Reflux esophagitis refers to inflammation, erosion, ulceration and fibrosis of the esophageal mucosa caused by the reflux of stomach and/or duodenal contents into the esophagus, and is classified as gastroesophageal reflux disease.
Diagnosis
In cases of retrosternal burning sensation or burning pain, the presence of GER can be determined by intraesophageal luminal pH measurement, intraesophageal luminal manometry, and gastroesophageal scintigraphy. application of an esophageal acid drip test will determine whether the symptoms are due to GER. If necessary, esophageal endoscopy and biopsy can be performed to clarify the diagnosis.
Qin Mingfang, Minimally Invasive Surgery Center, Nankai Hospital, Tianjin, China Zhang Chen, Minimally Invasive Surgery Center, Nankai Hospital, Tianjin, China
Reflux esophagitis should be differentiated from peptic ulcer, angina pectoris, esophageal cancer and esophageal fungal infection.
Treatment measures
(I) General treatment
Avoid smoking, alcohol, coffee, chocolate, acid food and excessive fat; avoid lying down immediately after meals; elevate the head of the bed 20-30cm when lying down; trouser belt should not be tied too tightly to avoid various states that cause excessive abdominal pressure.
(B) promote the emptying of the esophagus and stomach
1.Dopamine antagonists
These drugs can promote the emptying of the esophagus and office, and increase the tension of the LES. Such drugs include metoclopramide (gastric complex) and domperidone (morpholine), both 10-20 mg, 3-4 times a day, before bed and before meals. The former can lead to extrapyramidal neurological symptoms if taken in excessive doses or for a long time, so be cautious in elderly patients; the latter can also cause hyperprolactinemia and produce mastopathy, lactation and amenorrhea and other adverse reactions when taken for a long time.
2.Cisapride
10～20mg for 3～4 days, without adverse effects.
3.Cholinergic drugs
Uracholine can increase the tension of LES, promote the contraction of esophagus, accelerate the emptying of acidic food in the esophagus to improve the symptoms, 25mg each time, 3 to 4 times a day. This mouth can stimulate the secretion of gastric acid, long-term use should be cautious.
(C) Reduce gastric acid
1, acidophilus, can neutralize gastric acid, thus reducing the activity of pepsin and reducing the damage to the esophageal mucosa from acidic gastric contents. Alkaline drugs themselves also have the effect of increasing LES tension. Aluminum hydroxide gel 10-30ml and magnesium oxide 0.3g, 3-4 times daily. Alginic acid foam contains alginic acid, sodium alginate and acid making agent, which can float on the surface of gastric contents and can stop the reflux of gastric contents.
2, histamine H2 receptor antagonists, methandiamide, furosemide and famotidine can be used, the dose is 200mg, 3-4 / d; 150mg, 2 times / d and 30mg / d. The course of treatment are 6 to 8 weeks. This class of drugs can strongly inhibit the secretion of gastric acid and improve acid reflux in the gastroesophagus. If the above symptoms cannot be improved, the dose can be increased to 2 to 3 times.
3, proton pump inhibitors, these drugs can block the H+-K+-ATPase of the wall cells and meprazole and lansoprazole have been widely used in clinical, the former 20mg/d, the latter 30mg/d, can improve its symptoms.
(iv) Combination of drugs
The combination of esophageal and gastric emptying drugs and acidulants has a synergistic effect and can promote the healing of esophagitis. Dopamine antagonists or cisapride can also be used in combination with histamine H2 receptor antagonists or proton pump inhibitors.
The disease recurs in about 80% of cases within 6 months after the drug is discontinued because the LES tone is not fundamentally improved. If in the histamine H2 receptor antagonist, proton pump inhibitor or dopamine antagonist anti-days accounted for any one of the maintenance medication, or have symptoms when the timely use of drugs, can achieve better results.
(E) Surgical treatment
It is mainly applied to esophageal scar stenosis (feasible dilatation or surgical correction) and conditions such as ineffective medical treatment, recurrent bleeding, and recurrent concurrent pneumonia.
Pathogenesis
24-hour esophageal pH monitoring reveals that gastroesophageal reflux (GER) is present in normal people without any clinical symptoms, so it is called physiological GER.
It is characterized by: often occurring during the day but rarely at night; more reflux during or after meals; and a total reflux time of
The anti-reflux barrier at the esophagogastric junction is also known as the first anti-reflux screen, of which the most important structure is the lower esophageal sphincter (LES), a high-pressure area within 3-5 cm above the line of junction between the esophagus and stomach. The resting pressure there is about 2.0-4.0 kPa (15-30 mmHg), which constitutes a pressure barrier and plays a physiological role in preventing regurgitation of gastric contents into the esophagus. In normal subjects, an increase in intra-abdominal pressure can cause the LES contraction reflex through the vagus nerve, causing an exponential increase in LES pressure to prevent GER; low LES pressure and an increase in intra-abdominal pressure that does not cause a strong LES contraction response can lead to GER.
<0.8kPa is prone to reflux and is associated with GER in about 17-39% of people with reflux esophagitis. In addition, the incidence of GER increases with increased plasma progesterone levels during pregnancy, oral progesterone-containing contraceptive period and late menstrual cycle.
