BACKGROUND AND PATHOPHYSIOLOGY
Passage of the alimentary bolus from the stomach to the duodenum constitutes an important anatomical and functional transition point in the digestive process. The stomach functions as both a digestive organ and a temporary reservoir for the alimentary bolus. The stomach can be divided into a proximal half that functions as a reservoir, and via receptive relaxation, can accommodate changes in volume from the fasted to the postprandial state. Contractions in this region, together with the chemical action of hydrochloric acid and pepsin, further digest the triturated bolus. Weak contractions propel the bolus towards the antrum, where stronger contractions are coordinated with the duodenum and result in progressive emptying of the stomach across the pylorus. The rate of emptying is influenced by the physical nature of the meal, with liquids emptying more rapidly than solids, and foods with lower caloric density emptying more rapidly than foods with higher caloric density.
Abnormal gastric emptying into the duodenum may result in symptoms that require hospitalization for supportive care, diagnostic procedures, and therapeutic procedures. To simplify this review, the terms gastroparesis and dumping are utilized for delayed and accelerated gastric emptying, respectively. More detail is provided regarding hypertrophic pyloric stenosis (HPS), a common disorder of gastric emptying in infants.
Based on history alone, it is difficult to differentiate disorders of delayed from those of accelerated gastric emptying. Furthermore, as in many pediatric disorders, a child’s description of symptomatology may not be accurate or medically useful, and the presenting symptom may not be more specific than a “feeding disorder.”
Gastroparesis may present with vomiting that prompts consideration of small bowel obstruction. However, the typical symptoms are more vague and may include nausea, epigastric fullness, early satiety, pyrosis, and belching. Typically, vomiting does not occur during or immediately after ingesting a meal, which is a pattern more suggestive of rumination syndrome. Rapid gastric emptying may result in nausea, vomiting, epigastric fullness, and early satiety. Rapid emptying may also result in the classic dumping syndrome in a minority of patients, characterized by pallor, diaphoresis, or syncope. The etiology of this syndrome is thought to be rapid release of hyperosmolar fluid into the small bowel and resultant fluid shifts into the bowel. Patients have subsequent disordered glycemia, characterized by initial hyperglycemia, followed by hypoglycemia resulting from persistent elevated insulin levels when substrate absorption from the intestine rapidly declines.
Delayed gastric emptying has many potential causes (Table 78-1).
TABLE 78-1Differential Diagnosis of Delayed Gastric Emptying |Favorite Table|Download (.pdf) TABLE 78-1 Differential Diagnosis of Delayed Gastric Emptying
|Anatomic Obstruction ||Hypertrophic pyloric stenosis |
| ||Antral or duodenal webs |
| ||Ectopic pancreatic tissue |
| ||Antral polyp |
| ||Hyperplastic gastric folds |
| ||Duodenogastric intussusception |
| ||Bezoar |
|Metabolic or electrolyte disturbance ||Hypothyroidism |
| ||Hypokalemia |