Neuronal and astroglial injuries in patients undergoing coronary artery bypass grafting and aortic arch replacement during hypothermic cardiopulmonary bypass

More than 50% of patients suffer neuropsychologic impairment after cardiac surgery. We measured neuron-specific enolase (NSE) and S-100 protein (S-100) in patients' serum as putative markers of neuronal and astroglial cell injury, respectively. Group I (n = 13) underwent coronary artery bypass grafting (CABG) with mild hypothermic cardiopulmonary bypass (CPB); Group II (n = 6) underwent aortic arch replacement with deep hypothermic CPB; Group III (n = 8) underwent CABG under normothermia without CPB. During and after the operation, serum levels of NSE and S-100 were significantly increased only in Groups I and II (during CPB), NSE still being increased 12 h after surgery in Group II. This suggests that neuronal and astroglial cell injuries are more likely in patients undergoing CABG with mild hypothermic CPB or aortic arch replacement with deep hypothermic CPB than in those undergoing CABG under normothermia without CPB. However, these increases of NSE and S-100 failed to reflect clinical brain damage. Rather, an electroencephalogram, was only capable of detecting neurologic complications after surgery. Implications: Neuronal and astroglial cell injuries are likely to occur during coronary artery bypass grafting with mild hypothermic cardiopulmonary bypass (CPB) or aortic arch replacement with deep hypothermic CPB. Conversely, patients undergoing coronary artery bypass grafting without CPB under normothermic conditions may be less likely to suffer brain cell injury.     

Differential expression in markers for thrombin, platelet activation, and inflammation in cell saver versus systemic blood in patients undergoing on-pump coronary artery bypass graft surgery

OBJECTIVE: Elimination of cardiotomy suction increases reliance on cell-saver blood-conservation techniques. Reinfusion of processed cell-saver blood (PCSB) even without using cardiotomy field suction may contribute to thrombin, cytokines, platelet activators, and hemolytic factors measured systemically. DESIGN: This study was designed as a prospective, unblinded observational study of patients undergoing first-time, nonemergent on-pump coronary artery bypass graft surgery. SETTING: A university medical center. PARTICIPANTS: Fourteen patients were enrolled after informed consent. INTERVENTIONS: Arterial blood was sampled (1) before cardiopulmonary bypass, (2) immediately after bypass, and (3) 4 hours after bypass. PCSB, using the AutoLog (Medtronic, Inc, Minneapolis, MN), was sampled after bypass. MEASUREMENTS AND MAIN RESULTS: Blood and PCSB levels of prothrombin fragments 1.2, beta-thromboglobulin, interleukin-6, interleukin-8, polymorphonuclear leukocyte-elastase, neuron-specific enolase, and S-100beta were assayed by using enzyme-linked immunosorbent assay. Paired comparisons were performed by using paired t tests. Compared with postbypass blood, processed cell-saver blood (prepatient infusion) had higher levels of polymorphonuclear leukocyte-elastase, interleukin-8, neuron-specific enolase, and S-100beta (p 相似文献   

Central nervous system damage during cardiac surgery assessed by 3 different biochemical markers in cerebrospinal fluid.

Three cerebral biochemical markers, adenylate kinase (AK), neuron-specific enolase (NSE) and protein S-100, were determined in the cerebrospinal fluid (CSF) of male patients 24 h after coronary artery bypass grafting to investigate the extent of possible center nervous system (CNS) damage and relation to the type of oxygenator and the use of an arterial line filter. The patients were randomized into three groups for extracorporeal circulation (ECC); bubble oxygenator without an arterial line filter (Group I, n = 30), bubble oxygenator with a filter (Group II, n = 29) and a flat-sheet membrane oxygenator without a filter (Group III, n = 33). Pathologically high CSF levels of AK and NSE were found 24 h after ECC in respectively 93% and 95% of the patients. All protein S-100 concentrations were within the normal range. Isolated high CSF concentrations of AK, NSE and protein S-100 were observed in group I. Levels of AK and NSE were the lowest in group III, although there was no statistical difference between the groups. In conclusion, our study suggested that CNS damage caused by ECC involved neurons rather than glial cells. AK and NSE in the CSF seemed to be markers of ischaemic neuronal damage. Postoperative levels of biochemical markers in the CSF tended to be the lowest in the flat-sheet membrane oxygenator group.     

