| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
 
|
|
|
||
|
|
Anesth Analg 2007;104:51-58 © 2007 International Anesthesia Research Society doi: 10.1213/01.ane.0000246814.29362.f4
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
Abstract |
|---|
 Top Abstract IntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
BACKGROUND: Cerebral deoxygenation is associated with various adverse systemic outcomes. We hypothesized, by using the brain as an index organ, that interventions to improve cerebral oxygenation would have systemic benefits in cardiac surgical patients.
METHODS: Two-hundred coronary artery bypass patients were randomized to either intraoperative cerebral regional oxygen saturation (rSO2) monitoring with active display and treatment intervention protocol (intervention, n = 100), or underwent blinded rSO2 monitoring (control, n = 100). Predefined clinical outcomes were assessed by a blinded observer.
RESULTS: Significantly more patients in the control group demonstrated prolonged cerebral desaturation (P = 0.014) and longer duration in the intensive care unit (P = 0.029) versus intervention patients. There was no difference in overall incidence of adverse complications, but significantly more control patients had major organ morbidity or mortality (death, ventilation >48 h, stroke, myocardial infarction, return for re-exploration) versus intervention group patients (P = 0.048). Patients experiencing major organ morbidity or mortality had lower baseline and mean rSO2, more cerebral desaturations and longer lengths of stay in the intensive care unit and postoperative hospitalization, than patients without such complications. There was a significant (r2 = 0.29) inverse correlation between intraoperative rSO2 and duration of postoperative hospitalization in patients requiring 
10 days postoperative length of stay.
CONCLUSION: Monitoring cerebral rSO2 in coronary artery bypass patients avoids profound cerebral desaturation and is associated with significantly fewer incidences of major organ dysfunction.
|
Introduction |
|---|
|
TopAbstractIntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
The increasing age and incidence of preoperative comorbidity in patients presenting for coronary artery bypass (CAB) surgery increases the potential for stroke and other adverse perioperative outcomes (1). While the etiology of such adverse outcomes are multifactorial and incompletely understood, the interaction of embolic events and hypoperfusion in patients with cerebrovascular and systemic atherosclerotic disease can profoundly influence the response and viability of various organ systems. In several series it has been shown that >50% of patients presenting for CAB surgery have significant intracranial or extracranial disease (2,3).
The use of near-infrared reflectance spectroscopy (NIRS) for assessment of bifrontal regional cortical oxygen saturation (rSO2) has demonstrated correlation between CAB patients having low rSO2 values and cognitive dysfunction (4), prolonged hospital length of stay (LOS) (5), and most recently, perioperative cerebrovascular accident (CVA) (6). The cerebral oximeter used in this study has been cleared by the United States Food and Drug Administration for monitoring cerebral oxygen saturation (7), and in a range of patients and subjects, episodic and cumulative cerebral deoxygenation has been shown to correlate with a variety of adverse systemic outcomes. These include renal failure,1 overall well-being (8), prolonged ventilation (6,9), physical work load (10), nausea and vomiting (11),2 altitude sickness (12), cerebral functional activation testing (13), isocapnic hypoxia (14), and cardiac output (15). Dunham et al. (16) showed that cerebral oximeter readings correlated with cerebral perfusion pressure, Glasgow Outcome Score, and mortality in patients with traumatic brain injuries, and several other groups have demonstrated the ability of the device to provide an early warning of cerebral ischemia (17–19).
Given the above correlations between cerebral rSO2 and systemic outcomes, and because most of the intraoperative measures taken to optimize cerebral rSO2 potentially influence systemic perfusion (e.g., alterations in Paco2, flow rates, arterial blood pressure, etc.), we postulated, by using the brain as the index organ, that the majority of interventions to optimize cerebral oxygen saturation would have a beneficial systemic effect for enhancing global tissue perfusion and potentially improve outcomes. We therefore hypothesized that use of intraoperative NIRS monitoring with a predetermined treatment protocol designed to minimize decreases from baseline rSO2 values would result in improved outcomes in elective patients undergoing CAB surgery.
|
METHODS |
|---|
|
TopAbstractIntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
After IRB approval and obtaining written informed consent, patients were enrolled between September 2002 and April 2004. On the basis of inclusion criteria of age >18 yr, scheduled for primary elective CAB surgery with use of cardiopulmonary bypass (CPB), patients were recruited from the preoperative clinic with agreement and participation of all site-based cardiac surgeons, anesthesiologists, and all perfusionists. Patients were not routinely preoperatively screened for evidence of carotid artery disease.
