Gastroparesis is a syndrome characterized by delayed gastric emptying in the absence of a mechanical obstruction of the stomach. It is associated with the cardinal symptoms of nausea, vomiting, early satiety, belching, bloating, and/or upper abdominal pain. It is commonly associated with longstanding, poorly controlled diabetes.

Gastroparesis diabeticorum

Gastrointestinal autonomic neuropathy

Delayed gastric emptying

• Age-adjusted incidence of gastroparesis is 2.4 per 100,000 person-year for men and 9.8 per 100,000 person-year for women. The age-adjusted prevalence of definite gastroparesis is 9.6 per 100,000 persons for men and 38 per 100,000 persons for women
• Gastroparesis is seen more commonly in women, and there is no known genetic predisposition to the disease
• There are certain risk factors for development of gastroparesis, and diabetes is the most frequently recognized systemic disease. However, the most common form is idiopathic, where no detectable primary underlying abnormality is found. The idiopathic form accounts for approximately 50% of the patients with delayed gastric emptying
• Other risk factors include:
  1. Postviral, especially rotavirus and Norwalk virus
  2. Medications including narcotics, calcium channel blockers, and tricyclic antidepressants
  3. Postsurgical
  4. Neurologic illnesses, such as multiple sclerosis, brain stem stroke, or tumor, etc.
  5. Autoimmune gastrointestinal dysmotility
  6. Others such as mesenteric ischemia, scleroderma

• Patients with gastroparesis present with nausea, vomiting (vomitus may contain food ingested a few hours earlier), abdominal pain, early satiety, postprandial fullness, bloating, and in severe cases, weight loss. Although abdominal pain is a frequent symptom in patients with gastroparesis, it is rarely the predominant symptom.
• Interestingly, in patients with diabetes as the cause for gastroparesis, severe retching and vomiting are more commonly reported.
• Symptoms of gastroparesis are more pronounced in patients with type 1 diabetes, as compared with patients with type 2 diabetes.
• Physical examination findings may include epigastric distention or tenderness, but not guarding or rigidity. A succussion splash may be heard on auscultation by gently rocking the patient.

• Diabetic gastroparesis is thought to result from impairment of neural control of gastric function. Various mechanisms of nerve injury include inflammatory changes to the autonomic ganglia or dropout of myelinated fibers involving the vagus nerve.
• Acute hyperglycemia has been found to have effects on the gastric sensory and motor functions by causing altered gastric electrical activity. It can also result in relaxation of the proximal stomach and decreased pressure in the antrum and pylorus. All of these processes can contribute to the retardation of gastric emptying.
• Achieving euglycemia can correct the gastric emptying delay.
• The effect of chronic hyperglycemia on the stomach is less clear, but there is some evidence that gastric emptying of meals is slower in patients with high glycated hemoglobin levels.

• Functional dyspepsia¹
• Gastric outlet obstruction
• Cyclic vomiting syndrome
• Chronic use of cannabinoids
• Irritable bowel syndrome
• Rumination syndrome
• Eating disorders such as anorexia nervosa and bulimia

• Thorough history and physical examination.
  1. An associated history of poorly controlled blood sugars may be present.
  2. A history of retinopathy, nephropathy, and neuropathy may be present in association with diabetes.
• All medications that can delay gastric emptying should be stopped before formal workup.

No specific labs are needed to confirm the diagnosis, but the following can help to arrive at diagnosis:

• Hemoglobin A_1c (HbA_1c)
• Thyroid stimulating hormone (TSH)
• Total protein/albumin
• Hemoglobin
• Vitamin B₁₂
• Antinuclear antibody titers

• Initial imaging should be done to rule out a mass causing mechanical obstruction.
  1. Upper GI endoscopy is first line.
  2. Computed tomography (CT) enterography vs. magnetic resonance (MR) enterography may also be done to rule out mechanical obstruction from a small-bowel mass.
  3. Barium follow-through if CT or MR enterography unavailable.
• Food retained after overnight fasting may be suggestive of gastroparesis.
• After a mechanical obstruction has been ruled out, scintigraphic gastric emptying should be done as a confirmatory test.
  1. It is the simplest and most cost-effective test.
  2. Documenting the presence of delayed gastric emptying and assessing its severity is best done by measuring the delay in gastric emptying of solids.
  3. Patient is asked to ingest a standard, low-fat meal.
  4. Abnormal gastric emptying is defined as >10% gastric retention of solid food at 4 h and/or >60% at 2 h.
• ¹³C breath test can also be used to measure gastric emptying.
  1. Not as sensitive as the scintigraphy method
• An alternative testing modality, called the wireless motility capsule, is as sensitive and specific as scintigraphy, but it is rather expensive and has not been shown to offer any added clinical information that scintigraphy has already provided.
  1. It is an ingestible, wireless capsule that measures pH, pressure, and temperature as it traverses the GI tract. Gastric emptying of the capsule occurs with phase III of the migrating motor complex, signifying completion of the postprandial phase.

