Category Archives: Pediatric Gastroenterology Nutrition Topic

Best gastrostomy tube

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A recent report touts the feasibility of a one-step percutaneous gastrojejunostomy (GJ) as the latest advance in enteral access (JPGN 2012; 54: 820-21).  This reference describes a new variation in technical placement: gastropexy using t-fasteners to secure gastrostomy tube site and then advancing neonatal scope via gastrostomy site to advance guidewire for  GJ placement.  This technique was used in three infants.

Most centers have developed their own protocols for enteral access and it is likely that the familiar approach to that center will be safest for their patient population.  Recently, the subject of gastrostomy tube placement was extensively reviewed in our institution (see below) due to variation in care at two children’s hospitals.  In one hospital, the surgical group primarily placed laparascopic button gastrostomies and argued that better visualization led to lower complications like colonic interposition.  Furthermore, this approach was considered similar in cost effectiveness as the group would place a primary Mic-Key® (http://www.mic-key.com/home.aspx) thereby eliminating the need for anesthesia for a button placement.

The alternative approach utilized a Corflo® gastrostomy tube (http://www.corpakmedsystems.com/product_main/enteral_main.html#FeedingTubes).  The advantages of this approach were 1) less anesthetic time/a smaller operation, and 2) lower likelihood of tube dislodgment.  This group approach argued that dislodgment was the greatest risk and that there was no urgency for a button tube.

Despite a joint meeting of these groups weighing the pros and cons, there was not a single best gastrostomy tube.

My experience is that tube dislodgment is quite common with button tubes.  In addition, primary button tubes can be difficult to size when the patient is under anesthesia.  As such, it is my practice to discourage primary gastrostomy button placement.  In addition, most patients who need gastrostomy tubes can wait until they are good surgical candidates both in terms of cardiorespiratory status and size.

Resources:

Gtube Products:
• AMT clamp –helps eliminate tubing pullouts
www.amtinnovation.com

• Gtube washable pads
www.oley.org  (specific web address: http://oley.org/lifeline/TubetalkJF11.html)

Additional references:

  • -J Pediatr 2011; 159: 602. Preemptive gtube assoc with improved survival post Norwood. High number needed fundoplication.
  • -JPGN 2011; 53: 293. 95% success with PEG in infants 2.1-5.6kg
  • -JPEN 2011; 35: 50-55. Predictive factors of mortality after PEG.
  • -JPGN 2009; 49: 237. Gtube improves height & weight in Rett syndrome.
  • -Clin Gastro & Hep 2007; 5: 1372. PEG placement does NOT prolong life in dementia patients.
  • -Arch Dis Child 2006; 91: 478-82. PEG reduced hospitalizations for respiratory dz in 57 severely impaired children
  • -J Pediatr 2006; 149: 837. inreased risk of PEG in SMA type 1 -42% w aspiration; 17% death (2/12)
  • -Pediatrics 2004; 114: 458-61. Moratlity rate of 0.4% -one death related to sepsis/peritonitis & 5% complication rate.
  • -Teitelbaum JE, Gorcey SA, Fox VL. Combined endoscopic cautery and clip closure of chronic gastrocutaneous fistulas. Gastrointest Endosc. 2005;62(3):432-435
  • -JPGN 2006; 43: 624. Satisfaction with PEGs: 94% of parents viewed PEG as positive influence on child’s situation & 98% would have chosen PEG insertion again (n=121).
  • -Sullivan PB, Dev Med Child Neurol 2005; 47: 77-83. 57 CP pts -almost all had improved health/nutrition p gtube
  • -Gastroenterology 2001; 121: 970-1001 & JPEN 2004; 28: S16. Provision of nutrition does not, for the most part, favorably alter clinical outcome.
  • -Lancet 2005; 365: 755-763. Pts c stroke/PEG did not do better than those c stroke/NGT.
  • -Sullivan PB, Dev Med Child Neurol 2004; 46: 796-800. gtube improves QOL.

Gastrostomy Tube Review with annotated references: Laparoscopic gtube versus conventional PEG placement

 Zamakhshary et al.  JPS 2005; 40: 859-62.   i.  Retrospective review, n=119 (only 26 with laparoscopy =21%). (2002-2003)  ii.  States same operative time of ~53 min by combining 2nd procedure w PEG (in 77% w PEG).  It takes these authors a long time to perform PEG and gtube change procedures.  Also, it is not noted how many of these 2nd procedures were coordinated with other needed anesthesias.  (Many times a PEG is replaced at the time of another procedure.)   iii.   3 PEG with transcolonic tube, 2 failed PEG –one with peritonitis, 4 with tract disruption when PEG pulled.  Similar rate of local problems (eg granulation tissue).  ARTICLE does not detail when PEG tubes are pulled –VERY high rate of tract disruptions.   iv. Article missing key details regarding size of PEGs & gtube buttons which may impact complications.  v. Cited advantages according to authors:

  1. “eliminates” risk of hollow viscus injury (JH: this is NOT  accurate)
  2. Useful for small infants (<2kg) (JH: usually gtube NOT needed in <2kg)
  3. Enables “ideal” location (JH: this is NOT  accurate)
  4. Primary button ‘advantage’ (JH: DOES NOT cite potential pitfalls like button too tight, possibility of balloon breakdown, possibly higher rate of dislodgment)

 Vervloessem et al. JPS 2009; 18: 93-97.     i. Retrospective review: 1992-2008.  N=467.  ONLY 19 Lap PEG –thus limited ability to provide comparison.  ii. Cites 59 “major complications” due to PEG –Table 2, including “13” new cases of GERD after PEG (or worsened GERD).  Of the major complications, important complications included 1 sepsis death, 7 peritonitis, 5 gastrocolic fistulas, 4 major granulation tissue, and 11 buried bumpers.  iii.  States that VPS is risk factor for infection but does not state whether any Lap gtubes were done in these patients.  iv. Complication rate decreased over the years—p=0.003; thus PEG procedure became safer with time and experience.   Could not demonstrate a decrease in complications with lap gtube versus PEG.  Authors recommend lap PEG in specific situations such as previous abdominal surgery or if not a good puncture site.

 Segal et al. JPGN 2001; 33: 495-500.    i. Retrospective study, n=110 (1990-97). N=110 –ALL PEG (no LAP). Thus, limited utility in comparing two methods. ii. “44%” developed late complications with PEG.  Most common: 24 extruded tubes/buried tubes (would NOT be better with lap button); other important: cologastric fistula n=2, peritonitis.  Table 1 indicates that 75% of dislodgment were due to buttons not PEG.  12 of the complications were granulation tissue and proliferative gastric mucosa.  Buried tubes occurred 14 & 19 months after placement with button tube!!   iii.  Thus this article adds little to the discussion of PEG vs lap gtube.

Akay et al. JPS 2010; 45: 1147-52  i.  Retrospective review (2004-2008) n=238 (134 PEG, 104 LAP)  ii. PEG with higher complications;  authors were changing PEG after 6-8 weeks. iii.  6 patients had early PEG dislodgment –this is higher than expected.  iv. 1 patient with gastrocolic-cutaneous fistula with both PEG & with LAP.  v. Table 4 lists complications: similar stomal issues, 2 patients with leak after PEG exchange (too early! –see page 1152) vi. Cited advantages: “eliminating” risk of hollow viscus injury, allows for sutures, small infants (<2kg) & possible primary buttons.**These authors did not place primary buttons –this makes it difficult to draw any conclusions about PEG vs primary LAP button.  Many feel PEG tube is a better tube and less prone to dislodgment than button and guarantees appropriate size.

Lantz et al. Int J Pediatr 2010; ID# 507616, 1-4.   i. Literature review, included 54 studies that qualified (1995-2009).  N=4331 (1027 LAP, 3304 PEG).  Very few details given in this review.  ii.Fistulas in 1.27% of PEG vs 0% for LAP.  iii.  Lists significant limitations: different studies, not blinded, nonpublication bias.  iv.  “This study highlights the need …for trials, comparing PEG to” LAP. v.  Does not include the limitation that LAP technique developed later and with more experience less complications.  Except for gastrocolic-cutaneous fistulas –no specific information is given about complications.

Avitsland et al.  JPGN 2006; 43: 624-28.  i. Restrospective review. N=121 –all PEGs  ii.     PEG “safe technique…major complications rare.”  “Most children experience minor stoma-related complications.”  iii. 29 died due to other factors.  Of 85 with f/u, 21 able to remove gastrostomy.  iv. No early mortality (<30 days).  1 of 85 had tube dislodgment.  3 had tube migration into esophagus (in cases where tube was not endoscopically removed).  v.     Frequent tube site problems ~75% -most easily treated. vi. Parents with high satisfaction: 83/85 (98%) would choose PEG again, 80/85 (94%) stated PEG improved child’s situation

Gauderer M. JPS 2001; 36: 217-19.   i.  Focused literature search and personal 20 year experience. ii. >216,000 PEGs performed annually in U.S. according to article (~5000 children).  PEG procedure developed 1st for children. iii.  Suggested approach to PEG with or w/o fundoplication: “Because PEG is such a simple procedure, a well-accepted approach is to place gastrostomy initially in children who can tolerate nasogastric tube feedings and add an antireflux procedure later, if needed.”

