Gastroparesis is a heterogeneous disorder defined by delay in gastric emptying. Symptoms of gastroparesis are nonspecific, including nausea, vomiting, early satiety, bloating, and/or abdominal pain. Normal gastric motor function and sensory function depend on a complex coordination between the enteric and central nervous system. This article discusses the pathophysiology of delayed gastric emptying and the symptoms of gastroparesis, including antropyloroduodenal dysmotility, impaired gastric accommodation, visceral hypersensitivity, and autonomic dysfunction. The underlying pathophysiology of gastroparesis is complex and multifactorial. The article discusses how a combination of these factors leads to symptoms of gastroparesis.
Key points
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Symptoms of gastroparesis go beyond delay in gastric emptying.
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There is significant overlap between idiopathic gastroparesis and functional dyspepsia in terms of symptoms and pathophysiology.
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Abdominal pain is an under-recognized symptom of gastroparesis that is associated with decreased quality of life.
Gastroparesis is a heterogeneous disorder defined as delayed gastric emptying in the absence of a mechanical obstruction. Symptoms of gastroparesis include nausea, vomiting, bloating, early satiety, and/or abdominal pain.
Etiologies of gastroparesis
The most common forms of gastroparesis are idiopathic, diabetic, and postsurgical. In earlier studies, idiopathic gastroparesis comprised approximately 35% of all gastroparetic patients. However, a larger multicenter study found that 67% of patients had idiopathic gastroparesis. Additionally, other conditions can lead to gastroparesis ( Table 1 ). Independent of etiology, gastroparesis affects women more commonly than men.
| Etiology | N = 146 | % | Female (%) |
|---|---|---|---|
| 52 (12) | 35.6 (8.2) | 90.4 |
| Diabetes | 42 | 28.8 | 76.2 |
| Postsurgical | 19 | 13.0 | 73.7 |
| Parkinson disease | 11 | 7.5 | 81.8 |
| 7 | 4.8 | 85.7 |
| Intestinal pseudo-obstruction | 6 | 4.1 | 66.7 |
| 9 | 6.2 | 55.6 |
Etiologies of gastroparesis
The most common forms of gastroparesis are idiopathic, diabetic, and postsurgical. In earlier studies, idiopathic gastroparesis comprised approximately 35% of all gastroparetic patients. However, a larger multicenter study found that 67% of patients had idiopathic gastroparesis. Additionally, other conditions can lead to gastroparesis ( Table 1 ). Independent of etiology, gastroparesis affects women more commonly than men.
| Etiology | N = 146 | % | Female (%) |
|---|---|---|---|
| 52 (12) | 35.6 (8.2) | 90.4 |
| Diabetes | 42 | 28.8 | 76.2 |
| Postsurgical | 19 | 13.0 | 73.7 |
| Parkinson disease | 11 | 7.5 | 81.8 |
| 7 | 4.8 | 85.7 |
| Intestinal pseudo-obstruction | 6 | 4.1 | 66.7 |
| 9 | 6.2 | 55.6 |
Clinical manifestations
Symptoms of gastroparesis are variable and include nausea, vomiting, early satiety, bloating, postprandial fullness, abdominal pain/discomfort, and anorexia ( Table 2 ). However, despite its prevalence in gastroparesis, consensus publications have traditionally not considered pain as a predominant factor. Additionally, there is significant overlap between symptoms of gastroparesis and functional dyspepsia. In a recent multicenter study, 86% of patients with idiopathic gastroparesis met Rome III criteria for functional dyspepsia. Likewise, delayed gastric emptying has been found to present in 23% to 33% of patients with functional dyspepsia. Many of the patients had a previous cholecystectomy prior to the diagnosis of gastroparesis. Cholecystectomy was more common in patients with type 2 diabetes and idiopathic gastroparesis than in patients with type 1 diabetes. Patients who had a cholecystectomy had a higher prevalence of comorbidities including chronic fatigue, fibromyalgia, depression, and anxiety. These symptoms led to a worse quality of life.
| Symptom | % |
|---|---|
| Nausea | 80–92 |
| Vomiting | 66–84 |
| Bloating | 55–75 |
| Early satiety | 54–60 |
| Abdominal pain | 46–68 |
Patients with type 1 diabetes mellitus had increased vomiting and retching, whereas the idiopathic gastroparesis group had increased prevalence of early satiety, postprandial fullness, and abdominal pain ( Table 3 ).
