Neurocognitive and Psychiatric Issues Post Cardiac Surgery

Neurocognitive and Psychiatric Issues Post Cardiac Surgery

HLC 2277 1–7 REVIEW Heart, Lung and Circulation (2017) xx, 1–7 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2016.12.010 Neurocognitive and [...

170KB Sizes 1 Downloads 33 Views

HLC 2277 1–7

REVIEW

Heart, Lung and Circulation (2017) xx, 1–7 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2016.12.010

Neurocognitive and [1_TD$IF]Psychiatric Issues Post Cardiac Surgery

1 2 3

4

Q1

5 6 7 8 9 10 11 12 13 14 15 16 17 18

Q2

Ben Elias Indja a,b,c, Michael Seco, MBBS a[2_TD$IF],b,d, Richard Seamark, MBBS, FRANZCP e[2_TD$IF], Jason Kaplan, MBBS, FRACP f, Paul G. Bannon, MBBS, PhD, FRACS a,b,d,g, Stuart M. Grieve, FRANZCR, DPhil (Oxon) a,c,h, Michael P. Vallely, MBBS, PhD, FRACS a,b,d,f,g* a

Sydney Medical School, The University of Sydney, Sydney, NSW, Australia The Baird Institute of Applied Heart & Lung Surgical Research, Sydney, NSW, Australia c Sydney Translational Imaging Laboratory, Heart Research Institute, Charles Perkins Centre, University of Sydney, NSW, Australia d Royal Prince Alfred Institute of Academic Surgery, Sydney, NSW, Australia e Sunshine Coast Mental Health and Addiction Services, Nambour, NSW, Australia f Macquarie University Hospital, Sydney, NSW, Australia g Cardiothoracic Surgery Unit, Royal Prince Alfred Hospital, Sydney, NSW, Australia h Department of Radiology, Royal Prince Alfred Hospital, Sydney, NSW, Australia b

Received 24 November 2016; accepted 14 December 2016; online published-ahead-of-print xxx

[14_TD$IF]Neurocognitive and psychiatric complications are common following cardiac surgery and impact on patient quality of life, recovery from surgery, participation in rehabilitation and long-term mortality. Postoperative cognitive decline, depressive disorders, post-traumatic stress disorder and neurocognitive impairment related to silent brain infarcts have all been linked to the perioperative period of cardiac surgery, and potentially have serious consequences. The accurate assessment of these conditions, particularly in determining the aetiology, and impact on patients is difficult due to the poorly recognised nature of these complications as well as similarities in presentation with postoperative delirium. This review aims to summarise current understanding surrounding psychiatric disturbances following cardiac surgery including the impact on patient quality of life and long-term outcomes. Keywords

19 20 21

Introduction

22 23 24 25 26 27 28 29

Cardiac surgical procedures  Mental disorders  Neuropsychiatry  Postoperative cognitive dysfunction

Q4

Neurologic injury, including stroke and transient ischaemic attack are important complications of cardiac surgery. A number of techniques have developed with the aim of reducing neurologic injury during cardiac surgical procedures. These include off-pump coronary artery bypass grafting, antegrade cerebral perfusion and hypothermia during aortic arch surgery, and distal aortic perfusion and cerebrospinal fluid drainage in thoracoabdominal aortic surgery [1].

These techniques have positively impacted on overt neurologic outcomes, and the focus has begun to shift towards less well-understood and often subtle neuro-psychiatric complications such as postoperative cognitive dysfunction (POCD), depression, dementia, and post-traumatic stress disorder (PTSD). These disorders have a significant impact on postoperative quality of life, and potentially negate the expected improvement in quality of life following successful surgery [2]. They may also affect functional independence, resulting in an increase in care requirements, reduction in workforce participation, and increased reliance on social

*Corresponding author [3_TD$IF]at: The Baird Institute of Applied Heart & Lung Surgical Research, 305/100 Carillon Ave, Newtown NSW 2042, Australia[4_TD$IF]. Tel.: +61295503714, Fax: +61295197584 Email: [email protected] © 2017 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.

Please cite this article in press as: Indja BE, et al. Neurocognitive and [1_TD$IF]Psychiatric Issues Post Cardiac Surgery. Heart, Lung and Circulation (2017), http://dx.doi.org/10.1016/j.hlc.2016.12.010

30 31 32 33 34 35 36 37 38 39 40

HLC 2277 1–7

2

41 42 43 44 45 46 47 48 49 50 51

52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94

B.E. Indja et al.

welfare [3]. Furthermore, there is some evidence that POCD may be associated with an increased mortality long-term [3]. The precise aetiology of these conditions is not entirely clear but likely involves a number of mechanisms including cerebral hypoperfusion and oxygenation, microemboli causing silent brain infarcts or a systemic inflammatory response [4]. Known patient risk factors include age, preoperative cognitive function and cognitive reserve [5], and premorbid psychiatric disorders [6]. This review discusses the possible aetiology of these conditions and their effect on patient outcomes.

