bluuebunny/crossref_metadata_2025 huggingface dataset:
Sleeping Characteristics of Children Undergoing Outpatient Elective Surgery
Authors: Kain Zeev N. , Mayes Linda C. , Caldwell-Andrews Alison A. , Alexander Gerianne M. , Krivutza Dawn , Teague Barbara A. , Wang Shu-Ming
Published: November 2003

Background

A significant number of children undergoing anesthesia and surgery exhibit new-onset sleep-related problems postoperatively. The aim of this longitudinal cohort study was to expand previous research in this area by using a new objective technology.

Methods

This study compared children undergoing general anesthesia and outpatient surgery (n = 92) to a community-based control group of children (n = 77). Data regarding coping, temperament, anxiety, surgical procedures, and postoperative pain were collected. Subjects underwent actigraphy sleep monitoring for at least 3 nights before surgery and 5 postoperative days (POD). Sleep assessment was performed with actigraphy sleep monitoring and the Post Hospitalization Behavioral Questionnaire (PHBQ).

Results

Forty-three children (47%) in the surgery group experienced postoperative sleeping disturbances as determined by either the actigraphy or the PHBQ. Only 13 children (14.4%), however, experienced a decrease of at least 1 SD in percentage sleep as assessed by actigraphy. Postoperative pain scores on POD 1 and POD 2 were significantly higher among children who exhibited sleep problems as diagnosed by actigraphy (F = 4.283; P= 0.047). Also, children who exhibited actigraph-based sleep problems scored lower sociability-temperament (14.1 +/- 4.3 vs. 17.5 +/- 3.4; P= 0.04) scores compared with the community group and had a higher rate of change in their perioperative anxiety levels (group x time interaction, F = 5.1; P= 0.03).

Conclusion

A significant number of children undergoing outpatient surgery experience postoperative sleep-related problems. The clinical significance of this finding, however, is unclear.
Platelet PlA2Polymorphism and Platelet Activation Are Associated with Increased Troponin I Release after Cardiopulmonary Bypass
Authors: Rinder Christine S. , Mathew Joseph P. , Rinder Henry M. , Greg Howe J. , Fontes Manuel , Crouch Jill , Pfau Stephen , Patel Parag , Smith Brian R.
Published: November 2003

Background

The PlA2 polymorphism of platelet glycoprotein IIIa has been identified as a prothrombotic risk factor in a number of cardiovascular settings. The aim of this study was to determine whether the PlA2 polymorphism of platelet glycoprotein IIIa and degree of platelet activation were associated with more severe myocardial injury as indicated by troponin I release following cardiopulmonary bypass.

Methods

The PlA2 genotype was determined in 66 patients undergoing elective coronary artery bypass grafting requiring cardiopulmonary bypass. Troponin I concentrations and the percentage of circulating, activated (CD62P+) platelets were measured at predetermined intervals perioperatively.

Results

Forty-six patients were Pl(A1,A1), and 20 were Pl(A1,A2) or Pl(A2,A2). Patients with at least one PlA2 allele had significantly greater postoperative troponin I concentrations than PlA1 homozygotes (P = 0.006, analysis of variance). Peak troponin I concentrations also correlated significantly with the increase in circulating, activated platelets (P = 0.02, Spearman rank correlation).

Conclusions

The PlA2 allele of platelet glycoprotein IIIa is associated with higher troponin I concentrations following cardiopulmonary bypass surgery, suggesting that this platelet polymorphism contributes to perioperative myocardial injury.
Abnormal Echogenic Findings Detected by Transesophageal Echocardiography and Cardiorespiratory Impairment during Total Knee Arthroplasty with Tourniquet
Authors: Kato Nobuya , Nakanishi Kazuhiro , Yoshino Shinichi , Ogawa Ryo
Published: November 2003

Background

In patients undergoing total knee arthroplasty, intraoperative pulmonary embolic events are rare, and most occur following tourniquet deflation. This embolization can be observed using transesophageal echocardiography. However, the authors have encountered sudden decreases in arterial oxygen partial pressure while a tourniquet is still inflated. Therefore, the current investigation was designed to detect emboli during the tourniquet inflation phase and to identify the composition of the echogenic material.

Methods

Forty-six patients were randomly assigned to undergo total knee arthroplasty without (control, n = 24) or with a tourniquet (n = 22). Hemodynamic monitoring, blood gas analysis, and continuous transesophageal echocardiography were performed during the total knee arthroplasty procedure. Right jugular blood specimens were collected whenever echogenic material was seen in the atrium.

Results

In the tourniquet group, embolic events occurred in 27% of patients during femoral reaming and in 100% after tourniquet deflation. In the control group, emboli were detected in 54% of patients during femoral reaming. Most of the patients exhibited cardiopulmonary impairment after severe echogenic embolism, even while the tourniquet was inflated (two patients). None of the blood samples aspirated from the central catheters contained detectable material.

Conclusions

This prospective study showed that embolic events occurred during total knee arthroplasty, even while a tourniquet was inflated. An inflated tourniquet does not completely prevent pulmonary emboli.
Negative and Positive Inotropic Effects of Propofol via L-type Calcium Channels and the Sodium-Calcium Exchanger in Rat Cardiac Trabeculae
Authors: de Ruijter Wouter , M. Stienen Ger J. , van Klarenbosch Jan , de Lange Jacob J.
Published: November 2003

Background

Conflicting opinions are present in the literature regarding the origin of the negative inotropic effect of propofol on the myocardium. This study aims to resolve these discrepancies by investigating the inotropic effects of propofol the L-type calcium channels and the sodium-calcium exchanger (NCX).

