GastroparesisSyndrome is a group of clinical symptoms characterized by delayed gastric emptying. The examination does not reveal any organic lesions in the upper gastrointestinal tract or the upper abdomen. Depending on the cause, there are two types: primary and secondary. Primary, also known as idiopathic gastroparesis, mostly occurs in young women. Gastroparesis can be divided into two types: acute and chronic, depending on the urgency of onset and duration of the disease. Chronic cases are more common, with symptoms persisting or recurring for months or even more than 10 years.
Gastroparesis can be caused by primary gastric motility disorders (idiopathic gastroparesis) or secondary to certain systemic diseases and certain gastric surgery procedures. The mechanism of gastric emptying involves the close interaction of gastric smooth muscle, the intrinsic or extrinsic nervous system of the gastrointestinal tract, the central nervous system and hormones, and abnormalities of any of these factors can lead to gastroparesis.
The etiology and mechanism of primary gastroparesis are not yet clear, but the lesion may be located in the muscular layer of the stomach or the intermuscular plexus innervating the muscular layer; secondary cases often include: (1) diabetes mellitus; (2) connective tissue disease, such as progressive systemic sclerosis (PSS); (3) gastric surgery or vagotomy; (4) infection or metabolic abnormalities; (5) central nervous system diseases and certain drugs. In addition, reduced vagal tone and intestinal hormones and peptides may also play a role. The dysmotility of gastroparesis is often manifested as follows: 1. hypokinesis of the gastric sinus and delayed gastric emptying; 2. decreased proximal gastric compliance, resulting in decreased gastric accommodation; 3. decreased proximal gastric pressure, resulting in delayed gastric fluid emptying; 4. uncoordinated gastric, pyloric, and duodenal motility. Therefore, this disease mainly manifests as delayed gastric emptying. There are often symptoms such as early satiety, postprandial epigastric fullness and epigastric discomfort after eating.
What should be done to prevent gastroparesis syndrome? A low-fat, low-fiber diet should be given to facilitate gastric emptying by eating less and more meals, mainly liquids.
Bitter and spicy clay acupuncture point treatment bitter and spicy clay is pungent, hot, strong permeability, unblocking meridians, enhancing gastric motility, promoting gastric peristalsis, restoring coordinated movement of the stomach, pylorus and duodenum. It is safe and reliable for the treatment of gastric palsy. How to use: 5 grams of bitter spicy earth (reduce by half for infants and children), make a paste with rice vinegar or boiling water, knead it into a cake, heat it and paste it on the Shenjue point (navel), fix it with adhesive tape, once a day. Can also be used with the foot three li point, the effect is better. Stomach peristalsis is obviously enhanced half an hour after applying the acupuncture point and can be cured in 30-40 days. General treatment for patients with gastroparesis should be given a low-fat, low-fiber diet with few meals and fluids to facilitate gastric emptying. As smoking slows gastric emptying, smoking should be stopped. Drugs that delay gastric emptying should be avoided (Table). Table Drugs that cause delayed gastric emptying Treatment of primary disease Diabetes.
Gastric emptying function is measured by a number of tests, but currently it is considered that 1. radionuclide gastric emptying test is preferred. 2. intragastric manometry is performed only if the gastric emptying test is abnormal. In patients with gastroparesis, intragastric manometry can show abnormal gastric motility, most commonly when the postprandial gastric sinus is hypokinetic.3. Gastric electrogram is a non-invasive method of examination. The basic electrical rhythm of the stomach is a slow-wave potential 3 times per minute, which determines the frequency and direction of gastric muscle contraction. Once the slow-wave potential disappears, gastric action potential and gastric contraction cannot occur.
If there are symptoms of gastroparesis, especially vomiting a large amount of food several hours after meal, the preliminary diagnosis of gastroparesis can be made after barium X-ray and gastroscopy are normal or mechanical (organic) obstruction is excluded. A gastric emptying test, intragastric manometry or electrogram is required to confirm the diagnosis.
