7.1 Gastrointestinal Disorders: IBD, Celiac, Short Bowel & GERD

Inflammatory Bowel Disease in Children and Adolescents

Pediatric inflammatory bowel disease (IBD) is more aggressive than adult-onset disease, and nutrition sits at the center of both its presentation and its treatment. Roughly 20-25% of IBD is diagnosed before age 20, and incidence in children continues to rise.

Crohn's Disease vs. Ulcerative Colitis

Growth failure and delayed puberty are classic presenting signs of pediatric Crohn's disease and may precede abdominal pain or diarrhea by months or years. Any child with unexplained fall-off in height velocity, weight loss, iron deficiency, or perianal disease warrants an IBD workup. Growth deceleration reflects inflammation-driven anorexia, malabsorption, increased energy needs, and direct suppression of the growth hormone/IGF-1 axis by inflammatory cytokines.

Exclusive Enteral Nutrition (EEN)

For active luminal Crohn's disease, exclusive enteral nutrition — a complete liquid formula (polymeric, semi-elemental, or elemental) as the sole source of nutrition with no food — is the guideline-recommended first-line induction therapy in pediatrics, endorsed by both ESPGHAN/ECCO and NASPGHAN. The standard course is 6-8 weeks, and remission rates run around 80%, comparable to corticosteroids but with superior mucosal healing and none of the steroid toxicity. Proposed mechanisms include exclusion of dietary antigens and emulsifiers, favorable shifts in the microbiome and its metabolites, improved intestinal permeability, and direct anti-inflammatory effects. Beyond induction, EEN reverses growth failure and restores lean mass — the opposite of steroids, which suppress bone formation, drive appetite and fat gain, and do nothing for linear growth. When full EEN is not acceptable, partial enteral nutrition (about 50% of calories from formula) combined with structured food exclusion (the Crohn's Disease Exclusion Diet) is a validated alternative. The specific carbohydrate diet has small prospective studies and registry data suggesting symptom and inflammatory-marker improvement, but the evidence base remains limited; on the exam, treat it as adjunctive and incompletely validated rather than a replacement for proven therapy.

Micronutrients, Steroids, and Biologics

Active IBD produces predictable losses: iron (anemia of inflammation plus GI blood loss — favor IV iron when disease is active because oral iron is poorly absorbed in inflammation and may aggravate the mucosa), vitamin B12 (terminal ileal disease or resection), vitamin D (fat malabsorption, steroid exposure — check 25-OH vitamin D and replete aggressively for bone health), zinc (diarrheal losses; deficiency itself causes growth failure, taste changes, and poor wound healing), and folate (especially with sulfasalazine, which inhibits folate absorption). Corticosteroids remain useful for flares and for ulcerative colitis induction, but repeated courses in a growing child mean osteoporosis risk, adrenal suppression, cataracts, and further growth stunting — a key reason pediatric practice favors steroid-sparing strategies. Biologics, particularly anti-TNF agents (infliximab, adalimumab) and newer agents (vedolizumab, ustekinumab), are started earlier in pediatrics than in adults (top-down or accelerated step-up) specifically to protect growth potential before the epiphyses close. The dietitian's monitoring role includes serial weight, height velocity, pubertal staging, and at least annual micronutrient surveillance (CBC, ferritin, B12, folate, 25-OH vitamin D, zinc).

Celiac Disease

Celiac disease is an immune-mediated enteropathy triggered by gluten — the prolamins of wheat, barley, and rye — in genetically susceptible children, affecting roughly 1% of the population.

