Gastroesophageal reflux disease

Introduction to gastroesophageal reflux disease Gastro-esophageal reflux disease (GERD) refers to a disease in which the contents of the stomach and duodenum are reversed into the esophagus to cause clinical symptoms and/or esophageal inflammation. The reflux is mainly gastric acid and pepsin. There may be duodenal juice, bile acid, pancreatic juice, etc. The former is more common in clinical practice. The latter is mainly seen in postoperative gastrectomy, gastrointestinal anastomosis, and esophagojejunostomy. Patients with GERD may have only clinical symptoms. No esophageal inflammation, the clinical symptoms of esophageal inflammation are not necessarily parallel with the degree of inflammation. There are physiological and pathological points, pathological gastroesophageal reflux, mild cause discomfort, vomiting, severe cases can cause esophagitis and pulmonary inhalation syndrome, and even suffocation and death. basic knowledge The proportion of illness: 0.02% Susceptible people: no special people Mode of infection: non-infectious Complications: esophageal stricture congenital short esophagus pyloric obstruction hiccup

Causes of gastroesophageal reflux disease

(1) Causes of the disease

There are many factors that cause esophageal damage, which can be summarized as.

1. Esophageal hiatal hernia In the past 40 years, the role of esophageal hiatal hernia in the pathogenesis and pathophysiology of gastroesophageal reflux is a hot topic of research, representative research conclusions such as.

The risk of gastroesophageal reflux in esophageal hiatus hernia may be related to the following factors: 1 reducing acid scavenging capacity; 2 remaining gastric duodenal reflux refluxing into the esophagus; 3 damaging the sphincter of the esophagogastric junction The role of epidemiological investigations shows that in patients with moderate and severe GERD, the incidence of esophageal hiatal hernia is more, 50% to 60% of patients with esophageal hiatal hernia have endoscopic findings of esophagitis, >90% Patients with esophagitis seen in the mirror have esophageal hiatal hernia, the size of esophageal hiatal hernia and LES pressure, and the relationship between the two is the determinant of the ability to close the gastroesophageal junction. A patient with both LES pressure and a large esophageal hiatus hernia When the intra-abdominal pressure is suddenly increased, the chance of gastroesophageal reflux is many times higher than that of a patient with only LES pressure and no esophageal hiatus hernia. The study also proves that the size of the esophageal hiatus is increased and the LES pressure is more decline.

The modern concept supports the fact that for patients with reflux symptoms, the size of esophageal hiatal hernia is the main factor determining the degree of esophagitis. The effect of LES stress and gender is worse, but it is still a causative factor, 24hpH monitoring abnormality and The size of the esophageal hiatus hernia is clearly related.

2. The relationship between obesity and obesity and GERD is still unclear. Whether obese patients are more susceptible to esophageal hiatal hernia is not conclusive. There are many studies on the relationship between obesity and esophageal hiatal hernia, esophagitis, gastric emptying and pH monitoring. For example, Wright (1983) pointed out that body surface area has nothing to do with gastric emptying. Mercer (1985) believes that the average pressure gradient between the obese reflux and the esophagus and stomach is significantly larger than that of the non-refluxed thin person; Through the prolongation of time, the acid contact time of the esophageal mucosa was increased. Mercer (1987) also pointed out that there was no significant difference in the LES pressure between lean and fat people. Excessive obesity (more than 5% of body mass index) was more common in patients with esophageal hiatal hernia and esophagitis. Human (Stene Larsen, 1988), Maddox (1989) showed that compared with the control group, fat foods in the solid food and liquid foods were delayed in gastric emptying and esophageal emptying was delayed. Hutson (1993) found that the two groups were The gastric emptying rate was similar, and the average weight loss was 8.3%. The Rigaud (1995) study showed that the total number of reflux was significantly correlated with body mass index, fat intake, and delayed gastric emptying. Gastroesophageal reflux in obese patients was not Increase After dropping 10kg, the subjective performance and objective performance of reflux did not improve (Kjellin, 1996). After the weight loss of fat people, the average pH did not change (Mathus-Vliegen, 1996). It can be seen that the above results are inconsistent, but in any case, generally It is considered that the gastroesophageal reflux in fat people is more common. Regardless of the conclusions of many studies, the concept that obesity is a pathophysiological factor causing gastroesophageal reflux is widely accepted. Obviously, it is necessary to further obesity and reflux. A detailed study of the relationship between them.

3. Drinking alcohol can inhibit the acid scavenging ability of esophagus, impair esophageal motor function, and reduce LES pressure. Keshavarnzian (1987) demonstrated that intravenous application of ethanol 0.8g/kg can moderately reduce esophageal contraction amplitude, Hogan et al. (1972) Study, giving 350ml whiskey (containing 104g alcohol) can damage the esophageal push movement and reduce LES pressure, alcohol can reduce the function of clearing the esophageal acid, reduce the salivary secretion of the parotid gland, all have the effect of aggravating GERD, alcohol can cause normal Gastroesophageal reflux in healthy young volunteers, other evidences also suggest that drinking alcohol has the risk of increasing gastroesophageal reflux, both because of alcohol lowering LES pressure and lowering the acid scavenging capacity of the esophagus. According to observations of normal volunteers, the literature advocates avoiding Rapid drinking of more than 40 ~ 45g alcohol, can prevent gastroesophageal reflux, in addition, ethanol also affects gastric acid secretion and serum gastrin levels to varying degrees.

