摘要:

BackgroundSmoking changes numerous alveolar macrophage functions and is one of the most important risk factors for postoperative pulmonary complications. The current study tested the hypothesis that smoking impairs antimicrobial and proinflammatory responses in alveolar macrophages during anesthesia and surgery.MethodThe authors studied 30 smoking and 30 nonsmoking patients during propofol–fentanyl general anesthesia. Alveolar immune cells were harvested by bronchoalveolar lavage immediately and 2, 4, and 6 h after induction of anesthesia and at the end of surgery. The types of alveolar immune cell and macrophage aggregation were determined. The authors measured opsonized and unopsonized phagocytosis. Microbicidal activity was determined as the ability of the macrophages to killListeriamonocytogenes directly. Finally, RNA was extracted from harvested cells and cDNA was synthesized by reverse transcription. The expression of interleukin 1&bgr;, 6, and 8, interferon &ggr;, and tumor necrosis factor &agr; were measured by semiquantitative polymerase chain reaction using &bgr;-actin as an internal standard.ResultsThe fraction of aggregated macrophages increased significantly over time in both groups, whereas phagocytosis of opsonized and nonopsonized particles and microbicidal activity of alveolar macrophages decreased significantly. The changes, though, were nearly twice as great as in patients who smoked. Gene expression of all proinflammatory cytokines in alveolar immune cells except interleukin 6 increased 2- to 20-fold over time in both groups. The expression of interleukin 1&bgr;, interferon &ggr;, and tumor necrosis factor &agr;, however, increased only half as much in smokers as in nonsmokers.ConclusionSmoking was associated with macrophage aggregation but markedly reduced phagocytic and microbicidal activity—possibly because expression of proinflammatory cytokines was reduced in these patients. Our data thus suggest that smokers may have a limited ability to mount an effective pulmonary immune defense after anesthesia and surgery.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundRegional anesthesia and especially peribulbar anesthesia commonly is used for cataract surgery. Failure rates and need for reinjection remains high, however, with peribulbar anesthesia. Single-injection high-volume medial canthus episcleral (sub–Tenon’s) anesthesia has proven to be an efficient and safe alternative to peribulbar anesthesia.MethodsThe authors, in a blind study, compared the effectiveness of both techniques in 66 patients randomly assigned to episcleral anesthesia or single-injection peribulbar anesthesia. Motor blockade (akinesia) was used as the main index of anesthesia effectiveness. It was assessed using an 18-point scale (0–3 for each of the four directions of the gaze, lid opening, and lid closing, the total being from 0 = normal mobility to 18 = no movement at all). This score was compared between the groups 1, 5, 10, and 15 min after injection and at the end of the surgical procedures. Time to onset of the blockade also was compared between the two groups, as was the incidence of incomplete blockade with a need for supplemental injection and the satisfaction of the surgeon, patient, and anesthesiologist.ResultsEpiscleral anesthesia provided a quicker onset of anesthesia, a better akinesia score, and a lower rate of incomplete blockade necessitating reinjection (0 vs. 39%;P< 0.0001) than peribulbar anesthesia. Even after supplemental injection, peribulbar anesthesia had a lower akinesia score than did episcleral anesthesia. Peribulbar anesthesia began to wear off during surgery, whereas episcleral anesthesia did not.ConclusionMedial canthus single-injection episcleral anesthesia is a suitable alternative to peribulbar anesthesia. It provides better akinesia, with a quicker onset and more constancy in effectiveness.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundNonsurgical patients with sinus node dysfunction are at high risk for atrial tachyarrhythmias, but whether a similar relation exists for atrial fibrillation after coronary artery bypass graft surgery is not clear. The purpose of this study was to evaluate sinus nodal function before and after coronary artery bypass graft surgery and to evaluate its relation with the risk for postoperative atrial arrhythmias.MethodsSixty patients without complications having elective coronary artery bypass graft surgery underwent sinus nodal function testing by measurement of sinoatrial conduction time (SACT) and corrected sinus nodal recovery time (CSNRT). Patients were categorized based on whether postoperative atrial fibrillation developed.ResultsTwenty patients developed atrial fibrillation between postoperative days 1 through 3. For patients remaining in sinus rhythm (n = 40), sinoatrial conduction times were no different and corrected sinus nodal recovery times were shorter after surgery when compared with measurements obtained after anesthesia induction. Sinus node function test results before surgery were similar between the sinus rhythm and the atrial fibrillation groups. After surgery, patients who later developed atrial fibrillation had longer sinoatrial conduction times compared with the sinus rhythm group (P = 0.006), but corrected sinus nodal recover time was not different between these groups. A sinoatrial conduction time > 96 ms measured at this time point was associated with a 7.3-fold increased risk of postoperative atrial fibrillation (sensitivity, 62%; specificity, 81%; positive and negative predictive values, 56% and 85%, respectively; area under the receiver operator characteristic curve, 0.72).ConclusionsThese data show that sinus nodal function is not adversely affected by uncomplicated coronary artery bypass surgery. Patients who later developed atrial fibrillation, however, had prolonged sinoatrial conduction immediately after surgery compared with patients remaining in sinus rhythm. These results suggest that injury to atrial conduction tissue at the time of surgery predisposes to postoperative atrial fibrillation and that assessment of sinoatrial conduction times could provide a means of identifying patients at high risk for postoperative atrial fibrillation.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundAcoustic reflectometry can be used to create a “one-dimensional image” of a cavity, such as the airway and lung, with the image displayed as an area–length curve. This pilot study was undertaken to determine whether acoustic reflectometry could be used to distinguish between an endotracheal and an esophageal intubation.MethodsTen adult patients underwent general endotracheal anesthesia and neuromuscular blockade. The reflectometer wavetube was attached to an endotracheal tube, and a reflectometric profile was obtained of the endotracheal tube and the airway and lung cavity. After confirmation of tracheal intubation, a second endotracheal tube was placed in the esophagus. After four breaths were administered, a reflectometric profile of the endotracheal tube–esophagus cavity was obtained.ResultsThe acoustic reflectometric profiles for tracheal and esophageal intubation profiles were distinctive and characteristic. For an endotracheal tube–airway cavity, the profile shows a constant cross-sectional area throughout the length of the endotracheal tube, followed by a rapid rise in the area past the carina. For an esophageal intubation, the profile shows constant cross-sectional area throughout the length of the endotracheal tube, followed by a sudden decrease in the cross-sectional area to zero.ConclusionsIn this pilot study, acoustic reflectometry within seconds, and without resort to capnography, was able to generate characteristic and distinctive area–length profiles for both endotracheal and esophageal intubation. Acoustic reflectometry may have a role in the emergency imaging of the airway, and in the immediate detection of esophageal intubations, particularly in cases of cardiopulmonary arrest in which the usual techniques for confirmation of breathing tube placement fail.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundMidlatency auditory evoked potentials (MLAEP) show graded changes with increasing doses of hypnotics but little change with opioids. The effect of their combination on the MLAEP was evaluated. Also, the bispectral index (BIS) was compared with the ability of MLAEP to correlate with sedation and predict loss of consciousness.MethodsTwenty healthy volunteers were randomly assigned to receive stepped increases in propofol concentration (10 subjects) or propofol plus alfentanil 100 ng/ml (10 subjects). At baseline and at each targeted effect site concentration the mean MLAEP, BIS, measures of sedation, and drug concentration were obtained. The relation among MLAEP, BIS, and sedation score was determined. The prediction probability (Pk) was calculated and compared for BIS and MLAEP.ResultsThe BIS and MLAEP patterns showed significant changes (Pa and Nb decreased in amplitude and increased in latency) with increasing level of sedation (P< 0.0001). The BIS correlated better with sedation scores (0.884) than did the MLAEP (P< 0.05). Pa and Nb latencies showed the best correlation with sedation levels (0.685 and 0.658, respectively). The addition of alfentanil did not affect the relation between MLAEP and loss of consciousness (P> 0.15). The BIS (Pk= 0.952) was a better predictor of loss of consciousness than were Pa and Nb amplitude (P< 0.05) but were comparable to Pa and Nb latency (Pk= 0.869 and 0.873, respectively).ConclusionMLAEP changes, like the BIS, correlate well with increasing sedation produced by propofol, and these changes in the MLAEP are independent of the presence of an opioid. Among all the MLAEP parameters, Pa and Nb latencies are the best predictors of increasing sedation and loss of consciousness.