Infant Reflux, Colic, Food Protein Allergy & Constipation
Tell the normal spitty, fussy, or straining child from the one who needs a workup
Reflux: physiologic or disease?
Physiologic reflux. Effortless regurgitation in a comfortable, thriving infant (the happy spitter) is normal. It affects about half of young infants, peaks near 4 months, and resolves in most by 12 months and nearly all by 18 months. Management is reassurance, smaller and more frequent feeds without overfeeding, burping, and thickened feeds. No medication is needed, and the infant always sleeps supine.
GERD. Reflux becomes disease when it causes troublesome symptoms or complications: poor weight gain, feeding refusal, arching and irritability with feeds, hematemesis or anemia from esophagitis, chronic cough, wheeze, or recurrent pneumonia. Sandifer syndrome, paroxysmal torticollis and back arching, is often mistaken for seizures.
- Optimize feedingcorrect overfeeding, offer smaller feeds, thicken
- Milk-protein trial, 2–4 weeksstrict maternal dairy elimination if breastfed; extensively hydrolyzed formula if formula-fed (cow's milk protein allergy mimics GERD)
- Acid suppression, 4–8 weeks, or GI referralonly if symptoms persist
- TestingpH-impedance monitoring or endoscopy for refractory or complicated cases
PPIs do not reduce crying or spitting in healthy infants and increase the risk of pneumonia, gastroenteritis, fractures, and C. difficile. An upper GI series excludes anatomic problems such as malrotation but cannot diagnose GERD.
Red flags for another diagnosis: bilious or projectile vomiting, onset after 6 months or persistence beyond 18 months, GI bleeding, fever, lethargy, a bulging fontanelle or rapidly enlarging head, seizures, hepatosplenomegaly, distension, or chronic diarrhea. These point to obstruction (pyloric stenosis, malrotation), infection, raised intracranial pressure, or metabolic disease.
Infantile colic
Definition. The rule of 3s: crying more than 3 hours a day, more than 3 days a week, for more than 3 weeks in a healthy, well-fed infant with normal growth and a normal exam. Crying begins around 2–3 weeks, peaks near 6 weeks, and fades by 3–4 months, clustering in the late afternoon and evening, often with drawn-up legs, clenched fists, and a flushed face.
Exclude mimics. Undress and examine the infant for a hair tourniquet, corneal abrasion, fracture, incarcerated hernia, or infection before settling on colic.
Management. Reassurance, soothing (swaddling, rocking, white noise, a pacifier, car rides), reduced stimulation, and caregiver support and respite. Simethicone and repeated formula changes do not help.
Inconsolable crying is the leading trigger of abusive head trauma, which peaks at 2–4 months. Teach every caregiver to set the baby down safely in the crib and step away when overwhelmed, and screen for exhaustion and postpartum depression.
Food protein reactions in infants
| Feature | Allergic proctocolitis | FPIES | IgE-mediated milk allergy |
|---|---|---|---|
| Typical trigger | Cow's milk protein passed in breast milk (or in formula) | Cow's milk or soy formula; rice, oat | Cow's milk, egg, peanut |
| Timing | Onset at about 2–8 weeks | Repetitive vomiting 1–4 hours after ingestion | Minutes to 2 hours |
| Picture | Thriving, well baby with mucoid, blood-flecked stools | Pallor, lethargy, hypotonia, hypotension, hypothermia, later diarrhea; no hives or wheeze | Hives, angioedema, vomiting, wheeze, anaphylaxis |
| Treatment | Continue breastfeeding with strict maternal dairy elimination; extensively hydrolyzed formula if formula-fed | IV isotonic fluid boluses, ondansetron, steroids if severe; avoid the food | IM epinephrine; strict avoidance |
| Outlook | Blood clears within days to 2 weeks; most tolerate milk by about 1 year | Most outgrow it in early childhood | Many outgrow milk allergy |
FPIES pitfalls. The delayed vomiting and shock-like state are often mistaken for sepsis. Because the reaction is not IgE mediated, epinephrine and antihistamines do not help, and skin-prick or serum IgE tests are usually negative; the diagnosis rests on the history.
