Gastroesophageal reflux disease (hereinafter referred to as GERD) is a series of diseases caused by the reflux of stomach and duodenal contents into the esophagus or further into the airway, otorhinolaryngology and oral cavity for some reasons.
I. Epidemiology
1, incidence GERD is more common in Europe and the United States, as reported, 44 people in the United States have at least once a month reflux symptoms, 20 of the people Dad Sko Lia儆幸淮戳髦矗辉谖夜⒉÷式系停本更新厍戳飨喙寵物 (blowing M5 decorative glass).3, Shanghai is 7.68.
2.Age It is generally believed that the incidence of GESD increases with age, and the peak age of incidence is 40-60 years old.
3.Gender There are more males than females.
4, risk factors such as smoking, alcohol consumption, mental distress (such as fatigue, tension, anger, etc.), obesity, H. pylori and genetic factors.
II. Etiology and pathogenesis
(a) The simplified model of the digestive tract is: a pouch (stomach), two tubes (esophagus, intestinal tube), two mouths (cardia, pylorus), plus a meridian (vagus nerve). The esophagus goes in, the intestinal tube goes out, and the stomach stays a little; and the function of the vagus nerve is the fundamental guarantee of the proper function of the entire digestive tract. Normal people mostly have gastroesophageal reflux, but it does not cause transport to Cheltenham lining “Xuzibi (19) is a physiological gastroesophageal reflux in the wall. When the body’s defense mechanism is weakened, the pathological gastroesophageal reflux disease is caused by tissue damage to the relevant parts of the body, which affects the health and life of the person. To find the cause, there must be severe gastroesophageal reflux that needs to be treated.
(b) Why does severe GERD occur? We still need to look for the causes from the “two tubes, one pouch and one meridian”.
1, outlet (tube) malfunction.
(1) such as biliary tract, pylorus, duodenum inflammation (such as H. pylori infection, etc.), swelling, spasm
(1) such as inflammation of the bile duct, pylorus, duodenum (such as Helicobacter pylori infection, etc.), swelling, spasm, tumor, etc. can lead to narrowing of the outlet (duct), obstruction of gastric emptying, retention of z in the stomach, increased gastric pressure (more than acid reflux)
(2) or pylorus relaxation, or weak contraction of the gastric fundus resulting in backflow of duodenal fluid into the stomach (the cause of alkaline reflux).
2, the entrance (tube) relaxation: can not manage the upward impact of the reflux, such as
(1), lower esophageal scraping muscle (LES) relaxation. It is thought to be the main pathogenesis of this disease. The causes are mostly congenital factors: such as congenital dysplasia of the LES, hiatal hernia, etc.; acquired causes are very complex: such as drugs: gastrointestinal hormones (pancreatic u hormones, etc.), adrenergic stimulants; food: such as drinking alcohol, strong tea, fat, chocolate, etc.; other: such as smoking, gastric ulcer (increased gastric acid) and pregnancy, obesity, large amounts of ascites, etc. resulting in increased abdominal pressure, LES relaxation and other factors aggravate the herniation of the stomach into the esophagus (2), hiatal hernia.
(2), hiatal hernia; refers to the stomach rising into the thoracic cavity, so that the esophagogastric junction is located above the diaphragm. It is mostly a congenital factor. If the sliding hernia can cause incomplete closure of the esophagogastric junction, the spout is relaxed and easy to reflux.
3, pouch (gastric) dysfunction (or vagus nerve dysfunction): vagus nerve transient or persistent dysfunction can occur in the following situations
(1) weakened function weak contraction of the gastric sinus, gastric peristalsis, obstructed emptying, increased intragastric pressure, prone to reflux.
(2) hyperfunction Increased excitability of the vagus nerve, resulting in increased gastroduodenal secretion. High levels of gastric acid, pepsin and duodenal fluid can reduce LES tone and relax the spout, and can cause gastric spasm. Both are likely to cause reflux.
(3) Gastroduodenal retroperistalsis, will reflux.
The relationship between duodenal retroperistalsis, abnormal opening of the pylorus, and dysfunctional (weakened) gastric sinus movement determines the occurrence of bile reflux esophagitis and the amount of reflux.
4, genetic factors. The disease has obvious family predilection, manifested as LES dysplasia, hiatal hernia, vagus nerve dysfunction, etc.
