Who is responsible for operating room management and how do we measure how well we do it?

BACKGROUND: Managing the surgical process in the operating suite - often the most expensive unit in the hospital - is vital, yet challenging. While sensible management can improve efficiency, unclear managerial structures can hinder the optimal use of resources. Despite that, no previous data exists as to how the operating room management is organized and the performance monitored in our country. METHODS: A survey was sent to chief anesthesiologists and head nurses of 103 surgery units of 60 public hospitals regarding the current structures of daily management, as well as metrics and tools used for monitoring the performance of the operating room. RESULTS: The overall response rate was 87%. Nurses' and anesthesiologists' perceptions differed significantly on which care provider they held responsible for the daily operative management of the operating room. In doctors' opinion, that person was an anesthesiologist - either alone or in combinations - more often than in nurses' opinion (66% vs. 35%, P < 0.001). Anesthesiologists' involvement increased by the type and size of the hospital, being greatest in the university hospitals. Operating room performance was measured most often by number of procedures in a time unit, utilization and turnover time. Monitoring was complicated by old-fashioned information systems, and seldom seemed to lead to organizational changes. CONCLUSION: The structure of the daily operative management of an operating room needs redefining. There should be more focus on collaboration and communication between the care providers.

The validity of the static-charge-sensitive bed in the detection of fentanyl-induced respiratory depression.

BACKGROUND: Only a few methods for the measurement of breathing are non-invasive and do not interfere with measured parameters. The static-charge-sensitive bed (SCSB) could be such a monitor. The aim of this study was to evaluate the validity of the SCSB compared with the respiratory inductive plethysmograph (RIP) using a fentanyl-induced respiratory depression model. METHODS: Eight healthy male volunteers were infused with intravenous (i.v.) fentanyl (15 microg/kg/h) until a decrease in SpO2 below 90% for 1 min emerged. Breathing was continuously and simultaneously measured with SCSB and RIP. Oxygenation, hemodynamics, arterial blood gas analysis, and subjective opioid-related effects were monitored. Fentanyl concentration was measured from an arterial blood sample. The respiratory rate data of the SCSB (automated analysis and manual calculation) were compared with the corresponding RIP data, using analysis of variance for repeated measures. The validity of the SCSB compared with RIP was evaluated using an intra-class correlation coefficient. RESULTS: Mean fentanyl dose was 629 microg. A statistically significant association was found between the RIP and SCSB data in the manual SCSB analysis (P < 0.0001), but not in the automated SCSB analysis (P = 0.91). After adjusting for the effect of time and the SCSB method, an intra-class correlation coefficient between the manually calculated SCSB values and the RIP values was 0.66. CONCLUSION: Clinically significant changes in respiratory rate were detected with the SCSB, but the results had to be analyzed manually. The SCSB best suits situations, where comprehensive data are needed. It is not suitable for on-line respiratory monitoring, as the automated analysis did not calculate the respiratory rate correctly.

Pulmonary inflammatory mediators after sevoflurane and thiopentone anaesthesia in pigs.

BACKGROUND: Volatile anaesthetics have been shown to affect the release of pulmonary inflammatory mediators and exacerbate pulmonary injury after experimental aspiration. Thus, in theory, volatile anaesthetics may worsen inflammatory pulmonary injury and disease. We have previously described that no significant changes in alveolar ultrastructure are seen after sevoflurane anaesthesia. However, this does not exclude any possible physiological alterations. The aim of our study was to evaluate pulmonary inflammatory mediators in bronchoalveolar lavage (BAL) after sevoflurane and thiopentone anaesthesia in pigs with intact lungs. METHODS: Sixteen pigs were randomly selected to receive either a continuous thiopentone infusion (control group, n = 8) or sevoflurane (n = 8) at 4.0% inspiratory concentration (1.5 MAC) in air for 6 h. Bronchoalveolar lavage samples were collected at the end of the study to determine pulmonary inflammatory markers. RESULTS: Compared with thiopentone anaesthesia, significant increases in BAL leukotriene C4 (LTC4), NO3-, and NO2- levels were observed after sevoflurane anaesthesia. In addition, there was a significant decrease in total blood leukocyte count in sevoflurane-treated animals. CONCLUSION: We conclude that sevoflurane increases pulmonary LTC4, NO3-, and NO2- production in pigs, indicating an inflammatory response.