Upon arrival in the operating room (OR) the randomization envelope was opened and patients were assigned into either active treatment (intervention) or control (control) groups with cerebral oximetry monitoring using NIRS bilaterally (Invos 5100; Somanetics Corporation, Troy, MI) (7). After cleansing of the adjacent skin area with alcohol, an adhesive optode pad was placed over each fronto-temporal area. Resting baseline rSO2 values were obtained after waiting at least 1 min after placement of sensors once values had stabilized, with patients resting quietly and receiving 3–5 L of O2/min by nasal cannula. In the control group, the screen was electronically blinded and continuously recorded after verification of adequate signal strength and baseline values were calculated post hoc by taking the average of data over 1 min, 3 min after beginning recording. For the intervention group, an alarm threshold at 75% of the resting baseline rSO2 value was established. Continuous rSO2 values were stored on a floppy disk with a 15 s update for the duration of the intraoperative period. With application of the chest dressing, and before leaving the OR, monitoring was discontinued and optodes were removed.
After standardized premedication with 2 mg lorazepam SL, administration of supplemental O2, and titrated doses of midazolam (0.02–0.09 mg/kg), and after application and/or insertion of all routine monitors, including pulse oximetry, electrocardiogram, arterial and pulmonary artery manometry catheters, all patients were anesthetized with a narcotic-inhaled fast-track technique using fentanyl 10–30 µg/kg, isoflurane, and rocuronium for neuromuscular blockade, with a goal of early postoperative tracheal extubation. After induction of anesthesia, a urinary catheter and rectal and nasopharyngeal temperature probes were placed. Anesthetic management of clinical variables including heart rate, arterial blood pressure, ventilation, systemic oxygen saturation, temperature, depth of anesthesia, and related variables were done according to best clinical practice at the discretion of the attending anesthesiologist. Transesophageal echocardiography was performed routinely in all patients.
After administration of an initial bolus of heparin of 300–400 IU/kg to maintain activated clotting time above 480 s, and after either palpation or epiaortic scanning of the ascending aorta at the discretion of the attending surgeon, the ascending aorta was cannulated using a no. 21 Sarns® cannula with a single two-stage atrial cannula used for venous drainage. CPB was conducted using a 40-µm arterial line filter (Pall Biomedical, East Hills, NY), a nonsurface-modified membrane oxygenator with Capiox SX-18® integrated venous and cardiotomy reservoir, having a prime volume of 1750 mL, comprised of 500 mL Pentaspan®, 250 mL 20% mannitol, 1 L Ringer’s lactate solution, 5000 IU heparin, and 50 mEq NaHCO3, using a nonocclusive roller pump (Cobe Stockert®) and in- line monitoring of venous saturation and hematocrit (Hct). Aspirated cardiotomy blood was returned to the integrated cardiotomy reservoir during CPB. Steroids were not administered intraoperatively and aprotinin administration was at the discretion of attending physicians (Table 2). Flow rates of 2.0–2.5 L/min/m2 were used with rectal temperature maintained in 32°C–35°C "tepid" range during alpha-stat pH management and maintaining Pao2 in the range of 150–200 mm Hg. Combinations of antegrade and retrograde cold blood cardioplegia with a potassium concentration of 20 mEq/L were used for myocardial protection after application of aortic cross-clamp. Proximal anastamoses were performed either using a single aortic cross-clamp or with a separate application of a partial occlusion clamp to the aorta as shown in Table 2. A minimum concentration of isoflurane 0.5% (range: 0.5%–2.5%) was titrated continuously by vaporizer during CPB for anesthesia and to maintain mean arterial blood pressure (MAP) within 50–90 mm Hg. During CPB, activated clotting time, blood gases, Hct, glucose, and electrolyte values were analyzed for an average of four times: within 5 min after institution of CPB, after administration of cardioplegia, after 60 min of CPB, and before separation from CPB, or more frequently as clinically indicated. For all patients, best clinical practices aimed at maintenance of Hct 20%, blood glucose within the institutional normal range (3.4–11 mmol/L), MAP >50 mm Hg, and central venous pressure <10 mm Hg, were used specifically during CPB and throughout the intraoperative period. During rewarming arterial inflow temperatures did not exceed 37°C. A majority of patients were maintained with an infusion of 40–80 µg/kg/min propofol from chest closure until postoperative tracheal extubation in the intensive care unit (ICU).
|
In the intervention group, a prioritized intraoperative management protocol was used to maintain rSO2 values at or above 75% of the baseline threshold. With a decrease in rSO2, patient’s head position was checked to ensure that it had not been inadvertently rotated and the face was observed to detect plethora. If Paco2 or end-tidal CO2 was <35 mm Hg during positive pressure ventilation, ventilation was reduced to achieve Paco2 40 mm Hg. During CPB, alpha-stat management was used and if Paco2 was <40 mm Hg, steps were taken to increase it to 40 mm Hg by adjusting the oxygenator fresh gas sweep speed. If MAP was <50 mm Hg, 40 µg increments of phenylephrine were administered to achieve an MAP >60 mm Hg. If jugular venous pressure was >10 mm Hg during distal anastamoses, the heart was repositioned or MAP was increased to maintain cerebral perfusion pressure >50 mm Hg. If cardiac index was <2.0 L/m2/min the pump flow was increased to 2.5 L/m2/min. In patients with persistent rSO2 below treatment threshold Fio2 was increased, pulsatile perfusion was initiated, or propofol 50–100 mg bolus was administered. If Hct was below 20% red blood cell transfusion was administered.
