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BACKGROUND: In general emergency departments, advanced airway management of pediatric patients who are critically ill has been associated with increased adverse events given the varying exposure to pediatric patients and limited resources. Previous studies have shown significant improvement of simulated pediatric airway management in general emergency departments. The aim of this retrospective study was to determine the effect of an in situ simulation-based collaborative intervention program on the actual care of pediatric airway management in general emergency departments. METHODS: This was a retrospective study of pediatric subjects who were critically ill and required intubation at a diverse set of general emergency departments before referral to the academic medical center. The primary outcome was the quality of clinical care measured by adherence to best practices via a critical action checklist. Secondary outcomes included tracheal intubation associated adverse events and clinical outcomes. RESULTS: A total of 135 pediatric subjects (48 pre- and 87 post-intervention) who were transferred to the academic medical center from 9 general emergency departments between May 2014 and August 2019 were included in the analysis. The use of a cuffed endotracheal tube improved, from 44% to 72% (P = .001), whereas there was no significant change in the appropriate endotracheal tube size. Overall, severe tracheal intubation associated adverse events decreased, from 18.8% to 9.2% (P = .03), and post-intubation cardiac arrest events decreased, from 6.3% to 0% (P = .02). CONCLUSIONS: A simulation-based collaborative intervention program led to improvement in pediatric airway management and subject outcomes in general emergency departments. This model demonstrated the transfer of improvement from a simulated setting to a clinical setting and may be targeted in other clinical settings.

BACKGROUND Concern about the effects of inhaled, halogenated anesthetics on neurodevelopment of infants has renewed interest in regional anesthesia as an alternative to general anesthesia (GA). Infants undergoing percutaneous Achilles tenotomy (PAT) are well suited for spinal anesthesia (SP). METHODS Thirty infants (mean age: 2.3 mo) undergoing PAT with SP were compared with 15 infants (mean age: 2.0 mo) undergoing PAT with GA. Data collected included perioperative times, heart rate and blood pressure, and the administration of opioids. RESULTS Ten of 15 GA (67%) patients received perioperative opioids as opposed to 1 of 30 SP patients (3.3%) (P

Introduction: Posterior spinal fusion for idiopathic scoliosis is extremely painful, with no superior single analgesic modality. We introduced a methadone-based multimodal analgesia protocol, aiming to decrease the length of hospital stay (LOS), improve pain control, and decrease the need for additional opioids. Methods: We analyzed 122 idiopathic scoliosis patients with posterior instrumented spinal fusion. They were matched by age, sex, surgeon, and the number of levels fused before and after the implementation of the new protocol. This analysis included 61 controls (intrathecal morphine, gabapentin, intravenous opioids, and adjuncts) and 61 patients on the new protocol (scheduled methadone, methocarbamol, ketorolac/ibuprofen, acetaminophen, and oxycodone with intravenous opioids as needed). The primary outcome was LOS. Secondary outcomes included pain scores, total opioid use (morphine milligram equivalents), time to a first bowel movement, and postdischarge phone calls. Results: New protocol patients were discharged earlier (median LOS, 2 days) compared with control patients (3 days; P < 0.001). Total inpatient morphine consumption was lower in the protocol group (P < 0.001). Pain scores were higher in the protocol group on the day of surgery, similar on postoperative day (POD) 1, and lower by POD 2 (P = 0.01). The new protocol also reduced the median time to first bowel movement (P < 0.001), and the number of postdischarge pain-related phone calls (P < 0.006). Conclusion: Methadone-based multimodal analgesia resulted in significantly lower LOS compared with the conventional regimen. It also provided improved pain control, reduced total opioid consumption, and early bowel movement compared with the control group.