What diseases can be complicated by gastroparesis? Chronic mesenteric artery occlusion, diabetes mellitus, anorexia nervosa, progressive systemic sclerosis and cancer.
Gastroparesis, also known as gastroparesis syndrome, used to be called gastric paralysis, gastric weakness, gastric retention, etc. The definition of gastroparesis is vague and usually refers to an extreme delay in gastric emptying. Idiopathic gastroparesis is a type of gastroparesis with no clear history of metabolic disease, connective tissue disease, or other diseases, and with an unclear etiology, and is characterized by postprandial fullness, recurrent eructation, nausea, episodes of dry vomiting, or vomiting, with delayed gastric emptying, decreased sinus power, and abnormal gastric electrical activity, and has a better prognosis. Secondary gastroparesis refers to the occurrence of gastroparesis due to other diseases affecting gastrointestinal motility. It is commonly associated with diabetes mellitus, abdominal surgery, systemic lupus erythematosus, progressive systemic sclerosis, systemic amyloidosis, acute autonomic neuropathy, anorexia nervosa, long-term alcoholism, hypothyroidism and the use of certain drugs. People usually include idiopathic gastroparesis in the category of gastroduodenal dysfunctional diseases.
The etiology and mechanism of primary gastroparesis are not yet clear, but the lesion may be in the muscular layer of the stomach or the intermuscular plexus innervating the muscular layer.
Secondary cases often have.
①, diabetes mellitus.
②, connective tissue disease, such as progressive systemic sclerosis (PSS).
(iii), gastric surgery or vagotomy.
④, infections or metabolic abnormalities.
⑤, central nervous system diseases and certain drugs.
In addition, reduced vagal tone and intestinal hormones and peptides may also play a role. The level of gastrin and the function of gastrin receptors may be abnormal in gastroparesis.
I. Diabetic gastroparesis (DGP)
Abnormalities of the entire gastrointestinal tract motility are often present in diabetic patients. Gastroparesis occurs in approximately 40% of patients with type I or type II diabetes who are taking oral hypoglycemic drugs.
Ferroir observed decreased gastric motility on barium x-ray in diabetic patients. 1945 Rundles first clearly described the correlation between delayed gastric emptying and diabetes. 1958 Kassander first applied the term ” diabetic gastroparesis”.
Gastrointestinal motility disorders in patients with diabetic gastroparesis are characterized by the disappearance of mobile motor complex (MMC) phase III in the interdigestive phase and postprandial hypokinesis of the gastric sinus, uncoordinated contractions of the gastric sinus, pylorus and duodenum, and pyloric spasm, resulting in delayed emptying of gastric solids.
Delayed gastric emptying is mainly due to vagal nerve damage (autonomic neuropathy), and hyperglycemia also has an inhibitory effect on gastric emptying. Guy et al. found that the morphological changes of the vagus nerve in diabetic patients were a severe reduction in the density of unmyelinated axons and a thinning of the diameter of the residual axons. In other studies, no morphological abnormalities were found in the gastric wall or abdominal vagus nerve of diabetic patients. no abnormalities were found in the interosseous plexus of DGP patients. The ability of tranylcypromine and cisapride to stimulate contraction of the gastric sinus in patients with DGP suggests that the smooth muscle function of the sinus is intact.
Post-surgical gastroparesis
Gastric surgery is often accompanied by gastroparesis. The incidence of delayed gastric emptying after vagotomy is 5% to 10%, and 28% to 40% of gastric solid emptying is delayed after vagotomy plus pyloroplasty. Vagotomy reduces fundic diastolic function, sinus contraction, and coordinated pyloric diastolic function. This results in accelerated liquid emptying and delayed solid emptying of the stomach. However, highly selective (mural cell) vagotomy only prolongs the lag phase of solid emptying and has no effect on total gastric emptying.