• Nonpharmacologic therapy includes provision of nutritional support along with dietary modifications.
  1. Oral nutrition is preferred in mild disease. Diet should include small meals that are low in fiber (low-residue) and fat.
  2. Avoidance of carbonated beverages is recommended because these can lead to symptoms of bloating.
  3. Alcohol and tobacco smoking should also be stopped because these also delay gastric emptying.
  4. For patients with severe disease, a feeding jejunostomy tube may be considered. A successful trial of a nasojejunal feeding tube should precede placement.
  5. Optimize glucose and electrolyte levels.

• Prokinetic agents can be used to improve gastric motility.
  1. Metoclopramide and erythromycin are both available in intravenous and liquid form, which makes medication administration, tolerance, and efficacy more acceptable if patient symptoms are severe. Metoclopramide should generally not be used for over 12 wk because of the risk of tardive dyskinesia.
  2. The FDA has approved a nasal spray formulation of metoclopramide called Gimoti for diabetic gastroparesis in adults. Cost is a limiting factor.
  3. Domperidone is only available in the U.S. through investigational drug application due to increased risk of QT interval prolongation and arrhythmias.
• Antiemetic agents may also be needed for symptom relief in the acute setting.
  1. Phenothiazines, such as promethazine.
  2. 5-HT3 antagonists, such as ondansetron.
  3. Neurokinin receptor antagonist, such as aprepitant.
  4. Scopolamine patch.
• Intravenous fluid resuscitation may be required if signs or symptoms of dehydration are present due to persistent nausea and vomiting.
• Correct hyperglycemia even in the acute setting because delayed gastric emptying can be quickly corrected in the immediate setting.
• Discontinue medications that may delay gastric emptying.
  1. Pain medications.
     1. Avoid opioids.
     2. Tramadol may be used; however, one study showed that although gastric emptying was improved, colonic transit time was delayed.
  2. Incretin-based therapies and glucagon-like peptide 1 (GLP-1) analogues have been shown to retard gastric emptying.

• Metoclopramide should not be used for more than 12 wk unless the benefits outweigh the risks. Side effects include restlessness, anxiety, QT prolongation, and extrapyramidal effects such as dystonia and tardive dyskinesia.
• Erythromycin use is limited to 4 wk because longer use leads to tachyphylaxis. Similar effect is seen with the higher dose (250 mg) vs. a lower dose (40 mg).
• Pain management may need to be addressed for patients receiving chronic opioids.
  1. Low-dose tricyclic antidepressants, selective serotonin reuptake inhibitors, and pregabalin can be used as alternatives for long-term pain control.
• Endoscopic intrapyloric injection of botulinum toxin may be considered.
  1. Not shown to improve symptoms associated with diabetic gastroparesis but does have a modest effect on improving gastric emptying.
  2. Not approved as a mainstay treatment modality.
• Gastric electrical stimulation via a gastric electrical neurostimulator can be offered to patients with diabetic gastroparesis.
  1. Shown to improve symptom severity and gastric emptying.
  2. Approved as a humanitarian exemption device for patients with refractory symptoms.
• Surgical intervention.
  1. Venting gastrostomy, gastrojejunostomy, pyloroplasty, and gastrectomy are available.
  2. Rarely employed and is reserved for patients with severe, debilitating disease.

• Dietary modifications as described earlier
• Acupuncture
• Autonomic retraining

• Diabetic gastroparesis does not change over time, and it occurs with both liquids and digestible solids as well as with indigestible food residues. However, impaired gastric emptying of indigestible solids may be an earlier abnormality.²
• Gastroparesis can be one of the consequences of chronic, poorly controlled diabetes.
• Symptoms of nausea, vomiting, bloating, early satiety, and abdominal pain in a patient with chronic, poorly controlled diabetes should prompt the possibility of gastroparesis.
• The diagnostic study of choice is gastric scintigraphy, performed by the nuclear medicine department.
• Discontinue all medications that can slow gastric emptying, especially opioids.
• Improve blood sugar control and avoid hyperglycemia.
• Antiemetics with prokinetic properties, such as metoclopramide, are most helpful in relieving nausea and vomiting, in both the acute and chronic presentations.
• Refer to gastroenterology for consideration of botulinum toxin injection or gastric neurostimulator placement if patients have poorly controlled and refractory disease.

Focus on improved glycemic control in the long term.

• Gastroparesis Patient Association for Cures and Treatments (G-PACT)
• Association of Gastrointestinal Motility Disorders, Inc. (AGMD)

Diabetes Mellitus (Key Related Topic)

Diabetic Polyneuropathy (Key Related Topic)