Signs and Symptoms of Gastroparesis
Gastroparesis presents with a characteristic constellation of symptoms including nausea, vomiting, early satiety, postprandial fullness, bloating, abdominal pain, and weight loss, with nausea and vomiting typically being the most predominant and persistent manifestations. 1, 2
Cardinal Symptoms
Gastrointestinal Symptoms:
- Nausea and vomiting are the most predominant and persistent symptoms, particularly in medically refractory cases 1, 2
- Early satiety (inability to finish a normal-sized meal) is a defining feature 2, 3
- Postprandial fullness (uncomfortable sensation of fullness persisting after eating) is a core symptom 1, 2
- Bloating (subjective sensation of abdominal distension without necessarily visible distension) 1, 2
- Epigastric pain or discomfort occurs frequently and can be a prominent feature 1, 2
Systemic Manifestations:
- Weight loss and malnutrition develop in more severe cases due to inadequate oral intake 1, 2
- Anorexia (loss of appetite) can accompany the other symptoms 1
Important Clinical Distinctions
Symptom-Emptying Correlation: The American Gastroenterological Association emphasizes that symptoms correlate poorly with the degree of gastric emptying delay 2. This means severe symptoms can occur with mild emptying delays and vice versa. Exaggerated visceral perception, altered central processing, learned behaviors (including food aversion), and psychological distress can amplify symptom intensity independent of actual gastric emptying delay 1, 2.
Overlap with Functional Dyspepsia: Gastroparesis symptoms overlap significantly with functional dyspepsia, which is defined by bothersome epigastric pain, burning, postprandial fullness, or early satiation without structural disease 1. The key distinction is that functional dyspepsia has normal gastric emptying, whereas gastroparesis requires documented delayed emptying 2.
Pathophysiologic Contributors to Symptoms
Multiple mechanisms beyond delayed emptying contribute to symptom generation 1, 2:
- Impaired gastric accommodation (failure of the fundus to relax appropriately) 1, 2
- Antral hypomotility (reduced contractions in the distal stomach) 1, 2
- Antroduodenal and pyloric dyscoordination (uncoordinated contractions between stomach and duodenum) 1, 2
- Increased visceral perception (heightened sensitivity to normal gastric distension) 1, 2
- Vagal nerve injury (damage to the primary nerve controlling gastric function) 1, 2
Critical Diagnostic Caveats
Medication-Induced Mimics: Before diagnosing gastroparesis, exclude medication-induced symptoms, particularly from opioids and GLP-1 agonists, which can produce identical symptoms 1, 2. These must be discontinued or ruled out as causative factors.
Hyperglycemia Effects: In diabetic patients, hyperglycemia itself can slow gastric emptying and worsen symptoms 2. Blood glucose control must be assessed and optimized, as poor glycemic control frequently exacerbates symptoms 3.
Symptom Predominance Matters: Identify the predominant symptom to guide treatment: antiemetic agents for nausea/vomiting, neuromodulators for abdominal pain, and dietary modifications for early satiety and postprandial fullness 2. This symptom-directed approach is more effective than treating all symptoms uniformly.
Epidemiology and Clinical Context
Gastroparesis affects approximately 37.8 per 100,000 women and 9.6 per 100,000 men, with approximately 5 million U.S. adults suffering from gastroparesis-like symptoms 1. The most common etiologies are diabetic (25%), idiopathic (largest group), postsurgical, medication-induced, and post-viral 1, 4.