Background Elevated concentrations of cerebrospinal fluid (CSF) tau, a marker of axonal injury, have been associated with coma in severe malaria (cerebral malaria [CM]). However, it is unknown whether axonal injury is related to long-term neurologic deficits and cognitive impairment in children with CM. Methods Admission CSF tau concentrations were measured in 145 Ugandan children with CM and compared to clinical and laboratory factors and acute and chronic neurologic and cognitive outcomes. Results Elevated CSF tau concentrations were associated with younger age, increased disease severity (lower glucose and hemoglobin concentrations, malaria retinopathy, acute kidney injury, and prolonged coma duration, all P < .05), and an increased CSF:plasma albumin ratio, a marker of blood–brain barrier breakdown (P < .001). Admission CSF tau concentrations were associated with the presence of neurologic deficits at hospital discharge, and at 6, 12, and 24 months postdischarge (all P ≤ .02). After adjustment for potential confounding factors, elevated log10-transformed CSF tau concentrations correlated with worse cognitive outcome z scores over 2-year follow-up for associative memory (β coefficient, –0.31 [95% confidence interval [CI], –.53 to –.10]) in children Conclusions Acute axonal injury in children with CM is associated with long-term neurologic deficits and cognitive impairment. CSF tau concentrations at the time of the CM episode may identify children at high risk of long-term neurocognitive impairment.

Patients with dementia have been found to have substantial unmet palliative care (PC) needs, including behavioral concerns, pain, difficult decisions regarding treatment and placement, and caregiver burden.1–9 There is evidence that hospice10,11 can benefit patients with dementia and their families. In spite of this, few hospice programs have historically provided care to patients with dementia as their primary diagnosis. A 1995 survey found that only 21% of hospice programs had enrolled patients with a primary diagnosis of dementia and that 1% of all hospice patients had a primary dementia diagnosis.12 Rates of hospice referral of patients with dementia in nursing homes range from 6%13 to 22%9 and include 11% of home care clients.13 These low percentages may be because of the numerous barriers to providing hospice services to patients with dementia. Many healthcare providers and family members do not perceive dementia as a terminal disease,14 in spite of growing evidence that persons die of this disease.9 The memory and communication deficits in dementia make recognition and management of symptoms especially challenging.8 The caregiver experience involves substantial burden,4,15 extends over a prolonged time period, and has patterns of anticipatory grief and bereavement that differ from those of other illnesses,14–16 but most importantly, the hospice model and its funding were developed with the disease progression of cancer in mind. Many cancers, especially solid tumors, follow a predictable disease trajectory, with a period of marked decline in the final months. In contrast, patients with dementia often have a prolonged period of gradual decline.14,17 Finally, the criteria used to establish hospice eligibility for dementia have been found to be inaccurate in predicting mortality.18 The hospice criteria also assume that patients lose certain abilities in a predictable pattern and are therefore difficult to apply to many patients.18 These challenges make it difficult to prognosticate time to death, which is a requirement for the Medicare hospice benefit.12,19,20 Despite these challenges, the proportion of hospice patients with a primary diagnosis of dementia has risen from 6.8% in 200121 to 11.1% in 2008,22 even as the total number of patients that hospice serves has increased. The last decade has also seen tremendous growth in PC programs outside of the traditional hospice insurance benefit as an additional mechanism for providing care to patients with serious illnesses. Although this trend has been best documented in hospitals,23,24 home health agencies and hospices have also begun to offer PC services. PC outside of the hospice benefit provides another opportunity to provide care to patients with dementia,25,26 who may not quality for hospice until late in the disease but may have substantial unmet PC needs. Although the Medicare hospice eligibility criteria do not constrain service by PC programs, challenges involving prognostication, communication, and other concerns may persist.27 Little is known about the extent to which PC programs serve patients with a primary diagnosis of dementia or the barriers they face in providing this care. The primary goals of this study were to determine the extent to which hospice and nonhospice PC programs provide services for patients with dementia and to identify barriers to and facilitators of the provision of nonhospice PC to patients with dementia from the perspective of program administrators.

Aims: To assess how hippocampal volume (HV) from volumetric magnetic resonance imaging (vMRI) is related to the amyloid status at different stages of Alzheimer's disease (AD) and its relevance to patient care. Methods: We evaluated the ability of HV to predict the florbetapir positron emission tomography (PET) amyloid positive/negative status by group in healthy controls (HC, n = 170) and early/late mild cognitive impairment (EMCI, n = 252; LMCI, n = 136), and AD dementia (n = 75) subjects from the Alzheimer's Disease Neuroimaging Initiative Grand Opportunity (ADNI-GO) and ADNI2. Logistic regression analyses, including elastic net classification modeling with 10-fold cross-validation, were used with age and education as covariates. Results: HV predicted amyloid status only in LMCI using either logistic regression [area under the curve (AUC) = 0.71, p < 0.001] or elastic net classification modeling [positive predictive value (PPV) = 72.7%]. In EMCI, age (AUC = 0.70, p < 0.0001) and age and/or education (PPV = 63.1%), but not HV, predicted amyloid status. Conclusion: Using clinical neuroimaging, HV predicted amyloid status only in LMCI, suggesting that HV is not a biomarker surrogate for amyloid PET in clinical applications across the full diagnostic spectrum.

