ISSN NUMBER: 1938-7172
Issue 3.11

Michael A. Fiedler, PhD, CRNA

Contributing Editors:
Penelope S. Benedik PhD, CRNA, RRT
Joseph F. Burkard, DNSc, CRNA
Mary A. Golinski, PhD, CRNA
Gerard T. Hogan, Jr., DNSc., CRNA
Alfred E. Lupien, PhD, CRNA
Dennis Spence, PhD, CRNA
Steven R. Wooden, MS, CRNA

Assistant Editor
Jessica Floyd, BS

A Publication of Lifelong Learning, LLC © Copyright 2009

New health information becomes available constantly. While we strive to provide accurate information, factual and typographical errors may occur. The authors, editors, publisher, and Lifelong Learning, LLC is/are not responsible for any errors or omissions in the information presented. We endeavor to provide accurate information helpful in your clinical practice. Remember, though, that there is a lot of information out there and we are only presenting some of it here. Also, the comments of contributors represent their personal views, colored by their knowledge, understanding, experience, and judgment which may differ from yours. Their comments are written without knowing details of the clinical situation in which you may apply the information. In the end, your clinical decisions should be based upon your best judgment for each specific patient situation. We do not accept responsibility for clinical decisions or outcomes.

Table of Contents









Equipment & Technology

Kaki AM, Almarakbi WA


Does patient position influence the reading of the bispectral index monitor

Anesth Analg 2009;109:1843-1846

Kaki AM, Almarakbi WA




Purpose            The purpose of this study was to describe changes in BIS values associated with changes in patient position from neutral to head down or head up during stable general anesthesia.

Background            The Bispectral Index (BIS) monitor is purported to monitor the level of consciousness during general anesthesia. Multiple factors have been shown to alter BIS readings without affecting the actual depth of anesthesia. Head down position has been shown to increase intracranial pressure, intraocular pressure, and middle cerebral artery flow velocity. The authors observed changes in BIS readings with changes in patient position and wondered if the changes in BIS readings were due to changes in patient position or coincidental.

Methodology            This prospective, observational study examined the relationship between BIS readings and patient position during general anesthesia. Adult ASA physical status I and II patients scheduled for elective surgery with general anesthesia were enrolled. Those with hypertension, neurologic disease, previous head injury, glaucoma, or retinal detachment were excluded. A BIS monitor (Aspect Medical Systems, Norwood, MA) was applied. Impedance at all electrodes was within the manufacturer’s recommendations.

Anesthesia induction was standardized with fentanyl, propofol, and rocuronium followed by maintenance with 50% nitrous oxide, 1 MAC isoflurane and fentanyl. Normocapnia was maintained throughout the procedure.

BIS values were recorded at 5 minute intervals in four positions. Three readings were taken with the patient in neutral position (horizontal to the floor). The patient was then placed in a 30° head down tilt (Trendelenburg) and three BIS readings recorded. After returning the patient’s position to neutral again, an additional three readings were recorded before changing the patients position to 30° head up (reverse Trendelenburg) when the last three BIS readings were recorded.

Nonparametric statistical tests were used to compare BIS values in the various positions.

Result            There were significant changes in median BIS values with changes in position (P < 0.001). When position was changed from neutral to 30° head down BIS values increased 23%. When position was returned to neutral the BIS decreased 13%. Moving from neutral to 30° head up position resulted in an additional 15% decrease in the BIS value.

Conclusion            Changing patient position from neutral to 30° head down or head up significantly changed the reported BIS values despite a steady state general anesthetic. The authors attributed these findings to physiologic changes associated with changing cerebral blood flow in various positions.



I remain confused as to why so called “consciousness monitoring” has been accepted with a seeming lack of critical review. The literature is replete with evidence that consciousness monitors don’t monitor depth of anesthesia. Here is a partial list:

1.     Range of BIS values at loss of consciousness 51 – 79
            Anaesthesia 2003;58:531

2.     Unconsciousness produced with ketamine undetected by BIS

3.     Increased depth of anesthesia with nitrous oxide undetected by BIS
            Br J Anaesth 2004;92:167

4.     BIS insensitive to opioids
            Anesthesiology 2007;106:472

5.     Different values with different anesthetics at same depth of anesthesia
            Br J Anaesth 2003;91:329
            Anesth Analg 2004;99:1723

6.     BIS values decrease as patient is waking up
            Anesth Analg 2004;98:1036

7.     BIS decreases to 33 in awake, paralyzed patient
            Anesth Analg 2003;97:488

It appears that now we can add to this list changes in consciousness monitoring values when patient position is changed to head down or head up.

I love the idea of a monitor that reliably identifies a patient’s depth of anesthesia. I’m glad that manufacturers are spending research and development money on this technology. But, in my view, currently available “consciousness monitors” are the poster child for evidence based practice. If we all knew the evidence, we’d not be willing to believe that these devices provide information about a patient’s actual level of consciousness during general anesthesia.


Michael Fiedler, PhD, CRNA

© Copyright 2009 Anesthesia Abstracts · Volume 3 Number 11, November 30, 2009

Obstetric Anesthesia

Wang FZ, Shen XF, Guo XR, Peng YZ, Gu XQ, The Labor Analgesia Examining Group


epidural analgesia in the latent phase of labor and the risk of cesarean delivery: a five-year randomized controlled trial

Anesthesiology 2009;111:871-80

Wang FZ, Shen XF, Guo XR, Peng YZ, Gu XQ, The Labor Analgesia Examining Group


Purpose            The purpose of this study was to test the hypothesis that initiation of patient-controlled epidural analgesia (PCEA) during latent phase labor (at least 1 cm cervical dilation) does not increase the risk of prolonged labor or cesarean delivery when compared to initiation of PCEA at cervical dilation of at least 4 cm.

