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500 SECTION 17 THE DIGESTIVE SYSTEM The American Academy of Pediatrics recommends that is common in breast-fed infants as a result of colonization or primary care physicians apply fluoride varnish to the teeth infection of the mother’s nipples. Thrush in older...

500 SECTION 17 THE DIGESTIVE SYSTEM The American Academy of Pediatrics recommends that is common in breast-fed infants as a result of colonization or primary care physicians apply fluoride varnish to the teeth infection of the mother’s nipples. Thrush in older patients can of all children every 3–6 months, starting at the emergence occur but should suggest the possibility of an immunodefi- of the first tooth. Fluoride varnish is a concentrated fluoride ciency, broad-spectrum antibiotic or inhaled steroid use, or preparation that adheres to the teeth on contact with saliva. diabetes. It is painted onto the teeth with a small brush, after first dry- ing the tooth with a gauze pad, and has a prolonged cavity- prevention e%ect. Clinical Manifestations Thrush is easily visible as white plaques, often with a “fuzzy” CLEFT LIP AND PALATE appearance, on oral mucous membranes. When scraped with a tongue depressor, the plaques are difficult to remove and the Epidemiology underlying mucosa is inflamed and friable. Clinical diagnosis Cleft lip and palate occur separately or together and a%ect is usually adequate but may be confirmed by fungal culture approximately 1 in 700 infants. It is more common in Asians or potassium hydroxide smear. Oropharyngeal candidiasis is (1:500) and least common in Africans (1:2,500). Clefting sometimes painful (especially if associated with esophagitis) occurs with two possible patterns: isolated soft tissue cleft and can interfere with feeding. palate or cleft lip with or without associated clefts of the hard palate. Isolated cleft palate is associated with a higher risk of other congenital malformations. The combined cleft lip/palate Treatment type has a male predominance. Thrush is treated with topical nystatin or an azole antifun- gal agent such as fluconazole. When the mother’s breasts are infected and painful, consideration should be given to treat- Etiology ing the mother at the same time. Because thrush is commonly Cleft lip is due to hypoplasia of the mesenchymal tissues with self-limited in newborns, withholding therapy in asymptom- subsequent failure of fusion. There is a strong genetic compo- atic infants and treating only persistent or severe cases is a nent; the risk is highest in children with a%ected first-degree reasonable approach. relatives. Monozygotic twins are a%ected with only 60% concor- dance, suggesting other nongenomic factors. Environmental factors during gestation also increase risk, including drugs PEARLS FOR PRACTITIONERS (phenytoin, valproic acid, thalidomide), maternal alcohol and See The Digestive System: Pearls for Practitioners at the end of tobacco use, dioxins and other herbicides, and possibly high this section. altitude. Chromosomal and nonchromosomal syndromes are associated with clefting, as are specific genes in some families. Clinical Manifestations and Treatment 128 CHAPTER Cleft lip can be unilateral or bilateral and associated with cleft palate and defects of the alveolar ridge and dentition. When Esophagus and Stomach present, palatal defects allow direct communication between GASTROESOPHAGEAL REFLUX the nasal and oral cavities, creating problems with speech and feeding. Management includes squeeze-bottle feedings, spe- Etiology and Epidemiology cial nipples, nipples with attached shields to seal the palate, Gastroesophageal reflux (GER) is defined as the e%ortless ret- and gastrostomy in severe cases. Surgical closure of the cleft lip rograde movement of gastric contents upward into the esopha- is usually done by 3 months of age. Closure of the palate fol- gus or oropharynx. Physiologic GER (“spitting up”) is normal lows, usually before 1 year of age. Missing teeth are replaced by in infants. Nearly half of all infants are reported to spit up prostheses. Cosmetic results are often good, but they depend between 2 and 4 months of age. Infants who regurgitate meet on the severity of the defect. the criteria for physiologic GER so long as they maintain ade- quate