Comparison of epsilon aminocaproic acid and low-dose aprotinin in cardiopulmonary bypass: efficiency, safety and cost

BACKGROUND: In this study we compared the clinical efficiency, safety, and economic benefit of low-dose aprotinin with epsilon aminocaproic acid (EACA) in reducing bleeding after cardiopulmonary bypass operation. METHODS: In a double-blind, randomized study, 100 patients received low-dose aprotinin (2 x 10(6) kallikrein inhibitor units) or EACA (20 g). The surgical procedure was single- or double-valve replacement with or without coronary artery bypass grafts. RESULTS: Mediastinal chest drainage and transfusion requirements with both therapies were similar. There were no urgent reoperations to secure hemostasis in either group. Similar levels of D-dimer with both therapies indicate a similar inhibition of fibrinolysis. Release of troponin I was less in the low-dose aprotinin group 1 and 4 hours after bypass, although electrocardiographic measurements did not reflect this difference. Levels of S-100beta and neuron-specific enolase were similar with both therapies, confirming that there was no difference in the occurrence of any adverse neurologic events in either group. CONCLUSIONS: Low-dose aprotinin and EACA showed similar effects on the reduction of intraoperative and postoperative bleeding. The lower cost of EACA with no change in safety outcome suggests it is the preferred treatment.     

Cerebral inflammatory response during and after cardiac surgery

BACKGROUND AND OBJECTIVE: Neurological dysfunction is a common problem after cardiac surgery with cardiopulmonary bypass (CPB). Cerebral ischaemia associated with the use of CPB may result in a release of neuronal-ischaemic markers and a subsequent cerebral inflammatory response which may additionally release inflammatory cytokines. In order to locate the origin and to quantify the release of neuronal-ischaemic markers and cytokines we investigated arterial-cerebral venous concentration gradients during and after CPB in a clinical setting. METHODS: In twenty-five patients scheduled for coronary artery bypass grafting surgery we measured the plasma concentration of neuron-specific enolase, S-100beta protein as well as interleukins (IL) IL-6, IL-8 and IL-10 from arterial and cerebral venous blood samples prior to surgery (baseline), during hypothermic CPB at 32 degrees C, after termination of bypass, as well as 2, 4 and 6 h after admission to the intensive care unit. RESULTS: Arterial-cerebral venous concentration gradients of neuron-specific enolase, S-100beta, IL-6, IL-8 and IL-10 were neither detectable during nor after CPB. Compared to the baseline period, S-100beta and neuron-specific enolase significantly increased during hypothermic CPB. After termination of CPB, neuronal-ischaemic markers as well as cytokines were increased and remained elevated during the investigated time course without reaching baseline values. CONCLUSIONS: Although we found an overall increase in plasma concentrations of neuronal-ischaemic markers, IL-6, IL-8 and IL-10 during and after CPB, arterial-cerebral venous gradients were not detectable for any of these parameters. Our results suggest that the increase of investigated parameters associated with the use of CPB are not primarily caused by a cerebral inflammatory response but rather reflect a release from other sources in the systemic circulation.     

Influence of Methylprednisolone on Levels of Neuron-Specific Enolase in Cardiac Surgery: A Corticosteroid Derivative to Decrease Possible Neuronal Damage

