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).

GASTROPARESIS

Gastric outlet obstructions must be considered in the diagnosis of gastroparesis, particularly in younger children who may have the initial presentation of a congenital or acquired anatomical anomaly. Most common among these is hypertrophic pyloric stenosis (HPS),¹ which occurs at an annual incidence of 2 to 5 cases per 1000 infants and is the most common condition requiring operative correction in young infants. Infants typically present with “projectile” vomiting and variable degrees of toxicity depending on hydration and nutrition. Less impressive is the vomiting that may be seen with antral and duodenal webs. These are fenestrated, mucosal diaphragms that obstruct gastric outflow as a function of the fenestration diameter.² Less commonly, outlet obstruction may occur in association with ectopic pancreatic tissue,³ pyloric duplication cysts,⁴ polypoid tissue,⁵ or intermittent duodenogastric intussusception.⁶ Lastly, hyperplastic gastric folds have been known to obstruct antral outflow; conditions such as lymphocytic gastritis or viral infection (Menetrier disease) may result in such changes.⁷ Bezoars, when of sufficient size, may result in partial gastric outlet obstruction and delayed gastric emptying.⁸ These may include lactobezoars, trichobezoars, pharmacobezoars, and phytobezoars. Theoretically, large bezoars may also cause dumping if their main effect is a decrease in fundic compliance.

Metabolic problems may also result in ineffective gastric emptying. Hypothyroidism decreases antroduodenal motility that resolves upon treatment that restores the euthyroid state.⁹ Other metabolic abnormalities such as acid–base and electrolyte disturbances, by interacting with the gastrointestinal neuromuscular components, may result in impaired motility and delayed gastric emptying. This must be considered in settings such as diabetes mellitus or renal insufficiency.¹⁰ Note that metabolic alterations such as hypokalemia may be aggravated by recurrent vomiting, as may be found in hypertrophic pyloric stenosis, producing a vicious cycle of worsening gastric function.

Various types of medications cause a relative gastroparesis. Medications that may be used in hospital wards and operating rooms have profound untoward effects on the ability of the stomach to empty promptly. These may include opiates,¹¹ anticholinergics (imipramine),¹² and tricyclic antidepressants.¹³ Case reports and animal studies have also implicated benzodiazepines, anesthetics (propofol),¹⁴ and chemotherapy medications (cisplatin).¹⁵

Diseases primarily affecting the neuromuscular components of the gastrointestinal tract obviously may have a profound effect on gastric emptying. These might include primary central nervous system disease, vagotomy (planned or inadvertent), visceral myopathy, autonomic dysfunction (Riley-Day syndrome), systemic lupus erythematosus (SLE), myotonic dystrophy, or chronic idiopathic pseudoobstruction (CIPO). Mitochondrial disorders may frequently present with gastroparesis or a degree of dysmotility.¹⁶ Anorexia nervosa and bulimia are frequently associated with a secondary gastroparesis that responds to improved nutrition and weight gain.¹⁷ Infectious diseases that result in gastroparesis include viral gastritis and exposure to endotoxin from gram-negative bacteria.¹⁸ Duodenal tuberculosis causing obstructive poor gastric emptying has been reported.¹⁹

DUMPING SYNDROME

Dumping syndrome is most commonly seen in post-surgical states where the normal proximal compliance or distal tone of the stomach has been affected. In children, the most likely procedure by far to result in dumping syndrome is fundoplication.²⁰ Pyloroplasty is occasionally performed with a fundoplication, potentially resulting in more severe dumping.

Symptoms may not be very specific, especially in young children. In patients with recurrent, forceful vomiting, understanding the specific frequency, amounts, and contents of the emesis is critical toward determining if the case involves small bowel obstruction rather than a problem of gastric emptying. HPS has a unique demographic profile that suggests a predilection for firstborn males; however, this may be a demographic artifact and it is likely that the incidence of HPS is sporadic. Also associated with HPS is prenatal or early postnatal exposure to erythromycin.^{21, 22} Infants in whom prostaglandin E1 has been infused for maintenance of a patent ductus arteriosus are susceptible to developing obstructing antral hypertrophy.²³ Any history of intra-abdominal or thoracic operative procedures where vagal injury could have occurred is relevant toward diagnosing altered gastric emptying.

Physical examination should focus on determination of clinical hydration and general toxicity of the patient. Specific to HPS is the palpable mass that may be noticed along with strong, ineffective peristaltic gastric contractions. Palpation of this mass may be facilitated by sham feeding the infant with liquid that is then aspirated via nasogastric suction.