Alveolar integrity and ultrastructure in pigs remain undamaged after exposure to sevoflurane.

Previous studies have shown that both halothane and isoflurane have adverse but reversible effects on alveolar physiology. The present study was designed to test the hypothesis that also sevoflurane may affect alveolar integrity. Fifteen pigs were randomly selected to receive either thiopentone infusion (control group, n=8) or sevoflurane (n=7) at 4.0% inspiratory concentration (1.5 MAC) in air for 6 h. Tissue samples from the lungs were obtained at the end of the experiment. Both histopathological light microscopy and electron microscopy were used to assess the structural integrity of the alveoli. Pulmonary hemodynamics were comparable in both groups. Light microscopy showed no difference between the groups in the amount of alveolar macrophages, red blood cells or edema. Electron microscopy showed minor changes such as moderate local swelling of alveolar epithelium in both study groups. Alveolar type II cells were ultrastructurally unaltered in both study groups. We conclude that long-term, high concentration exposure to sevoflurane has no detrimental effect on the alveolar integrity in pigs.

The concentration-effect relationship of the respiratory depressant effects of alfentanil and fentanyl.

UNLABELLED: The relative potencies of fentanyl and alfentanil for respiratory depression were determined in eight healthy male volunteers in a double-blinded, randomized study with a cross-over design. The drugs were delivered by computer-driven infusion with logarithmically ascending plasma concentrations until the respiratory rate reached 2/min and/or oxygen saturation decreased below 85% with subjects breathing room air. Ventilation was measured with respiratory inductive plethysmography, indirect calorimetry, and arterial blood gas analysis, and plasma drug concentrations were determined. Pharmacodynamic modeling was performed using a fractional E(max) model for minute volume and respiratory rate and the concentrations producing 50% depression (i.e., apparent 50% effective concentration [EC(50)] values) were determined. Both drugs decreased ventilation in a similar manner, and drug infusions were terminated at mean +/- SD measured plasma concentrations of 254 +/- 88 ng/mL and 5.1 +/- 1.7 ng/mL for alfentanil and fentanyl, respectively. Alfentanil decreased minute volume from baseline by 54% +/- 19% and respiratory rate by 40% +/- 11% with EC(50) values of 234 +/- 57 ng/mL and 195 +/- 101 ng/mL. The respective decreases for fentanyl were 50% +/- 11%, 41% +/- 15%, and the estimated EC(50) values were 6.1 +/- 1.4 ng/mL and 3.5 +/- 1.4 ng/mL, respectively. Using the apparent EC(50) values, the calculated potency ratio for alfentanil:fentanyl was (mean and 95% confidence interval) 1:39 (1:31-1:46) for minute volume and 1:51 (1:34-1:68) for respiratory rate. This is analogous to the analgesic effect studied earlier. The findings support the notion of parallel analgesic and respiratory depressant effects of alfentanil and fentanyl. Therefore equianalgesic concentrations of both drugs will lead to equally pronounced respiratory depression. IMPLICATIONS: This double-blinded, randomized study evaluated the potency ratio of alfentanil and fentanyl-induced respiratory depression. The findings support the notion of parallel analgesic and respiratory depressant effects of alfentanil and fentanyl. Therefore equianalgesic concentrations of both drugs will lead to equally pronounced respiratory depression.

Spinal anesthesia with hypobaric bupivacaine for knee arthroscopies: effect of posture on motor block.

BACKGROUND AND OBJECTIVES: The clinical impact of patient positioning on motor block during unilateral spinal anesthesia was the focus of our study. It was assumed that a 45 degrees rotation toward the prone position would minimize blocking the ventral motor roots compared with using the conventional lateral decubitus position. METHODS: Spinal anesthesia with 3.4 mL of hypobaric 0.18% bupivacaine via a 27-gauge Whitacre needle was administered to 70 patients undergoing knee arthroscopy. The patients were kept either in a lateral decubitus position (group I) or rotated approximately 45 degrees toward the prone position (group II). No prophylactic vasopressors or infusions were used. The intensity of motor block (modified Bromage scale) was assessed for both the operative and the contralateral side. RESULTS: The patients in group I had a slightly more pronounced motor block, but statistical significance could be shown only 20 minutes following the block. There was no statistical difference between the groups in the need of additional analgesics during the operation. None of the patients needed general anesthesia. The hemodynamics were stable and none of the patients developed postspinal headache or backache. CONCLUSIONS: The position of the patient affects the spread of the spinal anesthesia when clearly hypobaric agents are used. However, this small modification in positioning of the patient did not lead to a clinically meaningful difference in the spread of the motor block.

