Diabetic gastroparesis

Introduction to diabetic gastroparesis Diabetic gastroparesis is a common symptom of diabetic gastrointestinal autonomic neuropathy. The clinical manifestations are chronic gastritis, gastric flaccid and gastric retention. Typical symptoms are bloating, early satiety, anorexia, belching, nausea, vomiting, and weight loss. Symptoms are usually more severe after a meal. Physical examination showed that the stomach area was full and could smell the sound of the water. X-ray examination showed signs of slowing, weakening of the stomach, dilatation or relaxation of the stomach, delayed emptying, and pyloric opening. Gastroscopic examination showed mucosal congestion, edema, and erosion of the stomach or antrum. Electrogastrogram examination has a weakened gastric motility. Traditional Chinese medicine for diabetic gastroparesis is called diabetes mellitus and stomach cramps. TCM syndrome differentiation and treatment of diabetic gastroparesis has obvious curative effect. basic knowledge The proportion of illness: 0.097% Susceptible people: no specific population Mode of infection: non-infectious Complications: gastric retention, reflux esophagitis

Causes of diabetic gastroparesis

(1) Causes of the disease

1. Physiology of gastrointestinal exercise

There are three movement functions of the stomach: storing food; grinding and stirring the food to make it into fine particles and thoroughly mixing with the gastric juice; and slowly and smallly discharging the chyme into the small intestine at a rate most suitable for digestion and absorption of the small intestine.

The smooth muscles of the stomach wall have longitudinal, circular and oblique lines. The thickest muscles are the thickest, and the contraction is also the most powerful. In the various parts of the stomach, the circumflex muscles of the antrum are most developed, and the contractile activity is also the most active. Therefore, the antrum is the most active. Motor function is the main driving force for gastric emptying.

There are two basic forms of stomach movement: tension contraction of the stomach and peristalsis of the stomach. The tension contraction of the stomach is particularly evident in the emptied stomach, which can cause a certain pressure in the stomach cavity to maintain the stomach and the fingers. The pressure gradient between the intestines helps the emptying of the digestive gastric juice; the peristalsis of the stomach can be divided into the gastric emptying movement during the digestive phase and the migrating motor complex (MMC) during the digestive phase. About 5 minutes after the stomach, the gastric emptying movement begins. The peristaltic wave starts from the cardia and spreads to the gastric antrum at a frequency of 3 times/min, and then to the pylorus. Usually a peristaltic wave can discharge 1 to 3 ml of fine-grained granules into the ten. In the duodenum, particles larger than 1 mm in diameter often cannot pass through the pylorus. The interdigestive transitional complex movement occurs after gastric emptying, presenting a regular periodic set of intense contractile activities. Originated from the antrum or duodenum, it spreads to the direction of the mouth and can spread to the proximal colon. The frequency of contraction activity is 3 times/min in the antrum of the stomach and 11 times/min in the duodenum. The conduction speed of the activity is about 2 to 5 cm/min. MMC usually takes place 4 to 6 hours after a meal, and occurs once every 2 hours. Each time MMC occurs, it is often accompanied by gastric juice, a large amount of bile and pancreatic secretion, and a peak of secretion of some gastrointestinal hormones (such as motilin). The occurrence process is divided into three phases. The first phase is the resting phase, which accounts for about 50% of the cycle. The phase II exhibits intermittent contraction activity, which accounts for about 40% of the cycle. The phase III is a group of continuous contraction activities, accounting for about 10 of the cycle. %, meal can terminate MMC, the mechanism of MMC has not been fully elucidated, many studies suggest that the autonomic nervous system, the periodic release of gastrointestinal hormones (especially motilin) and the secretion process of digestive juice, MMC function is Digestive gastric contents (such as swallowed saliva, gastric mucus, gastric mucosal exfoliation, food residue and undigested solid food) are discharged into the small intestine, and promote the emptying of the small intestine, under normal circumstances The residence time in the small intestine is about 3 to 8 hours. The abnormality of MMC can cause gastric juice and duodenal juice to be retained in the interdigestive phase, delay in intestinal emptying and excessive proliferation of bacteria in the small intestine and upper digestive tract.

