gastroparesis syndrome
Introduction
Introduction to gastroparesis syndrome Gastroparesis Syndrome refers to a group of clinical symptoms characterized by delayed gastric emptying, and no organic lesions in the upper digestive tract or upper abdomen are found in the examination. According to the cause can be divided into two types of primary and secondary. Primary, also known as idiopathic gastroparesis, occurs mostly in young women. According to the onset of illness and the length of the disease, the gastroparesis can be divided into acute and chronic. Clinically more common, symptoms persist or recurrent often for months or even more than 10 years. basic knowledge The proportion of illness: 0.003% Susceptible people: no special people Mode of infection: non-infectious Complications: Diabetic Anorexia nervosa
Cause
Causes of gastroparesis syndrome
Diabetes (20%):
Diabetic patients often have abnormal gastrointestinal motility, and about 40% of patients with type I or type II diabetes who take oral hypoglycemic agents have gastroparesis.
In 1937, Ferroir observed that X-ray barium examination of diabetic patients showed a decrease in gastric motility. In 1945, Rundles clearly described the correlation between gastric emptying delay and diabetes for the first time. In 1958, Kassander first applied "diabetic gastroparesis". A term.
Gastrointestinal dyskinesia in patients with diabetic gastroparesis is characterized by gastric digestive interval motor complex wave (MMC) phase III disappearance and postprandial gastric antrum movement, gastric antrum, pyloric and duodenal contraction inconsistency and pyloric fistula In order to delay the emptying of gastric solids, early gastric proximal diastolic dysfunction in DGP patients caused fluid emptying too fast, but the gastric emptying in the late gastric phase was also significantly delayed.
The cause of delayed gastric emptying in patients with DGP is mainly due to vagus nerve injury (autonomic neuropathy). Hyperglycemia also inhibits gastric emptying. After sham feeding or insulin-induced hypoglycemia in diabetic patients, gastric acid secretion reaction is reduced, suggesting vagus neuropathy. Guy et al found that the morphological changes of the vagus nerve in diabetic patients were severely reduced in the density of unmyelinated axons, and the diameter of residual axons became thinner. In other studies, no abnormalities were found in the stomach wall or abdominal vagus nerve of diabetic patients, and the muscles of DGP patients. There was no abnormal change in the interstitial plexus. Ramadylcholine and cisapride could stimulate the gastric antrum contraction in patients with DGP, suggesting that the antral smooth muscle function was intact.
Surgical factors (10%):
Gastric fistula is often accompanied by gastroparesis. The delayed gastric emptying rate after vagus nerve ablation is 5% to 10%. After vagus nerve cutting plus pyloric surgery, 28% to 40% of gastric solid emptying is delayed. The vagus nerve stem is cut. Gastric diastolic function, gastric antrum contraction, and coordinated pyloric diastolic function are all reduced, leading to accelerated gastric emptying and delayed solids emptying, but high selectivity (wall cell) vagotomy can only prolong the lag period of solid emptying. And has no effect on total gastric emptying.
In patients with peptic ulcer complicated with pyloric obstruction, about 30% of gastroparesis occurred after partial gastrectomy and vagus nerve ablation. The proximal gastric static pressure measurement was performed on these patients, and it was found that the low residual stomach tension is the main cause of gastric stagnation. The reason is that patients with Roux-en-Y syndrome also have delayed gastric emptying.
Gastric paralysis after surgery can occur in various types of gastric electrical slow wave rhythm abnormalities and MMC deficiency, and is also associated with delayed gastric emptying.
Anorexia nervosa (10%):
About 80% of patients with anorexia nervosa have delayed gastric solids emptying, but fluid emptying is normal, delayed gastric emptying is accompanied by nausea sinus rhythm disorder, low gastric fundus tension, postprandial plasma norepinephrine and neurotensin Decreased concentrations, as well as autonomic dysfunction, but with the same degree of weight loss and no psychiatric symptoms in patients with anorexia nervosa, there was no significant delay in emptying.
Gastric smooth muscle involvement (15%):
In addition to causing other systemic organ diseases, these diseases often have diffuse gastrointestinal smooth muscle involvement, causing intestinal motility dysfunction. Although esophageal involvement is more common, gastric smooth muscle may be involved and cause stomach paralysis.
Progressive systemic sclerosis often occurs with delayed gastric emptying. The development of gastrointestinal dyskinesia includes two stages, namely, initial stage neuropathy and muscle lesions due to myometrial fibrous tissue infiltration.
Dermatomyositis and polymyositis can cause delayed gastric emptying and/or fluid emptying, and the delay in gastric emptying is related to the degree of skeletal muscle weakness.
Most patients with myotonic dystrophy have delayed emptying of gastric solids and liquid foods. In this patient, the duodenum and proximal jejunal tension increases, and the contractile activity increases. It is believed to be caused by partial depolarization caused by smooth muscle damage. This theoretically increases the resistance to gastric emptying and delays gastric emptying.
Amyloidosis often has muscle infiltration of the gastrointestinal tract, causing motor dysfunction. In 1956, Intriere and Brown reported a case of primary amyloidosis involving only the stomach, in addition to myometrial involvement, amyloid neuropathy and vascular disease Intestinal ischemia caused by intestinal ischemia is also an important cause of dysfunction of the gastrointestinal tract. About 70% of the primary and 55% of the secondary amyloidosis have gastrointestinal symptoms.
