Opportunities for Diagnostic Improvement Among Pediatric Hospital Readmissions.

OBJECTIVES: Diagnostic errors, termed "missed opportunities for improving diagnosis" (MOIDs), are known sources of harm in children but have not been well characterized in pediatric hospital medicine. Our objectives were to systematically identify and describe MOIDs among general pediatric patients who experienced hospital readmission, outline improvement opportunities, and explore factors associated with increased risk of MOID. PATIENTS AND METHODS: Our retrospective cohort study included unplanned readmissions within 15 days of discharge from a freestanding children's hospital (October 2018-September 2020). Health records from index admissions and readmissions were independently reviewed and discussed by practicing inpatient physicians to identify MOIDs using an established instrument, SaferDx. MOIDs were evaluated using a diagnostic-specific tool to identify improvement opportunities within the diagnostic process. RESULTS: MOIDs were identified in 22 (6.3%) of 348 readmissions. Opportunities for improvement included: delay in considering the correct diagnosis (n = 11, 50%) and failure to order needed test(s) (n = 10, 45%). Patients with MOIDs were older (median age: 3.8 [interquartile range 1.5-11.2] vs 1.0 [0.3-4.9] years) than patients without MOIDs but similar in sex, primary language, race, ethnicity, and insurance type. We did not identify conditions associated with higher risk of MOID. Lower respiratory tract infections accounted for 26% of admission diagnoses but only 1 (4.5%) case of MOID. CONCLUSIONS: Standardized review of pediatric readmissions identified MOIDs and opportunities for improvement within the diagnostic process, particularly in clinician decision-making. We identified conditions with low incidence of MOID. Further work is needed to better understand pediatric populations at highest risk for MOID.

Sustainment of continuous pulse oximetry deimplementation: Analysis of Eliminating Monitor Overuse study data from six hospitals.

Using continuous pulse oximetry (cSpO2 ) to monitor children with bronchiolitis who are not receiving supplemental oxygen is a form of medical overuse. In this longitudinal analysis from the Eliminating Monitor Overuse (EMO) study, we aimed to assess changes in cSpO2 overuse before, during, and after intensive cSpO2 -deimplementation efforts in six hospitals. Monitoring data were collected during three phases: "P1" baseline, "P2" active deimplementation (all sites engaged in education and audit and feedback strategies), and "P3" sustainment (a new baseline measured after strategies were withdrawn). Two thousand and fifty-three observations were analyzed. We found that each hospital experienced reductions during active deimplementation (P2), with overall adjusted cSpO2 overuse decreasing from 53%, 95% confidence interval (CI): (49-57) to 22%, 95% CI: (19-25) between P1 and P2. However, following the withdrawal of deimplementation strategies, overuse rebounded in all six sites, with overall adjusted cSpO2 overuse increasing to 37%, 95% CI: (33-41) in P3.

A 7-Year-Old With Persistent Fever and Cough.

A previously healthy, fully immunized 7-year-old girl presented with a 7-week history of daily fevers and a worsening cough with persistently elevated inflammatory markers. Before admission, she had an unrevealing outpatient workup by infectious disease, rheumatology, pulmonology, and otorhinolaryngology for her fever and other symptoms. Multiple courses of antibiotics had no effect, but brief courses of steroids seemed to modestly alleviate her symptoms. At an outside hospital, a computed tomography neck and chest scan revealed mediastinal lymphadenopathy. She was subsequently transferred to the authors' institution. Her examination was notable for a febrile, tired-appearing girl in respiratory distress with a muffled voice and inspiratory stridor. Her laboratory tests revealed leukocytosis with left shift, microcytic anemia, and hypoalbuminemia, as well as elevated inflammatory markers, ferritin, and fecal calprotectin. Her peripheral smear, uric acid, and lactate dehydrogenase were all within normal limits. Infectious study results, including blood and urine cultures, cytomegalovirus serologies, and Bartonella serologies were negative. On the second read of her outside computed tomography imaging, her lymphadenopathy was felt to be nonpathologic. Based on a recommendation by rheumatology, an ophthalmologic examination was obtained, which revealed bilateral anterior uveitis; however, rheumatologic laboratory test results returned negative. Her fevers continued, and inflammatory markers remained elevated despite antibiotics. On day 6 of hospitalization, she developed worsening respiratory distress, necessitating intubation and transfer to the ICU. Repeat laryngoscopy and bronchoscopy revealed severe purulent tracheitis; however, throat cultures remained sterile. Her clinical deterioration without identification of an offending organism prompted additional evaluation for a systemic etiology.