[15_TD$IF]Postoperative Cognitive Dysfunction Cognitive dysfunction after cardiac surgery, while well known to occur, is less clearly understood with regards to the true incidence, causative factors involved, extent of the damage, and long-term implications and prognosis. Similar to clinically apparent stroke, embolic injury is likely to be a dominant mechanism of injury, however as demonstrated by an inconsistent correlation between POCD and new diffusion weighted imaging (DWI) cerebral ischaemic lesions [7], there are likely other factors involved. Cerebral hypoperfusion [8], systemic inflammatory response, CPB circuit [9], and cerebral hyperthermia [10] are all recognised as potential mechanisms of brain injury in the perioperative period. The definition of POCD is subject to considerable variation, which has made the true extent of this often sub-clinical brain injury difficult to determine. A 1995 statement of consensus for the diagnosis of POCD [11] recommended a core battery of tests, which included assessment of specific core cognitive domains including motor skill, verbal memory, attention and concentration, as well as assessing for effects of anxiety and depression, IQ testing, neurologic examination and accounting for learning effects and additional follow-up testing at least three months post procedure were all advocated. However in a review of POCD after cardiac surgery, which included 62 studies, high heterogeneity was found between the assessment batteries applied [12]. Further adding to heterogeneity was the finding that the statistical definition of POCD varied widely between studies with more than nine definitions (most notably including: percentage decline, standard deviation decline, factor analysis, individual test analysis) seen across the 62 studies with the threshold for cognitive decline being inconsistent between each [12]. Although heterogeneity in the definition of POCD remains, it can be generally described as a reduction in any cognitive domain following surgery [6_TD$IF]– typically thinking and memory, without an obvious state of confusion [13]. This is important so as to distinguish POCD from postoperative delirium, which can best be described as an acute and fluctuating confusional state, with reduced attention, disorientation, and additional symptoms such as hallucinations and inappropriate behaviour [14]. The reported incidence of POCD is highly variable, as would be expected with the

inconsistent definitions. A standard deviation (reduction of 1 SD) definition by Newman et al. has reported the incidence of POCD to be as high as 70% in the first week and 40% at 12 months [15]. Diagnosis of POCD early in the preoperative period is difficult due to many variables which may overestimate the diagnoses such as effects of anaesthetic drugs, narcotics and benzodiazepines [15] as well as misinterpretation of POCD in the presence of postoperative delirium [16]. Similarly, diagnosing POCD in the long-term has its own challenges, largely due to reduced cognition and associated increased incidence of silent brain infarcts (SBIs) with increasing age, potentially overestimating the effect of cognitive dysfunction actually related to the surgical procedure [17]. Cognitive dysfunction is a serious morbidity that can impact significantly on social function and independence. In a non-cardiac surgery study of POCD, in which 701 patients were followed up for 8.5 years, POCD present at one week postoperatively was associated with increased time receiving social welfare payments and earlier withdrawal from the labour market [3]. Self-care is an important factor of patient independence and their clinical outcomes [18] and in a study of patients with congestive heart failure, those who had cognitive impairment demonstrated difficulty in recognising symptom changes and thus had an impaired ability to make adequate self-care decisions over time [19]. Further to this, impairment of the executive function cognitive domain has been linked to a reduction in the ability to perform activities of daily living, specifically medication management [20], negatively impacting patient outcomes. In a long-term study of a median 11-year follow-up of patients following cardiac surgery, cognitive dysfunction present at six months was associated with increased long-term mortality [21], further demonstrating that the consequences of POCD are likely to have long-term implications that are more significant than just a transient postoperative state.

[7_TD$IF]Perioperative Depression Depression has been closely associated with cardiovascular disease, with major depressive disorder (MDD) reported to be present in up to 20% of patients [22]. It is not surprising, therefore, that depression is a notable comorbidity in patients undergoing cardiac surgery. Depression has been shown to be associated with extensive neural network abnormalities across the brain, hence both focal and global brain injuries may cause damage to these networks and predispose to increase risk of MDD [23]. Pre-morbid depressive disorders are the main risk factor for postoperative depression, with new postoperative depression relatively uncommon [24], so while cardiac surgery has not been shown to be a significant cause of depression it may be an important co-factor in inducing relapse as well as in contributing to postoperative morbidity and mortality. In a study of 309 patients undergoing CABG, 20% met the criteria for MDD prior to discharge; of this group 27% had a cardiac event within the first 12 months [25]. This was compared to 10% of the group without MDD [25]. Further to this,

Please cite this article in press as: Indja BE, et al. Neurocognitive and [1_TD$IF]Psychiatric Issues Post Cardiac Surgery. Heart, Lung and Circulation (2017), http://dx.doi.org/10.1016/j.hlc.2016.12.010

95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 114 115 116 117 118 119 120 121 122 123 124 125 126 127 128 129 130 131 132 133 134 135 136 137 138 139 140 141 142 143 144 145 146 147 148 149 150

HLC 2277 1–7

3

Neurocognitive and Psychiatric Issues Q3

151 152 153 154 155 156 157 158 159 160 161 162 163 164 165 166 167 168 169 170 171 172 173 174 175

176 177 178 179 180 181 182 183 184 185 186 187 188 189 190 191 192 193 194 195 196 197 198 199 200 201 202 203 204

depression scores assessed with Centre for Epidemiologic Studies Depression Scale (CES-D Scale) found a correlation between higher scores at one month, one year and five years to chest pain of cardiac origin in the five years following CABG [26]. Mortality is likely also affected with findings of new postoperative depressive symptoms being strongly associated with increased mortality and complications in the following two years [27]. This is not surprising as multiple studies have been able to show a link between preoperative depression and reduced postoperative mortality [28,29]. Depression may additionally be a risk factor for postoperative delirium, with Tully et al. [30] reporting that patients diagnosed with major depressive disorder had an odds ratio of 3.49 (95%CI 1.48–8.26, <0.01) for developing postoperative delirium after cardiac operations. This was further highlighted more recently in a cohort of CABG patients in which both delirium and reduced quality of life was correlated to preoperative depression [31]. With such evidence of the deleterious effects that MDD has following cardiac surgery, identification and appropriate management preoperatively may carry significant weight in reducing this population’s postoperative complications. However, more research is required regarding the efficacy and safety of antidepressants and psychological therapies with evidence currently conflicted in this area [32–35].