Constipation
Functional constipation. After a painful stool (hard stool, fissure, toilet training, avoiding school bathrooms), the child withholds by stiffening, crossing the legs, or standing on tiptoe. The rectum stretches, the urge fades, and stool hardens, producing infrequent (≤2 per week), large, painful stools, a palpable fecal mass, and overflow soiling (encopresis), which parents mistake for diarrhea. The diagnosis is clinical; X-rays and labs are unnecessary, and antidiarrheals are harmful.
- Disimpacthigh-dose oral PEG 3350 for 3–6 days, or enemas
- Maintaindaily PEG 3350 for months, titrated to one soft stool a day; wean slowly because relapse is common
- Behaviortoilet sitting for 5–10 minutes after meals, a footstool, and a reward chart
- Dietadequate fluid and fiber; avoid excess cow's milk
Other agents. Stimulants and glycerin suppositories are adjuncts; mineral oil is avoided in infants and in children at risk of aspiration (lipoid pneumonia).
Infant dyschezia: an infant under 9 months who strains and cries for 10 minutes or more before passing a soft stool is normal and needs no treatment.
| Feature | Functional constipation | Hirschsprung disease |
|---|---|---|
| Onset | Toilet training, school entry | From birth; meconium delayed beyond 48 hours |
| Rectal exam | Rectum packed with hard stool | Empty rectum; explosive release of stool and gas as the finger is withdrawn |
| Soiling | Common (overflow) | Rare |
| Growth and abdomen | Normal growth | Distension, poor growth, risk of enterocolitis |
| Next step | PEG and behavioral therapy | Rectal suction biopsy (absent ganglion cells) |
Other organic red flags. Hirschsprung disease is associated with Down syndrome. A sacral dimple or hair tuft, or an abnormal lower-extremity neurologic exam, suggests a tethered cord; hypothyroidism, celiac disease, and lead poisoning also cause constipation.
Rectal bleeding in children
| Cause | Typical age | Bleeding | Diagnosis and treatment |
|---|---|---|---|
| Anal fissure | Infants and toddlers (most common cause) | Painful defecation; bright red streaks on hard stool | Perianal inspection (posterior midline tear); stool softeners, sitz baths |
| Juvenile polyp | 2–10 years, peak 2–5 | Painless, intermittent bright red blood on normal stool; may prolapse | Colonoscopic polypectomy |
| Meckel diverticulum | Usually under 2 years | Painless, often brisk maroon or bright red bleeding | Tc-99m pertechnetate scan, then resection |
| Inflammatory bowel disease | Older children and adolescents | Bleeding with chronic diarrhea, pain, weight loss | ESR, CRP, fecal calprotectin; colonoscopy with biopsy |
Anal fissure. A hard stool tears the anoderm; treating the constipation breaks the pain-withholding cycle.
Juvenile polyp. Usually a single hamartomatous rectosigmoid polyp; removal is diagnostic and curative, and a solitary polyp carries no cancer risk. Five or more juvenile polyps suggest juvenile polyposis syndrome (SMAD4, BMPR1A), which does raise colorectal cancer risk.
Meckel diverticulum. A persistent vitelline (omphalomesenteric) duct remnant that follows the rule of 2s: 2% of people, about 2 feet from the ileocecal valve, about 2 inches long, 2 ectopic tissues (gastric and pancreatic), symptoms usually before age 2, and about 2:1 male. Acid from ectopic gastric mucosa ulcerates the adjacent ileum, and the same mucosa takes up pertechnetate on the scan. It can also be a lead point for intussusception or cause volvulus, obstruction, or diverticulitis that mimics appendicitis.
Inflammatory bowel disease. Suspect it with slowed growth, anemia, and perianal disease (Crohn). Other causes to weigh by age: swallowed maternal blood, necrotizing enterocolitis, and allergic proctocolitis in newborns and young infants; intussusception (currant-jelly stool), infectious colitis, and IgA vasculitis in older infants and children.