4. Smoking and smoking can lead to prolonged esophageal acid clearance, which is a decrease in saliva secretion. Even without reflux symptoms, smokers' acid clearance time is 50% longer than non-smokers; HCO-3 in smokers' saliva The content is only 60% of non-smokers of the same age. The reduction of saliva secretion in smokers is caused by anticholinergic action. Just as the patient uses anticholinergic drugs and saliva is reduced, esophageal pressure measurement shows that 2 consecutive cigarettes are smoked. The pressure of LES decreased, and the pressure returned to normal within 2 to 3 minutes after stopping smoking. Stanciu et al. (1972) observed 25 long-term smokers with heartburn symptoms by pressure measurement and pH monitoring. The LES pressure decreased significantly within 1 to 4 minutes after smoking. The pressure returned to the original level within 3 to 8 minutes after the end of smoking, and the number of reflux measurements measured by pH monitoring increased significantly. Pehl et al. (1997) studied 280 people with reflux symptoms and observed whether smoking and smoking cessation affected their pH monitoring. The results prove that there is no impact.

It is not yet certain that smoking can increase the risk of gastroesophageal reflux, but the literature exemplifies that smoking can reduce LES pressure, cough causes reflux, increases tLESRs, and reduces salivation, thus prolonging the pathophysiological mechanism of GERD. Esophageal acid clearance time, tobacco has a stimulating effect on the esophageal epithelium, etc. Many studies have shown that smoking increases the complications of reflux, such as erosive esophagitis, which also has the consequences of severe reflux, such as Barrett's esophagus and adenocarcinoma.

5. Drugs Many drugs affect the function of the esophagus and stomach, and promote the occurrence of reflux. The effects of these drugs are nothing more than changing the pressure of LES, affecting esophageal movement and gastric emptying.

(1) Anticholinergic drugs: The most important cholinergic neurotransmitter is acetylcholine, which acts directly on LES smooth muscle and increases its pressure. In addition, metoclopramide, domperidone and cisapride increase indirectly by releasing acetylcholine. LES pressure, acetylcholine antagonist atropine, can reduce LES pressure, easy to cause gastroesophageal reflux, there are experiments to prove that the application of atropine to reduce LES pressure, the mechanism of reflux caused by the increase in the number of tLESRs, and inhibit the tension of the foot However, atropine lowers the LES pressure and does not cause gastroesophageal reflux in normal people. It is to suppress tLESRs to reduce the reflux frequency.

(2) Theophylline: The most common jaundice affecting gastroesophageal reflux is caffeine and theophylline, which can reduce LES pressure. Experiments have shown that normal human oral theophylline can reduce LES pressure by 14% and cause reflux. Theophylline also stimulates gastric acid secretion and regurgitation occurs under low tension in the LES.

(3) Calcium channel blockers: 3 types of drugs with different structures, diltiazem, verapamil (isopidine) and nifedipine (heart pain), these drugs can relieve pain and discomfort caused by esophageal dyskinesia On the other hand, it causes reflux and esophagitis. Diltiazem can reduce the LES pressure in patients with achalasia. It has no effect on healthy adults and nutcracker esophageal patients, while nifedipine has no effect on cardia achalasia. In addition, the LES pressure is also reduced in normal people and nutcracker esophageal patients.

(4) Other drugs: There are many other drugs that work on LES and gastroesophageal reflux. Singh (1992) reported the pharmacological effects of benzodiazepines, and it is believed that alprazolam can inhibit the central nervous system. The nervous system causes deep sleep and loses acid scavenging function. Others such as diazepam, imidazodiazepine (intravenous anesthetic), hydroxydiazepam (tethicil) and other drugs inhibit the central nervous system and should be used with caution in patients with GERD.

Non-steroidal anti-inflammatory drugs have many effects on the gastrointestinal tract, including gastroesophageal reflux. Studies have shown that PGE2 inhibits LES pressure and reduces esophageal contractility, while PGF2 has the opposite effect. Therefore, non-steroidal anti-inflammatory drugs are given. Can interfere with the synthesis of prostaglandins, resulting in increased or decreased LES pressure.

The problem of reflux or lung aspiration caused by pre-anesthesia administration is worthy of attention. Hall (1975) used monkey and human studies to prove that morphine, dulantin, and diazepam all reduced LES pressure and increased the possibility of reflux, Penagini et al. (1997). The conclusion is reversed. It is believed that morphine does not affect LES pressure. In reflux patients, the number of tLESRs can be reduced. The effect of naloxone is completely opposite to that of morphine.

Gielkens (1998) observed that intravenous injection of amino acids caused a rapid decrease in LES pressure; the injection of amino acids into the stomach was similar, but the response was slow and transient, with no effect on the frequency of tLESRs, the number of reflux, and the duration of reflux, with amino acids affecting reflux and To reduce the pressure of LES, the mechanism may be due to the nitric oxide provided by L-arginine. For this reason, Horwhat (2000) believes that the cause of GERD is complicated, and it is not a simple mechanism or an ordinary chemical. Can cause it to happen.

