Towards a more intelligent model of providing pediatric trauma care: identifying temporal variations in trauma team activations.

BACKGROUND: Trauma centers are resource-intensive environments, and pediatric-specific personnel are often limited resources. Identifying the temporal patterns of pediatric traumas can help guide resource allocation strategies to optimize patient care. METHODS: We conducted a retrospective, single-institution analysis of 575 injured patients less than 18 years old that triggered a trauma team activation (TTA). TTA volume according to time of day and day of the week was analyzed using a mixed Poisson regression model and monthly patterns were analyzed using an analysis of variance. Subset analyses were conducted for children and teenagers. RESULTS: Across all days, the 6-hour time frame between 15:00 and 21:00 had significantly more activations than average, encompassing nearly half (47.2%) of all pediatric TTAs (p=0.01). Saturdays had significantly more activations than the daily average (Saturdays: 26.0/year, Other: 14.8/year, p<0.01). A pediatric TTA was 3.6 times more likely to occur between 15:00 and 21:00 on a Saturday than any other time. Volume of activation did not significantly differ by month (p=0.880). CONCLUSION: The volume of pediatric trauma activations varies significantly according to time of day and day of the week. These findings can direct or validate resource allocation strategies such as staffing physicians, nurses, and ancillary personnel according to TTA volume. TYPE OF STUDY: Retrospective cohort study. LEVEL OF EVIDENCE: Level III.

Continuous Digital Assessment for Weight Loss Surgery Patients.

We conducted a survey about recent surgical procedures on a large connected population and requested each individual's permission to access data from commercial wearable devices they may have been wearing around the time of the procedure. For subcohorts of 66-118 patients who reported having a weight loss procedure and who had dense Fitbit data around their procedure date, we examined several daily measures of behavior and physiology in the 12 weeks leading up to and the 12 weeks following their procedures. We found that the weeks following weight loss operations were associated with fewer daily total steps, smaller proportions of the day spent walking, lower resting and 95th percentile heart rates, more total sleep time, and greater sleep efficiency. We demonstrate that consumer-grade activity trackers can capture behavioral and physiological changes resulting from weight loss surgery and these devices have the potential to be used to develop measures of patients' postoperative recovery that are convenient, sensitive, scalable, individualized, and continuous.

Treatment of subcutaneous abscesses in children with incision and loop drainage: A simplified method of care.

PURPOSE: The aim of this study was to expand on our previous report of 115 patients after more than a decade-long experience using incision and loop drainage for pediatric subcutaneous abscess management. This report comprises the largest consecutive series of pediatric abscess patients from a single institution ever recorded. METHODS: A retrospective study was performed of all pediatric patients who underwent incision and loop drainage of subcutaneous abscesses at our institution between January 2002 and December 2014. TECHNIQUE: Two sub 5mm incisions were made at the periphery on the abscess. The abscess cavity was probed to break down loculations and drain pus. The abscess cavity was irrigated with normal saline. A loop drain was passed through one incision and brought out through the other. A simple absorbent dressing was applied over the drain. RESULTS: Five hundred seventy-six consecutive patients underwent loop drainage procedures. Mean values are as follows: age, 3.84years; duration of symptoms, 6.17days; postoperative length of stay (with 4 outliers excluded), 0.69days; drain duration, 8.38days; and number of postoperative visits, 1.28. Twenty-six patients had reoperations (4.5%), 2 of which were planned staged excisions of pilonidal cysts and 1 because of accidental home removal. CONCLUSIONS: Micro-incisions and loop drainage is a safe and effective treatment modality for subcutaneous abscesses in children. The findings eliminate the need for repetitive wound packing and simplify postoperative wound care. Loop drainage offers shorter time to discharge, lower recurrence rates, and minimal scarring. Additionally, there is expected cost reduction. We recommend this minimally invasive procedure to be the standard of care for subcutaneous abscesses in children. TYPE OF STUDY: Treatment study - retrospective review. LEVEL OF EVIDENCE: Level IV - case series with no comparison group.