nutrition and have no signs of respiratory complications or esophagitis. Contributing factors of infantile GER include Complications liquid diet; horizontal body position; short, narrow esopha- Speech is nasal as a result of the cleft palate. Surgical treatment gus; small, noncompliant stomach; frequent, relatively large- is e%ective, but it sometimes does not restore palatal function volume feedings; and an immature lower esophageal sphinc- completely. Speech therapy or, occasionally, the use of a speech- ter (LES). As infants grow, they spend more time upright, eat assisting appliance may help. Frequent episodes of otitis media more solid foods, develop a longer and larger diameter esoph- are common, as are defects of teeth and the alveolar ridge. agus, have a larger and more compliant stomach, and experi- ence lower caloric needs per unit of body weight. As a result, most infants stop spitting up by 9–12 months of age. THRUSH Gastroesophageal reflux disease (GERD) occurs when GER Epidemiology leads to troublesome symptoms or complications such as Oropharyngeal Candida albicans infection, or thrush, is com- poor growth, pain, or breathing difficulties. GERD occurs in mon in healthy neonates. The organism may be acquired in a minority of infants but is often implicated as the cause of the birth canal or from the environment. Persistent infection fussiness. GERD is seen in fewer than 5% of older children.  CHAPTER 128 Esophagus and Stomach 501 In older children, normal protective mechanisms against may have occult GER. A barium upper gastrointestinal (GI) GER include antegrade esophageal motility, tonic contraction series helps to rule out gastric outlet obstruction, malrota- of the LES, and the geometry of the gastroesophageal junc- tion, or other anatomic contributors to GER. Because of the tion. Abnormalities that cause GER in older children and brief nature of the examination, a negative barium study does adults include reduced tone of the LES, transient relaxations not rule out GER, nor does it rule it in as it is normal to have of the LES, esophagitis (which impairs esophageal motility), some reflux into the esophagus many times per day. A 24- increased intraabdominal pressure, cough, respiratory diffi- hour esophageal pH probe monitoring uses a pH electrode culty (asthma or cystic fibrosis), and hiatal hernia. placed transnasally into the distal esophagus, with continuous recording of esophageal pH. Data typically are gathered for 24 hours and analyzed for the number and temporal pattern Clinical Manifestations of acid reflux events. Esophageal impedance monitoring The presence of GER is easy to observe in an infant who spits records the migration of electrolyte-rich gastric fluid in the up. In older children, the refluxate is usually kept down by esophagus. Endoscopy is useful to evaluate for esophagitis, reswallowing, but GER may be suspected by associated symp- esophageal stricture, and anatomic abnormalities. toms, such as heartburn, cough, epigastric abdominal pain, dysphagia, wheezing, aspiration pneumonia, hoarse voice, failure to thrive, and recurrent hiccoughs or belching. In Treatment severe cases of esophagitis, there may be laboratory evidence In otherwise healthy young infants, no treatment is necessary. of anemia and hypoalbuminemia secondary to esophageal For infants with complications of GER, an H2 blocker or proton bleeding and inflammation. pump inhibitor may be o%ered (Table 128.1), but these have When esophagitis develops as a result of acid reflux, esoph- shown little benefit in infants with uncomplicated GER and/ ageal motility and LES function are impaired further, creating or fussiness. Prokinetic drugs, such as metoclopramide, occa- a cycle of reflux and esophageal injury. sionally are helpful by enhancing gastric emptying and increas- ing LES tone, but they are seldom e%ective and may lead to complications. When severe symptoms persist despite medica- Laboratory and Imaging Studies tion, or if life-threatening aspiration is present, surgical inter- A clinical diagnosis is often sufficient in children with clas- vention may be required. Fundoplication procedures, such as sic e%ortless regurgitation and no complications. Diagnostic the Nissen operation, are designed to enhance the antireflux studies are indicated