Srinivasan et al. JPGN 2009; 49: 584-88.   i.Prospectively collected data from observational study, n=601 (384 PEG insertions, 165 button conversions).  ALL pediatric. ii.  Complications:  PEG site erythema 15%, buried bumper migration (1 patient), 3 PEG dislodgments, one patient had laparotomy due to severe pain (no findings identified).   No procedure-related mortality.   iii.  49 of 384 removed –no longer needed.  iv. “The role of PEG is well established…our experience..PEG has been generally safe, with low procedure-related morbidity in children.”

Nutr Clin Pract 2005; 20 (6): 607-12.  Bankhead RR et al. i. Comparison of 91 patients.  23 PEG, 39 LAP, 29 open.  ii.   PEG had lowest complication rate

Surg Endosc 2006; 20: (8): 1248-51.  Ljungdahl M.                                         i.     Prospective, randomized study. N=70.  ii.  PEG with lower complication rate than surgical (open) gastrostomy –lower mortality & morbidity in adult patients.

UK Review Online: http://www.patient.co.uk/doctor/PEG-Feeding-Tubes-Indications-and-Management.htm   2009  i. Review of alternatives to PEG for gastrostomy insertion. There are alternative methods of gastrostomy tube insertion to PEG. They are: a) Laparoscopic insertion b) Open surgical technique c)Percutaneous radiologically guided gastrostomy (PRG) insertion. ii.  “There are reports over the years since introduction of PEG in the 1980s with often inconclusive results.21▪    A small study from Ireland and one from London favour PRG in patients with amyotrophic lateral sclerosis as it avoids the need for sedation or endoscopy.22,23▪  One meta-analysis suggested a higher success rate with PRG than with PEG, and less morbidity than either PEG or surgery.24 However a more recent comparison of a relatively small number of endoscopic, surgical and laparoscopic placement favoured PEG25 and another favoured PEG over PRG.26▪     A literature review suggested PEG as the procedure of choice for placement of gastrostomy tubes.27▪    A recent prospective randomized trial favoured PEG over surgical gastrostomy insertion.28▪     There is some evidence that polyurethane PEGs are less troublesome than silicone PEGs (less tube deterioration, less blockage).29▪    PEG is preferred in trauma patients.30▪                Antibiotic prophylaxis for PEG insertion appears to reduce the incidence of wound infection.19,20▪      Laparoscopic insertion was considered preferable to PEG by one study in children with PEG insertion having higher complication rate in children and often requiring repeat anaesthetics.31   An earlier study in children showed similar results for surgical, PRG and PEG insertion but did not look at the laparoscopic technique.32    A recent study from Norway found PEG insertion safe and very well tolerated by children and parents but made no comparison with other techniques.

Conclusions of review: PEG likely increases risk of gastrocolic fistulas (1-2%) but this has been reported with LAP as well.  The incidence is low.  No well-designed  studies have demonstrated superiority of LAP over PEG in terms of safety.  Potential drawbacks of LAP are likely underreported.  There have been cases of severe peritonitis at local hospitals following lap with primary gtube balloon misplacement.  Many feel PEG tube is a better tube and less prone to dislodgment than button (dislodgment is most frequent serious adverse event) and can be easily adjusted to  appropriate size.  To minimize complications, tube should not  be changed early.

Food choices, FODMAPs, and gluten haters

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Given the frequency of functional gastrointestinal diseases (FGID), including irritable bowel syndrome (IBS), dietary treatments that may improve symptoms receive a lot of attention.  A recent review of the role of food choices in the development and management of FGIDs is a useful reference (Am J Gastroenterol 2012; 107: 657-66 -thanks to Ben Gold for forwarding this article).

This review details specific dietary advice as well as the following specific physiologic effects of FODMAPs:

  • Osmotic effects
  • Bacterial fermentation
  • Motility effects
  • Prebiotic effects
  • Systemic effects –mild depression, tiredness
In addition, the review looks at other potential foods which could serve as a trigger for IBS symptoms, like gluten & summarizes why some IBS patients are gluten haters.  The authors acknowledge that gluten sensitivity, in the absence of celiac disease, does not have a known mechanism.  Until a reliable marker becomes available, the importance of gluten sensitivity for FGIDs is unknown.
Related posts:

What to make of FODMAPs

Gluten sensitivity without celiac disease

Is a biopsy necessary in Celiac disease?

