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Disorders of organs outside the gastrointestinal (GI) tract can produce symptoms and signs that mimic digestive tract disorders and should be considered in the differential diagnosis ( Table 332.1 ). In children with normal growth and development, treatment may be initiated without a formal evaluation based on a presumptive diagnosis after taking a history and performing a physical examination. Poor weight gain or weight loss is often associated with a significant pathologic process and usually necessitates a more formal evaluation.
ANOREXIA |
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VOMITING |
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DIARRHEA |
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CONSTIPATION |
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ABDOMINAL PAIN |
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ABDOMINAL DISTENTION OR MASS |
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JAUNDICE |
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Difficulty in swallowing is termed dysphagia. Painful swallowing is termed odynophagia . Globus is the sensation of something stuck in the throat without a clear etiology. Swallowing is a complex process that starts in the mouth with mastication and lubrication of food that is formed into a bolus. The bolus is pushed into the pharynx by the tongue. The pharyngeal phase of swallowing is rapid and involves protective mechanisms to prevent food from entering the airway. The epiglottis is lowered over the larynx while the soft palate is elevated against the nasopharyngeal wall; respiration is temporarily arrested while the upper esophageal sphincter opens to allow the bolus to enter the esophagus. In the esophagus, peristaltic coordinated muscular contractions push the food bolus toward the stomach. The lower esophageal sphincter relaxes shortly after the upper esophageal sphincter, so liquids that rapidly clear the esophagus enter the stomach without resistance.
Dysphagia is classified as oropharyngeal dysphagia and esophageal dysphagia. Oropharyngeal dysphagia occurs when the transfer of the food bolus from the mouth to the esophagus is impaired (also termed transfer dysphagia ). The striated muscles of the mouth, pharynx, and upper esophageal sphincter are affected in oropharyngeal dysphagia. Neurologic and muscular disorders can give rise to oropharyngeal dysphagia ( Table 332.2 ). Chiari malformations, Russell-Silver syndrome, and cri du chat may present with upper esophageal sphincter dysfunction, manifest by dysphagia with solids. The most serious complication of oropharyngeal dysphagia is life-threatening aspiration.
NEUROMUSCULAR DISORDERS |
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METABOLIC AND AUTOIMMUNE DISORDERS |
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INFECTIOUS DISEASE |
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STRUCTURAL LESIONS |
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OTHER |
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A complex sequence of neuromuscular events is involved in the transfer of foods to the upper esophagus. Abnormalities of the muscles involved in the ingestion process and their innervation, strength, or coordination are associated with transfer dysphagia in infants and children. In such cases, an oropharyngeal problem is usually part of a more generalized neurologic or muscular problem (botulism, diphtheria, neuromuscular disease). Painful oral lesions, such as acute viral stomatitis or trauma, occasionally interfere with ingestion. If the nasal air passage is seriously obstructed, the need for respiration causes severe distress when suckling. Although severe structural, dental, and salivary abnormalities would be expected to create difficulties, ingestion proceeds relatively well in most affected children if they are hungry.
Esophageal dysphagia occurs when there is difficulty in transporting the food bolus down the esophagus. Esophageal dysphagia can result from neuromuscular disorders or mechanical obstruction ( Table 332.3 ). Primary motility disorders causing impaired peristaltic function and dysphagia are rare in children. Eosinophilic esophagitis can present with esophageal dysphagia. Achalasia is an esophageal motility disorder with associated inability of relaxation of the lower esophageal sphincter, and it rarely occurs in children. Motility of the distal esophagus is disordered after surgical repair of tracheoesophageal fistula or achalasia. Abnormal motility can accompany collagen vascular disorders. Mechanical obstruction can be intrinsic or extrinsic. Intrinsic structural defects cause a fixed impediment to the passage of food bolus because of a narrowing within the esophagus, as in a stricture, web, or tumor. Extrinsic obstruction is caused by compression from vascular rings, mediastinal lesions, or vertebral abnormalities. Structural defects typically cause more problems in swallowing solids than liquids. In infants, esophageal web, tracheobronchial remnant, or vascular ring can cause dysphagia. An esophageal stricture secondary to esophagitis (chronic gastroesophageal reflux, eosinophilic esophagitis, chronic infections) occasionally has dysphagia as the first manifestation. An esophageal foreign body or a stricture secondary to a caustic ingestion also causes dysphagia. A Schatzki ring, a thin ring of mucosal tissue near the lower esophageal sphincter, is another mechanical cause of recurrent dysphagia, and again is rare in children.
