Cerebral sequelae of cardiac surgery

Current Opinion in Critical Care

Volumn 6, Issue 2, 2000, Pages 92-97

  Alston, R Peter ^a,b   Souter, Michael J ^c,d  

^a ROYAL INFIRMARY OF EDINBURGH   (United Kingdom)

^b UNIVERSITY OF EDINBURGH   (United Kingdom)

^c SOUTHERN GENERAL HOSPITAL   (United Kingdom)

^d UNIVERSITY OF GLASGOW   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

APROTININ; LIDOCAINE; NEURON SPECIFIC ENOLASE; PROPOFOL; PROTEIN S 100; REMACEMIDE;

BRAIN INJURY; BRAIN PROTECTION; COGNITIVE DEFECT; CORONARY ARTERY BYPASS GRAFT; DRUG MECHANISM; GENETIC SUSCEPTIBILITY; HEART SURGERY; HIGH RISK PATIENT; HUMAN; OXIDATIVE STRESS; POSTOPERATIVE COMPLICATION; REVIEW; STROKE;

EID: 0033913560     PISSN: 10705295     EISSN: None     Source Type: Journal    
DOI: 10.1097/00075198-200004000-00004     Document Type: Review

References (55)

1. 1 Newman SP, Harrison MJG (Eds): The brain and cardiac surgery. Amsterdam: Harwood Academic Publishers, 1999. A comprehensive account of the subject.
2. 2 Pua HL, Bissonnette B: Cerebral physiology in paediatric cardiopulmonary bypass. Can J Anaesth 1998, 45:960-978. A useful review of the important differences between adult and paediatric cardiac surgery, with the consequent need to alter anaesthetic and perfusion techniques.
3. 3 Newman MF, Laskowitz DT, Saunders AM, Grigore AM, Grocott HP: Genetic predictors of perioperative neurologic and neuropsychological injury and recovery. Semin Cardiothorac Vasc Anesths 1999, 3:34-46. Important review of genetic factors in the inflammatory and cellular response to physiological insult. Good introduction to the subject of apolipoprotein E.
4. 4 Wolman RL, Nussmeier NA, Aggarwal A, Kanchuger MS, Roach GW, Newman MF, et al.: Cerebral injury after cardiac surgery: identification of a group at extraordinary risk. Stroke 1999, 30:514-522. This prospective multicenter study of 273 patients distinguished between gross (16%) and more subtle (7%) neurologic change, attempting to relate these to distinct risk factors. Atherosclerotic disease and embolic risks featured prominently and both groups had prolonged hospital stays. The study's relevance is limited because the authors did not undertake neurocognitive testing.
5. 5 Sylivris S, Levi C, Matalanis G, Rosalion A, Buxton BF, Mitchell A, et al.: Pattern and significance of cerebral microemboli during coronary artery bypass grafting. Ann Thorac Surg 1998, 66:1674-1678.
6. 6 Brown WR, Moody DM, Challa VR: Cerebral fat embolism from cardiopulmonary bypass. J Neuropath Exp Neurol 1999, 58:109-119. Review of the genesis and manifestation of fat emboli during CPB.
7. 7 Brooker RF, Brown WR, Moody DM, Mammon JW Jr, Reboussin DM, Deal DD, et al.: Cardiotomy suction: a major source of brain lipid emboli during cardiopulmonary bypass. Ann Thorac Surg 1998, 65:1651-1655.
8. 8 Taylor RL, Borger MA, Weisel RD, Fedorko L, Feindel CM: Cerebral microemboli during cardiopulmonary bypass: increased emboli during perfusionist interventions. Ann Thorac Surg 1999, 68:89-93. Interesting study but one that requires repeating with different reservoirs because the design and arrangement may influence emboli formation.
9. 9 Bladin CF, Bingham L, Grigg L, Yapanis AG, Gerraty R, Davis SM: Transcranial doppler detection of microemboli during percutaneous transluminal coronary angioplasty. Stroke 1998, 29:2367-2370.
10. 10 Plochl W, Cook DJ: Quantification and distribution of cerebral emboli during cardiopulmonary bypass in the swine: the impact of PaCO2. Anesthesiology 1999, 90:183-190. Labeled microspheres were used to assess blood flow and emboli deposition because no model of embolus release exists. Increasing arterial carbon dioxide tension elevated cerebral blood flow and microsphere deposition in smaller vessels.
11. 11 Inoue S, Hayashi Y, Ohnishi Y, Kikumoto K, Minamino N, Kangawa K, et al.: Cerebral production of adrenomedullin after hypothermic cardiopulmonary bypass in adult cardiac surgery patients. Anesth Analg 1999, 88:1030-1035.