Methods

The effect of 20 microg/ml propofol on force development was determined in rat cardiac trabeculae at different pacing frequencies and different extracellular calcium concentrations. Postrest potentiation, sodium withdrawal during quiescence, and the NCX inhibitor KB-R7943 were used to study changes in the activity of the reverse mode of the NCX by propofol.

Results

The effect of propofol on steady state peak force depended on pacing frequency and calcium concentration. A negative inotropic effect was observed at pacing frequencies greater than 0.5 Hz, but a positive inotropic effect was observed at 0.1 Hz and low calcium, which cannot be explained by an effect on the L-type calcium channel. Propofol enhanced postrest potentiation in a calcium-dependent manner. Sodium withdrawal during quiescence and the use of the specific NCX inhibitor KB-R7943 provided evidence for an enhancement of calcium influx by propofol the reverse mode of the NCX.

Conclusions

The effects of propofol on the myocardium depend on pacing frequency and calcium concentration. The positive inotropic effect of propofol is associated with increased calcium influx the reverse mode of the NCX. The authors conclude that the net inotropic effect of propofol is the result of its counteracting influence on the functioning of the L-type calcium channel and the NCX.
Influence of Hemorrhage on Propofol Pseudo–Steady State Concentration
Authors: Kazama Tomiei , Kurita Tadayoshi , Morita Koji , Nakata Jun , Sato Shigehito
Published: November 2003

Background

A small induction dose has been recommended in cases of hemorrhagic shock. However, the influence of hemorrhage on the amplitude of plasma propofol concentration has not yet been fully investigated during continuous propofol infusion. The authors hypothesized that the effect of hemorrhage on plasma propofol concentration is variously influenced by the different stages of shock.

Methods

After 120 min of steady state infusion of propofol at a rate of 2 mg x kg(-1) x h(-1), nine instrumented immature swine were studied using a stepwise increasing hemorrhagic model (200 ml of blood every 30 min until 1 h, then additional stepwise bleeding of 100 ml every 30 min thereafter, to the point of circulatory collapse). Hemodynamic parameters and plasma propofol concentration were recorded at every step.

Results

Before total circulatory collapse, it was possible to drain 976 +/- 166 ml (mean +/- SD) of blood. Hemorrhage of less than 600 ml (19 ml/kg) was not accompanied by a significant change in plasma propofol concentration. At individual peak systemic vascular resistance, when cardiac output and mean arterial pressure decreased by 31% and 14%, respectively, plasma propofol concentration increased by 19% of its prehemorrhagic value. At maximum heart rate, when cardiac output and mean arterial pressure decreased by 46% and 28%, respectively, plasma propofol concentration increased by 38%. In uncompensated shock, it increased to 3.75 times its prehemorrhagic value.

Conclusions

During continuous propofol infusion, plasma propofol concentration increased by less than 20% during compensated shock. However, it increased 3.75 times its prehemorrhagic concentration during uncompensated shock.
Bupivacaine Attenuates Contractility by Decreasing Sensitivity of Myofilaments to Ca2+,in Rat Ventricular Muscle
Authors: Mio Yasushi , Fukuda Norio , Kusakari Yoichiro , Tanifuji Yasumasa , Kurihara Satoshi
Published: November 2003

Background

Bupivacaine exhibits a cardiodepressant effect, the molecular mechanism(s) of which have yet to be fully understood. Bupivacaine may directly act on contractile proteins and thereby decrease myofibrillar Ca2+ sensitivity.

Methods

Rat ventricular muscle was used. First, the effect of bupivacaine was examined on tetanic contractions in isolated intact myocytes. Next, Triton X-100-treated ventricular trabeculae were used to investigate the effect of bupivacaine on the pCa (= -log [Ca2+ ])-tension relation as well as on maximal Ca2+ -activated tension. Furthermore, to test whether bupivacaine inhibits the pathway downstream from Ca2+ binding to troponin C, tension was elicited in the skinned preparations by lowering the Mg-adenosine triphosphate (MgATP) concentration in the absence of Ca2+. The effect of bupivacaine on the pMgATP (= -log [MgATP])-tension relation was examined.

Results

In myocytes, 3 microm bupivacaine significantly (P < 0.01) increased intracellular Ca2+ concentration required for 5% cell shortening from the resting cell length. In skinned preparations, bupivacaine shifted the pCa-tension relation to the lower pCa side; the midpoint of the pCa curve (pCa50) was significantly (P < 0.05) changed by 10 and 100 microm bupivacaine. A highly correlated linear relation (R = 0.81; P< 0.0005) was present between pCa50 and maximal Ca2+ -activated tension. Bupivacaine (10 and 100 microm) significantly (P < 0.05) shifted the midpoint of the pMgATP-tension relation to the higher pMgATP side.

Conclusions

Bupivacaine decreases myofibrillar Ca2+ sensitivity in ventricular muscle, and this is coupled with the compound's inhibitory effect on the pathway beyond Ca2+ binding to troponin C, possibly on the actomyosin interaction. The current results may partly explain the overall cardiodepressant effect of bupivacaine in vivo.
Transmission through the Dorsal Spinocerebellar and Spinoreticular Tracts
Authors: Soja Peter J. , Taepavarapruk Niwat , Pang Walton , Cairns Brian E. , McErlane Shelly A. , Fragoso Miguel C.
Published: November 2003

Background

Most of what is known regarding the actions of injectable barbiturate anesthetics on the activity of lumbar sensory neurons arises from experiments performed in acute animal preparations that are exposed to invasive surgery and neural depression caused by coadministered inhalational anesthetics. Other parameters such as cortical synchronization and motor ouflow are typically not monitored, and, therefore, anesthetic actions on multiple cellular systems have not been quantitatively compared.

