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Diabetic gastroparesis
Diabetic gastroparesis, a chronic complication of diabetes mellitus, is marked by delayed gastric emptying in the absence of mechanical obstruction. Key risk factors include suboptimal glycemic control and obesity. Clinical manifestations typically encompass nausea, vomiting, abdominal discomfort, and early satiety. The diagnosis is one of exclusion, confirmed through scintigraphic evaluation of gastric emptying. Therapeutic intervention primarily involves conservative measures: stringent glycemic control, dietary adjustments, and avoiding substances that impede gastric emptying. Prokinetic agents may enhance gastric motility, while antiemetics offer symptomatic relief. In cases resistant to standard treatment, surgical intervention or parenteral nutrition might be necessitated.
Last updated: December 3, 2024
- Poor Glycemic Control:
- Specifically, sustained hyperglycemia exceeding 200 mg/dL.
- Obesity:
- Particularly relevant in patients with type 2 diabetes.
- Poor Glycemic Control (Sustained Hyperglycemia > 200 mg/dL):
- Leads to neuronal damage.
- Impairs neural control of gastric function, including:
- Dysfunction of interstitial cells of Cajal.
- Abnormal myenteric neurotransmission.
- Smooth muscle dysfunction.
- Vagal dysfunction.
- Results in antral motor coordination and function abnormalities:
- Decreased antral contractions.
- Pyloric spasms.
- Abnormal antroduodenal contractions.
- Culminates in delayed gastric emptying.
- Abnormal Small Bowel Motility:
- Contributes to increased or decreased gastric compliance.
- Further delays gastric emptying.
- Autonomic Neuropathy:
- Causes abnormal gastric electrical activity and altered visceral perception.
- Common Symptoms:
- Nausea and/or Vomiting: Due to delayed gastric emptying, food remains in the stomach for a prolonged period, triggering nausea and vomiting.
- Bloating: Results from the accumulation of undigested food and gas, leading to a sensation of abdominal fullness.
- Upper Abdominal Pain: Caused by gastric distension and disrupted motility. May also result from spasms or dysrhythmic contractions.
- Loss of Appetite: Often a consequence of prolonged gastric fullness and discomfort.
- Early Satiety: Occurs due to delayed emptying and reduced gastric accommodation, leading to a feeling of fullness after eating only a small amount.
- Examination Findings:
- Abdominal Distension: Visible enlargement of the abdomen, often a physical manifestation of bloating and gas accumulation.
- Epigastric Tenderness: Tenderness in the upper abdominal region upon palpation, indicative of underlying gastric irritation or distension.
- Succussion Splash: A sloshing sound heard during abdominal examination, suggesting retained gastric contents with fluid and gas, characteristic of delayed gastric emptying.
- Diagnostic Approach:
- Clinical evaluation to rule out other causes of gastroparesis-like symptoms.
- Assess for signs of neurological diseases, autoimmune disorders, or eating disorders.
- Review medications that may delay gastric emptying (like opioids).
- Inquire about history of bariatric surgery.
- Conduct laboratory studies as needed.
- Perform upper endoscopy to exclude mechanical obstruction.
- Laboratory Studies:
- HbA1c: To evaluate glycemic control.
- Additional studies based on clinical features may include:
- TSH: For hypothyroidism assessment.
- CBC: To check for infection or malignancy.
- Tests for chronic pancreatitis.
- Confirmatory Tests for Delayed Gastric Emptying:
- Preferred: Scintigraphic gastric emptying study.
- Alternatives:
- Wireless motility capsule test.
- Stable isotope breath test.
- Delayed gastric emptying is confirmed with > 10% retention after 4 hours.
- Prior to testing, stop medications affecting gastric emptying and ensure strict glucose control for accurate results.
- Nonpharmacological Management:
- Optimize diabetes treatment to achieve glycemic targets.
- Implement dietary modifications.
- Prescribe alternatives for medications that delay gastric emptying, including some diabetes medications (e.g., GLP-1 agonists, pramlintide).
- Pharmacotherapy:
- Prokinetics:
- Aim: Improve symptoms and gastric emptying.
- First line: Metoclopramide.
- How Metoclopramide Helps:
- Increases gastric motility by acting as a dopamine antagonist.
- Enhances antral contractions and relaxes the pyloric sphincter.
- Accelerates gastric emptying and reduces symptoms.
- How Metoclopramide Helps:
- Alternatives:
- Motilin Agonists (e.g., erythromycin, azithromycin).
- How Motilin Agonists Help:
- Stimulate motilin receptors in the gastrointestinal tract.
- Enhance gastric contractions, improving gastric emptying.
- How Motilin Agonists Help:
- Motilin Agonists (e.g., erythromycin, azithromycin).
- Antiemetics:
- Aim: Alleviate symptoms like nausea and vomiting.
- Options include 5-HT3 antagonists (e.g., ondansetron) and NK1 receptors antagonists (e.g., aprepitant).
- Prokinetics:
- Management of Refractory Diabetic Gastroparesis:
- Surgery:
- Jejunostomy tube placement for enteral feeding.
- Venting gastrostomy for symptom relief (bloating, vomiting).
- Gastric peroral endoscopic pyloromyotomy for severe cases.
- Surgery:
- Electrolyte imbalance
- Malnutrition
- Increased risk of postprandial hypoglycemia because of delayed food absorption
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