[8_TD$IF]Silent Brain Infarcts and Psychiatric Sequelae Silent brain infarcts (SBI) have been shown to be associated with cardiac surgery, evidenced by new ischaemic lesions detected by DWI postoperatively. The incidence of SBI after cardiac surgery is somewhat variably reported between 25– 50% [7] and appears associated with the type of procedure performed, with aortic valve replacement seemingly carrying the highest risk [36]. The sources of SBI associated with cardiac surgery, similar to stroke are multifactorial and likely include embolism, hypo-perfusion, systemic inflammatory response and microangiopathy [37]. While SBIs are not completely understood, there is growing evidence that with them comes increased risk of long- and short-term complications. The hypothesised link between SBIs and POCD has not been strongly established. Barber et al. demonstrated significant correlation between the burden of new DWI lesions and impairment of at least one cognitive domain at six weeks post operation [38], and Restrepo et al. were able to demonstrate a similar association [39]. In a study of cognitive dysfunction, SBIs in an elderly population were shown to correlate with a reduction in the attention domain, which was linked to disruption of the central cholinergic pathway [40]. However a number of studies of cardiac surgical procedures including CABG and AVR [41], transcatheter aortic valve implantation [42], and carotid revascularisation [43], have failed to show any significant correlation between the presence and number of new DWI lesions and POCD.

Numerous psychiatric conditions have been linked to SBIs including depression, mania and dementia. In a study of 194 patients with a variety of psychiatric conditions, SBIs were seen in 42.8% of patients receiving treatment for a depressive disorder [44], which supported previous findings by Yamashita et al. who reported the prevalence of SBI in major depression to be 48.6% [45]. For some time an association between depression and SBI has been known, which has largely been linked to depression onset with increasing age. In patients with pre-senile onset depression 51.4% have been observed to have SBIs, with this rate increasing to 97.3% of patients with senile onset depression [46]. Comparatively, only 22.6% of patients (mean age 56.7) with juvenile onset depression were shown to have SBIs present on MRI [46]. Further supporting this hypothesis was a finding from the Rotterdam study demonstrating that reduced cerebral blood flow velocity was predictive of depressive symptoms and disorders [47]. An important mechanism for the development of SBIs is thought to be due to impaired vasomotor reactivity of cerebral vessels leading to ischaemic injury [48]. Bipolar disorder is a growing concern in elderly patients and similar to late-onset depression, has been associated with vascular risk factors and white matter ischaemic lesions. Silent brain infarcts have been associated with mania, which have been seen in approximately half of patients diagnosed with bipolar disorder after the age of 50 [49]. Vascular risk factors, which are thought to be the cause of sub-clinical cerebral ischaemic lesions, have also been demonstrated to be an important cause of late-onset mania [50]. In a study comparing elderly patients who either had early onset or late onset bipolar disorder and age-matched controls, the lateonset group had the highest rate of silent white matter lesions on MRI, particularly in regions which have been associated with mood disorders [6_TD$IF]– the deep frontal and parietal regions, and the putamen [51]. In a meta-analysis, Beyer et al. found that 38.9% of bipolar patients had ischaemic lesions, compared to 18% of healthy controls [52]. The mean age of patients was around 34, which may account for this lower prevalence as compared to the previous studies of elderly populations. Interestingly, four of the studies were of child and adolescent populations, which reported an odds ratio of having SBIs of 5.7 for the bipolar disorder population as compared to healthy controls [52]. This meta-analysis also further supported the association of SBIs with unipolar depression and schizophrenia which both had similar rates of white matter hyper-intensities [52]. Silent brain infarcts have also been implicated in the development of dementia. The Rotterdam study reported that the presence of SBIs in the general population doubles the risk of dementia, and furthermore, patients with dementia accompanied by SBIs also had a quicker decline in cognitive function as compared to those without [53]. Further reported from the Rotterdam study was that an association between the location of the white matter lesions and the development of dementia may exist [6_TD$IF]– periventricular lesion severity was correlated with a higher risk of dementia, while lesions in the subcortical region did not [54]. Debette et al., who reviewed

Please cite this article in press as: Indja BE, et al. Neurocognitive and [1_TD$IF]Psychiatric Issues Post Cardiac Surgery. Heart, Lung and Circulation (2017), http://dx.doi.org/10.1016/j.hlc.2016.12.010

205 206 207 208 209 210 211 212 213 214 215 216 217 218 219 220 221 222 223 224 225 226 227 228 229 230 231 232 233 234 235 236 237 238 239 240 241 242 243 244 245 246 247 248 249 250 251 252 253 254 255 256 257 258 259 260 261

HLC 2277 1–7

4

262 263 264 265 266 267 268 269 270 271 272 273 274 275 276 277 278 279 280 281 282 283 284 285 286 287 288 289 290 291 292 293 294 295 296 297 298 299 300 301 302 303 304 305 306 307 308 309 310 311 312 313 314 315 316 317

B.E. Indja et al.

17 studies looking at SBIs and dementia, found that, comparable to the Rotterdam study, white matter lesions in the general population contributed to a higher risk of developing dementia, although this correlation was not seen in a high-risk population such as those with mild cognitive impairment or stroke [55]. There is obviously much overlap between patients undergoing cardiac surgical procedures and patients with vascular risk factors which lead to SBIs, thus studies specifically focussed on the incidence of these psychiatric conditions post-surgery associated with new infarct load are required for validation of this link. With new SBIs closely linked to cardiac procedures, the longer-term cognitive and psychiatric complications of these clinically silent lesions present a possible important cause of increased morbidity and mortality for patients following cardiac surgery.

