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Extracorporeal membrane oxygenation (ECMO) is used to treat severe hypoxemic respiratory failure and as a rescue therapy for patients with cardiopulmonary arrest within a narrow window of time. A failure modes and effects analysis (FMEA) was conducted to analyze the clinical and operational processes leading to delays in initiating ECMO. FMEA determined these highest-risk failure modes that were contributing to process failure: (1) ECMO candidacy not determined in time, (2) no or incomplete evaluation for ECMO prior to consult or arrest, (3) ECMO team not immediately available, and (4) cannulation not completed in time. When implemented collectively, a total of 4 interventions addressed more than 95% of the system failures. These interventions were (1) ECMO response pager held by a team required for decision, (2) distribution of institutionally defined inclusion/exclusion criteria, (3) educational training for clinicians consulting the ECMO team, and (4) establishment of a mobile ECMO insertion cart.

ObjectiveTo use a cluster analysis of [18F]AV‐1451 tau‐PET data to determine how subjects with Alzheimer's disease (AD) vary in the relative involvement of the entorhinal cortex and neocortex, and determine whether relative involvement of these two regions can help explain variability in age and clinical phenotype in AD.MethodsWe calculated [18F]AV‐1451 uptake in entorhinal cortex and neocortex in 62 amyloid‐positive AD patients (39 typical and 23 atypical presentation). tau‐PET (positron emission tomography) values were normalized to the cerebellum to create standard uptake value ratios (SUVRs). tau‐PET SUVRs were log‐transformed and clustered blinded to clinical information into three groups using K‐median cluster analysis. Demographics, clinical phenotype, cognitive performance, and apolipoprotein e4 frequency were compared across clusters.ResultsThe cluster analysis identified a cluster with low entorhinal and cortical uptake (ELo/CLo), one with low entorhinal but high cortical uptake (ELo/CHi), and one with high cortical and entorhinal uptake (EHi/CHi). Clinical phenotype differed across clusters, with typical AD most commonly observed in the ELo/CLo and EHi/CHi clusters, and atypical AD most commonly observed in the ELo/CHi cluster. The ELo/CLo cluster had an older age at PET and onset than the other clusters. Apolipoprotein e4 frequency was lower in the ELo/CHi cluster. The EHi/CHi cluster had the worst memory impairment, whereas the ELo/CHi cluster had the worst impairment in nonmemory domains.InterpretationThis study demonstrates considerable variability in [18F]AV‐1451 tau‐PET uptake in AD, but shows that a straightforward clustering based on entorhinal and cortical uptake maps well onto age and clinical presentation in AD. Ann Neurol 2018 Ann Neurol 2018;83:248–257

Abstract Cancer patient survivorship has become a significant topic within oncology care for both adult and pediatric patients. Starting in 2005, the Institute of Medicine recommended the use of survivorship care plans to assist patients transitioning from active treatment to the posttreatment phase of their cancer care, a critical time for many patients. Since 2014 there has been a mandate within the United States for adult cancer patients treated with curative intent to receive survivorship care plans comprised of a treatment summary and a follow-up plan to facilitate a better understanding among patients of what to expect after treatment. In addition to a general oncology survivorship care plan, specific care plans have been created for breast, lung, prostate, and colon cancers, as well as lymphoma. A survivorship care plan specific to adult neuro-oncology has been developed by a multidisciplinary and interprofessional committee, with approval from the Society for Neuro-Oncology Guidelines Committee. It has been published in compendium with this review of survivorship care planning and available as a fillable PDF on the Society of Neuro-Oncology Guidelines Endorsement web page (https://www.soc-neuro-onc.org/SNO/Resources/Survivorship_Care_Plan.aspx). Implementation of this survivorship care plan provides a unique opportunity to begin addressing the range of survivorship issues our neuro-oncology patients navigate from diagnosis to end of life.

The North American Consortium for the Study of End‐Stage Liver Disease's definition of acute‐on‐chronic liver failure (NACSELD‐ACLF) as two or more extrahepatic organ failures has been proposed as a simple bedside tool to assess the risk of mortality in hospitalized patients with cirrhosis. We validated the NACSELD‐ACLF's ability to predict 30‐day survival (defined as in‐hospital death or hospice discharge) in a separate multicenter prospectively enrolled cohort of both infected and uninfected hospitalized patients with cirrhosis. We used the NACSELD database of 14 tertiary care hepatology centers that prospectively enrolled nonelective hospitalized patients with cirrhosis (n = 2,675). The cohort was randomly split 60%/40% into training (n = 1,605) and testing (n = 1,070) groups. Organ failures assessed were (1) shock, (2) hepatic encephalopathy (grade III/IV), (3) renal (need for dialysis), and (4) respiratory (mechanical ventilation). Patients were most commonly Caucasian (79%) men (62%) with a mean age of 57 years and a diagnosis of alcohol‐induced cirrhosis (45%), and 1,079 patients had an infection during hospitalization. The mean Model for End‐Stage Liver Disease score was 19, and the median Child score was 10. No demographic differences were present between the two split groups. Multivariable modeling revealed that the NACSELD‐ACLF score, as determined by number of organ failures, was the strongest predictor of decreased survival after controlling for admission age, white blood cell count, serum albumin, Model for End‐Stage Liver Disease score, and presence of infection. The c‐statistics were 0.8073 for the training set and 0.8532 for the validation set. Conclusion: Although infection status remains an important predictor of death, NACSELD‐ACLF was independently validated in a separate large multinational prospective cohort as a simple, reliable bedside tool to predict 30‐day survival in both infected and uninfected patients hospitalized with a diagnosis of cirrhosis. (H epatology 2018;67:2367‐2374).