Cerebral oximetry monitoring was discontinued in the OR. To maintain postoperative blinding, no study group identifiers were included with the patient or in the patients’ charts. Postoperatively, all patients were transferred to an autonomous, protocol-driven, "closed" ICU, under the exclusive care of ICU physicians without direct reference to the attending surgeons or anesthesiologists. Criteria for discharge from the ICU comprised (a) hemodynamic stability defined as absence of IV inotropic drugs, removal of arterial and pulmonary artery or central venous catheters, and absence of unstable arrhythmias; (b) postextubation respiratory adequacy with maintenance of SaO2 >95% on 
5 L supplemental O2, and chest tube drainage <10 mL/h for 3 h with absence of air leak; (c) level of consciousness sufficient to protect the airway; and (d) urinary output 0.5 mL/kg/h.
As listed in Table 3, data on perioperative complications were compiled and registered concomitantly by an independent blinded observer using the same variables as modeled after the Society of Thoracic Surgeons (STS) database registry (1). These data included new, persistent Q-wave myocardial infarction, clinical stroke manifested as focal neurologic deficit persisting >24 h and confirmed by brain computed tomography imaging, prolonged ventilation defined as extubation >24 h and >48 h postoperatively, dialysis-dependent renal failure, re-exploration for bleeding, reoperation for any cause, arrhythmia requiring treatment, wound infection requiring specific antibiotic coverage, readmission to hospital within 30 days, or death. Data on ICU admission and discharge times, and tracheal extubation time in hours were obtained from the independent ICU database.
|
Sample size was based upon a projected incidence of overall postoperative complications of 40% as derived from unpublished results from a large study in a similar cardiac surgical population (6). As an a priori assumption, we hypothesized that a 50% reduction in the incidence of overall complications would be associated with active NIRS cerebral oximetry, and accepting P < 0.05 for statistical significance and a ß error of 0.2, we determined that 97 patients in each group were required for this study. Randomization was by means of sealed opaque envelopes assigning treatment allocation and placed in computer-generated random order which were drawn in sequence as each patient was enrolled in the study and were opened in the OR at the time of surgery.
Cerebral desaturation was defined as a decrease in saturation values below 70% of baseline for 1 min or longer (20). To minimize the probability of patients reaching these levels, interventions to improve cerebral oxygenation were administered when rSO2 decreased to <75% of baseline for >15 s. Mean and minimum values of rSO2, as well as area under the curve of rSO2 values <75% of baseline (AUCrSO2 <75% baseline) and AUC of rSO2 values less than absolute 40% (AUCrSO2 <40%) were determined. An index of the degree and duration of desaturations was determined by examining the incidence of prolonged desaturations where the AUC of rSO2 values <70% of baseline was >150% minute duration (AUCrSO2 <70% baseline >150% min).
Categorical values are presented as numbers (percentage) and were analyzed using contingency table analysis, Fisher’s exact test, 
2, and Wilcoxon’s rank sum tests as appropriate. Continuous variables are presented as mean ± sd using unpaired t-test or ANOVA for analysis with P < 0.05 required for statistical significance. Bonferroni correction was applied to P value if multiple comparisons of data were made.
|
RESULTS |
|---|
|
TopAbstractIntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
A total of 206 patients provided written informed consent but, because of emergency surgery (n = 2) or lack of technical support (n = 4), 200 patients were randomized and had rSO2 monitors applied. The primary analysis undertaken was "intent-to-treat" without exclusion of any patients once randomization had occurred. As shown in Table 1, the mean age of patients in each group was similar, and there were no significant differences in preoperative demographic or morphometric data, or in individual or cumulative categorical risk factors for cardiovascular, respiratory, renal, or neurologic events.
|
As shown in Table 2, the number of distal anastamotic grafts was similar between groups, and six patients (intervention = 2, C = 4; P = 0.682) underwent concomitant procedures, including one Bentall and three ventricular remodeling in the Control group and one mitral valve replacement and one apical bullectomy in the intervention group. Additionally, 13 patients underwent coronary grafting as a beating heart procedure (intervention = 5, C = 8; P = 0.289) without the use of CPB. For all patients, the average duration of postoperative ventilation and postoperative LOS was similar, while the ICU LOS was 1.87 ± 2.7 vs 1.25 ± 0.8 days (P = 0.029), for control versus intervention groups, respectively.
