BL 16 ± 4 pg ml−1 mmHg−1, P = 0.84) and were steeper during LBNP for noradrenaline (LBNP 28 ± 6 pg ml−1 mmHg−1 versus BL 9 ± 6 pg ml−1 mmHg−1, P = 0.01). These data indicate that central hypovolaemia elicits a relative leucocytosis with a predominantly neutrophil‐based response. Additionally, our results indicate that LBNP models the stimulus–response relationship between central venous pressure and [WBC] observed during BL.

In humans, intra-arterial ATP infusion in limbs mimics many features of exercise hyperemia. However, it remains unknown whether ATP can evoke the prolonged vasodilation seen during exercise. Therefore, we addressed two questions during a continuous 3-h brachial artery infusion of ATP [20 μg·100 ml forearm volume (FAV) −1 ·min −1 ]: 1) would skeletal muscle blood flow remain robust or wane over time (tachyphylaxis); and 2) would the hyperemic response to moderate-intensity exercise performed during the ATP administration be blunted compared with that during control (saline) infusion. Nine participants (25 ± 1 yr) performed one trial consisting of seven bouts of rhythmic handgrip exercise (20 contractions/min at 20% of maximum), two bouts during saline (control), and five bouts during 180 min of continuous ATP infusion. Five minutes of ATP infusion resulted in a 710% increase in forearm vascular conductance (FVC) from control (4.8 ± 0.77 vs. 35.0 ± 5.7 ml·min −1 ·100 mmHg −1 ·dl FAV −1 , P < 0.05). Contrary to our expectations, FVC did not wane over time with values of 35.0 ± 5.7 and 36.0 ± 7.7 ml·min −1 ·100 mmHg −1 ·dl FAV −1 ( P > 0.05), seen prior to the exercise bouts at 5 vs. 150 min, respectively. During superimposed exercise, FVC increased from 35.0 ± 5.7 to 49.6 ± 5.4 ml·min −1 ·100 mmHg −1 ·dl FAV −1 at 5 min and 36.0 ± 7.7 to 54.5 ± 5.0 at 150 min ( P < 0.05). Our findings demonstrate ATP vasodilation is prolonged over time without tachyphylaxis; however, exercise hyperemia responses remain intact. Our results challenge the metabolic theory of exercise hyperemia, suggesting a disconnect between matching of blood flow and metabolic demand.

Study Design Retrospective study. Objective Efficient use of operating room time is important, as delays during induction or recovery increase time not spent operating while in the operating room. We identified factors that increase anesthetized, nonoperative time by utilizing a database of over 5,000 consecutive neurosurgical spine cases. Methods Surgical records were searched to identify all spine surgeries performed between January 2010 and July 2012. Anesthetized, nonoperative time was calculated from the anesthesia record and compared with both patient and procedure characteristics to determine any significant relationships Results There were 5,515 surgical cases with a mean age of 60.5 and mean body mass index (BMI) of 29.7; 3,226 (58%) were male subjects. There were 1,176 (21%) fusion cases, and level of pathology was predominantly lumbar (4,010 cases, 73%). Fusion cases had a significantly longer total anesthetized, nonoperative time (fusion: 98 minutes, nonfusion: 76 minutes, mean difference: 22 minutes, p < 0.0001). Significant factors affecting anesthetized, nonoperative time in nonfusion cases include age greater than 65 years (mean difference 5 minutes, p < 0.0001), American Society of Anesthesiologists (ASA) grade, and BMI (BMI < 25: 72 ± 1.2 minutes, BMI 25 to 29: 74 ± 0.6 minutes, BMI 30 to 39: 79 ± 0.6 minutes, BMI 40 + : 87 ± 1.8 minutes, p < 0.0001). Similarly, for fusion operations, age > 65 years significantly increased nonoperative time (mean difference 6 minutes, p < 0.01), as did increasing ASA (mean difference 9 minutes, p < 0.0001) and increasing BMI. Conclusion Patient and surgical factors, including ASA grade, BMI, level of pathology, and surgical approach, have noticeable effects on anesthetized, nonoperative times in spine surgery.