if there are persistent symptoms or com- anatomy of the LES. In children with a severe neurologic defect plications or if other symptoms suggest the possibility of GER who cannot tolerate oral or gastric tube feedings, placement in the absence of regurgitation. A child with recurrent pneu- of a feeding jejunostomy may be considered as an alternative monia, chronic cough, or apneic spells without overt emesis to fundoplication. In older children, lifestyle changes should TABLE 128.1 Treatment of Gastroesophageal Reflux THERAPIES COMMENTS CONSERVATIVE THERAPIES Towel on caregiver’s shoulder Cheap, effective; useful only for physiologic reflux Thickened feedings Reduces number of episodes, enhances nutrition Smaller, more frequent feedings Can help some; be careful not to underfeed child Avoidance of tobacco smoke and alcohol Always a good idea; may help reflux symptoms Abstaining from caffeine Inexpensive, offers some benefit Positional therapy—upright in seat, elevate Prone positioning with head of crib or bed up is helpful, but not for young infants because of risk of SIDS Weight loss when indicated Increased weight (especially abdominal) increases intraabdominal pressure, leading to reflux MEDICAL THERAPY Proton pump inhibitor Effective medical therapy for heartburn and esophagitis H2-receptor antagonist Reduces heartburn, less effective for healing esophagitis Metoclopramide Enhances stomach emptying and LES tone; real benefit is often minimal SURGICAL THERAPY Nissen or other fundoplication procedure For life-threatening or medically unresponsive cases Feeding jejunostomy Useful in child requiring tube feeds; delivering feeds downstream eliminates GERD GERD, Gastroesophageal reflux disease; LES, lower esophageal sphincter; SIDS, sudden infant death syndrome. 502 SECTION 17 THE DIGESTIVE SYSTEM be discussed, including cessation of smoking, weight loss, not eating or exercising before bed, and limiting intake of ca%eine, carbonation, and high-fat foods. If lifestyle changes are ine%ec- tive in reducing symptoms, proton pump inhibitor therapy is e%ective in reducing symptoms and supports healing. EOSINOPHILIC ESOPHAGITIS Etiology and Epidemiology This chronic immune-mediated disorder is characterized by infiltration of eosinophils into the mucosa of the esopha- gus. It is thought to be triggered by non–immunoglobulin E (IgE)–mediated allergic reactions to ingested foods or aeroal- lergens. Eosinophilic esophagitis (EoE) may have a familial component; no specific gene has yet been identified. Incidence appears to be increasing with estimated prevalence of more than 50 per 100,000 children. It is more common in males than females and in patients with history of atopy. FIGURE 128.1 Histologic image of eosinophilic esophagitis. Note the large number of eosinophils within the lamina propria. Clinical Manifestations The presentation of EoE often varies with age. In young chil- dren, it may present with oral aversion, vomiting, and failure to thrive. In school-age children, it may present with vague abdominal pain or vomiting. In adolescents and adults, it pre- sents with dysphagia and food impactions. These symptoms are attributed to the inflammatory response in the esophagus leading to edema and poor esophageal motility. Laboratory and Imaging Studies Diagnosis requires multilevel esophageal biopsies via flexible endoscopy with the finding of more than 15 eosinophils per high-power field (Fig. 128.1). Treatment with high-dose pro- ton pump inhibitor therapy is recommended to exclude the possibility that findings are secondary to severe acidic esopha- geal injury or by evaluating for acid reflux by pH probe testing. Proton pump responsive esophageal eosinophilia (PPI-REE) is a subset of EoE that has histologic response to high-dose proton pump inhibitor therapy. Gross findings at endoscopy may include normal appearance, esophageal linear furrow- FIGURE 128.2 Endoscopic picture of eosinophilic esophagitis. ing, trachealization, and eosinophilic abscesses (Fig. 128.2). White plaques on the surface are collections of eosinophils (eosino- A barium study may reveal a food impaction in an acutely philic abscesses). Linear furrowing is also seen. symptomatic patient or esophageal stricture in someone with chronic disease. e%ective, but it often requires