Propulsion of the gastrointestinal (GI) luminal contents 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, which is modulated by motor input from the brain through the sympathetic and parasympathetic branches of the autonomic nervous system. GI motor function develops between 26 and 36 weeks of intrauterine life, but it is not fully developed until 36 weeks’ gestation. Thus, it is not unusual for preterm infants to have poor gastric emptying (GE) and feeding intolerance. 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, recurrent abdominal pain to severe chronic intestinal pseudo-obstruction syndrome (CIP) with intestinal failure.
MOTOR DISORDERS OF THE STOMACH
Motor disorders of the stomach can result from either gastric emptying that is too rapid or too slow. 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. The act of swallowing initiates gastric accommodation (receptive relaxation) such that the stomach fundus expands to receive the ingested food. This reflex is mediated by vagal pathways and can also be initiated by gastric distension, duodenal distension, or nutrient infusion into the small bowel. Pharmacological inhibition of gastric accommodation induces early satiety and weight loss.
A gradual increase in the proximal stomach muscle tone transfers the food into the distal stomach. Liquids are transferred rapidly from the proximal to the distal stomach and emptied into the duodenum by series of antral peristaltic contractions. In contrast, solids are emptied at a relatively slower rate. There is a significant lag phase in the delivery of solids from the stomach into the duodenum, as food particles first need to be grounded into a thick chyme, consisting of particles 1 to 2 mm in diameter. The strong antral contractions that typically occur at a rate of 3 per minute help to ground and mix the food before it is emptied into the duodenum.
Gastroparesis is a gastric motility disorder characterized by delayed GE of solids and/or liquids in the absence of any mechanical obstruction.
PATHOGENESIS AND EPIDEMIOLOGY
Disorders that can cause slow emptying are listed in Table 402-1; drug-induced, postsurgical, and postviral gastroparesis are the 3 most common causes. However, 70% of pediatric patients are diagnosed with idiopathic gastroparesis. GE can be delayed in preterm infants due to immaturity of the enteric nervous system. In older children, it can follow infections such as rotavirus, Epstein-Barr virus, and cytomegalovirus. Delayed GE also has been reported in children with eosinophilic gastroenteropathy and following injury to the vagal nerve or its branches during surgery.