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POSTOPERATIVE COGNITIVE DYSFUNCTION
V.H. SHARIPOVA, A.A. VALIHANOV
ПОСЛЕОПЕРАЦИОННАЯ КОГНИТИВНАЯ ДИСФУНКЦИЯ
В.Х. ШАРИПОВА, А.А. ВАЛИХАНОВ
Republican Research Centre of Emergency Medicine
Postoperative cognitive disfunction is often occurring phenomenon after surgeries or other interventions. In common population of patients its frequency at discharge reaches 30-40%. In spite of occurrence frequency and important clinical, social value, etiology, pathophysiology and methods of postoperative cognitive disfunction's decreasing still remain arguable. The review presents the most important moments of postoperative cognitive disfunction on the base of researches data which have been published fro recent 15 years.
Key-words: postoperative cognitive disfunction, anesthesia, cognitive functions.
Послеоперационная когнитивная дисфункция - важный часто встречающийся феномен после операций или других интервенций. В общей популяции больных ее частота при выписке достигает 30-40%. Несмотря на частоту встречаемости и важную клиническую и социальную значимость, этиология, патофизиология и методы уменьшения послеоперационной когнитивной дисфункции продолжают вызывать споры. В обзоре рассматриваются наиболее важные моменты послеоперационной когнитивной дисфункции на основании данных работ, опубликованных в последние 15 лет. Ключевые слова: послеоперационная когнитивная дисфункция, анестезия, когнитивные функции.
Postoperative cognitive dysfunction (POCD) is an important and well recognized medical condition that may follow surgery [5] or other procedures and has serious clinical and social impacts. This phenomenon was firstly described by Bedford in 1955 under the designation "adverse cerebral effects of anesthesia on old people" [8]. POCD was associated with increased risk of mortality, premature retirement from labour and social dependency [69]. Its prevalence among general population after non-cardiac surgery is significant [75,83], but more abundant among elderly[7], with an average incidence of 30 - 40% at hospital discharge and 5 - 12% at 3 months for noncardiac surgeries [47]. According to recent reports the prevalence of POCD after cardiac surgery at hospital discharge was 30 - 65% and after few months, the reported incidences were still high enough, 20 - 40% [15,27,49]. Despite such high incidence and significant impacts on patients the term POCD is neither included in the Diagnostic Statistical Manual nor in International Classification of Diseases [ICD-10].
DEFINITION AND ASSESSMENT
Cognition is defined as the mental processes of perception, memory, and information processing, which allows the individual to acquire knowledge, solve problems, and plan for the future. It comprises the mental processes required for everyday living and should not be confused with intelligence. Cognitive dysfunction is thus impairment of one or more of these processes [55].
Currently there is no standardized definition of POCD; the closest term in ICD-10 is "mild cognitive impairment". By Ingrid R POCD is defined as a new cognitive impairment arising after a surgical procedure [25]. Its diagnosis requires both pre- and post-operative psychometric testing. A deviation from normal cognition; however the definition of
the extent of deviation varies among studies. Furthermore, the cognitive changes in POCD are subtle and manifold and must be confirmed by a battery of neuropsychological tests. The most commonly seen manifestations are memory impairment and impairment performance on intellectual tasks. Hence the diagnosis cannot be made on purely clinical grounds.
The diagnosis of POCD is verified by psychometric testing performed pre- and postoperatively to assess cognitive performance. They include learning and memory, language, executive function, complex attention, perceptual-motor function and social cognition [64]. A comprehensive clinical neuropsychological examination may take two and a half hours. Different combinations of the following tests are generally used in the assessment of POCD.
• the Auditory Verbal Learning Test (a word learning test to assess short-time and long-time memory),
• the Trail Making Test (to assess executive functioning, visual search speed, speed of processing, mental flexibility and ability to perform multiple tasks),
• the Digit Span Test (to measure the working memory),
• the Digit-Letter Replacement Test (to assess learning ability and speed of general information processing),
• the Stroop Test (to examine selective attention capacity),
• the Four-Field Test (to assess the psychomotor reaction time)
• and the Paper and Pencil Memory Test (to examine sensomotor speed and the speed of recall).