Class I alcohol dehydrogenases (ADHs) are the principal enzymes responsible for ethanol metabolism in humans. Genetic polymorphism at the ADH1B locus (old nomenclature ADH2) results in isozymes with quite different catalytic properties. The frequency of the ADH1B*2 allele varies among ethnic groups. ADH1B*2 is most often observed in Asian populations, and has been shown to be protective against alcoholism. The Jewish population has a higher frequency of the ADH1B*2 allele and lower rates of alcohol-related problems as compared to other Caucasian populations. Thus, it would be of interest to determine whether the ADH1B*2 allele is associated with alcohol consumption and its subjective effects in this group. Four groups of Jewish subjects (male and female college-age samples, and male and female general samples) were recruited from the same region of the United States. All subjects completed a questionnaire to delineate alcohol consumption and its subjective consequences. Genotype at the ADH1B locus was determined for each participant. ADH1B*2 allele frequencies were similar for the Jewish college-age and general population samples. Men in both the college-age and general population in the ADH1B*2 group reported more unpleasant reactions following alcohol consumption than men in the ADH1B*1 group. Men in the general population in the ADH1B*2 group drank alcohol less frequently than men who were homozygous ADH1B*1; there was a similar trend among the women. The ADH1B polymorphism is associated with unpleasant reactions after alcohol consumption, and frequency of alcohol consumption in these Jewish samples. © 2002 Wiley-Liss, Inc.

The inbred preferring (iP) and nonpreferring (iNP) rat strains were derived from the selectively bred alcohol-preferring (P) and alcohol-nonpreferring (NP) lines. Previously, 381 iP × iNP F2 progeny were generated to identify quantitative trait loci (QTLs) influencing alcohol consumption and preference. Saccharin consumption (ml/48 h) and saccharin intake (ml/kg/day) were also measured in the F2 sample and were significantly correlated with both alcohol consumption and preference (all r ≥ .20, p < .0001), suggesting that there might be some QTLs influencing both saccharin and alcohol phenotypes. We have performed a genome screen using F2 animals with extreme saccharin or alcohol consumption to identify QTLs contributing to saccharin-related phenotypes. Lod scores greater than 2.0 were found on chromosomes 3, 16 and 18 in this sample. Additional genotyping was performed in these regions in the full sample of 381 F2 progeny to further characterize these putative QTLs. On chromosome 3, the maximum lod score in the full sample was 2.7 with saccharin consumption. This QTL appears to overlap with a QTL identified for alcohol consumption in the iP and iNP lines and has pleiotropic effects on both phenotypes. Interestingly, this region of rat chromosome 3 is syntenic with mouse chromosome 2, where a QTL influencing alcohol preference has been previously reported. The QTL on chromosome 16 has a maximum lod score of 4.0 with saccharin intake and 2.6 with saccharin consumption. The QTL on chromosome 18 has a maximum lod score of 2.7 with saccharin consumption. Taken together, these data provide the first results of a genome screen for QTLs contributing to saccharin phenotypes in the rat.

As part of a four-center NIMH Genetics Initiative on Bipolar Disorder, a genome screen using 365 markers was performed on 540 DNAs from 97 families, enriched for affected relative pairs. This is the largest uniformly ascertained and assessed linkage sample for this disease, and includes 232 subjects diagnosed with bipolar I (BPI), 32 with schizo-affective, bipolar type (SABP), 72 with bipolar II (BPII), and 88 with unipolar recurrent depression (UPR). A hierarchical set of definitions of affected status was examined. Under Model I, affected individuals were those with a diagnosis of BPI or SABP, Model II included as affected those fitting Model I plus BPII, and Model III included those fitting Model II plus UPR. This data set was previously analyzed using primarily affected sib pair methods. We report the results of nonparametric linkage analyses of the extended pedigree structure using the program Genehunter Plus. The strongest finding was a lod score of 2.5 obtained on chromosome 10 near the marker D10S1423 with diagnosis as defined under Model II. This region has been previously implicated in genome-wide studies of schizophrenia and bipolar disorder. Other chromosomal regions with lod scores over 1.50 for at least one Model Included chromosomes 8 (Model III), 16 (Model III), and 20 (Model I). Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:18-23, 2000