Gastroparesis (20%):
In some cancer patients, gastroparesis can be part of the cancer syndrome, Chinn et al reported 7 cases of lung carcinoid, 6 of which developed gastroparesis, histological examination showed intermuscular plexus degeneration, neurons and axons Decreased, inflammatory cells such as lymphocytes and plasma cells infiltrated, glial cells proliferated, and submucosal plexus was not affected. Libefrski et al recently reported 2 cases of mesenteric artery occlusion, severe gastroparesis in patients with chronic gastrointestinal tract, accompanied by gastric electrical rhythm disorder and related symptoms. Gastric solid row of patients 6 months after bypass vascular grafting The air and stomach electrical rhythm returned to normal and the symptoms disappeared. That is, the unexplained gastroparesis accounts for about 50% of patients with delayed gastric emptying. These patients can be roughly divided into two groups: one group is diagnosed as functional dyspepsia, and the other group is diffuse gastrointestinal smooth muscle involvement. There is a dysfunction of the entire gastrointestinal tract. In addition to gastroparesis, there are often multiple diagnoses such as irritable bowel syndrome or pseudo-intestinal obstruction.
Gastroesophageal reflux (10%):
About 60% of patients with gastroesophageal reflux disease have delayed gastric emptying, and it is unclear whether this abnormality is primary or secondary.
Pathogenesis
The etiology of primary gastroparesis, the mechanism is not clear, but the lesion may be in the muscular layer of the stomach or the myenteric plexus that innervates the muscular layer; secondary ones often have:
Diabetes; connective tissue disease, such as progressive systemic sclerosis (PSS); stomach surgery or vagotomy; infection or metabolic abnormalities; central nervous system diseases and certain drugs, in addition, vagus nerve tension and intestinal hormones Peptide substances may also play a role, and motilin levels and motilin receptor function may be abnormal during gastroparesis.
The cause of gastroparesis may be primary gastric motor dysfunction (esthetic gastroparesis), secondary to some systemic diseases and some stomach surgery hands, gastric emptying mechanism involves gastric smooth muscle, gastrointestinal The intrinsic or external nervous system, the close interaction of the central nervous system and hormones, abnormalities of either factor can lead to paralysis of the stomach.
Prevention
Gastroparesis prevention
Should be given a low-fat, low-fiber diet, eat less meals, mainly liquid, in order to facilitate the emptying of the stomach, because smoking can slow down the gastric emptying, should quit smoking, should try to avoid the use of drugs that can delay gastric emptying.
Complication
Gastroparesis syndrome complications Complications Diabetic anorexia nervosa
Easy to develop chronic mesenteric artery occlusion, diabetes, anorexia nervosa, progressive systemic sclerosis and cancer.
Symptom
Symptoms of gastroparesis syndrome Common symptoms Upper abdominal discomfort Stomach accommodating weakening Stomach sinus low stomach emptying delay early fullness
1. The gastric antrum is low and the gastric emptying is delayed.
2. The proximal end of the stomach is less compliant, which weakens the gastric containment.
3. The pressure at the proximal end of the stomach is reduced, which delays the emptying of the gastric fluid.
4. The stomach, pylorus, and duodenum movements are not coordinated. Therefore, the disease mainly manifests as delayed gastric emptying, often with early satiety, fullness after the meal, and symptoms of upper abdominal discomfort after eating.
Examine
Examination of gastroparesis syndrome
1. Determination of gastric emptying function
There are many methods for the examination of gastric emptying function. It is currently considered that the radionuclide gastric emptying test should be the first choice. For patients with dyspepsia of unknown cause, if conditions permit, the routine labeling of solid and liquid gastric emptying should be carried out. The test is of great value for the diagnosis of the diagnosis, and is also an important objective evaluation method for observing the efficacy of the prokinetic drugs. The intubation method and the X-ray barium meal or the X-ray-proof marker inspection method have been used less because of more defects. It can be used to measure gastric emptying, which may be widely used in the future. Ultrasound measurement of gastric emptying is currently only used as a research method due to its high technical requirements.
2. Intragastric pressure measurement
Only when the gastric emptying test is abnormal, the examination is performed. The gastric pressure measurement in patients with gastroparesis can show abnormal gastric movement, and the lowering of gastric antrum movement after meal is the most common, and patients with gastroparesis after partial gastrectomy, The proximal gastric pressure measurement showed a low underlying tension.
3. Electrogastrogram
The surface electrogastrogram is a non-invasive method. The basic electrical rhythm of the stomach is the slow wave potential 3 times per minute, which determines the frequency and conduction direction of the gastric muscle contraction. Once the slow wave potential disappears, the gastric action potential and Stomach contraction can not occur, it has been found that various types of gastroparesis can occur abnormal gastric electrical rhythm, such as gastric tachycardia, gastric hyperactivity and gastric electrical rhythm disorder, these abnormalities can lead to delayed gastric emptying, some promote Dynamic drugs can restore it to normal.
Diagnosis
Diagnosis and differentiation of gastroparesis syndrome
If you have symptoms of gastroparesis, especially after a small number of meals, you still vomit a lot of food. After X-ray barium meal and gastroscopy are normal or mechanical (organic) obstruction is excluded, you can generally make a preliminary diagnosis of gastroparesis. Diagnosis requires gastric emptying test, intragastric pressure or electrogastrogram.
Should be differentiated from gastric organic lesions, endoscopic examination of this disease without organic lesions.