(C) Why does reflux produce a series of symptoms (i.e. GERD)? The occurrence of GERD is closely related to the following factors in addition to the above-mentioned anatomical and physiological variation of the digestive tract.
(1) Weakened or damaged body’s own defense function (anti-reflux barrier), including.
(1), the weakened function of the esophagus’ own peristalsis (e.g., in the elderly), which decreases the ability to automatically clear reflux, delaying the time for reflux to damage the esophageal mucosa.
(2), esophageal contouring dysfunction: for example, saliva secretion is reduced (1000-1500ml/h in normal people), which cannot effectively flush and neutralize acidic and alkaline reflux to the esophagus, which can easily cause damage to the esophagus.
(3) Damage to the anti-reflux barrier of the esophageal mucosa: the squamous epithelial cells of the esophageal mucosa are weakened by the acidic or alkaline reflux, and cannot effectively resist the erosion from outside.
2. The high acid content of the regurgitant|stimulates acid-sensitive receptors in the esophageal (distal) mucosa, activating the vagal reflex arc from the esophagus to the lungs, causing bronchospasm and asthma (esophagus and trachea are homologous in the embryonic stage).
3, Acid or alkaline regurgitant is inhaled into the airway through the larynx as an allergen and excites or aggravates asthma.
4.After the regurgitant reaches a certain part of the arrythmus, the stimulation, obstruction, infection, etc. produced and the physiological and pathological changes of the part r of the arrythmus are secondary, triggering the corresponding clinical symptoms.
5, the elderly due to muscle relaxation, muscle strength decreased, esophageal peristaltic function decreased; coupled with obesity, constipation, and gastric emptying delay, etc. to promote the increase in gastric pressure, aggravate the destruction of the anti-reflux barrier, so that GERD increased; the elderly saliva points to reduce, so that the esophageal clearance function decreased.
III. Clinical manifestations
The symptoms of GERD patients are related to the quality and quantity of the refluxed material, the location of the organ it reaches, the time it stays and the damage it causes, as well as the reactivity of the organism. Refluxes often include bile, duodenal fluid, gastric contents and gastrointestinal putrefaction ∑Tanyuan Blossom and Blossom, and (10) the supply of careful and careful products.
GERD has a wide range of clinical manifestations, which can be divided into four categories: first, symptoms of the gastrointestinal tract mainly due to reflux, including vomiting, belching, acid reflux and regurgitation; second, symptoms of esophagitis due to irritation of the esophagus by reflux, including heartburn, retrosternal pain and dysphagia; third, symptoms of extra-esophageal reflux irritation other than esophagitis, such as cough, asthma, otorhinolaryngology and oral symptoms; fourth, other manifestations, such as pharyngeal Foreign body feeling, cotton ball feeling, blockage feeling, etc., but no real swallowing difficulties.
The following list is only the symptoms that GERD patients may have, not everyone has them. This article describes them in terms of the anatomical sites (tissues and organs) where the reflux may reach, and possibly in chronological order. The frequency of each type of symptom (to be counted).
Some patients have pre-reflux symptoms, such as abdominal, abdominal pain, anorexia and other dyspeptic symptoms.
(a) Reflux (containing gastric gas) reaches the esophagus (upper part) through the cardia :.
1, stimulate the esophageal mucosa, causing acute and chronic inflammation can be out of F heartburn, thorny mackerel (12) yuk choke ⒈ punishment base Ⅰ crab (6) cheer mowing (9) electron world selection (6) car music cut buck take S fishy shun broken annihilation Gancher Qian poke to eat the main symptoms of esophagitis.
The following are mostly referred to as extraesophageal symptoms of GERD. Clinical also many, and more harmful.
2. Stimulation of acid-sensitive receptors in the esophageal mucosa activates the vagal plexus from the esophagus to the trachea, causing bronchospasm to severe coughing, shortness of breath, and wheezing. As mentioned later, the inhalation of micro-particles directly into the airway during reflux is also an important cause of coughing and wheezing. Furthermore, acid infiltration of the esophagus causes the release of transmitters from cholinergic nerve endings that act on the airway (bronchial) microvasculature, resulting in increased glandular secretion, vascular exudation, and sputum! In addition, the increased intra-abdominal pressure due to coughing can in turn aggravate or induce asthma!!! In this way, a continuous feedback loop is established between GERD and chronic cough, making the two aggravate each other.
