Prior recommendations for ethanol locks have favored silicone central lines over polyurethane due to concerns of increased breakage rates when ethanol locks are used with polyurethane catheters. However, a recent small study indicates that this may be incorrect.
A 10‐year retrospective study with 10 children comprising 85 CVCs and 13,227 catheter days
Key findings:
Breakages were the most common complication: polyurethane 1.46/1000 vs silicone 3.76/1000 catheter days. Silicone catheters had a significantly higher breakage rate (adjusted rate ratio [RR], 2.86; 95% confidence interval [CI], 2.84–2.88; P < .001)
Polyurethane catheters had higher rates of occlusion (adjusted RR, 0.14; 95% CI, 0.07–0.28; P < .001) and displacements.
There were no differences in the overall catheter replacement rates and any other catheter‐related outcomes.
This prospective observational study provides helpful outcome data for infants (n=80) born with congenital duodenal obstruction (CDO).
Key findings (also see infographic below):
Though there was an 8.4% overall mortality, there were no deaths directly attributed to CDO. 69% had associated anomalies.
Median length of stay after repair was 20 days; at 28 days following repair, 76% had been discharged home
Failure to achieve full enteral feeds was NOT related to CDO (due instead to other gastrointestinal anomalies). Mean time for full feeds was 13 days post-op; 90% reached full enteral feeds at 28 days.
Repair type: 80% had duodenoduodenostomy, 14% had duodenojejunostomy, the others: membrane incision (n=1), membrane resection (n=2), and duodenoplasty (n=2)
My take: This data will inform clinicians of expected outcomes in this population. I hope this cohort is followed long-term to provide more information about long-term outcomes including frequency of pancreatitis.
Using a prospective database with 27,100 endoscopies, the authors evaluated a clinical care guideline to reduce unnecessary medical care following endoscopy.
Key findings:
Post-endoscopy fever (PEF) occurred in 0.55% (n=150)
ONLY 6 of these 150 PEFs (0.4%) were attributed to a procedure complication: 3 had perforations (all with abdominal pain), 2 had aspiration (both had emesis at time of endoscopy) and 1 had a positive blood culture (though had undergone a liver biopsy as well as endoscopy)
The authors published their care guideline (Figure 1) which stratifies risk based on whether the procedure was an interventional (high risk) vs diagnostic (low risk), ASA class, duration of fever, concomitant immunosuppression (eg. steroids), and associated symptoms including vomiting, diarrhea, bleeding, new abdominal pain, impact on activities of daily living, and hydration
Interestingly, the authors note that their cohort had a total of 23 perforations, but only 3 presented with fever
Using the care guideline resulted in a “significant shift in the prevalence of Grade 2 and above (requiring hospital use) to Grade 1 (clinical observation and reassurance) adverse events, dropping ED visits and admissions by 43.6% and 76.4% respectively for the post-endoscopy fever patients.” This shift was not associated with any observed negative patient outcomes or missed diagnoses.
My take: The authors note that fever is often related to release of inflammatory cytokines which can occur with endoscopy in the absence of complications. The authors methodical guideline to post-procedure fever provides a logical approach to this common problem.
Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician. Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure. This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.
Related article: AE Wiskin et al. Clin Nutrition 2021; https://doi.org/10.1016/j.clnesp.2020.12.029. Prevalence of Home Parenteral Nutrition in childrenKey finding: In 2019, 389 children received HPN (home parenteral nutrition) in the UK; this is nearly double the number last reported in 2012 and is a prevalence of 30 per million children (Thanks to Kipp Ellsworth for this reference)
In total, 59% of children with BMI z-score <−0.5 had moderate-severe osteopenia and only 18% of those with higher z-scores.
Osteopenia was associated with lower BMI z-score (−0.8 ± 1.2 vs −1.8 ± 1.1, P < 0.001) and higher PCDAI (33.7 ± 15.2 vs 25.7 ± 16.5; P = 0.009)
None of the higher risk patients were receiving long-term corticosteroids
Limitations: retrospective study with relatively small sample size, pubertal stage not recorded, variability in DXA studies, and lack of followup information
My take: The authors have NOT shown that identification of osteopenia at the time of diagnosis improves outcome of Crohn’s disease or bone disease. This is why I disagree with their recommendation to routinely screen children with BMI z-score <−0.5. In those in which finding osteopenia may influence treatment, then a DXA study would be worthwhile.
A recent large retrospective study (R Mandile et al. JPGN 2021; 72: 282-287. Seronegative Villous Atrophy in Children: Clinical and Immunohistochemical Features) provides information about conditions, besides celiac disease (CD) which present with villous atrophy. 64 of 1282 pediatric patients were seronegative with villous atrophy; seronegative was defined as testing negative twice for serology (TTG IgA/EMA or if IgA-deficient, IgG antibody serology).
Key findings:
Diagnoses were: inflammatory bowel diseases (IBD) (21/64), food allergy (8/64), infections (7/64, of which 3 HIV infections), immune deficiency (3/64), short bowel syndrome (3/64), congenital diarrhea (2/64), other/inconclusive diagnosis (8/64). In addition, there were 12 with Gastro-Esophageal Reflux Disease (GERD) & the authors speculate that perhaps hyperacidity could play a role in some of these cases.
Only one quarter of the seronegative patients had an increased number of intraepithelial lymphocytosis (IELs)
Among those with villous atrophy attributed to IBD, this was nearly equally-split between Crohn’s disease and ulcerative colitis, 10 and 11 patients respectively (according to Table 1)
The authors note that the ~5% of patients with seronegative villous atrophy with alternative diagnosis than Celiac disease may be an overestimation as more individuals are being diagnosed without biopsy based on serology
Despite the large cohort, there are still other rare conditions that were not identified in this study (eg. autoimmune enteropathy, CTLA4B deficiency,drug-induced enteropathy, and tropical sprue)
My take: This article provides a good starting point for patients with villous atrophy and negative serology.
During the study period 12,744 children underwent an EGD with biopsies. Of those, we identified 426 children with LD (3%).
Among the LD (compared to control group), 5% had celiac disease (vs 0%, P < 0.001), 9% had Crohn disease (3%, P = 0.003) and 3% had Helicobacter pylori gastritis (1%, P = 0.021).
A recent study (PT Reeves et al. J Pediatr 2021; 229: 118-126. Full text link: Development and Assessment of a Pictographic Pediatric Constipation Action Plan) highlighted patient education efforts. “This study focused on the design and assessment of a low literacy pictographic CAP for the care of functional constipation in children.”
My take: I agree with the authors that a simple plan like this has “the potential to become an important tool to be used in the care of children with functional constipation, improving both quality-of-care and clinical outcomes.”
This QR code provides 9 minute explanation of constipation and action plan:
Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician. Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure. This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition
The authors utilized three databases for children aged 2 months to 18 years: Medicaid Databases from Arizona (2009-2017) and Wisconsin (2005-2014) (public insurance databases) and The Truven Health Analytics MarketScan Commercial Claims and Encounters Database (2009-2015) (a nationwide private insurance database).
Key findings:
There were 126 002 and 367 256 children 5 years of age or younger with pediatric feeding disorders (PFD) with public and private insurance, respectively
In 2014, the annual prevalence of PFD was 1 in 23, 1 in 24, and 1 in 37 in children under 5 years in the publicly insured cohorts in Wisconsin, Arizona, and the privately insured cohort, respectively.
The prevalence of PFD in children <5 years (range: 27-44 per 1000 children) exceeds the prevalence of U.S. children with autism spectrum disorder (~17 per 1000 children at age 8 year) and eating disorders like anorexia nervosa and bulimia (8 and 13 per 100,000 persons per year).
In an associated editorial (pg 13-14), Rachel Rosen notes that “despite their high prevalence, the lack of studies funded by the National Institutes of Health…is striking.”
My take: This study provides useful data on PFD prevalence. PFD have a wide range of associated diseases, including prematurity, neurologic disorders/developmental delay, congenital heart disease, chronic lung disease, autism, and congenital bowel disorders. In some, PFD are related to poorly-understood feeding aversions.
In The Shawshank Redemption, Andy Dufresne (Tim Robbins) manages to escape prison by crawling through 500 yards of a filthy sewage pipe. It seems like a similar effort will be needed to find out how to benefit from fecal transplantation when given for problems like irritable bowel syndrome and metabolic disease/obesity. Some recent studies and associated editorials are noted below.
Key finding: At week 12, 56% of patients given donor stool reported improvement in both primary endpoints compared with 26% of patients given placebo (P = .03).
This editorial stresses that trials of FMT in IBS have had inconsistent results and risks are unclear. “How many clinicians inform patients receiving FMT that the donor microbiota might include components that increase (or decrease) one’s risk of colorectal cancer?” Part of the problem is “due, in part, because a normal microbiome has not been defined.”
In this randomized controlled trial with 90 participants, autologous FMT (aFMT) significantly attenuated weight regain in the green-Mediterranean group (aFMT, 17.1%, vs placebo, 50%; P = .02) and improved insulin resistance: insulin rebound (aFMT, –1.46 ± 3.6 μIU/mL vs placebo, 1.64 ± 4.7 μIU/mL; P = .04) (Graphical abstract below)
In mice, Mankai-modulated aFMT in the weight-loss phase compared with control diet aFMT, significantly prevented weight regain and resulted in better glucose tolerance during a high-fat diet–induced regain phase (all, P < .05).
“These findings add support to the current body of evidence that the gut microbiota have a role in weight gain and metabolism. However, many questions remain. Indeed, although studies have shown varying degrees of effectiveness of FMT in the improvement of metabolic parameters in human participants, there has been no evidence yet that FMT can induce weight loss in obese patients.”
“The finding that maintenance of weight loss was only seen in the one dietary group consuming the Mediterranean diet plus green tea and Mankai supplement who received autologous FMT, would suggest that specific microbial profiles may be involved and that weight loss per se may not result in the required microbial profiles.”
Figure 1 from editorial: Challenges associated with the use of fecal microbial transplantation (FMT) as treatment
My take: Both of these studies show that modulation of the fecal microbiome may be helpful under the right set of circumstances to help with both irritable bowel syndrome and metabolic syndrome. However, ‘hundreds of yards’ of more research is needed to determine if this is really feasible and to assure that the benefits outweigh the potential risks.
Background: “Up to 20% of people worldwide develop gastrointestinal symptoms following a meal, leading to decreased quality of life, substantial morbidity and high medical costs”
“Here we show that a bacterial infection and bacterial toxins can trigger an immune response that leads to the production of dietary-antigen-specific IgE antibodies in mice, which are limited to the intestine. Following subsequent oral ingestion of the respective dietary antigen, an IgE- and mast-cell-dependent mechanism induced increased visceral pain. This aberrant pain signaling resulted from histamine receptor H1-mediated sensitization of visceral afferents. Moreover, injection of food antigens (gluten, wheat, soy and milk) into the rectosigmoid mucosa of patients with irritable bowel syndrome induced local oedema and mast cell activation.”
My take: This study shows how innocuous food can trigger pain after an intestinal infection.