Methods

The activities of antidromically identified dorsal spinocerebellar and spinoreticular tract neurons, neck motoneurons, and cortical neurons were monitored extracellularly before, during, and following recovery from the anesthetic state induced by thiopental in intact, chronically instrumented animal preparations.

Results

Intravenous administration of 15 mg/kg, but not 5 mg/kg, of thiopental to awake cats induced general anesthesia that was characterized by 5-10 min of cortical synchronization, reflected as large-amplitude slow-wave events and neck muscle atonia. However, even though the animal behaviorally began to reemerge from the anesthetic state after this 5-10-min period, neck muscle (neck motoneuron) activity recovered more slowly and remained significantly suppressed for up to 23 min after thiopental administration. The spontaneous activity of both dorsal spinocerebellar and spinoreticular tract neurons was maximally suppressed 5 min after administration but remained significantly attenuated for up to 17 min after injection. Peripheral nerve and glutamate-evoked responses of dorsal spinocerebellar and spinoreticular tract neurons were particularly sensitive to thiopental administration and remained suppressed for up to 20 min after injection.

Conclusions

These results demonstrate that thiopental administration is associated with a prolonged blockade of motoneuron output and sensory transmission through the dorsal spinocerebellar and spinoreticular tracts that exceeds the duration of general anesthesia. Further, the blockade of glutamate-evoked neuronal responses indicates that these effects are due, in part, to a local action of the drug in the spinal cord. The authors suggest that this combination of lumbar sensory and motoneuron inhibition underlies the prolonged impairment of reflex coordination observed when thiopental is used clinically.
Protein Tyrosine Kinase-Dependent Modulation of Isoflurane Effects on Cardiac Sarcolemmal KATPChannel
Authors: Stadnicka Anna , Kwok Wai-Meng , Warltier David C. , Bosnjak Zeljko J
Published: November 2003

Background

Cardiac adenosine triphosphate-sensitive potassium (K(ATP)) channels and protein tyrosine kinases (PTKs) are mediators of ischemic preconditioning, but the interaction of both and a role in myocardial protection afforded by volatile anesthetics have not been defined.

Methods

Whole cell and single channel patch clamp techniques were used to investigate the effects of isoflurane and the PTK inhibitor genistein on the cardiac sarcolemmal K(ATP) channel in acutely dissociated guinea pig ventricular myocytes.

Results

At 0.5 mm internal ATP, genistein (50 microm) elicited whole cell K(ATP) current (22.5 +/- 7.9 pA/pF). Genistein effects were concentration-dependent, with an EC50 of 32.3 +/- 1.4 microm. Another PTK inhibitor, tyrphostin B42, had a similar effect. The inactive analog of genistein, daidzein (50 microm), did not elicit K(ATP) current. Isoflurane (0.5 mm) increased genistein (35 microm)-activated whole cell K(ATP) current from 14.5 +/- 3.1 to 32.5 +/- 6.6 pA/pF. Stimulation of receptor PTKs with epidermal growth factor, nerve growth factor, or insulin attenuated genistein and isoflurane effects, and the protein tyrosine phosphatase inhibitor orthovanadate (1 mm) prevented their actions on K(ATP) current. In excised inside-out membrane patches, and at fixed 0.2 mm internal ATP, genistein (50 microm) increased channel open probability from 0.053 +/- 0.016 to 0.183 +/- 0.039, but isoflurane failed to further increase open probability (0.162 +/- 0.051) of genistein-activated channels. However, applied in the presence of genistein and protein tyrosine phosphatase 1B (1 microg/ml), isoflurane significantly increased open probability to 0.473 +/- 0.114.

Conclusions

These results suggest that the PTK-protein tyrosine phosphatase signaling pathway may be one of the regulators of cardiac sarcolemmal K(ATP) channel and may play a role in modulating its responsiveness to isoflurane. Relative importance of this modulation for cardioprotection by volatile anesthetics remains to be established.
What Is the Minimum Training Required for Successful Cricothyroidotomy?
Authors: Wong David T. , Prabhu Atul J. , Coloma Margarita , Imasogie Ngozi , Chung Frances F.
Published: November 2003

Background

A correctly performed cricothyroidotomy may be lifesaving in a cannot-ventilate, cannot-intubate situation. However, many practicing anesthesiologists do not have experience with cricothyroidotomy. The purpose of this study was to determine the minimum training required to perform cricothyroidotomy in 40 s or less in mannequins.

Methods

After informed consent, participants were shown a demonstration video and asked to perform 10 consecutive cricothyroidotomy procedures on a mannequin using a preassembled percutaneous dilational cricothyroidotomy set. Each attempt was timed from skin palpation to lung insufflation. Cricothyroidotomy was considered successful if it was performed in 40 s or less, and the cricothyroidotomy time was considered to have plateaued when there were no significant reductions in cricothyroidotomy times in three consecutive attempts.

Results

One hundred two anesthesiologists participated in the study. There was a significant reduction of cricothyroidotomy times over the 10 attempts (P < 0.0001) and between three consecutive attempts until the fourth attempt (P < 0.03). The cricothyroidotomy times plateaued by the fourth attempt, while the success rate plateaued at the fifth attempt (94, 96, 96, and 96% at the fourth, fifth, sixth, and seventh attempts, respectively).