Reflux cough (or GERD-associated cough) is characterized by chronic, paroxysmal coughing, or symptoms of increased intracranial pressure such as back pain, leg pain, or headache due to severe coughing; spitting of large amounts of white foamy sputum or coughing up food residues; worsening after eating or sudden attacks during sleep at night; or reflux symptoms such as heartburn, belching, or acid reflux; other respiratory diseases can be excluded or treated as such (hormones, bronchial dilators, antibiotics, etc.) are ineffective; cough symptoms disappear or are significantly relieved after anti-reflux treatment.
(b) The reflux is then directed upward, into the laryngopharynx, and the following six conditions can occur.
1. Impacting the entrance pharynx.
(1) into the pharynx: acute and chronic pharyngitis, pharyngeal foreign body sensation can occur; long-term stimulation of the pharyngeal mucosa by stomach acid can lead to chronic hyperplasia, hypertrophy, mucosal white spots, etc.
(2) Through the pharynx to the oral cavity.
(1) Vomiting, belching (gas reflux), acid reflux (acid reflux), regurgitation (patient without nausea and vomiting action), or vomiting of bile (alkaline reflux) may occur.
② oral mucosal lesions: erosion, incurable recurrent oral ulcers, lichen planus, mucosal white spots, etc.; ③ acid erosion of teeth, dental caries; unexplained halitosis, etc.
2, impact into the nasopharynx: into the top of the nasopharynx: (pharyngeal fossa, pharyngeal bullae mouth)
It can cause eustachian tube inflammation, swelling, and canal obstruction; patients can develop otalgia (sometimes become the cause of persistent, non-smellable tinnitus), ear occlusion, exudative otitis media, purulent otitis media and other ear diseases. According to the note: Some people in Shanghai have found gastric fluid components in the ear secretions.
3. Entering the nasal cavity through the posterior nasal aperture.
(1) stimulate the nasal mucosa, congestion, edema, hypertrophy, can appear nasal congestion, runny nose, snorting and other symptoms of allergic rhinitis and nasal turbinate hypertrophy, nasal polyps, etc.
(2) Obstruction of the natural opening of the paranasal sinuses, resulting in acute and chronic sinusitis, cysts, polyps, tumors, etc.
(3) Obstruction of the natural opening of the nasolacrimal duct, causing acute and chronic dacryocystitis and ocular conjunctivitis
(4) Impacting the epiglottis (laryngeal surface) via the laryngopharynx forward: it can cause the taking of the bilirubin
(5) Spraying downward into the laryngeal cavity (vocal fissure) through the epiglottis: it can cause laryngeal spasm, laryngeal pain, foreign body feeling, dysphonia, laryngeal polyp, etc. in chronic cases.
(6) The laryngeal valve (laryngeal opening) and then downward impact on the trachea, bronchus, into the lungs: can cause.
(1) violent coughing and coughing up sputum, which may contain food residues.
② Bronchospasm, cough, chest tightness, shortness of breath.
③ aspiration pneumonia, chronic inflammation of lung bronchus, emphysema, pulmonary atelectasis and other lung function damage.
It is currently believed that gastroesophageal reflux causing asthma may be related to the following mechanisms.
1. Reflux theory (i.e., microinhalation theory of intraesophageal reflux): trace amounts of intraesophageal reflux (gastric acid) enter the trachea: one can stimulate vagal nerve receptors in the airway causing bronchospasm; second, acidic (or alkaline) reflux stimulates and damages the respiratory mucosa causing chemical inflammation; or thus brings in bacteria in the gastrointestinal tract causing bacterial inflammation; third, due to reflux stimulation, the airway mucosa reactivity is increased and enhances the sensitivity of asthma patients to various triggering factors.
2. Reflex theory: Reflux does not enter the airway (or only the distal esophagus): firstly, it can also reflexively cause bronchospasm through the vagus plexus (widely distributed in the esophagus and trachea) and increase the resistance; secondly, reflux causes damage to the esophageal mucosa, the surface mucosa of the esophagus is eroded and the vagus nerve endings are exposed, which increases the sensitivity to the reflux and is more likely to reflexively and indirectly cause bronchospasm after stimulation.
