Peptic ulcers are chronic ulcers that occur mainly in the bulb of the stomach and duodenum, but also in the lower esophagus, near the gastrojejunal anastomosis, and in Meckle’s diverticulum. The formation of these ulcers is related to the digestive action of gastric acid and pepsin, so they are called peptic ulcers. The majority of this disease (more than 95%) occurs in the stomach and duodenum and is also known as gastroduodenal ulcer. Among them, the age of onset of gastric ulcers is greater than that of duodenal ulcers.
A deceased person in 167 BC in China is the earliest case available. The patient died of peritonitis caused by perforation of the prepyloric ulcer. Gastric ulcers were first recorded in 1586 and duodenal ulcers in 1688. In the 1960s, the annual incidence in the United States was approximately 3,500,000; its characteristics were.
(1) single or multiple ulcers occur in certain favored sites of the stomach and duodenum; (2) a chronic, prolonged course that alternates between healing and recurrence; (3) gastroduodenal ulcer disease is a chronic pathological state unique to humans; and (4) based on the different clinical characteristics of gastric and duodenal ulcer disease, it is suggested that the two may have their own different pathogenic links and processes.
The epidemiology of peptic ulcers, especially duodenal ulcers, has changed significantly in the last 20 years. It is characterized by.
(1) a trend of non-decreasing incidence; (2) a greater decrease in men than in women; (3) an increase in the average age of patients by 2 to 10 years; (4) an increase in the rate of emergency manual surgery and a decrease in the rate of elective surgery; and (5) a shift from previous intractable ulcerative pain to comorbidities such as perforation, bleeding and pyloric obstruction in surgical cases. This may be related to the invention and application of H2 receptor blocking agents. Therefore, surgeons should pay attention to pharmacological treatment along with good surgery in order to achieve good results.
1, Pathogenesis.
H. pylori infection is a common pathogenic and recurrence-causing factor for gastric and duodenal ulcers.
1.1 Gastric ulcer.
Patients are mostly associated with a reduced number of mural cells and low gastric acid secretion. It is usually believed that the occurrence of gastric ulcers is related to the weakening of their mucosa and mucosal barrier function (mucus, alkaline fluid secretion, rate of prostaglandin synthesis within the mucosa).
Currently, gastric ulcers can be divided into 3 separate types according to the response to clinical manifestations and treatment.
Type I: Gastric body ulcer. The ulcers are located in the distal 1/2 of the stomach, near the junction of the gastric body and sinus, mostly in the lesser curvature of the stomach. Patients are mostly accompanied by low gastric acid and are mostly considered to be gastritis type; Type II: i.e., a compound ulcer in which gastric ulcer and duodenal ulcer coexist; Type III: anterior pyloric ulcer. The ulcer is located in the posterior pyloric canal of the gastric sinus. Patients tend to have high gastric acid, consistent with the clinical and therapeutic response of duodenal ulcer patients.
(1) The doctrine of gastric sinus stasis (antral stasis) is proposed. Gastric ulcer is caused by some factors that lead to low function of vagal motor fibers, delayed gastric emptying causing sinus stasis, and gastric contents (mainly gastric acid and pepsin) stimulating the gastric sinus causing gastrin release. And the secretion of gastric acid increases, eventually forming ulcers. This theory can explain the occurrence of type II gastric ulcers very well. However, the disadvantage is that it cannot explain why most gastric ulcer patients do not have delayed gastric emptying.
② Bile reflux theory: Due to the reflux of duodenal contents into the stomach, the damage to the epithelial cells of the gastric mucosa caused by bile and hemolytic lecithin in the bile, the mucosal barrier of the gastric wall is destroyed. Recent studies have found that this result will cause reverse diffusion of H+ into the mucosa and stimulate the release of histamine from mast cells in the mucosa, causing even higher H+ in the stomach; at the same time, it can also cause capillary dilation of the gastric wall and inflammatory edema of the mucosa. In addition, the enhanced acidic environment stimulates the activation of pepsin elements to cause self-digestion, thus facilitating the development of ulcers. From animal experiments, it has been found that the drainage of bile into the stomach can cause chronic inflammatory changes in the gastric mucosa, while the damage to the gastric mucosa caused by the entry of duodenal contents into the stomach is more severe than that caused by bile alone. It was also found that gastric ulcers are often combined with gastric sinusitis, and the closer to the pylorus, the more severe the gastritis; it was also found that the higher the location of the ulcer in the stomach, the more extensive the gastritis. The reflux of duodenal fluid and pyloric insufficiency are related. Therefore, recently, scholars hold the view of “duodenal fluid reflux”.