Analysis of cumulative postoperative complications within the first 30 days after surgery, as shown in Table 3, was derived from the independent ICU and cardiac surgical databases and comprised new onset myocardial infarction, use of an intraaortic balloon pump, CVA, mediastinitis, septicemia, wound infection, prolonged ventilatory time >24 h and >48 h, arrhythmia requiring treatment, reoperation for bleeding, any other surgical reintervention, renal failure requiring dialysis, sternal dehiscence, mediastinitis, >7 days duration of postoperative hospitalization, readmission to hospital within 30 days, and death.
Fewer patients suffered a stroke in the intervention group (n = 1) compared with patients in the control group (n = 4). Four patients with stroke were tracheally extubated within 24 h postoperatively while one patient with postoperative stroke required ventilation for >24 h but was tracheally extubated within 48 h. Patients with CVA averaged 7.4 ± 6.8 days in ICU and 23.2 ± 12.3 days in the hospital postoperatively.
To compare the incidence and severity of adverse outcomes between groups, a secondary analysis of the incidence of perioperative major organ morbidity and mortality (MOMM) was undertaken as determined from the STS 30-day operative mortality and morbidity risk model (1). MOMM was defined as incidence of stroke, renal failure requiring dialysis, prolonged ventilation >48 h, deep sternal infection, reoperation, and death and demonstrated significantly (P = 0.048) fewer patients having one or more such complications in the intervention group (n = 3) than in the control group (n = 11) (Fig. 1). As shown in Table 4, the exclusion of the six patients who underwent concomitant procedures did not directionally influence the relative incidence of either MOMM or overall complications, with 10 of 96 patients in the control group versus two of 98 patients in the intervention groups experiencing MOMM (P = 0.017). Patients with MOMM had significantly longer ICU LOS (6.15 ± 5.8 vs 1.23 ± 0.43) and overall hospital LOS (17.80 vs 5.71 days, P = 0.003) than those without.
|
|
Technical failure resulted in loss of rSO2 data from the floppy discs of six patients, with resultant NIRS data from 194 patients for cerebral rSO2 analysis. As shown in Table 2, there were no significant differences in resting baseline, mean or minimum rSO2 values between the control and intervention groups. Significantly (P = 0.014) more patients in the control group (n = 6) had prolonged desaturations (AUC<70%>150 min%) than in the intervention group (n = 0), and patients having prolonged desaturations tended to have a more frequent MOMM (33% vs 7%, P = 0.070) compared with patients without such prolonged desaturations. Patients experiencing MOMM also had lower baseline rSO2 (64.66% vs 70.04%, P = 0.008), lower nadir rSO2 (41.5% vs 46.4%, P = 0.017), significantly more profound desaturations (AUC<40% 21.93 vs 4.91%min, P = 0.02), and a trend for more prolonged cerebral desaturation (AUC<70%>150 min% 14.3% vs 2.2%, P = 0.07) than patients without such complications. Mean rSO2 trended lower in those patients with any complication (n = 56; Table 3) compared with those without complications (n = 144) being 61.9% ± 7% vs 64.0% ± 6.4% (P = 0.056), respectively. As shown in Figure 2, post hoc analysis of all patients irrespective of group demonstrated a significant correlation (r2 = 0.29, P < 0.05) between mean intraoperative rSO2 and duration of postoperative LOS in those patients requiring prolonged hospitalization of 10 or more days. Overall there was a trend for mean rSO2 in those patients with postoperative LOS 10 days (n = 17) to be lower than in patients (n = 183) with postoperative LOS < 10 days (60.43% ± 7.7% vs 63.79% ± 6.6%; P = 0.0716).
|
In 56 of 100 patients in the intervention group, there were one or more episodes of cerebral desaturation which were treated with predefined interventions with an overall success rate of 80.4% (45/56 patients). Of these patients, 2 required 1 intervention, 10 required 2 interventions, 4 required 3 interventions, and 40 required >3 interventions. As shown in Table 5, the three most frequent interventions for increasing rSO2 were increasing MAP, increasing pump flow, and normalizing Paco2, respectively. These interventions were effective in restoring rSO2 to within 75% of baseline values in >50% of instances used.
|
|
DISCUSSION |
|---|
|
TopAbstractIntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
This randomized, prospective, blinded study was designed to evaluate the impact of cerebral oximetry monitoring and an intervention protocol on clinical outcomes in patients undergoing elective CAB surgery. Several limitations of this study must be considered. Cerebral oximetry monitoring was not continued into the ICU. Although this was essential to maintenance of blinding, it limited the extent and duration of interventions that were used while the patients were ventilated to the intraoperative period. Also, because of resource limitations, there was no formal assessment of cognitive or neurologic outcomes, clinically apparent stroke being detected on routine postoperative assessment rather than specifically sought using cognitive testing and a structured and systematic pre- and postoperative neurologic examination, as we have previously described (21). Such sensitive organ-specific assessments may well have increased the sensitivity of this study to detect significant differences in neurobehavioral outcomes, in addition to detecting differences in overall clinical morbidities as described.
