Gastrointestinal · Year 2 · from Gastrointestinal
Case 2: Gastroparesis
Patient Presentation
Demographics: 55-year-old male
Chief Complaint: Nausea, vomiting, and early satiety for 6 months
History of Present Illness: The patient reports persistent nausea, bloating, and feeling full after only a few bites of food. He vomits 2-3 times weekly, often recognizing food eaten many hours earlier. He has lost 20 pounds over 6 months due to reduced oral intake. Symptoms worsen with fatty or fibrous foods.
Past Medical History: Type 2 diabetes mellitus for 18 years (HbA1c 9.2%), peripheral neuropathy, hypertension, hyperlipidemia
Medications: Metformin, glipizide, lisinopril, atorvastatin
Physical Examination
- Vital Signs: BP 132/84 mmHg, HR 88 bpm, BMI 26
- General: Cachectic-appearing male
- Abdomen: Mildly distended, succession splash present, mild epigastric tenderness, no peritoneal signs
- Neurologic: Decreased sensation in stocking distribution bilaterally
Workup and Results
- Upper Endoscopy: Retained food in stomach despite 12-hour fast; no gastric outlet obstruction, no ulcers or masses
- Gastric Emptying Scintigraphy: 78% retention at 2 hours (normal <60%), 45% retention at 4 hours (normal <10%)
- HbA1c: 9.2%
Gastric emptying scintigraphy at 4 hours showing significant retained radiotracer in the stomach (45% retention), indicating markedly delayed gastric emptying consistent with gastroparesis.
Image Source: Case courtesy of Radiopaedia.org
Diagnosis
Diabetic Gastroparesis
Clinical Correlation to Motility Physiology
Diabetic autonomic neuropathy damages vagal nerve fibers that coordinate gastric motility. The proximal stomach (fundus) normally provides reservoir function through receptive relaxation mediated by vagal inhibitory neurons releasing NO and VIP. The distal stomach (antrum) generates grinding contractions at 3 cycles per minute, driven by interstitial cells of Cajal (ICC) pacemaker activity modulated by vagal cholinergic input. In diabetic gastroparesis, impaired vagal function and potential ICC loss result in poor fundic accommodation and weak antral contractions, leading to retained gastric contents, nausea, and vomiting.
Treatment
- Glycemic optimization (reduces acute hyperglycemia-induced slowing)
- Dietary modifications: small, frequent, low-fat, low-fiber meals; liquid nutritional supplements
- Metoclopramide 10 mg before meals (with caution regarding tardive dyskinesia)
- Consider gastric electrical stimulation (Enterra) for refractory symptoms
- Pyloric interventions (G-POEM) for selected patients