bluuebunny/crossref_metadata_2025_split huggingface dataset:
Femoral-Sciatic Nerve Blocks for Complex Outpatient Knee Surgery Are Associated with Less Postoperative Pain Before Same-day Discharge
Authors: Williams Brian A. , Kentor Michael L. , Vogt Molly T. , Williams John P. , Chelly Jacques E. , Valalik Stacey , Harner Christopher D. , Fu Freddie H. 
Published: November 2003

Background
Outpatient knee surgery has come to involve increasingly complex procedures. The authors present observational data from a nerve block algorithm designed for the care of outpatients undergoing knee surgery. The aim of this report is to demonstrate differences in pain and unplanned hospital admission associated with surgical complexity and nerve blocks used.

Methods
Day-of-surgery outcomes were studied for 1,200 consecutive outpatients undergoing routine arthroscopy or one of six complex outpatient knee procedures. Nerve blocks were administered on the basis of anticipated pain from open incisions in the femoral and sciatic nerve distributions. Regression analysis was used to determine factors associated with postoperative pain and unplanned hospital admissions, and patients were categorized as having received femoral and sciatic nerve blocks (FSB), femoral nerve block only (FNB), or no nerve blocks.

Results
Patients undergoing more complex (vs. less invasive) knee surgery were at greater risk for pain (P </= 0.004), whereas the use of FSB (vs. FNB or no block) was associated with less pain (P < 0.01). When no nerve blocks were used, more complex (vs. less invasive) knee surgery was associated with a 10-fold greater risk of hospital admission (P = 0.001). In the regression analyses, more complex surgery (P < 0.001) was associated with increased risk of admission, and the use of FNB or FSB (vs. no block) was associated with a 2.5-fold reduction in unplanned admissions (P = 0.009).

Conclusions
For complex knee surgery, the use of FSB was associated with less pain; the use of FNB or FSB (vs. no block) was associated with fewer hospital admissions.
Quantitative Sensory Testing and Human Surgery
Authors: Wilder-Smith Oliver H. G. , Tassonyi Edömer , Crul Ben J. P. , Arendt-Nielsen Lars 
Published: November 2003

Background
Altered central nervous system sensory processing (neuroplasticity) is a basic mechanism underlying postoperative pain that can be made visible using quantitative sensory testing. Using quantitative sensory testing, the authors investigated how perioperative analgesia affects postoperative neuroplasticity and how this relates to clinical pain measures.

Methods
Patients undergoing back surgery received placebo, fentanyl, or ketorolac (n = 15 per group) before isoflurane-nitrous oxide anesthesia. Preoperatively to 5 days postoperatively, we measured thresholds to electrical skin stimulation at the incision site, arm, and leg; pain scores; and morphine patient-controlled analgesia consumption.

Results
Decreased pain thresholds versus preoperatively were seen 5 days postoperatively, with decreases greater for ketorolac (-63%; P = 0.00005 vs. preoperatively) than placebo (-45%; P = 0.008 vs. preoperatively) but nonsignificant for fentanyl (-36%; P = 0.9 vs. preoperatively). Mainly nonnociceptive thresholds were increased up to 24 h postoperatively. Postoperative clinical pain measures were similar across drug groups. Postoperative pain tolerance threshold changes did not correlate with preoperative clinical pain measures but were inversely related to preoperative thresholds for placebo and ketorolac but not fentanyl.

Conclusions
Without analgesia, neuroplasticity after surgery was inhibitory the first 24 h and followed at 5 days by excitation. Fentanyl efficiently preempted this hyperalgesia, but hyperalgesia was greater with ketorolac than with placebo. Clinical pain measures neither reflected the different effects of ketorolac and fentanyl on postoperative neuroplasticity nor permitted prediction of postoperative neuroplasticity. The information obtained by perioperative quantitative sensory testing is separate from and additional to that from clinical pain measures and may enable more mechanism-based approaches to surgical analgesia management in the future.
Supraspinal Contribution to Development of Both Tonic Nociception and Referred Mirror Hyperalgesia
Authors: Chen Hui-Sheng , Li Meng-Meng , Shi Juan , Chen Jun 
Published: November 2003

Background
The roles of descending facilitatory pathway from the rostral medial medulla (RMM) in development of persistent spontaneous nociception and hyperalgesia were evaluated in the bee venom (BV) test and the formalin test.