Background            Current evidence supports the safety and lack of increased risk of cesarean delivery, with epidural analgesia (EA)placement in laboring women with cervical dilation of 2 cm or more. The National Institute for Health and Clinical Excellence guidelines suggest that women should not be denied EA during the latent first stage of labor (time from beginning of regular contractions to some cervical change). However, data from these guidelines does not address placement of EA at less than 2 cm dilation.

Methodology            A prospective randomized controlled trial of 12,793 nulliparous women requesting EA who were randomized to have placement of EA during latent phase (at least 1 cm dilation) or active phase (at least 4 cm dilation) labor. Subjects in both groups were administered meperidine 25 mg IM as needed until reaching the appropriate cervical dilation. After a negative test dose, subjects received a 15 mL bolus of 0.125% ropivicaine with 0.3 mcg/mL sufentanil followed by PCEA of 10 mL every 15 minutes with an hourly limit of 30 mL. No background infusion was administered. The primary outcome was method of delivery; vaginal vs. cesarean delivery. Secondary outcomes included indication for cesarean delivery, rate of instrument-assisted vaginal delivery, time to vaginal delivery, VAS pain scores, meperidine administration, satisfaction, oxytocin requirement, side effects and complications from EA, and infant outcomes. Primary analysis was based on an intention-to-treat and per protocol populations. Parametric and nonparametric tests were used to analyze the results; Kaplan-Meir cumulative-event curves were used to analyze different lengths of labor, and multivariable logistic regression used to identify predictors of cesarean delivery.

Result            A total of 12,793 subjects were enrolled; 164 subjects were excluded, and 6,274 subjects in the latent analgesia group and 6,355 in the active analgesia group completed the study. Demographic variables, meperidine consumption, oxytocin use and maximum dose, highest sensory level, temperature, and infant outcomes were similar between the groups. Rate of cesarean delivery (latent group: n = 1,486 (23.3%) vs. n = 1,456 (22.8%), P= 0.51), instrument-assisted vaginal delivery (latent group: n = 753 (11.8%) vs. active group n = 814 (12.7%), P = 0.10), and length of labor (latent group: M = 11.3 ± 4.5 h vs. active group M = 11.8 ± 4.9, P = 0.90) were similar between the groups.

Kaplan-Meir curves revealed no difference between groups in time to: vaginal delivery, first stage of labor, latent phase of first stage of labor, active phase of first stage of labor, second stage of labor, cesarean delivery or instrument-assisted vaginal delivery, respectively.

Average VAS pain scores during latent phase (latent group: 32 (26-40) vs. active group: 48 (33-65), P = 0.18) and active phase (latent group: 28 (20-40) vs. active group: 25 (20-45), P = 0.80) were similar. Nausea and vomiting was significantly lower in the latent group. Median satisfaction scores were significantly higher in the latent phase group (latent group: 84 (66-95) vs. active phase: 62 (50-75), P = 0.01). Adjusted odds ratio (OR) found an association between age (OR = 1.46), weight (OR = 1.67), height (OR = 1.25) and oxytocin use (mU/min) (OR = 2.20) and cesarean delivery (P < 0.05).

Conclusion            Initiation of EA with PCEA demand only dosing during latent labor at cervical dilation of 1 cm or more does not prolong labor or increase the risk of cesarean delivery when compared to initiation at active phase labor with 4 cm or more cervical dilation in nulliparous women.


The question of when to initiate epidural analgesia has long been an issue anesthesia providers have long struggled with. In the past arbitrary cervical dilation of 4-5 cm was recommended because of concern EA would slow the progress of labor and increase the risk for cesarean delivery. Fortunately, recent well designed randomized controlled trials have demonstrated early EA in spontaneous or induced labor, with various EA methods, does not slow the progress of labor or increase the risk for cesarean delivery.1-3 This study adds to this body of knowledge by demonstrating that early EA during latent labor does not increase the risk of cesarean delivery.

This study is probably the largest EA study examining differences in cesarean delivery rates based on time of placement. It is a well designed study with strong level of evidence (Level 1). However, as Flood points out, readers should be cautious when interpreting a large number of secondary outcomes because large sample sizes increase the chance of finding small statistically significant, but clinically irrelevant findings. 4 Rather these secondary outcomes should be considered exploratory, hypothesis generating results to evaluate in future research.

Having said that, I do think some of the secondary outcomes are important to discuss. First, in this study pain scores during latent labor were slightly higher (though not statistically different) in the active group (48 vs. 28) when compared to the latent group. During active phase VAS pain scores were almost the same (28 vs. 25). This most likely demonstrates better analgesia in the latent group with early EA placement. However, one would expect pain scores to be even lower with EA in both groups. This may be a function of the demand-only PCEA method used. In my opinion, if a background continuous infusion had been used pain scores may have been lower.

Second, overall maternal satisfaction with analgesia scores was significantly lower in the active group (84 vs. 62). I believe this provides further evidence supporting the superiority of EA for latent phase labor when compared to opioids. Patient satisfaction is a difficult concept to measure, and I suspect the higher rate of nausea and vomiting in the active group may have influenced this result.

