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Addressing Diabetic Gastroparesis

By: Gwen Y. Reyes-Amurao, MDAddressing Diabetic Gastroparesis

Although not commonly discussed as a complication of diabetes, one of its most serious ones is diabetic gastroparesis. This is defined as a delay in gastric emptying in the absence of mechanical obstruction in the stomach. Because of recent studies, this disease seems to affect females more than males, and often present in their 40s to 50s with Type 1 diabetes. Gastroparesis typically develops after at least 10 years of diabetes, especially in patients with evidence of autonomic dysfunction. For a better understanding of how this comes about, the entire process of digestion must be understood.

In normal digestion, the stomach contracts to help break down ingested food and move it into the small intestine. This is regulated by complex mechanisms between smooth muscles, the   enteric system, and vagus nerve. The stomach is divided into functional components, namely the fundus or the proximal part, and the corpus or body and antrum known as the distal part. When food is ingested, a process known as peristalsis or peristaltic propulsions of the esophagus brings the food into the fundus. This, in turn, relaxes in order to accommodate the food. Once the increased filling is detected by certain receptors in the stomach, further accommodation is triggered. All these processes and reflexes are mediated through the vagus nerve.

Diabetes can cause gastroparesis due to the known effects on the nervous system, in this case, vagus nerve damage. When the vagus nerve is affected, the muscles in the stomach and other parts of the digestive tract are unable to function properly. This leads to impaired fundic  (fundus) accommodation, irregular contractions of gastric muscles, and decreased motility, all of which slows down the movement of food through the digestive system and delays gastric emptying time.

Manifestations of Diabetic Gastroparesis

In the early stages of the disease, symptoms may be minimal and hardly observable. As it worsens, symptoms become more common and may include any of the following:

  • Nausea
  • Vomiting of undigested food
  • Heartburn
  • Gastroesophageal reflux or GERD
  • Early satiety or feeling full despite eating small amounts of food
  • Bloating
  • Loss of appetite
  • Unintentional weight loss
  • Stomach spasms
  • Unstable blood sugar levels

Once the symptoms become more severe, nutritional deficiency often results. Although the pain symptoms are relatively vague and non-specific, they are very similar to the other types of neuropathic pain and are often chronic and respond poorly to current forms of therapy.

Associated Risks and Complications

According to the Mayo Clinic, the damage to the nervous system leads to the unpredictability of gastroparesis. This makes it more difficult for a person with diabetes to manage their blood sugar levels. Gastroparesis can also cause several other complications, such as:

  • Severe dehydration from frequent and persistent vomiting.
  • Malnutrition due to loss of appetite and inability to effectively absorb nutrients.
  • Bezoars or undigested food that hardens and remains in the stomach, which can lead to further nausea and vomiting and can be dangerous and life-threatening once it blocks the passage of food into the small intestine.
  • Unpredictable blood sugar changes. Gastroparesis per se is not the cause of diabetes. However, frequent changes in the rate and amount of food passing into the small bowel might cause erratic changes in blood sugar levels.
  • Decreased quality of life. Because symptoms often come and go, an acute attack can make it difficult for a person to function normally.

Although having diabetes alone will already increase one’s risk of developing gastroparesis, those who have Type 1 diabetes are more at risk than those with Type 2, but once the second type has persisted for 10 years or longer, this increases their risk as well. Diabetics who have a coexisting autoimmune disease or history of surgeries involving the gastrointestinal tract,      especially around the esophagus, stomach, and small intestine area, are also more likely to    develop such a condition.

Diagnosing the Condition

The American Diabetic Association mentions diagnostic tests that can detect and help diagnose the presence of diabetic gastroparesis once symptoms are reported, such as barium swallow or x-ray, barium beefsteak meal, gastric manometry, upper endoscopy and ultrasound, and radioisotope gastric-emptying scan.

Treating Gastroparesis

When addressing diabetic gastroparesis, the most important goal of treatment aside from alleviation of symptoms is the management of blood glucose levels to prevent morbidities and mortalities. Some of the medications used to address this condition include prokinetics, anti-nauseants, and pain modulation therapies,  although diet and lifestyle modification seems to play an important role in addressing this condition.


Prokinetics are the most commonly used medications to address this condition. These basically improve gastric emptying to help alleviate symptoms in the diabetic patient. Currently, there are two types of prokinetic drugs that are given in gastroparesis, anti-dopaminergic and serotoninergic prokinetics. Domperidone and metoclopramide are both well-known anti-dopaminergic variants that help improve gastric emptying. Domperidone works through the peripheral nervous system, while metoclopramide works centrally, crossing the blood-brain barrier and increasing the risk of neurologic side effects.

In a study conducted by the Journal of Clinical Gastroenterology and Hepatology, it was concluded that there was enough evidence to recommend domperidone use in diabetic gastroparesis. In another study by the Journal of Clinical Therapeutics, when efficacy, tolerability, and impact on quality of life of domperidone in the management of  gastroparesis was determined, the results showed that after 4 weeks of domperidone therapy, patients who responded to it experienced significant improvements in quality of life as evidenced by a deterioration in manifestations and significant improvements in the upper GI symptoms.

Aside from dopaminergic prokinetics, serotonergic prokinetic cisapride, can also be given in those suffering from this condition. This works mainly as a mediator of peristalsis or movement in the gut and is one of the most common medications given in gastroparesis. 

Pain Therapy

Because other neuropathies are already detected prior to developing gastroparesis, medications for the treatment of pain in diabetic neuropathy such as gabapentin and pregabalin have displayed improvement in diabetic gastroparesis symptoms as well.


Surgical resection of the stomach for severe refractory gastroparesis has been described in some studies, although mostly recommended for post-vagotomy or post-surgical gastroparesis. Because of the invasiveness and morbidity of such a procedure, surgical removal of part of the stomach is often not recommended and may warrant further study.

Dietary changes

Gastroenterology specialists or gastroenterologists would often recommend to make necessary dietary changes since something as simple as these can help manage one’s symptoms. Some helpful tips would be:

  • Eating frequent, smaller meals instead of three larger meals each day
  • Chewing food thoroughly
  • Limiting high-fiber foods, such as broccoli, which take longer to digest
  • Sticking to mainly low-fat food
  • Eating well-cooked vegetables instead of raw vegetables
  • Drinking juices or taking in soups and pureed foods that are easier to swallow
  • Avoiding alcohol and carbonated drinks
  • Eating slowly
  • Sitting upright or taking a walk after meals

In the end, the goal of therapy and management for individuals who suffer from diabetic gastroparesis no matter what the presentation, is the improvement of one’s symptoms. Although a relatively newer complication compared to others, the fact that it has been recognized is a significant development, which will hopefully lead to more studies which will help improve the overall quality of life.

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