[7_TD$IF]PTSD, Chronic Perioperative Stress and HRQL Exposure to a high level of stress occurs in the perioperative period surrounding cardiac procedures, particularly in the ICU environment. Highlighted by Schelling et al., who found that notwithstanding successful cardiac procedures, up to 20% of patients did not have improvement in the HRQL scores [56]. Of 148 patients, 20 had new PTSD six months after their surgery and this was strongly correlated to preoperative stress levels and CPB time (150 vs 120 minutes, median values, p[9_TD$IF]<0.01) [56]. Overall, the total study population showed significant improvement in HRQL scores (almost exclusively related to physical function scores), however the patients with new postoperative PTSD did not show the same improvement due to reduced mental health function. Critical illness related corticosteroid insufficiency (CIRCI) is a corticosteroid insufficiency that is seen in acute illness, including septic shock and post cardiac surgery [57]. This is a poorly understood condition; during critical illness states the normal cortisol response is maintained, and there are even decreased levels of corticosteroid-binding globulin leading to an increase in plasma free corticosteroid available [58]. However, at some point, an impaired response or signalling occurs and likely factors thought to be involved include inadequate corticosteroid release as well as tissue resistance to both corticosteroids and ACTH [59]. In the early postoperative period after cardiac surgery, patients with prolonged reduction in circulating corticosteroids have been found to have a higher incidence of PTSD and chronic stress [60]. Weis et al. demonstrated that hydrocortisone administration in the perioperative period (initial dose prior to anaesthesia induction, followed by a gradually reduced infusion over the first four postoperative days) was able to reduce chronic stress symptoms, improve HRQL scores and reduce incidence of PTSD at a six-month follow-up [61]. Improvements in both physical and mental health functions were seen on the HRQL questionnaire in the hydrocortisone group suggesting that stressors may have an impact on patient physical health. There is no clear explanation for these findings, however,

contributing factors may include: [1] stress masking the physical benefits of the successful operation; [2] stress increasing allostatic load [62]; [3] stress resulting in decreased compliance with medications resulting in actual physical impairment [63]. In addition to the long-term benefits, the hydrocortisone group also demonstrated short-term benefits as compared to the control group [6_TD$IF]– reduced ICU stay, lower TISS score, reduced norepinephrine requirements and lower concentrations of pro-inflammatory cytokine IL-6 [60]. Schelling et al. supported these findings by similarly demonstrating the protective benefit of perioperative hydrocortisone administration in reducing chronic stress symptoms and PTSD at six months following cardiac surgery [60].

318

Postoperative Delirium

331

Postoperative delirium is a well-known complication of cardiac surgery [64]. Reported incidence varies widely according to age, population, type of operation and the diagnostic criteria used. Similar to POCD, clinical diagnostic tests vary in their structure as well as selected threshold for diagnosis, thus all these factors result in a wide reported incidence from 6% to over 50% [65]. Similarities also exist between hypothesised aetiology of delirium and POCD [6_TD$IF]– duration of CPB [66], postoperative systemic inflammatory response, history of stroke and micro-emboli [67]. However, there is mixed evidence, with Rudolph et al. showing that an intraoperative micro-emboli load of the middle cerebral artery detected by transcranial Doppler (TCD) had no association with postoperative delirium in patients undergoing CABG, nor did they find an association with CPB time [68]. Similarly, in a systematic review of studies which examined the relationship between intraoperative micro-emboli and cognitive impairment, there was no definitive causal link with the authors concluding that micro emboli may only play a small role at best [69]. And in a separate systematic review looking at risk factors for postoperative delirium following cardiac surgery, CPB time was not found to have an association [70]. In this same review a number of risk factors were found to have a strong level of evidence toward postoperative delirium, notably age, pre-existing cognitive or psychiatric conditions, previous stroke, complexity of cardiac surgery and mechanical ventilation time [70]. Length of aortic cross clamp time has also been shown to have a positive correlation to patients developing severe delirium [71]. Furthermore, in non-cardiac surgery, delirium has been associated with intraoperative hypotension, blood loss and number of blood transfusions and hypothermia [72], all of which are common factors associated with cardiac surgery [68]. Postoperative delirium negatively impacts patient shortand long-term outcomes. Short-term outcomes include increased recovery time, which can be separated into longer intensive care stay, and increased hospital stay [67] as well as prolonging the required time for mechanical ventilation [73]. Longer term, there is a potential association between delirium in the intensive care postoperatively and cognitive impairment [74]. Additionally, higher 12-month mortality is significantly associated with delirium, particularly in

332

Please cite this article in press as: Indja BE, et al. Neurocognitive and [1_TD$IF]Psychiatric Issues Post Cardiac Surgery. Heart, Lung and Circulation (2017), http://dx.doi.org/10.1016/j.hlc.2016.12.010

319 320 321 322 323 324 325 326 327 328 329 330

333 334 335 336 337 338 339 340 341 342 343 344 345 346 347 348 349 350 351 352 353 354 355 356 357 358 359 360 361 362 363 364 365 366 367 368 369 370 371 372 373