Providers should remember other factors such as macrosomia, dysfunctional labor, and fetal malposition increase labor pain are more likely than timing of when EA is initiated, to increase the risk for cesarean delivery.2 Overall, this is an excellent study which provides evidence anesthesia providers can use when discussing the options and risks of EA with parturients.


 Dennis Spence PhD, CRNA

1. Wong CA, Scavone BM, Peaceman AM, et al. The risk of cesarean delivery with neuraxial analgesia given early versus late in labor. N Engl J Med 2009; 352:655-65.

2. Wong CA, McCarthy RJ, Sullivan JT, Scavone BM, Gerber SE, Yaghmour EA. Early compared with late neuraxial analgesia in nulliparous labor induction: a randomized controlled trial. Obstet Gynecol 2009;113:1066-74.

3. Ohel G, Gonen R, Vaida S, Barak S, Gaitini L. Early versus late initiation of epidural analgesia in labor: Does it increase the risk of cesarean section? A randomized controlled trial. Am J Obstet Gynecol 2006; 194:600-5.

4. Flood, P. Primary versus secondary outcomes in gargantuan studies. Anesthesiology 2009; 111;704-5.

The views expressed in this article are those of the author and do not reflect official policy or position of the Department of the Navy, Department of Defense or the United States Government.


© Copyright 2009 Anesthesia Abstracts · Volume 3 Number 11, November 30, 2009

Djabatey EA, Barclay PM

Difficult and failed intubation in 3,430 obstetric general anaesthetics

Anaesthesia 2009;64:1168-1171

Djabatey EA, Barclay PM


Purpose            This retrospective audit was performed to quantify the incidence of difficult and failed maternal intubation in an institution where general anesthesia was frequently used for cesarean section.

Background            Failed intubation is involved in over half the maternal deaths directly attributable to anesthetic causes. The increased risk of general anesthesia is a significant reason that regional anesthetic techniques are favored for cesarean section. Probably partly due to these facts, the proportion of cesarean sections performed with regional anesthesia in the United Kingdom has increased in the past 25 years from 50% to 95%. Over the same time period, the incidence of failed intubation in pregnant women has increased to a reported 1:250 laryngoscopies. Countries that report high rates of general anesthesia for cesarean section also report lower rates of failed intubation in obstetrics (OB). The reported incidence of failed maternal intubation in South Africa, for example, is 1:750; fully two thirds less often than reported in the USA. A number of factors may have contributed to the currently reported high incidence of failed intubation in labor and delivery.

In pregnant women, general anesthesia is largely reserved for emergency cases. The time pressure associated with emergencies may lead to an inadequate airway assessment. The dominant use of regional anesthesia in OB results in some physicians completing an anesthesia residency having done fewer than six general anesthetics in OB. The reusable gum elastic bougie has been replaced by a less effective disposable version in many institutions. Increased use of Laryngeal Mask Airways (LMAs) has reduced anesthesia providers experience with endotracheal intubation, especially during training. In some localities, laws restricting the number of hours an anesthesia trainee may be required to be in the clinical area have also reduced the procedural experiences available to anesthetists in training.

Methodology            While the data was generated in a teaching hospital, upper level trainees or attending anesthesiologists were present to provide assistance during all inductions.

Data was collected from a custom report generated by an electronic medical record database over an eight year period. The data was combined with information from the hospital’s Adverse Clinical Event database.

Result            A total of 3,430 rapid sequence inductions were performed, 86% for cesarean section and the remainder for a variety of other obstetric surgeries. Sodium pentothal and succinylcholine was used for all inductions.

There were no failed intubations or esophageal intubations among the 3,430 patients. There were 23 “difficult intubations,” for an incidence of 1:156. In 9 patients a difficult intubation was anticipated as a result of the pre-anesthetic airway assessment. Three patients had an awake fiberoptic intubation. In the remaining 14 patients, a difficult airway was unanticipated. In each of these 14 cases there was either evidence of inadequate airway assessment, the airway assessment was poorly documented, or the airway assessment wasn’t documented at all.

Conclusion            In a series of 3,430 general anesthetics in an obstetric operating room, there were no failed intubations. This produces, at the upper end of a 95% confidence interval, a maximum incidence of failed intubation in OB of 1:1,143; less than a quarter of the incidence reported in the USA. The authors attributed this relatively low incidence of failed intubation to greater experience with intubating pregnant women due to their higher rate of general anesthesia for cesarean section.


This is a simple and thought provoking report. It gets my attention immediately because I would expect there to have been about 14 failed intubations in this number of OB general anesthetics. That they had none is a little bit amazing. I immediately wanted to know how they did it!

On the matter of difficult intubations, the authors emphasized the importance of a proper pre-anesthetic airway assessment. Indeed, some of the three awake fiberoptic intubations they performed may well have been a failed intubation if it were not for a good pre-anesthetic airway assessment. What they didn’t talk about, and what I’d really like to know, is how quick they were to choose an awake fiberoptic intubation. In my experience it is exceedingly rare to choose this method of airway management as a primary approach in a pregnant patient. Perhaps part of the reason their OB failed intubation rate was so low was that they were willing to go to very conservative airway management on the first attempt.