Save a life with free allergy education

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Food allergy affects 4-8% of children and allergic reactions can be fatal.  In fact, the main cause of poor outcome with accidental food allergy exposure is delay in the use of epinephrine.  To improve parental knowledge and overall management of food allergies, a group of allergists, nurses and dieticians has developed and validated educational materials (J Pediatr 2012; 160: 651-6).  In addition, they have made these materials available at no cost online:

To validate their materials, the authors enrolled 60 parents of newly referred children with a prior food allergy.  The measured outcome was demonstration of an autoinjector for epinephrine.  The correct number of steps in the use of the autoinjector increased from a 3.4 to 5.95 score (max score 6).  In addition, at 1 year, the score remained high, 5.47.  Knowledge tests improved as well: from 9.2 to 12.4 (out of 15); at one year, the score was 12.7.  On a practical basis, the frequency of allergic reactions was reduced as well.  The annualized allergic reaction rate dropped from 1.77 (historical data) to 0.42 after the instruction.

The article also relates that some of the material relied on previous educational material, in particular the food allergy emergency plan available from the Food Allergy & Anaphylaxis Network (www.foodallergy.org).

Materials available include information on specific allergic disorders, avoiding allergens, management in and outside home, and living a safe/healthy life.  In addition, an educational video is available.

Additional references:

  • -Bock SA et al. J Allergy Clin Immunol 2007; 119: 1016-8. Poor outcome with accidental food allergy exposure is delay in the use of epinephrine.
  • -J Pediatr 2011; 158: 578.  Oral food challenges allowed 84% to return foods to diet.  n=125.
  • -Clin Gastro & Hep 2010; 8: 755.  Review of food allergy (vs intolerance) in adults.  Gives list of hypoallergenic diet , pg 758.
  • -Pediatrics 2009; 124: 1549-55.  3.9% of US kids w food allergy.  Nat’l surveys.
  • -NEJM 2008; 359: 1252 Review. Usual age of resolution: eggs  @ 7yr (75%), milk @ 5yr (76%); wheat/soy -rarely cause IgE-mediated allergies 80% resolve by 5yrs>  More  persistent allergens:  peanuts/tree nuts/sesame seeds = persistent in 80-90% at 5yrs, fish = persistent.
  • -Pediatrics 2003; 111: 1591-1680.  (supplement) Pediatric Good Allergy symposium
  • -Pediatrics 2003; 111:829-835. Infants c food-induced enterocolitis often have multiple food allergies (cereal, veggie, poultry, meat)  IgE based tests are negative (skin prick & IgE Abs
  • -Gastroenterology 2001; 120: 1023-25; 1026-40.  AGA position paper; technical review.
  • -J Allergy Clin Immmunol 1999; 103: 717-728 &981-9.  Pathogenesis &  Dx/ mgt.

VTE with IBD

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In our children’s hospital, work is underway to systematically screen children for risk factors for venous thromboembolism (VTE) and to establish an algorithm to lower the risk of a VTE with either mechanical or pharmacologic treatments. One of the risk factors has been the presence of inflammatory bowel disease (IBD).  The absolute risk of IBD for VTE is not clear.  However, a recent study relates the risk among a large Danish population of adults and children (Gut 2011; 60: 937-43).

The study included 49,799 patients with IBD (14,211 Crohn’s, 35,229 UC) and compared with 477,504 members of the general population.  VTE risk for IBD was increased with HR of 2.0.  The incidence of VTE increased with age; however, the RR was higher in younger patients.  Among those less than 20 years, HR was 6.6 for VTE; HR 6.0 for DVT and 6.4 for PE.  In this age group, “unprovoked” VTE had HR of 4.5.  Unprovoked VTE was defined as event occurring without malignancy, recent surgery, pregnancy or fracture.

Although the relative risk is increased, the authors caution that the absolute risk in younger patients is low.  In those IBD patients less than 20 years, the incidence rate was 8.9 per 10,000 person years.  In contrast, in those IBD patients older than 60, the incidence rate was 54.6 per 10,000 person years.  There did not seem to be a significant difference between Crohn’s disease and ulcerative colitis in absolute or relative risk. The authors conclude that in those IBD patients younger than 20 years without ‘other VTE risk factors or limited mobility, the benefits of prophylaxis may no longer outweigh the risks.”  In older patients (>60 years), even outpatients experiencing flares might benefit from VTE prophylaxis.

Additional references:

  • -NEJM 2012; 366: 860 (letter to editor). Authors emphasize importance of VTE with UC, especially during flares.
  • -Lancet 2010; 375: 657-63. VTE with active IBD and in remission.
  • -Clin Gastroenterol Hepatol 2008; 6: 41-5. Thrombosis with IBD.
  • -Gut 2004; 53: 542-8. IBD -risk factor for VTE?
  • -Gut 2004; 53 (suppl 5): v1-16. IBD guidelines for management.

More on PNAC

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In a previous blog entry (PNAC, PNALD, and IFAC), reduction in intralipids was shown to improve parenteral nutrition associated cholestasis (PNAC).  This change in the use of parenteral nutrition (PN) and others are emphasized in a review article by the American Pediatric Surgical Association (J Ped Surg 2012; 47: 225-40).