HLC 2277 1–7

5

Neurocognitive and Psychiatric Issues

374 375 376 377 378 379 380 381 382 383 384 385 386 387 388 389 390 391 392 393 394 395

elderly patients. Martin et al. were able to demonstrate a strong link between delirium and perioperative stroke and separately to this, a higher stroke rate in the preceding 10 years [75]. Also significantly affected was a notable lack in increase of HRQL scores following CABG in patients who suffered delirium compared to the significant increase seen in non-delirious patients at 18 months follow-up [76]. Health care costs are also significantly increased due to postoperative delirium, which includes costs of longer intensive care and overall hospital stay, and higher intensive care costs, regardless of length of stay [77]. Due to the multi-factorial mechanisms resulting in postoperative delirium, it is difficult to accurately predict patient risk prior to surgery. Additionally to this, the high heterogeneity in diagnostic criteria adds to the complexity. DSM-IV, ICD-10, and the Memorial Delirium Assessment Scale criteria, have all been shown to have different positive diagnostic rates across a single cohort [78]. In addition to this, the unavoidable subjective nature of these assessments adds to the heterogeneity of results. Prevention and management of postoperative delirium is therefore difficult with the present knowledge due to the highly variable aetiology.

[8]

[9]

[10]

[11]

[12]

[13] [14]

[15]

[16]

[17]

396

Conclusion

397

409

Neurologic injury has been the main focus of cardiac surgery complications, albeit in the more overt forms of stroke and transient ischaemic attacks. With improvements seen in these areas the focus has shifted towards the subtler neurocognitive and psychiatric complications such as POCD, depression, dementia and PTSD for which similar mechanisms have been proposed, yet current understanding and evidence is not adequate. Psychiatric sequelae following cardiac surgery have a clear impact on patient quality of life, and potential to impact long-term outcomes. Thus, improved understanding is required to more accurately assess the prevalence, understand causative factors and develop potential preventative measures.

410

References

398 399 400 401 402 403 404 405 406 407 408

411 412 413 414 415 416 417 418 419 420 421 422 423 424 425 426 427 428 429

[1] Seco M, Edelman JJ, Van Boxtel B, Forrest P, Byrom MJ, Wilson MK, et al. Neurologic injury and protection in adult cardiac and aortic surgery. Journal of Cardiothoracic and Vascular Anesthesia 2015;29(1):185–95. [2] Phillips-Bute B, Mathew JP, Blumenthal JA, Grocott HP, Laskowitz DT, Jones RH, et al. Association of neurocognitive function and quality of life 1 year after coronary artery bypass graft (CABG) surgery. Psychosomatic Medicine 2006;68(3):369–75. [3] Steinmetz J, Christensen KB, Lund T, Lohse N, Rasmussen LS, Group I. Long-term consequences of postoperative cognitive dysfunction. Anesthesiology 2009;110(3):548–55. [4] van Harten AE, Scheeren TW, Absalom AR. A review of postoperative cognitive dysfunction and neuroinflammation associated with cardiac surgery and anaesthesia. Anaesthesia 2012;67(3):280–93. [5] Gao L, Taha R, Gauvin D, Othmen LB, Wang Y, Blaise G. Postoperative cognitive dysfunction after cardiac surgery. Chest 2005;128(5):3664–70. [6] Rao V, Lyketsos CG. Psychiatric aspects of traumatic brain injury. The Psychiatric Clinics of North America 2002;25(1):43–69. [7] Sun X, Lindsay J, Monsein LH, Hill PC, Corso PJ. Silent brain injury after cardiac surgery: a review: cognitive dysfunction and magnetic resonance

[18]

[19]

[20]

[21]

[22]

[23]

[24]

[25]

[26]

[27]

[28]

[29]

[30]