There are available some composite tests as well which cover major aspects of cognitive performance and take significantly less time (5 - 15 minutes) than individual tests for each cognitive function. Some of them are Mini Mental State Exam (MMSE), Mini Cognitive Test (Mini-Cog),
General Practitioner Assessment of Cognition (GPCOG) and Erzigkeit's Short Cognitive Performance Test [42]. But the disadvantages of such composite tests are lack of sensitivity and specificity (around 80%) and in some cases they may be not sufficient to detect mild cognitive impairment.
Chung et al used untraditional method, driving simulator, after general anesthesia to assess cognitive performance [9]
Choice of tests is important because different cognitive tests differ in their susceptibility to confounders such as practice and floor and ceiling effects [56]. Floor effects occur when a test is too difficult, resulting in low baseline scores, and compromising the chances of detecting a postoperative decline, particularly when a decline is defined in absolute terms. Ceiling effects happen when the tests are too easy, so that some subjects are able to achieve maximum scores despite cognitive decline. Interpretation of tests may also have a critical influence on reported incidences of POCD. The out-come in a given patient or group when using a specific test battery depends strongly on the statistical methods used to define the cut-off point between POCD and normal variation in cognitive function [40]. Widely used analytic criteria are a percentage change from baseline in a defined number of tests (usually a decline > 20% in two or more tests) or an absolute decline from baseline scores greater than a defined proportion of the standard deviation of the two or more tests (usually > 1 SD, calculated from baseline scores) [61].
There is no consensus on the optimal time intervals for testing patients for POCD. In previous studies, cognitive function was measured beginning 1 day to as long as 5 years after surgery. The time interval at which a diagnosis of POCD holds the greatest clinical significance has not been determined, nor have any studies invalidated the importance of conducting assessments at a specific time point. Surgery-related factors may affect test performance in the immediate postoperative period, including acute pain [20,82], the use of drugs nausea, limited mobility, and fatigue. Thus, it has been recommended that patients should not be assessed for POCD until at least one week postoperatively [19,57].
Pathophysiology, etiology and risk factors of POCD
The exact pathophysiology of POCD is not fully understood, but recent available data shows that causative factors include the surgical experience [31] or potential neurotoxic effects of anesthesia [79]. Alosco M.L. et al. and Seminowicz D.A. et al. in separate studies reported postoperative cognitive improvements relative to preoperative function has even been reported after surgery and anesthesia [3,63]. According to much of recent available research it is believed that POCD has multifactorial pathophysiology which may include: genetic predisposition, immune response to surgery induced inflammation, neurotoxic effect of anesthetics, systemic and neural inflammation, intraoperative brain hypoxia, low level of education, advanced age and alcohol abuse.
Whether patients have a genetic predisposition for development of POCD genotype is not fully understood because findings from studies to date are conflicting. Abildstrom H. et al. in a large found no link between apolipoprotein E (Associated with Alzeimer's disease
and cognitive decline) genotype and POCD measured at one week or 3 months after surgery was conducted in patients undergoing noncardiac surgery [2]. However, this study likely underestimated the incidence of POCD since they considered any patients who were not "fit enough for testing" as not having POCD. Recently, McDonagh et al.conducted a study in 394 older patients undergoing non-cardiac surgery and similarly reported that apolipoprotein E4 was not associated with POCD measured at 6 weeks or at one year after surgery[13]. The results of Leung J et al. on apolipoprotein E4are in contrast to our work in 190 older patients undergoing noncardiac surgery, in which, the presence of one copy of the E4 allele was associated with an increased risk of early postoperative delirium [34].