This review tries to provide evidence-based guidelines for PNAC with ratings of the evidence for each of their recommendations.

A summary of their findings is given in Figure 1 of the article.  Key points:

  • PN duration is a significant predictor for cholestasis
  • NEC & sepsis both play a role in the development of PNAC
  • Insufficient data to determine if antibiotics used to decrease bacterial translocation/hepatocyte damage may be beneficial
  • Fat emulsion restriction may reduce PNAC without detriment to growth
  • Fish-oil based lipid emulsions are safe and effective for PNAC.  “Despite the promise of Omegaven…the literature is insufficient to provide a recommendation higher than grade C.”  (Grade C= “possibly effective, ineffective, or harmful;” requires at least 2 convincing class III studies [class III studies generally are non-randomized non-blinded studies]).  Information to obtain Omegaven:

http://www.oley.org/documents/How_Physicians_Can_Obtain_Omegaven.pdf
http://www.oley.org/lifeline/PN_Liver_Disease.html

  • Strong evidence that higher initial protein load does not increase the risk of PNAC
  • Strong evidence that trophic feeds are beneficial to reduce PNAC
  • Weak/conflicting evidence that there is any benefit of Aminosyn over Trophamine
  • Weak evidence to support the routine removal of copper or manganese from PN as a prophylactic strategy to prevent PNAC
  • Weak evidence to support prophylactic cycling of PN to reduce PNAC.  There are also concerns about the development of hypoglycemia in preterm infants off of PN
  • Use of CCK is not recommended
  • Oral bile acids may result in improvement
  • Erythromycin may promote motility and facilitate enteral feeds, thereby reducing PNAC

Common to be “D-ficient”

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Many of the children that a pediatric gastroenterologist sees are at risk for Vitamin D deficiency, including children with inflammatory bowel disease, cystic fibrosis, celiac disease, and liver diseases.  In addition, vitamin D deficiency is widespread: in U.S. 50% of children aged 1-5 years and 70% 6-11 years are vitamin D deficient or insufficient. A thorough review on this “D-lightful” vitamin was in a recent JPEN (JPEN J Parenter Enteral Nutr 2012; 9S-19S).

History: In 1822 Sniadecki recognized children in urban but not rural Poland developed rickets. He postulated the effects of the sun as the reason for rickets; his idea was dismissed.  In 1920s, the concept of irradiating milk to prevent rickets emerged. In 1950s, outbreak of hypercalcemia in infants in Great Britain was thought to be related to vitamin D fortification and curtailed this practice in Europe.  However, these cases were likely due to Williams syndrome.

Sources of vitamin D: oily fish (salmon), cod liver oil, some mushrooms, egg yolk, & sunlight. Exposure of an adult in a bathing suit to one minimal erythemal dose (MED) is equivalent to ingesting 20,000 IUs of Vitamin D. (The minimal dose that induces any visible reddening at that point is defined as one MED.)

Effect of sunscreen: A sun protection factor (SPF) of 30 absorbs approximately 98% of solar ultaviolet radiation & thus lowers vitamin D production by 98%.

Ethnicity: Melanin is an effective SPF.  A person of african-american descent, on average, has an SPF of 15, which reduces vitamin D production by 90%.

Age: Aging decreases 7-dehydrocholesterol in human skin.  Due to this, the elderly produce much less vitamin D.  For example, a 70 year old has a 75% reduction compared to a 20 year old.

Forms of vitamin D:  25-hydroxyvitamin D (25OH-D) is the major circulating form of vitamin D & physicians measure 25OH-D. 25OH-D is metabolized in kidney to 1,25-dihydroxyvitamin D (1,25OH-D), also called calcitriol.  This is the most biologically-active and is responsible for increasing intestinal calcium absorption and mobilizing calcium from bone.  However, 1,25OH-D provides no information vitamin D deficiency; it can be elevated or normal in deficiency states.

  • Cholecalciferol (vitamin D-3) is formed in the skin from 5-dihydrotachysterol.
  • Ergocalciferol (Vitamin D-2) is the form in Drisdol (8000 IU/mL) & Ergocalciferol Capsules (1.25 mg =50,000 USP Units)

Vitamin D deficiency:  The exact numbers are debated.  The institute of medicine (IOM) has considered individuals deficient if 25OH-D is <20 ng/mL.  The Endocrine Society and the author suggest vitamin D deficiency as <20 ng/mL & insufficiency as <30 ng/mL.  The author recommends ideal levels between 40-60 ng/mL.

