Anesthesia and analgesia
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Anesthesia and analgesia · Apr 1998
Comparative StudySuccessful strategies for improving operating room efficiency at academic institutions.
In this prospective study, we evaluated the etiology of operating room (OR) delays in an academic institution, examined the impact of multidisciplinary strategies to improve OR efficiency, and established OR timing benchmarks for use in future OR efficiency studies. OR times and delay etiologies were collected for 94 cases during the initial phase of the study. Timing data and delay etiologies were analyzed, and 2 wk of multidisciplinary OR efficiency awareness education was conducted for the nursing, surgical, and anesthesia staff. After the education period, timing data were collected from 1787 cases, and monthly reports listing individual case delays and timing data were sent to the Chiefs of Service. For the first case of the day, patient in room, anesthesia ready, surgical preparation start, and procedure start time were significantly earlier (P < 0.01) in the posteducation period compared with the preeducation period, and the procedure start time for the first case of the day occurred, on average, 22 min earlier than all other procedures. For all cases combined, turnover time decreased, on average, by 16 min. Unavailability of surgeons, anesthesiologists, and residents decreased significantly (P < 0.05) as causes of OR delays. Anesthesia induction times were consistently longer for the vascular and cardiothoracic services, whereas surgical preparation time was increased for the neurosurgical and orthopedic services (P < 0.05). Identification of the etiology of OR inefficiency, combined with multidisciplinary awareness training and personal accountability, can improve OR efficiency. The time savings realized are probably most cost-effective when combined with more flexible OR staffing and improved OR scheduling. ⋯ We achieved significant improvements in operating room efficiency by analyzing operating room data on causes of delays, devising strategies for minimizing the most common delays, and subsequently measuring delay data. Personal accountability, streamlining of procedures, interdisciplinary team work, and accurate data collection were all important contributors to improved efficiency.
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Anesthesia and analgesia · Apr 1998
Comparative StudyIsoflurane and pentobarbital reduce the frequency of transient ischemic depolarizations during focal ischemia in rats.
Repetitive transient ischemic depolarizations (IDs) during focal cerebral ischemia are thought to contribute to ischemic damage. Isoflurane and pentobarbital reduce injury (versus the nonanesthetized state) after focal cerebral ischemia. The mechanism by which these drugs reduce injury is not known. This protective effect might be mediated by a reduction in the number of IDs. We measured the frequency of IDs during focal cerebral ischemia in animals anesthetized with isoflurane or pentobarbital and compared it with that in N2O/fentanyl anesthetized animals and in animals in which the N-methyl-D-aspartate receptor antagonist MK801 (dizocilpine) was given. Focal cerebral ischemia was induced by the occlusion of the middle cerebral artery for a period of 2 h. Cortical infarct volumes were determined after 3 h of reperfusion by image analysis of 2,3,5-triphenyl tetrazolium-stained coronal brain sections. The infarct volume was significantly greater in the N2O/fentanyl group than in the other three groups. Infarct volumes in the isoflurane, pentobarbital, and MK801 groups were similar. The frequency of IDs was significantly greater in the N2O/fentanyl group than in the other three groups, and was the least in the MK801 group. There was a direct correlation between the number of IDs and the volume of tissue injury. The data indicate that the protective effect of isoflurane and pentobarbital might, in part, be determined by their ability to reduce IDs during focal ischemia. However, the observation that the infarct volume was similar in the MK801, isoflurane, and pentobarbital groups, despite a greater frequency of IDs in the latter two groups, suggests that mechanisms other than a simple reduction in the number of IDs probably also play a role in anesthetic-mediated cerebral protection. ⋯ Transient ischemic depolarizations during focal ischemia contribute to brain injury. Both isoflurane and pentobarbital reduced the frequency of these depolarizations. Isoflurane- and pentobarbital-mediated reduction in the frequency of depolarizations might, in part, mediate the previously documented neuroprotective effect of these drugs.
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Anesthesia and analgesia · Apr 1998
Bacterial colonization and infection rate of continuous epidural catheters in children.