Methods
Bilateral lesions of the RMM with ibotenic acid, a soma-selective neurotoxin, were performed to study their effects on the spontaneous pain-related behaviors and hyperalgesia, which were determined by counting the number of flinching reflex per 5 min (1 h) and by measuring paw withdrawal thermal latency (PWTL) and mechanical threshold (PWMT) to radiant heat and von-Frey filaments to both hind paws in conscious rats, respectively.

Results
1) Bilateral lesions of the RMM produced a similarly significant inhibition of persistent spontaneous flinching reflexes in the BV test and the formalin test; however, the inhibitory effect occurred in the late 50 min (11-60 min), but not the first 10 min (0-10 min) following intraplantar injection of either BV or formalin. 2) Bilateral lesions of the RMM prevented the development of the BV-induced referred mirror heat hyperalgesia occurred in the noninjected paw, but had no effect on the primary heat and mechanical hyperalgesia occurred in the injected paw.

Conclusions
The present results provide a new line of behavioral evidence that tonic activation of descending facilitatory pathway contributes to the establishment of 1) the BV and formalin-induced persistent spontaneous nociception; and 2) the BV-induced referred mirror heat hyperalgesia and the central sensitization, but not the primary heat and mechanical hyperalgesia.
Spinal Adrenergic and Cholinergic Receptor Interactions Activated by Clonidine in Postincisional Pain
Authors: Duflo Frédéric , Conklin Dawn , Li Xinhui , Eisenach James C. 
Published: November 2003

Background
Previous pharmacologic and molecular studies suggest that the alpha(2)-adrenoceptor subtype A is the target for spinally administered alpha(2)-adrenergic agonists, i.e., clonidine, for pain relief. However, intrathecally administered alpha(2) C antisense oligodeoxynucleotide was recently reported to decrease antinociception induced by clonidine in the rat, suggesting non-A sites may be important as well. The current study sought to determine the subtype of alpha(2) adrenoceptors activated by clonidine in a rodent model for human postoperative pain, and to examine its interaction with spinal cholinergic receptors.

Methods
Postoperative hypersensitivity was produced in rats by plantar incision of the hind paw and punctuate mechanical stimuli were applied around the wound 24 h after surgery. Effects of intrathecal clonidine and 2-(2,6-diethylphenylamino)-2-imidazoline (ST91) on withdrawal thresholds to the stimulus were determined. To examine the adrenoceptor subtype and its interaction with spinal cholinergic receptors, animals were intrathecally pretreated with vehicles BRL44408 (an alpha(2) A subtype-preferring antagonist), ARC239 (an alpha(2) non-A subtype-preferring antagonist), atropine (a muscarinic antagonist), and mecamylamine (a nicotinic antagonist).

Results
Intrathecal ST91 showed a significantly greater efficacy when compared with clonidine. The analgesic effect of clonidine was diminished by pretreatment with either adrenoceptor antagonist, whereas the effect of ST91 was solely blocked by ARC239 pretreatment. Atropine and mecamylamine abolished the effect of clonidine effect but not the effect of ST91.

Conclusions
Both alpha(2) A and alpha(2) non-A adrenoceptors, as well as spinal cholinergic activation, are important to the antihypersensitivity effect of clonidine after surgery. ST91 is more efficacious in this model than clonidine and relies entirely on alpha(2) non-A adrenoceptors.
Operating Room Utilization Alone Is Not an Accurate Metric for the Allocation of Operating Room Block Time to Individual Surgeons with Low Caseloads
Authors: Raja Srinivasa N. , Dexter Franklin , Macario Alex , Traub Rodney D. , Lubarsky David A. 
Published: November 2003

Introduction
Many surgical suites allocate operating room (OR) block time to individual surgeons. If block time is allocated to services/groups and yet the same surgeon invariably operates on the same weekday, for all practical purposes block time is being allocated to individual surgeons. Organizational conflict occurs when a surgeon with a relatively low OR utilization has his or her allocated block time reduced. The authors studied potential limitations affecting whether a facility can accurately estimate the average block time utilizations of individual surgeons performing low volumes of cases.

Methods
Discrete-event computer simulation.