While this report certainly doesn’t begin to establish cause and effect between experience intubating pregnant women and their lower incidence of failed intubation in OB, the authors make a good circumstantial case that greater experience is the reason for their success rate. But, having been an anesthesia educator for many years, I must comment on one aspect of that argument. They cited a change in law limiting the hours their trainees could be in the clinical area as a reason for decreased experience. They go on to specify that OB anesthesia coverage was provided by 9 trainees prior to the law going into effect but 14 trainees after the law went into effect. They needed to increase their staffing by 55% to bring trainee clinical hours into compliance with legal limits. All clinical experience does not contribute to an improvement of clinical care; it must be good clinical experience. There comes a point where being tired and physically exhausted impedes one’s clinical performance and the ability to learn. If previous clinical hours were sufficient to render their trainees lethargic, I don’t accept reduced clinical hours as a cause of inexperience. Being awake in the OR may well have improved learning from the experiences they had, even if there were fewer of them.

Perhaps the aspect of this report that has the greatest implications for clinical practice and risk reduction in OB anesthesia is the apparent premise of their argument – that their rate of failed intubation in OB was due to more experience with intubation of OB patients. Any way you look at it, current evidence says that the risk of failed intubation is higher in OB patients; even if how much higher varies with experience. Furthermore, the single greatest anesthetic cause of maternal mortality is airway problems during general anesthesia for cesarean section. Thus, anything we can do to reduce the need for general anesthesia and intubation reduces the risk of the number one source of anesthetic mortality in pregnant women as a group. To say that increased experience intubating pregnant women reduces the risk of failed intubation is a catch-22. To reduce the risk for all pregnant women in general we must gain more experience intubating a few specific pregnant women; increasing their risk of death. I draw two conclusions from this line of thinking. First, it is up to our educators to design methods that maximize the learning that occurs with whatever number of OB airway experiences can be had. For example, research has shown that simply visualizing and mentally running through a procedure such as endotracheal intubation before physically performing it results in better performance during the actual procedure. Second, this supports the concept of having anesthetic specialists in whom the experience with, in this case, intubating pregnant women is concentrated. Specialists have an opportunity to get better at critical tasks due to concentrated learning and more extensive clinical experience.

The single biggest contribution of this report may be that it demonstrates that the incidence of failed intubation in OB patients is due to factors other than the anatomy of pregnant women which we cannot control. External factors that we can control can thus be manipulated to reduce the risk of failed intubation in this patient population.

Michael Fiedler, PhD, CRNA

© Copyright 2009 Anesthesia Abstracts · Volume 3 Number 11, November 30, 2009


McKay A, Gottschalk A, Ploppa A, Durieux ME, Groves DS


Systemic lidocaine decreased the perioperative opioid analgesic requirements but failed to reduce discharge time after ambulatory surgery

Anesth Analg 2009;109:1805-1808

McKay A, Gottschalk A, Ploppa A, Durieux ME, Groves DS


Purpose            The purpose of this study was to examine the effects of perioperative lidocaine infusion on pain and opioid consumption in ambulatory surgery patients.

Background            Postoperative pain can delay patient discharge and result in unplanned hospital admission. Postoperative pain has a significant inflammatory component and local anesthetics modulate inflammation. Some inpatient studies have shown reduced pain and shorter hospital stay when lidocaine was included as part of a general anesthetic.

Methodology            This prospective, double-blind, randomized study included ASA class I-III adult patients scheduled for outpatient surgery with general anesthesia. The general anesthetic was standardized for all patients in regards to opioids, ketorolac, and prophylaxis of nausea and vomiting. All patients received 1.5 mg/kg lidocaine slow IV during induction of general anesthesia. Following induction, the lidocaine group received an infusion of 2 mg/kg/h intraoperatively and during the first hour postoperatively. Control patients received an equal volume infusion of saline. In the Post Anesthesia Recovery Unit (PACU), pain was assessed every 15 minutes with a visual analogue scale (VAS). Discharge readiness was assessed every 15 minutes with the modified Aldrete score.

Result            Fifty-six patients were included in the analysis. Demographic data, type of surgery, and duration of surgery were comparable between groups. Lidocaine patients received an average of 517 ± 203 mg lidocaine by infusion.

In the lidocaine group, opioid use was approximately 30% lower intraoperatively (P = 0.017), 50% lower in the PACU (P = 0.015), but no different than placebo control during the first 24 hours after discharge (P = 0.76). In the PACU, lidocaine patients tended to report less pain than placebo control patients. There was no difference in patient reports of nausea or vomiting between groups.

Conclusion            Lidocaine is safe, inexpensive, and may be useful as a component of immediate postoperative analgesia in outpatients.



The methodology and statistical analysis of a study has everything to do with the conclusions that can be drawn. This study clearly shows a reduction in opioid use, both intraoperatively and in the PACU, for patients who received a lidocaine infusion. Since neither the anesthesia provider nor the PACU nurses knew whether the patient was receiving lidocaine or not, the 30% and 50% reduction in opioids administered to lidocaine patients is fairly impressive. But because of the way patient pain was measured and analyzed, I’m hesitant to accept the study’s claims of reduced pain in lidocaine patients. The fact that PACU staff ended up administering less pain medicine to lidocaine patients is at least an indirect indicator that their pain was less intense than placebo control patients.