The above shows that GERD may cause asthma, but not all GERD patients will have asthma complications, because in addition to the aforementioned first barrier, there is also a second barrier in the human body – the anti-reflux function outside the esophagus; it can effectively prevent the micro aspiration of reflux in the esophagus into the airway, even if a small amount enters the airway, there is still a sufficient gadfly which is Χ cloud A malefactor
The anti-reflux function outside the esophagus determines the occurrence of reflux asthma or not, mostly through the neuroreflex mechanism, so there is a reflex theory. This includes
(1) When GERD occurs, the vocal cords and arytenoid cartilage are invaginated, and the invaginated arytenoid cartilage reaches the base of the epiglottis, which prevents reflux from entering the closed vocal hilum.
(2) During reflux, sudden localized or even widespread dilatation of the esophagus can reflexively cause closure of the vocal fold.
(3) Other anti-reflux mechanisms: including the cough reflex and ciliary movements on the mucosal surfaces of the trachea and bronchi.
Attachment: clinical symptoms of bile reflux gastritis due to duodenal fluid reflux: (1) discomfort and fullness in the stomach, aggravated after meals; (2) chilling of the stomach; (3) may be accompanied by abdominal, ke (5) incurrence of this choice (1) tucking (Huanglong) (10) just gusseted woven (6) j decompensation, wasting, etc.; (4) in severe cases, gastric bleeding, vomiting blood, black stool.
IV. Examination and diagnosis
At present, the diagnosis of GERD mainly relies on a comprehensive medical history (clinical features) and the efficacy judgment after drug (PPI) test treatment (which can be used as a diagnostic basis for acid reflux). Some tests can confirm the diagnosis, but they are expensive and not easy to purchase, such as 24h esophageal PH monitor. Commonly used examination methods are
(a) General examination (physical examination): pay attention to whether the patient is too obese, whether there are complications such as stomatitis, acid erosion of teeth, pharyngitis, chronic cough, and excessive sputum. Chest X-ray, ECG (mandatory for patients with a history of chest pain episodes gastroduodenal); children patients should be asked whether vomiting, nocturnal crying, anorexia and developmental status.
(b), upper gastrointestinal tract ^ meal X-ray: pay attention to the presence of reflux of intestinal contents into the esophagus during abdominal pressure; esophageal hiatal hernia or esophageal stricture; and to understand duodenal problems and exclude masses.
(iii) Endoscopy and biopsy: Approximately 50% of patients can lace up and ramie GERD based on what they see under endoscopy, but a negative result cannot exclude the presence of GERD. Fiberoptic gastroscopy can observe the condition of the esophageal mucosa, whether the spout is relaxed, the presence of hiatal hernia, and gastric and decubitus lesions. Patients with alkaline reflux may see a high volume of gastric juice with a grass-green color; gastric mucosa is congested, edematous, and eroded; in some cases, the pyloric portal may also be seen to be open and bile is refluxing from the duodenum through the pyloric portal to the stomach. Endoscopically, the esophageal mucosal lesions can be classified into five grades.
Grade 1: normal mucosa.
Grade 1: a non-fused lesion in one or several areas of the lower esophagus that exhibits congestion, or is accompanied by exudation.
Grade 2: a fused lesion, but not yet a pericyclic lesion, manifesting as congestion, erosion and exudation.
Grade 3: a pericyclic lesion with a table F of erosions and exudations.
Grade 4: shows chronic lesions with ulceration, stricture, and Barrett’s esophagus. That is: after the mucosa of the ulcer heals in chronic reflux patients, the new epithelium is replaced by the columnar epithelium of the esophagogastric junction (not the original squamous epithelium), and when the columnar epithelium of the upper cardia exceeds 3 cm, it is called Barrett’s esophagus, which is prone to carcinogenesis!
(d) Esophageal acid drip test: the patient takes a sitting position, cuttings nasogastric tube. If there is no discomfort, then drip 0.1ml of hydrochloric acid in the same way for 15min, and if there is pain or burning sensation behind the sternum, it is positive. Use sparingly.
(E), esophageal manometry: LES degree and site, LES pressure, LES relaxation pressure, esophageal body pressure, upper esophageal scraping muscle pressure (UES) can be measured.
and if it is <6mmHg, t is easy to reflux.
