Motor Disorders of the Stomach, Small Bowel, and Colon

Manu R. Sood and Casey M. Calkins

Propulsion of the luminal contents along the gastrointestinal tract requires coordinated contractions of the intestinal smooth muscle in response to input from the enteric neurons. The enteric nervous system is capable of independent function that is modulated by motor input from the brain. Gastrointestinal motor function develops between 26 to 36 weeks of gestation, but it is poorly developed before 30 weeks and not fully developed until 36 weeks gestation. Thus, it is not unusual for preterm infants to have poor gastric emptying and feeding intolerance.¹ GI motility disorders result from weak or uncoordinated contractions due to abnormalities of the neuromuscular apparatus or abnormal sensory and motor input from the brain. These disorders range in severity from mild disorders, such as recurrent abdominal pain, to severe, such as chronic idiopathic pseudo-obstruction syndrome with intestinal failure.²

Motor disorders of the stomach can result from either too rapid or too slow gastric emptying. The stomach is a complex electromechanical chamber, and the rate of gastric emptying is influenced by the meal consistency, calorie concentration, and central neural and hormonal input mechanisms. There is a significant lag phase in the delivery of solids from the stomach into the duodenum, as food particles first need to be ground into a thick chyme, consisting of particles 1 to 2 mm in diameter. The strong antral contractions help to grind and mix the food before it is emptied into the duodenum. Following passage of the food into the small intestine, rhythmic contractions of the small intestine mix the chyme, allowing maximum mucosal exposure of nutrients, and propels the food to the cecum. Fluid is absorbed as the undigested colonic contents pass distally to the cecum where segmenting waves allow fluid absorption. Following meals and upon awakening, high-amplitude propagating contractions occur that propel colonic contents into the rectum, initiating the need to defecate.

DELAYED GASTRIC EMPTYING (GASTROPARESIS)

CLINICAL FEATURES AND DIFFERENTIAL DIAGNOSIS

Early satiety, postprandial fullness and discomfort, reduced calorie intake with weight loss, and halitosis are all symptoms of delayed gastric emptying.³ When gastric emptying is marked, food ingested several hours or sometimes days earlier may be vomited. Anatomic obstruction of the gastric outlet or proximal small bowel can present similarly to motor disorders. If these are excluded, then a variety of disorders may cause slow emptying, as listed in Table 407-1. Diabetic, postsurgical, and idiopathic causes are the 3 most common forms of gastroparesis.

Delayed gastric emptying should be differentiated from gastrointestinal obstruction. Aerophagia can present with abdominal distension and dyspeptic symptoms, but normal gastric emptying.⁷ The child either voluntarily or unconsciously swallows excessive amounts of air with saliva or may swallow excessive air due to a swallowing disorder. Sometimes in aerophagia the abdominal and gastric distension gradually worsen during the day and improve overnight.

DIAGNOSTIC EVALUATION

Abdominal X-ray examination often reveals a large dilated stomach, but both aerophagia and anatomic obstruction can present similarly. Upper GI contrast study is required to exclude a gastric outlet obstruction and if severely prolonged, suggests gastroparesis (eFig. 407.1 ). Diagnosis of gastroparesis is best determined using a radioisotope-labeled solid meal with scintigraphic imaging for at least 2 hours, and preferably 4 hours, postprandially. Most commonly, a 99mTc sulfur colloid-labeled egg sandwich with imaging at 0, 1, 2, and 4 hours is used in adults or adolescents. Radioisotope-labeled milk is used for infants.⁸ Due to the difficulties encountered in performing reliable scintigraphic emptying studies in infants and children, breath tests to assess gastric emptying using a carbon 13 octanoic acid-labeled test meal is being used as an alternative to scintigraphy.⁹ Antroduodenal manometry enables a direct record of the gastric antrum contractions and evaluation of the gastric motor response to a meal and drugs, such as erythromycin. Ultrasound has also been used to evaluate gastric emptying in young infants, but it is not as reliable as other methods.

TREATMENT

Treatment of delayed gastric emptying is challenging.¹⁰ The aims of treatment are to control symptoms and to maintain adequate nutrition and hydration. Administration of small meals consisting of liquids (which often empty better), low fat, and fiber, is often helpful. Diabetic patients must control blood glucose levels since symptom exacerbation is frequently associated with poor glycemic control. Treatment with the prokinetic metoclopramide may be helpful, but side effects of tardive dyskinesia may limit use. Domperidone (not readily available in the United States) is preferable to metoclopramide due to a lower risk of side effects. If this regimen is unsuccessful, then alternative prokinetic agents erythromycin or tegaserod may be considered. Antiemetic agent may be helpful to control nausea, with orally dissolving odansetron being particularly effective. Symptom modulators such as low-dose tricyclic antidepressants can be tried to reduce symptoms, but these do not improve gastric emptying. If all medical therapy fails, other therapeutic options include the injection of botulinum toxin into the pylorus, placement of a feeding jejunostomy, and/or placement of a gastric electrical stimulator.

In premature infants administration of either small, frequent feeds or slow nasogastric drip often allows adequate nutritional support until emptying improves with maturation. Breast milk empties faster than formula feeds.⁶ Nasojejunal tube feeding may be necessary if the infant is unable to tolerate gastric feeds. In infants, prokinetic agents are of limited value. Erythromycin, a motilin receptor agonist, accelerates gastric emptying and improves feeding intolerance but is associated with an increased risk of pyloric stenosis with erythromycin use in infancy. Metoclopramide and domperidone may increase emptying but have neurologic side effects.

Table 407-1. Conditions Associated with Delayed Gastric Emptying in Children

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