2. Characteristics of gastrointestinal motility dysfunction in diabetic patients

The gastric emptying delay in diabetic patients has been confirmed by many studies and there are few studies on gastrointestinal dysfunction in the digestive phase of diabetic patients. Beijing Tongren Hospital found about 70 gastrointestinal motility in the digestive period of diabetic patients. % of patients with diabetes have interdigestive gastrointestinal dyskinesia. These dyskinesias are mainly caused by MMC stage III loss, in which stage III antrum loss is most obvious, and instead of phase II prolongation, and antrum contraction Attenuation, in addition to gastric emptying and MMC abnormalities, there are obvious abnormalities in gastric electrical activity in diabetic patients. The body of the stomach and the heart also have pacing function, which can produce spontaneous rhythmic electrical activity, ie slow wave Potential, the frequency of normal slow wave potential is 3 times / min, diabetic patients often show tachycardia (more than 4 ~ 5 times / min, and lasted more than 1min), gastric hyperactivity (less than 2 times / min, And for more than 1min) or mixed gastric rhythm disorder (gastropia alternates with gastric hyperactivity).

Although many diabetic patients have gastrointestinal dysfunction, there are fewer clinical manifestations, the severity of gastrointestinal dyskinesia and age, disease duration, clinical manifestations and some common complications (such as kidney, peripheral nerve, fundus lesions, etc.) Lack of a clear and consistent relationship, the emergence of gastrointestinal dysfunction often precedes the appearance of clinical symptoms and complications.

(two) pathogenesis

Normal gastrointestinal motility is regulated by many factors, including the intrinsic properties of the gastrointestinal tract and the annular muscle layer, the extraintestinal and intestinal neurological factors, and the role of endocrine and paracrine substances. Of particular importance is the enteric nervous system. It plays a major regulatory role in normal gastrointestinal movements.

Diabetic autonomic neuropathy

Diabetic autonomic neuropathy is a common complication of diabetes. It is found in about 50% of diabetic patients. Autonomic neuropathy often affects the digestive tract, causing motor dysfunction in the esophagus, stomach, small intestine, large intestine, etc., which can be manifested as nausea, vomiting, and fullness. Abdominal pain, bloating, heartburn, difficulty swallowing, diarrhea, constipation, etc., especially with diabetes gastroparesis as a prominent phenomenon.

2. Glucose metabolism and endocrine dysfunction

There is evidence that gastric emptying is regulated by blood glucose concentration. The relationship between blood glucose concentration and gastric emptying rate in patients with type 1 and type 2 diabetes is reversible, causing hyperglycemia in normal people. The results of pressure measurement show: stomach The amplitude of sinus pressure wave is reduced, the abnormality of gastric antrum activity and the amplitude of pyloric pressure wave increase in MMC stage III, so hyperglycemia may delay the gastric emptying of non-digestible solid granule food in patients with diabetic gastroparesis. In addition, hyperglycemia can inhibit Vagus nerve activity, which may be another important cause of autonomic dysfunction, in addition, abnormalities in diabetic gastric electrical activity may be associated with hyperglycemia, and healthy people may cause significant tachycardia when blood glucose reaches 12.88 mmol/L. It shows that blood sugar changes can destroy the activity of normal pacemaker. After studying for type 1 diabetes patients with nausea, it is found that patients with blood glucose concentration over 12.6mmol/L have gastric electrical rhythm disorder accounting for 75%, while blood glucose control is 6.72mmol. At least 38% of gastric electrical rhythm disorders occur below /L, and studies have shown that endogenous prostaglandins may cause the formation of gastric slow wave rhythm disorders, endogenous Leptin may damage the slow wave rhythm of dogs, while indomethacin prevents tachycardia in healthy volunteers caused by hyperglycemia. It can be seen that patients with diabetic gastroparesis have at least one type of slow wave rhythm disorder and It is related to endogenous prostaglandins and can be corrected by synthetic inhibitors of prostaglandins.

3. Other factors

Diabetes-induced microcirculatory disorders are important pathophysiological basis for complications. Studies have shown that patients with type 2 diabetes, regardless of their gastroscopy and pathology confirmed normal or chronic superficial gastritis, with laser Doppler The endoscopic probe of blood flow meter (Swedish) directly measured the gastric mucosal blood flow (GMBF) from the endoscopic biopsy hole, which was significantly lower than that of healthy people without diabetes and GMBF of chronic superficial gastritis. Mucosal biopsy confirmed gastric mucosal blood vessels. The basement membrane is thickened significantly, and the endothelial cells are significantly swollen, revealing that diabetic microangiopathy is already present in patients with "normal stomach" without gastrointestinal symptoms. Microcirculatory disturbances also affect microcirculation perfusion of autonomic and enteric nervous systems. The occurrence and development of cockroaches may play a catalytic role.