(B) Disorders of esophageal acid scavenging function
Normal esophageal acid contouring function consists of two parts: esophageal emptying and saliva neutralization. When acidic gastric contents are refluxed, only one to two times (about 10-15 seconds) of secondary peristalsis of the esophagus is required to empty almost all of the refluxed material. The small amount of acid remaining in the esophageal mucosal trap can then be neutralized by saliva (about 1,000 to 1,500 ml per hour of saliva with pH 6 to 8 enters the stomach through the esophagus in normal people). The function of esophageal acid contouring is to reduce the time limit for the esophageal mucosa to be immersed in gastric acid, so it has the effect of preventing reflux esophagitis. It has been found that most abnormal esophageal emptying occurs early in esophagitis, while esophagitis due to reduced salivary secretion is rare. Salivary secretion almost stops during nighttime sleep, and secondary peristalsis of the esophagus rarely occurs, and the acid contouring of the esophagus at night is significantly delayed, so the risk of GER is more serious at night.
(C) Damage to the anti-reflux barrier function of esophageal mucosa
The anti-reflux barrier function of esophageal mucosa is composed of the following factors.
1. pre-epithelial factors including mucus layer, HCO-3 concentration on the mucosal surface;
2. Epithelial factors include epithelial cell membranes and intercellular junctional structures, as well as epithelial transport, intracellular buffers, cellular metabolism, and other functions;
3, post-epithelial factors refer to the internal basal acid status and blood supply of the tissue. When these defensive barriers are damaged, esophagitis can be caused even under normal reflux conditions. It has been found that the weakened ability of esophageal epithelial cells to proliferate and repair is one of the major causes of reflux esophagitis.
(iv) Gastroduodenal malfunction
1. abnormal gastric emptying The incidence of delayed gastric emptying in patients with reflux esophagitis is above 40%, but the causal relationship between the two is still debated.
2. Gastroduodenal reflux
Under normal conditions, esophageal squamous epithelial cells have a keratinized surface layer that prevents H+ infiltration into the mucosa to protect the mucosal surface of the esophagus from damage by acidic reflux. When the pyloric sphincter tone and LES pressure are low at the same time, hydrochloric acid and pepsin in gastric juice, bile acid, pancreatic juice and hemolytic lecithin in duodenal juice can simultaneously reflux into the esophagus and erode the keratinized layer of esophageal epithelial cells, and make them thin or fall off. The H+ and pepsin in the regurgitant penetrate deep into the esophageal tissue through the new squamous epithelial cell layer, causing esophagitis.
Therefore, reflux esophagitis is usually the result of the combined action of refluxed bile and gastric acid on the esophageal mucosa, and pylorus and LES dysfunction must exist before bile can cause esophageal injury; most people with reflux esophagitis are accompanied by gastritis. Sliding esophageal hiatal hernia is often complicated by LES and pylorus dysfunction; duodenal ulcer is often accompanied by high gastric acid secretion, which leads to spasm of the gastric sinus and pylorus dysfunction, so it is also complicated by this disease. Obesity, large amount of ascites, late pregnancy, and increased intragastric pressure can trigger this disease.
Pathological changes
The mucosa of the esophagus is bleeding, edematous, brittle and easily bleeding. In acute esophagitis, the mucosal epithelium is necrotic and peels off, forming erosions and superficial ulcers. In severe cases, the entire epithelial layer can be shed, but generally does not exceed the mucosal muscle layer. In chronic esophagitis, mucosal erosion can be followed by fibrosis and can involve the entire esophageal wall beyond the mucosal muscle layer. Repeated formation of esophageal mucosal erosions, ulcers and fibrosis can lead to scarring of the esophagus. Microscopically, basal cell hyperplasia of the squamous epithelium is seen, with milk penetration extending to the surface layer of the epithelium with vascular proliferation and neutrophil infiltration of the lamina propria. In cases of esophageal stricture, scar formation can occur in either the submucosa or the muscular layer. In severe esophagitis, the basal layer of the mucosal epithelium is seen to be disrupted, and because the ulcer is too large, the squamous epithelium at the edge of the ulcer is unable to repair the ulcer by re-epithelialization, and the form of epithelial hyperplasia is called Barrett’s esophagus. Ulcers that occur in Barrett’s epithelium are called Barrett’s ulcers.
Clinical manifestations
(A) Burning sensation or pain behind the sternum
is the main symptom of the disease. The symptoms occur about 1 hour after eating and can be triggered by semi-recumbency, forward bending of the torso or strenuous exercise, and can disappear after taking acid suppressants, while overheated and acidic food can aggravate it. In cases of acid deficiency, the burning sensation is mainly caused by bile reflux, and the effect of acid suppressants is not effective. The severity of the burning sensation does not necessarily correspond to the severity of the lesion. In severe esophagitis, especially in those with scar formation, there may be no or only a mild burning sensation.
(B) Gastric and esophageal reflux
Acidic fluid or food reflux from the stomach and esophagus into the pharynx or mouth after a meal, when lying with the body flexed forward, or when sleeping in bed at night. This symptom mostly appears before the onset of burning sensation or burning pain behind the sternum.