As shown in Table 2, there were significantly more patients in the intervention group who received 2 m KIU "pump dose" aprotinin administration. Although 6 m KIU "full dose" aprotinin has been associated with decreased incidences of stroke and overall mortality (22,23), this has not been demonstrated for lower aprotinin dosages (24), and is thus unlikely to have influenced clinical outcomes in the current study. It may also be that monitoring alone, by an overall increase in vigilance, may have improved clinical management and outcomes. Since cerebral oximetry patches and a monitor were present intraoperatively in both the control and intervention groups, the improvements in clinical outcomes demonstrated in the intervention group were unlikely to have been due to any such nonspecific "study effect" (i.e., Hawthorne effect) (25).
This study was powered to detect a 50% decrease in the incidence of overall complications assuming an incidence of 40% in control patients, whereas the observed incidence of complications was 30% with a nonsignificant decrease to 23% in intervention group patients. While the number of patients experiencing any complications did not differ significantly between groups, there was significantly less major organ morbidity or death in patients in whom cerebral oxygen saturation was monitored and treated. As seen in Table 2, this resulted in a significant shortening of ICU LOS, and a trend to fewer patients having prolonged hospitalization in the intervention as compared with the control group. As shown in Table 4, for those patients who underwent CAB alone (n = 194) the incidence of MOMM was also significantly lower in the intervention group.
The overall incidence of 11% MOMM seen in the control group of the present study is comparable with that reported in the STS database-derived analysis of similar variables in which an incidence of major organ morbidity of 13.4% was observed, demonstrating that, in the intervention group, cerebral oximetry monitoring was associated with improved outcomes (1). This corroborates the fundamental hypothesis of this study, by using the brain as the index organ, that most of the interventions undertaken to optimize cerebral perfusion would have a similarly beneficial effect on systemic tissue perfusion and clinical outcomes. This is consistent with the correlation demonstrated in Figure 2 between duration of prolonged postoperative hospitalization and mean intraoperative rSO2 reflecting an association between fewer intraoperative cerebral oxygen saturations and a more complicated postoperative course.
The reduction in the number of patients experiencing MOMM, and the trend for fewer patients requiring prolonged hospitalization observed in the intervention group is consistent with the improvement in outcomes reported by Casati et al. (26) in a randomized blinded study of elderly patients undergoing major abdominal surgery. In that prospective study, involving 122 patients over the age of 65 yr, patients in the control group with intraoperative desaturations experienced significantly longer time to postoperative recovery room discharge and longer hospital LOS compared with patients in the treatment group. Patients in the control group experiencing cerebral desaturations also had a significantly lower Mini Mental Status Examination score compared with treatment group patients (26).
The present study was not powered to assess stroke rate. However, the results observed here, with a stroke rate of 4% in the control group and 1% in the intervention group, while not statistically significant, are directionally comparable with the results of Goldman et al. (6). In that study, cerebral oximetry was used in 1034 patients undergoing cardiac surgical procedures as compared with 1245 patients who underwent cardiac surgery without cerebral oximetry in the preceding 18 mo interval. It demonstrated significantly fewer permanent strokes and that the proportion of patients requiring prolonged ventilation was significantly smaller in the study group
In our study, the significant difference between groups in the incidence of prolonged cerebral desaturations, as demonstrated by six of the control group versus none of the intervention group patients having AUC<70%>150 min%, is consistent with the impact of cerebral oximetry monitoring to optimize cerebral perfusion. As a consequence of the nature of coronary revascularization surgery, e.g., during maneuvers to assess graft length, or for application and release of aortic clamps, pump flow is often profoundly decreased or stopped transiently, with a consequent abrupt decrease in rSO2. The rSO2 signal rapidly responds to such perturbations in cerebral perfusion and the goal of the treatment protocol in the intervention group was to minimize the duration and extent of such cerebral desaturations.
In many patients, interventions to increase pump flow, increase MAP, or normalize Paco2 were sufficient to rapidly return rSO2 to within the baseline range whereas, for others, multiple interventions were required at various intervals with an overall success rate of 80%. Since there was no difference in blood transfusion rates between the control and intervention groups, patients undergoing cerebral oximetry were not at increased risk of receiving blood transfusion as a consequence of monitoring cerebral oxygen saturation.
Not all studies of cerebral oximetry have indicated clinical benefit, however. In a review of cerebral oximetry by Taillefer and Denault (27), they tabulated results of NIRS studies based on a literature search as of February 2004. The authors analyzed and grouped together studies using any type and generation of NIRS device. No discrimination was made based on the device being investigated and they concluded that evidence of clinical effectiveness was lacking. Also, because of the date the paper was drafted, it did not include the final results of more recent studies (4,6,26).