Diagnosis

• Serology first: tissue transglutaminase IgA (tTG-IgA) is the screening test of choice in children over age 2, drawn while the child is still consuming a gluten-containing diet — starting a gluten-free diet before testing normalizes serology and histology and invalidates the workup. Always pair it with a total IgA level, because selective IgA deficiency (10-15 times more common in celiac patients) causes false-negative tTG-IgA; if IgA is low, use IgG-based tests such as deamidated gliadin peptide IgG or tTG-IgG.
• Genetics: essentially all celiac patients carry HLA-DQ2 and/or HLA-DQ8; a negative result effectively excludes celiac disease, which is useful for risk-stratifying screened relatives or for patients who already stopped gluten before testing.
• Biopsy vs. no-biopsy: US guidance (NASPGHAN) still generally requires upper endoscopy with duodenal biopsies showing villous atrophy for diagnosis. ESPGHAN permits a no-biopsy pathway in children when tTG-IgA is at least 10 times the upper limit of normal and a second blood sample confirms a positive endomysial antibody (EMA); HLA testing is optional in that pathway.
• Screening associations: screen asymptomatic children who have type 1 diabetes (about 5-10% also have celiac), Down syndrome, Turner syndrome, Williams syndrome, autoimmune thyroid disease, or a first-degree relative with celiac disease.

Treatment and Nutrition Management

The only treatment is a strict, lifelong gluten-free diet excluding wheat, barley, rye, and their derivatives (malt, brewer's yeast, most conventional soy sauce, many processed foods). Oats are tolerated by most patients but must be labeled gluten-free because of cross-contact with wheat during growing and milling; introduce them once the diet is established. Cross-contact education covers shared toasters, colanders, fryers, condiment jars, cutting boards, and bulk bins. Nutritional risks at diagnosis mirror the proximal small-bowel injury: iron deficiency is most common, along with folate, B12, vitamin D and calcium (osteopenia is frequent at diagnosis), and zinc. Catch-up growth in children typically occurs within 1-2 years on a strict diet, and follow-up tTG-IgA should fall and normalize over roughly 6-12 months, confirming adherence. A gluten-free diet is not automatically healthy: many gluten-free products are low in fiber, iron, folate, and B vitamins (they are not enriched like wheat flour) and higher in fat and sugar, so build the diet on naturally gluten-free whole grains (rice, quinoa, buckwheat, corn, millet) rather than processed substitutes. Persistent symptoms despite apparent adherence most often mean ongoing gluten exposure.

Short Bowel Syndrome and Intestinal Failure

Short bowel syndrome (SBS) is the leading cause of pediatric intestinal failure — the inability of the gut to absorb enough fluid, electrolytes, and nutrients to sustain life and growth without parenteral support. In children the major etiologies are necrotizing enterocolitis (NEC), gastroschisis, midgut volvulus, and intestinal atresia, all capable of causing massive small-bowel loss in the newborn period.

Adaptation and Weaning Parenteral Nutrition

After resection the remnant bowel undergoes adaptation — villous hyperplasia, crypt deepening, dilation, and slowed transit — over roughly 1-3 years, driven by luminal nutrients, pancreatobiliary secretions, and trophic hormones (glucagon-like peptide-2 is a key factor and is concentrated in the distal ileum and colon, one reason a preserved colon and intact ileocecal valve improve prognosis). Predictors of successful weaning include residual small-bowel length, presence of the ileocecal valve and colon, and absence of liver disease.

The weaning strategy follows a consistent logic:

• Start trophic (minimal enteral) feeds early, even 10-20 mL/kg/day, to stimulate adaptation and protect the liver.
• Continuous enteral feeds maximize mucosal contact time in a short gut; as tolerance grows, compress the hours and add bolus and oral feeds to develop normal eating skills.
• Advance enteral volume in small increments while watching stool or stoma output — an increase of more than about 50%, or output persistently above roughly 40-50 mL/kg/day, signals the advance exceeded absorptive capacity.
• As enteral tolerance improves, reduce parenteral nutrition (PN) hours or days rather than concentration, moving toward a cycled overnight schedule.
• For children with a colon in continuity, solids and soluble fiber help: colonic bacteria ferment fiber to short-chain fatty acids that supply energy and stimulate adaptation.
• Elemental or extensively hydrolyzed formulas are often used early, though many children tolerate intact protein as adaptation proceeds; lactose is usually tolerated better than expected and need not be routinely restricted when the colon is present.