Esophageal manometry cannot respond to the presence of reflux, but it can directly respond to pressure changes in the lumen of the esophagus, understand the peristaltic function of the esophagus, the pressure of the lower esophageal scrapers and the frequency of transient LES relaxation, and exclude some functional esophageal diseases. It is mostly used to determine the site of LES before acid measurement and to understand the function of LES before anti-reflux surgery.
(vi) 24h esophageal PH monitoring.
The application of portable PH recorder and continuous monitoring of esophageal PH for 24 hours in physiological state can provide guest evidence of the presence of acid reflux in the esophagus and is recognized as an important diagnostic basis for GERD. Especially in patients with atypical symptoms, or patients with typical symptoms but ineffective treatment, must be checked.
Method: The esophageal pressure is measured first to determine the LES site, and the electrode is placed 5em above the LES through the nose with a portable PH monitor and connected to a box outside the body. After 24 hours of monitoring, the computer analyzes, displays, stores and prints.
There is usually one electrode on the catheter, but there are also multiple electrodes on the catheter, i.e., the stomach, distal esophagus and proximal (upper sphincter) can be monitored simultaneously. In addition to detecting acid reflux in the lower esophagus it is also possible to measure acid exposure below the upper esophageal sphincter (UES). This can be used to detect aspiration due to reflux in patients with chronic cough, asthma, or hoarseness.
Result determination: A normal intraesophageal pH of 5?5 to 7?0 < 4 is considered an indicator of acid reflux. < p="">
Six parameters are commonly used.
1, the total percentage time of PH <4 in 24h; (the highest positive rate)
2. upright position: percentage time with PH <4; < p="">
3, supine position: percent time with PH <4; < p="">
4, total number of refluxes in 24h.
5, number of refluxes with L longer than 5 min.
6, duration of reflux for the most L
In conclusion, 24h esophageal PH monitoring can show whether the patient has pathological reflux and can detect gastroesophageal reflux ~pieces where PH drops from above 4 to below 4; while reflux with PH ≥ 4 (alkaline reflux), t cannot be identified.
(vii), nuclear scan: make the patient lie flat, drink a test meal calibrated with nuclear, and scan under a scintillation camera, which can quantitatively detect gastroesophageal reflux. The advantage of this technique is that it is simple, fast, painless, and can rapidly detect postprandial reflux (61); the disadvantage is that the sensitivity and specificity are not high, and because reflux is mostly intermittent, most reflux is difficult to capture.
(H) Intragastric aspirate determination: used to diagnose alkaline reflux. The method is cuttings gastric tube aspiration: a fasting, two postprandial gastric juice, the determination of bile acid content; such as fasting basic gastric acid secretion (BAO) <3?0mmol / h, bile acid > 30ug / mlt can confirm the diagnosis
(ix) 24h esophageal impedance DPH monitoring: This is a latest technology introduced from Germany in recent years. It combines esophageal impedance monitoring and PH monitoring together, and can determine various forms of gastroesophageal reflux, such as acid reflux, alkaline reflux, gas reflux and mixed reflux. It is still in the initial stage in China.
V. Treatment.
(a) General treatment: Adjustment of raw put way should be the basic measure for the treatment of GERD. It has obvious effect on 25% of patients.
1. Raise the head of the bed 15-20cm when sleeping. i.e. use gravity to remove the acid refluxed to the esophagus as soon as possible and reduce the reflux at night.
2, control: fat, chocolate, strong tea, carbonated drinks, acid food, etc. because they can reduce LES tension; tobacco, alcohol can weaken the acid contouring function of the esophagus, reduce LES pressure, weaken the protective function of the esophageal epithelium and aggravate the injury.
3, 3 hours before bedtime, not full, reduce abdominal pressure, reduce night reflux.
4, adjust psychological factors, such as tight, anxiety, sadness, depression and other emotions only should be, to alleviate the central nervous (brain) to the adverse reaction of the gastrointestinal vegetative nerves; improve sleep, do more outdoor activities, strengthen physical exercise, and actively participate in social activities.
(ii), drug treatment.
Objective: to reduce reflux and relieve symptoms; to reduce the damage of reflux on esophageal mucosa, to enhance the anti-reflux defense function of esophageal mucosa, to cure esophagitis; to prevent recurrence; to prevent and treat important complications.