Alteration of Mammary Gland Development and Gene Expression by In Utero Exposure to Cadmium.

Environmental exposure to estrogens and estrogen like contaminants during early development is thought to contribute to the risk of developing breast cancer primarily due to an early onset of puberty; however, exposure during key developing windows may also influence the risk of developing the disease. The goal of this study was to ask whether in utero exposure to the metalloestrogen cadmium alters mammary gland development due to acceleration of puberty onset or to an effect on early development of the mammary gland. The results show that, in addition to advancing the onset of puberty, in utero exposure to the metalloestrogen cadmium altered mammary gland development prior to its effect on puberty onset. In utero exposure resulted in an expansion of the number of mammosphere-forming cells in the neonatal mammary gland and an increase in branching, epithelial cells, and density in the prepubertal mammary gland. In the postpubertal mammary gland, there was a further expansion of the mammary stem/progenitor cell population and overexpression of estrogen receptor-alpha (ERα) that was due to the overexpression and altered regulation of the ERα transcripts derived from exons O and OT in response to estradiol. These results suggest that in utero exposure to cadmium increases stem/progenitor cells, cell density, and expression of estrogen receptor-alpha that may contribute to the risk of developing breast cancer.

Outcomes in 132 patients following laparoscopic total mesorectal excision (TME) for rectal cancer with greater than 5-year follow-up.

INTRODUCTION: The role of laparoscopic TME for rectal cancer is still questioned as a safe and adequate cancer operation. Currently, multicenter randomized prospective trials are underway to evaluate this. We analyze our long-term results using laparoscopic TME in the treatment of rectal cancer to evaluate its oncologic outcomes. METHODS: A prospective laparoscopic database was queried to identify all patients operated upon for rectal cancer from April 1997 to September 2007. In total, 151 patients were identified. Metastatic disease excluded 19 patients, leaving 132 patients to be analyzed for perioperative and 5-year oncologic outcomes. Procedures included LAR, n = 35; transanal abdominal transanal proctosigmoidectomy, n = 77; and APR, n = 20. All surgeries were TME or pTME. RESULTS: Laparoscopic TME was performed on 89 men (67%), mean age 61 (22-85). Preoperative chemoradiation was administered in 119 (90.2 %) with median dose of 5500 cGy (3800-10,080). Mean EBL was 300 ml, and 4.5% were transfused. Seven patients (5.3%) underwent conversion, 5 to lap-assisted, with a 1.5% conversion rate to open. Pathologic stage of disease: complete response: 24%; I: 36%; II: 22%; III: 18%. There were no mortalities. Overall morbidity was 23.5%, with no anastomotic leaks and 5 (3.8%) delayed anastomotic stricture/fistula. There were no port site recurrences. Mean follow-up was 69.4 months (7.6-168.0). Overall LR was 5.3% (n = 7). There was only one isolated LR (0.8%). Mean time to local recurrence was 13.9 months. Metastatic rate was 18.2%. By stage, disease-specific survival was: CR 86.3%; I: 87.4%; II: 86.4%; III: 77.4%. Overall, 5-year survival was 84.8%. CONCLUSION: The long-term data confirm that laparoscopic TME can be performed with lasting low local recurrence (5.3 %) and excellent 5-year survival (84.8%). This report's importance stems from it representing one of the largest experiences of rectal cancer treated by laparoscopic TME with greater than 5-year follow-up reported in the literature.

Alteration of mammary gland development and gene expression by in utero exposure to arsenic.

Early life exposure to estrogens and estrogen like contaminants in the environment is thought to contribute to the early onset of puberty and consequently increases the risk of developing breast cancer in the exposed female. The results of this study show that in utero exposure to the metalloestrogen arsenite altered mammary gland development prior to its effect on puberty onset. In the prepubertal gland, in utero exposure resulted in an increase in the number of mammosphere-forming cells and an increase in branching, epithelial cells, and density. In the postpubertal gland, in utero exposure resulted in the overexpression of estrogen receptor-alpha (ERα) that was due to the increased and altered response of the ERα transcripts derived from exons O and OT to estradiol. These results suggest that, in addition to advancing puberty onset, in utero exposure to arsenite alters the pre- and postpubertal development of the mammary gland and possibly, the risk of developing breast cancer.