Conclusion

Practice on mannequins leads to reductions in cricothyroidotomy times and improvement in success rates. By the fifth attempt, 96% of participants were able to successfully perform the cricothyroidotomy in 40 s or less. While clinical correlates are not known, the authors recommend that providers of emergency airway management be trained on mannequins for at least five attempts or until their cricothyroidotomy time is 40 s or less. The most appropriate retraining intervals have yet to be determined for optimal cricothyroidotomy skill retention.
Effects of Isoflurane and Propofol on Glutamate and GABA Transporters in Isolated Cortical Nerve Terminals
Authors: Westphalen Robert I. , Hemmings Hugh C.
Published: November 2003

Background

Depression of glutamate-mediated excitatory transmission and potentiation of gamma-aminobutyric acid (GABA)-mediated inhibitory transmission appear to be primary mechanisms by which general anesthetics produce anesthesia. Since effects on transmitter transport have been implicated in anesthetic actions, the authors examined the sensitivity of presynaptic glutamate and GABA transporters to the effects of a representative volatile (isoflurane) and a representative intravenous (propofol) anesthetic.

Methods

A dual-isotope (l-[3H]glutamate and [14C]GABA) approach allowed simultaneous comparisons of anesthetic effects on three independent assays of glutamate and GABA transporters in adult rat cerebral cortex: transmitter uptake into isolated nerve terminals (synaptosomes), transmitter binding to lysed and washed synaptosomes (synaptic membranes), and carrier-mediated release (reverse transport) of transmitter from preloaded synaptosomes using a modified superfusion system.

Results

Isoflurane produced small but statistically significant inhibition of l-[3H]glutamate and [14C]GABA uptake, while propofol had no effect. Inhibition of uptake by isoflurane was noncompetitive, an outcome that was mimicked by indirectly affecting transporter function through synaptosomal depolarization. Neither isoflurane nor propofol affected l-[3H]glutamate or [14C]GABA binding to synaptic membranes or Ca(2+)-independent carrier-mediated l-[3H]glutamate or [14C]GABA release (reverse transport).

Conclusions

These findings suggest that isoflurane and propofol at clinical concentrations do not affect excitatory glutamatergic transmission or inhibitory GABAergic transmission directly effects on their presynaptic neuronal transporters.
Isoflurane Decreases ATP Sensitivity of Guinea Pig Cardiac Sarcolemmal KATPChannel at Reduced Intracellular pH
Authors: Stadnicka Anna , Bosnjak Zeljko J.
Published: November 2003

Background

Volatile anesthetics can protect the myocardium against ischemic injury by opening the adenosine triphosphate (ATP)-sensitive potassium (K(atp)) channels. However, direct evidence for anesthetic-channel interaction is still limited, and little is known about the role K(atp) channel modulators play in this effect. Because pH is one of the regulators of K(atp) channels, the authors tested the hypothesis that intracellular pH (pHi) modulates the direct interaction of isoflurane with the cardiac K(atp) channel.

Methods

The effects of isoflurane on sarcolemmal K(atp) channels were investigated at pHi 7.4 and pHi 6.8 in excised inside-out membrane patches from ventricular myocytes of guinea pig hearts.

Results

At pHi 7.4, intracellular ATP (1-1,000 microm) inhibited K(atp) channels and decreased channel open probability (Po) in a concentration-dependent manner with an IC(50) of 8 +/- 1.5 microm, and isoflurane (0.5 mm) either had no effect or decreased channel activity. Lowering pHi from 7.4 to 6.8 enhanced channel opening by increasing Po and reduced channel sensitivity to ATP, with IC shifting from 8 +/- 1.2 to 45 +/- 5.6 microm. When applied to the channels activated at pHi 6.8, isoflurane (0.5 mm) increased Po and further reduced ATP sensitivity, shifting IC(50) to 110 +/- 10.0 microm.

Conclusions

Changes in pHi appear to modulate isoflurane interaction with the cardiac K(atp) channel. At pHi 6.8, which itself facilitates channel opening, isoflurane enhances channel activity by increasing Po and reduces sensitivity to inhibition by ATP without changing the unitary amplitude of single channel current or the conductance. These results support the hypothesis of direct isoflurane-K(atp) channel interaction that may play a role in cardioprotection by volatile anesthetics.
Interaction of Isoflurane with the Dopamine Transporter
Authors: Votaw John , Byas-Smith Michael , Hua Jian , Voll Ronald , Martarello Laurent , Levey Allan I. , Bowman F. DuBois , Goodman Mark
Published: November 2003

Background

Isoflurane administration is known to increase extracellular dopamine (DA) concentration. Because the dopamine transporter (DAT) is a key regulator of DA, it is likely affected by isoflurane. This study investigates the hypothesis that isoflurane inhibits DA reuptake by causing DAT to be trafficked into the cell.

Methods

Rhesus monkeys were scanned with positron emission tomography (PET) using [18F]FECNT (a highly specific DAT ligand) while anesthetized with 1% isoflurane. The isoflurane was increased to 2%, and the animals were rescanned. Uptake was analyzed with the tissue reference method using the cerebellum as the reference tissue to determine the binding potential in the putamen. Immunohistochemistry and Western blot analyses were performed in rats to determine if isoflurane administration would change the total amount of DAT. Rats breathed air plus 2% isoflurane for 30 min, and then striatal DAT assays were rapidly performed. immunocytochemistry experiments were performed using human embryonic kidney (HEK) cells stably transfected with human DAT. The cells were exposed to 4% isoflurane for 1 h while the location of DAT was observed with fluorescent confocal microscopy.