Consequences of deficiency:

Osteoporosis, Osteopenia, Rickets (see references below): Bone weakening occurs due to loss of phosphorus from the kidneys.  Vitamin D deficiency lowers accrual of calcium in skeleton and leads to osteoporosis, osteopenia, and rickets. Imaging for rickets: the best single radiographic view for infants and children younger than 3 years is an anterior view of the knee that reveals the metaphyseal end and epiphysis of the femur and tibia. This site is best because growth is most rapid in this location, thus the changes are accentuated.

Nonskeletal consequences: vitamin D deficiency is associated with increased risk for preeclampsia, URIs, asthma, diabetes (type 1), multiple sclerosis, hypertension, and schizophrenia.

Treatment:

  • Infants who are breastfed should be receiving supplemental vitamin D, 400 IU/day.
  • Adults/children (>1 year) RDA 600 IU/day –mostly from diet per IOM. Yet author states, “it is unrealistic to believe that diet alone can ….provide this requirement.”
  • In vitamin D deficient patients: (initial treatment) 2000 IU/day or 50,000 IU/week for 6 weeks.
Toxicity from vitamin D (from NEJM 2010; 364: 248-254.): “Toxicity from vitamin D supplementation is rare and consists principally of acute hypercalcemia, which usually results from doses that exceed 10,000 IU per day; associated serum levels of 25-hydroxyvitamin D are well above 150 ng per milliliter (375 nmol per liter). The tolerable upper level of daily vitamin D intake recently set by the Institute of Medicine (IOM) is 4000 IU.”

Additional references:

  • -Pediatrics 2008; 122: 398. Should give 400 IU/day to breastfed babies. Consequences of Vit D deficiency: increased risk for DM, multiple sclerosis, cancer (breast, prostate,colon), rickets, and schizophrenia. Article lists vit D content of foods (high in cod liver oil, shrimp, fortified milk, many fish). Severe deficiency when < 5ng/mL, deficient if < 15 ng/mL; probably should be >32 ng/mL. Causes of vit D deficiency: decreased synthesis (due to lack of sun -skin pigmentation, sunscreen/clothing, geography, clouds), decreased intake, decreased maternal stores & breastfeeding, malabsorption (eg celiac, CF, EHBA, cholestasis), increased degradation; treatment of rickets: double-dose of vitamin d (~1000 IU/day for babies & 5000 for older kids) x 3-4 months along with calcium (30-75/mg/kg/day). Follow Ca/phos/alk phos monthly. Alternatively, give ~100,000 units over 1-5 days.
  • -JPEN J Parenter Enteral Nutr. 2011;35:308-316-Results: The study included 504 IBD patients (403 Crohn’s disease [CD] and 101 ulcerative colitis [UC]) who had a mean disease duration of 15.5 years in CD patients and 10.9 years in UC patients; 49.8% were vitamin D deficient, with 10.9% having severe deficiency. Vitamin D deficiency was associated with lower HRQOL (regression coefficient –2.21, 95% confidence interval [CI], –4.10 to –0.33) in CD but not UC (regression coefficient 0.41, 95% CI, –2.91 to 3.73). Vitamin D deficiency was also associated with increased disease activity in CD (regression coefficient 1.07, 95% CI, 0.43 to 1.71). Conclusions: Vitamin D deficiency is common in IBD and is independently associated with lower HRQOL and greater disease activity in CD. There is a need for prospective studies to assess this correlation and examine the impact of vitamin D supplementation on disease course.
  • -JPGN 2011;53: 361. similar prevalence of low Vitamin D as general population –58% with less than 32.
  • -JPGN 2011; 53: 11. Guidelines for bone disease with inflammatory bowel disease.
  • -Pediatrics 2010; 125: 633. Increasing Vit D deficiency noted in minority children. n=290. 22% w levels <20, 74% <30.
  • -Hepatology 2011; 53: 1118. Good vitamin D levels are another favorable predictive factor in antiviral response to Hep C along with IL28B.
  • -NEJM 2010; 364: 248-254. Vitamin D insufficiency. Levels between 20-30 may be OK -not enough evidence to determine conclusively whether this level is detrimental
  • -J Pediatr 2010; 156: 948. High rate among african americans with asthma, 86%. n=63.
  • -Pediatrics 2009; 124:e362. n=6275. 9% of pediatric patients vit D deficient & 61% were insufficient.
  • -Pediatrics 2009; 124:e371. n=3577. low 25OH-D levels inversely assoc with SBP/metabolic syndrome.
  • -NEJM 2009; 360: 398. case report of rickets
  • -J Pediatr 2003; 143: 422 & 434
  • -Pediatrics 2003; 111: 908. 200 IU Vit D recommended for all breastfed infants.
  • -J Pediatr 2000;137: 153 & 143.. Nutritional rickets–primarily in blacks; rec vitamin D 400 IU per day.