In conclusion, we demonstrated that treatment of declining rSO2 prevented prolonged desaturations and was associated with a shorter ICU LOS and a significantly reduced incidence of MOMM. The intervention protocol undertaken to return rSO2 to baseline resulted in a rapid improvement in rSO2 in most cases, and did not add undue risk to the patient. While none of the interventions undertaken are outside the range of good clinical practice, it is clear that in the absence of feedback from a specific indicator of end-organ compromise (e.g., cerebral desaturations), the ability of the clinician to detect and optimize otherwise silent but potentially adverse perturbations in clinical variables remains limited. This is consistent with previous retrospective case–control studies (6; also see footnote 1), and indicates a clinical benefit to monitoring and managing cerebral oxygen saturation during CAB surgery.
|
ACKNOWLEDGMENTS |
|---|
The authors acknowledge the support of the cardiac surgical, perfusion, respiratory technology, and anesthesiology staff at University Hospital. Mr. R.A. Widman, an employee of Somanetics Corporation, assisted with collection of NIRS data as well as statistical analysis of the data.
|
Footnotes |
|---|
1Alexander HC, Kronenefeld MA, Dance GR. Reduced postoperative length of stay may result from using cerebral oximetry monitoring to guide treatment (abstract). Ann Thorac Surg 2002;73:373-C.
2Amosu O, Bhavani-Shankar K. Cerebral oxygenation during cesarean section (abstract). Anesthesiology 2000;92 (Suppl):A85.
Accepted for publication September 12, 2006.
Supported in part by Canadian Institutes of Health Research grant MOP37914, and a grant from Somanetics Corporation.
Presented in part at the 27th Annual Meeting of Society of Cardiovascular Anesthesiologists, May 2005 and at Outcomes Key West Symposium, May 2005.
Disclosures: Dr. Murkin has received lecture/travel fees from neuromonitoring companies, including Somanetics, but has no stock equity, consulting agreements, or other financial interests in Somanetics. None of the other authors have any relevant disclosures.
|
REFERENCES |
|---|
|
TopAbstractIntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
- Shroyer AL, Coombs LP, Peterson ED, et al. The Society of Thoracic Surgeons: 30-day operative mortality and morbidity risk models. Ann Thorac Surg 2003;75:1856–64.
[Abstract/Free Full Text] - Uehara T, Tabuchi M, Kozawa S, Mori E. MR angiographic evaluation of carotid and intracranial arteries in Japanese patients scheduled for coronary artery bypass grafting. Cerebrovasc Dis 2001;11:341–5.[Web of Science][Medline]
- Yoon BW, Bae HJ, Kang DW, et al. Intracranial cerebral artery disease as a risk factor for central nervous system complications of coronary artery bypass graft surgery. Stroke 2001;32:94–9.
[Abstract/Free Full Text] - Yao FF, Tseng CA, Ho CA, et al. Cerebral oxygen desaturations is associated with early postoperative neuropsychological dysfunction in patients undergoing cardiac surgery. J Cardiothorac Vasc Anesth 2004;18:552–8.[Web of Science][Medline]
- Edmonds HL Jr. Multi-modality neurophysiologic monitoring for cardiac surgery. Heart Surg Forum 2002;5:225–8.[Web of Science][Medline]
- Goldman S, Sutter F, Ferdinand F, Trace C. Optimizing intraoperative cerebral oxygen delivery using noninvasive cerebral oximetry decreases the incidence of stroke for cardiac surgical patients. Heart Surg Forum 2004;7:E376–E381.[Web of Science][Medline]
- Kim M, Ward D, Cartwright C, et al. Estimation of jugular venous O2 saturation from cerebral oximetry or arterial O2 saturation during isocapnic hypoxia. J Clin Monit 2000;16:191–9.
- Madsen PL, Nielsen HB, Christiansen P. Well-being and cerebral oxygen saturation during acute heart failure in humans. Clin Physiol 2000;20:158–64.[Web of Science][Medline]
- Austin EH III, Edmonds HL Jr, Auden SM, et al. Benefit of neurophysiologic monitoring for pediatric cardiac surgery. J Thorac Cardiovasc Surg 1997;114:707–15.
[Abstract/Free Full Text] - Nielsen H, Boushel R, Madsen P, Secher H. Cerebral desaturations during exercise reversed by O2 supplementation. Am J Physiol 1999;277:H1045–H1052.