③ Junction theory: from the structure of the gastric wall, there are two junction areas at the gastric bend. One is the junction of gastric sinus and mucosa of wall cells; the other is the junction of longitudinal muscle fibers and oblique muscle fibers. This theory suggests that gastric ulcers mostly occur in the junctional overlap zone of different mucosa or muscles.
1.2 Duodenal ulcers.
Gastric acid and pepsin are the main damage factors. The concept of “no acid means no ulcer” has been around for more than 100 years and is still accepted today.
Regarding the pathogenesis of duodenal ulcers.
The ulcerogenic effect of pepsin is less important than that of gastric acid. Gastric acid secretion is increased in 1/3-1/2 of duodenal ulcer patients. It is commonly believed that the development of chronic duodenal ulcer is associated with mucosal damage caused by high gastric acid and high pepsinogen secretion. However, the relationship between ulcer disease and gastric acid secretion is not simply linear in absolute numbers, but may be the result of a combination of increased stimulation of gastric acid secretion and decreased inhibition of gastric acid secretion.
It is thought that the factors that may cause enhanced gastric acid secretion include
a. Increased number of mural cells, i.e., high PCM. The number of mural cells in patients with small duodenal ulcers has been described in the literature as approximately 1.8×1 billion; almost twice as many as in normal subjects. This causes an increase in MAO that is significantly associated with the number of mural cells, resulting in a hyperacidic secretory state.
b. Increased stimulation and excitability of mural cell secretion activity. This is manifested by increased cholinergic stimulation via the vagus nerve and increased activity of gastrin release from G cells in the gastric sinus. The former is mainly manifested by fasting nocturnal hypersecretion in ulcer patients; the latter is manifested by higher than normal gastrin values measured in patients with duodenal ulcer, thus causing gastric acid secretion.
c. Increased sensitivity of mural cells to acid-producing stimuli. The increased gastric acid secretion refers to the increased responsiveness of the wall cells to normal vagal and sinus gastrin stimulation, resulting in excessive gastric acid secretion. It has also been suggested that this increased sensitivity is related to the enhanced calcium content or stimulation of the second messenger of gastric acid secretion.
d. Weakening of the negative feedback or inhibitory mechanism of gastric acid secretion leads to increased relative gastric acid secretion. This may involve a defective feedback mechanism of gastric acid secretion itself or a weakened function of some gastrointestinal hormones that inhibit gastric acid secretion.
e. The pathogenic role of Helicobacter pylori (Hp), i.e., the Hp infection-gastritis-ulcer formation theory of infection.
In 1993, Australian scholars Marshall and Warren first isolated this bacterium from the gastric mucosa of patients with gastric disease and suggested that the bacterium may be the causative agent of chronic gastritis and peptic ulcer. There are two theories, namely: Leaking roof hypothesis: Hp causes upper gastrointestinal tract injury by damaging the local mucosal barrier of the gastroduodenum; Levi’s gastrin-link hypothesis: Hp increases gastrin secretion and release in the fundus of the stomach and increases acidity in the stomach, causing gastroduodenal injury. Hp infection is one of the causes of chronic gastritis, DU and GU, and is a worldwide problem. The prevalence of infection increases with age. Our country is one of the countries with a high rate of infection, with a natural population rate of 40% to 60%. Hp is mainly transmitted orally, but there are also studies suggesting the possibility of transmission through the birth canal. hp mainly inhabits the mucus layer of the gastric sinus and the epithelium, and it can produce a variety of enzymes and toxins (urease, peroxidase, proteolytic enzymes, lipase, phospholipase, vacuolar toxin and lipopolysaccharide). Therefore, Hp infection must be removed in order to cure ulcers.
(2) Weak inhibition mechanism of gastric acid secretion: In duodenal patients, their duodenum is weakened by the specific pH-sensitive mechanism of gastric acid inhibition, and gastric emptying is accelerated, resulting in pH imbalance in the duodenum.
In addition, increased intake of smoking, caffeine, and alcohol is also associated with the development of duodenal ulcers. It has been shown that alcohol has a destructive effect on the defense mechanism of the gastric mucosa. Excessive alcohol consumption can lead to acute gastritis.
2.Treatment.
In principle, the treatment of gastric ulcer is based on the application of surgery. The main purpose of surgery is to reduce gastric acid secretion, which is not necessarily suitable for the treatment of gastric ulcer from the pathogenesis. Drug therapy is limited to duodenal ulcers without complications.