6. There are gastrointestinal reactions in a series of physiological changes in pregnancy with pregnancy, the most common of which is gastroesophageal reflux, 48% to 79% of pregnant women have gastroesophageal reflux during pregnancy (Nagler, 1962; Bassey, 1977), due to the lack of large-scale population survey, the exact number is still unknown. In a group of 607 prenatal surveys, the symptoms of reflux are gradually increased during pregnancy: 22% in the first 3 months and 39% in 3 months. In the last 3 months, 72%, the researchers believe that the hormone-related esophageal distal clearing function during pregnancy is impaired, which is the main cause of reflux.

Nagler et al (1961) have studied LES stress during pregnancy and found that half of pregnant women with reflux symptoms have low LES pressure, progressive decline during pregnancy, and return to normal after delivery. Later, Van Theil (1977) also had the same The discovery of scholars on the role of estrogen and progesterone in the process of gastroesophageal reflux during pregnancy, in animal experiments and humans have observed that estrogen alone does not cause LES pressure drop, and estrogen and pregnancy The combination of ketones caused a significant drop in LES pressure, and Filippone (1983) also achieved the same result in men, that is, combining the two hormones can reduce the LES pressure, while using one alone is not.

The mechanical compression of the uterus during pregnancy seems to be less important for the occurrence of reflux, because the symptoms do not improve after the fetal head falls (into the basin), but in the past it was thought that the increase in the uterus increased the intra-abdominal pressure and also increased the pressure in the stomach. High and delayed gastric emptying, Spence (1967) study confirmed that pregnant women's gastric pressure twice as many as men, children and non-pregnant women, and immediately decreased after delivery, considered to be caused by uterine compression during pregnancy, but Lind (1968) Studies have shown that LES stress in non-pregnant and non-reflux symptoms in pregnant women and women without reflux symptoms is elevated due to elevated intra-abdominal pressure, but only in patients with reflux symptoms, LES pressure decreases. Difference, the author failed to explain, Varl Thiel (1981) observed cirrhosis and ascites pressure in male patients, no reflux and heartburn symptoms before and after diuresis, LES pressure before ascites increased, after the ascites turned to normal, These observations suggest that, in the case of extremely high intra-abdominal pressure, like the abdomen of a pregnant woman, it can only increase the pressure of LES, but it does not promote the occurrence of gastroesophageal reflux, and also studies the gastric emptying and intestinal transit function of pregnant women, although Progesterone relaxation smoothing But could not confirm the presence of delayed gastric emptying pregnant women, pregnancy can not be sure the relationship between gastrointestinal motility disorders and gastroesophageal reflux.

At present, it seems that the reflux during pregnancy is related to the effect of progesterone on LES, rather than mechanical compression. Progesterone levels increase during pregnancy, return to normal after delivery, and reflux symptoms relieve themselves.

(two) pathogenesis

In order to carry out digestion, one or more enzymes exist in various parts of the digestive tract. A certain pH environment is the basic condition for ensuring the activity of the enzyme. However, the pH environment of each organ is not uniform. Under normal circumstances, there is a flap between the organs. Mechanism, the isolation of these pH environment, esophageal and gastric isolation mechanism in the esophagogastric junction, the LES and other mechanisms in this part of the stomach with high acidity (pH 1-3) and the acidity of the esophagus (pH 5 ~ 6) Isolation, the same example is seen in the pyloric isolation of the acidity of the stomach and the alkaline duodenum (pH6), isolation is not only the separation of the acidity of the organ, but also ensure that the food in the digestive tract "single direction "Sports, because food reflux (ie, the destruction of unidirectional movement, or reflux) also caused a disorder in the pH environment.

The biological valve mechanism is not a simple mechanical structure. It has very complicated factors (such as nerves, hormones, and the organ's own tissue structure). In regulating the isolation function of these organs, any regulation of dysfunction and obstacles can lead to organ content. Countercurrent flow occurs in the countercurrent between the esophagus and the stomach, that is, gastroesophageal reflux. GERD has the following pathophysiological changes.

1. Anti-reflux barrier dysfunction The main abnormal change of GERD is that the anti-gastroesophageal reflux barrier can not prevent the gastric content and/or duodenal juice from flowing back into the esophagus. The anti-reflux barrier function may be due to the following factors. The role is formed.

(1) LES smooth muscle function is weakened: LES smooth muscle function is the main pathophysiological change of GERD, the cause of which is still unknown. The gastrin or choline stimulating agent stimulates the sphincter of GERD patients, and its effect is not obvious. The smooth muscle contraction function of the sphincter is reduced, but not the obvious atrophy of the smooth muscle. For example, whether the LES smooth muscle of patients with scleroderma and esophageal inflammation are related to this is difficult, because the LES pressure is still low after the healing of esophageal inflammation, and after medical treatment The fact that the recurrence rate is high does not support the theory of inflammation and pathogenesis.

The LES pressure measured at the pressure transition point is very large, from 8 to 26 mmHg (Zaninotto, 1988), and the LES resting pressure below 6 mmHg is considered to be pathologically low, but this condition is only seen in 60% of GERD patients, According to statistics, GERD patients have reflux, and only 18% to 23% are formed by low LES pressure (Dent, 1988; Dodds, 1982), indicating that there are factors other than LES in the occurrence of reflux.

(2) LES becomes shorter: In addition to the pressure value factor, the shorter LES can also cause the cardia to be incompletely closed. According to the measurement of 324 patients with abnormal reflux, the LES length is shorter than 2cm. For pathological changes (Zaninotto, 1988), the length of the LES in the abdomen is less than 1 cm and is also considered a mechanical defect in the sphincter.