The use of bupivacaine and fentanyl for spinal anesthesia for urologic surgery.

We evaluated the effect of 25 microg of fentanyl added to bupivacaine on sensory and motor block. By using a double-blinded study design, 80 men undergoing urologic surgery were randomized into the following four groups: Group I, bupivacaine 10 mg; Group II, bupivacaine 10 mg + fentanyl 25 microg; Group III, bupivacaine 7.5 mg + fentanyl 25 microg; Group IV, bupivacaine 5 mg + fentanyl 25 microg. The final volume of intrathecal injectate was adjusted to 2. 5 mL with sterile distilled water. Spinal anesthesia was administered with the 27-gauge Whitacre needle at the L2-3 interspace with the patient in the sitting position. Neural block was assessed by using pinprick and a modified Bromage scale. The degree of motor block was more profound in Group II compared with Group I at the end of operation. In Group IV, there was no motor block at the end of operation in any of the patients. The median level of the upper limit of the sensory block was higher than T(7) in all groups before the start of surgery. The addition of 25 microg of fentanyl to 5 mg of bupivacaine resulted in short-acting motor block. When 25 microg of fentanyl was added to 10 mg of bupivacaine, it increased the intensity and duration of motor block. Only 5 (6. 3%) of the patients needed supplemental analgesia during the operation. ¿abs¿

Morphine-induced cardiovascular stimulation: the effects of two doses on healthy subjects.

UNLABELLED: In humans, morphine induces hypotension, probably because of histamine liberation. Earlier animal studies have, however, suggested that morphine can induce immediate cardiovascular stimulation when given as a sole medication. The aim of this study was to evaluate the initial effects of morphine on circulation, oxygen consumption, and plasma histamine and catecholamine concentrations. Oxycodone was used as a reference drug. Eight healthy volunteers received, in a random, cross-over, double-blinded fashion: 0.07 mg/kg morphine (M1); 0.14 mg/kg morphine (M2); 0.14 mg/kg oxycodone (O); and placebo (P) as a 2-min IV injection for pain. Mean arterial blood pressure (MAP), heart rate (HR), and oxygen consumption (VO(2)) were recorded. Plasma histamine and catecholamine concentrations were determined. Both M1 and M2 elicited an initial, but transient, increase in MAP from 84 +/- 5 to 96 +/- 9 mm Hg (P < 0.05) and from 83 +/- 8 to 100 +/- 10 mm Hg (P < 0.05), respectively. A parallel increase in HR was also seen after M1 (from 62 +/- 12 to 70 +/- 10 bpm, P < 0.05) and M2 (from 67 +/- 9 to 78 +/- 8 bpm, P < 0.05). After M2, this was accompanied by a simultaneous increase in VO(2) from 295 +/- 39 mL/min to 322 +/- 61 mL/min (P < 0.05). After O, as well as P, no increase in MAP or HR was detected. Plasma histamine and catecholamine concentrations were not clearly affected by any of the treatments. We conclude that the immediate effect of morphine on the hemodynamics of healthy volunteers was stimulation, not hypotension. This effect was not seen in conjunction with oxycodone, a morphine-like mu-receptor agonist. IMPLICATIONS: In this double-blinded, randomized study, we evaluated whether morphine could induce immediate cardiovascular stimulation, as seen previously in animal studies. In healthy volunteers, during a painful stimulus, morphine caused an initial, transient hemodynamic stimulation, accompanied by increased oxygen consumption, without detectable release of histamine or catecholamines into the plasma. Oxycodone caused only minor hemodynamic alterations.

Barbiturate anesthesia and brain proton spectroscopy.