Results
Neither 3 months nor 1 yr of historical data were enough to be able to identify surgeons who had persistently low average OR utilizations. For example, with 3 months of data, the widths of the 95% CIs for average OR utilization exceeded 10% for surgeons who had average raw utilizations of 83% or less. If during a 3-month period a surgeon's measured adjusted utilization is 65%, there is a 95% chance that the surgeon's average adjusted utilization is as low as 38% or as high as 83%. If two surgeons have measured adjusted utilizations of 65% and 80%, respectively, there is a 16% chance that they have the same average adjusted utilization. Average OR utilization can be estimated more precisely for surgeons performing more cases each week.

Conclusions
Average OR utilization probably cannot be estimated precisely for low-volume surgeons based on 3 months or 1 yr of historical OR utilization data. The authors recommend that at surgical suites trying to allocate OR time to individual low-volume surgeons, OR allocations be based on criteria other than only OR utilization (e.g., based on OR efficiency).
Simulation Study of Rested Versus Sleep-deprived Anesthesiologists
Authors: Howard Steven K. , Gaba David M. , Smith Brian E. , Weinger Matthew B. , Herndon Christopher , Keshavacharya Shanthala , Rosekind Mark R. 
Published: November 2003

Background
Sleep deprivation causes physiologic and subjective sleepiness. Studies of fatigue effects on anesthesiologist performance have given equivocal results. The authors used a realistic simulation environment to study the effects of sleep deprivation on psychomotor and clinical performance, subjective and objective sleepiness, and mood.

Methods
Twelve anesthesia residents performed a 4-h anesthetic on a simulated patient the morning after two conditions of prior sleep: sleep-extended (EXT), in which subjects were allowed to arrive at work at 10:00 AM for 4 consecutive days, thus allowing an increase in nocturnal sleep time, and total sleep deprivation (DEP), in which subjects were awake at least 25 h. Psychomotor testing was performed at specified periods throughout the night in the DEP condition and at matched times during the simulation session in both conditions. Three types of vigilance probes were presented to subjects at random intervals as well as two clinical events. Task analysis and scoring of alertness were performed retrospectively from videotape.

Results
In the EXT condition, subjects increased their sleep by more than 2 h from baseline (P = 0.0001). Psychomotor tests revealed progressive impairment of alertness, mood, and performance in the DEP condition over the course of the night and when compared with EXT during the experimental day. DEP subjects showed longer response latency to vigilance probes, although this was statistically significant for only one probe type. Task analysis showed no difference between conditions except that subjects "slept" more in the DEP condition. There was no significant difference in the cases' clinical management between sleep conditions. Subjects in the DEP condition had lower alertness scores (P = 0.02), and subjects in the EXT condition showed little video evidence of sleepiness.

Conclusions
Psychomotor performance and mood were impaired while subjective sleepiness and sleepy behaviors increased during simulated patient care in the DEP condition. Clinical performance between conditions was similar.
Propofol Increases Phosphorylation of Troponin I and Myosin Light Chain 2 via Protein Kinase C Activation in Cardiomyocytes
Authors: Kanaya Noriaki , Gable Brad , Murray Paul A. , Damron Derek S. 
Published: November 2003

Background
Troponin I (TnI) and myosin light chain 2 (MLC2) are important myofibrillar proteins involved in the regulation of myofilament calcium (Ca2+) sensitivity and cardiac inotropy. The objectives of this study were to determine the role of protein kinase C (PKC) in mediating propofol-induced changes in actomyosin adenosine triphosphatase activity in cardiac myofibrils and to examine the extent to which propofol alters the phosphorylation of TnI and MLC2 in cardiomyocytes.

Methods
Freshly isolated adult rat ventricular myocytes were used for the study. Cardiac myofibrils were extracted for assessment of actomyosin adenosine triphosphatase activity and phosphorylation of TnI and MLC2. Western blot analysis for PKC-alpha was performed on cardiomyocyte subcellular fractions. Simultaneous measurement of intracellular free Ca2+ concentration ([Ca2+](i)) and myocyte shortening was assessed using fura-2 and video edge detection, respectively.