either nasogastric or gastrotomy administration because of its poor palatability. Systemic glucocorticoids can decrease symptoms, but long- Treatment and Prognosis term use is discouraged due to concerns for potential com- Exposure to identified causative antigens needs to be elimi- plications. Swallowed “topical” glucocorticoids administered nated. Identification can be difficult, as typical allergy testing via a metered-dose inhaler (fluticasone) or mixed as a slurry (skin prick, radioallergosorbent test [RAST], and immunocap (budesonide) have shown benefit. Candida esophagitis or oral assays) only identifies IgE-mediated antigens. Atopic patch thrush are the most common side e%ects. testing may be more reliable but is not standardized and can Endoscopy can be used to relieve food impactions and to dilate be difficult to perform. One approach is to eliminate from the esophageal strictures secondary to EoE. The prognosis for EoE is diet cow’s milk, soy, wheat, eggs (four-food elimination diet) largely unknown. Symptoms tend to wax and wane over time. or additionally peanuts and fish/shellfish (six-food elimination diet), as these are the most common causative dietary antigens. Alternatively, eliminating the most common allergen first Complications (cow’s milk) can be e%ective for a number of patients. Repeat Failure to thrive or weight loss may be seen due to difficulty endoscopies are often necessary to document efficacy of these in eating. Food impactions are a common complication in eliminations. An elemental diet can also be used and is very the older child and may require endoscopic removal. Chronic  CHAPTER 128 Esophagus and Stomach 503 inflammation of the esophagus can predispose to esophageal the tube coiled in the esophageal pouch. Air can be injected strictures. through the tube to outline the atretic pouch. Barium should not be used because of extreme risk of aspiration, but a tiny ESOPHAGEAL ATRESIA AND amount of dilute water-soluble contrast agent can be given TRACHEOESOPHAGEAL FISTULA carefully, then suctioned when the defect is clearly shown. Etiology and Epidemiology The esophagus and trachea develop in close proximity to each Treatment and Prognosis other during weeks 4–6 of fetal life. Defects in the mesenchyme The treatment of TEF is surgical. The fistula is divided and separating these two structures result in a tracheoesophageal ligated. The esophageal ends are approximated and anastomo- fistula (TEF), often in association with other anomalies (renal, sed. In some cases, primary anastomosis cannot be performed heart, spine, limbs). This defect occurs in about 1 in 3,000 live because of a long gap between the proximal and distal esoph- births. TEF is not thought to be a genetic defect. agus. Various techniques have been described to treat this problem, including pulling up the stomach, elongating the esophagus by myotomy, and simply delaying esophageal anas- Clinical Manifestations tomosis and providing continuous suction to the upper pouch The most common forms of TEF occur with esophageal atresia; while allowing for growth. the “H-type” TEF without atresia is uncommon, as is esopha- geal atresia without TEF (Fig. 128.3). Associated defects include the VACTERL association—vertebral anomalies (70%), anal Complications atresia (imperforate anus) (50%), cardiac anomalies (30%), The surgically reconstructed esophagus is not normal and is TEF (70%), renal anomalies (50%), and limb anomalies (poly- prone to poor motility, GER, anastomotic stricture, recurrent dactyly, forearm defects, absent thumbs, syndactyly) (70%). fistula, and leakage. The trachea also is malformed; tracheo- A single-artery umbilical cord is often present. Infants with malacia and wheezing are common. esophageal atresia have a history of polyhydramnios, exhibit drooling, and have mucus and saliva bubbling from the nose ESOPHAGEAL FOREIGN BODIES and mouth. Patients with a TEF are vulnerable to aspiration pneumonia. When TEF is suspected, the first feeding should be Etiology and Epidemiology delayed until a diagnostic study is performed. Young children often place nonfood items in the mouth. When these items are swallowed, they may become lodged in the esophagus at the thoracic inlet or at the LES. The most com- Laboratory and Imaging Studies mon objects