Abd pain 2/2 activation of visceral nerves (innervate hollow viscera & mesentery; poorly localizing), or somatic nerves (innervate parietal peritoneum; focal).

Pain can be referred to abd from other structures (i.e., pleuritis in lower lobe PNA, Strep. pharyngitis). (Pediatr Clin North Am 2006;53:107)

History w/ assoc sxs, signs, & physical are important to narrow differential

Concerning sx: Anorexia (appendicitis), bilious emesis (obstruction), rebound or guarding (peritonitis), assoc findings of palpable purpura (HSP) or ecchymosis on abdomen or back (pancreatitis). Fever can be concerning but nonspecific.

Localized pain can be helpful for localization, but is often nonspecific.

Etiologies and working differential varies based on age. See specific topics for Rx.

Evaluation is dependent on history (associated symptoms & signs) & physical exam

PMH of abd surgery raises risk of incarcerated hernia or obstruction 2/2 adhesion

Always consider the possibility of child abuse.

Damage to mucosal lining of upper GI tract 2/2 imbalance btw protective fxn of mucus and bicarb secretion and damage from gastric acid and pepsin, +/- external factors (NSAIDs, EtOH, other mucotoxic agents) or H. pylori infection.

Acid secretion is mediated by stimulation of parietal cells by acetylcholine (vagal), histamine, and gastrin (Zollinger-Ellison syndrome).

H. pylori (gram neg spiral rod) adapted to mucous layer; infxn possibly resulting in damage of intestinal mucosa 2/2 urease secretion (hydrolyzes urea to ammonia and bicarbonate) disrupts epithelial cell fxn; +/- vacuolating cytotoxin.

H. pylori w/ ∼ 50% prevalence worldwide (from 10% [U.S. avg] to 80% w/ higher rates in lower socioeconomic groups); only 10%–15% infected develop PUD

Evidence suggests acquisition of H. pylori infection occurs in childhood (by 5–10 yo)

There is often a family history of peptic ulcer disease; unclear why

Other etiologies less common overall (can be more prevalent in inpts); stress related (severe illness, burn), 2/2 ↑ ICP (Cushing ulcer) or 2/2 NSAID and other drugs.

Generally p/w recurrent epigastric pain and can be assoc w/ postprandial or nocturnal abd pain, vomiting or food regurgitation.

In severe cases can present with failure to thrive, upper GI bleed, or chronic anemia.

Controversial whether H. pylori infxn can cause acute abd pain; NSAID- and drug-induced gastritis and ulcer formation can. (Pediatrics 1999;103:192)

Initial eval w/ CBC diff (assess for anemia), ESR (IBD), LFTs, electrolytes (if recurrent vomiting), and stool evaluation for O and P (if exposure/diarrhea)

If PUD suspected, send H. pylori IgG; can’t distinguish btw current & prior infxn.

Stool antigen testing where available is highly sensitive (98%) and specific (99%)

Urea breath testing (UBT): Radio-labeled urea is ingested and then CO₂ exhalation is measured; good functional test and can be used to assess for cure

Gold standard upper GI endoscopy and bx, radiographic UGI studies less sensitive

If H. pylori +; rx w/ PPI (1–2 mg/kg/d) w/ any 2 of the following; amoxicillin 50 mg/kg/d, clarithromycin 15 mg/kg/d, and/or metronidazole 20 mg/kg/d

Studies show 75%–80% cure rate w/ 7 d of triple therapy, suggesting rx for 14 d

Atrophic gastritis +/- metaplasia; high risk if PPI use w/o eradication; gastric CA risk

Gastric CA: Seen in 1% of H. pylori infected, likely via above mechanism

Gastric mucosa-associated lymphoid tissue lymphoma (MALT): Rarer, only 0.1%

Reverse peristalsis 2/2 activation of vomiting center (VC) in medulla or chemoreceptor trigger zone (CTZ) in area postrema (floor IVth ventricle).

Assess for dehydration; Mod (5%–10% BW) w/ irritability, cool ext, dry mucous membranes, sunken eyes, dec skin turgor (1–2 sec skin pinch), Severe (>10% BW) w/ lethargy, >2 sec skin pinch, cold ext, deep acidotic breathing, HoTN, tachy.

Definitive management as well as diagnostic testing depends on underlying etiology.

Nonbilious emesis: Generally less concerning; some emergencies, pyloric stenosis

Bilious emesis is almost always concerning sx warranting further evaluation.