12. 12 Degirmenci B, Durak H, Hazan E, Karabay O, Derebek E, Yilmaz M, et al.: The effect of coronary artery bypass surgery on brain perfusion. J Nuc Med 1998, 39:587-591. Radiologic assessment of postoperative cerebral perfusion suggesting a relation between frontal hypoperfusion and neuropsychological changes. Persisting symptoms resolved with improvement of perfusion at 5-month follow-up, but significance of this finding is limited by the small study population.
13. 13 Abdul-Khaliq H, Blasig IE, Baur MO, Hohlfeld M, Alexi-Meskhishvili V, Lange PE: Release of the cerebral protein S-100 into blood after reperfusion during cardiac operations in infants: is there a relation to oxygen radical-induced lipid peroxidation? J Thorac Cardiovasc Surg 1999, 117:1027-1028. A prospective study of 58 infants, looking at malondialdehyde as an index of lipid peroxidation, and demonstrating a correlation with S-100 levels over the course of the procedure. It suggests activation of inflammatory mechanisms, which may increase release of S-100 across a compromised cell membrane.
14. 14 Grocott HP, Sheng H, Miura Y, Sarraf-Yazdi S, Mackensen GB, Pearlstein, et al.: The effects of aprotinin on outcome from cerebral ischemia in the rat. Anesth Analg 1999, 88:1-7.
15. 15 Murkin JM: Etiology and incidence of brain dysfunction after cardiac surgery. J Cardiothorac Vasc Anesth 1999, 13:12-17. A worthwhile discussion of etiology from an established expert in the field.
16. 16 Ashraf S, Bhattacharya K, Tian Y, Watterson K: Cytokine and S100b levels in paediatric patients undergoing corrective cardiac surgery with or without total circulatory arrest. Eur J Cardiothorac Surg 1999, 16:32-37.
17. 17 Baumgartner WA, Walinsky PL, Salazar JD, Tseng EE, Brock MV, Doty JR, et al.: Assessing the impact of cerebral injury after cardiac surgery: will determining the mechanism reduce this injury? Ann Thorac Surg 1999, 67:1871-1873.
18. 18 Tseng EE, Brock MV, Kwon CC, Annanata M, Lange MS, Troncoso JC, et al.: Increased intracerebral excitatory amino acids and nitric oxide after hypothermic circulatory arrest. Ann Thorac Surg 1999, 67:371-376.
19. 19 Tseng EE, Brock MV, Lange MS, Troncoso JC, Lowenstein CJ, Blue ME, et al.: Nitric oxide mediates neurologic injury after hypothermic circulatory arrest. Ann Thorac Surg 1999, 67:65-71. Both of the above references (18 and 19) used a canine model to demonstrate increased release of glutamate and nitric oxide induction. Administration of a nitric oxide synthase inhibitor decreased apoptosis and neuronal loss with improved neurologic function.
20. 20 Arrowsmith JE, Harrison MJG, Newman SP, Stygall J, Timberlake N, Pugsley WB: Neuroprotection of the brain during cardiopulmonary bypass. A randomized trial of remacemide during coronary artery bypass in 171 patients. Stroke 1998, 29:2357-2362. The logical sequelae to the studies of Tseng et al. [18,19•], with a randomized prospective study of remacemide. There are some methodologic reservations, because the number of patients showing deficit were below that estimated for the sample size calculation. However, this was anticipated by the authors and so change in performance was used as an outcome measure. There were increased levels of minor CNS disturbances which, to date, seem to be an inevitable side effect NMDA antagonists. Improvements were subtle and should be weighed against the adverse effects encountered (See accompanying Hindman and Todd editorial [37]).
21. 21 Yoshitake A, Goto T, Baba T, Shibata Y: Analysis of factors related to jugular venous oxygen saturation during cardiopulmonary bypass. J Cardiothorac Vasc Anesth 1999, 13:160-164. This study examined 140 patients prospectively to analyze factors affecting jugular venous desaturation during CPB. Although cerebral perfusion pressure did not affect oxygen extraction during stable hypothermia, it did during rewarming. Preoperative cerebrovascular disease had an adverse effect during initiation of CPB.