are coins. Smaller coins may pass harmlessly into The simplest test for TEF is to gently attempt to place a 10 F or the stomach, where they rarely cause symptoms. Other com- larger tube via the mouth into the stomach. The passage of the mon esophageal foreign bodies include food items, small toys tube is blocked at the level of the atresia. A chest x-ray reveals or toy parts, button batteries, and other small household items. Esophageal atresia Esophageal atresia H-type TEF with distal TEF with no TEF (4%) (85%) (8%) Esophageal atresia Esophageal atresia with with proximal TEF proximal and distal TEF (2%) (1%) FIGURE 128.3 Various types of tracheoesophageal fistulas (TEF) with relative frequency (%). 504 SECTION 17 THE DIGESTIVE SYSTEM Children with a prior history of esophageal atresia or with tongue and lips and often are expelled before swallowing. Less poor motility secondary to GER or EoE are more prone to food caustic agents, such as bleach and detergents, cause less serious impactions, which seldom occur in the normal esophagus. injury. Pill ulcers occur when certain medications (tetracy- clines and nonsteroidal antiinflammatory drugs [NSAIDs]) are swallowed without sufficient liquids, allowing prolonged Clinical Manifestations direct contact of the pill with the esophageal mucosa. Some children are asymptomatic, but most exhibit some degree of drooling, food refusal, or chest discomfort. Older children usually can point to the region of the chest where they Clinical Manifestations feel the object to be lodged. Respiratory symptoms tend to be Caustic burns cause immediate and severe mouth pain. The minimal, but cough or wheezing may be present, especially child cries out, drools, spits, and usually drops the container when the esophagus is completely blocked by a large object, immediately. Burns of the lips and tongue are visible almost such as a piece of meat, which presses on the trachea. immediately. These burns clearly indicate the possibility of esophageal involvement, although esophageal injury can occur in the absence of oral burns. Symptoms may not be present; Diagnosis further evaluation by endoscopy usually is indicated with any Plain chest and abdominal radiographs should be taken when significant history of caustic ingestion. Pill injury causes severe foreign body ingestion is suspected. Metallic objects are eas- chest pain and often prominent odynophagia and dysphagia. ily visualized. A plastic object often can be seen if the child is given a small amount of dilute x-ray contrast material to drink, although endoscopy is probably safer and more definitive. Laboratory and Imaging Studies A chest x-ray should be obtained to rule out aspiration and to inspect for mediastinal air. The child should be admitted to Treatment the hospital and given intravenous (IV) fluids until endoscopy. Endoscopy is ultimately necessary in most cases to remove The true extent of burns may not be endoscopically apparent a retained esophageal foreign body. Various devices can be immediately, but delayed endoscopy can increase the risk of used to remove the object, depending on its size, shape, and perforation. Most endoscopists perform the initial endoscopy location. Coins usually are grasped with special-purpose for- soon after injury, when the patient has been stabilized. The ceps and removed. Nets, baskets, and snares also are available. extent of injury and severity of the burn should be carefully Whenever objects that may threaten the airway are being determined. Risk of subsequent esophageal strictures is related recovered, endoscopy should be performed with endotracheal to the degree of burn and whether the injury is circumferential. intubation and under general anesthesia. Removal is usually not necessary if the object is small and located in the stomach, as it will most likely pass without complication. Endoscopy is Treatment emergent for removal of any esophageal foreign body if the A nasogastric tube can be placed over a guide wire at the time patient has airway compromise. Due to high risk of compli- of the initial endoscopy to provide a route for feeding and to cations, emergent removal is required for esophageal button stent the esophagus. Systemic steroid use has not been found to batteries or multiple magnets. be beneficial in