imaging diffusion-weighted imaging findings. Journal of the American College of Cardiology 2012;60(9):791–7. Caplan LR, Hennerici M. Impaired clearance of emboli (washout) is an important link between hypoperfusion, embolism, and ischemic stroke. Archives of Neurology 1998;55(11):1475–82. Hogue Jr CW, Palin CA, Arrowsmith JE. Cardiopulmonary bypass management and neurologic outcomes: an evidence-based appraisal of current practices. Anesthesia and Analgesia 2006;103(1):21–37. Grocott HP, Mackensen GB, Grigore AM, Mathew J, Reves JG, PhillipsBute B, et al. Postoperative hyperthermia is associated with cognitive dysfunction after coronary artery bypass graft surgery. Stroke; a Journal of Cerebral Circulation 2002;33(2):537–41. Murkin JM, Newman SP, Stump DA, Blumenthal JA. Statement of consensus on assessment of neurobehavioral outcomes after cardiac surgery. The Annals of Thoracic Surgery 1995;59(5):1289–95. Rudolph JL, Schreiber KA, Culley DJ, McGlinchey RE, Crosby G, Levitsky S, et al. Measurement of post-operative cognitive dysfunction after cardiac surgery: a systematic review. Acta Anaesthesiologica Scandinavica 2010;54(6):663–77. Tsai TL, Sands LP, Leung JM. An Update on Postoperative Cognitive Dysfunction. Advances in Anesthesia 2010;28(1):269–84. Inouye SK, van Dyck CH, Alessi CA, Balkin S, Siegal AP, Horwitz RI. Clarifying confusion: the confusion assessment method. A new method for detection of delirium. Annals of Internal Medicine 1990;113(12): 941–8. Newman MF, Mathew JP, Grocott HP, Mackensen GB, Monk T, WelshBohmer KA, et al. Central nervous system injury associated with cardiac surgery. Lancet 2006;368(9536):694–703. Rudolph JL, Marcantonio ER, Culley DJ, Silverstein JH, Rasmussen LS, Crosby GJ, et al. Delirium is associated with early postoperative cognitive dysfunction. Anaesthesia 2008;63(9):941–7. Fanning JP, Wong AA, Fraser JF. The epidemiology of silent brain infarction: a systematic review of population-based cohorts. BMC Medicine 2014;12:119. Lee CS, Tkacs NC, Riegel B. The influence of heart failure self-care on health outcomes: hypothetical cardioprotective mechanisms. The Journal of Cardiovascular Nursing 2009;24(3):179–87. quiz 88-9. Hajduk AM, Lemon SC, McManus DD, Lessard DM, Gurwitz JH, Spencer FA, et al. Cognitive impairment and self-care in heart failure. Clinical Epidemiology 2013;5:407–16. Alosco ML, Spitznagel MB, Raz N, Cohen R, Sweet LH, Colbert LH, et al. Executive dysfunction is independently associated with reduced functional independence in heart failure. Journal of Clinical Nursing 2014;23 (5-6):829–36. Tully PJ, Baune BT, Baker RA. Cognitive impairment before and six months after cardiac surgery increase mortality risk at median 11 year follow-up: a cohort study. International Journal of Cardiology 2013;168 (3):2796–802. Thombs BD, Bass EB, Ford DE, Stewart KJ, Tsilidis KK, Patel U, et al. Prevalence of depression in survivors of acute myocardial infarction. Journal of General Internal Medicine 2006;21(1):30–8. Korgaonkar MS, Fornito A, Williams LM, Grieve SM. Abnormal structural networks characterize major depressive disorder: a connectome analysis. Biological Psychiatry 2014;76(7):567–74. McKhann GM, Borowicz LM, Goldsborough MA, Enger C, Selnes OA. Depression and cognitive decline after coronary artery bypass grafting. Lancet 1997;349(9061):1282–4. Connerney I, Shapiro PA, McLaughlin JS, Bagiella E, Sloan RP. Relation between depression after coronary artery bypass surgery and 12-month outcome: a prospective study. Lancet 2001;358(9295):1766–71. Borowicz Jr L, Royall R, Grega M, Selnes O, Lyketsos C, McKhann G. Depression and cardiac morbidity 5 years after coronary artery bypass surgery. Psychosomatics 2002;43(6):464–71. Peterson JC, Charlson ME, Williams-Russo P, Krieger KH, Pirraglia PA, Meyers BS, et al. New postoperative depressive symptoms and long-term cardiac outcomes after coronary artery bypass surgery. The American Journal of Geriatric Psychiatry: official journal of the American Association for Geriatric Psychiatry 2002;10(2):192–8. Stenman M, Holzmann MJ, Sartipy U. Relation of major depression to survival after coronary artery bypass grafting. The American Journal of Cardiology 2014;114(5):698–703. Ho PM, Masoudi FA, Spertus JA, Peterson PN, Shroyer AL, McCarthy Jr M, et al. Depression predicts mortality following cardiac valve surgery. The Annals of Thoracic Surgery 2005;79(4):1255–9. Tully PJ, Baker RA, Winefield HR, Turnbull DA. Depression, anxiety disorders and Type D personality as risk factors for delirium after cardiac

Please cite this article in press as: Indja BE, et al. Neurocognitive and [1_TD$IF]Psychiatric Issues Post Cardiac Surgery. Heart, Lung and Circulation (2017), http://dx.doi.org/10.1016/j.hlc.2016.12.010

430 431 432 433 434 435 436 437 438 439 440 441 442 443 444 445 446 447 448 449 450 451 452 453 454 455 456 457 458 459 460 461 462 463 464 465 466 467 468 469 470 471 472 473 474 475 476 477 478 479 480 481 482 483 484 485 486 487 488 489 490 491 492 493 494 495 496 497 498 499 500 501 502 503 504 505

HLC 2277 1–7

6

506 507 508 509 510 511 512 513 514 515 516 517 518 519 520 521 522 523 524 525 526 527 528 529 530 531 532 533 534 535 536 537 538 539 540 541 542 543 544 545 546 547 548 549 550 551 552 553 554 555 556 557 558 559 560 561 562 563 564 565 566 567 568 569 570 571 572 573 574 575 576 577 578 579 580

B.E. Indja et al.

[31]

[32]

[33]

[34]

[35]

[36]

[37]

[38]

[39]

[40]

[41]

[42]

[43]

[44]

[45]

[46]

[47]

[48]

[49]

[50]