(C) Difficulty in swallowing
In the initial stage, intermittent dysphagia can often occur due to secondary esophageal spasm caused by esophagitis. In the later stage, due to narrowing of the esophageal scar, the burning sensation and burning pain may gradually decrease and be replaced by permanent dysphagia, which may cause blockage or pain at the glabella when eating solid food.
(iv) Bleeding and anemia
In severe esophagitis, bleeding may occur due to esophageal mucosal erosion, mostly chronic and small amount of bleeding. Long-term or massive bleeding can lead to iron deficiency anemia.
Complications
In addition to complications such as esophageal stricture, bleeding and ulceration, regurgitated gastric juice can also erode the pharynx, vocal cords and trachea and cause chronic pharyngitis, chronic vocal cords and bronchitis, which is clinically known as Delahunty’s syndrome. Gastric reflux and aspiration into the respiratory tract can also lead to aspiration pneumonia. Recent studies have shown that GER is associated with some recurrent episodes of asthma, cough, nocturnal apnea, and angina-like chest pain.
Ancillary tests
(i) Esophageal acid drip test
The patient is placed in a sitting position and a gastric tube is placed through the nasal cavity. When the end of the tube reaches 30-35 cm, first drip saline, about 10 ml per minute, for 15 minutes. If the patient has no special discomfort, switch to 0.1N hydrochloric acid and drip at the same rate for 30 minutes. During the acid drip, a positive reaction is defined as a painful or burning sensation behind the sternum, which occurs mostly within the first 15 minutes of the acid drip. If a positive reaction is repeated twice and can be relieved by drops of saline, it can be judged that there is acid GER, and the sensitivity and specificity of the test are about 80%.
(B) Intraluminal pH measurement of esophagus
A pH electrode placed in the lumen is gradually pulled into the esophagus and placed at about 5 cm above the LES. Under normal conditions, the pH in the stomach is very low. At this time, the patient is asked to take a supine position and make movements to increase the pressure in the abdominal pain, such as closing the mouth, covering the nose, exhaling deeply or flexing the legs, and blowing the nose 3 to 4 times. If the pH in the esophagus drops to below 4 times, it indicates the presence of GER. Also, inject 300ml of 0.1N hydrochloric acid into the gastric cavity. Before injecting hydrochloric acid and 15 minutes after injecting, ask the patient to lie on his back and make abdominal pressure increasing movements respectively. In the presence of GER, the pH in the lumen of the esophagus decreased significantly after the injection of hydrochloric acid. In recent years, 24-hour esophageal pH monitoring has become a standard for determining the presence or absence of acidic GER, including the percentage of pH<4 in the esophagus, the percentage of pH<4 in the prone and standing positions, the number of times pH<4, the number of times pH<4 lasts more than 5 minutes, and the longest duration. Our normal 24-hour esophageal pH monitoring for pH<4 is less than 6% of the time, the number of times it lasts more than 5 minutes is ≤3, and the longest duration of reflux is 18 minutes. These parameters can help determine the presence or absence of acid reflux and help elucidate the relationship between chest pain and pulmonary disease and acid reflux.
(iii) Intraluminal pressure measurement in the esophagus
Intraluminal esophageal pressure is usually measured using a continuous perfusion catheter system filled with water to estimate the function of the LES and esophagus. For pressure measurement, the pressure catheter is first inserted into the stomach, and later, the catheter is withdrawn at a rate of 0.5 to 1.0 cm/min and the intraesophageal pressure is measured. In normal people, the LES pressure at rest is about 2~4kPa (15~30mmHg), or the ratio of LES pressure to pressure in the gastric lumen is >1. When the LES pressure at rest is <0.8kPa (6mmHg), or the ratio between the two is <1, it indicates LES insufficiency or the presence of GER.
(iv) Gastro-esophageal scintigraphy
This method can estimate the gastric-esophageal reflux. A pneumatic lap band is placed on the patient’s abdomen and 300 ml of acidified orange juice solution containing 300 μCi99mTc-Sc (containing 150 ml of orange juice and 0.1 N
HCL150ml) and drink another 15-30ml of cold boiled water to remove residual test solution from the esophagus and visualize upright. In normal people, no radioactivity exists above the stomach after 10 to 15 minutes. Otherwise, it indicates the presence of GER. The sensitivity and specificity of this method is about 90%.
(e) Barium swallow X-ray examination of the esophagus is less sensitive and has more false negatives.
(F) Endoscopy and biopsy
Endoscopy and biopsy are of great value to determine whether there are pathological changes of reflux esophagitis and whether there is bile reflux whether there is the severity of the pathology of reflux esophagitis. According to Savary and Miller grouping criteria inflammatory lesions of reflux esophagitis can be divided into 4 grades: grade I is a single or several non-fused lesions, manifested as erythema or superficial erosion; grade II is a fused lesion, but not diffuse or circumferential; grade III lesions diffuse circumferential, with erosion but no stenosis; grade IV shows chronic lesions, manifested as ulceration, stenosis, fibrosis, shortening of the width of the esophagus and Barrett esophagus.