I’m left scratching my head about one aspect of this study. Why did patients in BOTH groups receive a 1.5 mg/kg bolus of lidocaine during induction? Lidocaine was the study drug! It didn’t need to be given to the control group. Administering it during induction may have changed the results of the study markedly. Would even more opioid have been needed in the placebo control group if they hadn’t had the induction lidocaine bolus? Did the induction bolus of lidocaine have anything to do with the reason there was no difference in opioid use in the first 24 hours post discharge?

A reduction in inflammation and, thus, reduced pain is not the only explanation for the reduction in opioid use seen in the lidocaine infusion group. Noticeably missing from the author’s literature review was anything about the CNS depressive and general anesthetic effects of lidocaine. While I’m not recommending it, lidocaine has be administered in doses sufficient to cause significant CNS depression and even general anesthesia. Perhaps the reason for a reduction in intraoperative opioid administration was simply deeper anesthesia. Perhaps the reason for a reduction in PACU opioid administration was simply CNS depression. Neither level of consciousness nor level of sedation was measured or reported in this study, so we don’t really know if lidocaine patients were really in less pain or simply less awake.

All in all, while some other studies do suggest a role for lidocaine in reducing postoperative pain, this study doesn’t make me want to run a lidocaine infusion throughout a general anesthetic for postoperative pain control. While the cost of lidocaine is low, there are some risks and the benefit observed in this study doesn’t seem worth the work to me.


Michael Fiedler, PhD, CRNA

© Copyright 2009 Anesthesia Abstracts · Volume 3 Number 11, November 30, 2009

Yardeni IZ, Beilin B, Mayburd ELevinson Y, Bessler H



The effect of perioperative intravenous lidocaine on postoperative pain and immune function

Anesth Analg 2009;109:1464-1469

Yardeni IZ, Beilin B, Mayburd E

Levinson Y, Bessler H




Purpose            The purpose of this study was to test the hypothesis that administering intravenous lidocaine before surgical incision and intraoperatively would reduce postoperative pain.

Background            Postoperative pain results in physiologic, immunologic, and psychologic changes. Tissue injury results in inflammatory reactions, increased levels of proinflammatory substances, and hyperalgesia. Intravenous lidocaine has an anti-inflammatory effect. It has been shown to produce postoperative analgesia, reduce opioid consumption, accelerate recovery of bowel function, and facilitate rehabilitation postoperatively.

Methodology            Healthy women aged 45 years to 70 years old scheduled for transabdominal hysterectomy were included in this prospective, randomized, double-blind study. Exclusion criteria included hypertension, arrhythmias, diabetes, and patients previously taking medications with immunosuppressive or antiinflammatory properties. The lidocaine group received a bolus of 2 mg/kg IV lidocaine 20 minutes before induction of general anesthesia followed by an infusion of lidocaine 1.5 mg/kg/h. The control group received an equal bolus and infusion volume of normal saline. The infusions were terminated at the end of surgery. Postoperatively, all patients received Patient Controlled Epidural Analgesia (PCEA) with 0.1% bupivacaine plus 2 µg/mL fentanyl; background infusion 6 mL/h, demand 3 mL, lockout 10 min. No IV opioids or antiinflammatory drugs were given for postoperative pain.

All patients received a standardized general anesthetic beginning with PO lorazepam, IV midazolam and induction with fentanyl, propofol, and vecuronium. General anesthesia was maintained with 50% nitrous oxide, fentanyl, and isoflurane titrated to maintain blood pressure within 20% of baseline (end tidal concentrations between 0.6% and 1.2%).

Pain was assessed by Visual Analogue Scale (VAS) at rest and with coughing at six time periods; 4, 8, 12, 24, 48, and 72 hours postoperatively.

Result            Sixty-five women were enrolled in the study; five were excluded from analysis due to the presence of inflammatory confounders. The groups were demographically similar.

Average intraoperative fentanyl administration was 249 µg in the lidocaine group and 283 µg in the control group (P=NS). Postoperatively, VAS pain scores were no different between groups at rest or during coughing at the 12 hour assessment and beyond. At 4 hours postoperatively, VAS pain scores were 4.0 and 5.3 at rest and during coughing respectively in the lidocaine group vs. 4.53 and 6.13 in the control group. At 8 hours postoperatively, VAS pain scores were 3.7 and 5.0 at rest and during coughing respectively in the lidocaine group vs. 4.27 and 5.37 in the control group.

During the first 24 hours postoperatively, lidocaine patients received an average of 229 mL of PCEA solution and pressed the demand button an average 28 times. Control patients received an average of 247 mL of PCEA solution and pressed the demand button an average 35 times. These differences were not significant.

Conclusion            The lidocaine group experienced less pain than the control group in the immediate postoperative period.



I couldn’t disagree with the investigators conclusion on postoperative pain more, on either clinical or statistical grounds. The investigators did “find” a statistically significant reduction in VAS pain scores in the lidocaine group at 4 and 8 hours postoperatively. But to produce this result they made a common mistake in the analysis of VAS data. The number produced when patients describe their pain with a VAS is simply an order, much like the order in which runners finish a race. It is not linear and the difference between any two numbers isn’t necessarily the same. That is to say, 2 is not necessarily twice as much as 1 and 5 is not necessarily 20% more than 4. As a result, nonparametric statistical tests should be used to compare VAS scores. But even if the differences in VAS pain scores had been statistically significant, I don’t believe them to be clinically significant. At 4 hours, the differences between the lidocaine and control groups were 0.53 and 0.83 at rest and during coughing respectively. At 8 hours, 0.57 and 0.37. These difference in VAS scores are tiny and patients tend to clump VAS scores together in these ranges so there isn’t much difference in the numbers to begin with. Further evidence that pain wasn’t clinically significantly different is found in the actual use of PCEA bupivacaine and fentanyl. The differences in PCEA solution infused and the number of demand button presses wasn’t even statistically significant.