Both sphincter length and resting pressure affect the pressure vector volume, which is a key factor in the ability of the sphincter to close. It has been shown that the LES pressure vector volume is significantly lower in patients with GERD (Stein, 1991).

(3) Changes in control mechanisms: LES pressure is regulated by factors such as nerves and hormones. For example, when excessive force is applied, the increase in LES pressure is not due to the sphincter sphincter sputum ES or even the contraction of the foot, so this neuromodulation mechanism is also Regulating the resting pressure of LES, human LES is mainly controlled by tonic cholinergic innervation, which innervates the vagus nerve, and atropine reduces the sphincter pressure by about 50% (Dodds, 1981; Mittal, 1990).

There are several hormones that affect LES resting pressure, gastrin, motilin can increase LES pressure, while cholecystokinin, secretin and vasopressin are opposite, GERD patients have significantly lower motilin levels. There is a delay in gastric emptying.

However, the low level of motilin causes GERD, or the reflux disease causes low levels of motilin. The reason is not clear.

Reduce LES pressure and slow down gastric emptying foods, drugs and hormones, etc.: 1 food: fat, chocolate, high-fiber foods, 2 drugs: anticholinergic drugs, nitrates, theophylline, nicotine (smoking), Receptor blockers, calcium channel blockers, left dopa, anesthetics, 3 hormones/others: progesterone, estrogen, cholecystokinin, somatostatin, beta receptor agonist, prostaglandin E1, E2.

Gastroesophageal reflux disease prevention

The lifestyle change aims to reduce acid reflux and reduce contact time between the reflux and the esophageal mucosa.

1. Excessive obesity will increase abdominal pressure and promote reflux, so avoid eating high-fat foods that promote reflux, and lose weight.

2. Eat less meals, do not eat within 4 hours before going to bed, so that the night stomach contents and stomach pressure are reduced to a minimum, if necessary, raise the bed head 10cm, which is very important for the reflux during the nighttime supine Use gravity to remove harmful substances in the esophagus.

3. Avoid long-term increase in life.

Gastroesophageal reflux disease complications Complications esophageal stenosis congenital short esophageal pyloric obstruction hiccup

1. Esophageal stricture Patterson (1983) statistics that about 80% of esophageal stenosis is caused by digestive diseases. Esophageal stricture is a serious complication of late GERD, and approximately 10% of patients receiving drug therapy develop esophageal stenosis (Marks, 1996). In addition, 7.0% to 22.7% of patients with statistical reflux esophagitis may have esophageal stenosis.

This complication of GERD is most common in 60 to 80 years old. Esophageal stricture is more common in patients with duodenal reflux, except for esophageal injury caused by repeated acid exposure. Most patients have LES functional defects and have hiatal hernia. The severity of GERD is slightly related to the formation of stenosis. The literature reports that esophageal stenosis is more likely to occur in Caucasian patients and men in GERD patients. The use of non-steroidal anti-inflammatory drugs often forms esophageal stenosis (el-Serag, 1997). The incidence of esophageal stenosis caused by GERD in China is unknown, and it is estimated that it is not as much as reported abroad.

Esophageal stricture is formed by repeated peptic ulcers in the esophageal wall. Inflammation begins with mucosal congestion, edema, and erosion, further forming ulcers in the esophageal wall. The inflammation of the ulcer is generally deep into the submucosa, and can further destroy the superficial muscle layer. In severe cases, it involves the entire esophageal wall and causes inflammation around the esophagus. Submucosal fibroblasts were most infiltrated, and the connective tissue formed thickened and fibrosis of the esophageal wall, resulting in narrowing of the esophagus and shortening of the longitudinal direction. The scar tissue replaced the normal esophageal wall tissue. The muscle layer can also shrink due to embolization of the blood vessels in the wall.

There are sometimes deep ulcers in the stenosis, and there is a layer of granulation tissue and purulent fibrin exudate at the bottom of the ulcer. Although local blood vessels are narrowed by subendocardial fibrosis, they can be attacked to cause severe bleeding. If the ulcer heals, it is replaced by glandular epithelial repair. Ulcers can also be perforated. Stenosis often coincides with Barrett's esophagus. Inflammation of the esophageal wall, such as involving part of the muscular layer or the entire muscular layer, may form esophageal stricture. In theory, the destruction of the longitudinal muscles leads to the shortening of the esophagus and becomes a short esophagus. The fibrosis of the circumflex muscle forms an esophageal stenosis, so the short esophagus and stenosis often coexist. Both can be accompanied by hiatal hernia.

The stenosis occurs mostly in the lower esophagus near the esophagogastric junction; the high stenosis is seen in the Barrett's esophagus. There are two types: one is located at the junction of the squamous epithelium and the Barrett epithelium, which is the result of reflux esophagitis; the first type is located in the columnar epithelium. Within the scope of the lining, chronic Barrett ulcers form later.

Short stenosis, usually 1 ~ 2cm or > 2cm, the location is close to the esophagogastric junction. The elderly can reach 5cm or longer, but it is rare. The lumen is less than 3 mm, and the stenosis is longer than 3 cm, which is severe stenosis. According to statistics, about 75% are short segmental stenosis, 14% are annular stenosis, and 11% are long segmental stenosis.

