44 - Optimal Intraoperative Technique to Prevent Postoperative Delirium

Delirium after surgery is an increasing concern for older adults, caregivers, and health care providers. It is characterized by inattention, confusion, and altered mental state. Delirium is not only disturbing for patients and families during the acute episode but has significant long-term consequences, including an association with long-term cognitive and functional impairment and mortality. In this chapter, we review recommendations and evidence for (1) screening for high-risk patients, (2) medications to avoid, (3) medications to prevent delirium, (4) choice of anesthetic type, (5) electroencephalography (EEG)-guided anesthetic depth, (6) blood pressure control, and (7) cerebral perfusion monitoring. Our final recommendations are to discuss the risk for postoperative delirium with patients. Screen patients for preexisting cognitive impairment and develop protocols for anesthetic management. Be aware of the Beers list criteria medications. Do not apply enhanced recovery after surgery (ERAS) protocols without thinking thorough whether the measures are appropriate for an older adult. Avoid unnecessary deep planes of anesthesia. Optimize pain control. Finally, screen for delirium in the postoperative period or preoperatively in emergency cases

Hierarchical Cluster Analysis Identifies Distinct Physiological States After Acute Brain Injury

Background Analysis of intracranial multimodality monitoring data is challenging, and quantitative methods may help identify unique physiological signatures that inform therapeutic strategies and outcome prediction. The aim of this study was to test the hypothesis that data-driven approaches can identify distinct physiological states from intracranial multimodality monitoring data. Methods This was a single-center retrospective observational study of patients with either severe traumatic brain injury or high-grade subarachnoid hemorrhage who underwent invasive multimodality neuromonitoring. We used hierarchical cluster analysis to group hourly values for heart rate, mean arterial pressure, intracranial pressure, brain tissue oxygen, and cerebral microdialysis across all included patients into distinct groups. Average values for measured physiological variables were compared across the identified clusters, and physiological profiles from identified clusters were mapped onto physiological states known to occur after acute brain injury. The distribution of clusters was compared between patients with favorable outcome (discharged to home or acute rehab) and unfavorable outcome (in-hospital death or discharged to chronic nursing facility). Results A total of 1704 observations from 20 patients were included. Even though the difference in mean values for measured variables between patients with favorable and unfavorable outcome were small, we identified four distinct clusters within our data: (1) events with low brain tissue oxygen and high lactate-to-pyruvate ratio-values (consistent with cerebral ischemia), (2) events with higher intracranial pressure values without evidence for ischemia (3) events which appeared to be physiologically "normal," and (4) events with high cerebral lactate without brain hypoxia (consistent with cerebral hyperglycolysis). Patients with a favorable outcome had a greater proportion of cluster 3 (normal) events, whereas patients with an unfavorable outcome had a greater proportion of cluster 1 (ischemia) and cluster 4 (hyperglycolysis) events (p < 0.0001, Fisher-Freeman-Halton test). Conclusions A data-driven approach can identify distinct groupings from invasive multimodality neuromonitoring data that may have implications for therapeutic strategies and outcome predictions. These groupings could be used as classifiers to train machine learning models that can aid in the treatment of patients with acute brain injury. Further work is needed to replicate the findings of this exploratory study in larger data sets

Does the melatonin receptor 1B gene polymorphism have a role in postoperative delirium?

INTRODUCTION:Patients undergoing cardiac surgery are at high risk for postoperative delirium, which is associated with longer hospital and intensive care lengths of stays, increased morbidity and mortality. Because sleep disturbances are common in delirium, melatonin has been an area of interest in the treatment of delirium. The rs10830963 single nucleotide polymorphism of the melatonin receptor 1B gene can cause pathological dysfunction of this receptor and is associated with delayed morning offset of melatonin. We hypothesized patients undergoing aortic cardiac surgery who have the risk genotype of a melatonin receptor 1B polymorphism would have a higher incidence of postoperative delirium. METHODS:Ninety-eight patients undergoing aortic root or valve surgery underwent analysis for melatonin receptor 1B single nucleotide polymorphism, rs10830963. Using a validated method, CHART-DEL, all charts were retrospectively reviewed and scored for the presence of delirium while blinded to the results of the melatonin receptor 1B gene polymorphism. RESULTS:Genotyping for melatonin receptor 1B polymorphism was acceptable in 76 subjects of European descent of which 18 (23.7%) had delirium. Four of seven subjects with the risk genotype had delirium versus only 20.3% of subjects without the risk genotype. This carried an odds ratio of 5.2 (1.0, 26.1), p = 0.050. CONCLUSION:This observation suggests a role of the risk genotype of a melatonin receptor 1B polymorphism in the development of postoperative delirium. These hypotheses generating results warrant further prospective studies in a larger cohort group with delirium, circadian rhythm and melatonin assessments

Defining a Taxonomy of Intracranial Hypertension Is ICP More Than Just a Number?