BACKGROUND AND PURPOSE: Thiopentone reduces CBF and metabolic rate. Still, it is widely used for sedation during MR spectroscopy. We investigated whether barbiturate anesthesia and preanesthetic fasting have an effect on metabolic ratios in proton MR spectroscopy of the brain. METHODS: Eight healthy, consenting, male volunteers were studied twice in a random, crossover fashion. The study sessions were conducted during fasting (F) and nonfasting (nonF), with glucose infusion mimicking the fed state. During both sessions, two sets of spectroscopic data were collected, one during the awake state (F or nonF) and one under barbiturate anesthesia (F+B or nonF+B), using TEs of 135 and 270. Spectral areas of N-acetylaspartate (NAA), choline-containing compounds (Cho), and creatine plus phosphocreatine (Cr) were calculated, and the presence of lactate or lipid was noted. Venous blood samples for glucose, beta-hydroxybutyrate, lactate, and electrolytes were collected. RESULTS: Barbiturate anesthesia caused a 42% reduction in blood lactate levels during fasting, but not during glucose infusion. There were no differences in NAA/Cho, NAA/Cr, or in Cho/Cr between the groups F, nonF, F+B, or nonF+B. No lactate or lipid resonances were detected. CONCLUSION: Barbiturate anesthesia with preanesthetic fasting can be used for proton spectroscopy at TEs of 135 or 270 without interference from NAA/Cho, NAA/Cr, or Cho/Cr or from the appearance of lactate or lipid.

Effects of tramadol and meperidine on respiration, plasma catecholamine concentrations, and hemodynamics.

STUDY OBJECTIVE: To evaluate the effects of high analgesic doses of tramadol and meperidine on respiration, plasma catecholamine concentrations, and hemodynamic parameters. STUDY DESIGN: Randomized, double-blind, cross-over, controlled volunteer study. SETTING: Laboratory at a university hospital. SUBJECTS: 8 healthy male volunteers. INTERVENTIONS: Tramadol was given as a 150 mg bolus plus a succeeding 3-hour steady infusion of 250 mg (83.3 mg/hr). Meperidine was given in a similar manner as a bolus dose of 112.5 mg plus 187.5 mg in a 3-hour steady infusion (62.5 mg/hr). Experimental pain was induced using a tourniquet. MEASUREMENTS AND MAIN RESULTS: Respiration was studied noninvasively with respiratory inductive plethysmography and pulse oximetry. Arterial line was used for measurement of hemodynamics and blood sampling. Tramadol did not have any clinically significant effects on respiration, breathing pattern, or hemodynamics, but an increase in plasma epinephrine levels was noted. Meperidine bolus decreased tidal volume (p < 0.05, difference from baseline) and pulse oxygen saturation (from 97% to 94%, p < 0.05), but during the succeeding infusion, the respiratory drive, measured as mean inspiratory flow, was enhanced (p < 0.05 difference from baseline), and the respiratory parameters returned to baseline level. No change in hemodynamics was noted, but a significant increase in plasma norepinephrine and epinephrine levels (from 0.9 to 1.6 nmol/L and from 0.3 to 0.8 nmol/L, respectively; p < 0.05) was observed after meperidine administration. Tramadol caused nausea more often than meperidine (p < 0.05, between treatments). CONCLUSIONS: Tramadol exhibited a minimal effect on respiration and breathing pattern in healthy volunteers. The respiratory effects of meperidine bolus were predictable with decreasing tidal volume and pulse oxygen saturation. In contrast, during meperidine infusion, adequate respiration was preserved despite the large amount of meperidine infused.

Comparison of the analgesic effects of intrabursal oxycodone and bupivacaine after acromioplasty.