Abstract   Background: Cerebral injury is a well-known complication after cardiac surgery with cardiopulmonary bypass (CPB), especially in adult patients. Specific biochemical markers like neuron-specific enolase (NSE) and S-100β protein were developed previously for early detecting neuronal damage after CPB. Corticosteroids are shown to reduce multisystemic deleterious effects of cardiopulmonary bypass due to their anti-inflammatory characteristics. The aim of this study is to demonstrate the decrease of serum neuron-specific enolase levels in patients who received corticosteroids before CPB. Methods: Thirty patients scheduled for elective coronary bypass surgery were included in the study. Patients were divided randomly into two groups as the control group (n = 15) who underwent a standard coronary bypass surgery without any additional medication and the study group (n = 15) who received 1 gm of methylprednisolone before CPB. Blood samples for analysis of serum NSE, interleukin-6 (IL-6), and IL-10 were drawn before CPB, 4 and 24 hours after the end of extracorporeal circulation. Results : Serum cytokine and NSE levels were significantly increased after CPB above their normal range in both groups. In the study group, IL-6 and NSE levels were significantly reduced while IL-10 levels were much higher after CPB. High NSE levels significantly correlated with IL-6 levels in the control group. Conclusion: The lower levels of NSE in patients who received methylprednisolone may suggest that corticosteroids might be useful in decreasing possible neuronal damage during heart surgery. However, we were not able to demonstrate an adverse neurological outcome.     

Is there a relationship between serum S-100beta protein and neuropsychologic dysfunction after cardiopulmonary bypass?

OBJECTIVES: Over the past decade, the glial protein S-100beta has been used to detect cerebral injury in a number of clinical settings including cardiac surgery. Previous investigations suggest that S-100beta is capable of identifying patients with cerebral dysfunction after cardiopulmonary bypass. Whether detection of elevated levels S-100beta reflects long-term cognitive impairment remains to be shown. The present study evaluated whether perioperative release of S-100beta after coronary artery operations with cardiopulmonary bypass could predict early or late neuropsychologic impairment. METHODS: A total of 100 patients undergoing elective coronary bypass without a previous history of neurologic events were prospectively studied. To exclude noncerebral sources of S-100beta, we did not use cardiotomy suction or retransfusion of shed mediastinal blood. Serial perioperative measurements of S-100beta were performed with the use of a new sensitive immunoluminometric assay up to 8 hours after the operation. Patients underwent cognitive testing on a battery of 11 tests before the operation, before discharge from the hospital, and 3 months later. RESULTS: No significant correlation was found between S-100beta release and neuropsychologic measures either 5 days or 3 months after the operation. CONCLUSION: Despite using a sensitive immunoluminometric assay of S-100beta, we found no evidence to support the suggestion that early release of S-100beta may reflect long-term neurologic injury capable of producing cognitive impairment.     

Elevated levels of s-100beta correlate with neurocognitive outcome after cardiac surgery

AIM: S-100beta is a specific astroglial protein whose serum level increases after cerebral injury. The purpose of this study was to investigate the correlation between elevated levels of S-100beta and the neurocognitive outcome after cardiac surgery. METHODS: Fifty consecutive patients undergoing elective coronary artery bypass grafting were studied. Serum S-100beta levels were measured on induction of anaesthesia, at the 15(th) minute, at skin closure and on the 1(st) postoperative day. Neurocognitive outcome was evaluated by STAI-T and Zung tests preoperatively and by Mini-mental state examination every postoperative day until discharge. Neurocognitive tests and S-100beta levels were correlated within the scope of risk factors by Pearson correlation. RESULTS: Serum S-100beta was not detected preoperatively. Peak serum S-100beta levels were reached at skin closure in 36 of 50 patients (72%). In 24 hours, serum S-100beta disappeared in 25 patients but was still elevated in 11 (22%). A highly significant correlation was demonstrated between the duration of CPB and peak serum S-100beta levels (r=0.91). There was a weak correlation between age and peak S-100beta levels (r=0.62). Nine patients (18%) had a positive MMSE test which correlated well with persistent high serum S-100 levels (r=0.98). CONCLUSIONS: Serum S-100beta is a promising early biochemical marker for cerebral injury following cardiac surgery within a good correlation with the CPB time, age and especially with neurocognitive tests.     