Treatment of nausea: (N Engl J Med 2005;352:817) based on etiology

Passage of gastric contents to esophagus, can be nml (GER), or pathologic (GERD).

Intermittent relaxation of LES, acid refluxing to esophagus w/ esophagitis, chronically causes change from columnar to squamous (Barrett)

Prevalence physiologic reflux ∼50% at 0–3 mo, 67% by 4 mo, 5% at 12 mo, and in children 3–17 yo, rates vary from 1.4%–8.2%

Infants: Vomiting, FTT, irritability, asthma, ALTE, recurrent PNAs

Children/adolescent: Abd pain retrosternal CP, dysphagia, regurg, asthma/cough

H&P only, unless complications present or dx in question

UGI: Not sensitive or specific for GERD but identifies malro, esophageal/antral webs, pyloric stenosis, Schatzki rings, hiatal hernia.

Esophageal pH probe: Checks freq and duration of acid exposure. Reflux index = % time Ph <4 (most valid tool), upper nml 0–11 mo 11.7%, 1–9 yo 5.4%, adults 6%

Endoscopy: Visualize and bx esophagus and duodenum for inflamm and complications

Empiric Rx: widely used but not validated for any sx presentation in children

Evidence for 2 wk trial of hypoallergenic formula for formula fed infants

Thickening agents do not improve reflux index, do dec # of vomiting events

Positioning (if >1 yr): Left-side positioning and elevation of head of bed in sleep

Lifestyle Δ (child/adoles): No caffeine, chocolate, spicy food, tobacco, EtOH

Acid suppression: PPIs >H₂RAs; if long-term PPI, check for H. pylori (risk of atrophic gastritis w/ chronic >6 mo PPI use and untreated H. pylori)

Prokinetic: Aside from cisapride (limited access) no prokinetics show benefit

Surgical Rx: Case series show generally favorable outcomes.

Respiratory (asthma, apnea, ALTE, cough), ENT (sinusitis, dental erosions, laryngitis), esophageal strictures, Barrett, adenoCA, UGI bleeding.

∼2/3 of children w/ asthma improve to some degree w/ rx for GERD

Neurologically impaired at high risk of recurrent aspiration (PNA, pulm fibrosis)

Gastric outlet obstruction 2/2 hypertrophy and edema of pyloric canal, and antropyloric muscle spasm → vomiting, dehydration and hypochloremic, hypokalemic, metabolic alkalosis; thought to be an acquired condition.

Incidence of 1 in 250–1000, M 4–8×’s > F, caucasian predilection

Mean age 3 wk, but anytime birth to 5 mo; begins w/ regurgitation → nonbilious vomiting +/- projectile vomiting

Classically w/ “olivelike” mass palpated in epigastric region, pathognomonic; not always appreciable; exam enhanced by NGT decomp and prone positioning

US is study of choice, pyloric thickness >4 mm, length >16 mm w/ sens 89%, spec 100%; may need repeat US given operator variability.

Most common cause of metabolic alkalosis in infancy; hypochloremic metabolic alkalosis 2/2 acid loss from vomiting and decreased HCO₃ secretion.

Excess bicarb can be excreted in urine w/ obligate Na loss, followed by H₂O, also 2° hyperaldo 2/2 inc renin release causes distal H⁺ secretion and paradoxic aciduria.

Can have low or nml K but usually total body K depletion

Reverse metabolic derangements and volume status.

Pyloromyotomy is curative, incision through serosa and mucosal layer.

Intraluminal bleeding at any site from oropharynx to the anus; definition of upper GI bleed as proximal to the ligament of Treitz and lower GI bleed as distal.

Can p/w bloody vomit (hematemesis), “coffee ground” emesis, hematochezia (BRBPR; LGIB or rapid UGIB (>20% blood volume)) or melana (tarry black 2/2 digestion, darkness correlates w/ time to pass); R/o other site (nasopharynx).

Check for false coloring; red food coloring, fruit juice, beets can make vomit or stool red; Pepto-Bismol, iron, grape juice, spinach, and blueberry can make it black.

Anal fissure: Most common cause LGIB <2 yo. Blood coated stool. Painful.

Food allergy: 3 different mechanisms; cow’s milk and soy most likely offenders

Necrotizing enterocolitis: Risk factors, prematurity, sepsis, LBW, HoTN, asphyxia

Infectious enterocolitis: Bacterial, viral, or parasitic pathogens. C. diff w/ Abx hx.