Results

The [18F]FECNT binding potential in rhesus monkeys decreased by 63 +/- 6% (SEM, n = 5) when isoflurane was increased from 1 to 2% as compared with no significant change (0.7 +/- 2.5%; SEM, n = 5) when the isoflurane concentration was not changed (P < 0.001). No difference in DAT staining between isoflurane-treated and control rats was apparent from visual inspection, and quantitative Western blot analyses showed no significant change in total DAT protein. After isoflurane treatment, focal puncta of intense fluorescence was visible inside the HEK cells.

Conclusions

The experiments indicate that DAT is trafficked into the cell by isoflurane without changing the total amount of DAT in the striatum. The PET data are consistent with this finding, provided that intracellular DAT acquires a conformation that has low affinity for [18F]FECNT. Thus, [18F]FECNT appears to be an excellent agent for measuring plasma membrane-expressed DAT and evaluating DAT trafficking.
Supraspinal Antinociceptive Effects of μ and δ Agonists Involve Modulation of Adenosine Uptake
Authors: Pham Thao , Carrega Louis , Sauze Nicole , Fund-Saunier Odile , Devaux Christiane , Peragut Jean-Claude , Saadjian Alain , Guieu Régis
Published: November 2003

Background

The modulation of extracellular adenosine concentration by opioids provides evidence that the antinociceptive effects of these compounds involve endogenous adenosine. The aim of this study was to determine whether there is a relation between the inhibition of brain synaptosome adenosine uptake by opioid agonists and the analgesic effects of these compounds.

Methods

The authors used the hot plate and tail-pinch tests to evaluate in mice (C57BL/6 females; weight, 25-30 g) the effects of caffeine, a nonspecific adenosine receptor antagonist, on the antinociceptive effect induced by the intracerebroventricular administration of oxymorphone as a mu agonist, SNC80 as a delta agonist, or U69593 as a kappa agonist. They also investigated the effect of these opioid receptor agonists on the uptake of adenosine by whole brain synaptosomes.

Results

Caffeine decreased the analgesic effects induced by oxymorphone or SNC80 but not those induced by U69593. Oxymorphone and SNC80 inhibited adenosine uptake by brain cells, but U69593 did not.

Conclusion

The antinociceptive effects obtained with mu or delta (but not kappa) agonists administered supraspinally were indicative of the involvement of modulation of adenosine uptake.
Prospective study on Incidence and Functional Impact of Transient Neurologic Symptoms Associated with 1%Versus 5% Hyperbaric Lidocaine in Short Urologic Procedures
Authors: Tong Doris , Wong Jean , Chung Frances , Friedlander Mark , Bremang Joseph , Mezei Gabor , Streiner David
Published: November 2003

Background

The objectives of this study were to compare the incidence, onset, duration and pain scores of transient neurologic symptoms (TNS) with 1% versus 5% hyperbaric lidocaine in spinal anesthesia for short urological procedures in a large prospective study. This study would also evaluate patient satisfaction, and impact of TNS on functional recovery to assess the clinical significance of TNS.

Methods

This was a multicenter, double-blind, randomized controlled trial. Four hundred fifty-three patients undergoing short transurethral procedures were randomized to receive 1% or 5% hyperbaric lidocaine. Eighty milligrams of 1% or 5% hyperbaric lidocaine was administered. During the first 3 days after surgery, the presence of TNS, its intensity and duration, and patient functional level were recorded. An intention-to-treat analysis was used.

Results

There was no difference in the incidence of TNS (21% vs. 18%) between 1% versus 5% lidocaine. Patients with TNS had significantly higher pain scores (5.3 +/- 3 vs. 2.3 +/- 3) than patients without TNS during the first 24 h. This difference in pain scores persisted until 72 h postoperatively. There was a significant difference in the daily activities functional scores (2.2 +/- 1 vs. 1.4 +/- 0.8) of TNS non-TNS patients during the first 24 h postoperatively.

Conclusions

There was no difference in the incidence of TNS between the 1% versus 5% spinal lidocaine groups. Pain scores were higher in patients with TNS than those who did not have TNS. During the first 48 h postop, a small proportion of patients who had TNS experienced functional impairment of walking, sitting, and sleeping.
Spinal Anesthesia
Authors: Imarengiaye Charles O. , Song Dajun , Prabhu Atul J. , Chung Frances
Published: November 2003

Background

The ability of patients to walk without assistance after spinal anesthesia is a determining factor in the time to discharge following ambulatory surgery. The authors compared clinical markers of gross motor recovery with objective data of functional balance after spinal anesthesia.

Methods

Twenty-two male patients with American Society of Anesthesiology physical status I or II who were scheduled for perineal surgery were studied during recovery from spinal anesthesia to compare the predictive accuracy of clinical markers of ambulatory readiness (e.g., full knee flexion and extension) with that of an objective method of measurement focused on functional balance. Lumbar puncture was performed at the L2-L3 or L3-L4 interspace using a 25-gauge Whitacre needle, with patients in the sitting position. A 3-ml mixture of 5 mg bupivacaine (heavy) and 10 microg fentanyl was injected. Block regression and restoration of motor function were assessed and recorded. Functional balance was measured using a computerized force platform method.