The strongest conclusion one can draw from the data in this study is that a lidocaine bolus and infusion may result in a slight trend towards less postoperative pain. Unless we can figure out how to make that effect bigger without overdosing patients on lidocaine, I question the benefit of the intervention. It also adds to the anesthesia workload without producing much patient benefit. I was excited when I first saw study titles indicating that systemic lidocaine might prevent postoperative pain. The two studies in this issue of Anesthesia Abstracts have left me unimpressed.


Michael Fiedler, PhD, CRNA



© Copyright 2009 Anesthesia Abstracts · Volume 3 Number 11, November 30, 2009


Hiller DB, DiGregorio G, Ripper R, Kelly K, Massad M, Edelman L, Edelman G, Feinstein DL & Weinberg GL


Epinephrine impairs lipid resuscitation from bupivacaine overdose: A threshold effect

Anesthesiology 2009;111:498-505

Hiller DB, DiGregorio G, Ripper R, Kelly K, Massad M, Edelman L, Edelman G, Feinstein DL & Weinberg GL



Purpose            The aim of this study was to determine whether different doses of epinephrine influenced the effectiveness of lipid emulsion therapy in the setting of massive bupivacaine overdose.

Background            The use of lipid emulsion has been successfully advocated for the resuscitation of bupivacaine overdose; several case reports have supplied evidence of its clinical efficacy. However, because lipid therapy is often used as “last ditch” therapy, these authors thought to investigate whether the high doses of epinephrine (equivalent to those administered during a difficult code situation) may adversely affect the effectiveness of lipid therapy.

Methodology            Thirty rats were randomly assigned to 1 of 6 groups: saline-control, lipid-control, and lipid PLUS a single dose of epinephrine (1, 2.5, 10, or 25 mcg/kg). Thus, there were 5 rats in each group. The rats were anesthetized with isoflurane and overdosed with bupivacaine (20 mg/kg over 20 seconds, a dose that in rats causes asystole that is unrecoverable with CPR alone).  CPR was initiated for 3 minutes in all subjects prior to resuscitation with the assigned drug regimen. Chest compressions were stopped when the native rate-pressure product (RPP) ≥ 30% of baseline, which was considered an adequate reflection of the return of spontaneous circulation. In all groups, chest compressions stopped at 10 minutes; over the next 5-minute period, rats were evaluated for evidence of recovery. At 15 minutes, blood was drawn for analysis and rats were euthanized.

Result            The only groups in which all of the animals had full circulation restored at the 10-minute mark were the lipid control group and the two groups who received the lowest doses of epinephrine (1 and 2.5 mcg/kg) with the lipid treatment. Rats who received 10 and 25 mcg/kg of epinephrine with lipids had statistically lower recovery profiles (outcome measurement RPP, P < 0.001) at both the 10 and 15-minute measurement points. At 15 minutes post-resuscitation, rats in the saline control and 10 and 25 mcg/kg epinephrine groups had significantly decreased pH (7.21, 7.2, 7.13), base excess (-7.0, -5.8, -10.6), and HCO3 (20.1, 21.7, 16.1 mmol/L) along with decreased arterial PO2 (170, 61, 104 mmHg) compared to the lipid control group (pH 7.31, BE -1.4, HCO3 25.4 mmol/L, 308 mmHg). All subjects receiving epinephrine initially responded favorably, however, by the 7.5-minute mark, subjects with the higher epinephrine doses deteriorated and those who received the smaller doses recovered.

Conclusion            A single dose of epinephrine (in the rat model, 10 mcg/kg or higher) decreases the effectiveness of lipid resuscitation from bupivacaine overdose.


This research may represent the beginning of a fundamental shift in the concept of resuscitation from local anesthetic overdose, and possibly a shift in the concept of resuscitation from any cause. A largely ignored body of research has demonstrated that epinephrine is probably no better than placebo in resuscitating a pulseless patient and that the more epinephrine given, the more deleterious the outcome. A strong dose-response relationship between epinephrine dose, elevated serum lactate and drops in RPP was seen in this study; these events occurred in the presence of well-oxygenated blood. In the single study that failed to show the benefit of lipid in conjunction of high dose epinephrine, the study design included a period of apnea (AKA asphyxia and cellular hypoxia). These data make me wonder whether there is a causal link between epinephrine in large doses and hypoxia at the cellular level. Could these be the same reasons why we avoid vasopressors in patients undergoing digit/limb replantation or flap reconstruction?


Resuscitation of bupivacaine overdose is one area in which double-blinded, randomized controlled trials in humans are not possible, so evaluating the evidence from animal trials is our only option.  For practice settings in which peripheral nerve blocks play a large role, it seems clear that lipid emulsion should be immediately available in the event of an intravascular injection. Based on this animal study, clinicians must consider lipid use early in the resuscitation period and use caution in dosing epinephrine. The benefit of lipids far outweighs the relatively benign risk associated with acute short-term administration in the resuscitation setting.