Intracranial pressure (ICP) monitoring and control is a cornerstone of neuroanesthesia and neurocritical care. However, because elevated ICP can be due to multiple pathophysiological processes, its interpretation is not straightforward. We propose a formal taxonomy of intracranial hypertension, which defines ICP elevations into 3 major pathophysiological subsets: increased cerebral blood volume, masses and edema, and hydrocephalus. (1) Increased cerebral blood volume increases ICP and arises secondary to arterial or venous hypervolemia. Arterial hypervolemia is produced by autoregulated or dysregulated vasodilation, both of which are importantly and disparately affected by systemic blood pressure. Dysregulated vasodilation tends to be worsened by arterial hypertension. In contrast, autoregulated vasodilation contributes to intracranial hypertension during decreases in cerebral perfusion pressure that occur within the normal range of cerebral autoregulation. Venous hypervolemia is produced by Starling resistor outflow obstruction, venous occlusion, and very high extracranial venous pressure. Starling resistor outflow obstruction tends to arise when cerebrospinal fluid pressure causes venous compression to thus increase tissue pressure and worsen tissue edema (and ICP elevation), producing a positive feedback ICP cycle. (2) Masses and edema are conditions that increase brain tissue volume and ICP, causing both vascular compression and decrease in cerebral perfusion pressure leading to oligemia. Brain edema is either vasogenic or cytotoxic, each with disparate causes and often linked to cerebral blood flow or blood volume abnormalities. Masses may arise from hematoma or neoplasia. (3) Hydrocephalus can also increase ICP, and is either communicating or noncommunicating. Further research is warranted to ascertain whether ICP therapy should be tailored to these physiological subsets of intracranial hypertension

Frailty Is Associated With Postoperative Delirium But Not With Postoperative Cognitive Decline in Older Noncardiac Surgery Patients

Postoperative cognitive dysfunction (POCD) and delirium are the most common perioperative cognitive complications in older adults undergoing surgery. A recent study of cardiac surgery patients suggests that physical frailty is a risk factor for both complications. We sought to examine the relationship between preoperative frailty and postoperative delirium and preoperative frailty and POCD after major noncardiac surgery. We performed a prospective cohort study of patients >65 years old having major elective noncardiac surgery with general anesthesia. Exclusion criteria were preexisting dementia, inability to consent, cardiac, intracranial, or emergency surgery. Preoperative frailty was determined using the FRAIL scale, a simple questionnaire that categorizes patients as robust, prefrail, or frail. Delirium was assessed with the Confusion Assessment Method for the intensive care unit (CAM-ICU) twice daily, starting in the recovery room until hospital discharge. All patients were assessed with neuropsychological tests (California Verbal Learning Test II, Trail Making Test, subtests from the Wechsler Adult Intelligence Scale, Logical Memory Story A, Immediate and Delayed Recall, Animal and Vegetable verbal fluency, Boston Naming Test, and the Mini-Mental Status Examination) before surgery and at 3 months afterward. A total of 178 patients met inclusion criteria; 167 underwent major surgery and 150 were available for follow-up 3 months after surgery. The median age was 70 years old. Thirty-one patients (18.6%) tested as frail, and 72 (43.1%) prefrail before surgery. After adjustment for baseline cognitive score, age, education, surgery duration, American Society of Anesthesiologists (ASA) physical status, type of surgery, and sex, patients who tested frail or prefrail had an estimated 2.7 times the odds of delirium (97.5% confidence interval, 1.0-7.3) when compared to patients who were robust. There was no significant difference between the proportion of POCD between patients who tested as frail, prefrail, or robust. After adjustment for baseline cognition, testing as frail or prefrail with the FRAIL scale is associated with increased odds of postoperative delirium, but not POCD after noncardiac surgery

Comparison of optical measurements of critical closing pressure acquired before and during induced ventricular arrhythmia in adults