Selective breeding has been employed to develop high-alcohol-drinking (HAD) and low-alcohol-drinking (LAD) rat lines from the heterogeneous N/Nih rat. Within-family selection and a rotational breeding design were used to discourage inbreeding (Li et al, 1993). To identify quantitative trait loci (QTLs) contributing to alcohol consumption, reciprocal HAD and LAD matings in conjunction with F1 intercrosses were used to create 459 F2 progeny. Using selective genotyping of 151 F2 progeny with extreme alcohol consumption scores and a novel least squares method developed by Haley et al (1994), five chromosomal regions (1, 5, 10, 12, and 16) were identified with lod scores greater than 2.0. Genotyping of the entire sample of 459 F2 progeny produced maximum lod scores of 3.5 on chromosome 5, 2.4 on chromosome 10, 4.7 on chromosome 12 and 2.9 on chromosome 16. The evidence of linkage to chromosome 1 diminished substantially to a maximum lod score of 0.5 when all F2 progeny were genotyped. This study is the first genome-wide study for QTLs underlying alcohol consumption that has employed noninbred lines. Further localization of these QTLs will likely provide insight and candidate genes for the study of human alcoholism.

Selective breeding for voluntary alcohol consumption was utilized to establish the alcohol-preferring (P) and alcohol-nonpreferring (NP) rat lines. Inbreeding was initiated after 30 generations of selection and, after 19 generations of inbreeding, 384 F2 intercross progeny were created to identify quantitative trait loci (QTLs) influencing alcohol consumption. We had reported previously a QTL on Chromosome (Chr) 4; additional markers genotyped on Chr 4 have increased the maximum lod score from 8.6 to 9.2. This QTL acts in an additive fashion and continues to account for approximately 11% of the phenotypic variability. The 95% confidence interval is 12.5 cM and includes the candidate gene, neuropeptide Y. Subsequent to the identification of the QTL on Chr 4, a genome scan was completed to identify additional QTLs influencing alcohol consumption. A lod score of 2.5 was obtained on Chr 3, syntenic to a region previously reported for alcohol preference in mice. Analysis of Chr 8 produced a lod score of 2.2 near the dopamine D2 and serotonin 1b receptors, which have been previously reported as candidate genes for alcohol preference. Evidence for linkage to alcohol consumption was not found on any other chromosome. It therefore appears likely that, in addition to the QTL on Chr 4, multiple loci of small to moderate effect, such as those on Chrs 3 and 8, underlie the difference in alcohol consumption in the P/NP lines.

Objectives. Among patients who arrive at an emergency department (ED) with pain, over half remain in moderate or severe pain at ED discharge. Our objectives were to identify ED physicians' prescribing patterns when discharging patients with common musculoskeletal conditions and to determine if disparities in opioid prescribing exist. Design. Five-year retrospective investigation. Setting. An urban, academic ED with approximately 100,000 annual visits, where physicians write discharge prescriptions, including over-the-counter medications, using a computerized order entry system. Patients. Adult patients who were discharged home from an ED with fractures (clavicle or long bone fractures) or non-fracture musculoskeletal diagnoses (sprains, strains, sciatica, or back pain). Outcome Measures. Patient demographics and pain medications prescribed for use at home. Results. The study sample included 13,335 patients with a mean age of 39 years. Half were female; 52% were white; 39% were black; and 7% were Hispanic. Among fracture patients, 77% received an opioid prescription, 2% received a non-opioid prescription, and 21% received no analgesic prescription. The percentages for patients with non-fracture diagnoses were 65% (opioids), 18% (non-opioid analgesics), and 17% (no analgesic). Patients aged 80 years and older were significantly less likely to receive opioid prescriptions. Although prescribing by race for fractures was similar, significantly fewer black and Hispanic patients with non-fracture diagnoses received opioid prescriptions, compared with white patients. Conclusions. Approximately one fifth of patients in the fracture and non-fracture groups did not receive an analgesic prescription. Age greater than 80 years and minority race/ethnic status were associated with lower rates of opioid prescribing.