2. Short esophageal short esophagus is seen in patients with long-term GERD, or patients who have had multiple anti-reflux surgery before. Wall inflammation and fibrosis lead to shortening of the esophagus and may be associated with esophageal stenosis.

3. Barrett's esophagus due to gastroesophageal reflux and acidic gastric juice (gastric acid) caused by the formation of squamous epithelial ulcers in the lower esophagus and squamous epithelial destruction, and then the lesion was replaced by columnar epithelial uplift. Endoscopic examination of the pink small tongue-shaped columnar epithelium in the lower esophagus

4. The Schatzki ring Schatzki ring occurs at the junction of the squamous epithelium and the columnar epithelium. The ring has a scaly epithelium and a columnar epithelium below. The ring is thin and is measured on esophageal radiographs, usually less than 5mm. Because the Schatzki ring is significantly retracted into the lumen, it has symptoms of dysphagia.

The cause of the Schatzki ring is unknown, may be a congenital variation, but there is also evidence that people with Schatzki ring have a lot of GERD, so it is considered a complication of GERD. Since the person with this ring can only have difficulty swallowing and no GERD symptoms, most GERD patients do not find this ring, so the relationship between this disease and GERD remains to be explored.

5. Extra-esophageal complications

(1) Laryngeal complications: According to statistics, ENT patients with laryngeal symptoms and vocal dysfunction, about half of the gastroesophageal reflux is the cause of the disease, or the relevant factors of the onset. Throat symptoms associated with reflux include chronic vocal difficulties, intermittent vocal difficulties, vocal cord fatigue, broken sounds, long-term throat clearing habits, excessive laryngeal mucus, nasal discharge, chronic cough, difficulty swallowing, and sputum. Reflux as a cause or synergistic factor includes reflux laryngitis, subglottic stenosis, laryngeal cancer, vocal cord contact ulcer or granuloma, post-vocal stenosis, unilateral or bilateral sacral cartilage fixation, paroxysmal throat, Pharyngeal sacral sign, vocal cord nodules, polypoid degeneration, laryngeal cartilage softening, laryngeal skin disease (pachydermia laryngis) and leukoplakia.

(2) Chronic cough Gastroesophageal reflux is an important cause of chronic cough, ranking the third cause of the cough, from children to adults. The occurrence of chronic cough is related to both respiratory aspiration and neuroreflex. The afferent and efferent pathways of nerve reflex are vagus nerves.

More than half of GERD's cough is a dry cough. After 24 hours of pH monitoring, it is found that cough is often seen in awake and upright positions, rather than at night. Patients often do not have symptoms of gastroesophageal reflux, such as heartburn, acid reflux, etc., so 50% to 75% of patients deny a history of reflux. Coughing is often the only symptom with long-term pH monitoring, but it can also have typical reflux symptoms, or atypical symptoms such as chest pain, nausea, asthma, and hoarseness.

(3) Asthma: Among the asthma patients, the incidence of GERD has different investigation reports. Perrin-Foyolle et al (1989) found that 65% of patients with 150 asthmatic patients had reflux symptoms. Connell (1990) reported that 72% of consecutive 189 asthma patients had heartburn symptoms, and half of the patients had heartburn symptoms during supine supine position. 18% had a burning sensation in the throat at night. Field et al (1996) reported that 77% of 109 asthma patients had heartburn symptoms, 55% had nausea, 24% had dysphagia, and 37% required at least one anti-reflux medication. In another 527 adult asthma patients reported by 6 hospitals in 4 countries, 362 (69%) of patients with gastroesophageal reflux were confirmed by esophageal pH monitoring. Endoscopy continued to observe 186 asthma patients, 39% had esophageal mucosal erosion or ulceration, and 13% had Barrett's esophagus. Esophageal hiatus hernia is an indirect manifestation of gastroesophageal reflux, and 50% of asthma patients have hiatal hernia. A total of 783 children with asthma in 8 studies, through a short-term pH test, long-term pH monitoring or radiographic observation of esophageal hiatal hernia, found that there were gastroesophageal reflux from 47% to 64%, an average of 56%, and reports The incidence of adults is similar (Sontag, 1999). It can be seen from the above materials that gastroesophageal reflux and asthma often coexist. In children or adult asthma patients, the incidence of gastroesophageal reflux is very high, which is worthy of attention and attention of clinicians.

(4) Oral complications: acidic stomach contents stay in the mouth can cause oral diseases, of which tooth erosion is the most prominent. The acid acts on the teeth for a long time, which forms tooth erosion, which is a chemical change process of long-term acid exposure. At first, the surface of the enamel is eroded and the gloss disappears. The enamel is gradually destroyed by the corrosive effect of the year. The dentin which is soft in texture and poor in acid resistance is exposed to acid. Under the action of acid, the dentin is destroyed more. fast. Allergic to temperature changes, sweets and acidic foods. Jarvinen (1988) studied 109 patients with upper gastrointestinal symptoms. 55% of patients with reflux esophagitis had oral symptoms such as burning sensation, tongue sensitivity and painful ulcers. Another 117 patients with reflux, through their mouth, teeth and salivary glands, most patients often feel dry mouth, tooth sensitivity, non-specific oral itching or burning sensation, or pharyngeal symptoms (Meurman, 1994 year). In addition to gingivitis and periodontitis, patients with reflux can also increase salivary glands due to long-term acid reflux, especially the parotid gland. The reason for the enlargement of the parotid gland may be caused by repeated acid reflux to stimulate the mouth and excessive secretion of the parotid gland.