NEUROMUSCULAR |
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GERD |
INTRINSIC LESIONS |
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EXTRINSIC LESIONS |
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When dysphagia is associated with a delay in passage through the esophagus, the patient may be able to point to the level of the chest where the delay occurs, but esophageal symptoms are usually referred to the suprasternal notch. When a patient points to the suprasternal notch, the impaction can be found anywhere in the esophagus.
Regurgitation is the effortless movement of stomach contents into the esophagus and mouth. It is not associated with distress, and infants with regurgitation are often hungry immediately after an episode. The lower esophageal sphincter prevents reflux of gastric contents into the esophagus. Regurgitation is a result of gastroesophageal reflux through an incompetent or, in infants, immature lower esophageal sphincter. This is often a developmental process, and regurgitation or “spitting” resolves with maturity. Regurgitation should be differentiated from vomiting, which denotes an active reflex process with an extensive differential diagnosis ( Table 332.4 ).
INFANT | CHILD | ADOLESCENT |
---|---|---|
COMMON | ||
Gastroenteritis Gastroesophageal reflux Overfeeding Anatomic obstruction * Systemic infection † Pertussis syndrome Otitis media |
Gastroenteritis Systemic infection Gastritis Toxic ingestion/poisoning Pertussis syndrome Medication Reflux (GERD) Sinusitis Otitis media Anatomic obstruction * Eosinophilic esophagitis |
Gastroenteritis GERD Systemic infection Toxic ingestion/poisoning/marijuana Gastritis Sinusitis Inflammatory bowel disease Appendicitis Migraine Pregnancy Medications Ipecac abuse, bulimia Concussion |
RARE | ||
Adrenogenital syndrome Inborn errors of metabolism Brain tumor (increased intracranial pressure) Subdural hemorrhage Food poisoning Rumination Renal tubular acidosis Ureteropelvic junction obstruction Pseudoobstruction |
Reye syndrome Hepatitis Peptic ulcer Pancreatitis Brain tumor Increased intracranial pressure Middle ear disease/labyrinthitis Chemotherapy Achalasia Cyclic vomiting (migraine) Esophageal stricture Duodenal hematoma Inborn error of metabolism Pseudoobstruction Gastroparesis |
Reye syndrome Hepatitis Peptic ulcer Pancreatitis Cholecystitis Brain tumor Increased intracranial pressure Concussion Middle ear disease/labyrinthitis Chemotherapy Cyclic vomiting (migraine) Biliary colic Renal colic Porphyria Diabetic ketoacidosis Adrenal insufficiency Pseudoobstruction Intestinal tumor Gastroparesis Achalasia Superior mesentery artery syndrome Distal intestinal obstruction syndrome |
* Includes malrotation, pyloric stenosis, intussusception, Hirschsprung disease, adhesions, hernias.
Anorexia means prolonged lack of appetite. Hunger and satiety centers are located in the hypothalamus; it seems likely that afferent nerves from the GI tract to these brain centers are important determinants of the anorexia that characterizes many diseases of the stomach and intestine (see Chapter 47 ). Satiety is stimulated by distention of the stomach or upper small bowel, the signal being transmitted by sensory afferents, which are especially dense in the upper gut. Chemoreceptors in the intestine, influenced by the assimilation of nutrients, also affect afferent flow to the appetite centers. Impulses reach the hypothalamus from higher centers, possibly influenced by pain or the emotional disturbance of an intestinal disease. Other regulatory factors include hormones, ghrelin, leptin, and plasma glucose, which, in turn, reflect intestinal function (see Chapter 47 ).
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