Gastric Stimulation For Gastroparesis

Clinical Presentation

Gastric stimulation is a treatment option typically reserved for refractory cases of gastroparesis. Estimates from Minnesota in 2007 suggest that the prevalence of confirmed gastroparesis per 100,000 people is 37.8 for women and 9.8 for men. However, estimates based on symptom profiles provide evidence that there may be a large number of undiagnosed cases, which could significantly increase the prevalence.

Gastroparesis is a syndrome defined by specific symptomology combined with delayed gastric emptying without gastric ulceration or mechanical outlet obstruction. Gastroparesis can be classified into subtypes based on etiology, but all subtypes have similar symptom profiles. The most commonly encountered subtypes are idiopathic gastroparesis and diabetic gastroparesis. Patients with diabetic gastroparesis tend to present with other complications associated with chronic hyperglycemia, such as neuropathy, retinopathy, or cardiac autonomic abnormalities. Conversely, patients with idiopathic gastroparesis do not have an identifiable underlying disorder that is thought to cause the delay in gastric emptying.

The most common symptoms of gastroparesis are nausea, vomiting, and early satiety, which are reported in greater than 90%, 84%, and 60% of patients, respectively. Additional symptoms are consistent with slowed gastric motility and are frequently reported in patients with gastroparesis: early satiety, postprandial fullness, bloating, and upper abdominal pain. Patients’ symptoms can be episodic or persistent, mild, or severe. Although always unpleasant, if symptoms are persistent and severe, they can lead to serious medical problems. Weight loss, malnutrition, and dehydration are the potential poor outcomes of uncontrolled gastroparesis. There are standardized methods for evaluating the symptom progress for gastroparesis. The most common is the Gastroparesis Cardinal Symptom Index (commonly abbreviated to GCSI). Tools such as this can be helpful for monitoring treatment response and patient status.

One important mimicker of gastroparesis is functional dyspepsia. Both can present with similar symptom profiles, yet the treatment strategies are quite different. As such, it is important for providers to distinguish between the two. One clinical clue is a patient’s interpretation of associated abdominal pain. Though common in both disorders, it is thought to be a very prominent symptom for a patient with functional dyspepsia, while being of lesser significance to a patient with gastroparesis. However, the symptomatic nuances between these disorders, though informative, are not enough to establish an accurate diagnosis. Such subtle differences between the two conditions further stresses the importance of performing more objective testing to demonstrate delayed gastric emptying and confirm the diagnosis of gastroparesis.

In addition to treating gastroparesis, there has been recent investigation of gastric stimulation’s role in treating obesity. Multiple systematic reviews have shown promising results for its efficacy, but most sources agree that more robust clinical trials are needed before it can become an acceptable treatment option. Due to the relative novelty of gastric stimulation as a treatment for obesity, a detailed review of this approach will not be provided in this chapter.

Anatomy

Functional gastric emptying is dependent on a variety of factors. Extrinsically, changes in autonomic innervation, endocrine signaling, or psychosomatic responses can change the rate of gastric emptying. Intrinsic factors such as the enteric nervous system, distension of the duodenum, or variations in the tonicity, fat content, or pH of the chyme solution can influence emptying as well. While any of these factors can lead to gastroparesis, increased scrutiny has been given to a few target areas. Injury to the vagus nerve in particular is known to result in poor autonomic regulation. Functional loss of peristaltic pacemaker cells or of specific enzymes like nitric oxide synthetase can disrupt gastric coordination via abnormal signaling in the enteric nervous system. Microvascular damage, seen commonly in diabetics, can lead to autonomic neuropathy and smooth muscle atrophy in the gastrointestinal system. With so many possibilities for dysfunction and the continued need for therapeutic advancement, it will continue to be important to learn more about the physiology of gastroparesis.