Laparoscopic sleeve gastrectomy as first-line surgical treatment for morbid obesity among adolescents.

BACKGROUND: The increasing prevalence of obesity has necessitated the increasing use of bariatric surgery in the adolescent population. Outcomes following laparoscopic sleeve gastrectomy (LSG) among adolescents, however, have not been well-studied. We report outcomes following LSG as a first-line surgical therapy in patients under 21years of age. METHODS: All patients who underwent LSG as a primary surgical option for morbid obesity were identified at the University of Illinois at Chicago between 2006 and 2014. Standard clinicopathologic and outcomes data were recorded. RESULTS: We identified 18 patients (13 females, 5 males) who underwent LSG. Mean patient age was 17.8±1.7years. Mean BMI among all patients was 48.6±7.2kg/m2 and did not differ by gender (P=0.68). One patient (5.6%) experienced a 30-day perioperative complication (pulmonary embolism). Median LOS following LSG was 3days (IQR: 2, 3). 2 patients (11.1%) were readmitted within 30-days because of feeding intolerance that resolved without invasive intervention. At a median follow-up of 10.6 (range: 0-38) months, percent excess weight loss (%EWL) among all patients was 35.6%. Among patients with at least 2years follow-up (n=3), %EWL was 50.2%. CONCLUSIONS: Laparoscopic sleeve gastrectomy in morbidly obese adolescents is a safe and feasible option. Short- and long-term weight loss appears to be successful following LSG. As such, LSG should be strongly considered as a primary surgical treatment option for all morbidly obese adolescents. LEVEL OF EVIDENCE: Level IV.

A 13-Month-Old With Xanthogranulomatous Pyelonephritis With Features of Renal Malakoplakia.

Xanthogranulomatous pyelonephritis is an uncommon chronic inflammatory renal disorder caused by chronic infection with gram-negative bacteria leading to destruction of the renal parenchyma and replacement with foamy lipid-laden macrophages. Renal malakoplakia is another rare form of chronic inflammatory granulomatous disease in the kidney associated with infection usually occurring in adults with immunocompromised status or debilitating disease. It is hallmarked by the finding of foamy histiocytes with distinctive basophilic inclusions (Michaelis-Gutmann bodies). We present a case of a 13-month-old male with history of congenital hydronephrosis who presented with clinical and radiologic findings suggestive of xanthogranulomatous pyelonephritis. However, further pathologic studies revealed the presence of Michaelis-Gutmann bodies, which are pathognomonic for renal malakoplakia. With this case we hope to bring further evidence to support that these two conditions are not mutually exclusive but rather represent two pathologic processes on the same disease spectrum.

Induction of fibroblast growth factor 10 (FGF10) in the ileal crypt epithelium after massive small bowel resection suggests a role for FGF10 in gut adaptation.

We have previously reported that fibroblast growth factor 10 (FGF10) is crucial for the survival and proliferation of progenitor cells during embryonic gastrointestinal development. We sought to characterize the potential role of FGF10 signaling in the adaptive response following small bowel resection. Adult wild-type and Fgf10(LacZ) mice underwent 50% small bowel resection (SBR) or sham operation. Tissues were harvested 24 or 48 hr after surgery for histology, immunohistochemistry, and in situ hybridization. After SBR, Fgf10 expression was demonstrated in the epithelium at the base of the crypts. Moreover, there was a statistically significant increase in proliferating cells and goblet cells after SBR. In vitro studies using rat intestinal epithelial crypt (IEC-6) cells exposed to medium with or without recombinant FGF10 showed increased proliferation and phosphorylation of Raf and AKT with the addition of FGF10. Our results suggest that FGF10 may play a therapeutic role in diseases involving intestinal failure.

The fibroblast growth factor pathway serves a regulatory role in proliferation and apoptosis in the pathogenesis of intestinal atresia.