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundCore hypothermia develops after the induction of general anesthesia, but intraoperative vasoconstriction usually prevents its progression. However, diabetes mellitus is often associated with autonomic neuropathy, which leads to abnormal peripheral neurovascular function. Accordingly, we tested the hypothesis that diabetic patients experience a greater reduction in core temperature during general anesthesia than nondiabetic patients.MethodsWe studied 36 nondiabetic patients (control group) and 27 diabetic patients (diabetic group) undergoing elective abdominal surgery. Both groups were divided into young (< 60 yr) and older age (≥ 60 yr) groups. Standard noninvasive autonomic tests (heart rate variation at deep periodical breathing, Valsalva maneuver, and head-up tilt) were carried out for each patient. The relation between the results of these tests of autonomic function and the tympanic membrane temperature during general anesthesia was assessed in relation to peripheral vasoconstriction.ResultsThirteen patients in the diabetic group showed abnormal responses to two or more of the basal autonomic function tests (patients with autonomic dysfunction). Changes in core temperature among the groups were similar at 90 min after the induction of anesthesia. However, the core temperature of the diabetic patients with autonomic dysfunction was lower from 120 min (35.1°C) onward compared with the young or older nondiabetic patients and the diabetic patients with normal autonomic function. Peripheral vasoconstriction, evaluated using the forearm–fingertip skin surface temperature gradient, was delayed in patients with autonomic dysfunction compared with the others.ConclusionsThe current results indicate that diabetic autonomic neuropathy is associated with more severe intraoperative hypothermia. We postulate that diabetic patients become more hypothermic because their peripheral neuropathy delays the onset of thermoregulatory vasoconstriction and reduces its efficacy once triggered. These patients may therefore fail to develop a normal core temperature plateau.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThe influence of spread of spinal anesthesia on the duration of spinal blockade has been suggested but never investigated specifically. Because elimination of local anesthetic from subarachnoid space is probably dependent of the surface available for its diffusion and vascular absorption, the current study was designed to evaluate the hypothesis that with a same dose of hyperbaric bupivacaine, a higher anesthetic level would result in a shorter duration of spinal blockade than a lower level.MethodsThree milliliters (15 mg) of hyperbaric bupivacaine, 0.5%, was injected intrathecally in 40 patients classified as American Society of Anesthesiologists physical status I or II scheduled for lower limb surgery during spinal anesthesia. To obtain significantly different anesthetic levels, the patients were positioned randomly either horizontally or with the torso elevated 30°. Regression of sensory level and motor blockade, the appearance of pain at the operative site, and hemodynamic changes were evaluated.ResultsThe maximum cephalad spread of sensory blockade (expressed as the median with ranges in parentheses) was significantly higher in the horizontal group than in the group with 30-degree elevation of the torso,i.e., T3.5 (T1–T9)versusT10 (T6–L1), with respectively significantly faster regression times (mean ± SD) by two segments (216 ± 46 minvs.253 ± 64 min) and to segment L4 (269 ± 53 minvs.337 ± 58 min), as well as shorter time to complete motor blockade recovery (173 ± 34 minvs.233 ± 58 min) and faster appearance of pain at the operative site (221 ± 68 minvs.271 ± 56 min).ConclusionThe results indicate that with the same dose of hyperbaric bupivacaine, the duration of spinal blockade is longer in patients with restricted spread.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThe authors hypothesized that patients with cerebrovascular abnormalities or metabolic disorders may experience abnormality in cerebral circulation more frequently than patients without these risks. The current study attempted to assess jugular venous bulb oxygen saturation (SjvO2) in patients with preexisting diabetes mellitus or stroke undergoing normothermic cardiopulmonary bypass.MethodsThirty-nine patients undergoing elective coronary artery bypass graft surgery were studied, including 19 age-matched control patients, 10 diabetic patients, and 9 patients with preexisting stroke A 4.0-French fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to continuously monitor internal SjvO2. Hemodynamic parameters and arterial and jugular venous blood gases were measured at seven time points: (1) after the induction of anesthesia and before the start of surgery, (2) just after the beginning of cardiopulmonary bypass, (3) 20 min after the beginning of bypass, (4) 40 min after the beginning of bypass, (5) 60 min after the beginning of bypass, (6) just after the cessation of bypass, and (7) at the end of the operation.ResultsNo significant differences were seen in mean arterial pressure, arterial carbon dioxide tension (PaCO2), or hemoglobin concentration among the three groups during the study. The SjvO2value did not differ among the three groups after anesthesia induction and before surgery, just after the beginning of cardiopulmonary bypass, 60 min after the beginning of bypass, just after the end of bypass, or at the end of the operation. Significant differences between the control group and the diabetic and stroke groups were observed, however, at 20 min and 40 min after the beginning of bypass (at 20 min: control group 62.2 ± 6.8%, diabetes group 48.4 ± 5.1%, stroke group 45.9 ± 6.3%; at 40 min: control group 62.6 ± 5.2%, diabetes group 47.1 ± 5.2%, stroke group 48.8 ± 4.1% [values expressed as the mean ± SD];P< 0.05). Also, values in the diabetes and stroke groups were decreased at 20 min and 40 min after the beginning of bypass compared with before the start of surgery.ConclusionsA reduced SjvO2value was observed more frequently in patients with preexisting diabetes mellitus or stroke during normothermic cardiopulmonary bypass. It is possible that cerebral circulation during normothermic bypass is altered in patients with risk factors for cerebrovascular disorder.