Penelope S Benedik PhD, CRNA, RRT


Brull SJ. Lipid emulsion for the treatment of local anesthetic toxicity: Patient safety implications. Anesth Analg 2008;106:1337-1339


Rate-pressure product = systolic pressure x heart rate; an indicator of myocardial oxygen consumption. In humans, the RPP should not exceed 12000.

© Copyright 2009 Anesthesia Abstracts · Volume 3 Number 11, November 30, 2009

Quality Improvement

Lewthwaite BJ


What do nurses know about postoperative nausea and vomiting?

Medsurg Nurs 2009;18:110-113

Lewthwaite BJ


Purpose            Nurses at St. Boniface general hospital (SBGH), a tertiary care hospital in western Canada, undertook this postoperative nausea and vomiting (PONV) learning project to assess nurses understanding of PONV.

Background            Postoperative nausea and vomiting affects 20%-30% of patients in a low-risk population (having fewer than two risk factors for PONV) and can affect as much as 70%-80% of persons in a high-risk population, with three or more risk factors. Nurses on a gynecologic unit report that many of their patients experience nausea and vomiting after surgery, however, do these nurses also understand why their patient population is at high risk for PONV? Many health care providers and centers, however, continue to fall short in addressing this troublesome and potentially harmful surgical complication. Although nurses spend a great deal of time addressing PONV, the literature suggests they lack sufficient knowledge to provide evidence-based interventions to patients experiencing this postoperative complaint.

Methodology            In 2007, a survey was distributed to all nurses who worked in a postoperative setting or had the potential to care for patients following surgery. Goals of the study were to identify knowledge gaps, stimulate an interest in the identification and treatment of PONV, and increase nurses’ ability to match the most suitable treatment to the likely cause of PONV. This was a descriptive non-experimental correlation cross-facility study.

Result            From a pool of 665 nurses, 396 full or part-time nurses participated in this survey. The response rate was 36.89% and deemed acceptable for the survey. Results indicated that this group of nurses was practicing with approximately 61.34% of the necessary knowledge to assist with PONV treatments effectively. Statements 12 and 13 relating to nursing practice most often received correct responses (91.8%), with statements 3 and 17 relating to knowledge of PONV correctly answered the least often (10.3% and 29.5% respectively).

Conclusion            Findings from this survey were used as the foundation for a systemic education program on PONV. A presentation was made to approximately 370 health care practitioners. It included the etiology and risk factors of PONV, an extensive review of pharmacological and non-pharmalogical treatment options, recommended nursing interventions, survey results, and answers to a post-test of 20 true-false statements. This study focused on the knowledge and practice nurses require when dealing with PONV, a common complaint.



This collaborative effort by anesthesia providers and pharmacists during sessions to educate nurses led to a sharing of expertise and exposure between practitioners and nurses. Often, anesthesia providers work independently and fail to appreciate the value of each member of the health care team. These types of education sessions allow anesthesia providers and pharmacists time to dialogue with nursing personnel, especially concerning the medications and treatment algorithms commonly used in clinical practice. Nurses can also learn more about PONV risk factor assessment tools and be prepared for high risk patients and introduce timely interventions.


Joseph F. Burkard, DNSc, CRNA

© Copyright 2009 Anesthesia Abstracts · Volume 3 Number 11, November 30, 2009

Respiration & Ventilation

Talab HF, Zabani IA, Abdelrahman HS, Bukhari WL, Mamoun I, Ashour MA, Bin Sadeq B, El Sayed SI



Intraoperative ventilatory strategies for prevention of pulmonary atelectasis in obese patients undergoing laparoscopic bariatric surgery

Anesth Analg 2009;109:1511-16

Talab HF, Zabani IA, Abdelrahman HS, Bukhari WL, Mamoun I, Ashour MA, Bin Sadeq B, El Sayed SI




Purpose            The aim of this study was to assess the effects of a post-induction alveolar recruitment maneuver and varying levels of PEEP on postoperative outcomes in a sample of morbidly obese patients undergoing laparoscopic bariatric surgery.

Background            Anesthesia-induced atelectasis has been identified as the explanation for the increase in shunt fraction that occurs after anesthesia induction. Over the last several decades, multiple researchers have demonstrated the extent and effects of atelectasis on intra- and post-operative pulmonary function with computed tomography and magnetic resonance imaging in pediatric, adult, lean, and obese populations. In the last decade, research has focused on the successful treatment and prevention of anesthesia-induced atelectasis. Atelectasis increases as a higher FIO2 is used to preoxygenate the patient prior to induction. To treat this alveolar collapse, alveolar recruitment maneuvers (also known as a vital capacity maneuver, VCM) are given by manually inflating the lung to a peak inspiratory pressure 40 cm H2O with up to a 15 second pause. This has implications for frequent users of the laryngeal mask airway since the VCM cannot be accomplished with an LMA in use. The VCM can effectively reinflate collapsed alveoli, however unless PEEP and/or a gas mixture less than 100% oxygen is delivered subsequent to the maneuver, atelectasis will reaccumulate within about 10 minutes. Vital capacity maneuvers with an FIO2 less than 1.0 are also recommended prior to extubation. Additionally, and not unexpectedly, obese patients develop more intraoperative atelectasis and it lasts longer into the postoperative period. The missing piece in this large body of literature is whether the “usual” versus a “reexpansion” intraoperative ventilation technique will actually affect postoperative outcomes.