Biochemical markers for brain damage after cardiac surgery -- time profile and correlation with cognitive dysfunction

BACKGROUND: Cerebral dysfunction is common after cardiac surgery and may be reflected in increasing blood concentrations of neuron specific enolase (NSE) and S-100 beta protein. The aim of the study was to determine the optimal timing of blood sampling. METHODS: We studied 15 patients undergoing coronary artery bypass grafting. Serum concentrations of NSE and S-100 beta protein were measured before surgery and after 12, 18, 24, 30, and 36 h. Neuropsychological testing was performed before surgery, at discharge from hospital and after 3 months. RESULTS: Serum concentrations of both NSE and S-100 beta protein increased significantly. At the first postoperative test, seven patients had cognitive dysfunction and a significant correlation was found between the composite z-score and the increase in the NSE level after 36 h (R = 0.76, P=0.001). The median increase in NSE after 36 h was 4.1 microg/l in patients having cognitive dysfunction and 0.9 microg/l in the remaining patients (P<0.05). No significant correlation was found between cognitive dysfunction and the increase in S-100 beta protein. After 3 months, no statistically significant correlation was found between either NSE or S-100 beta protein and cognitive dysfunction. CONCLUSION: NSE seems to be a useful blood marker for early cognitive dysfunction after coronary artery bypass grafting, optimal timing of blood sampling being at approximately 36 h postoperatively.     

Limitation of thrombin generation, platelet activation, and inflammation by elimination of cardiotomy suction in patients undergoing coronary artery bypass grafting treated with heparin-bonded circuits

OBJECTIVE: Reports evaluating the efficacy of heparin-bonded circuits to blunt inflammation, platelet dysfunction, and thrombin generation in response to cardiopulmonary bypass have varied. We hypothesized that this variability may in part be related to the use of cardiotomy suction, which has been demonstrated to reintroduce procoagulant and proinflammatory factors into the systemic circulation during cardiopulmonary bypass. A prospective, randomized study was undertaken to evaluate the specific effects of cardiotomy suction. METHODS: Thirty-six patients undergoing first-time, nonemergency coronary artery bypass grafting with cardiopulmonary bypass were randomly assigned to one of three treatment groups: group I, non-heparin-bonded circuits with the use of cardiotomy suction (n = 12); group II, Duraflo II (BCR-3500; Jostra Bentley Corp, Irvine, Calif) heparin-bonded circuits with cardiotomy suction (n = 12); and group III, Duraflo II heparin-bonded circuits without cardiotomy suction (n = 12). Thrombin generation, neutrophil activation (polymorphonuclear elastase), platelet activation (beta-thromboglobulin), and neuronal injury (neuron-specific enolase) were analyzed by enzyme-linked immunosorbent assays after cardiopulmonary bypass and compared with prebypass levels. Results are presented as mean +/- SEM. RESULTS: Prebypass levels of all markers were similar among treatment groups. However, postbypass levels were significantly and consistently highest in group I relative to groups II and III. Thrombin generation levels were 5.0 +/- 0.9 nmol/L in group I, 3.0 +/- 0.6 nmol/L in group II, and 1.5 +/- 0.1 nmol/L in group III (P <.05 vs group II and P <.001 vs group I). Polymorphonuclear elastase levels were 307 +/- 64 microg/L in group I, 128 +/- 24 microg/L in group II (P <.05 vs group I), and 75 +/- 14 microg/L in group III (P <.001 vs group I). beta-Thromboglobulin levels were 2692 +/- 401 IU/mL in group I, 912 +/- 99 IU/mL in group II (P =.001 vs group I), and 646 +/- 133 IU/mL in group III (P =.001 vs group I). Neuron-specific enolase levels were 9.8 +/- 0.9 ng/mL in group I, 10.5 +/- 1.6 ng/mL in group II, and 4.2 +/- 0.5 ng/mL in group III (P =.001 vs groups I and II). CONCLUSIONS: Use of cardiotomy suction resulted in significant increases in thrombin, neutrophil, and platelet activation, as well as the release of neuron-specific enolase, after cardiopulmonary bypass. Limiting increases in these markers would be best accomplished by eliminating cardiotomy suction and routinely using heparin-bonded circuits whenever possible.     

