Comparison of Direct Patient Care Costs and Quality Outcomes of the Teaching and Nonteaching Hospitalist Services at a Large Academic Medical Center.

PURPOSE: To compare costs of care and quality outcomes between teaching and nonteaching hospitalist services, while testing the assumption that resident-driven care is more expensive. METHOD: Records of inpatients with the top 20 Medicare Severity Diagnosis-Related Groups admitted to the University Teaching Service (UTS) and nonteaching hospitalist service (NTHS) at Houston Methodist Hospital from 2014-2015 were analyzed retrospectively. Direct costs of care, length of stay (LOS), in-hospital mortality (IHM), 30-day readmission rate (30DRR), and consultant utilization were compared between the UTS and NTHS. Propensity score matching and case mix index (CMI) were used to mitigate differences in baseline characteristics. To compare outcomes between matched groups, the Wilcoxon rank sum test and chi-square test were used. A sensitivity analysis was conducted using multivariable regression analysis. RESULTS: From the overall study population of 8,457 patients, 1,041 UTS and 3,123 NTHS patients were matched. CMI was 1.07 for each group. The UTS had lower direct costs of care per case ($5,028 vs. $5,502, P = .006), lower LOS (4.7 vs. 5.2 days, P = .0002), and lower consultant utilization (1.0 vs. 1.6, P ≤ .0001) versus the NTHS. The UTS and NTHS 30DRR (17.2% vs. 19.3%, P = .110) and IHM (2.9% vs. 3.7%, P = .206) were comparable. The multivariable regression analysis validated the matched data and identified an incremental cost savings of $333/UTS patient. CONCLUSIONS: Patients of an academic hospitalist service had significantly shorter LOS, fewer consultants, and lower direct care costs than comparable patients of a nonteaching service.

Repeatability of anorectal manometry in healthy volunteers and patients.

BACKGROUND: Anorectal manometry is used extensively in the assessment of patients with disorders of the pelvic floor. The present study investigated the repeatability of anorectal manometry in healthy volunteers and patients. PATIENTS AND METHODS: A total of 30 healthy volunteers (15 men and 15 women) and 10 patients with fecal incontinence (4 men and 6 women) underwent perfusion manometry and volumetry. Intraindividual variability was evaluated using the intraindividual correlation coefficient (ICC). Interindividual variability was expressed as the standard deviation from the calculated mean values. RESULTS: We found a high intraindividual correlation for the squeezing pressure (ICC 0.75-0.95), vector volume (ICC 0.88-0.97), and rectal perception (ICC 0.82-0.98). The anal resting pressure showed moderate repeatability (ICC 0.60-0.72). However, with regard to sphincter asymmetry, rectal compliance, and the rectoanal inhibitory reflex, a wide range of variability was found. In the female volunteers, the squeezing pressure and vector volume were lower than in those in the male volunteers. The anal pressure, vector volume, thresholds for urgency, and the maximum tolerable volume were lower in the incontinent patients than in the healthy volunteers. CONCLUSIONS: The squeezing pressure, vector volume, and rectal perception allow a reliable analysis of anal sphincter function. Sphincter asymmetry, rectal compliance, and the rectoanal inhibitory reflex were of limited diagnostic value.

Neurologic phenotype of Schimke immuno-osseous dysplasia and neurodevelopmental expression of SMARCAL1.

Schimke immuno-osseous dysplasia (OMIM 242900) is an uncommon autosomal-recessive multisystem disease caused by mutations in SMARCAL1 (swi/snf-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a-like 1), a gene encoding a putative chromatin remodeling protein. Neurologic manifestations identified to date relate to enhanced atherosclerosis and cerebrovascular disease. Based on a clinical survey, we determined that half of Schimke immuno-osseous dysplasia patients have a small head circumference, and 15% have social, language, motor, or cognitive abnormalities. Postmortem examination of 2 Schimke immuno-osseous dysplasia patients showed low brain weights and subtle brain histologic abnormalities suggestive of perturbed neuron-glial migration such as heterotopia, irregular cortical thickness, incomplete gyral formation, and poor definition of cortical layers. We found that SMARCAL1 is highly expressed in the developing and adult mouse and human brain, including neural precursors and neuronal lineage cells. These observations suggest that SMARCAL1 deficiency may influence brain development and function in addition to its previously recognized effect on cerebral circulation.

Cerebellar atrophy in Schimke-immuno-osseous dysplasia.

Schimke-immuno-osseous dysplasia is an autosomal-recessive multisystem disorder with the prominent clinical features disproportionate growth failure, progressive renal failure, and T-cell immunodeficiency. Neurological symptoms caused by transient ischemic attacks (TIAs) and strokes are a typical clinical finding in severe SIOD. Cerebral ischemia and white matter changes, moyamoya phenomena and absence of a cerebellar hemisphere and partial absence of the cerebellar vermis have been described in patients with severe SIOD. We present three SIOD patients with atrophy of the caudal parts of the cerebellar vermis (posterior lobule) and of the cerebellar hemispheres. We hypothesize that these cerebellar abnormalities are a continuum of the ongoing vascular disease in severe SIOD.

Schimke immuno-osseous dysplasia: a cell autonomous disorder?

SMARCAL1 (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a-like protein 1) encodes a SWI/SNF ATP-dependent chromatin remodeling protein. Mutations in SMARCAL1 cause the autosomal-recessive multisystem disorder Schimke immuno-osseous dysplasia (SIOD); this suggests that the SMARCAL1 protein is involved in the development or maintenance of multiple organs. Disease within these many tissues could arise by a cell autonomous or a cell non-autonomous mechanism. Consistent with a cell autonomous mechanism, we did not find any disease recurrence in transplanted organs or protection of other tissues by the organ grafts. In order to better understand the role of SMARCAL1 during normal development and in the pathogenesis of SIOD, we characterized the spatial and temporal expression of the murine homolog (Smarcal1). The Smarcal1 mRNA and protein were expressed throughout development and in all tissues affected in patients with SIOD including the bone, kidney, thymus, thyroid, tooth, bone marrow, hair, eye, and blood vessels. Significantly, the expression profile of Smarcal1 in the mouse has led us to reexamine and identify novel pathology in our patient population resulting in changes in the clinical management of SIOD. The expression of Smarcal1 in affected tissues and the non-recurrence of disease in grafted organs lead us to hypothesize a cell autonomous function for SMARCAL1 and to propose tissue-specific mechanisms for the pathophysiology of SIOD.