It is difficult to study the oral complications of GERD patients because there are many causes that can cause oral lesions and are difficult to identify.

Symptoms of gastroesophageal reflux disease Common symptoms Anti-acid stomach pressure increase dysphagia Heartburn burning pain Heart nausea Heartburn Heart hoarse upper gastrointestinal bleeding

Patients with severe symptoms of GERD have a better understanding of their condition and can take their own medication to relieve symptoms; patients with mild symptoms may not know much about their illness, only when they have an objective examination, the disease is found, GERD Symptoms are light and heavy in most people. Of course, some people develop drug dependence. Once the drug is stopped, the symptoms recur. There is no evidence that the longer the patient's medical history, the more serious the complications, and 25% of the benign stenosis of the esophagus secondary to GERD. No or few prodromal symptoms.

In the 1960s, patients with esophageal hiatal hernia who had a history of 20 years were followed up. Many patients lost symptoms over time, and 15% of patients who reported follow-up for 3 years (including treatment or no treatment) had 15%. Symptoms disappeared. These conditions were not associated with esophagitis at the beginning of treatment. Esophagitis seen under endoscopy sometimes appeared during follow-up and sometimes disappeared, and its endoscopic findings were not related to symptoms.

Postlethwait (1986) summarized 5,000 patients reported in the literature, the symptoms of GERD were: heartburn 58%, nausea 44%, hernia 30%, dysphagia 28%, anemia 19%, pharyngeal symptoms 18%, respiratory symptoms 16 %, hematemesis 14%, major bleeding 12%, Clark (1986) comprehensive literature 2178 patients with GERD symptoms: heartburn 85%, of which 81% increased with body position, 47% cough, 37% dysphagia, 35% bronchitis, 23% nausea, 2l% nausea and vomiting, 16% asthma and pneumonia, 3% hoarseness, the latter group of statistical heartburn symptoms seem to be more in line with the actual situation, also reflects the universality of GERD respiratory complications, most literature reports heartburn symptoms Above 80%, as in 2260 cases of GERD collected by Henderson (1980), heartburn symptoms were 88%.

1. Heartburn is the most common symptom of GERD. It has different vocabulary expressions, such as pyrosis and sour regurgitation. It is the result of contact with stimulating substances in the esophageal mucosa, mainly acid. For example, 0.1mol/L When HCl is infused into the esophagus, most people can experience the feeling of heartburn, such as stopping the injection of acid, or changing the saline, alkaline solution, burning heart quickly disappears, the columnar epithelium in the esophagus, such as Barrett's esophagus, is not sensitive to acid contact, typical In the case, heartburn occurs 1 to 2 hours after a meal, and the ingredients of the food have a great influence on the symptoms. Hard liquor, sweet food, acidic food, rough food, greasy food, tea and coffee are easy to cause heartburn. Occurrence, eating a large amount is more prone to heartburn symptoms, pregnant women often have a heartburn feeling, is due to the effects of hormone changes during pregnancy, this symptom continues until after delivery, when heartburn occurs, taking baking soda can quickly relieve symptoms; drinking milk is also It can work quickly, because milk can neutralize stomach acid on the one hand, and can cause esophageal peristalsis to remove the reflux in the esophagus. When swallowing the heart, swallowing saliva frequently to alleviate the disease. It has the same mechanism.

Patients with "reflux symptoms" but no esophagitis, often because of excessive sensitivity of their esophageal mucosa, reflux is not serious, in acute esophagitis, heartburn symptoms are often sudden, and no precursors, such as recurrent heartburn symptoms That is the performance of GERD, but the frequency and severity of heartburn symptoms do not help to understand the damage of the esophageal mucosa, not as accurate as seen by endoscopy.

2. nausea (re-acidification) regurgitation means that the contents of the stomach or esophagus are returned to the pharynx or mouth without force. It is also a common symptom of GERD, like heartburn symptoms, normal people are eating stimulating stomach acid. Occasionally, there may be acid reflux after the secretion of more food. It is a physiological phenomenon and will not cause damage. Unlike vomiting, the nausea is not accompanied by nausea, retching, belching, and strong contraction of the abdomen and ankle. Can be accompanied by heartburn, GERD patients with force, bending, hernia or abdominal compression, can also form this symptom (Parkman, 1995), if the reflux is purely stomach content, it is a sour liquid; if mixed with bile, It is a bitter taste liquid. When the fasting reflux is mostly acidic, it is called acid reflux. If the bile color is found on the pillow, it indicates that there is reflux at night.

3. Swallowing pain swallowing pain occurs immediately after swallowing, especially when eating hot food, acidic food, drink, although the literature reports that 50% of GERD patients have this symptom, but erosive esophagitis and esophageal ulcer are not so Symptoms, in addition to reflux esophagitis, other causes of esophagitis also swallowing pain, such as esophagitis caused by pills, infectious esophagitis.