Comparative study on cerebral injury after open heart surgery in patients with congenital and rheumatic heart disease

Alongwiththedevelopmentofscienceandtechnology,intracardiacoperationsbecomemuchsaferthanever.Althoughthemortalityrateofthepatientsreceivingintracardiacoperationwith helpofcardiopulmonarybypass(CPB)hasdecreased butneurologicalcomplicationsoccurfrequently.Neurologicalcomplicationshavebeenidentifiedsince theearlydayswhenemployingcardiacsurgery.1And neurologicalcomplicationsaftertheemploymentofCPB areimportantfatalcomplicationsofnon cardiovascular originatpresent.2Theincidenceofneuropsychologica…     

Serum S100B protein levels are correlated with subclinical neurocognitive declines after carotid endarterectomy

OBJECTIVE: Carotid endarterectomy (CEA) is an effective means of stroke prevention among appropriately selected patients; however, neuropsychometric testing has revealed subtle cognitive injuries in the early postoperative period. The purpose of this study was to establish whether serum levels of two biochemical markers of cerebral injury were correlated with postoperative declines in neuropsychometric test performance after CEA. METHODS: Fifty-five consecutive patients underwent a battery of neuropsychometric tests 24 hours before and 24 hours after elective CEA. Two patients were excluded because of postoperative strokes. The pre- and postoperative serum levels of S100B protein and neuron-specific enolase for injured patients, defined as those who exhibited significant declines in neuropsychometric test performance (n = 12), were compared with the levels for uninjured patients (n = 41). RESULTS: There were no significant differences in the baseline S100B levels for the two groups. Injured patients exhibited significantly higher S100B levels, compared with uninjured patients, at 24, 48, and 72 hours after surgery (P < 0.05). There were no significant differences in neuron-specific enolase levels for injured and uninjured patients at any time point. CONCLUSION: These data suggest that subtle cerebral injuries after CEA, even in the absence of overt strokes, are associated with significant increases in serum S100B but not neuron-specific enolase levels. Analyses of earlier time points in future studies of subtle cognitive injuries and biochemical markers of cerebral injury after CEA may be revealing.     

Neuroprotection is associated with beta-adrenergic receptor antagonists during cardiac surgery: evidence from 2,575 patients

OBJECTIVE: To determine the impact of perioperative beta-adrenergic receptor (betaAR) antagonist administration on neurologic complications. DESIGN: Observational database analysis. SETTING: A clinical investigation at a single tertiary academic medical center. PARTICIPANTS: Elective coronary artery bypass graft surgical patients operated on in the period 1994-1996. INTERVENTIONS: Patients were divided into 2 groups: (1) patients given betaAR antagonist-blocking drugs in the perioperative period, including during operation, and (2) patients not given betaAR antagonists. MEASUREMENTS AND MAIN RESULTS: betaAR antagonist use in 2,575 consecutive patients undergoing coronary artery bypass graft surgery (1994-1996) was determined using the Cardiovascular Database and Anesthesia Information System Database. Outcome variables were postoperative stroke, coma, and transient ischemic attack. Of patients, 113 (4.4%) had postoperative neurologic complications, including stroke (n = 44), coma (n = 12), and transient ischemic attack (n = 3). Of patients, 2,296 (89%) received perioperative betaAR antagonist therapy, and 279 (11%) did not. Adverse neurologic events occurred in 3.9% (n = 90) of patients who received perioperative betaAR antagonists and 8.2% (n = 23) of patients who did not receive betaAR antagonists (odds ratio, 0.45; 95% confidence interval, 0.28 to 0.73; p = 0.003, unadjusted.) Severe neurologic outcomes (stroke and coma) occurred in 1.9% (n = 44) of patients who received betaAR antagonists and 4.3% (n = 12) of patients who did not receive betaAR antagonists (odds ratio, 0.43; 95% confidence interval, 0.23 to 0.83; p = 0.016). CONCLUSION: Use of beta-adrenergic antagonists was associated with a substantial reduction in the incidence of postoperative neurologic complications. A prospective randomized trial is needed to verify this potentially important neuroprotective strategy in cardiac surgery.     