Diabetic gastroparesis prevention

Active and effective treatment of diabetes is the best way to prevent diabetic gastroparesis.

Diabetic gastroparesis complications Complications, gastric retention, reflux esophagitis

Due to delayed gastric emptying, gastric retention may occur. Repeated gastrolithic formation may occur. When the lower esophageal sphincter pressure is reduced, gastric-esophageal reflux symptoms (such as acid reflux, anti-feeding, heartburn, etc.) may occur. Sexual esophagitis.

Symptoms of diabetic gastroparesis Common symptoms Esophageal reflux symptoms, nausea, heartburn, abdominal pain, early onset

Most patients have no obvious clinical symptoms. Less patients have early satiety, nausea, vomiting, abdominal distension, etc. The severity of symptoms varies from person to person. The degree of symptoms in the same patient is also affected by many factors, which may be related to diabetes autonomic nerve. Lesions cause a decrease in sensitivity to afferent nerve pathways. Gastric retention due to delayed gastric emptying may result in repeated gastrolithic formation. Gastro-esophageal reflux symptoms may occur when the lower esophageal sphincter pressure is reduced (eg, acid reflux, anti-acid Food, heartburn, etc.), severe cases of reflux esophagitis, abnormal MMC can cause the above symptoms can also cause abnormal intestinal and colon emptying, causing abdominal pain, constipation, diarrhea and other symptoms.

Examination of diabetic gastroparesis

Indirect measurement techniques: plasma and breath test.

Scintillation scanning technology

Beginning in 1966, with 99mTc and 111In double-labeled solid and liquid test meals, gastric emptying rate (GERS) and gastric half emptying time (GETl/2) at various times can be measured. The empty time is 30 to 45 minutes, and the solid food is 60 to 110 minutes. Before the start of gastric emptying, there is usually a lag period with very little emptying. This period is equivalent to grinding the food to the fine particles that can pass through the pylorus. At the time, patients with diabetic gastroparesis have a half-empty stomach time, gastric emptying rate and lag phase are significantly prolonged, so this method is the gold standard for gastric emptying.

2. Gastrointestinal pressure measurement technology

Gastrointestinal pressure measurement technology is mainly used for the detection of gastrointestinal systolic function, including the time of contraction activity, contraction intensity, contraction frequency, and coordination of contraction. It can be called the gold standard for the determination of gastrointestinal contractile activity, gastrointestinal pressure measurement. Hydraulic capillary perfusion system and airbag pressure measuring system can be used. The former is widely used. In addition, there is a dynamic gastrointestinal pressure monitoring and recording system designed and manufactured by solid pressure sensor, which can perform continuous gastrointestinal pressure measurement for more than 24 hours.

3. Ultrasonic examination technology

For non-invasive examination, the patient is easy to accept, can dynamically observe the liquid gastric emptying, gastric peristalsis and digestion of food through the pylorus, can be repeated many times.

4. Electrogastrogram technique

It can provide valuable information for gastric motility and gastric emptying. It can be used as an important screening test for diabetic gastroparesis. It can also be used to observe the scientific comparison before and after gastric motility drug treatment.

5. Radiology technology

Indirect data on digestive phase movement can be obtained by measuring the emptying of solid material that is not digested and impervious to X-rays (wrapped polyethylene pellets).

6. Impedance technology.

7. Magnetic resonance imaging technology.

Diagnosis and diagnosis of diabetic gastroparesis

diagnosis

With the deepening of research in the field of gastrointestinal motility and the application of new technologies, the diagnosis of gastroparesis is more accurate, and it is based on functional tests of gastrointestinal tract.

Differential diagnosis

1. Gastroptosis: patients often have abdominal distension and upper abdominal discomfort; abdominal pain is mostly persistent pain, often occurs after meals, and is related to food intake; nausea and vomiting often occur during postprandial activities, especially when eating too much.

2. Chronic gastric torsion: patients with chronic gastric torsion often have non-specific symptoms such as stomach discomfort, indigestion, burning sensation, upper abdominal fullness or abdominal sputum, more than post-meal induction, although patients rarely have symptoms of gastroesophageal reflux However, esophagitis can often be found by endoscopy. The pain of intermittent gastric torsion is similar to that of acute gastric torsion, but to a lesser extent. Because of its transient characteristics, it is often mistaken for the origin of pancreaticobiliary tract. Patients with intermittent upper abdominal pain, especially those with vomiting or vomiting should consider chronic intermittent gastric torsion.

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