reducing stricture formation. Broad-spectrum antibiotics should be prescribed if infection is suspected. Complications Sharp objects may lacerate or perforate the esophagus; smooth Complications objects present for a long time also may result in perforation Esophageal strictures, if they occur, usually develop within 1–2 due to ulceration. Corrosive objects, such as zinc-containing months and can be treated with endoscopic dilation. There is a pennies and button batteries, can cause considerable local tis- risk of perforation during dilation. When esophageal destruc- sue injury and esophageal perforation. Magnets can lead to tion is severe, surgical reconstruction of the esophagus using perforation and fistula formation when they connect between stomach or intestine may be necessary. adjacent loops of bowel. PYLORIC STENOSIS CAUSTIC INJURIES AND PILL ULCERS Etiology and Epidemiology Etiology and Epidemiology Pyloric stenosis is an acquired condition caused by hypertro- In adolescents, caustic ingestion injuries are usually the result phy and spasm of the pyloric muscle, resulting in gastric outlet of suicide attempts. In toddlers, ingestion of household clean- obstruction. It occurs in 6–8 per 1,000 live births, has a 5:1 ing products typically is accidental. Injurious agents include male predominance, and is more common in first-born chil- drain cleaners, toilet bowl cleaners, dishwasher and laundry dren. Its cause is unknown. detergents, and powerful bleaching agents. Childproof lids for commercial products o%er some protection but have not elim- inated the problem. Lye-based drain cleaners, especially liquid Clinical Manifestations products, cause the worst injuries because they are swallowed Infants with pyloric stenosis typically begin vomiting during easily and liquefy tissue rapidly. Full-thickness burns can occur the first weeks of life, but onset may be delayed. The emesis in seconds. Granular products are less likely to cause esopha- becomes increasingly frequent and forceful as time passes. geal injury during accidental exposures because they burn the Vomiting di%ers from spitting up because of its extremely  CHAPTER 128 Esophagus and Stomach 505 FIGURE 128.4 Pyloric stenosis. Note the huge, gas-filled stomach extending across the midline, with minimal air in the intestine down- stream. (Courtesy Warren Bishop, MD.) forceful and often projectile nature. The vomited material never FIGURE 128.5 Ultrasound image of infant with pyloric stenosis. contains bile because the gastric outlet obstruction is proximal Large, fluid-filled stomach (S) is seen at right, with an elongated, thick- to the duodenum. This feature di%erentiates pyloric stenosis ened pylorus. The length of the pylorus is marked by the red arrows; the wall thickness is marked by the yellow arrows. from most other obstructive lesions of early childhood. A%ected infants are ravenously hungry early in the course of the illness but become more lethargic with increasing malnutrition and containing 5% dextrose and potassium chloride when urine dehydration. The stomach becomes massively enlarged with output is observed. In pyloromyotomy (often by laparoscope), retained food and secretions, and gastric peristaltic waves are the pyloric muscle is incised longitudinally to release the often visible in the left upper quadrant. A hypertrophied pylo- constriction. rus (the “olive”) may be palpated. As the illness progresses, very little of each feeding is able to pass through the pylorus, and the PEPTIC DISEASE child becomes progressively thinner and more dehydrated. Etiology and Epidemiology Acid-related injury can occur in the esophagus, stomach, or Laboratory and Imaging Studies duodenum. Table 128.2 lists risk factors for peptic ulcer dis- Repetitive vomiting of purely gastric contents results in ease in children. Helicobacter pylori is responsible for more loss of hydrochloric acid; the classic laboratory finding is a than half of ulcers in the stomach and duodenum in adults. hypochloremic, hypokalemic metabolic alkalosis with ele- H. pylori plays a significant but lesser role in childhood ulcer vated blood urea nitrogen (BUN) secondary to dehydration. disease. Risk factors for acquisition of H. pylori are low socio- Jaundice with unconjugated hyperbilirubinemia may also economic