Complications and Adjunct Therapies

Intestinal failure-associated liver disease (IFALD) is the major long-term PN complication. Protective strategies include maximizing enteral intake (the single most effective measure), cycling PN, aggressively preventing central-line infections, limiting soybean-oil lipid to about 1 g/kg/day, and using mixed-oil emulsions (SMOF) or fish-oil emulsion (Omegaven) for established cholestasis. Teduglutide, a GLP-2 analog approved for children 1 year and older with PN-dependent SBS, enhances mucosal growth and absorption and can reduce PN volume and infusion days. Surgical serial transverse enteroplasty (STEP) lengthens and tapers dilated, poorly functioning bowel and may improve absorption and motility in selected patients. Long-term monitoring mirrors the losses: fat-soluble vitamins (A, D, E, K), vitamin B12 with terminal ileal loss, zinc, iron, selenium, copper, and manganese. Oral aversion is nearly universal in infants who missed early oral feeding; prevent and treat it with early non-nutritive sucking, small oral tastes even during PN dependence, and occupational or speech feeding therapy, because durable weaning off PN ultimately requires a child who will eat.

GERD in Infants, Constipation, and Encopresis

Physiologic Reflux vs. GERD

Regurgitation is normal in infancy: more than half of infants spit up daily, peaking around 4 months and resolving by 12 months in the great majority as the lower esophageal sphincter matures, feeds thicken with solids, and the child spends more time upright. This physiologic GER — the happy spitter who grows well — needs no testing, no medication, only reassurance. Gastroesophageal reflux disease (GERD) exists only when reflux causes troublesome symptoms or complications: poor weight gain, feeding refusal, esophagitis, or respiratory complications.

Conservative management comes first per AAP/NASPGHAN guidance:

• Smaller, more frequent feeds; avoid overfeeding.
• Thickening feeds reduces visible regurgitation. The traditional recipe — 1 tablespoon of rice cereal per ounce of formula — adds substantial calories and carries arsenic-exposure concerns with heavy use, so many clinicians prefer commercial thickeners (bean gum-based products work in breast milk, where amylase breaks down cereal starch) or pre-thickened anti-regurgitation formulas.
• Upright positioning after feeds; never prone or side-lying sleep — safe-sleep rules trump reflux concerns.
• A 2-4 week trial of extensively hydrolyzed formula (or maternal elimination of milk and soy in breastfed infants) when cow's milk protein allergy (CMPA) overlap is suspected, because CMPA and reflux symptoms are nearly indistinguishable in young infants.
• Avoid acid suppression (proton pump inhibitors, H2 blockers) in infants with uncomplicated regurgitation. Trials show no benefit over placebo for irritability, and acid suppression increases risks of respiratory and GI infections and fractures; reserve a time-limited trial for documented esophagitis or clear red flags.

Sandifer syndrome — dystonic posturing, arching, and head tilting with feeds — is a neurologic-appearing presentation of GERD frequently misdiagnosed as seizures. Warning signs demanding workup rather than reassurance include bilious or projectile vomiting, hematemesis, weight loss or failure to thrive, onset after 6 months of age, persistence beyond 12-18 months, and neurologic abnormalities.

Constipation and Encopresis

Functional constipation affects up to 30% of children and most often begins at toilet training, with transitions such as school entry, or after a painful stool triggers a withholding cycle. Chronic withholding stretches the rectum, blunts sensation, and leads to encopresis — involuntary overflow soiling of liquid stool leaking around a fecal mass, which signals impaction rather than behavioral defiance. Management pairs medication with behavior: disimpaction first (high-dose polyethylene glycol 3350 or a clean-out protocol), then months of maintenance osmotic laxative (PEG 3350 is first-line), scheduled toilet sitting after meals to exploit the gastrocolic reflex, positive reinforcement rather than punishment, and adequate fluid plus age-appropriate fiber (the age + 5 to 10 grams per day rule of thumb). Fiber and fluid alone will not fix an established withholding cycle; the behavioral component and prolonged maintenance therapy are what prevent relapse.