| Symptom | Idiopathic (%) | Type 1 DM (%) | Type 2 DM (%) |
|---|---|---|---|
| Nausea | 84.3 | 84.6 | 94.9 a |
| Vomiting | 59.8 | 88.5 a | 91.5 a |
| Bloating | 57.5 | 56.4 | 62.7 |
| Early satiety | 57.5 | 47.4 | 74.6 a |
| Abdominal pain | 76.0 | 60.3 a | 69.5 |
| Weight loss | 46.5 | 52.6 | 52.5 |
Not all patients with chronic nausea and vomiting have a delay in gastric emptying. The Gastroparesis Registry enrolled 106 patients (25%) with normal emptying and chronic nausea and vomiting. The symptoms in patients with normal gastric emptying, including nausea, vomiting and abdominal pain, had a similar severity as in patients with delayed gastric emptying. The majority of patients in either the normal or delayed gastric emptying group satisfied Rome III criteria for functional dyspepsia. Both groups remained equally symptomatic at 48-week follow-up.
In addition to nausea and vomiting, abdominal pain is a major symptom in patients with gastroparesis. Abdominal pain often has been an overlooked symptom in patients with gastroparesis. Classical teaching dictates that patients with pain predominance should undergo additional evaluation for other causes. This in part may be due to the overlap between idiopathic gastroparesis and functional dyspepsia and the broad differential diagnoses for abdominal pain. However, in a large multicenter cohort study, the prevalence of moderate-to-severe abdominal pain (approximately 60%) was similar between patients with idiopathic and diabetic gastroparesis. In this study, 20% of patients with gastroparesis reported pain predominance compared with 44% reporting nausea/vomiting predominance. The presence of pain predominance was associated with decreased quality of life and increased depression and anxiety. The delay in gastric emptying was similar in patients with predominant pain and predominant nausea and vomiting. Moderate-to-severe abdominal pain was more prevalent in idiopathic gastroparesis and in those patients who did not have an infectious prodrome. Compared with patients with predominant nausea/vomiting, the patients with pain had greater use of opiates and less use of antiemetics.
Measures of symptom severity
The Patient Assessment of Upper Gastrointestinal Disorders Symptoms (PAGI-SYM) was developed to assess symptom severity of upper gastrointestinal (GI) symptoms in patients with gastroesophageal reflux disease (GERD), dyspepsia, and gastroparesis. The PAGI-SYM consists of 20 questions and 6 subscales: heartburn/regurgitation, nausea/vomiting, postprandial fullness/early satiety, bloating, upper abdominal pain, and lower abdominal pain. The subscale scores are calculated by taking the mean of the items in each of the subscales.
The Gastroparesis Cardinal Symptom Index (GCSI) is derived from the PAGI-SYM and validated as a tool to assess patient-derived symptom severity in patients with upper gut symptoms. Based on review of the literature, physician interviews, and patient focus groups, the GCSI was constructed with 9 items that categorized gastroparesis into 3 subscales: nausea/vomiting, postprandial fullness/early satiety, and bloating. The purpose of the GCSI is to provide a patient-reported tool that can be used in clinical trials to assess patient responses to therapy. However, the GCSI does not address the impact of pain on treatment outcomes.
Psychological dysfunction is associated with increased severity of symptoms as measured with the Beck Depression Inventory and the State–Trait Anxiety Inventory. All 3 indexes were greater for GCSI scores greater than 3.1. The measures of psychological dysfunction were not different for diabetic or idiopathic gastroparesis and were not related to the severity of gastric retention. Nausea, vomiting, bloating, and postprandial fullness were increased in patients with higher depression or anxiety inventories.
Normal gastric motor function
Normal GI function depends on a complex coordination between smooth muscles of the gastric fundus, antrum, pylorus, and duodenum under the control of the enteric (intrinsic) and central (extrinsic) nervous systems. Central nervous system control of digestion is mediated through the autonomic nervous system. Parasympathetic control is mediated through the vagus, while sympathetic control is mediated through the spinal cord at T5 to T10 via the celiac ganglia. Vagal efferents arise from the dorsal motor nucleus and terminate in the myenteric plexus. The vagus effects gastric motility indirectly via the enteric nervous system rather than direct innervation of gastric smooth muscles.
Distention of the antrum by a solid meal triggers the fundus to relax to store food as the rest of the meal enters the stomach. This accommodation response effectively increases the gastric volume without raising the intragastric pressure. Tonic contractions of the proximal stomach transfer food to the gastric antrum, where high amplitude contractions break down the food into particles 1 to 2 mm in size through trituration. These particles are able to pass through the pylorus into the duodenum. Particles greater than 2 mm that cannot pass the pylorus during the postprandial phase are cleared during the interdigestive period by phase 3 of the migrating motor complexes (MMCs), which are cyclical contractions of the antrum and small bowel that propel undigestable solids distally.
Motor dysfunction anywhere in the stomach may delay gastric emptying.
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