status and poor sanitation, with the highest inci- occur. Plain abdominal x-rays typically show an enlarged stom- dence in developing countries. Nonulcer dyspepsia includes ach and diminished or absent gas in the intestine (Fig. 128.4). upper abdominal symptoms (pain, bloating, nausea, early sati- Ultrasound examination shows marked elongation and thick- ety) in the absence of gastric or duodenal ulceration. Nonulcer ening of the pylorus (Fig. 128.5). A barium upper GI series dyspepsia is not associated with H. pylori infection. GER (see also may be obtained whenever doubt about the diagnosis Chapter 128) allows acidic gastric contents to injure the esoph- exists; this shows a “string sign” caused by barium moving agus, resulting in esophagitis. Esophagitis is characterized by through an elongated, constricted pyloric channel. retrosternal and epigastric burning pain and is best diagnosed by endoscopy. It can range from minimal, with only erythema and microscopic inflammation on biopsy, to superficial ero- Treatment sions and, finally, to frank ulceration. Treatment of pyloric stenosis includes IV fluid and elec- trolyte resuscitation followed by surgical pyloromyotomy. Before surgery, dehydration and hypochloremic alkalosis Clinical Manifestations must be corrected, generally with an initial normal saline Typical symptoms are listed in Table 128.3. The presence of fluid bolus followed by infusions of half-normal saline recurrent burning epigastric and retrosternal pain is a risk 506 SECTION 17 THE DIGESTIVE SYSTEM TABLE 128.2 Risk Factors for Peptic Ulcer Disease Helicobacter pylori infection | TABLE 128.3 Peptic Disorders, Symptoms, and Clinical Investigation SYNDROME AND Drugs ASSOCIATED SYMPTOMS CLINICAL INVESTIGATIONS NSAIDs, including aspirin ESOPHAGITIS Tobacco use Retrosternal and epigastric Endoscopy Bisphosphonates location Therapeutic trial of acid-blocker Burning pain therapy Potassium supplements Sensation of regurgitation pH probe study Family history Dysphagia, odynophagia Sepsis NONULCER DYSPEPSIA Head trauma Upper abdominal location Endoscopy Burn injury Fullness Therapeutic trial of acid-blocker Bloating therapy Hypotension Nausea Upper GI series to ligament of NSAIDs, Nonsteroidal antiinflammatory drugs. Treitz—rule out malrotation CBC, ESR, amylase, lipase, abdominal ultrasound PEPTIC ULCER DISEASE factor for esophagitis. With duodenal ulcers, pain typically occurs several hours after meals and often awakens patients “Alarm” symptoms Endoscopy—mandatory with at night. Eating tends to relieve the pain. Gastric ulcers di%er Weight loss alarm symptoms in that pain is commonly aggravated by eating, resulting in Hematemesis Test for Helicobacter pylori weight loss. GI bleeding from either can occur. Many patients Melena, heme-positive stools CBC, ESR, amylase, lipase, abdominal ultrasound report symptom relief with antacids or acid blockers. Chronic vomiting Microcytic anemia Nocturnal pain Laboratory and Imaging Studies Other symptoms—same as for Endoscopy can be used to diagnose the underlying condition. esophagitis and nonulcer dyspepsia Empiric therapy with H2 blockers or proton pump inhibi- tors can be used but may delay diagnosis of conditions such CBC, Complete blood count; ESR, erythrocyte sedimentation rate; GI, as H. pylori. For patients with chronic epigastric pain, the gastrointestinal. possibilities of inflammatory bowel disease, anatomic abnor- mality such as malrotation, pancreatitis, and biliary disease CYCLIC VOMITING SYNDROME should be ruled out by appropriate testing when suspected (see Chapter 126 and Table 128.3 for recommended studies). Etiology and Epidemiology Testing for H. pylori can be performed by biopsy during Cyclic vomiting syndrome (CVS) presents with intermittent endoscopy with use of a urease test or presence histologically episodes of prolonged nausea and vomiting with periods of on tissue. If endoscopy is not done, noninvasive tests for infec- health in between. It can occur at any age but is diagnosed most tion can be done with reasonable accuracy with H. pylori fecal frequently in preschool to school-age children. It is thought to antigen and 13C urea breath tests. be a migraine variant; many patients have a positive family his- tory of migraines, and some with CVS will eventually develop