Commonly used drugs.
1.Lower stomach acid: for acid reflux
(1) neutralize gastric acid with an acidifier (a weak alkaline drug) to reduce the activity of pepsin and decrease the damage to the esophageal mucosa from acid reflux. In addition, alkaline drugs themselves have the effect of increasing LES tone.
(2) H2 receptor antagonist q agents (H2RAS).
Principle: These drugs compete with histamine for H2 receptors on gastric lining cells and bind to them to inhibit the acid secretion effect of histamine stimulated lining cells and reduce gastric acid secretion.
At present, there are four kinds of H2 receptor blockers widely used in clinical practice: cimetidine, ranitidine, famotidine, and nizatidine.
(3) Proton pump inhibitor (PPI).
Principle: There are many H+-K+ ATPases (also known as proton pumps) distributed on the cell membrane of the secretory tubules of the gastric wall cells, which can pump the extracellular K+ into the cells and pump the intracellular H+ out; H+ and Cl+ combine to form gastric acid. Proton pump inhibitor (PPI) can inhibit the activity of this enzyme and produce stronger and longer-lasting acid inhibiting effect than H2 receptor inhibitor.
Representative drugs: omeprazole, lansoprazole, mixed toltrazole, esomeprazole, etc.
2.Promote the emptying of esophagus and stomach: power drugs Clinically used for various types of GERD (acid reflux, alkaline reflux, gas reflux or mixed reflux)
(1) Dopamine antagonists: These drugs can increase LES tension and promote the emptying of the esophagus and stomach. Package scraping: ① Metoclopramide (Gastrodipine) for a generation, 10-20mg, 3-4 times/day, should not be used for a long time in the elderly. (2) Domperidone (Marginalin) for the second generation, 10-20mg, 3-4 times / day; take before bed or before meals. Women should not be used for a long time.
(2) cisapride (Prebux capsule), mosapride: for the third generation of power drugs, through the intestinal plexus postganglionic nerve fibers release acetylcholine to inhibit duodenal retrograde peristalsis, increase the pyloric scraping muscle force, promote burst esophagus, gastric peristalsis and emptying. 10 ~ 20mg, 3 ~ 4 times / day, no adverse reactions.
(3) Cholinergic drugs: enhance LES force, promote esophageal contraction and accelerate emptying. Such as uracholide, 25mg, 3-4 times / day.
(4) new drugs: trimebutine maleate (Shu Li Qi Neng), the role is to adjust the gastrointestinal nerve function, when weak can be enhanced, when hyperactive back to normal. It is very ideal gastrointestinal motility drugs.
3.Mucosal protective agents.
(1) Aluminum thioglycollate: It is a topical agent that can adhere to the surface of esophageal mucosa and (provide physical barrier) resist the leaching of acidic reflux on esophageal mucosa. Does not affect the secretion of gastric acid and pepsin, and has no effect on LES pressure.
(2) magnesium aluminum carbonate: can be combined with reflux bile acid salt in an acidic environment, reduce the damage to the gastric mucosa, mostly used for alkaline reflux.
4, other: most of the combination of drugs, such as H peal RAS plus power drugs; or PPI plus power drugs, etc.. Patients with pulmonary infection still need to use antibiotics and other comprehensive treatment.
(C), surgical treatment.
Surgical indications.
1, cases with serious complications, such as asthma, laryngospasm.
2.Cases with esophageal hiatal hernia and other factors causing cardia relaxation.
3, cases with typical symptoms and ineffective conservative treatment; or effective drug treatment, but the patient does not original L-phase medication.
Surgical options 1, fundoplication: the purpose is to repair the hiatal hernia, shrink the spouting mouth, increase the fundic force, enhance the LES force, and control reflux. 2, radiofrequency therapy: the method is to cut a radiofrequency treatment catheter into the esophagogastric junction (i.e. LES site) under endoscopic guidance, and apply the radiofrequency treatment instrument for multi-level, multi-point cautery. The main principle of action is to cause tissue destruction through thermal energy. Regeneration, guide collagen fiber contraction, reconstruction, and block the nerve pathway, thus increasing the thickness and pressure of the lower esophageal scraping muscle, reducing transient scraping muscle relaxation, to prevent the effect of gastroesophageal reflux.