22. 22 Hanel F, von Knobelsdorff G, Werner C, Schutte AM, Esch J: Hypercapnia prevents jugular bulb desaturation during rewarming from hypothermic cardiopulmonary bypass. Anesthesiology 1999, 89:19-23. In a presumable effect upon cerebral blood flow, hypercapnia prevented cerebral venous desaturation, suggesting that a primary imbalance between caliber-dependent flow and temperature-related demand occurs during rewarming. Cerebral vascular reactivity to carbon dioxide tension is obviously preserved.
23. 23 Cook DJ: Changing temperature management for cardiopulmonary bypass. Anesth Analg 1999, 88:1254-1271. A comprehensive review of thermal management during CPB by an established researcher.
24. 24 Kadoi Y, Kawahara F, Saito S, Morita T, Kunimoto F, Goto F, Fujita N: Effects of hypothermic and normothermic cardiopulmonary bypass on brain oxygenation. Ann Thorac Surg 1999, 68:34-39.
25. 25 Engelman RM, Fleet ABP, Rousou JA, Flack JE, Deaton DW, Pekow PS, Gregory CA: Influence of cardiopulmonary bypass perfusion temperature on neurologic and hematologic function after cardiopulmonary artery bypass grafting. Ann Thorac Surg 1999, 67:1547-1556. An interesting study, although flawed by an unexplained high degree of selection attrition (291 out of 1,777 screened). The authors employed the Mathew score, a multiscale assessment of cognitive function elemental skills and disability derived from stroke methodology. Persistent dysfunction occurred in 36% and did not relate to perfusion temperature or length of procedure. Consequently, there may be reservations on the sensitivity of the scale. The increased fibrinolysis inducing rebleeding in warm patients was of particular interest.
26. 26 Conroy BP, Lin CY, Jenkins LW, DeWitt DS, Zornow MH, Uchida T, Johnston WE: Hypothermic modulation of cerebral ischemic injury during cardiopulmonary bypass in pigs. Anesthesiology 1998, 88:390-402. A porcine model of cerebral ischemia during bypass was used to assess the cerebroprotective effect of hypothermia on compromised cerebrovascular perfusion. Detailed and invasive monitoring of cerebral metabolism established that adverse metabolic effects occurred at a perfusion temperature of 34 and 37°C, but not at 28 and 31°C. This is an interesting finding in the context of the current popularity of "tepid hypothermia," thought to be a protective compromise between hypothermia and normothermia.
27. 27 Souter MJ, Andrews PJD, Alston RP: Jugular venous desaturation following cardiac surgery. Br J Anaes 1998, 81:239-241. Of 22 monitored patients, 15 experienced jugular bulb desaturations in the post-operative period, in considerable excess of durations reported peroperatively. However, this finding is limited by the lack of neurocognitive testing.
28. 28 Millar SA, Alston RP, Souter MJ, Andrews PJD: Aerobic, anaerobic and combination estimates of cerebral hypoperfusion during and after cardiac surgery. Br J Anaes 1999, 83:936-999.
29. 29 Irikura K, Miyasaka Y, Nagai S, Yuzawa I, Morii S, Fujii K: Moderate hypothermia reduces hypotensive, but not hypercapnic vasodilation of pial arterioles in rats. J Cereb Blood Flow Metab 1998, 18:1294-1297.
30. 30 Pesonen EJ, Peltola KI, Korpela RE, Sairanen HI, Leijala MA, Raivio KO, Andersson SHM: Delayed impairment of cerebral oxygenation after deep hypothermic circulatory arrest in children. Ann Thorac Surg 1999, 67:1765-1770. Cerebral desaturation occurred at 2 and 6 hours postoperatively following hypothermic circulatory arrest in 10 children. Also, neutrophil activation occurred 30 minutes postoperatively. This adds strength to the argument that physiologic insults trigger a sequence of pathologic events extending into the postoperative period.