Results

The majority of patients maintained motor function and proprioception sensation at the onset of surgical anesthesia, as indicated by performance on clinical tests of function: 96% were able to perform the straight leg increase; 82, 77, and 91%, respectively, were able to perform full knee flexion and extension, perform heel-to-shin maneuvers, and identify joint position in the supine position. Postoperatively, clinical return of motor function occurred much earlier than recovery of functional balance. At 60 min after onset of spinal anesthesia, 22 patients (100%) had recovered sensory and gross motor function, but only 36% could stand, and 8% could walk without assistance (P < 0.01). At 150-180 min after onset, 96-100% of patients achieved the levels of functional balance that permitted adequate ambulation.

Conclusions

The results suggest that the recovery time to unassisted ambulation is longer than has been assumed, and that the standard clinical markers of gross motor function are poor predictors of functional balance following ambulatory surgery.
Do They Understand? (Part I)
Authors: Tait Alan R. , Voepel-Lewis Terri , Malviya Shobha
Published: November 2003

Background

Central to the tenet of informed consent is the quality of disclosure of information by the investigator and the understanding thereof by the research subject or his or her surrogate. This study was designed to measure parents' understanding of the elements of informed consent for clinical studies in which their children had been approached to participate.

Methods

The study sample consisted of 505 parents who had been approached for permission to allow their child to participate in a clinical anesthesia or surgery study. Regardless of whether the parent consented (consenters, n = 411) or declined (nonconsenters, n = 94) to their child's participation in a study, they were interviewed to determine their understanding of 11 elements of consent. Two independent assessors who were familiar with the study protocols scored the parents' levels of understanding.

Results

Parents perceived their overall understanding of the elements of consent as high (8.7 +/- 1.6; 0-10 scale); however, this represented a significant overestimation compared with the assessors' measures of parental understanding (7.3 +/- 1.8; P< 0.0001). Furthermore, consenters had greater understanding than nonconsenters (7.6 +/- 1.6 vs 6.1 +/- 1.9; P< 0.001). Several predictors of understanding were identified, including whether the parent consented, education level, clarity of disclosure, child in previous study, age of parent, parent listened to disclosure, and degree to which parent read the consent document. The day on which consent was sought had no impact on the level of understanding.

Conclusions

Parents approached for permission to allow their child to participate in a research study had less than optimal understanding of the elements of consent. As such, investigators must make every effort to enhance understanding and ensure that parents have sufficient information to make informed decisions regarding their child's participation in research studies.
Teaching with a Video System Improves the Training Period but Not Subsequent Success of Tracheal Intubation with the Bullard Laryngoscope
Authors: Shulman G. Brent , Nordin Ned G. , Connelly Neil Roy
Published: November 2003

Background

The Bullard laryngoscope is useful for the management of a variety of airway management scenarios. Without the aid of a video system, teaching laryngoscopy skills occurs with indirect feedback to the instructor. The purpose of this study was to determine if use of a video system would speed the process of learning the Bullard laryngoscope or improve the performance (speed or success) of its use.

Methods

Thirty-six anesthesia providers with no previous Bullard laryngoscope experience were randomly divided into two groups: initial training (first 15 intubations) with looking directly through the eyepiece (n = 20), or with the display of the scope on a video monitor (n = 16). The subjects each then performed 15 Bullard intubations by looking directly through the eyepiece.

Results

There was not an overall significant difference in laryngoscopy or intubation times between the groups. When only the first 15 intubations were considered, the laryngoscopy time was shorter in the video group (26 +/- 24) than in the nonvideo group (32 +/- 34; P< 0.04). In the first 15 patients, there were fewer single attempts at intubation (67.9% vs 80.3%; P< 0.002) and more failed intubations (17.2% vs 6.0%; P< 0.0001) in the nonvideo group.

Conclusions

In conclusion, the authors have shown that use of a video camera decreases time for laryngoscopic view and improves success rate when the Bullard laryngoscope is first being taught to experienced clinicians. However, these benefits are not evident as more experience with the Bullard laryngoscope is achieved, such that no difference in skill with the Bullard laryngoscope is discernible after 15 intubations whether a video system was used to teach this technique.
Redistribution of Microcirculatory Blood Flow within the Intestinal Wall during Sepsis and General Anesthesia
Authors: Hiltebrand Luzius B. , Krejci Vladimir , tenHoevel Marcus E. , Banic Andrej , Sigurdsson Gisli H.
Published: November 2003

Background

Hypoperfusion of the intestinal mucosa remains an important clinical problem during sepsis. Impairment of the autoregulation of microcirculatory blood flow in the intestinal tract has been suggested to play an important role in the development of multiple organ failure during sepsis and surgery. The authors studied microcirculatory blood flow in the gastrointestinal tract in anesthetized subjects during early septic shock.

Methods

Eighteen pigs were intravenously anesthetized and mechanically ventilated. Regional blood flow in the superior mesenteric artery was measured with ultrasound transit time flowmetry. Microcirculatory blood flow was continuously measured with a six-channel laser Doppler flowmetry system in the mucosa and the muscularis of the stomach, jejunum, and colon. Eleven pigs were assigned to the sepsis group, while seven animal served as sham controls. Sepsis was induced with fecal peritonitis, and intravenous fluids were administered after 240 min of sepsis to alter hypodynamic sepsis to hyperdynamic sepsis.