Hirschsprung disease: 10%–30% develop enterocolitis w/ fever, bloody diarrhea

Meckel diverticulum: 2/2 incomplete obliteration of omphalomesenteric duct

Intussusception: Usually <2 yo, colicky abd pain, “sausage shaped” abd mass w/ late finding of “currant jelly stool.” See ED Chapter.

Polyps: Outside of infant age group these are the most common source for LGIB

IBD: Almost all UC and ¼ of Crohn have LGIB, 1 in 4 present before 20 yo

Angiodysplasia: Vascular ectasia; assoc syndromes (Osler-Weber-Rendu, Turner)

Hemorrhoids: Rare in childhood, assess for portal HTN; common after adolescence

Henoch-Schönlein purpura: Typically 4–7 yo (but any age) systemic small vessel vasculitis w/ abd pain and bloody stools, “palpable purpura.” +/- renal and joint

HUS: Microangiopathic hemolytic anemia, thrombocytopenia, ARF usually preceded by bloody diarrhea. (90% D+HUS w/ shiga-like toxin vs. atypical HUS/D-HUS w/o)

Tachycardia most sensitive sign of acute, severe blood loss

HoTN and decreased capillary refill are ominous late findings (>30% blood vol loss)

With infants who are breast-feeding, ask mother about presence of breast lesions

Hemorrhagic disease of newborn; hx. child born at home, no Vit K presents DOL 1–5

Variceal bleed 2/2 extrahepatic portal HTN; no cirrhotic stigmata, + splenomegaly

Check skin for petechiae or purpura (coagulopathy or HSP), spider angiomata (liver dz), hemangiomas or telangiectasias (Osler-Weber-Rendu).

Confirm w/ hemoccult for stool guaiac or gastroccult w/ vomitus

False neg w/ vit C, false + w/ red meat, veg w/ peroxidase (broccoli, radish, turnips)

NGT lavage useful if returns blood/coffee grounds = UGIB; can miss duodenal ulcer

Isolated increase in BUN can be a sign of gastric bleeding and absorption

Plain films: KUB/upright for free air (perforation), pneumatosis intestinalis (NEC), air fluid levels (obstruction).

Upper GI and small bowel follow through best for structural lesions.

Endoscopy: Indicated w/ acute UGIB necessitating transfusion or recurrent bleeding or as first step in evaluation of LGIB; contraindicated in clinically unstable patient

Rectosigmoidoscopy/Colonoscopy: Useful if not active major bleeding

Barium enema: For Hirschsprung dz, IBD, polyps, dx and rx of intussusception.

Nuclear medicine (Technetium-99 pertechnetate): Labels ectopic gastric mucosa, best for Meckel diverticulum or intestinal duplication.

Angiography: Must be >0.5 mL/min for detection

Abdominal US +/- Doppler: For specific evaluation (i.e., liver dz or portal HTN)

In immune compromised consider assessment for CMV, HSV, or Candida esophagitis

Acute management: Volume resuscitation w/ 2 large bore IVs, IV bolus w/ NS or LR, transfusion, if present correct coagulopathies (FFP, platelets)

UGIB: Basically 2 sources (1) Mucosal (-itis, ulcers, Mallory-Weiss) (2) Variceal

LGIB: Etiology specific (stool softeners for fissure, Abx for infectious colitis)

> nml stool output (>10 cc/kg/d), usually ↑ # BMs/d; WHO crit >3 stools/d.

Young infants have intestinal mucosa permeable to water; have greater net fluid loss.

80% fluid absorption at small bowel; processes affecting SB have rapid dehydration

4 basic processes: secretory, cytotoxic, osmotic, and inflammatory

Secretory: 2/2 infectious enterotoxin (cholera), metabolic/endocrine (hyperthyroid, VIPoma, ZES), or exogenous toxic agent (colchicines)

Cytotoxic: 2/2 destruction of mucosal cells of small intestine, generally 2/2 viral infection (rota, Norwalk), similar underlying changes in celiac disease

Osmotic: Seen in malabsorptive conditions, unabsorbed substance in lumen reaches osmotically active concentration causing water influx. (i.e., lactose intolerance)

Inflammatory: 2/2 damage to intestinal lining w/ bloody stools, fecal leukocytes, and tenesmus, generally involves large intestine and terminal ileum

Hx recent consumption raw milk, salad, undercooked meat/poultry, unpurified H₂O, recent Abx, immunocompromise, sick contacts, FHx GI dz (IBD), blood in stool