We tested the hypothesis that markers of coagulation activation are greater during lower body negative pressure (LBNP) than those obtained during blood loss (BL). We assessed coagulation using both standard clinical tests and thrombelastography (TEG) in 12 men who performed a LBNP and BL protocol in a randomized order. LBNP consisted of 5-min stages at 0, −15, −30, and −45 mmHg of suction. BL included 5 min at baseline and following three stages of 333 ml of blood removal (up to 1,000 ml total). Arterial blood draws were performed at baseline and after the last stage of each protocol. We found that LBNP to −45 mmHg is a greater central hypovolemic stimulus versus BL; therefore, the coagulation markers were plotted against central venous pressure (CVP) to obtain stimulus-response relationships using the linear regression line slopes for both protocols. Paired t-tests were used to determine whether the slopes of these regression lines fell on similar trajectories for each protocol. Mean regression line slopes for coagulation markers versus CVP fell on similar trajectories during both protocols, except for TEG α° angle (−0.42 ± 0.96 during LBNP vs. −2.41 ± 1.13°/mmHg during BL; P < 0.05). During both LBNP and BL, coagulation was accelerated as evidenced by shortened R-times (LBNP, 9.9 ± 2.4 to 6.2 ± 1.1; BL, 8.7 ± 1.3 to 6.4 ± 0.4 min; both P < 0.05). Our results indicate that LBNP models the general changes in coagulation markers observed during BL.

Endogenous female sex hormones influence muscle sympathetic nerve activity (MSNA), a regulator of arterial blood pressure and important factor in hypertension development. Although ≈80% of American women report using hormonal contraceptives sometime during their life, the influence of combined oral contraceptives (OCs) on MSNA and systemic hemodynamics remains equivocal. The goal of this study was to determine whether women taking OCs have altered MSNA and hemodynamics (cardiac output and total peripheral resistance) at rest during the placebo phase of OC use compared with women with natural menstrual cycles during the early follicular phase. We retrospectively analyzed data from studies in which healthy, premenopausal women (aged 18–35 years) participated. We collected MSNA values at rest and hemodynamic measurements in women taking OCs (n=53; 25±4 years) and women with natural menstrual cycles (n=74; 25±4 years). Blood pressure was higher in women taking OCs versus those with natural menstrual cycles (mean arterial pressure, 89±1 versus 85±1 mm Hg, respectively; P =0.01), although MSNA was similar in both groups (MSNA burst incidence, 16±1 versus 18±1 bursts/100 heartbeats, respectively; P =0.19). In a subset of women in which detailed hemodynamic data were available, those taking OCs (n=33) had similar cardiac output (4.9±0.2 versus 4.7±0.2 L/min, respectively; P =0.47) and total peripheral resistance (19.2±0.8 versus 20.0±0.9 U, respectively; P =0.51) as women with natural menstrual cycles (n=22). In conclusion, women taking OCs have higher resting blood pressure and similar MSNA and hemodynamics during the placebo phase of OC use when compared with naturally menstruating women in the early follicular phase.

Hypoglycemia results in a reduction in cardiac baroreflex sensitivity and a shift in the baroreflex working range to higher heart rates. This effect is mediated, in part, by the carotid chemoreceptors. Therefore, we hypothesized hypoglycemia-mediated changes in baroreflex control of heart rate would be blunted in carotid body–resected patients when compared with healthy controls. Five patients with bilateral carotid body resection for glomus tumors and 10 healthy controls completed a 180-minute hyperinsulinemic, hypoglycemic (≈3.3 mmol/L) clamp. Changes in heart rate, blood pressure, and spontaneous cardiac baroreflex sensitivity were assessed. Baseline baroreflex sensitivity was not different between groups ( P >0.05). Hypoglycemia resulted in a reduction in baroreflex sensitivity in both the groups (main effect of time, P <0.01) and responses were lower in resected patients when compared with controls (main effect of group, P <0.05). Hypoglycemia resulted in large reductions in systolic (−17±7 mm Hg) and mean (−14±5 mm Hg) blood pressure in resected patients that were not observed in controls (interaction of group and time, P <0.05). Despite lower blood pressures, increases in heart rate with hypoglycemia were blunted in resected patients (interaction of group and time, P <0.01). Major novel findings from this study demonstrate that intact carotid chemoreceptors are essential for increasing heart rate and maintaining arterial blood pressure during hypoglycemia in humans. These data support a contribution of the carotid chemoreceptors to blood pressure control and highlight the potential widespread effects of carotid body resection in humans.