Maekawa K et al. showed in prospective study [41] that preoperative existence of low grey matter volume and white matter lesions on MRI were associated with higher incidence of POCD after elective cardiac surgery. In a study using standardized assessment tools and good statistical design, Evered et al. compared the occurrence of POCD after CABG [on-pump; general anesthesia], coronary angiography [sedation only], and total hip arthroplasty [spinal and light general anesthesia]; the incidence of POCD after 3 months was 16%, 21% and 16% respectively. Unexpectedly, the least invasive procedure performed only with sedation was associated with the highest incidence of POCD. This suggests that neither the intensity of surgical or procedural intervention nor the type of anesthesia alone can predict the occurrence of POCD [15].
It has been believed that the surgical experience might induce POCD through surgery-induced systemic inflammation via activation of the immune system and release of proinflammatory cytokines [e.g. IL-1B, IL-6, TNF]. The latter are thought to violate the integrity of blood brain barrier and induce inflammation in the hippocampus, an area known to mediate memory and learning [60,73]. This response is even more exaggerated in the diseased brain [11,12,14]. Terrando et al. showed that a peripheral surgical procedure in mice activates the inflammatory TNF /NF-kB signal cascades, leading to the release of cytokines that impair the integrity of the blood-brain barrier [73]. Data by Rosczyk H.A. et al. in animal study support the concept that inflammation is a possible pathogenic mechanism for POCD [76].
To date, there is very little direct evidence that POCD is the result of cerebral inflammation caused by neuronal injuries, systemic inflammation, or a combination of the two. Several groups have measured biomarkers of neuronal injury such as neuron specific enolase, S100B and nuclear factor kB, after cardiac surgery with CPB [28,45], and have found elevated plasma levels, but with varying correlations between these markers and cognitive function. Unfortunately, these biomarkers remain non-specific with regard to neuronal injury. In the case of S100B, the assay has been shown to cross-react with non-neuronal molecules [18].
General anesthetics could potentially lead to memory impairment through hyperphosphorylation of tau-protein, an important protein involved in the pathogenesis
of Alzheimer's disease. Earlier studies attributed neuroinflammation to surgery only [10,74], but a more recent study has suggested anesthetic mediation as well. The putative neurotoxicity of anesthetic drugs in children has been studied in order to determine whether anesthesia in childhood might lead to behavioral abnormalities, learning disorders, and cognitive impairment in later years. The results of the findings that have been obtained are currently debated; in any case, twin studies by Stratmann G et al. have failed to yield any definitive evidence that anesthetic drugs are neurotoxic [71]. Earlier studies suggested an association between general anesthesia and a higher incidence of cognitive dysfunction relative to epidural anesthesia [22,4]. However, recent studies concluded that there was no relationship between anesthetic techniques and the magnitude or pattern of postoperative cognitive dysfunction [50,58]. Some studies report that opioids like fentanyl, sufentanil and remifentanil can be neurotoxic in rats [29]. Fentanyl is associated with delirium [6], but there seems to be no clear relationship between fentanyl dosage and the incidence of POCD 3 or 12 months postoperatively [67]. There is no convincing evidence that anesthetic agents cause inflammation resulting in POCD; indeed, control animals in recent studies that received isoflurane or neuroleptanesthesia, but no surgical procedures, showed neither cytokine activation, nor behavioural changes associated with POCD [74,80]. In Uzbekistan EshonovO. Sh.et. al. studied prevalence of POCD after total intravenous anesthesia with ketamine, fentanyl and droperidol in 192 patients. They reported 45% incidences of POCD after surgery [1]