- Berlac PA, Rasmussen YH. Per-operative cerebral near-infrared spectroscopy (NIRS) predicts maternal hypotension during elective caesarean delivery in spinal anaesthesia. Int J Obstet Anesth 2005;14:26–31.[Medline]
- Hadolt I, Litscher G. Noninvasive assessment of cerebral oxygenation during high altitude trekking in the Nepal Himalayas (2850–5600 m). Neurol Res 2003;25:183–8.[Web of Science][Medline]
- Kwee IL, Nakada T. Dorsolateral prefrontal lobe activation declines significantly with age. Functional NIRS study. J Neurol 2003;250:525–9.[Web of Science][Medline]
- Kolb JC, Ainslie PN, Ide K, Poulin MJ. Protocol to measure acute cerebrovascular and ventilatory responses to isocapnic hypoxia in humans. Respir Physiol Neurobiol 2004;141:191–9.[Web of Science][Medline]
- Hoffman GM, Ghanayem NS, Tweddell JS. Noninvasive assessment of cardiac output. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 2005;8:12–21.
- Dunham CM, Ransom KJ, Flowers LL, et al. Cerebral hypoxia in severely brain-injured patients is associated with admission Glasgow Coma Score, computed tomographic severity, cerebral perfusion pressure, and survival. J Trauma 2004;56: 482–91.[Web of Science][Medline]
- Papadimos TJ, Marco AP. Cerebral oximetry and an unanticipated circulatory arrest (letter to the editor). Anaesthesia 2004;59:309–10.[Web of Science][Medline]
- Fukada J, Morishita K, Kawaharada N, et al. Isolated cerebral perfusion for interoperative cerebral malperfusion in type A aortic dissection. Ann Thorac Surg 2003;75:266–8.
[Abstract/Free Full Text] - Janelle GM, Mnookin S, Gravenstein N, et al. Unilateral cerebral oxygen desaturations during emergent repair of DeBakey type 1 aortic dissection: potential aversion of a major catastrophe. Anesthesiology 2002;96:1263–5.[Web of Science][Medline]
- Higami T, Kozawa S, Asada T, et al. Retrograde cerebral perfusion versus selective cerebral perfusion as evaluated by cerebral oxygen saturation during aortic arch reconstruction. Ann Thorac Surg 1999;67:1091–6.
[Abstract/Free Full Text] - Murkin JM, Martzke JS, Buchan AM, et al. A randomized study of the influence of perfusion technique and pH management strategy in 316 patients undergoing coronary artery bypass surgery. II. Neurological and cognitive outcomes. J Thorac Cardiovasc Surg 1995;110:349–62.
[Abstract/Free Full Text] - Sedrakyan A, Treasure T, Elefteriades JA. Effect of aprotinin on clinical outcomes in coronary artery bypass graft surgery: a systematic review and meta-analysis of randomized clinical trials. J Thorac Cardiovasc Surg 2004;128:442–8.
[Abstract/Free Full Text] - Levi M, Cromheecke ME, de Jonge E, et al. Pharmacological strategies to decrease excessive blood loss in cardiac surgery: a meta-analysis of clinically relevant endpoints. Lancet 1999;354: 1940–7.[Web of Science][Medline]
- Smith PK, Muhlbaier LH. Aprotinin: safe and effective only with the full-dose regimen. Ann Thorac Surg 1996;62:1575–7.
[Free Full Text] - Seminowicz DA. Believe in your placebo. J Neurosci 2006;26: 4453–4.
[Free Full Text] - Casati A, Fanelli G, Pietropaoli P, et al. Continuous monitoring of cerebral oxygen saturation in elderly patients undergoing major abdominal surgery minimizes exposure to potential hypoxia. Anesth Analg 2005;101:740–7.