Results

In the control group, all monitored flow data remained stable throughout the study. During the hypodynamic phase of sepsis, cardiac output, superior mesenteric artery flow, and microcirculatory blood flow in the gastric mucosa decreased by 45%, 51%, and 40%, respectively, compared to baseline (P < 0.01 in all). Microcirculatory blood flow in the muscularis of the stomach, jejunum, and colon decreased by 55%, 64%, and 70%, respectively (P < 0.001 in all). In contrast, flow in the jejunal and colonic mucosa remained virtually unchanged. During the hyperdynamic phase of sepsis, there was a threefold increase in cardiac output and superior mesenteric artery flow. Blood flow in the gastric, jejunal, and colonic mucosa also increased (22%, 24%, and 31% above baseline, respectively). Flow in the muscularis of the stomach returned to baseline, while in the jejunum and colon, flow in the muscularis remained significantly below baseline (55% and 45%, respectively, P< 0.01).

Conclusions

It appears that in early septic shock, autoregulation of microcirculatory blood flow is largely intact in the intestinal mucosa in anesthetized pigs, explaining why microcirculatory blood flow remained virtually unchanged. This may be facilitated through redistribution of flow within the intestinal wall, from the muscularis toward the mucosa.
Neutrophils Pretreated with Volatile Anesthetics Lose Ability to Cause Cardiac Dysfunction
Authors: Hu Guochang , Vasiliauskas Tomas , Salem M. Ramez , Rhone Douglas P. , Crystal George J.
Published: November 2003

Background

Volatile anesthetics can precondition the myocardium against functional depression and infarction following ischemia-reperfusion. Neutrophil activation, adherence, and release of superoxide play major roles in reperfusion injury. The authors tested the hypothesis that pretreatment of neutrophils with a volatile anesthetic, i.e., simulated preconditioning, can blunt their ability to cause cardiac dysfunction.

Methods

Studies were performed in 60 buffer-perfused and paced isolated rat hearts. Left ventricular developed pressure served as an index of myocardial contractility. Polymorphonuclear neutrophils and/or drugs were added to coronary perfusate for 10 min, followed by 30 min of recovery. Platelet-activating factor was used to stimulate neutrophils. Pretreatment of neutrophils consisted of incubation with 1.0 minimum alveolar concentration (MAC) isoflurane or sevoflurane for 15 min, followed by washout. Additional studies were performed with 0.25 MAC isoflurane. Effects of superoxide dismutase were compared to those of volatile anesthetics. Superoxide production was measured by spectrophotometry. Neutrophil adherence to coronary vascular endothelium was estimated from the difference between neutrophils administered and recovered in coronary venous effluent.

Results

Activated neutrophils caused marked, persistent reduction (> 50%) in left ventricular developed pressure. Isoflurane and sevoflurane at 1.0 MAC and superoxide dismutase abolished this effect. Isoflurane and sevoflurane reduced superoxide production of activated neutrophils by 29% and 33%, respectively, and completely prevented the platelet-activating factor-induced increases in neutrophil adherence. Isoflurane at 0.25 MAC blunted, but did not abolish, the neutrophil-induced decreases in left ventricular developed pressure.

Conclusion

Neutrophils pretreated with 1.0 MAC isoflurane or sevoflurane lost their ability to cause cardiac dysfunction, while those pretreated with a concentration of isoflurane as low as 0.25 MAC were partially inhibited. This action of the volatile anesthetics was associated with reductions in superoxide production and neutrophil adherence to the coronary vascular endothelium. Our findings suggest that inhibitory actions on neutrophil activation and neutrophil-endothelium interaction may contribute to the preconditioning effects of volatile anesthetics observed in vivo during myocardial ischemia-reperfusion.
Assessment of the Lower Limit for Cerebral Perfusion Pressure in Severe Head Injuries by Bedside Monitoring of Regional Energy Metabolism
Authors: Nordström Carl-Henrik , Reinstrup Peter , Xu Wangbin , Gärdenfors Anna , Ungerstedt Urban
Published: November 2003

Background

In patients with severe traumatic brain lesions, the lower limit for cerebral perfusion pressure (CPP) is controversial. The aim of this prospective study was to assess this limit from bedside measurements of cerebral energy metabolism and to clarify whether the penumbra zone surrounding a focal lesion is more sensitive to a decrease in CPP than less-injured areas.

Methods

Fifty patients with severe head injury were included after evacuation of an intracranial hematoma and/or focal brain contusion. They were treated according to intensive care routine (Lund concept), including continuous monitoring of intracranial pressure. One microdialysis catheter was inserted in less-injured brain tissue ("better" position), and one or two catheters were inserted into the boundary of injured cerebral cortex ("worse" position). Concentrations of glucose, pyruvate, and lactate were analyzed and displayed bedside and were related to CPP (n = 29,495).

Results

Mean interstitial glucose concentration was unaffected by the level of the CPP within the studied ranges. Increases in lactate concentration (P = 0.0008) and lactate-pyruvate ratio (P = 0.01) were obtained in the "worse" but not in the "better" position at CPP less than 50 mmHg compared with the same positions at CPP greater than 50 mmHg.

Conclusions

The study results support the view that CPP may be reduced to 50 mmHg in patients with severe traumatic brain lesions, provided that the physiologic and pharmacologic principles of the Lund concept are recognized. In the individual patient, preservation of normal concentrations of energy metabolites within cerebral areas at risk can be guaranteed by intracerebral microdialysis and bedside biochemical analyses.
Influence of Erythrocyte Concentrate Storage Time on Postsurgical Morbidity in Cardiac Surgery Patients
Authors: Leal-Noval Santiago R. , Jara-López Irene , García-Garmendia José L. , Marín-Niebla Ana , Herruzo-Avilés Angel , Camacho-Laraña Pedro , Loscertales Jesús
Published: November 2003

Background

The transfusion of erythrocytes that have been stored for long periods of time can produce visceral ischemia and favor the acquisition of postsurgical infections. To estimate the role of the duration of storage of erythrocytes on morbidity in cardiac surgery, we performed an observational study.