migraine headaches. Triggers to an episode often include viral Treatment illnesses, lack of sleep, stressful or exciting events (holidays, If H. pylori is present in association with ulcers, it should birthdays, vacations), physical exhaustion, and menses. be treated with a multidrug regimen, such as omeprazole- clarithromycin-metronidazole (or amoxicillin). Other proton pump inhibitors may be substituted when necessary. Bismuth Clinical Manifestations compounds are e%ective against H. pylori and can be consid- Episodes can start at any time but will often start in the early ered in addition to the abovementioned therapies. In North morning hours. Episodes are similar to each other in tim- America, only the subsalicylate salt is available, the use of ing and duration. Repetitive vomiting can last hours to days. which raises some concerns about Reye syndrome and poten- Patients can also have abdominal pain, diarrhea, and head- tial salicylate toxicity. Tetracycline is useful in adults but aches. Those a%ected are typically pale, listless, and prefer to should be avoided in children less than 8 years of age. In the be left alone. They may have photo- or phonophobia. absence of H. pylori, esophagitis and peptic ulcer disease are treated with a proton pump inhibitor, which yields higher rates of healing than H2-receptor antagonists. Gastric and duodenal Laboratory and Imaging Studies ulcers heal in 4–8 weeks in at least 80% of patients. Esophagitis There are no specific tests for CVS, which is diagnosed requires several months of proton pump inhibitor treatment based on the history and the exclusion of other disorders. for optimal healing. Diagnoses that should be considered include malrotation with  CHAPTER 129 Intestinal Tract 507 intermittent volvulus, uteropelvic junction (UPJ) obstruction, abdomen and rotates counterclockwise around the superior EoE, intracranial mass lesions, and metabolic disorders. Rome mesenteric artery until the cecum arrives in the right lower IV criteria for diagnosis are outlined in Table 126.5. quadrant. The duodenum rotates behind the artery and ter- minates at the ligament of Treitz in the left upper quad- rant. The base of the mesentery becomes fixed along a broad Treatment attachment posteriorly, running from the cecum to the lig- For the acute episode, supportive treatment includes hydration; ament of Treitz (Fig. 129.1A). When rotation is incomplete dark, quiet environment; and antiemetics such as ondanse- or otherwise abnormal, “malrotation” is present. Incomplete tron. In addition, abortive therapy using antimigraine med- rotation occurs when the cecum stops near the right upper ications such as triptans or antiemetics such as ondansetron quadrant and the duodenum fails to move behind the mes- can be used. For those with frequent or prolonged episodes, enteric artery; this results in an extremely narrow mesenteric prophylactic therapy should be considered, such as cyprohep- root (see Fig. 129.1B) that makes the child susceptible to tadine, tricyclic antidepressants, β blockers, or topiramate. midgut volvulus, causing intestinal obstruction or mesen- teric artery occlusion and intestinal infarction (Fig. 129.2). It is also common for abnormal mesenteric attachments (Ladd PEARLS FOR PRACTITIONERS bands) to extend from the cecum across the duodenum, See The Digestive System: Pearls for Practitioners at the end of causing partial obstruction. this section. Clinical Manifestations About 60% of children with malrotation present with symp- CHAPTER 129 toms of bilious vomiting during the first month of life. The remaining 40% present later in infancy or childhood. The Intestinal Tract emesis initially may be due to obstruction by Ladd bands without volvulus. When midgut volvulus occurs, the venous MALROTATION drainage of the gut is impaired; congestion results in ische- mia, pain, tenderness, and often bloody emesis and stools. Etiology and Epidemiology The bowel undergoes ischemic necrosis, and the child may During early fetal life, the midgut is attached to the yolk appear septic. Physicians must be alert to the possibility of sac and loops outward into the umbilical cord. Beginning volvulus in patients with vomiting, fussiness, abdominal pain, at around 10 weeks of gestation, the bowel re-enters the or shock.