Gastroparesis occurs in approximately 30% of patients with peptic ulcer combined with pyloric obstruction after major gastrectomy and vagotomy. In patients with Roux-en-Y syndrome, delayed gastric emptying of the remnant stomach is also observed.
Various types of abnormal gastric slow-wave rhythms and MMC deficits can occur in postoperative gastroparesis and are also associated with delayed gastric emptying.
Anorexia nervosa
About 80% of patients with anorexia nervosa have delayed gastric solid emptying, but normal liquid emptying. Delayed gastric emptying is associated with disturbances in sinus rhythm, low fundic tone, decreased postprandial plasma norepinephrine and neurohypophyseal concentrations, and impaired autonomic function. However, patients with the same degree of weight loss without psychiatric symptoms as those with anorexia nervosa do not have significant delayed emptying.
Diseases involving gastric smooth muscle
In addition to other systemic organ lesions, these diseases often involve diffuse gastrointestinal smooth muscle involvement, resulting in impaired motor function of the intestinal tract. Although esophageal involvement is more common, gastric smooth muscle can also be involved and cause gastroparesis.
Delayed gastric emptying often occurs in progressive systemic sclerosis. The progression of this gastrointestinal motility disorder consists of two stages, namely the initial neuropathy and myopathy due to infiltration of fibrous tissue in the muscular layer.
Dermatomyositis and polymyositis can cause delayed emptying of gastric solids and/or liquids, 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 solid and liquid food. The increased tone and contractile activity of the duodenum and proximal jejunum in this disease is thought to be due to partial depolarization due to smooth muscle damage, which could theoretically increase the resistance to gastric emptying and delay gastric emptying .
In 1956, Intriere and Brown reported a case of primary amyloidosis involving only the stomach. In addition to myxomatous involvement, amyloid neuropathy and intestinal ischemia due to vascular lesions are also important causes of gastrointestinal motility disorders. Gastrointestinal symptoms occur in approximately 70% of primary and 55% of secondary amyloidosis.
V. Gastroesophageal reflux disease
About 60% of patients with gastroesophageal reflux disease have delayed gastric emptying, and it is not clear whether this abnormality is primary or secondary.
Carcinoid syndrome
In some tumor patients, gastroparesis can be part of the syndrome with carcinoid tumor. chinn et al. reported 7 cases of pulmonary carcinoid tumor, 6 of which had gastroparesis. Histological examination showed degeneration of the intermuscular plexus, reduction of neurons and axons, infiltration of inflammatory cells such as lymphocytes and plasma cells, and proliferation of glial cells, while the submucosal plexus was not affected.
VII. Ischemic gastroparesis
We recently reported 2 patients with mesenteric artery occlusion and chronic ischemia of the gastrointestinal tract who developed severe gastroparesis with disturbance of gastric electrical rhythm and associated symptoms. Six months after bypass vascular grafting, the patient’s gastric solid emptying and gastric electrical rhythm returned to normal and the symptoms disappeared.
Idiopathic gastroparesis
Gastroparesis of unknown origin accounts for approximately 50% of patients with delayed gastric emptying. These patients can be roughly divided into two groups: one with a diagnosis of functional dyspepsia and the other with diffuse gastrointestinal smooth muscle involvement, in which there is a dynamic disorder of the entire gastrointestinal tract and, in addition to gastroparesis, there are often multiple diagnoses such as irritable bowel syndrome or pseudo-intestinal obstruction.
Clinical manifestations
Gastroparesis is often characterized by
Hypokinesis of the gastric sinus and delayed gastric emptying.
The proximal gastric compliance is reduced, making the stomach less accommodating.
Reduced proximal gastric pressure, which delays gastric fluid emptying.
Gastric, pyloric, and duodenal motility are not coordinated. Therefore, the disease is mainly characterized by delayed gastric emptying. Symptoms such as early satiety, postprandial epigastric fullness and epigastric discomfort after eating are often present.