Many authors compared patients receiving GA with those having regional anesthesia [RA] or neuroaxialanesthesia. A review of seventeen clinical studies [48,59] find no significant difference in the incidence of POCD after GA compared to RA. The main criticism of these studies is that RA is often combined with sedation, frequently deep sedation. Initially regional anesthesia without deep sedation [i.e. BIS>80 was shown to result in a substantially lower occurrence of delirium compared with [65]. Therefore, Silbert et al. [66] prospectively compared the incidence of POCD after GA for Extracorporeal Shockwave Lithotripsy [ESWL] with the use of spinal anesthesia without sedation. The incidence of POCD was almost three times as high after spinal anesthesia. At 1 week, POCD was 11.9% after spinal vs. 4.1% after GA; at 3 months the incidence was 19.6% and 6.8% for spinal and GA, respectively. The investigators could not conclude superiority of one technique over the other; clearly POCD could not be avoided through the use of RA without sedation. This and other findings after minimally invasive interventions point to a likely effect of hospitalization on patient functional status. Physician deconditioning has long been recognized as a consequence of hospital stays [21,62]
Depth of GA has been investigated as an influential factor for POCD. Two separate studies by Farag E. et al. and Jianxiong An et al. suggested that deeper level of anesthesia monitored by BiSpectral Index [BIS] to values between 3040 result in better cognitive outcome than lighter values
[i.e. 50-60] [17,32]. The main criticisms of this work are relatively small sample sizes and that assessment for POCD was done in the early postoperative period [4-6 weeks and 5 days, respectively]. Additionally, only 3 neuropsychological tests were used for assessment in the first study instead of a full battery of tests. The CODA trial [COgnitive Dysfunction after Anesthesia] is a prospective randomized study of 921 patients. The patients were divided into a BIS-titrated group with a target of 40-60 versus BIS-blinded group. The BIS-titrated group had less delirium, less POCD and decreased anesthetic delivery than the BIS-blinded group, where BIS values were lower than in the BIS-guided group [44]. Radtke F. M. et al. in a large prospective study found an association between low BIS values and higher incidence of delirium but not POCD [54]. More alarmingly, two studies by Lindholm M.L. et al. and Leslie K. et al. have linked low BIS values with mortality [33,39].
Old Age is considered to be a major risk factor for POCD in the available literature. Strom et al outlined seven mechanisms to explain the higher incidence of POCD in older subjects [72]. This includes decreased brain volume, decreased density of the blood-brain barrier, decreased neurogenesis, decreased baseline cognition, decreased cognitive reserve, increased likelihood of inflammation, and cerebrovascular disease. Elderly patients are more susceptible to sepsis, and when they develop sepsis, the morbidity and mortality are significantly greater than in younger patients [43]. It is thus highly likely that in humans the micro-vascular endothelium is primed by ageing, making the elderly more susceptible to the harmful effects of inflammation [81].
Hypoxia and hypotension are mechanisms that could induce cerebral ischemia and were examined in ISPOCD1 study [46] and were not found to be significant risk factors for POCD. However, direct measurement of cerebral oxygen desaturation predicts POCD in cardiac [68] and noncardiac surgery and might be useful in selected cases [38,85]. Showers of micro emboli during cardiac surgery, especially during cardiopulmonary bypass, were thought to represent a mechanism of subtle ischemia and POCD [53]. MRI is a useful modality for detecting cerebral ischemia and micro-infarcts caused by micro-emboli. Knipp et al. [27] prospectively examined 39 patients undergoing CABG by neuropsychological testing and MRI preoperatively and up to 3 years after the surgery. They found ischemic cerebral lesions in 51% of patients, but they failed to find an association between these lesions and POCD. Due to the small population studied, further large scale studies are needed to confirm these findings and their clinical significance.
Cognitive reserve and a patient>s propensity in developing adverse postoperative neurological outcomes need to be considered when discussing the pathophysiology of POCD. A hypothetical construct coined "cognitive reserve" has been used to describe models of cognitive aging and situations where the brain sustains injury [70,78]. Surrogates of cognitive reserve have included education level, occupational attainment, and performance on tests of knowledge (such as vocabulary). The association between lower occupational attainment and incident dementia has
been found in a number of studies. Although cognitive reserve is typically invoked as an important concept in dementia research, there is also evidence that cognitive reserve may play a protective role against POCD.