4. Chest pain in patients with GERD needs to be differentiated from cardiogenic chest pain. The pain is in the back of the sternum, under the xiphoid or upper abdomen, and often radiates to the chest, back, shoulders, neck, jaw, ears and arms (Figure 10). About 30% of people suspected of having cardiogenic chest pain have no heart disease after cardiology examination. This unexplained chest pain can be related to microcirculatory angina, esophageal disease, lung disease, musculoskeletal lesions and mental factors. The chest pain caused by various causes is collectively referred to as "syndrome X", including microvascular angina pectoris of the heart, esophageal disorders, estrogen deficiency and mental disorders in women, and several studies have shown that gastroesophageal reflux is unknown. The most common cause of chest pain. In the past, esophageal dyskinesia (such as esophageal diffuse fistula and nutcracker esophagus) was considered to be the most common cause of esophageal chest pain, but clinical practice has shown that 50% to 70% of these patients with chest pain have abnormalities. Acid exposure, 20% to 60% of people with chest pain are associated with reflux, and proton pump inhibitor (PPI) or high dose H2 receptor antagonists improve chest pain in many patients. For those who are known to have "heart disease", those who fail with standard treatment for gastroesophageal reflux, and those with esophageal dyskinesia, the first thing to do is to exclude pain from the heart; secondly, to learn more about the history and behavior. Physical examination to exclude lung disease, musculoskeletal lesions or mental factors; third, to understand the history of gastroesophageal reflux disease, esophageal pH monitoring, endoscopy and experimental anti-reflux therapy to determine gastroesophageal reflux.

5. Dysphagia Dysphagia is a manifestation of impaired esophageal transmission function. 40% of patients with long-term GERD have this symptom. Dysphagia is also a sign of esophageal stricture and Schatzki ring. Generally speaking, solid food causes dysphagia as luminal obstruction. As a result, the symptoms caused by liquid food suggest the presence of esophageal dyskinesia, such as progressive aggravation of dysphagia and weight loss, should consider the occurrence of cancer.

6. 20% of patients with endoscopic bleeding due to reflux symptoms have erosive esophagitis, reflux esophagitis caused by mucosal damage is very rare, most reports of upper gastrointestinal bleeding, erosive esophagitis bleeding Only 10% or less, but the bleeding caused by other esophageal diseases accounted for more than 30%, of which the most patients with esophageal varices and Mallory-Weiss syndrome, some patients with erosive esophagitis are prone to bleeding, Such as the elderly, chronic renal insufficiency, the application of anticoagulants or AIDS patients, esophageal hiatal hernia complicated with ulcers (called Cameron ulcer) is the cause of unhealed upper gastrointestinal bleeding, which occurs due to the gastric wall ischemia at the level of the hernia Although bleeding is not caused by GERD itself, it is often associated with esophageal hiatal hernia and simultaneous gastroesophageal reflux symptoms. This patient has a large esophageal hiatus hernia, and patients often have iron deficiency anemia.

Gastroesophageal reflux disease examination

Esophageal mucosal biopsy

Esophageal mucosal biopsy and cytology are of limited value in the evaluation of patients with GERD. Unless Barrett's esophagus and suspected carcinogenesis are suspected to be Barrett's esophagus, they should be systematically examined to exclude poor differentiation and cancer. Patients should also adopt Endoscopic follow-up, once every 1 or 2 years, is the current treatment of Barrett's esophagus.

2. Pathological examination

Ismail-Beigi et al (1970) studied four groups of people using a biopsy method. They established a histopathological diagnostic criteria for GERD: 1 squamous epithelial basal cell layer thickness increased, normally accounting for 10% of epithelial thickness (from 5 %14%), if more than 15%, indicating the presence of reflux inflammation; 2 inherent membrane nipple extension, under normal circumstances, the nipple is less than 66% of the epithelial thickness, beyond this limit is abnormal, and later Kobayashi (1974) also booked A similar diagnostic criteria for esophagitis, that is, the basal cell layer thickness should exceed 50% of the epithelium, and the intrinsic membrane nipple extension length exceeds 50% of the epithelial thickness. The explanation for this pathological change is that the surface cells of the esophageal epithelium are affected by the reflux. The damage of the detachment requires basal cell proliferation in order to repair these epithelium; the intrinsic membrane nipple extension is to increase the local blood supply.

The presence of neutrophilic and eosinophilic cells in the esophageal lamina propria of GERD is important for the diagnosis of reflux esophagitis, but eosinophils are not an intrinsic feature of reflux esophagitis, eosinophilia and addiction. Patients with acid cell gastroenteritis can also find obvious eosinophilic infiltration. Only after these two conditions can they be regarded as a histological diagnostic criteria for reflux esophagitis, and the sinus is found in the esophageal epithelium or the lamina propria. Neutral cells usually indicate that the inflammation is more serious. Many authors believe that the mild neutrophils of reflux esophagitis do not occur frequently, so it is not reliable as a basis for diagnosis. In addition, the intrinsic membrane nipple is superficially telangiectasia. Intradermal growth and red blood cell infiltration into the epithelium are also a diagnostic marker of early esophagitis.

In the stage of inflammation progression and erosion formation, endoscopically, there are strips of erosion along the long axis of the esophagus, which can also be flaky fusion. Histological examination reveals epithelial necrosis of the lesion area, forming a superficial epithelial defect, which is inflammatory. Covered with cellulose membrane, neutrophils and lymphocytes, plasma cell infiltration, inflammatory changes are mainly restricted to the mucosal muscle layer, and superficial capillary and fibroblast proliferation can be seen in the superficial parts, forming chronic inflammation or healing. Granulation tissue.