surgery. The Australian and New Zealand Journal of Psychiatry 2010; 44(11):1005–11. Humphreys JM, Denson LA, Baker RA, Tully PJ. The importance of depression and alcohol use in coronary artery bypass graft surgery patients: risk factors for delirium and poorer quality of life. Journal of Geriatric Cardiology 2016;13(1):51–7. Baumeister H, Hutter N, Bengel J. Psychological and pharmacological interventions for depression in patients with coronary artery disease. The Cochrane Database of Systematic Reviews 2011;(9):CD008012. Tully PJ, Cardinal T, Bennetts JS, Baker RA. Selective serotonin reuptake inhibitors, venlafaxine and duloxetine are associated with in hospital morbidity but not bleeding or late mortality after coronary artery bypass graft surgery. Heart, Lung and Circulation 2012;21(4): 206–14. Xiong GL, Jiang W, Clare R, Shaw LK, Smith PK, Mahaffey KW, et al. Prognosis of patients taking selective serotonin reuptake inhibitors before coronary artery bypass grafting. The American Journal of Cardiology 2006;98(1):42–7. Stenman M, Holzmann MJ, Sartipy U. Antidepressant use before coronary artery bypass surgery is associated with long-term mortality. International Journal of Cardiology 2013;167(6):2958–62. Floyd TF, Shah PN, Price CC, Harris F, Ratcliffe SJ, Acker MA, et al. Clinically silent cerebral ischemic events after cardiac surgery: their incidence, regional vascular occurrence, and procedural dependence. The Annals of Thoracic Surgery 2006;81(6):2160–6. Fanning JP, Wesley AJ, Wong AA, Fraser JF. Emerging spectra of silent brain infarction. Stroke; a Journal of Cerebral Circulation 2014;45 (11):3461–71. Barber PA, Hach S, Tippett LJ, Ross L, Merry AF, Milsom P. Cerebral ischemic lesions on diffusion-weighted imaging are associated with neurocognitive decline after cardiac surgery. Stroke; a Journal of Cerebral Circulation 2008;39(5):1427–33. Restrepo L, Wityk RJ, Grega MA, Borowicz Jr L, Barker PB, Jacobs MA, et al. Diffusion- and perfusion-weighted magnetic resonance imaging of the brain before and after coronary artery bypass grafting surgery. Stroke; a Journal of Cerebral Circulation 2002;33(12):2909–15. Ishikawa H, Meguro K, Ishii H, Tanaka N, Yamaguchi S. Silent infarction or white matter hyperintensity and impaired attention task scores in a nondemented population: the Osaki-Tajiri Project. Journal of Stroke and Cerebrovascular Diseases: the official journal of National Stroke Association 2012;21(4):275–82. Knipp SC, Matatko N, Schlamann M, Wilhelm H, Thielmann M, Forsting M, et al. Small ischemic brain lesions after cardiac valve replacement detected by diffusion-weighted magnetic resonance imaging: relation to neurocognitive function. European Journal of Cardio-Thoracic Surgery: official journal of the European Association for Cardio-Thoracic Surgery 2005;28(1):88–96. Knipp SC, Kahlert P, Jokisch D, Schlamann M, Wendt D, Weimar C, et al. Cognitive function after transapical aortic valve implantation: a singlecentre study with 3-month follow-up. Interactive Cardiovascular and Thoracic Surgery 2013;16(2):116–22. Wasser K, Pilgram-Pastor SM, Schnaudigel S, Stojanovic T, Schmidt H, Knauf J, et al. New brain lesions after carotid revascularization are not associated with cognitive performance. Journal of Vascular Surgery 2011;53(1):61–70. Avdibegovic E, Becirovic E, Selimbasic Z, Hasanovic M, Sinanovic O. Cerebral cortical atrophy and silent brain infarcts in psychiatric patients. Psychiatria Danubina 2007;19(1-2):49–55. Yamashita H, Fujikawa T, Yanai I, Morinobu S, Yamawaki S. Cognitive dysfunction in recovered depressive patients with silent cerebral infarction. Neuropsychobiology 2002;45(1):12–8. Fujikawa T, Yamawaki S, Touhouda Y. Incidence of silent cerebral infarction in patients with major depression. Stroke; a Journal of Cerebral Circulation 1993;24(11):1631–4. Direk N, Koudstaal PJ, Hofman A, Ikram MA, Hoogendijk WJ, Tiemeier H. Cerebral hemodynamics and incident depression: the Rotterdam Study. Biological Psychiatry 2012;72(4):318–23. Bakker SL, de Leeuw FE, de Groot JC, Hofman A, Koudstaal PJ, Breteler MM. Cerebral vasomotor reactivity and cerebral white matter lesions in the elderly. Neurology 1999;52(3):578–83. Fujikawa T, Yamawaki S, Touhouda Y. Silent cerebral infarctions in patients with late-onset mania. Stroke; a Journal of Cerebral Circulation 1995;26(6):946–9. Cassidy F, Carroll BJ. Vascular risk factors in late onset mania. Psychological Medicine 2002;32(2):359–62.