Significance: The critical closing pressure (CrCP) of cerebral circulation, as measured by diffuse correlation spectroscopy (DCS), is a promising biomarker of intracranial hypertension. However, CrCP techniques using DCS have not been assessed in gold standard experiments. Aim: CrCP is typically calculated by examining the variation of cerebral blood flow (CBF) during the cardiac cycle (with normal sinus rhythm). We compare this typical CrCP measurement with a gold standard obtained during the drops in arterial blood pressure (ABP) caused by rapid ventricular pacing (RVP) in patients undergoing invasive electrophysiologic procedures. Approach: Adults receiving electrophysiology procedures with planned ablation were enrolled for DCS CBF monitoring. CrCP was calculated from CBF and ABP data by three methods: (1) linear extrapolation of data during RVP ( CrCP RVP ; the gold standard); (2) linear extrapolation of data during regular heartbeats ( CrCP Linear ); and (3) fundamental harmonic Fourier filtering of data during regular heartbeats ( CrCP Fourier ). Results: CBF monitoring was performed prior to and during 55 episodes of RVP in five adults. CrCP RVP and CrCP Fourier demonstrated agreement ( R = 0.66 , slope = 1.05 (95%CI, 0.72 to 1.38). Agreement between CrCP RVP and CrCP Linear was worse; CrCP Linear was 8.2 ± 5.9    mmHg higher than CrCP RVP (mean ± SD; p < 0.001 ). Conclusions: Our results suggest that DCS-measured CrCP can be accurately acquired during normal sinus rhythm

Continuous non-invasive optical monitoring of cerebral blood flow and oxidative metabolism after acute brain injury

Rapid detection of ischemic conditions at the bedside can improve treatment of acute brain injury. In this observational study of 11 critically ill brain-injured adults, we employed a monitoring approach that interleaves time-resolved near-infrared spectroscopy (TR-NIRS) measurements of cerebral oxygen saturation and oxygen extraction fraction (OEF) with diffuse correlation spectroscopy (DCS) measurement of cerebral blood flow (CBF). Using this approach, we demonstrate the clinical promise of non-invasive, continuous optical monitoring of changes in CBF and cerebral metabolic rate of oxygen (CMRO ). In addition, the optical CBF and CMRO measures were compared to invasive brain tissue oxygen tension (PbtO ), thermal diffusion flowmetry CBF, and cerebral microdialysis measures obtained concurrently. The optical CBF and CMRO information successfully distinguished between ischemic, hypermetabolic, and hyperemic conditions that arose spontaneously during patient care. Moreover, CBF monitoring during pressor-induced changes of mean arterial blood pressure enabled assessment of cerebral autoregulation. In total, the findings suggest that this hybrid non-invasive neurometabolic optical monitor (NNOM) can facilitate clinical detection of adverse physiological changes in brain injured patients that are otherwise difficult to measure with conventional bedside monitoring techniques

Sleep, self‐reported ocular health, and cognition in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) and SOL‐Investigation of Neurocognitive Aging (SOL‐INCA)

/Proposal Background Visually impaired individuals may experience increased frequency of sleep/wake disorders, fragmented sleep, insomnia, and short sleep duration. Visual impairment and sleep disorders can have downstream effects on cognitive functioning. Method Sample included n = 590 (unweighted) HCHS/SOL Miami Field Center participants ages 45‐74 at baseline who returned for cognitive examination on average 7‐years later (SOL‐INCA). Participants completed validated ocular (National Eye Institute Visual Functioning Questionnaire; NEI‐VFQ), validated sleep questionnaires for sleepiness, insomnia, sleep duration and objective measures of sleep apnea visit‐1 (2008‐2011). They also completed a battery of neurocognitive tests for verbal episodic learning and memory (Brief Spanish English Verbal Learning Test), verbal fluency (Controlled Oral Word Association), processing speed and executive function (Digit Symbol Substitution) at visit‐1 and at SOL‐INCA. Two additional measures of processing speed/executive functioning were added at SOL‐INCA(Trails‐A, ‐B). We examined global cognitive performance and change using a regression‐based reliable change index, adjusting for the time lapse between visit 1 and SOL‐INCA (all measured in z‐score units). We used regression models to test whether (1) participants with sleep disorders have an increased risk for visual impairment, (2a) ocular health is associated with worse baseline and average 7‐years cognitive function and/or cognitive decline, and (2b) sleep attenuates any of these associations. Result Sleepiness (β = 0.04; p<0.01) and insomnia (β = 0.03; p<0.001) were linked to worse ocular health, and the associations were robust to adjustment for sociodemographic characteristics, acculturation, behavioral risk measures, and health conditions. Worse ocular health was linked to lower global cognitive function at baseline (β = ‐0.14; p<0.001) and on average 7‐years later (β = ‐0.16; p<0.01). The associations were consistent across all considered cognitive domains and robust to demographic adjustments. Ocular health was also associated with a change in verbal fluency (β = ‐0.17; p<0.05), but no change was observed in other cognitive domains. Sleep disorders did not attenuate any of the reported associations. Conclusion Self‐reported ocular health was independently associated with worse language, memory, and executive function and predicted 7‐year cognitive decline in the language domain