Methodology            This was a double-blind, randomized controlled study of 66 healthy obese subjects, BMI 30 to 50 kg/m2 and age between 20 and 50 years, undergoing laparoscopic bariatric surgery. Subjects were induced after preoxygenation with 100% oxygen; all subjects received a VCM immediately after intubation and were randomly allocated to zero-end expiratory pressure (ZEEP), 5 cmH2O PEEP (PEEP 5), or 10 cmH2O PEEP (PEEP 10). Intraoperative ventilation consisted of tidal volume 8 to 10 mL/kg based on ideal body weight with FIO2 0.50 with the designated end-expiratory pressure. At the end of surgery, the FIO2 was increased to 1.0 and subjects were “fully reversed” from neuromuscular blocking agents before extubation. Arterial blood gases were drawn with subjects awake prior to induction on room air and before discharge from PACU. CT scans at “just above the diaphragm” were performed after subjects were discharged from PACU. CT scans were assessed specifically for atelectasis and/or evidence of barotrauma. Atelectasis was quantified into lamellar (< 3mm thickness), plate (3 to 10 mm), segmental (> 10 mm but less than lobar), and lobar (involving the entire lower lobe). A 35% reduction in atelectasis was considered a clinically important result.

Result            There was no difference between groups based on age, sex, ASA status, BMI, or duration of surgery. The ZEEP, PEEP 5, and PEEP 10 groups had 19, 19, and 20 subjects each respectively, after 8 subjects were removed for protocol violations. There were no differences in mean arterial pressure and heart rate between groups at any time point during the perioperative period. There was no difference in A-a gradient between groups preoperatively, but postoperatively, the A-a gradient at PEEP 10 was significantly less than at PEEP 5 or ZEEP (PEEP 10, 29.85 ± 18; PEEP 5, 53 ± 30; ZEEP, 63 ± 35; P < 0.05). The length of stay in PACU and number of patients who required 100% oxygen in PACU was significantly less in the PEEP 10 group (66 minutes, 1 patient) compared to PEEP 5 (77 minutes, 3 patients) or ZEEP (88 minutes, 5 patients) (p < 0.05). During the first 48 hours postoperatively, no patients in the PEEP 10 group had significant desaturation, bronchospasm or chest infection, while 3 patients in the PEEP 5 group and 4 patients in the ZEEP group had these postoperative complications (c2 and significance not reported). Postoperatively, the PEEP 10 group had fewer subjects with segmental and lobar atelectasis (4 and 0 subjects) versus the PEEP 5 group (9 and 0 subjects) or the ZEEP group (13 and 1 subjects) (p < 0.05), while the PEEP 10 group had more lamellar atelectasis (11 subjects) versus the PEEP 5 (4 subjects) and ZEEP (2 subjects) groups (P < 0.05). Two subjects in the PEEP 10 group had no atelectasis while all subjects in the PEEP 5 and ZEEP groups had some measurable atelectasis. No barotrauma was detected by CT scan in any group.

Conclusion            This study provided preliminary data that the application of PEEP 10 following a VCM and using an FIO2 of 0.50 is beneficial both intra- and postoperatively to obese patients undergoing laparoscopic bariatric surgery.


Comment  I have had many discussions with physician colleagues who deny the usefulness of the well-documented research on the prevention and treatment of intraoperative atelectasis (a bit of which is referenced below). “Who cares? There is no evidence that anesthesia-induced atelectasis impacts outcomes . . . just put the patients on oxygen in the PACU and they do fine.” Up until now, my response was that our job is to provide surgical conditions with as homeostatic an environment as possible, which includes using the VCM and PEEP to maintain alveolar patency, that is, to awaken the patient in a condition as close to their preanesthetic condition as possible. This study now provides early findings that these intraoperative interventions do make a difference in outcomes both physiologically and in facility utilization and cost. If extrapolated across the obese patient population for all surgeries, the impact of these preventive and treatment strategies would be staggering.

One caveat about the results deserves note: while the authors state in the text that there were no preoperative group differences, Table 2 (which is labeled extremely poorly) has the apparent mean BMI of the PEEP 5 group (44.53 ± 6.99) statistically different from the BMI of PEEP 10 group (38.3 ± 6.85, p < 0.05). This could provide a partial explanation of the apparent benefits of PEEP 10; these subjects were “smaller” overall than the subjects in the PEEP 5 group. However, because the BMI and outcome data from the ZEEP and PEEP 5 groups were statistically similar, one might infer that the benefit of PEEP 10 is real. Unfortunately this discrepancy was neither acknowledged nor commented upon by the authors.



Penelope S Benedik PhD, CRNA, RRT


Coussa M et al. Prevention of atelectasis formation during the induction of general anesthesia in morbidly obese patients. Anesth Analg 2004;98:1491-1495.

Edmark, Kostova-Aherdan, Enlung & Hedensteirna. Optimal oxygen concentration during induction of general anesthesia. Anesthesiology 2003;98:28-33.

 Neumann et al. Positive end-expiratory pressure prevents atelectasis during general anesthesia even in the presence of a high inspired oxygen concentration. Acta Anaesthesiol Scand, 1999;43:295-301.

Rothen et al. Dynamics of re-expansion of atelectasis during general anesthesia. Br J Anaesth, 1999;82:551-6.

Tokics et al. J Appl Physiol 1996;81:1822-33.



© Copyright 2009 Anesthesia Abstracts · Volume 3 Number 11, November 30, 2009