BACKGROUND/PURPOSE: Intestinal atresia occurs in 1:5000 live births and is a neonatal challenge. Fibroblast growth factor receptor 2b (Fgfr2b) is a critical developmental regulator of proliferation and apoptosis in multiple organ systems including the gastrointestinal tract (GIT). Fgfr2b invalidation results in an autosomal recessive intestinal atresia phenotype. This study evaluates the role of Fgfr2b signaling in regulating proliferation and apoptosis in the pathogenesis of intestinal atresia. METHODS: Wild-type and Fgfr2b-/- embryos were harvested from timed pregnant mice. The GIT was harvested using standard techniques. Terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling) was used to evaluate apoptosis and bromodeoxyuridine to assess proliferation by standard protocols. Photomicrographs were compared (Institutional Animal Care and Use Committee-approved protocol 32-02). RESULTS: Wild-type and mutant GIT demonstrate that deletion of the Fgfr2b gene results in inhibition of epithelial proliferation and increased apoptosis. Inhibited proliferation and increased apoptosis are specific to those tissues of normal Fgfr2b expression, corresponding to the site of intestinal atresia. CONCLUSIONS: The absence of embryonic GIT Fgfr2b expression results in decreased proliferation and increased apoptosis resulting in GIT atresia. The regulation of proliferation and apoptosis in intestinal cells as a genetically based cause of intestinal atresia represents a novel consideration in the pathogenesis of intestinal atresia.

Osteochondroma causing diaphragmatic rupture and bowel obstruction in a 14-year-old boy.

Exostosis, also known as osteochondroma, results from a disorder of the growth-plate where bone grows away from the growth axis and forms an irregular projection. This abnormality most commonly occurs around the femur, scapula, humerus, and ribs. Although hemothorax and diaphragmatic rupture are known complications of exostosis growth, we present herein the first known report of an inward-facing exostosis in a 14-year-old boy with hereditary multiple exostosis causing diaphragmatic rupture and a bowel obstruction requiring operation. Most exostoses are asymptomatic and as such require no further treatment. However, when they are threatening to cause mass effects (such as frictional bursitis, local entrapment of vessels, and tendons or nerves) or symptomatic, surgical resection is the appropriate treatment.

Fibroblast growth factor-10 serves a regulatory role in duodenal development.

PURPOSE: Duodenal obstruction occurs in 1 of 6000 live births and requires urgent surgical intervention. Duodenal atresia previously has been ascribed to a developmental failure of luminal recanalization; however, the cause of duodenal atresia remains incompletely understood. Although familial intestinal atresias have been described and syndromic associations are known, no specific genetic link has been established. Fibroblast growth factor-10 (Fgf10) is a known regulatory molecule relevant to mesenchymal-epithelial interactions, and mice deficient in Fgf10 demonstrate congenital anomalies in several organ systems including the gastrointestinal tract. The authors hypothesized that Fgf10 could serve a regulatory role in establishing normal duodenal development. METHODS: Wild-type mice with beta-galactosidase under the control of the Fgf10 promoter were harvested from timed-pregnancy mothers. The expression of Fgf10 in the duodenum during development was evaluated by developing the embryos in X-Gal solution. Wild-type and mutant Fgf10(-/-) embryos were harvested from timed-pregnancy mothers at 18.5 days postconception (near term) and were analyzed for duodenal morphology (Institutional Animal Care and Use Committee-approved protocol 32-02). Photomicrographs were reviewed. RESULTS: Fibroblast growth factor-10 is active in the duodenum at a late stage of development. The Fgf10(-/-) mutants demonstrate duodenal atresia with a variable phenotype similar to clinical findings. The duodenum fails to develop luminal continuity and has proximal dilation. The phenotype occurs in an autosomal recessive pattern with incomplete penetrance (38%). CONCLUSIONS: Fibroblast growth factor-10 serves as a regulator in normal duodenal growth and development. Its deletion leads to duodenal atresia and challenges traditionally accepted theories of pathogenesis. This novel, genetically mediated duodenal malformation reflects an animal model that will allow further evaluation of the pathogenesis of this surgically correctable disease. By studying the mechanism of Fgf10 function in foregut development, the authors hope to better understand these anomalies and to explore possible therapeutic alternatives.

Colonic atresia without mesenteric vascular occlusion. The role of the fibroblast growth factor 10 signaling pathway.

BACKGROUND/PURPOSE: Colonic atresia occurs in 1:20,000 live births, offering a neonatal surgical challenge. Prenatal expression of fibroblast growth factor 10 (Fgf10), acting through fibroblast growth factor receptor 2b (Fgfr2b), is critical to the normal development of the colon. Invalidation of the Fgf10 pathway results in colonic atresia, inherited in an autosomal recessive pattern. Classically, disturbance of the mesenteric vasculature has been thought to cause many forms of intestinal atresia. The purpose of this study was to evaluate the role of vascular occlusion in the pathogenesis of colonic atresia. METHODS: Wild type (Wt), Fgf10(-/-), and Fgfr2b(-/-) mutant mouse embryos were harvested from timed pregnant mothers. Immediately following harvest, filtered India ink was infused via intracardiac microinjection. The gastrointestinal tract was dissected, and photomicrographs of the mesenteric arterial anatomy were taken at key developmental time points. RESULTS: Photomicrographs after India ink microinjections demonstrate normal, patent mesenteric cascades to the atretic colon at the time points corresponding to the failure of colonic development in the Fgf10(-/-) and Fgfr2b(-/-) mutants. The mesenteric arterial anatomy of the colon demonstrates no difference between the Wt and mutant colonic atresia. CONCLUSIONS: The absence of embryonic expression of Fgf10 or its receptor Fgfr2b results in colonic atresia in mice. India ink microinjection is a direct measure of mesenteric arterial patency. Colonic atresia in the Fgf10(-/-) and Fgfr2b(-/-) mutants occurs despite normal mesenteric vascular development. Thus the atresia is not the result of a mesenteric vascular occlusion. The patent colonic mesentery of the Fgf10(-/-) and Fgfr2b(-/-) mutants challenges an accepted pathogenesis of intestinal atresia. Although colonic atresia can occur as a result of vascular occlusion, new evidence exists to suggest that a genetic mechanism may play a role in the pathogenesis of this disease.

Fibroblast growth factor receptor 2 IIIb invalidation--a potential cause of familial duodenal atresia.

BACKGROUND/PURPOSE: Duodenal atresia (DA) occurs in 1 in every 6,000 live births and represents a significant surgically correctable cause of intestinal obstruction in the neonate. Familial or congenital DA has been reported, implying that at least some cases of DA are the result of genetic, heritable abnormalities. The genes controlling duodenal development are incompletely understood. Fibroblast growth factor receptor 2IIIb (Fgfr2b) is known to play a critical role in the development of multiple organ systems including other gastrointestinal tract (GIT) structures. This study shows the key role of Fgfr2b in normal duodenal development and the pathogenesis of DA. METHODS: Wild type (Wt) and Fgfr2b-/- embryos were harvested from timed pregnant mothers at stage E18.5 and were analyzed for duodenal phenotype. RESULTS: Inactivation of Fgfr2b results in DA. DA is present in the Fgf2b-/- mutants with a 35% penetrance. The duodenal phenotype of the Fgf2b-/- mutants ranges from normal to a mucosal web, type I, and type III atresia. CONCLUSIONS: Fgfr2b is a critical regulatory gene in the development of the duodenum. Fgfr2b invalidation (Fgfr2b-/- mutant) results in a reproducible, autosomal recessive duodenal atresia phenotype with incomplete penetrance and a variable phenotype.