2. prof. siti chasnak pocd 2016-updateprofsiti
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Anesthesiologists should concern about the risk of POCD by making prevention and attentive to the potential risk factors. It should be remembered that research in animal models which represent the specific characteristics of POCD in human remains unclear. With many factors still unknown, there is still a chance for sinchronized preclinical and clinical research on POCD.
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2. prof. siti chasnak pocd 2016-updateprofsiti
- 1. POSTOPERATIVE COGNITIVE DYSFUNCTION What should we know? Siti Chasnak Saleh Airlangga Univ./Soetomo Hospt. Surabaya 03/08/16 1
- 2. Characterization of POCD Memory impairment as identified by a reduced ability to learn or recall information. Disturbance in executive functioning Disturbance in attention or speed of information processing Impairment of perceptual-motor abilities Impairment in language GERIATRIC & AGING 2003;vol 6 no 10 03/08/16 2
- 3. 03/08/16 3 POCD • Not detected until days or weeks after anesthesia. • Duration of several weeks to permanent • Diagnosis is only warranted if: - corroborated with neurophychological testing - evidence of greater memory loss than one would expect due to normal aging
- 4. 4 Long-term postoperative cognitive dysfunction in the elderly: ISPOCD1 study JT Moller P Cluitmans LS Rasmussen P Houx H Rasmussen J CanetJT Moller P Cluitmans LS Rasmussen P Houx H Rasmussen J Canet P Rabbitt J Jolles K Larsen CD Hanning O Langeron T Johnson PM LauvenP Rabbitt J Jolles K Larsen CD Hanning O Langeron T Johnson PM Lauven PA Kristensen A Biedler H van Beem O Fraidakis, JH SilversteinPA Kristensen A Biedler H van Beem O Fraidakis, JH Silverstein JEW Beneken JS Gravenstein for the ISPOCD investigatorsJEW Beneken JS Gravenstein for the ISPOCD investigators THE LANCET 1998;351:857-861 • Collaborative research effort: – Members from 8 European countries and USA – 13 hospitals • Research conducted from 1994 - 1996 International Study of Postoperative Cognitive Dysfunction 03/08/16
- 5. 5 0 5 10 15 20 25 30 Percentage(%) Early Late Controls Patients Lancet 1998: 351-357 * * * p < 0.004 Incidence of POCD in patients and control One week 3 months 03/08/16
- 6. 03/08/16 6 INCIDENCE OF POCD (according age group n=1082) Age (yr) 1 Week 3 months 18 – 39 36.6% 5.7% 40 - 59 30.4% 5.6% > 60 41.4% 12.7% Monk et al: Anesthesiology 2008; 108:18-30.
- 7. Risk factors for POCD Risk factors Patient Advence age, pre-existing cerebral, cardiac or vascular disease, preoperative mild mild cognitive impairment (MCI), low educational level, history of alcohol abuse Surgery Extensive surgical procedure, intra-or postoperative complication, secondary surgery Anesthesia Long-acting anesthetic, marked disturbance of homeostasis, organ ischemia due to hypoxia and hypoperfusion, intra-or postoperative anesthesiological complication. Dtsch Arztedl Int 2014; 111(8): 119-125 03/08/16 7
- 8. Predictors of POCD: 3 Months After Surgery NS0.046History of MI NS0.021Baseline Co-morbidity NS0.009ASA Physical Status NS0.003History of Stroke 2.51 (p=0.057)0.001Age 0.86 (p=0.028)< 0.001Years of Education NS0.028NYHA Status NSNSAnesthesia Time NSNSBaseline MMSE NSNSGender NSNSSurgery Type Multivariate Odds RatioUnivariate P valueRisk Factors for POCD Multivariate c-statistic = 0.671 (p = 0.003) Monk et al. Anesthesiology 2001; 95: A-50
- 9. Preoperative factors • Age • Pre-existing diseases • Low level if education • Cognitive function Hospital associated factors • Change in environment • Length of hospital stay • Sleep deprivation (noise and monitoring) Postoperative factors • Inflammatory response • Postoperative pain • Stress-induced sleep disturbances • Opioids Interventions • Minimal invasive surgery • Pain control - non-opioid • Early discharge • Pharmacological sleep improvement • Reduction in nighttime noise POCD Pathogenic mechanism for POCD and possible intervention Act Anaesthesiol Scand 2010, 54:951-95603/08/16 9
- 10. Continuum from Normal Aging through Mild Cognitive Impairment to Dementia Mild cognitive impairment Dementia Age Function Normal Aging 03/08/16 10
- 11. Threshold Theory for Cognitive Decline LesionLesion LesionLesionProtective Factor Case A Case B BrainReserveCapacity A:: Protective factor (greater brain reserve capacity), lower test sensitivity, no impairment B: Vulnerability factor (less brain reserve capacity), higher test sensitivity, impairment Satz, Neuropsychology 1993:(7);273. Functional impairment cutoff 03/08/16 11
- 12. 03/08/16 12
- 13. 03/08/16 13 Mayo Clin Proc. 2011;86(6):885-893 Pathogenesis of cognitive decline
- 14. Proposed Mechanisms for Neuroinflammation and POCD J Anesth Perioper Med 2014; 1: 97-103.03/08/16 14
- 15. 03/08/16 15 Eckenhoff R, Prog Neuro-Psychopharm & Bio Psych, 2012
- 16. Anesthetic Risk Factors for POCD • Cholinergic neurons in the basal forebrain regulate normal memory • Choline reserves ↓ with aging • Anesthetic agents affect release of CNS neurotransmitter – acetylcholine, dopamine, norepinephrine • Difficult to postulate effects of anesthesia on memory, since mechanisms of general anesthesia are poorly understood. 03/08/16 16
- 17. 03/08/16 17 Rossi et al .Anesth Analg 2014;119:947–55)
- 18. • Not been able to clearly link general anesthesia & POCD • Suggesting neurotoxicity from animal studies, but not fully explain POCD in humans • Drugs effect may play a role in postoperative cognitive decline & analgesics Anesthesia 03/08/16 18
- 19. 03/08/16 19 Conclusion Anesthesiologists should concern about the risk of POCD by making prevention and attentive to the potential risk factors. It should be remembered that research in animal models which represent the specific characteristics of POCD in human remains unclear. With many factors still unknown, there is still a chance for sinchronized preclinical and clinical research on POCD.