[51] Tamashiro JH, Zung S, Zanetti MV, de Castro CC, Vallada H, Busatto GF, et al. Increased rates of white matter hyperintensities in late-onset bipolar disorder. Bipolar Disorders 2008;10(7):765–75. [52] Beyer JL, Young R, Kuchibhatla M, Krishnan KR. Hyperintense MRI lesions in bipolar disorder: A meta-analysis and review. International Review of Psychiatry 2009;21(4):394–409. [53] Vermeer SE, Prins ND, den Heijer T, Hofman A, Koudstaal PJ, Breteler MM. Silent brain infarcts and the risk of dementia and cognitive decline. The New England Journal of Medicine 2003;348(13):1215–22. [54] Prins ND, van Dijk EJ, den Heijer T, Vermeer SE, Koudstaal PJ, Oudkerk M, et al. Cerebral white matter lesions and the risk of dementia. Archives of Neurology 2004;61(10):1531–4. [55] Debette S, Markus HS. The clinical importance of white matter hyperintensities on brain magnetic resonance imaging: systematic review and meta-analysis. BMJ 2010;341:c3666. [56] Schelling G, Richter M, Roozendaal B, Rothenhausler HB, Krauseneck T, Stoll C, et al. Exposure to high stress in the intensive care unit may have negative effects on health-related quality-of-life outcomes after cardiac surgery. Critical Care Medicine 2003;31(7):1971–80. [57] Schelling G, Roozendaal B, Krauseneck T, Schmoelz M, D DEQ, Briegel J. Efficacy of hydrocortisone in preventing posttraumatic stress disorder following critical illness and major surgery. Annals of the New York Academy of Sciences 2006;1071:46–53. [58] Beishuizen A, Thijs LG, Vermes I. Patterns of corticosteroid-binding globulin and the free cortisol index during septic shock and multitrauma. Intensive Care Medicine 2001;27(10):1584–91. [59] Cooper MS, Stewart PM. Corticosteroid insufficiency in acutely ill patients. The New England Journal of Medicine 2003;348(8):727–34. [60] Schelling G, Kilger E, Roozendaal B, de Quervain DJ, Briegel J, Dagge A, et al. Stress doses of hydrocortisone, traumatic memories, and symptoms of posttraumatic stress disorder in patients after cardiac surgery: a randomized study. Biological Psychiatry 2004;55(6):627–33. [61] Weis F, Kilger E, Roozendaal B, de Quervain DJ, Lamm P, Schmidt M, et al. Stress doses of hydrocortisone reduce chronic stress symptoms and improve health-related quality of life in high-risk patients after cardiac surgery: a randomized study. The Journal of Thoracic and Cardiovascular Surgery 2006;131(2):277–82. [62] McEwen BS. Mood disorders and allostatic load. Biological Psychiatry 2003;54(3):200–7. [63] Shemesh E, Yehuda R, Milo O, Dinur I, Rudnick A, Vered Z, et al. Posttraumatic stress, nonadherence, and adverse outcome in survivors of a myocardial infarction. Psychosomatic Medicine 2004;66(4):521–6. [64] Blachy PH, Starr A. Post-Cardiotomy Delirum. The American Journal of Psychiatry 1964;121:371–5. [65] Lin Y, Chen J, Wang Z. Meta-analysis of factors which influence delirium following cardiac surgery. Journal of Cardiac Surgery 2012;27(4):481–92. [66] Rolfson DB, McElhaney JE, Rockwood K, Finnegan BA, Entwistle LM, Wong JF, et al. Incidence and risk factors for delirium and other adverse outcomes in older adults after coronary artery bypass graft surgery. The Canadian Journal of Cardiology 1999;15(7):771–6. [67] Guenther U, Theuerkauf N, Frommann I, Brimmers K, Malik R, Stori S, et al. Predisposing and precipitating factors of delirium after cardiac surgery: a prospective observational cohort study. Annals of Surgery 2013;257(6):1160–7. [68] Rudolph JL, Babikian VL, Treanor P, Pochay VE, Wigginton JB, Crittenden MD, et al. Microemboli are not associated with delirium after coronary artery bypass graft surgery. Perfusion 2009;24(6):409–15. [69] Martin KK, Wigginton JB, Babikian VL, Pochay VE, Crittenden MD, Rudolph JL. Intraoperative cerebral high-intensity transient signals and postoperative cognitive function: a systematic review. American Journal of Surgery 2009;197(1):55–63. [70] Gosselt AN, Slooter AJ, Boere PR, Zaal IJ. Risk factors for delirium after on-pump cardiac surgery: a systematic review. Critical Care 2015;19:346. [71] Andrejaitiene J, Sirvinskas E. Early post-cardiac surgery delirium risk factors. Perfusion 2012;27(2):105–12. [72] Marcantonio ER, Goldman L, Orav EJ, Cook EF, Lee TH. The association of intraoperative factors with the development of postoperative delirium. The American Journal of Medicine 1998;105(5):380–4. [73] Stransky M, Schmidt C, Ganslmeier P, Grossmann E, Haneya A, Moritz S, et al. Hypoactive delirium after cardiac surgery as an independent risk factor for prolonged mechanical ventilation. Journal of Cardiothoracic and Vascular Anesthesia 2011;25(6):968–74. [74] Jackson JC, Gordon SM, Hart RP, Hopkins RO, Ely EW. The association between delirium and cognitive decline: a review of the empirical literature. Neuropsychology Review 2004;14(2):87–98.

Please cite this article in press as: Indja BE, et al. Neurocognitive and [1_TD$IF]Psychiatric Issues Post Cardiac Surgery. Heart, Lung and Circulation (2017), http://dx.doi.org/10.1016/j.hlc.2016.12.010

581 582 583 584 585 586 587 588 589 590 591 592 593 594 595 596 597 598 599 600 601 602 603 604 605 606 607 608 609 610 611 612 613 614 615 616 617 618 619 620 621 622 623 624 625 626 627 628 629 630 631 632 633 634 635 636 637 638 639 640 641 642 643 644 645 646 647 648 649 650 651 652 653 654 655

HLC 2277 1–7

7

Neurocognitive and Psychiatric Issues

656 657 658 659 660 661 662

[75] Martin BJ, Buth KJ, Arora RC, Baskett RJ. Delirium: a cause for concern beyond the immediate postoperative period. The Annals of Thoracic Surgery 2012;93(4):1114–20. [76] Loponen P, Luther M, Wistbacka JO, Nissinen J, Sintonen H, Huhtala H, et al. Postoperative delirium and health related quality of life after coronary artery bypass grafting. Scandinavian Cardiovascular Journal 2008;42(5):337–44.

[77] Milbrandt EB, Deppen S, Harrison PL, Shintani AK, Speroff T, Stiles RA, et al. Costs associated with delirium in mechanically ventilated patients. Critical Care Medicine 2004;32(4):955–62. [78] Kazmierski J, Kowman M, Banach M, Fendler W, Okonski P, Banys A, et al. The use of DSM-IV and ICD-10 criteria and diagnostic scales for delirium among cardiac surgery patients: results from the IPDACS study. The Journal of Neuropsychiatry And Clinical Neurosciences 2010;22(4):426–32.

Please cite this article in press as: Indja BE, et al. Neurocognitive and [1_TD$IF]Psychiatric Issues Post Cardiac Surgery. Heart, Lung and Circulation (2017), http://dx.doi.org/10.1016/j.hlc.2016.12.010

663 664 665 666 667 668 669