Food as medicine

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Two recent articles add some useful information regarding enteral therapy for Crohn’s disease (Inflamm Bowel Dis 2012; 18: 246-53 & JPGN 2012; 54: 298-305).

The first article enrolled 34 children with newly-diagnosed Crohn’s disease.  Patients were divided into elemental and polymeric formula groups and followed in a prospective, double-blind randomized controlled trial for two years.  Measures of improvement included the PCDAI as well as fecal calprotectin and fatty acids.  Both groups of patients responded clinically.  93% (14/15) of the elemental formula group achieved remission based on PCDAI scores (<11) and 79% (15/19) of the polymeric formula group.  The initial treatment was use of formula (along with only clears) either by NG or oral for 6 weeks.  All patients had NG placed at time of endoscopy and if sufficient oral intake was demonstrated (for 2 days), NG was removed.  All subjects had small bowel and colonic disease.  Although calprotectin levels decreased, they remained very elevated.  In the EF group, the median calprotectin dropped from 2023 μ/g to 1113 μ/g, though only one patient had a level below 400; similarly in the PF group the calprotectin dropped from 1929 μ/g to 1134 μ/g, and only two patients had a level below 400.  Some to the reasons why changes in diet may be useful have been alluded to in a previous post: Eat your veggies…if you don’t want to get sick.

The second reference is a clinical guideline on the use of exclusive enteral nutrition EEN).  The introduction notes that 65% of European pediatric gastroenterologists use EEN compared to 4% for North American pediatric gastroenterologists.  In pediatric trials, EEN and corticosteroids were considered ‘equally effective’ in a pediatric meta-analysis which included five randomized controlled trials (n=147).  However, a Cochrane review favored corticosteroid treatment over EEN in a meta-analysis that included adult and pediatric patients (n=192 EEN, n=160 corticosteroids).  According to the authors, small studies have demonstrated other potential advantages of EEN including higher rates of mucosal healing and better linear growth.  With regard to mucosal healing, the initial cited study casts with ongoing elevated calprotectin indicates that this does not occur in the majority of children with EEN therapy.  Other caveats:

  • Disease location: some evidence favors small bowel disease rather than colonic disease
  • Formula composition: does not seem to matter whether elemental or polymeric
  • Duration of therapy: majority treat for 6-8 weeks of EEN.  The authors recommend at least 8 weeks
  • Time for response: Inflammatory markers improve in a little as a week, remission typically 2-4 weeks
  • Concomitant medications: many places initiate immunomodulator treatment; others cycle EEN
  • Start with goal 120% of ‘maintenance’ nutrient needs.  On 1st day, authors recommend starting at 1/2 goal volume and gradually increase over 1-2 days
  • Partial enteral nutrition (PEN) (eg. overnight feedings & normal daytime diet) has been helpful in improving growth and may improve remission rates.
Why not EEN or PEN? Potential barriers include cost, difficulty changing diet, fear of tube feedings, and more acceptable alternatives.  At the same time, some of these barriers could be overcome.  Quality of life measures have improved in children receiving enteral nutrition.

The use of more top-down therapy may affect all of the above considerations (Only one chance to make first impression).

Additional references:

  • -Cochrane Database Syst Rev 2007; CD000542.  Enteral nutritional therapy vs corticosteroids to induce remission in Crohn’s disease.
  • -Gastroenterology 2011; 141: 742. AGA guidelines on use of enteral nutrition in wide variety of conditions.
  • -Gastroenterology 2008; 135 : 1005. omega-3 fatty acids ineffective in Crohn’s dz for maintaining remission.
  • -Pediatr Res 2007; 61: 356-60.  Enteral nutrition effect on protein turnover in adolescents with Crohn’s disease.
  • -J Pediatr 2000; 136: 285-91. Nutritional Rx w polymeric diet is effective w/in 8 weeks in 32/37.
  • -Scand J Gastro 2001; 36: 383-8. Elemental & polymeric diets successful in maintaining remission in ~43% of adults with complete steroid withdrawal
  • -JPEN 1992; 16: 499. improved wt,ht, decreased prednisone, decreased CDAI
  • -JPGN 2000; 31 (supp 2) A291. Polymeric vs elemental diet.
  • -JPGN 2002; 35: 339-40. Lactase deficiency – same prevalence in IBD as in RAP.
  • -JPGN 2000; 31: 3 & 8. EN about as effective as steroids for primary Rx.