- 20. 03/08/16 20
Editor's Notes
- The largest prospective study evaluating cognitive dysfunction after non-cardiac surgery was published in The Lancet in March of 1998. This study was a collaborative research effort from 13 hospitals in 8 different European countries and the United States. It was conducted from 1994 through 1996 and the senior author on this manuscript was Dr. J. S. Gravenstein at the University of Florida.
- These investigators found that postoperative cognitive dysfunction occurred in 26% of patients at one week after surgery and in 10% of patients at three months after surgery, which was significantly higher than the 3% of control patients at each time point.
- Univariate predictors of cognitive dysfunction at 3 months after surgery included: Lower educational level, Older age, History of stroke, Higher ASA physical status class, Higher New York Heart Association class, and History of a previous myocardial infarction. When logistic regression was performed using the significant univariate indicators for cognitive decline, only lower educational level and older age remained significant.
- In recent years, neurologists have described a transitional state between normal aging and dementia called mild cognitive impairment or MCI. While all elderly individuals experience some gradual cognitive decline with normal aging, there are certain elders who experience greater memory loss than one would expect for their age but do not meet the criteria for dementia. When these people are observed longitudinally, they progress to dementia at an accelerated rate compared with healthy, age-matched individuals. It is possible that the elderly patients who experience postoperative cognitive problems have mild cognitive impairment prior to surgery and the stress of the perioperative period pushes them over their “functional cliff.”
- In the past decade, neuropsychologists have used the concept of a threshold theory to explain why some elderly people are vulnerable to cognitive deterioration while others remain cognitively intact their entire lives. The basis of the threshold theory is that an individual’s brain reserve capacity determines cognitive changes during aging. In this slide, you can see two hypothetical cases. In case A, the individual has greater reserve capacity and presumably redundant neural networks. In this case, a lesion occurs but remains subthreshold and the patient continues to function normally. In case B, a similar brain lesion occurs, but the individual has less brain reserve and can no longer function normally after the insult.
- Factors and molecular events associated with the pathogenesis of cognitive decline. CNS = central nervous system; DAMPs = damage- associated molecular patterns; HMGB-1 = high mobility group box chromosomal protein 1; IL-1 = interleukin 1; PMN = polymorphonuclear leukocytes; TNF = tumor necrosis factor α; TNFR = tumor necrosis factor α receptor; TLR = toll-like receptor.
- Surgery has been shown to engage the innate immune system and activate a cascade of pro-inflammatory mediators, including alarmins, cytokines and eicosanoids. These molecules exert effects on the humoral and neuronal signaling overall contributing to the neuroinflammatory response. These processes are mediated not only by activation of resident microglia but also by infiltration of peripheral cells into the brain parenchyma via a disrupted BBB. This pro-inflammatory milieu and glia dysfunction impair neuronal activity and synaptic plasticity, impinging on processes of long- term potentiation, neurotransmission, and receptor function at the synapse. In combination, these pathological hallmarks contribute to learning and memory impairments following surgical trauma.
- Exposure to anesthesia has been suggested as a possible cause of postoperative cognitive decline. Evidence suggests that cholinergic neurons in the basal forebrain regulate normal memory function. Choline reserves decrease with aging and this is felt to be the primary reason that the elderly are more prone to delirium following surgery. Anesthetic agents affecting the release of central nervous system transmitters such as acetylcholine, dopamine, and norepinephrine could potentially impair memory, especially in elderly patients. However, the mechanisms of general anesthesia are poorly understood making it difficult to postulate the effects of anesthesia on memory.
- Perioperative changes in serum anticholinergic activity (ΔSAA) in patients with and without postoperative cognitive dysfunction (POCD). Most patients have small changes in SAA, and patients with and without POCD show both perioperative decreases and increases in SAA, suggesting that SAA is unlikely to be an important factor in the development of POCD in the majority of these patients.