Results
Propofol (30 microM) reduced the Ca2+ concentration required for activation of actomyosin adenosine triphosphatase activity, and this effect was abolished by bisindolylmaleimide I. In addition, propofol stimulated dose-dependent phosphorylation of TnI and MLC2. PKC activation with phorbol myristic acetate also stimulated an increase in phosphorylation of TnI and MLC2. The actions of propofol and phorbol myristic acetate together on phosphorylation of TnI and MLC2 were not additive. PKC inhibition with bisindolylmaleimide I attenuated phorbol myristic acetate- and propofol-induced phosphorylation of TnI and MLC2. Propofol stimulated translocation of PKC-alpha from cytosolic to membrane fraction. Propofol caused a shift in the extracellular Ca2+-shortening relationship, and this effect was abolished by bisindolylmaleimide I.

Conclusions
These results suggest that propofol increases myofilament Ca2+ sensitivity via a PKC-dependent pathway involving the phosphorylation of MLC2.
Fetal Plasma Concentrations after Intraamniotic Sufentanil in Chronically Instrumented Pregnant Sheep
Authors: Strümper Danja , Durieux Marcel E. , Gogarten Wiebke , Van Aken Hugo , Hartleb Kristian , Marcus Marco A. E. 
Published: November 2003

Background
Rapid progress is being made in fetal surgery. Because the fetus is capable of pain perception after the 26th week of gestation, adequate postoperative fetal pain management is essential. The preferred approach would provide fetal analgesia without affecting the mother. Intraamniotically administered sufentanil may be an interesting option if it achieves therapeutic plasma concentrations (PCs) in the fetus but not the mother.

Methods
After approval of the study, 25 or 50 microg sufentanil was administered intraamniotically in 10 chronically instrumented pregnant ewes. Maternal and fetal vital signs, arterial blood gases, and uterine blood flow were recorded over 120 min. Sufentanil PCs were determined before and 1, 3, 5, 10, 15, 30, 45, 60, 90, and 120 min after injection. Statistical analysis was performed using one- or two-way analysis of variance followed by Dunnett or Tukey test, as appropriate (P < 0.05; data presented as median [95% confidence interval]).

Results
After 25 microg sufentanil, fetal PC stabilized at 134 +/- 89 pg/ml (after 10 min), and maternal PCs stabilized at 44 +/- 11 pg/ml (after 15 min). After 50 microg sufentanil, fetal PCs stabilized at 134 +/- 35 pg/ml (after 15 min), and maternal PCs reached 80 +/- 25 pg/ml (at 30 min). Injection of 25 microg sufentanil intraamniotically did not affect maternal or fetal hemodynamics, uterine blood flow, or arterial blood gases. Fetal heart rate increased after administration of 50 microg sufentanil (maximum change at 10 min: +16 +/- 12%).

Conclusion
The sheep fetus absorbs sufentanil after intraamniotic instillation. Significantly greater PCs were obtained in the fetal lamb as compared with the ewe. This suggests that investigation of intraamniotic opioids for fetal analgesia might be worthwhile.
Intraspinal Adenosine Induces Spinal Cord Norepinephrine Release in Spinal Nerve-ligated Rats but not in Normal or Sham Controls
Authors: Bantel Carsten , Li Xinhui , C. Eisenach James 
Published: November 2003

Background
Intrathecal adenosine is antinociceptive under conditions of central sensitization, but not in response to acute stimuli in normals. The reasons for this selective circumstance of action remain unclear, but some evidence links adenosine's antinociceptive effects to release of norepinephrine by terminals in the spinal cord. The purpose of this study was to test whether spinal adenosine induces norepinephrine release selectively in settings of hypersensitivity.

Methods
Rats randomly assigned to spinal nerve ligation, sham operation, or no operation were anesthetized. A microdialysis fiber was implanted in the spinal cord dorsal horn at the L5-L6 level and perfused with artificial cerebrospinal fluid. After washout and a baseline sample period, adenosine at various concentrations was infused through the fiber for 150 min, and samples were collected every 15 min.

Results
In ligated, but not in sham or normal animals, adenosine perfusion increased norepinephrine in spinal cord microdialysates in a concentration-dependent manner. The effects of adenosine plateaued after 75 min and remained stable until the end of the experiment. Intravenous injection of selective adenosine A1 and A2 receptor antagonists revealed that adenosine's effect on spinal norepinephrine release was A1 receptor mediated.