Background: Hamstring autograft size <8 mm has been shown to be a predictor for failure after anterior cruciate ligament (ACL) reconstruction. The ability to predict graft size preoperatively is helpful in counseling patients about the possible need for graft augmentation. Purpose: To determine whether preoperative ultrasound (US) measurements of hamstring tendons can predict intraoperative graft diameter during ACL reconstruction. Study Design: Cohort study (diagnosis); Level of evidence, 2. Methods: Twenty patients undergoing unilateral isolated ACL reconstruction were prospectively enrolled in the study (10 males, 10 females; mean ± SD age, 22.8 ± 6.6 years; height, 175.1 ± 7.1 cm; weight, 81.4 ± 14.2 kg; body mass index, 26.5 ± 4.1 kg/m 2 ). Hamstrings were assessed by US, and double-looped semitendinosus-gracilis hamstring size was independently calculated with a freehand selection method on a nonmagnified US image by 2 orthopaedic surgeons. Intraoperative autograft size was determined with a standard graft-sizing tool. Intra- and interrater reliability was measured with intraclass correlation coefficients (ICCs) and standard error of the measure (SEM). A receiver operating characteristic curve was calculated to assess the ability of the US measurement to predict intraoperative measurements. Results: The mean autograft diameter by US was 8.9 ± 0.98 mm, while the mean intraoperative hamstring graft size was 8.1 ± 0.89 mm. There was excellent intrarater (ICC 2,1 = 0.95, SEM = 0.32 mm) and interrater (ICC 2,1 = 0.88, SEM = 0.55 mm) reliability for US measurements. Receiver operating characteristic analysis showed that US did not consistently quantify graft size. Graft size did not significantly correlate with height, weight, or body mass index in our sample ( P > .05). Conclusion: These results suggest that preoperative US imaging of the hamstring tendons is unreliable in predicting intraoperative graft diameter.

AbstractBackgroundPositron emission tomography ligands are now available that bind to tau proteins in the brain, providing the exciting opportunity to assess the presence and distribution of tau in vivo in living patients.MethodsThis manuscript performed a systematic review of studies that have performed tau PET imaging in patients with parkinsonian disorders. PubMed was searched through November 13, 2017 and the review included case reports and patient‐control studies.ResultsMost tau‐PET studies have utilized the [18F]AV‐1451 ligand, with a few using the [11C]PBB3 and [18F]THK‐5351 ligands. Elevated cortical tau‐PET uptake has been observed in Parkinson's disease dementia and dementia with Lewy bodies, presumed to be related to Alzheimer's disease‐related pathology. Mild patterns of tau‐PET uptake have been observed in subcortical structures in progressive supranuclear palsy and subcortical structures and motor cortex in corticobasal syndrome, although discrepancy with autoradiographic studies that show lack of binding to 4‐repeat tau and “off‐target” binding observed in subcortical structures limit the interpretation of these findings. Findings in frontotemporal dementia with tau mutations are variable, but elevated signal is most pronounced in mutations with deposition of both 3 and 4‐repeat tau. Elevated tau‐PET uptake has also been observed in multiple system atrophy, a synucleinopathy.ConclusionThe value of the current generation of tau‐PET ligands varies across parkinsonian syndromes, depending upon underlying variability in tau pathology and “off‐target” binding. More work is needed to understand the biological basis of binding and more specific tau PET ligands are needed to study parkinsonian disorders.

The purpose of the present investigation was to study the effects of inhibition of monoamine oxidase (MAO) and/or catechol- O-methyltransferase (COMT), enzymes involved in the degradation of dopamine (DA) and serotonin (5-HT), on intrarenal DA and 5-HT, as reflected in the renal interstitial fluid (RIF) microdialysate and urine, and on renal function. Inhibition of MAO selectively increased RIF 5-HT from 3.16 ± 0.38 to 8.03 ± 1.83 pg/min ( n = 7, P < 0.05), concomitant with decreases in mean arterial blood pressure and glomerular filtration rate (2.09 ± 0.18 to 1.57 ± 0.22 ml/min, n = 7, P < 0.05). Inhibition of COMT significantly increased RIF DA (3.47 ± 0.70 to 8.68 ± 1.96 pg/min, n = 9, P < 0.05), urinary DA (2.00 ± 0.16 to 2.76 ± 0.26 ng/min, n = 9, P < 0.05), and absolute excretion of sodium (6.42 ± 2.00 to 9.82 ± 1.62 μmol/min, n = 10, P < 0.05). Combined inhibition of MAO and COMT significantly increased RIF DA, urinary DA, and urinary 5-HT, which was accompanied with increases in urine flow rate, and absolute (3.03 ± 0.59 to 8.40 ± 1.61 μmol/min, n = 9, P < 0.01) and fractional excretion of sodium. We conclude that inhibition of MAO selectively increases RIF 5-HT. COMT appears to be more important than MAO in the metabolism of intrarenal DA. Physiological increases in intrarenal DA/5-HT induced by inhibition of their degrading enzymes are accompanied with significant alterations of renal function.