31. 31 Taggart DP, Browne SM, Halligan PW, Wade DT: Is cardiopulmonary bypass still the cause of cognitive dysfunction after cardiac operations? J Thorac Cardiovasc Surg 1999, 118:414-420. A pertinent and provocative assessment of the role of CPB in the genesis of cognitive change. It should be read with the accompanying commentary by Murkin [32] for a thorough appraisal of arguments and criticism of the methodology.
32. 32 Murkin JM: Commentary on Taggart et al: is cardiopulmonary bypass still the cause of cognitive dysfunction after cardiac operations ? J Thorac Cardiovasc Surg 1999, 118:420-421.
33. 33 Newman MF, Croughwell ND, White WD, Sanderson I, Spillane W, Reves JG: Pharmacologic electroencephalographic suppression during cardiopulmonary bypass: a comparison of thiopental and isoflurane. Anesth Analg 1998, 86:246-251.
34. 34 Selnes OA, Goldsborough MA, Borowicz LM, Enger C, Quaskey SA, McKhann GM: Determinants of cognitive change after coronary artery bypass surgery: a multifactorial problem. Ann Thorac Surg 1999, 67:1669-1676. A comprehensive study of the influence of pre-, peri-, and postoperative factors upon eight cognitive domains in 127 patients. A number of interesting findings arise, but they are inadequately discussed and there are some statistical reservations on the validity of multiple comparisons. The study is followed by a cogent commentary from Stump.
35. 35 Selnes OA, Goldsborough MA, Borowicz LM, McKhann GM: Neurobehavioural sequelae of cardiopulmonary bypass. Lancet 1999, 353:1601-1606.
36. 36 Limburg M, Wijdicks EFM, Li H: Ischemic stroke after surgical procedures: clinical features, neuroimaging, and risk factors. Neurology 1998, 50:895-901. Although this article relates to general surgical procedures, it is worth reading for precisely that reason as it provides some context on the neurologic changes that occur in and around the time of surgery.
37. 37 Hindman BJ, Todd MM: Improving neurologic outcome after cardiac surgery. Anesthesiology 1999, 90:1243-1247. A critical discussion that has especial reference to the efficacy and risk/benefit ratio of protective measures.
38. 38 Gaudino M, Glieca F, Alessandrini F, Cellini C, Luciani N, Pragliola C, et al.: Individualized surgical strategy for the reduction of stroke risk in patients undergoing coronary artery bypass grafting. Ann Thorac Surg 1999, 67:1246-1253. An interesting concept developing the rationale of categorizing patients according to risk of neurologic damage on the basis of preoperative assessment and altering surgical management accordingly. This prospective study of 2,326 patients resulted in a reduction of adverse neurologic events, but with an increase in asymptomatic ischemic recurrence, diagnosed on scintillography at 3-year follow-up.
39. 39 Murkin JM, Newman SP, Stump DA, Blumenthal JA: Statement of consensus on assessment of neurobehavioral outcomes after cardiac surgery. Ann Thorac Surg 1995, 59:1289-1295.
40. 40 Roach GW, Newman MF, Murkin JM, Martzke J, Ruskin A, Li J, et al.: Ineffectiveness of burst suppression therapy in mitigating perioperative cerebrovascular dysfunction. Anesthesiology 1999, 90:1255-1264. This study contradicts previous work that suggested a protective role for propofol, and validates the view that pharmacologic metabolic suppression is inadequate to protect the vulnerable brain in extreme conditions.
41. 41 Browne SM, Halligan PW, Wade DT, Taggart DP: Cognitive performance after cardiac operation: implications of regression toward the mean. J Thorac Cardiovasc Surg 1999, 117:481-485. This study merits reading for a discussion of the role of regression toward mean, which is a largely unacknowledged problem in sequential testing. There are, however, important limitations to group mean analysis that are not discussed.
42. 42 Ashraf S, Bhattacharya K, Zacharias S, Kaul P, Kay PH: Serum S100beta release after coronary artery bypass grafting: roller versus centrifugal pump. Ann Thorac Surg 1998, 66:1958-1962.