[Abstract/Free Full Text] - Taillefer MC, Denault AY. Cerebral near-infrared spectroscopy in adult heart surgery: systematic review of its clinical efficacy. Can J Anaesth 2005;52:79–87.[Web of Science][Medline]
This article has been cited by other articles:
|
|
 |
|
  R. Kazan, D. Bracco, and T. M. Hemmerling Reduced cerebral oxygen saturation measured by absolute cerebral oximetry during thoracic surgery correlates with postoperative complications Br. J. Anaesth., December 1, 2009; 103(6): 811 - 816. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. P. Grocott PRO: Temperature Regimens and Neuroprotection During Cardiopulmonary Bypass: Does Rewarming Rate Matter? Anesth. Analg., December 1, 2009; 109(6): 1738 - 1740. [Full Text] [PDF]
|
|
|
|
 |
|
 H. A. Vohra, A. Modi, and S. K. Ohri Does use of intra-operative cerebral regional oxygen saturation monitoring during cardiac surgery lead to improved clinical outcomes? Interactive CardioVascular and Thoracic Surgery, August 1, 2009; 9(2): 318 - 322. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. S. Shuler, W. M. Reisman, T. E. Whitesides Jr., T. L. Kinsey, E. M. Hammerberg, M. G. Davila, and T. J. Moore Near-Infrared Spectroscopy in Lower Extremity Trauma J. Bone Joint Surg. Am., June 1, 2009; 91(6): 1360 - 1368. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Smith and C. Elwell Near-Infrared Spectroscopy: Shedding Light on the Injured Brain Anesth. Analg., April 1, 2009; 108(4): 1055 - 1057. [Full Text] [PDF]
|
|
|
|
|
|
B. D. Kussman, D. Wypij, J. A. DiNardo, J. W. Newburger, J. E. Mayer Jr, P. J. del Nido, E. A. Bacha, F. Pigula, E. McGrath, P. C. Laussen, et al. Cerebral Oximetry During Infant Cardiac Surgery: Evaluation and Relationship to Early Postoperative Outcome Anesth. Analg., April 1, 2009; 108(4): 1122 - 1131. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. P. Slater, T. Guarino, J. Stack, K. Vinod, R. T. Bustami, J. M. Brown III, A. L. Rodriguez, C. J. Magovern, T. Zaubler, K. Freundlich, et al. Cerebral Oxygen Desaturation Predicts Cognitive Decline and Longer Hospital Stay After Cardiac Surgery Ann. Thorac. Surg., January 1, 2009; 87(1): 36 - 45. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. D. Tobias Cerebral Oximetry Monitoring with Near Infrared Spectroscopy Detects Alterations in Oxygenation Before Pulse Oximetry J Intensive Care Med, November 1, 2008; 23(6): 384 - 388. [Abstract] [PDF]
|
|
|
|
|
|
G. M. T. Hare, A. K. Y. Tsui, A. T. McLaren, T. E. Ragoonanan, J. Yu, and C. D. Mazer Anemia and Cerebral Outcomes: Many Questions, Fewer Answers Anesth. Analg., October 1, 2008; 107(4): 1356 - 1370. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. C. Santo, A. Barrios, U. Dandekar, P. Riley, P. Guest, and R. S. Bonser Near-Infrared Spectroscopy: An Important Monitoring Tool During Hybrid Aortic Arch Replacement Anesth. Analg., September 1, 2008; 107(3): 793 - 796. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. W. Hong, J. K. Shim, Y. S. Choi, D. H. Kim, B. C. Chang, and Y. L. Kwak Prediction of cognitive dysfunction and patients' outcome following valvular heart surgery and the role of cerebral oximetry Eur. J. Cardiothorac. Surg., April 1, 2008; 33(4): 560 - 565. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. W. Fischer Recent Advances in Application of Cerebral Oximetry in Adult Cardiovascular Surgery Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2008; 12(1): 60 - 69. [Abstract] [PDF]
|
|
|
|
|
|
P. Meybohm, G. Hoffmann, J. Renner, A. Boening, E. Cavus, M. Steinfath, J. Scholz, and B. Bein Measurement of Blood Flow Index During Antegrade Selective Cerebral Perfusion with Near-Infrared Spectroscopy in Newborn Piglets Anesth. Analg., March 1, 2008; 106(3): 795 - 803. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Denault, A. Deschamps, and J. M. Murkin A Proposed Algorithm for the Intraoperative Use of Cerebral Near-Infrared Spectroscopy Seminars in Cardiothoracic and Vascular Anesthesia, December 1, 2007; 11(4): 274 - 281. [Abstract] [PDF]
|
|
|
|
|
|
J. M. Murkin Cerebral Autoregulation: The Role of CO2 in Metabolic Homeostasis Seminars in Cardiothoracic and Vascular Anesthesia, December 1, 2007; 11(4): 269 - 273. [Abstract] [PDF]
|
|
|
|
 |
|
 G. M. T. Hare, C. D. Mazer, J. S. Hutchison, A. T. McLaren, E. Liu, A. Rassouli, J. Ai, R. E. Shaye, J. A. Lockwood, C. E. Hawkins, et al. Severe hemodilutional anemia increases cerebral tissue injury following acute neurotrauma J Appl Physiol, September 1, 2007; 103(3): 1021 - 1029. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. B. Nielsen and J. Borglum Cerebral Oxygenation in Heart Surgery Anesth. Analg., August 1, 2007; 105(2): 537 - 537. [Full Text] [PDF]
|
|
|
|
|
|
J. M. Murkin, D. Bainbridge, and R. Novick Adequacy of Brain Oxygen Saturation for Goal-Directed Therapy Anesth. Analg., August 1, 2007; 105(2): 538 - 539. [Full Text] [PDF]
|
|
|
|
|
|
E. C. Nemergut and W. J. Mauermann Do the Data Really Support the Conclusion? Anesth. Analg., August 1, 2007; 105(2): 536 - 537. [Full Text] [PDF]
|
|
|
|
|
|
M. Dworschak Adequacy of Brain Oxygen Saturation for Goal-Directed Therapy Anesth. Analg., August 1, 2007; 105(2): 537 - 538. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