Somatosensory evoked potentials and biochemical markers of neuronal deficits in patients undergoing carotid endarterectomy under regional anesthesia

OBJECTIVE OF THE STUDY: Carotid endarterectomy (CEA) remains the standard procedure for primary and secondary prevention of stroke. Somato-sensory evoked potentials (SEP) are frequently used in carotid endarterectomy under general anaesthesia and recommended for monitoring cerebral functions. The aim of the study was to compare changes in SEP and serum levels of S-100 beta protein and neuron-specific enolase (NSE) with perioperative clinical neurological deficits in patients undergoing regional anaesthesia (RA). PATIENTS AND METHODS: After approval of the ethics committee of the Otto-von-Guericke-University, Magdeburg fifty patients undergoing elective CEA under RA were prospectively investigated. RA was performed by combined deep and superficial cervical plexus blockade. SEP was monitored continuously during the surgical procedure. A more of 50 % decrease of potentials (N 20 / P 25 amplitude) compared to potentials before clamping was considered to be significant. Arterial blood samples were collected preoperatively, before declamping and on the first postoperative day to determine serum levels of S-100 beta and NSE. RESULTS: 12 patients developed intraoperatively neurological deficits with carotid clamping. The symptoms were transient and regressed in one minute after shunting. One patient was discharged with persistent hemiparesis. In 8 of 12 patients (66 %) with neurological deficits a more of 50 % decrease of potentials was observed. In one patient with loss of consciousness and hemiparesis changes in SEP or decrease in N 20 / P 25 amplitude were absent. Decrease in amplitude was in patients with intraoperative neurological deficits with 78 % versus 34 % in patients without any deficits significantly reduced (p = 0.01). The sensitivity of monitoring was 67 % at a specificity of 74 %. Serum levels of S-100 beta increased before declamping between patients with and without any neurological deficits significantly (p = 0.02). On the first postoperative day, increased levels of S-100 beta correlated with decrease in amplitude (p = 0.001). CONCLUSION: Compared to SEP, CEA under regional anaesthesia is a safer method to detect patients with cerebral ischaemia before irreversible cellular brain damage occurs. Measuring blood levels of S-100 beta could help to evaluate patients with risk to develop cerebral ischaemia during clamping.     

Markers of nerve tissue injury in the cerebrospinal fluid in patients with lumbar disc herniation and sciatica

STUDY DESIGN: The light subunit of neurofilament protein, S-100 protein, neuron-specific enolase, and glial fibrillary acidic protein were determined in the cerebrospinal fluid in patients with lumbar disc herniation and in control patients. OBJECTIVES: To determine whether nerve root injury caused by disc herniation increases the levels of nerve and glial cell injury markers in the cerebrospinal fluid. SUMMARY OF BACKGROUND DATA: Markers of nerve tissue injury can be analyzed in the cerebrospinal fluid, allowing characterization of the cell types involved and the degree of disease in patients with neurologic disorders. METHODS: Cerebrospinal fluid samples were obtained by preoperative lumbar puncture in patients who underwent surgery for lumbar disc herniation and in patients who underwent lower extremity surgery (control group), neurofilament protein (light subunit) and glial fibrillary acidic protein were analyzed by enzyme-linked immunosorbent assay and S-100 protein and neuron-specific enolase by radioimmunoassay and luminescence immunoassay, respectively. In the disc herniation group the concentrations of the four markers were evaluated regarding possible correlation to patient history, computed tomographic findings, and clinical findings. RESULTS: Cerebrospinal fluid concentration of neurofilament protein (light subunit) and S-100 were increased in the disc herniation group compared with that in control subjects (1158 +/- 383 ng/L vs. 152 +/- 14 ng/L, P < 0.01; 1963 +/- 231 ng/L vs. 1003 +/- 152 ng/L, P < 0.05, respectively). No statistical differences in neuron-specific enolase and glial fibrillary acidic protein concentrations were observed between the groups. Disc herniation patients with fewer than 3 months' duration of subjective symptoms had higher neurofilament protein levels than did patients with longer duration. None of the markers was related to preoperative clinical or computed tomographic findings. Patients with persistent neurologic findings at follow-up 2-3 months after surgery had higher levels of neurofilament protein before surgery compared with-those without sequelae. CONCLUSIONS: Patients with disc herniation and sciatica have increased concentrations of neurofilament protein and S-100 in the cerebrospinal fluid, which indicates damage of axons and Schwann cells in the affected nerve root.     