Coarse fiber food
It is advisable to adhere to the dietary treatment, small amount of meals, 6~8 meals per day, to make up for the lack of three meals; to choose foods rich in water-soluble food fiber, such as konjac, fruits, algae gel, etc., in order to facilitate gastrointestinal motility.
Avoid – Do not eat foods that are too dry, too hard or rich in coarse fiber.
If there are symptoms of gastroparesis, especially vomiting large amounts of food several hours after a meal, a preliminary diagnosis of gastroparesis can usually be made after a normal barium X-ray and gastroscopy or after excluding mechanical (organic) obstruction.
Gastric emptying test, intragastric manometry or electrogram are required to confirm the diagnosis.
Measurement of gastric emptying function
There are many methods of gastric emptying tests, but the radionuclide gastric emptying test is currently considered to be the first choice.
Intragastric manometry
This test is only performed if the gastric emptying test is abnormal. Intragastric manometry can show abnormal gastric motility in patients with gastroparesis, most commonly when there is hypokinesis of the gastric sinus after meals.
Gastric electrogram
The body surface electrogram is a non-invasive test. The basic electrical rhythm of the stomach is a slow-wave potential that occurs 3 times per minute and determines the frequency and direction of gastric muscle contraction.
Related ancillary tests
Scintigraphy: Liquid and solid test meals are labeled with 99TC and 111 molybdenum binucleotides and scanned by a λ-scintillometer to measure gastric emptying rate (GERS) and gastric half emptying time (GET1/2) at different times.
Wire technique: Gastric emptying of undigested solids was measured by taking test meals containing impermeable X-ray markers and measuring the number of retained markers in the stomach at different times.
Real-time ultrasound test: gastric emptying was observed by measuring the change in gastric sinus volume after a liquid test meal.
Respiration test: Gastric emptying is indirectly measured by measuring the amount of CO2 labeled by using nuclear carbon to label substances that are not absorbed in the stomach but are rapidly absorbed in the duodenum, which oxidizes and then expels CO2 through the respiratory tract.
Gastric image study: MRI gastric image study provides real-time human pyloric passage time and volumetric emptying information associated with gastric contraction.
Intestinal absorption test: The amount of acetaminophen is measured indirectly by using the principle that it is not absorbed in the stomach but is rapidly absorbed in the duodenum.
Gastric impedance measurement: The gastric impedance method is used to determine gastric emptying because the electrical conductivity of the test meal is different from that of the surrounding tissue. When the test meal is expelled from the stomach, it reflects different electrical impedance changes in the upper abdomen to indirectly determine gastric emptying
Gastric magnetic tracer method: The gastric emptying time is indirectly determined by taking a test meal containing a magnetic tracer to form a weak magnetic field in the stomach and using a fluxgate magnetic needle to measure the weakening gastric magnetic field with the emptying of the test meal.
Digestive tract pressure measurement
Intragastric manometry is useful diagnostically, not only to help establish a diagnosis, but also to monitor the course of a motility disorder. The methods used to determine intragastric pressure include catheterization, balloon notation, and radio telemetry. Of these, the catheter method is the most commonly used. A manometric catheter is inserted into the stomach and duodenum, a capillary perfusion system is applied, and upper gastrointestinal pressure is measured by a physiologic polysynthesizer. Most patients are found to have abnormalities in gastric or gastrointestinal pressure, mainly in the form of decreased postprandial phasic contractions, increased pyloric activity before and after meals, pyloric spasm, retrograde duodenal-pyloric-sinus contractions and irregular contractions of the proximal jejunum.
Treatment
Bitter and spicy earth acupressure treatment
Bitter and spicy earth
Bitter spicy clay is pungent, hot and penetrating, unblocks the meridians, enhances gastric motility, promotes gastric peristalsis and restores coordinated movement of the stomach, pylorus and duodenum. It is safe and reliable for treating gastroparesis with acupuncture points.