STUDY OBJECTIVES: To compare the peripheral analgesic effect of oxycodone, an opioid agonist, to the effect of bupivacaine infiltration and parenteral oxycodone administration in conjunction with shoulder surgery. DESIGN: Prospective, randomized, double-blind study. SETTING: University teaching hospital. PATIENTS: 42 ASA physical status I and II patients scheduled for shoulder surgery with general anesthesia. INTERVENTIONS: Patients were randomized to three study groups: at the end of the surgery patients received either 10 ml of 0.5% bupivacaine (group BIB) or 5 mg of oxycodone in 10 ml of saline (group OIB) in the subacromial bursa; or 5 mg of oxycodone intramuscularly (group OIM). Postoperative analgesia was provided by patient-controlled analgesia (PCA). MEASUREMENTS AND MAIN RESULTS: The fentanyl requirements were recorded for the 24-hour postoperative period and the total perioperative period. Postoperative pain was assessed by visual analog scale for pain (VASP). Plasma oxycodone concentrations were measured in groups OIB and OIM. The total perioperative fentanyl consumption was significantly lower in groups BIB (0.97 +/- 0.09 mg) and OIB (1.23 +/- 0.12 mg) than in group OIM (1.61 +/- 0.12 mg) (p = 0.01 and 0.048, respectively). Groups BIB and OIB were similar (p = 0.34). The absorption of oxycodone was significantly lower after subacromial than after intramuscular administration. CONCLUSION: Intrabursal oxycodone and intrabursal bupivacaine reduced perioperative analgesic requirements similarly. Intrabursal oxycodone may offer an effective, simple, and safe method for postoperative analgesia after shoulder surgery.

Successful treatment of whiplash-type injury induced severe pain syndrome with epidural stimulation: a case report.

Chronic severe cervico-facial pain syndrome associated with a whiplash-type injury was successfully treated with epidural spinal cord stimulation. The patient had been in pain for 9 years, responding temporarily only to stellate ganglion blocks. The patient has now been painless for 18 months. We have been unable to find a similar case reported in the literature to date.

Effect of clonidine on changes in plasma catecholamine concentrations and oxygen consumption caused by the cold pressor test.

This study was designed to investigate whether clonidine could attenuate the increase in oxygen consumption (VO2), arterial pressure (AP) and plasma catecholamines in response to the cold pressor test (CPT), an intense stimulation of the sympathetic nervous system. Six volunteers were given clonidine (2 micrograms kg-1 and 4 micrograms kg-1) and placebo i.m. in a random, double-blind, cross-over manner. Both clonidine doses decreased plasma catecholamine concentrations (P < 0.01), but only the higher dose of clonidine attenuated the CPT-induced absolute increase in plasma catecholamine concentration compared with the placebo group (P < 0.01). VO2 and AP decreased and were less after clonidine 4 micrograms kg-1 when compared with clonidine 2 micrograms kg-1 and placebo (P < 0.05) throughout the observation period. Thus, although clonidine 4 micrograms kg-1 attenuated the catecholamine response, the increases in VO2 and AP in response to CPT were similar in all groups.

The effect of clonidine or midazolam premedication on perioperative responses during ketamine anesthesia.

UNLABELLED: The use of ketamine as a sole anesthetic induces marked central sympathetic stimulation, causing increased heart rate, blood pressure (BP), and oxygen consumption (VO2). Both alpha 2-agonists and benzodiazepines have been used to attenuate these potentially harmful ketamine-induced responses. This double-blind, randomized, placebo-controlled study was designed to compare the perioperative metabolic, hemodynamic, and sympathoadrenal responses to IM clonidine (2 micrograms/kg) and midazolam (70 micrograms/kg) premedication during ketamine anesthesia. VO2 was measured continuously using indirect calorimetry in 30 ASA physical status I patients. The patients received ketamine, mivacurium, and fentanyl for the induction of anesthesia. Anesthesia was maintained using a ketamine infusion and fentanyl boluses i.v. Preoperatively, both VO2 and BP decreased significantly after the administration clonidine and midazolam compared with placebo (P < 0.01). Intraoperatively, VO2 was higher in the midazolam group than in the placebo and clonidine groups (P < 0.05). Postoperatively, there were no significant differences in BP and VO2, although they stayed at lower level in the clonidine group during the whole postoperative period. Clonidine decreased pre- and postoperative plasma catecholamine concentrations (P < 0.05). Our results indicate that a midazolam-ketamine combination may induce potentially harmful metabolic stimulation, whereas the sympatholytic effects of clonidine on ketamine-anesthetized patients may be beneficial, as perioperative VO2 was decreased. IMPLICATIONS: Ketamine causes sympathetic stimulation with an ensuing increase in oxygen consumption. Anticipating that clonidine might attenuate this response, we measured oxygen consumption in patients undergoing surgery during ketamine anesthesia. Patients treated with a clonidine-ketamine combination had lower intra- and postoperative oxygen consumption than those treated with a midazolam-ketamine combination.