Continuous epidural infusions are widely used for postoperative analgesia in children. We prospectively studied the incidence of bacterial colonization of caudal and lumbar epidural catheters, as well as the incidence of serious systemic and local infection, in 210 children after short-term epidural analgesia. Using aseptic technique, epidural catheters were inserted into either the lumbar or the caudal epidural space based on the preferences of the anesthesia team and/or clinical indication. The integrity of the catheter and overlying transparent dressing site was evaluated by a member of the pediatric pain service at least once a day. The catheters were aseptically removed if the patient had a fever greater than 39 degrees C, if the dressing was compromised, or when epidural analgesia was no longer required. The subcutaneous portion of the catheter was semiquantitatively cultured. Cellulitis (erythema, swelling, purulent discharge, pustule formation, or tenderness) was diagnosed by examination of the epidural insertion site. The mean (+/- SD) age of patients in the caudal catheter group (n = 170) was 3 +/- 3 yr; their mean weight was 13 +/- 11 kg. The mean (+/- SD) age of patients in the epidural catheter group (n = 40) was 11 +/- 4 yr; their mean weight was 36 +/- 23 kg. All catheters remained in place for 3 +/- 1 days (range 1-5 days). There was no serious systemic infection (meningitis, epidural abscess, or systemic sepsis). Of all epidural catheters, 35% (73 of 210) were colonized. Gram-positive colonization was similar in caudal (25%; 43 of 170) and lumbar (23%; 9 of 40) catheters. Gram-negative organisms were cultured from 16% of the caudal catheters (27 of 170) and 3% of the lumbar catheters (1 of 40). In patients treated with caudal epidural catheters, children aged >3 yr were less likely to have colonized epidural catheters than younger children. Age did not affect the probability of developing cellulitis at the insertion site. Although patients aged <3 yr with caudal catheters had a slightly greater risk of cellulitis than children aged >3 yr (14% vs 9%), this association was very weak (P = 0.33). We observed that, despite bacterial colonization of caudal and lumbar epidural catheters, serious systemic and local infection after short-term epidural analgesia did not occur in our study. ⋯ Continuous epidural infusions are widely used for postoperative analgesia in children. We found no serious systemic infections after short-term (3 days) continuous epidural analgesia in children.
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Anesthesia and analgesia · Apr 1998
Comparative StudyAntinociceptive potentiation and attenuation of tolerance by intrathecal co-infusion of magnesium sulfate and morphine in rats.
N-methyl-D-aspartate (NMDA) antagonists, such as MK801, delay the development of morphine tolerance. Magnesium, a noncompetitive NMDA antagonist, reduces postoperative morphine requirements. The present study was designed to evaluate the effects of intrathecal co-administration of magnesium sulfate with morphine on antinociceptive potentiation, tolerance, and naloxone-induced withdrawal signs. Magnesium sulfate (40-60 microg/h) co-administration for 7 days, similar to MK801 (10 nmol/h), prevented the decline in antinociceptive response compared with morphine (20 nmol/h). Magnesium sulfate (60 microg/h) produced no antinociception, but co-infused with morphine (1 nmol/h), it resulted in potentiated antinociception compared with morphine throughout the 7-day period. Probe morphine doses after 7-day infusions demonstrated a significantly greater 50% effective dose value for morphine 1 nmol/h (109.7 nmol) compared with saline (10.9 nmol), magnesium sulfate 60 microg/h (10.9 nmol), and magnesium sulfate 60 microg/h plus morphine 1 nmol/h (11.2 nmol), which indicates that magnesium had delayed morphine tolerance. Morphine withdrawal signs after naloxone administration were not altered by the co-infusion of magnesium sulfate. Cerebrospinal fluid magnesium levels after intrathecal magnesium sulfate (60 microg/h) for 2 days increased from 17.0 +/- 1.0 microg/mL to 41.4 +/- 23.6 microg/mL, although serum levels were unchanged. This study demonstrates antinociceptive potentiation and delay in the development of morphine tolerance by the intrathecal coinfusion of magnesium sulfate and morphine in the rat. ⋯ The addition of magnesium sulfate, an N-methyl-D-aspartate antagonist, to morphine in an intrathecal infusion provided better analgesia than morphine alone in normal rats. These results suggest that intrathecal administration of magnesium sulfate may be a useful adjunct to spinal morphine analgesia.