Usage
5g of bitter spicy earth (reduce by half for infants), make a paste with rice vinegar or boiling water, knead it into a cake, heat it and stick it on the Shenjue point (navel), fix it with adhesive tape, once a day. Can also be used with the foot three li point, the effect is better. Stomach peristalsis is obviously enhanced in half an hour after applying the acupuncture point, and it can be cured in 30-40 days.
General treatment
Patients with gastroparesis should be given a low-fat, low-fiber diet with few meals and mainly liquids to facilitate gastric emptying. As smoking slows gastric emptying, smoking should be stopped. Drugs that delay gastric emptying should be avoided as much as possible.
Diabetic gastroparesis Hyperglycemia should be controlled as much as possible, and some patients may improve their symptoms due to the control of hyperglycemia. Malageleda et al. reported a case of gastroparesis that disappeared after lung tumor resection and normalized gastric motility. As mentioned earlier, ischemic gastroparesis due to chronic mesenteric artery occlusion can be completely normalized after revascularization.
Prokinetic drugs
The use of prokinetic drugs is currently the most effective treatment route for most patients with gastroparesis. Prokinetic drugs are a class of drugs that restore, enhance and coordinate the systolic activity of the smooth muscles of the digestive tract and accelerate the rotation of substances in the lumen.
Carbamylmethylcholine increases the frequency and amplitude of gastric contractions, but nuclear gastric emptying tests have shown that it does not accelerate gastric emptying, so it is not considered a prokinetic drug.
These drugs can increase the frequency and amplitude of gastric sinus contraction and enhance the coordination of sinus and duodenal contraction, and are used to treat various types of gastroparesis, which can accelerate gastric emptying and improve clinical symptoms. However, the effect of long-term treatment with gastrofacial and domperidone is not very rational, while cisapride still has good efficacy in long-term application.
In recent years, the prokinetic effect of erythromycin has attracted more attention. Erythromycin acts as a gastrin receptor agonist to stimulate gastrointestinal motility, inducing a postprandial phase similar to the MMC III phase during the interdigestive period, causing powerful contractions of the gastric sinus, reducing pyloric pressure, improving the coordination of sinusoduodenal contractions, and promoting the emptying of solid food (including larger particles of undigested food).
In 1993, Richards et al. used erythromycin for the first time to treat idiopathic gastroparesis with good efficacy, and demonstrated that erythromycin, whether given intravenously, orally for a short period of time (4 weeks) or orally for a long period of time (1 to 11 months), can increase gastric solid emptying and improve clinical symptoms without significant side effects. There are no significant side effects. Erythromycin has been shown to be effective for anorexia nervosa, post-vagotomy, progressive systemic sclerosis, and gastroparesis due to chemotherapy for cancer.
For the administration of erythromycin, Camilleri recommends 3 mg/kg body weight intravenously every 8 hours, followed by 250 mg orally three times daily for up to 10 days once the patient is able to tolerate food. Patients who can tolerate erythromycin may continue to take the drug for several months as long as it is beneficial and there are no side effects.
The side effects of erythromycin include nausea, vomiting, and diarrhea. Ventricular tachycardia has been reported at high doses. Erythromycin can also cause subclinical presynaptic inhibition of the neuromuscular junction, which can worsen the condition in patients with myasthenia gravis. The induction of resistant strains of erythromycin needs to be considered for long-term use, but the prokinetic but not antimicrobial activity of erythromycin derivatives EM-523 and EM-574 can solve this problem.
Gastrin Peeters et al. treated six patients with severe diabetic gastroparesis with intravenous infusion of gastrin, resulting in significantly faster gastric emptying of both liquids and solids. Therefore, gastrodin may provide a new tool for the treatment of gastroparesis in the future.
Prokinetic drugs with different mechanisms of action can be combined if necessary, or several drugs can be used alternately to avoid side effects and rapid tolerance reactions due to high doses or long-term application of a single drug.