When the esophagus is ulcerated, it is isolated, or fused, and spreads to the submucosa, less invading the muscle layer. The surface of the ulcer is exudative cellulite, the bottom of the ulcer is necrotic tissue, and the underlying is a new capillary, a proliferating fiber. Cells, chronic inflammatory cells or granulation tissue composed of varying amounts of neutrophils, for a long time, the bottom of the ulcer is repaired by scar tissue formed by granulation tissue.

3. Bilirubin monitoring

In recent years, studies have found that the symptoms and complications of GERD patients are related to the duplication of duodenal contents. The reflux of duodenogastroesophageal reflux (DGR) contains trypsin, lysolecithin and cholic acid. If the substance is mixed with the stomach content (protease, hydrochloric acid), it is considered to aggravate the damage to the esophageal mucosa. Studies on animals and humans have shown that the bile acid present in the esophagus can cause esophagitis in an acidic environment, and bile salts or Whether trypsin can damage the mucosa in an alkaline environment is inconclusive.

The biggest difficulty in studying DGR is the lack of tools to correctly identify such reflux. In the past, endoscopic examination, radionuclide scanning and esophageal pH monitoring were used to study the results. The results were inaccurate. Sexual reflux, but there are many factors that can cause pH>7, where excessive salivation is a major cause of pH>7, such as pH electrode stimulation, acid reflux, tooth infection, etc., which increase salivary secretion and Its pH rises.

The most sensitive discovery of the DGR method is bilirubin monitoring. In recent years, Bilitec 2000 (Medttonic-Synectics) has been introduced, which can effectively measure duodenal reflux and quantitatively detect duodenal reflux. Bilirubin, a monitoring device made with fiber-optic light-guide technology, provides 24-hour portable monitoring of duodenal reflux under physiological conditions, and can be used in combination with a pH electrode to measure the duodenum. Bilirubin and pH changes in the stomach.

Film degree exam

X-ray barium meal angiography

Esophageal barium meal imaging is generally not easy to show abnormalities of the esophageal mucosa, or can only show heavier inflammatory changes, such as thickening of mucosal folds, erosion, esophageal ulcers, etc., mild esophageal inflammation is not sensitive

Esophageal barium meal imaging has diagnostic significance for combined esophageal hiatus hernia and esophageal stricture. Image features of esophageal stricture: A. stenotic esophageal lumen; B. stenosis lacks dilatation ability, and can not be dilated with smooth muscle relaxant; The symmetrical lumen is thinned, and the upper lumen is moderately enlarged. Sliding esophageal hiatus is seen below the stenosis. Stenosis such as asymmetry and narrow internal mucosa are obviously irregular, indicating the possibility of cancer.

2. Endoscopy

Endoscopy is the best way to observe the esophageal injury and establish the diagnosis of erosive esophagitis and Barrett's esophagus. Endoscopy in patients with suspected GERD is the preferred method. Patients with heartburn, acid reflux symptoms, endoscopy can be 45 Erosive esophagitis is shown in % to 60% of patients; other patients may have non-erosive esophagitis, such as esophageal mucosal edema, hyperemia or normal manifestations.

(1) Endoscopic Savary and Miller staging methods.

Stage I: Single or isolated erosion with erythema and/or exudation.

Stage II: erosion or ulcer fusion, but not involving the esophagus for the entire week.

Stage III: The lesion involved the esophagus for the entire week without esophageal stricture.

Stage IV: Chronic lesions or ulcers, with esophageal wall fibrosis and stenosis, short esophagus, and/or Barrett's esophagus.

(2) Los Angeles classification method:

Class A: Mucosal damage in one or more places, no more than 5mm in each place.

Grade B: There is at least one mucosal destruction of more than 5 mm on the mucosal folds, but there is no fusion between the mucosal folds.

Grade C: There is a fusion failure between mucosal folds at two or more places, and no full-week damage has been formed.

Grade D: Mucosal destruction throughout the week.

In patients with atypical symptoms and extra-esophageal symptoms, erosive esophagitis is rare, and patients with unexplained chest pain and normal coronary vessels, although 50% have GERD, erosive esophagitis only accounts for 10% or less.

Endoscopic esophagitis is reported to be 30% to 40% of patients with GERD who have asthma at the same time. A study by Larrain (1991) indicates that esophagitis is found in 33% of asthma patients, mainly non-erosive esophagitis.

GERD

GERDpHBarrett

3.pH

pHpH24pH24

LESLES5cm

(upper esophageal sphincterUES)UESUES15cmUESLES5cmLES5cm20cmpH<46%1.2%;1.1%0%

50%(Weinei1988)

GERD24pHGERDGERDGERD103(Katz1987)12%(Schnatz1996)5(Katz1987)

4.

LESLESGERDGERDLESBarrett4%GERDLES30mmHg(ineffective esophageal motilityIEM)30%GERDKatzIEMGERD35%IEMNlissenIEMToupetBelsey 4

5.

99mTcValsalva

Shay(1991)61%pH15%

14%90%65%60%90%()pH

diagnosis

pH

PH

Differential diagnosis

1.pHLES

2.GERD

(1)

(2)GERD

(3)

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