Alcohol abuse and an anxious, depressed basal mood have been identified as further risk factors for POCD. In a randomized trial, Hudetz et al. showed that patients with a history of alcohol abuse had worse cognitive impairment after surgery than patients with no such history [23].
Pharmacological methods of reducing incidence of POCD
Anti-inflammatory and neuroprotective therapies have been investigated for their potential to prevent POCD. Vacas et al. studied in animals that neutralizing antibody to alarmin prevented the inflammatory response and decreased the incidence of memory deficits [77]. Li SY et al. reported that minocycline decreased isoflurane-induced cognitive impairment in aged rats [35]. Zhang J et al. studied in 344 rats attenuating effect of amantadine on learning and memory impairment after surgical intervention [84]. Efficacy of low dose bolus ketamine in decreasing incidence of POCD after cardiac surgery was reported by Hudetz J et al.[24]. The effects of dexamethasone on the incidence of POCD are varying. Fang Q. et al. [16] reported a beneficial effect of low dose [0.1 mg/kg] dexamethasone on the incidence of POCD but a harmful effect with high dose [0.2 mg/kg] administration. In another study Ottens T.H. et al. [51] reported that high dose [1 mg/kg] dexamethasone is not beneficial. Yet another study showed that 8 mg of IV dexamethasone can significantly decrease the incidence of POCD in elderly patients who undergo cardiac surgery. Other drugs including ondansetron, ketoprofen, ACE inhibitors, and resveratrol could have beneficial effects according to recent studies [26,36,37,52].
CONCLUSION
POCD remains poorly defined and poorly understood. There are not still universally accepted criteria for diagnosis. Furthermore no testing methods of POCD are accepted as standard. While many potential explanations are suggested, a definitive pathophysiology has not been described, and a direct causal relationship has not been firmly established between the disease and any suggested insult. Furthermore, no definitive perioperative or, more specifically, anesthetic strategy has been shown to definitively improve the incidence or severity of POCD.
Additionally no measuring instruments for cognitive impairment have yet become established as part of routine clinical practice in anesthesiology departments. Due to time and labour-intensiveness of existing diagnostic test, there is a need for composite test with high specificity and sensitivity.
The prognostic significance of POCD remains a hotly debated topic, especially in light of recent data showing that patients with early POCD were at higher risk of mortality after discharge.
While both anesthesia and surgery have been associated with POCD, there are other factors that appear to contribute as well. For example, prolonged hospital stays, sleep deprivation in the hospital, and postoperative pain may all
contribute to POCD. Minimizing length-of-stay, carefully managing post-operative pain, and improving patient sleep-efforts may help with this disease. Implementation of fasttrack policy in orthopedic surgery could decrease early POCD [30].
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ОПЕРАЦИЯДАН СУЧНГИ КОГНИТИВ ДИСФУНКЦИЯ
В.Х. Шарипова, А.А. Валиханов Республика шошилинч тиббий ёрдам илмий маркази
Операциядан сунги когнитив дисфункция - операциялардан ёки бош°а интервенциядан сунг куп учрайдиган му^им феномен. Шифохонадан чи°аётган беморларнинг умумий популяциясида 30-40% ^олатларда кузатилади. Операциядан сунги когнитив дисфункциянинг ю°ори частотаси *амда му^им клиник ва ижтимоий а^амиятига °арамасдан, унинг этиологияси, патофизиологияси ва ми°дорини камайтириш масалалари ечилмаган. Ушбу шархда охирги 15 йилда чоп этилганишлар асосида операциядан сунги когнитив дисфункциянинг энг му^им жаб^алари ёритилган.
Контакт А.А. Валиханов, врач-анестезиолог РНЦЭМП. Tel: +99891-191-02-68 Email: abror_27@mail.ru