Rest easy with enteral nutrition

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Exactly how long can we leave enteral formulas (ready-to-feed) hang while families rest?  Probably 12 hours according to a recent article (Nutr Clin Pract 2011; 26: 451).  This prospective study involving 30 pediatric patients studied the outcomes in those who received continuous enteral feedings using decanted formula for a minimum of 12 hours.  In this study, patients received both polymeric and peptide based formulas.  Cultures of the formula were obtained.  Among 111 usable cultures, 100 showed no growth, 6 had growth considered below FDA threshold for contamination & 5 (in two patients) had coliforms identified.  No patient developed clinical symptoms.  In these two patients, the authors speculate that contamination occurred due to a combination of exogenous source (touching) as well as possible endogenous source (retrograde movement of bacteria from patient’s gastrointestinal tract).

This small study lends support to extended hang times of up to 12 hours as long as the feeding sets are carefully managed with aseptic technique, clean gloves & avoiding touching formula.  Instead of more frequent changes to formula, this approach can allow parents to sleep while their children receive enteral nutrition and for nurses to pursue other activities for hospitalized patients.

The context for the study was a FDA recommendation for an 8-hour hang time based on conservative recommendations from manufacturers.  The FDA recommendation may have been influenced by a report in 2001 of an enteral powdered formula contaminated with Enterobacter sakazakii which lead to the death of a premature infant.

It should be noted that ready-to-feed enteral formulas are commercially sterilized prior to hanging whereas powdered formulas cannot be commercially sterilized.

Additional references:

  • -MMWR 2002; 51: 297-300.
  • -J Hosp Infect 2005; 59: 311-316.

Eat your veggies…if you don’t want to get sick

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Maybe your mother was right –you should eat your vegetables!   For a long time, it has been known that dietary changes can be used to treat Crohn’s disease.  The specifics about what type of diet and the reasons for how diet promotes a healthy gastrointestinal tract are being unraveled.  A person’s diet affects their microbiome; and, a number of recent articles have highlighted the microbiome in both functional and nonfunctional disorders (see below).

An even more fascinating article is in last week’s New England Journal of Medicine (NEJM 2012; 366: 181).  This article discusses two publications which show how certain dietary components interact with intestinal immune receptors.

  • Kiss EA et al. Science 2011 October 27 (Epub ahead of print).
  • Li Y et al. Cell 2011; 147: 629-40.

This NEJM article implicates a typical ‘Western’ diet as a contributor to inflammatory bowel disease (IBD).  However, a diet high in vegetables may prevent or reduce inflammation.  One mechanism whereby vegetables affect the GI tract is through the AhR (aryl hydrocarbon) receptor.  Some vegetables, like broccoli, cabbage, and brussel sprouts, are natural ligands for this receptor.  A mouse model has shown that AhR deficiency “results in increased epithelial vulnerability, immune activation, and altered composition of the microbiota.”  In addition, AhR is down-regulated in the intestinal tissue of persons with IBD.  AhR ligands are associated with increased interleukin-22 which promotes intestinal integrity.

Additional work regarding the optimal diet are ongoing.  There has been an interest in a ‘carbohydrate specific diet.’  This year’s NASPGHAN meeting (abstract #48)  presented data on this diet from a retrospective study.  This poster described five patients on monotherapy (diet alone) and at 6 months –good results in four patients (80%).  A few prospective studies are underway; in fact, a prospective study with patients from our office will be presented at this year’s DDW.  Initial results look promising (personal communication from lead investigator, Stan Cohen).

Additional references:

  • -Gastroenterology 2010; 139: 1816, 1844.  Microbiome & affect on IBD vs mucosal homeostasis.
  • -J Pediatr 2010; 157: 240.  Microbiota in pediatric IBD -increased E coli and decreased F praunsitzil in IBD pts.
  • -Gastro 2011; 141: 28, 208.  GM-CSF receptor (CD116) defective expression & function in 85% of IBD pts. n=52.
  • -Scand J Gastro 2001; 36: 383-8.  Elemental & polymeric diets successful in maintaining remission in ~43% of adults with complete steroid withdrawal.
  • -Clin Gastro & Hepatology 2006; 4: 744.  10 weeks of exclusive modulen (along with clears) had 79% response rate (n=37).  Better histologic response than steroids.
  • -J Pediatr 2000; 136: 285. Nutritional treatment w polymeric diet is effective w/in 8 weeks in 32/37.
  • -JPGN 2000; 31: 3 & 8.  EN about as effective as steroids for primary Rx.
  • -Can J Gastroenterol 1998; 12(8):544-49. Patients, diets and preferences in
    a pediatric population with Crohn’s disease.
  • -Gastroenterology 1988; 94:603-610. Chronic intermittent elemental diet improves growth failure in  children with Crohn’s disease.
  • -JPGN 1989; 8:8-12. Nutritional support for pediatric patients with inflammatory bowel disease.
  • -J Pediatr 2000; 136: 285-91. The role of nutrition in treating pediatric Crohn’s disease in the new millennium.