Effect of clonidine and dexmedetomidine premedication on perioperative oxygen consumption and haemodynamic state.

Premedication has been shown to affect both oxygen consumption and metabolic rate. We have compared the perioperative metabolic and haemodynamic effects of two alpha 2-agonists, clonidine and the more selective dexmedetomidine, in 30 ASA I patients undergoing plastic surgical procedures under general anaesthesia. Patients were premedicated with clonidine 4 micrograms kg-1 (n = 10), dexmedetomidine 2.5 micrograms kg-1 (n = 10) or saline (n = 10) i.m. The doses of clonidine and dexmedetomidine were intended to be equipotent. The maximum decrease in preoperative oxygen consumption was 8% and decreases in systolic and diastolic arterial pressures were 11% from baseline after clonidine and dexmedetomidine. During operation, the maximum reduction in heart rate was 18% in the clonidine and dexmedetomidine groups compared with the placebo group. After operation, the maximum decrease in systolic arterial pressure was 11%, diastolic arterial pressure 15% and oxygen consumption 17% in the clonidine and dexmedetomidine groups compared with placebo. In summary, both clonidine 4 micrograms kg-1 and dexmedetomidine 2.5 micrograms kg-1 decreased perioperative oxygen consumption effectively, with a similar haemodynamic profile.

Anticholinergic drugs: effects on oxygen consumption and energy expenditure.

Premedication has been shown to affect both oxygen consumption (VO2) and energy expenditure (EE). The metabolic responses to anticholinergic drugs have not been studied. In this study the effects of anticholinergic drugs on VO2 and EE (calculated from the measured rates of VO2 and carbon dioxide production [VCO2]: EE [kcal/d] = 3.581 x VO2 [L/d] + 1.448 x VCO2 [L/d] - 32.4) were measured in six healthy female volunteers. They were given intramuscular atropine (15 micrograms/kg), glycopyrrolate (8 micrograms/kg), scopolamine (8 micrograms/kg), and placebo in a random double-blind cross-over design. The consecutive sessions were at least 1 wk apart for each subject. VO2 and EE were measured using an indirect calorimetry (Deltatrac). Cardiovascular responses were assessed using standard noninvasive monitoring. Plasma drug concentrations were analyzed using a sensitive modification of radioreceptor assay. Subjective responses were measured with visual analog scale (VAS). Atropine and glycopyrrolate induced a significant increase in heart rate with a simultaneous decrease in pressure rate quotient (PRQ), while scopolamine caused a significant decrease in heart rate with a simultaneous increase in PRQ. Scopolamine significantly decreased both VO2 and EE, whereas glycopyrrolate increased VO2. Atropine had no significant effect on metabolic variables. Only scopolamine induced sedation in this study. In conclusion, atropine, glycopyrrolate, and scopolamine differ not only in their cardiovascular and central nervous system effects, but also in their effects on metabolism.

Clinical and metabolic responses to different types of premedication.

Clinical and metabolic responses to three types of premedication were studied in ASA physical status I patients given any one of the following: (a) 0.5 mg of atropine and 50 mg of meperidine given intramuscularly plus an oral placebo tablet (n = 14), (b) 10 mg of oral diazepam and an intramuscular placebo (2 mL NaCl, concentration = 0.9) (n = 14), or (c) oral and intramuscular placebo (n = 14). Based both on subjective estimates (tiredness, fear, anxiety, dryness of mouth) and, especially, on metabolic responses (energy expenditure, oxygen consumption), oral diazepam appears to be superior to the combination of an opiate (meperidine) plus an anticholinergic (atropine). Atropine plus meperidine significantly increased energy expenditure above predicted values (2061 +/- 365 vs 1714 +/- 361 kcal/24 h, P = 0.004), calculated using the Harris-Benedict equation, based on sex, weight, height, and age, as well as increased oxygen consumption above levels seen with diazepam premedication (160 +/- 29 vs 137 +/- 17 mL.min-1. m-2). These findings indicate an iatrogenic stress factor induced by premedication with atropine plus meperidine.