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundBody temperature often is ignored during regional anesthesia, despite evidence that hypothermia occurs commonly. Because hypothermia is associated with adverse clinical outcomes, it is important to recognize predictors of hypothermia and to monitor and control body temperature in patients at risk. The current study was designed to determine the predictors of core hypothermia in patients receiving spinal anesthesia for radical retropubic prostatectomy.MethodsForty-four patients undergoing radical retropubic prostatectomy were studied. A lumbar intrathecal injection of 18–22 mg bupivacaine, 0.75%, with 20 &mgr;g fentanyl was given. No active warming measures were used other than intravenous fluid warming. The following clinical variables were assessed as potential predictors of core (tympanic) temperature at admission to the postanesthesia care unit: duration of surgery, average ambient operating room temperature, body habitus, age, and spinal blockade level.ResultsThe mean core temperature at admission to the postanesthesia care unit was 35.1 ± 0.6°C (range, 33.6–36.3°C). Duration of surgery, ambient operating room temperature, and body habitus were not predictors of hypothermia. A high level of spinal blockade and increasing age were predictors of hypothermia. For each incremental increase in block level, core temperature decreased by 0.15°C, and for each increase in age, core temperature decreased by 0.3°C.ConclusionsAlthough high-level spinal blockade has been associated with decreased thermoregulatory thresholds, no previous study has shown that a higher level of blockade is associated with a greater magnitude of core hypothermia in the clinical setting. As with general anesthesia, advanced age is associated with hypothermia during spinal anesthesia.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundSeveral investigations have shown that volatile anesthetics can reduce ischemic cerebral injury. In these studies, however, neurologic injury was evaluated only after a short recovery period. Recent data suggest that injury caused by ischemia is a dynamic process characterized by continual neuronal loss for a prolonged period. Whether isoflurane-mediated neuroprotection is sustained after a longer recovery period is not known. The current study was conducted to compare the effect of isoflurane on brain injury after short (2-day) and long (14-day) recovery periods in rats subjected to focal ischemia.MethodsFasted Wistar-Kyoto rats were anesthetized with isoflurane and randomly allocated to an awake (n = 36) or an isoflurane (n = 34) group. Animals in both groups were subjected to focal ischemia by filament occlusion of the middle cerebral artery. Pericranial temperature was servocontrolled at 37°C throughout the experiment. In the awake group, isoflurane was discontinued and the animals were allowed to awaken. In the isoflurane group, isoflurane anesthesia was maintained at 1.5 times the minimum alveolar concentration. After 70 min of focal ischemia, the filament was removed. Animals were killed 2 days (awake, n = 18; isoflurane, n = 17) and 14 days (awake, n = 18; isoflurane, n = 17) after ischemia. The volumes of cerebral infarction and selective neuronal necrosis in the animals were determined by image analysis of hematoxylin and eosin–stained coronal brain sections.ResultsCortical and subcortical volumes of infarction were significantly less in the isoflurane 2-day group (26 ± 23 mm3and 17 ± 6 mm3, respectively) than in the awake 2-day group (58 ± 35 mm3,P< 0.01; and 28 ± 12 mm3,P< 0.01, respectively). By contrast, cortical and subcortical volumes of infarction in the awake (41 ± 31 mm3and 28 ± 16 mm3, respectively) and isoflurane (41 ± 35 mm3and 19 ± 8 mm3, respectively) 14-day groups were not different (cortex,P= 0.99; subcortex,P= 0.08). The volume of cortical tissue in which selective neuronal necrosis was observed, however, was significantly less in the isoflurane 14-day group (5 ± 4 mm3) than in the awake 14-day group (17 ± 9 mm3,P< 0.01). The total number of necrotic neurons in the region of selective neuronal necrosis was significantly smaller in the isoflurane 14-day group than in the awake 14-day group (P< 0.01).ConclusionCompared with the awake state, isoflurane reduced the extent of infarction assessed 2 days after focal ischemia in rats. At 14 days, however, only selective neuronal necrosis, but not infarction, was reduced by isoflurane. These results suggest that isoflurane delays but does not prevent cerebral infarction caused by focal ischemia. Isoflurane may attenuate the delayed development of selective neuronal necrosis in periinfarct areas in this animal model.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID