INTRODUCTIONState and federal laws have been enacted to protect the mother's right to breastfeed and provide breastmilk to her infant. The Patient Protection and Affordable Care Act requires employers to provide hourly waged nursing mothers a private place other than a bathroom, shielded from view, free from intrusion. Minimum requirement for a lactation room would be providing a private space other than a bathroom. Workplace lactation accommodation laws are in place in 24 states, Puerto Rico, and the District of Columbia. These requirements benefit the breast-pumping mother in an office, but what about the breast-pumping mother who travels? Of women with a child under a year, 55.8% are in the workforce. A significant barrier for working mothers to maintain breastfeeding is traveling, and they will need support from the workplace and the community. This study aimed to determine which airports offer the minimum requirements for a breast-pumping mother: private space other than a bathroom, with chair, table, and electrical outlet.STUDY DESIGNA phone survey was done with the customer service representative at 100 U.S. airports. Confirmatory follow-up was done via e-mail.RESULTSOf the respondents, 37% (n=37) reported having designated lactation rooms, 25% (n=25) considered the unisex/family restroom a lactation room, 8% (n=8) offer a space other than a bathroom with an electrical outlet, table, and chair, and 62% (n=62) answered yes to being breastfeeding friendly.CONCLUSIONSOnly 8% of the airports surveyed provided the minimum requirements for a lactation room. However 62% stated they were breastfeeding friendly. Airports need to be educated as to the minimum requirements for a lactation room.

There is very limited data on the indications, applications and risks of performing endoscopic ultrasound (EUS) in children. Major limiting factor has been lack of clear indications and difficulty in obtaining adequate training. EUS has a role both as a diagnostic tool and also guiding therapeutic interventions. In this role EUS can have the most impact. One provider (AQ) completed a dedicated adult therapeutic endoscopy training program at a high volume EUS center. Between 2005 and 2008 we performed 175 EUS examinations in children. Age ranges were 2mo-16yrs. 100 upper and 75 lower endoscopy/EUS performed, including: 18 EGD/dilations, 8 EGD/mucosectomy, 9 UGI-bleeding, 8 EUS-pancreatic, 4 EUS-cystgastrostomy, 9 colon/dilations, 5 lower-GI bleeding, 15 colonic polypectomies. Out of 76 interventional studies, 2 acute procedure related complications noted (2.5%): mucosal tear during balloon dilation in a Crohn's ileal stricture and bleeding after romoval of a large duodenal polyp in a patient with Peutz-Jegher's. With adequate training and staff support, establishing a viable pediatric EUS program is feasible. Improved patient outcomes and reduced need for surgical interventions in these children were noted results from our experience. Tabled 1Interventional EUS procedures in children Procedure description Indication Complication ⁎ denotes both acute and long term complications directly related to procedure. Upper EUS with dilation Esophageal Crohn's Peptic strictures Achalasia Schatzky's rings Caustic injury Duodenal web Pyloric stricture recurrence none recurrence none none none none Upper EUS with mucosectomy/polypectomy Esophageal tubular duplication Esophageal polyp Esophageal duplication cyst Gastric polyp Antral nodule Duodenal web Duodenal polyp none none none none none none bleeding EUS pancreatobiliary Recurrent pancreatitis Pancreatic psudocyst Necrotizing pancreatitis none none pancreatic none Lower EUS dilation Stricturing Crohn's disease Post surgical strictures perforation, recurrence none Lower EUS mucosectomy/polypectomy Rectal inflammatory polyps Hamartomatous polyps Adenomatous polyps none none none denotes both acute and long term complications directly related to procedure. Open table in a new tab

Journal of Pediatric Gastroenterology and NutritionVolume 35, Issue 1 p. 99-101 Short Communications Crohn's Disease and Acute Lymphoblastic Leukemia in A Two-Year-Old Child Jolie Limon, Jolie Limon Section of Hematology/Oncology, Davis, California, U.S.A.Search for more papers by this authorDouglas S. Taylor, Douglas S. Taylor Section of Hematology/Oncology, Davis, California, U.S.A.Search for more papers by this authorMichael Haight, Michael Haight Section of Gastroenterology, Department of Pediatrics, School of Medicine, University of California, Davis, California, U.S.A.Search for more papers by this authorDaniel C. West, Corresponding Author Daniel C. West [email protected] Section of Hematology/Oncology, Davis, California, U.S.A.Address correspondence and requests for reprints to Daniel C. West, M.D., Department of Pediatrics, University of California, Davis 2516 Stockton Blvd., Sacramento, CA 95817, U.S.A. (e-mail: [email protected]).Search for more papers by this author Jolie Limon, Jolie Limon Section of Hematology/Oncology, Davis, California, U.S.A.Search for more papers by this authorDouglas S. Taylor, Douglas S. Taylor Section of Hematology/Oncology, Davis, California, U.S.A.Search for more papers by this authorMichael Haight, Michael Haight Section of Gastroenterology, Department of Pediatrics, School of Medicine, University of California, Davis, California, U.S.A.Search for more papers by this authorDaniel C. West, Corresponding Author Daniel C. West [email protected] Section of Hematology/Oncology, Davis, California, U.S.A.Address correspondence and requests for reprints to Daniel C. West, M.D., Department of Pediatrics, University of California, Davis 2516 Stockton Blvd., Sacramento, CA 95817, U.S.A. (e-mail: [email protected]).Search for more papers by this author First published: 01 July 2002 https://doi.org/10.1002/j.1536-4801.2002.tb07737.xRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. REFERENCES 1Mir-Madjlessi SH, Farmer RG, Easley KA, et al. Colorectal and extracolonic malignancy in ulcerative colitis. 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Ms. Green, the mother of a 2-week-old infant, calls the lactation consultant with concerns that “my baby doesn’t like my milk.” Baby Patric was born at 41 weeks gestation, the product of a spontaneous vaginal delivery, weighing 3.8 kg at birth. At 2 weeks of age, Patric is well above birth weight, weighing 4.4 kg. Patric has been exclusively breastfed since birth, with feedings going well. Ms. Green has a 3-year-old daughter who was breastfed for 4 months. Ms. Green then decided to switch her daughter to soy formula because of unending colic, which Ms. Green reports as “disappearing overnight” once she stopped breastfeeding. Because of her daughter’s past history, Ms. Green is worried that “there is something wrong with my milk” as this baby is also very colicky. Ms. Green states that for the past few days, Patric has been showing increasingly more signs of colic, with his fussiness and apparent discomfort getting worse. “About the only time he isn’t crying is when he’s asleep or nursing,” she states. She reports Patric’s stools as very runny, and they have started to appear “mucus-like” as well. Ms. Green does not think she could bear to go through 4 months of colic like she did with her daughter, and yet she very much wants her son to be breastfed. “What’s wrong with my milk?” Ms. Green asks desperately. Response

The authors report on a neonate with gastroschisis repaired at birth who later had abdominal distension, emesis, feeding intolerance, and an abnormal stooling pattern. Total colon and partial small bowel aganglionosis (TCAS), or Hirschsprung's disease, was diagnosed subsequently. This is the first report of this combination of gastrointestinal anomalies. J Pediatr Surg 36:638-640. Copyright © 2001 by W.B. Saunders Company.

Introduction: Propofol was introduced in 1982 and it has been used in over 250 million patients. From 1991 to 1994, seven cases of postoperative pancreatitis related to propofol use were reported to the FDA. In a series of 4 patients with no underlying pancreatic disease undergoing non-abdominal surgery, 2 died due to severe pancreatitis. The manufacturer claims that a causal relationship between propofol and postoperative pancreatitis is unlikely. However, in a sub-population of high risk patients with a past history of pancreatic disease this could be a potentially dangerous drug. Methods: We cared for LB, a 16 y/o female with cystic fibrosis and pancreas divisum. She had multiple procedures including ERCPs, with and without propofol. We retrospectively extensively reviewed her chart. At her initial presentation in 6/96, 3 ERCPs were performed using Demerol and Versed. She underwent stent placement, sphincterotomy, stent replacement and stent removal. After the first procedure her amylase and lipase increased dramatically and took 3 days to return to baseline. No problems were noted after the second ERCP. In 7/97 her pancreatitis recurred, and for the first time she received propofol for ERCP with dilatation of the minor papilla. Her amylase did not increase much, but she did take longer to recover. In 1/99 she had 2 procedures with propofol induction, sinus surgery using 90 mg of propofol. and 10 days later a PASport placement with 150 mg of propofol. After the first procedure she had minor complaints and a slight increase in amylase, and after the second procedure she developed pancreatitis. Her enzyme elevation and symptoms lasted 2 months. She eventually underwent 2 more ERCPs without propofol, one with sphincterotomy of the minor papilla and stent placement, and one for stent removal. Neither of these procedures gave her more than a small elevation in amylase which lasted less than a day. Results: We find that in this high risk patient 2 procedures for non-abdominal problems using propofol precipitated severe pancreatitis. Subsequent ERCPs avoiding propofol did not cause such problems. Discussion: Propofol is often used for sedation and is considered safe. Previous pancreatitis is not currently considered a contraindication for its use. We feel that propofol should be suitably labelled to caution against its use in patients with known or suspected pancreatic disease. Also, amylase and lipase should be checked in any patient who complains of abdominal pain after they have received propofol.

OBJECTIVETo determine the safety and efficacy of anabolic therapy to prevent or reverse wasting and malnutrition in human immunodeficiency virus (HIV)-infected pediatric patients. The anabolic steroid, oxandrolone, was evaluated because of its safe and effective use in other pediatric conditions.METHODSNine HIV-positive children who were malnourished or at risk for malnutrition (4 females, 5 males; 4-14 years of age) took oxandrolone for 3 months (.1 mg/kg/day orally). Quantitative HIV ribonucleic acid polymerase chain reaction and CD4(+) T-cell levels, complete blood cell count (CBC) and chemistry profile, endocrinologic studies, resting energy expenditure, respiratory quotient, nutritional measures, body composition assessment with quantitative computed tomography, and skinfold body composition measurements were determined before treatment, during treatment (3 months), and for 3 months after treatment. Statistical analyses were completed using the Friedman two-way analysis of variance and Spearman correlation tests.RESULTSNo adverse clinical or laboratory events or changes in Tanner staging or virilization occurred. Quantitative HIV ribonucleic acid polymerase chain reaction and CD4(+) T-cell levels did not change significantly. Insulin-like growth factor 1 increased, suggesting an anabolic effect of treatment. The rate of weight gain increased during treatment and was maintained after treatment. Linear growth continued and was maintained throughout treatment, whereas bone age did not increase significantly. Anthropometric assessments indicated an increase in muscle mass and a decrease in fat while patients were on treatment, and a mild decrease of muscle and increased fat posttreatment. Likewise, computed tomography scan results demonstrated similar changes in muscle mass. Resting energy expenditure and respiratory quotient remained stable throughout treatment and follow-up. No significant changes were seen in the quality of life questionnaire.CONCLUSIONSTreatment with oxandrolone for 3 months in HIV-infected children was well-tolerated, safe, and associated with markers of anabolism. The latter effect was maintained partially for 3 months after discontinuation of a 3-month course of therapy. Additional studies are needed to assess the potential benefits and risks of a longer course of therapy or a higher dose of oxandrolone in HIV-infected children.

A self-expanding metallic stent (Wallstent) was used to relieve obstruction of the common bile duct in a young male with a desmoplastic small cell tumor of the abdomen. Two months after insertion and following a course of chemotherapy the lower end of the stent eroded the mucosa of the second part of the duodenum causing severe gastrointestinal hemorrhage which necessitated laparotomy and trimming of the stent. This complication may have been due to shrinking of the tumor as well as thrombocytopenia following chemotherapy.

FAP is an autosomal dominant condition with a prevalence of 1 in 8-10.000 births and is linked to a mutation/deletion in the Adenomatous Polyposis Coli (APC) gene on chromosome 5. The risk of colon cancer in untreated FAP approaches 100%. Thus, screening of at risk individuals is crucial. We investigated using DNA testing for FAP to reduce the frequency and cost of endoscopic screening of at risk individuals. METHODS: We computed the cost of annual colonoscopy performed in a hospital based endoscopy suite and an ambulatory endoscopy suite. The costs were derived from reported charges for professional fees, supplies, medications, nursing, room and pathology fees. We assumed that an individual underwent annual colonoscopy from age 10-25 yrs (a 15 yr screening period), as per the current recommendations. We then calculated the cost of a modified screening program by adding the cost of performing the current genetic test available for FAP to the cost of performing modified endoscopic screening for individuals who were negative for an APC mutation. The modified schedules included baseline colonoscopy, and then colonoscopy either every 3 yrs, every 5 yrs, or no further procedures. The total costs of these screening approaches were then compared. RESULTS: We demonstrated a considerable reduction in cost over a 15 yr period when an individual did not carry an APC mutation and when procedures were done in an ambulatory endoscopy suite. The cost comparison analysis over the expected 15 yr screening period is given in the table. CONCLUSIONS: There were significant cost savings when at risk individuals for FAP undergo DNA screening. We speculate that utilization of genetic testing for FAP will result in improved patient acceptance and participation in a screening program.

Dietary protein-induced colitis is a frequent cause of rectal bleeding in infants. The exact pathogenic mechanism is unknown but the disorder has been thought to be due to an allergic response. Rectal mucosal edema and eosinophilia are typically found but there are no specific markers currently available. Because eosinophil degranulation, as evidenced by the release of major basic protein, has been implicated in hypersensitivity disorders, we aimed to assess major basic protein deposition as a marker of dietary protein-induced colitis occurring in young infants. Suction rectal biopsies from five infants aged 1 to 7 months with findings consistent with dietary protein-induced colitis were compared histologically with five age matched controls who underwent rectal biopsies to rule out Hirschsprung's disease. An established indirect immunofluorescent staining method was used to identify tissue major basic protein. Comparable rectal deposition of major basic protein was found for the controls and colitic patients. Mucosal eosinophilia but not mast cell content was more prominent in the colitic patients (P < .05) than in the controls. Some of the colitic infants had elevated serum IgE levels (1 of 5), positive RAST for milk (2 of 5), and peripheral blood eosinophilia (1 of 5). Our findings do not support the concept that dietary protein-induced colitis of infancy is due solely to an immediate hypersensitivity response. The results also indicate that major basic protein is probably not a marker or likely primary mediator of this disorder.

Department of Pediatrics USC Medical School and Children's Hospital of Los Angeles Los Angeles, California

To assess the utility of the serum aspartate aminotransferase/alanine aminotransferase (AST/ALT) ratio in a group of infants with liver disorders, we retrospectively analyzed the charts of 73 infants with chronic liver disorders. Patients were considered as having either a good outcome (n = 40) or a poor outcome (n = 33), based upon the clinical course. AST and ALT in serum were measured simultaneously at the time of initial presentation and at various follow-up visits during the first 13 months after birth. At presentation (mean age 1.65 months), there was no difference in the AST/ALT ratios between the good (1.61 +/- 0.62; mean +/- SD) and poor (1.65 +/- 0.78) outcome groups (P = 0.81). However, over time, the AST/ALT ratio increased in patients in the poor-outcome group and decreased in patients in the good-outcome group. Calculating the AST/ALT ratio appears to be an easy, early, and reliable prognostic indicator for infants with hepatic disease, and may be a useful measure for evaluating liver-disease patients.

Twenty-one infants less than 6 months of age with gastrointestinal symptoms of cow milk and/or soy protein-based infant formula intolerance (diarrhea in 14, hematochezia in 16, emesis in 8, failure to thrive in 4, and colic in 10) were treated clinically with a whey protein hydrolysate formula. Six patients improved when placed directly on the formula, and 15 remained asymptomatic or improved when given the whey hydrolysate formula following initial treatment with a casein hydrolysate or elemental formula. Eighteen had supporting evidence of an allergic basis for their symptoms, including a family history of allergies in 6, a clinical challenge with the offending formula in 1, laboratory tests consistent with atopy in 11, and/or rectal biopsy with histologic allergic features in 7. The whey hydrolysate formula may be an acceptable alternative to soy or casein hydrolysate formulas in most infants with gastrointestinal symptoms of cow milk and/or formula intolerance.