Gastroparesis is a disorder that is characterized by slow or delayed transit of food from the stomach to the small intestines. Diabetes is one of the most important causes of gastroparesis.

The primary aim of management of diabetic gastroparesis is to improve stomach emptying and regain control of blood glucose levels. This is because delayed emptying of the stomach causes erratic absorption of glucose from food and worsens the high blood sugar that is characteristic of diabetic patients.

Mechanism of diabetic gastroparesis

The underlying mechanism of gastroparesis in diabetes mellitus patients is not clearly understood. This is because the associations between the pathology of the condition and the severity of the symptoms are not often in coordination.

Several mechanisms that underlie the condition have been proposed. Some of these include:-

Autonomic neuropathy

One of the most well known mechanisms of diabetic gastroparesis is autonomic neuropathy. High blood sugar tends to damage blood vessels that in turn supply nutrients to the nerves. Due to damage to blood vessels the nerves may be damaged. This is called neuropathy.

When the vagus nerve is damaged the stomach emptying is hampered. This also causes a rebound increase in sympathetic nervous system activity. Neuropathy is common in patients with diabetes, affecting 60% of patients.

This neuropathy reduces autonomic ganglia and unmyelinated nerves and leads to loss of myelinated fibers in the vagal and sympathetic nerve trunks. But the severity of neuropathy does not always correlated with the severity of the symptoms. This indicates that neuropathy alone is not the cause of gastroparesis.

Dysfunction of the enteric nervous system

There may be a dysfunction of the enteric nervous system due to diabetes

Dysfunction of hormonal and neurotransmitter control mechanisms

There may also be an underlying dysfunction of hormonal and neurotransmitter control mechanisms. There have been studies showing alterations of release of hormones like motilin, cholecystokinin, somatostatin and glucagon.

Motilin increases the contractions of the upper part of the stomach and cholecystokinin and glucagon reduce movement of the stomach muscles.

Treatment of diabetic gastroparesis

The main aim of treating diabetic gastroparesis is to maintain a tight blood sugar control. Treatment includes dietary changes, insulin, oral medications to reduce blood sugar and in more severe cases, a feeding tube and parenteral nutrition or injected and infused liquid nutrition.

Diet changes include six smaller meals a day rather than three large ones. Liquid or pureed meals may be advised. This will keep the blood glucose levels stable. Liquid meals provide all the nutrients found in solid foods, but can pass through the stomach more easily and rapidly.

Food is usually absorbed slowly and unpredictably in patients with diabetic gastroparesis. This leads to unpredictable fluctuations in blood sugar. More insulin or changes in insulin formulation may be advised for better blood sugar control.

Insulin may be advised after a meal instead of traditional before meal injections. Insulin injections may be catering to the blood glucose levels in these patients rather than fixed doses.

Symptoms of nausea and vomiting are controlled using prokinetic and anti-nausea agents like Metoclopramide, Domperidone etc. Motilin receptor agonists, such as erythromycin, azithromycin, clarithromycin, act as prokinetics, that improve delayed gastric emptying by accelerating muscle contractions of the stomach and duodenum.

Mild gastroparesis with easily controlled symptoms is generally controlled with dietary modifications whereas moderate or severe gastroparesis requires prokinetic medications.