Clinical significance of serum S-100β protein level after pediatric cardiac surgery

OBJECTIVE: The serum S-100 beta protein level is a specific marker of damage to the central nerve system (CNS). We studied its significance in pediatric cardiac surgery as a possible marker of CNS damage. METHODS: Subjects were 18 consecutive pediatric patients aged 12 days to 13 years (mean: 2.8 years) undergoing open-heart surgery. We measured the serum S-100 beta protein level using ELISA (SRL Co. Ltd., Tokyo) immediately after inducing anesthesia and immediately, 12 hours, and 24 hours after weaning from cardiopulmonary bypass (CPB). RESULTS: None had postoperative neurological symptoms. The prebypass serum S-100 beta protein level showed a significant logarithmic correlation with patient age. All patients showed increased S-100 beta protein immediately after weaning from CPB, and multiple regression analysis showed that bypass time and cyanosis were significant factors in such as increase. Cyanosis was the only factor in increased S-100 beta protein levels 12 and 24 hours after weaning from CPB. The peak S-100 beta protein level showed a significant exponential correlation with bypass time. CONCLUSION: Serum S-100 beta protein elevated immediately after weaning from CPB correlated with bypass time but not with neurological symptoms. Physiological changes other than substantial brain damage caused by CPB may increase the serum S-100 beta protein level. Prebypass data on neonates and infants showed serum S-100 beta protein increased without brain damage supporting this hypothesis.     

Blood S-100 protein concentration in children undergoing cardiac surgery

OBJECTIVES: To investigate plasma levels of the betabeta isomer of S-100 protein and to assess the relationship between post-cardiopulmonary bypass (CPB) levels of this marker and a variety of perioperative and patient factors in children undergoing cardiac surgery. DESIGN: Prospective study. SETTING: University hospital. PARTICIPANTS: Twenty-five children. INTERVENTIONS: Blood samples (2 mL) for S-100 determinations were collected after the induction of anesthesia, 30 minutes after aortic cross-clamping, 1 hour after the termination of CPB, and 5 and 24 hours after the operation. Electroencephalogram activity was recorded, and neurologic examination was performed on all children 1 day before and 10 days after the operation. Lowest values of nasopharyngeal temperature, mean arterial pressure, arterial carbon dioxide tension (PaCO2), pH, and hematocrit during CPB were recorded. MEASUREMENTS AND MAIN RESULTS: The overall change in S-100 during the study period was found to be statistically significant (p < 0.0001). Correlation between deltaS-100 and age (r = -0.45; p = 0.04), body surface area (r = -0.63; p = 0.002), nasopharyngeal temperature (r = -0.55; p = 0.01), and PaCO2 (r = -0.55; p = 0.009) was statistically significant in infants and children. Multivariate regression analysis indicated significant effects of PaCO2 and body surface area on deltaS-100 levels and area under the curve values. CONCLUSION: In contrast to newborns, infants and older children showed prominent increases in S-100 protein concentration. Lack of pathologic electroencephalogram findings and neurologic signs in the postoperative period precludes the clinical use of S-100 protein concentration as a sensitive marker of cerebral injury.     

