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Motility Disorders of the Stomach and Small Intestine
Gastric Motility
Anatomy and Physiology
The gastric fundus, body, antrum, and pylorus must contract and relax in a coordinated manner to produce satisfactory gastric function and emptying ( Figs. 65.1 and 65.2 ). The thinner fundus receptively relaxes to store food and liquids and then contracts to empty liquids from the stomach. The gastric pacemaker, which is located in the body along the greater curvature, stimulates both the filling and mixing of food in the body and antrum. The antrum strongly and periodically contracts against the closed pylorus to grind solid food particles down to a small size. The antrum peristalses at a frequency of three cycles per minute and propels small particles and liquids into the duodenum as the pylorus opens. Consequently, the stomach has three motile regions that coordinate to empty the stomach. The fundus receptively relaxes and subsequently contracts, and the body then fills and mixes. The antropyloroduodenal complex triturates and then empties into the duodenum as the pyloric sphincter opens.
Noncontractile gastric slow waves originate from the gastric pacemaker at a frequency of three waves per minute and propagate in both circumferential and longitudinal directions. The network of interstitial cells of Cajal (ICCs) in the myenteric plexus initiates the slow wave and then conducts it to the smooth muscle layer by inducing depolarization. A deeper region of intramuscular ICCs is located in the muscularis propria. These serve to amplify the gastric slow wave signal to reach an action potential level through activation of calcium channels resulting in muscle contractions. Thus the ICCs in the myenteric plexus initiate the slow wave frequency in the smooth muscle, and the intramuscular ICCs propagate the slow wave and permit peristalsis.
Gastric emptying comes under neural and hormonal control. The enteric nervous system (ENS; the “second brain”) runs along the course of the stomach and intestines, contains over 100 million neurons, and can function independently of the central nervous system (CNS). It consists of two plexuses, submucosal (Meissner) and myenteric (Auerbach), which help direct the smooth muscle. The vagus nerve connects the ENS and the CNS. Several hormones, such as gastrin, cholecystokinin (CCK), glucagon-like peptide (GLP)-1 and GLP-2, peptide YY, and others, also influence gastric motility; a full review of these hormones is beyond the scope of this chapter and is described elsewhere.
Gastroparesis
Gastroparesis is objectively delayed gastric emptying in the absence of organic causes such as stricture, ulcer, tumor, or mechanical obstruction, and in the absence of other causes such as functional dyspepsia, rumination syndrome, cyclic vomiting syndrome, or bulimia/anorexia nervosa. Official diagnosis requires both objectively confirmed delayed gastric emptying and associated symptoms of nausea, vomiting, bloating, and pain.
Mechanisms
Recent research has demonstrated the synergistic effect of multiple mechanisms in causing gastroparesis. With gastroparesis, both abnormal peristaltic contractile activity and abnormal electrical slow waves are usually present. Antral hypomotility, likely a neuropathic process reflecting the loss of ICCs, commonly occurs in diabetic patients, with evidence linking it to those with Parkinson disease as well. Although the fundus has minimal contractile activity, its normally firm tone facilitates food movement to the body; a lax fundus—shown to result from both vagotomy and diabetes—delays passage of chyme. In contrast, impaired pyloric relaxation, seen primarily in type 1 diabetics, can trap contents in the stomach. The stomach and duodenum must act together, with the pylorus and duodenum relaxing as the antrum contracts. Disruptions in this concert or the various neurohormonal factors that coordinate the process also lead to gastric dysmotility.
Epidemiology and Etiology
Gastroparesis has an overall prevalence of 24 per 100,000 Americans. The disease affects females more often than males (4 : 1), with the onset of symptoms beginning at an average age of 34 years. There were 16,736 primary hospitalizations for gastroparesis in 2009 (up 18-fold from 1994), at a cost of an average $25,000 per hospitalization.
The most common etiology of gastroparesis is, unfortunately, idiopathic, representing half of all cases. Diabetes causes about 25% of cases. Gastroparesis typically develops after 10 or more years of diabetes; patients almost always present with various symptoms of autonomic dysfunction as well as increased incidence of microvascular disease. In the community, around 5% of type 1 diabetics and 1% of type 2 diabetics develop gastroparesis (numbers from patients with more advanced disease receiving care at tertiary centers are much higher: 40% and 15%, respectively). Improved glycemic control does not appear to relieve gastroparesis, with symptoms and emptying time unchanged in patients despite better management of blood sugars. Gastroparesis does not appear to cause increased mortality in diabetic patients but does serve as a marker for increased morbidity and mortality, likely due to shared effects of microvascular disease.
Postsurgical sequelae (especially with intended or inadvertent vagotomy) cause approximately 13% of gastroparesis cases. The remaining patients suffer from a variety of less common causes: radiation, viral disease (e.g., Norwalk), connective tissue disorders (e.g., scleroderma), paraneoplastic syndromes, infiltrative diseases (e.g., amyloidosis), and neurologic disorders (e.g., Parkinson disease, ~7.5% of cases). Specific therapies for these rare etiologies are not addressed in this chapter.
Clinical Presentation
The predominant symptoms are similar regardless of etiology: nausea (80% to 92%) and vomiting (66% to 85%), abdominal bloating (55% to 75%) and early satiety (54% to 60%). Previously underestimated, epigastric abdominal pain is present in almost 90% of patients, is worsened by eating (72%), occurs nocturnally (74%), and often disturbs sleep (66%). Abdominal pain is not usually treated satisfactorily by gastric electrical stimulation or by prokinetic drugs. Some studies suggest diabetic patients have more vomiting and idiopathic patients have more satiety, but the differences are not significant enough to affect diagnosis or management. Symptoms frequently overlap with functional dyspepsia, a condition that shares similar pathophysiology and presentation and can be difficult to distinguish even with objective testing. The Gastroparesis Cardinal Symptom Index (GCSI) is a validated tool used to assess patients' severity of symptoms. Differential diagnoses for these symptoms include gastroparesis, dumping syndrome, functional dyspepsia, ulcer disease, malignancy, gastroesophageal reflux disease, rumination syndrome, cyclic vomiting syndrome, bulimia, and mechanical gastric outlet obstruction.
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