Methods

All patients (n = 897) undergoing cardiac surgery during three consecutive years were included. Morbidity (main outcome measure) was evaluated by means of four surrogate measures: duration of stay in the intensive care unit longer than 4 days, mechanical ventilation time longer than 1 day, perioperative myocardial infarction rate, and severe postoperative infection rate. The mean duration of storage of all erythrocytes transfused and the duration of storage of the oldest unit transfused were used as storage variables.

Results

After considering multiple confounding variables related to patient severity, illness, and surgical difficulty, the duration of storage of erythrocytes was found to be associated neither with a more prolonged stay in the intensive care unit or mechanical ventilation time nor with increased rates of perioperative infarction, mediastinitis, or sepsis. However, each day of storage of the oldest unit was associated with an increment of the risk of pneumonia of 6% (95% confidence interval, 1-11; P = 0.018). The cutoff point of maximum sensitivity and specificity (54.8 and 66.9%) associated with a greater risk for pneumonia corresponded to 28 days of storage for the oldest unit (odds ratio, 2.74; 95% confidence interval, 1.18-6.36; P = 0.019).

Conclusions

Prolonged storage of erythrocytes does not increase morbidity in cardiac surgery. However, storage for longer than 28 days could be a risk factor for the acquisition of nosocomial pneumonia.
The Effects of Hydration on Core Temperature in Pediatric Surgical Patients
Authors: Ezri Tiberiu , Szmuk Peter , Weisenberg Marian , Serour Francis , Gorenstein Arcadi , Sessler Daniel I.
Published: November 2003

Background

Reduced vascular volume might influence body temperature by diverting heat flow from peripheral tissues to the central organs. We therefore tested the hypothesis that mild hypovolemia helps to prevent intraoperative hypothermia in pediatric patients.

Methods

Twenty-two pediatric patients (aged 1-3 yr) undergoing prolonged minor surgery were randomly assigned to conservative (n = 12) or aggressive (n = 10) perioperative fluid management. The conservative group fasted 8 h before surgery and received a crystalloid at 1 ml. kg-1. h-1 during surgery. The aggressive group was allowed to drink liquids until 3 h before surgery and was given a maintenance crystalloid at 8 ml. kg-1. h-1. Anesthesia was induced and maintained with halothane in nitrous oxide. Ambient temperature was kept near 25 degrees C, but the patients were not actively warmed. During recovery from anesthesia, additional fluid was given to the conservative group so that perioperative fluid totaled 9.5 ml. kg-1. h-1 in both groups.

Results

Intraoperative body weight remained unchanged in the aggressive group and decreased only 1% in patients managed conservatively. Heart rate was slightly greater in the conservative group (107 +/- 9 vs. 95 +/- 4 beats/min, P = 0.002), but blood pressure was similar. Esophageal temperature in patients whose fluid was managed conservatively increased significantly, by 0.4 +/- 0.3 degrees C, to 37.1 degrees C; in contrast, temperature in the aggressive group decreased significantly, by 0.4 +/- 0.2 degrees C, to 36.4 degrees C (P < 0.001 between groups). Temperatures remained significantly different 1 h after surgery.

Conclusions

Conservative fluid management, which decreased body weight by only 1%, prevented reduction in core body temperature, presumably by reducing dissipation of metabolic heat from the core thermal compartment to peripheral tissues.
Neuraxial Morphine May Trigger Transient Motor Dysfunction after a Noninjurious Interval of Spinal Cord Ischemia
Authors: Kakinohana Manabu , Marsala Martin , Carter Christopher , Davison J. Kenneth , Yaksh Tony L.
Published: November 2003

Background

A patient underwent repair of a thoracoabdominal aortic aneurysm. Epidural morphine, 4 mg, was given for pain relief. After anesthesia, the patient displayed lower extremity paraparesis. This effect was reversed by naloxone. The authors sought to confirm these observations using a rat spinal ischemia model to define the effects of intrathecal morphine administered at various times after reflow on behavior and spinal histopathology.

Methods

Spinal cord ischemia was induced for 6 min using an intraaortic balloon. Morphine or saline, 30 microg, was injected intrathecally at 0.5, 2, or 24 h after reflow. In a separate group, spinal cord temperature was decreased to 27 degrees C before ischemia. After ischemia, recovery of motor function was assessed periodically using the motor deficit index (0 = complete recovery; 6 = complete paraplegia).

Results

After ischemia, all rats showed near-complete recovery of function by 4-6 h. Intrathecal injection of morphine at 0.5 or 2 h of reflow (but not at 24 h) but not saline caused a development of hind limb dysfunction and lasted for 4.5 h (motor deficit index score = 4-6). This effect was reversed by intrathecal naloxone (30 microg). Intrathecal morphine administered after hypothermic ischemia was without effect. Histopathological analysis in animals that received intrathecal morphine at 0.5 or 2 h after ischemia (but not at 24 h) revealed dark-staining alpha motoneurons and interneurons. Intrathecal saline or spinal hypothermia plus morphine was without effect.

Conclusions

These data indicate that during the immediate reflow following a noninjurious interval of spinal ischemia, intrathecal morphine potentiates motor dysfunction. Reversal by naloxone suggests that this effect results from an opioid receptor-mediated potentiation of a transient block of inhibitory neurons initiated by spinal ischemia.