Surgical treatment
Surgery may be used for a small number of patients with refractory gastroparesis. Significant symptom relief has been reported in some patients with idiopathic gastroparesis after major gastrectomy and gastrojejunostomy. Yeung et al. reported a diabetic patient with refractory gastroparesis after vagotomy and pyloroplasty for duodenal ulcer, resulting in intractable nausea and vomiting, which was not treated with prokinetic drugs and was treated with percutaneous gastrostomy cannulation under X-ray fluoroscopy. long-term remission.
Other treatments
Gastric Pacing can normalize the disturbed slow wave rhythm of gastric electricity, thus restoring normal gastric motility. However, its technical problems and its role in the treatment of gastroparesis need further study.
If the symptoms of gastroparesis are present, especially vomiting large amounts of food even after a few minutes of meal, the preliminary diagnosis of gastroparesis can be made after the X-ray barium meal and gastroscopy are normal or mechanical (organic) obstruction is excluded. To confirm the diagnosis, gastric emptying test, intragastric manometry or gastroelectrographic examination is required.
Ancillary tests 1. gastric emptying function measurement 2. intragastric manometry 3. gastric electrogram 4. 3D gastric balance repair method
Recommended recipes
Pineapple and Bitter Melon Soup
Pineapple and bitter melon soup
Ingredients: 25g fresh or canned pineapple slices, 35g bitter melon, 5g carrot, water
Seasoning: a little salt
Production process.
Wash all ingredients; cut pineapple into thin slices (if canned pineapple, then cut into small pieces); remove seeds from bitter melon and slice; peel and slice carrots and set aside.
Put water into a pot, turn on medium heat, add bitter melon, carrot and pineapple into the pot, wait for the water to boil, then turn the heat to cook the ingredients, add a little salt to taste as appropriate.
Precautions before treatment
I. General treatment
Patients with gastroparesis should be given a low-fat, low-fiber diet, with few meals and fluids to facilitate gastric emptying. As smoking can slow down gastric emptying, smoking should be stopped.
Treatment of primary disease
Diabetic gastroparesis should control hyperglycemia as much as possible, and some patients can improve their symptoms due to the control of hyperglycemia. Malageleda et al. reported a case of gastroparesis after lung tumor resection in which the symptoms of gastroparesis disappeared and gastric motility returned to normal. As mentioned earlier, ischemic gastroparesis due to chronic mesenteric artery occlusion can be completely restored after revascularization.
III. Prokinetic drugs
The application of prokinetic drugs is currently the most effective treatment route for most patients with gastroparesis. Shenzhen Pengcheng gastrointestinal experts said that prokinetic drugs are a class of drugs that can restore, enhance and coordinate the contraction activity of the smooth muscle of the digestive tract and accelerate the rotation of substances in the lumen.
Fourth, surgical treatment
For a small number of patients with refractory gastroparesis can be treated surgically. There are reports of significant symptom reduction after major gastrectomy and gastrojejunostomy in some patients with idiopathic gastroparesis. Yeung et al. reported a diabetic patient with refractory gastroparesis after vagotomy and pyloroplasty for duodenal ulcer, resulting in intractable nausea and vomiting, which was treated with percutaneous gastrostomy tube under X-ray fluoroscopy and achieved long-term remission.
V. Other therapies
Gastric Pacing can normalize the disturbed gastric slow wave rhythm and restore normal gastric motility, and it has been tried to treat postoperative gastroparesis with disturbed gastric rhythm with certain efficacy. However, its technical problems and its role in the treatment of gastroparesis need further study.
Prevention
How should gastroparesis syndrome be prevented? A low-fat, low-fiber diet with few meals and fluids should be given to facilitate gastric emptying, and since smoking slows gastric emptying, smoking cessation should be given, and drugs that delay gastric emptying should be avoided.
Complications
What are the possible complications of gastroparesis syndrome? Chronic mesenteric artery occlusion, diabetes mellitus, anorexia nervosa, progressive systemic sclerosis and cancer