43. 43 Gao F, Harris DN, Sapsed-Byrne S: Time course of neurone-specific enolase and S-100 protein release during and after coronary artery bypass grafting. Br J Anaes 1999, 82:266-267.
44. 44 Schmitt B, Bauersfeld U, Schmid ER, Tuchschmid P, Molinari L, Fanconi S, Bandtlow C: Serum and CSF levels of neuron-specific enolase (NSE) in cardiac surgery with cardiopulmonary bypass: a marker of brain injury? Brain Develop 1998, 20:536-539.
45. 45 Anderson RE, Hansson LO, Vaage J: Release of S100b during coronary artery bypass grafting is reduced by off-pump surgery. Ann Thorac Surg 1999, 67:1721-1725.
46. 46 Kilminster S, Treasure T, McMillan T, Holt DW: Neuropsychological change and S-100 protein release in 130 unselected patients undergoing cardiac surgery. Stroke 1999, 30:1869-1874. An assessment of correlation between neurocognitive change and S-100 release. Generally, most patients improve their scores with repeated testing, and a failure to improve is suggested as a surrogate endpoint. This, in turn, did correlate with increased S-100 levels, but neuropsychological tests accounted for only 23% of the variance associated with S-100 release. This may be due to insensitivity of the testing process or, more likely, may reflect the poor specificity of S-100.
47. 47 Wunderlich MT, Ebert AD, Kratz T, Goertler M, Jost S, Herrmann M: Early neurobehavioral outcome after stroke is related to release of neurobio-chemical markers of brain damage. Stroke 1999, 30:1190-1195.
48. 48 Raabe A, Grolms C, Seifert V: Serum markers of brain damage and outcome prediction in patients after severe head injury. Br J Neurosurg 1999, 13:56-59.
49. 49 Rasmussen LS, Christiansen M, Hansen PB, Moller JT: Do blood levels of neuron-specific enolase and S-100 protein reflect cognitive dysfunction after coronary artery bypass? Acta Anaesthesiol Scand 1999, 43:495-500. A prospective study of 35 patients undertaken by researchers with experience in assessment of cognitive deterioration. S-100 increases correlated with duration of CPB, but only NSE increase was related to cognitive dysfunction on discharge from hospital. Fourteen percent of patients had persistent cognitive dysfunction at 3 months postoperatively and this was unrelated to either marker.
50. 50 Gazzolo D, Vinesi P, Geloso MC, Marcelletti C, Iorio FS, Cipriani A, et al.: S100 blood concentrations in children subjected to cardiopulmonary bypass. Clin Chem 1998, 44:1058-1060.
51. 51 Nussmeier NA, Arlund C, Slogoff S: Neuropsychiatric complications after cardiopulmonary bypass: cerebral protection by a barbiturate. Anesthesiology 1986, 64:165-170.
52. 52 Souter MJ, Andrews PJD, Alston RP: Propofol does not ameliorate cerebral venous oxyhemoglobin desaturation during hypothermic cardiopulmonary bypass. Anesth Analg 1998, 86:926-931. A prospective study of 30 patients in whom propofol not onely failed to prevent jugular venous desaturation during rewarming on CPB but was associated with an increased cerebral lactate production, suggesting increased anaerobic metabolism.
53. 53 Taylor KM: Central nervous system effects of cardiopulmonary bypass. Ann Thorac Surg 1998, 66:S20-28. A review of current thinking.
54. 54 Wang D, Wu X, Zhong Y, Zhou Y, Shan G, Hu X, et al.: Effect of lidocaine on improving cerebral protection provided by retrograde cerebral perfusion: a neuropathologic study. J Cardiothorac Vasc Anesth 1999, 13:176-180.
55. 55 Mitchell SJ, Pellett O, Gorman DF, Butterworth J: Cerebral protection by lidocaine during cardiac operations. Ann Thorac Surg 1999, 67:1117-1124. Worth reading in conjunction with the pathologic study [54], as it demonstrates a possible protective role for lidocaine in a prospective randomised and blinded study of 65 patients. The lidocaine group suffered significantly more disease, but demonstrated better neuropsychologic dysfunction at 10 days, 10 weeks, and 6 months postoperatively.