Gastroparesis and chronic intestinal pseudo-obstruction are chronic conditions characterized by intermittent, waxing and waning symptoms and signs of gastric or intestinal obstruction in the absence of any mechanical lesions to account for the findings. They are caused by a heterogeneous group of endocrine disorders (diabetes mellitus, hypothyroidism, cortisol deficiency), postsurgical conditions (vagotomy, partial gastric resection, fundoplication, gastric bypass, Whipple procedure), neurologic conditions (Parkinson disease, muscular and myotonic dystrophy, autonomic dysfunction, multiple sclerosis, postpolio syndrome, porphyria), rheumatologic syndromes (progressive systemic sclerosis), infections (postviral, Chagas disease), amyloidosis, paraneoplastic syndromes, medications, and eating disorders (anorexia); a cause may not always be identified.
A. Symptoms and Signs
Gastric involvement leads to chronic or intermittent symptoms of gastroparesis with postprandial fullness (early satiety), nausea, and vomiting (1–3 hours after meals). Upper abdominal symptoms correlate poorly with the severity of gastric emptying and may be attributable to impaired proximal gastric accommodation after meals, visceral hypersensitivity to gastric distention, afferent nerve dysfunction, gastric electrical rhythm disturbances, or concomitant small intestinal dysmotility. Patients with predominantly small bowel involvement may have abdominal distention, vomiting, diarrhea, and varying degrees of malnutrition. Abdominal pain is not common and should prompt investigation for structural causes of obstruction. Bacterial overgrowth in the stagnant intestine may result in malabsorption. Colonic involvement may result in constipation or alternating diarrhea and constipation.
Plain film radiography may demonstrate dilation of the esophagus, stomach, small intestine, or colon resembling ileus or mechanical obstruction. Mechanical obstruction of the stomach, small intestine, or colon is much more common than gastroparesis or intestinal pseudo-obstruction and must be excluded with endoscopy or CT enterography, especially in patients with prior surgery, recent onset of symptoms, or abdominal pain. In cases of unclear origin, studies based on the clinical picture are obtained to exclude underlying systemic disease. Gastric scintigraphy with a low-fat solid meal remains the preferred method for assessing gastric emptying. Gastric retention of 60% after 2 hours or more than 10% after 4 hours is abnormal. A wireless motility capsule and a nonradioactive or 13-C labeled breath test using blue-green algae (Spirulina platensis) also are available. Small bowel manometry is useful for distinguishing visceral from myopathic disorders and for excluding cases of mechanical obstruction that are otherwise difficult to diagnose by endoscopy or radiographic studies.
There is no specific therapy for gastroparesis or pseudo-obstruction. Acute exacerbations are treated with nasogastric suction and intravenous fluids. Long-term treatment is directed at maintaining nutrition. Patients should eat small, frequent meals that are low in fiber, milk, gas-forming foods, and fat. Foods that are well tolerated include tea, ginger ale, soup, white rice, potatoes and sweet potatoes, fish, gluten-free foods, and applesauce. Some patients may require liquid enteral supplements. Agents that reduce gastrointestinal motility (opioids, anticholinergics) should be avoided. In diabetic patients, glucose levels should be maintained below 200 mg/dL, as hyperglycemia may slow gastric emptying even in the absence of diabetic neuropathy, and amylin and GLP-1 analogs (exenatide or pramlintide) should be discontinued. Currently available prokinetic agents have shown limited improvement of gastric emptying or upper gastrointestinal symptoms in patients with gastroparesis. Metoclopramide (5–20 mg orally or 5–10 mg intravenously or subcutaneously four times daily) may enhance gastric emptying but not small bowel dysmotility. Since the use of metoclopramide for more than 3 months is associated with a less than 1% risk of tardive dyskinesia, patients are advised to discontinue the medication if neuromuscular side effects, particularly involuntary movements, develop. Older patients are at greatest risk. Domperidone (20–30 mg four times daily) is another antidopaminergic agent that enhances gastric emptying and has efficacy as an antiemetic agent. Unlike metoclopramide, it does not cross the blood-brain barrier and therefore is devoid of neuropsychiatric side effects. Although unavailable in the United States, it is available in most other countries, where its use is preferred. In 2019, a small, blinded, crossover trial involving 34 patients with confirmed gastroparesis showed that prucalopride, a serotonin 5-HT4-receptor agonist (currently FDA approved for treatment of chronic constipation), significantly improved gastric emptying and symptoms after 2 weeks of therapy (2 mg daily orally) compared with placebo. Uncontrolled studies report symptom improvement with modalities that reduce intrapyloric pressure, including botulinum toxin injection, laparoscopic myotomy, and endoscopic myotomy. Bacterial overgrowth should be treated with intermittent antibiotics. Patients with predominant small bowel distention may require a venting gastrostomy to relieve distress. Some patients may require placement of a jejunostomy for long-term enteral nutrition. Patients unable to maintain adequate enteral nutrition require TPN or small bowel transplantation. Difficult cases should be referred to centers with expertise in this area.
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