Conclusions
This is the first study to provide direct evidence that adenosine is able to release norepinephrine in spinal cord dorsal horns in living animals. However, this effect was only seen in animals after spinal nerve ligation. These data are consistent with behavioral studies demonstrating that adenosine's antinociceptive effects in rats after spinal nerve ligation is totally dependent on intact spinal noradrenergic terminals and can be blocked by spinal alpha 2-adrenergic receptor antagonists.
Antihyperalgesic and Side Effects of Intrathecal Clonidine and Tizanidine in a Rat Model of Neuropathic Pain
Authors: Kawamata Tomoyuki , Omote Keiichi , Yamamoto Hiroki , Toriyabe Masaki , Wada Kohsuke , Namiki Akiyoshi 
Published: November 2003

Background
Although intrathecal clonidine produces pronounced analgesia, antinociceptive doses of intrathecal clonidine produce several side effects, including hypotension, bradycardia, and sedation. Intrathecal tizanidine, another alpha(2)-adrenergic agonist, has provided antinociception without producing pronounced hemodynamic changes in animal studies. However, it has been unclear whether antihyperalgesic doses of intrathecal clonidine and tizanidine produce hypotension and bradycardia in a neuropathic pain state. This study was designed to evaluate the antihyperalgesic effects and side effects of intrathecal clonidine and tizanidine in a rat model of neuropathic pain.

Methods
Male Sprague-Dawley rats were chronically implanted with lumbar intrathecal catheters, and the sciatic nerve was loosely ligated. After 21-28 days after surgery, the rats received intrathecal clonidine (0.3, 1.0, and 3.0 microg) and tizanidine (1.0, 2.0, and 5.0 microg), and the antihyperalgesic effects of thermal and mechanical stimuli were examined. In addition, the changes in blood pressure and heart rate, sedation level, and other side effects after intrathecal administration of drugs were recorded.

Results
The administration of 3.0 microg intrathecal clonidine or 5.0 microg tizanidine significantly reversed both thermal and mechanical hyperalgesia. The administration of 3.0 microg intrathecal clonidine, but not 5.0 microg tizanidine, significantly decreased mean blood pressure and heart rate and produced urinary voiding. A greater sedative effect was produced by 3.0 microg intrathecal clonidine than by 5.0 microg tizanidine.

Conclusion
The antihyperalgesic dose of intrathecal clonidine and the antinociceptive doses produced several side effects. Intrathecal tizanidine at the dose that reversed hyperalgesia would be preferable for neuropathic pain management because of absence of hypotension and bradycardia and lower incidence of sedation.
Variability in Surgical Caseload and Access to Intensive Care Services
Authors: McManus Michael L. , Long Michael C. , Cooper Abbot , Mandell James , Berwick Donald M. , Pagano Marcello , Litvak Eugene 
Published: November 2003

Background
Variability in the demand for any service is a significant barrier to efficient distribution of limited resources. In health care, demand is often highly variable and access may be limited when peaks cannot be accommodated in a downsized care delivery system. Intensive care units may frequently present bottlenecks to patient flow, and saturation of these services limits a hospital's responsiveness to new emergencies.

Methods
Over a 1-yr period, information was collected prospectively on all requests for admission to the intensive care unit of a large, urban children's hospital. Data included the nature of each request, as well as each patient's final disposition. The daily variability of requests was then analyzed and related to the unit's ability to accommodate new admissions.

Results
Day-to-day demand for intensive care services was extremely variable. This variability was particularly high among patients undergoing scheduled surgical procedures, with variability of scheduled admissions exceeding that of emergencies. Peaks of demand were associated with diversion of patients both within the hospital (to off-service care sites) and to other institutions (ambulance diversions). Although emergency requests for admission outnumbered scheduled requests, diversion from the intensive care unit was better correlated with scheduled caseload (r = 0.542, P < 0.001) than with unscheduled volume (r = 0.255, P < 0.001). During the busiest periods, nearly 70% of all diversions were associated with variability in the scheduled caseload.

Conclusions
Variability in scheduled surgical caseload represents a potentially reducible source of stress on intensive care units in hospitals and throughout the healthcare delivery system generally. When uncontrolled, variability limits access to care and impairs overall responsiveness to emergencies.