Regional cerebral oxygen saturation is a sensitive marker of cerebral hypoperfusion during orthotopic liver transplantation

Neurological complications contribute significantly to morbidity and mortality of patients after orthotopic liver transplantation (OLT). One possible cause of postoperative neurological complications is cerebral ischemia during the surgical procedure. In this study, we investigated the relationship between intraoperative changes in regional cerebral oxygen saturation (rSo(2)) and postoperative values of neuron-specific enolase (NSE) and S-100, which are specific variables that indicate cerebral disturbances due to hypoxia/ischemia. The rSo(2) was monitored continuously by near-infrared spectroscopy in 16 patients undergoing OLT. In addition, NSE and S-100 were determined in arterial blood before surgery and 24 h after reperfusion of the donor liver. Interestingly, clamping of the recipient's liver led to a significant decline in rSo(2) in eight patients, whereas the others tolerated clamping without major changes in rSo(2). The decrease in rSo(2) after clamping correlated significantly with postoperative increases in NSE (r(2) = 0.57) and S-100 (r(2) = 0.52). However, there were no significant differences between patients with and without rSo(2) decline concerning hemodynamic variables. There were no significant correlations between DeltarSo(2) and cardiac output (r(2) = 0.20), NSE and cardiac output (r(2) = 0.37), or S-100 and cardiac output (r(2) = 0.24). Monitoring of rSo(2) may be a useful noninvasive tool to estimate disturbances in rSo(2) during OLT.     

Subtle brain damage cannot be detected by measuring neuron-specific enolase and S-100beta protein after carotid endarterectomy

OBJECTIVE: To assess whether subtle brain damage after carotid endarterectomy could be detected using serum levels of neuron-specific enolase (NSE) or S-100beta protein. DESIGN: Prospective noninterventional study. SETTING: University hospital. PARTICIPANTS: Twenty-two patients undergoing carotid endarterectomy and 16 patients undergoing repair of abdominal aortic aneurysm. INTERVENTIONS: Serum levels of NSE and S-100beta protein were measured in all patients before surgery and postoperatively at 12, 24, 36, and 48 hours. In patients undergoing carotid endarterectomy, neuropsychologic testing was performed before surgery and postoperatively at discharge from the hospital and after 3 months using a neuropsychologic test battery. MEASUREMENTS AND MAIN RESULTS: Compared with abdominal aortic surgery patients, the preoperative serum concentration of NSE was significantly higher in carotid artery surgery patients. Postoperatively, the NSE serum level decreased significantly after uncomplicated carotid artery surgery, and the level was then similar to that in the aortic surgery patients. Before operation, the S-100beta protein levels were similar in the two groups, but a significant increase was seen in aortic surgery patients postoperatively. Neuropsychologic testing after uncomplicated carotid artery surgery revealed cognitive dysfunction in 2 of 20 (10%) of the patients after 5 days and 3 of 16 (19%) of the patients after 3 months. There was no correlation between the change in cognitive function and the changes in blood levels of either NSE or S-100 protein. CONCLUSIONS: Subtle brain damage after carotid artery surgery could not be detected by measuring blood levels of NSE and S-100beta protein. The NSE level was significantly higher before carotid artery surgery and decreased postoperatively to the level observed in aortic surgery.     

Predictors of type II neurologic complications after coronary artery bypass graft surgery

The study objective was to determine predictors, and adverse outcomes of postoperative type II neurologic complications. An 11-year cohort (N=12,706) study with 595 coronary artery bypass graft (CABG) patients with a neurologic complication, and 7793 patients without any neurologic complications was conducted. This study examined 26 potential risk factors and 13 outcome variables. Logistic regression analysis found that patients were more likely to experience a neurologic complication after CABG if they were older than 70 years of age [odds ratio (OR), 3.8; 95% confidence interval (CI), 3.1-4.5; P < 0.001], had a previous intervention within 10 days before surgery (OR, 3.4; 95% CI, 1.4-8.3; P = 0.008), or had a higher creatinine level (OR, 0.9; 95% CI, 0.95-0.99; P = 0.013). Additionally, there was a significant difference between CABG patients with and without neurologic complications on 12 outcome variables. Type II neurologic complications after CABG are common and associated with an increased risk of postoperative morbidity and mortality.