2.1 Pharmacological treatment.
According to the location and size of the ulcer and the level of gastric acid secretion, drug therapy is feasible in patients with good general condition, small ulcers and no malignant evidence. Internal treatment is effective, and the ulcer is usually healed within 8 weeks, but the recurrence rate is high, with a recurrence rate of 40% within 2 years, of which 70% recurs within 1 year. The understanding of the pathogenesis and natural history of peptic ulcers and their treatment has been revolutionized in the past 20 years by scientific evaluation of the natural history of peptic ulcers and the effectiveness of various treatments, the vigorous development of new drugs, and the widespread use of endoscopy.
Tracing the history, the treatment of peptic ulcer can be divided into three stages.
① Acid suppression therapy. Treatment is directed at the increase in gastric acid secretion, the main cause of ulcer development. This is the earliest treatment method applied and has been shown to be effective so far.
②Strengthening gastric mucosa defense treatment. By enhancing the defense and self-healing ability of gastric mucosa, the treatment effect is similar to that of antacids; moreover, it is possible to reduce recurrence more effectively than antacid treatment.
(iii) Antibacterial therapy. Recent studies have shown that in most cases of peptic ulcer, H. pylori may play an important pathogenic role. Removal of this bacterium not only helps the ulcer heal, but also reduces recurrence and even alters the natural course of the disease. Given that the transmission route of H. pylori is mainly oral, it is unrealistic to hope to kill it permanently with antibacterial antibacterial; therefore, the study of H. pylori immunization vaccine may provide us with a way to completely eliminate H. pylori. Currently, some scholars have been engaged in this area of research, however, no successful reports have been made.
2.1.1 Treatment of peptic ulcers aims to
(1) to relieve symptoms; (2) to promote healing; (3) to prevent recurrence; and (4) to prevent complications. From the present treatment results, for most cases without complications, the current treatment, including maintenance treatment, can effectively relieve symptoms and promote healing; in terms of reducing the recurrence rate, little progress has been made; whether the occurrence of complications such as bleeding, perforation and obstruction can be reduced is yet to be determined.
2.1.2 Treatment for gastric acid secretion conditions.
2.1.2.1 For those with low gastric acid, mucosal protective agents are mainly chosen.
For example.
Aluminum thioglycollate (Sucra lfate) has good efficacy for gastric ulcer and is equivalent to cimetidine for duodenal ulcer. The main advantage of this drug is that it is safe and can be the drug of choice for the treatment of peptic ulcers in pregnant women.
Carbenoxolone, a licorice preparation, is more commonly used to treat gastric ulcers and occasionally duodenal ulcers. It is less effective than other drugs.
Tri-potassium dicitrato-bismuthate has been used clinically for more than 20 years, but only in recent years has it received attention. Among the many gastric drugs, it is the only one that can kill H. pylori. Trade names include Dilaudid and De-Nol. Its main advantage is that it reduces the rate of ulcer recurrence. The recurrence rate within one year of stopping the drug is 39%-76%.
2.1.2.2 For people with high gastric acidity, gastric acid secretion inhibition should be used.
①H2 receptor antagonist: It not only inhibits histamine-stimulated acid secretion, but also partially inhibits gastrin- and acetylcholine-stimulated acid secretion. However, gastric acid secretion resumes rapidly after drug discontinuation, and even rebound secretion occurs. The latter may be associated with ulcer recurrence after drug discontinuation. The recurrence rate within one year of drug discontinuation is 60% to 100%. Clinically used H2 receptor antagonists include: cimetidine, taganet, ranitidine, ranitidine, zantac, famotidine, (pepcid), which have different relative strengths of action, but there is no significant difference in clinical efficacy.
②Toxoplasma receptor antagonists: non-selective M1 and M2 receptor antagonists, such as atropine and probenecid, have been used to treat peptic ulcers for many years. The disadvantage is the limited efficacy with side effects. Since the introduction of H2 receptor antagonists, these drugs have been used less frequently. Quazepam (prienzepin) is a relatively selective M1 receptor antagonist that is much more powerful in suppressing acid secretion than smooth muscle, cardiac muscle, and salivary gland secretion. In recent years this drug has been used to treat duodenal ulcers, but is less effective than H2 receptor antagonists.
(3) H+-K+-ATPase inhibitors: (acid pump inhibitors, proton pump inhibitors) suberimidazole (omeprazol), omeprazole, losec (losec) are the first acid pump inhibitors used in clinical practice. It is stronger than H2 receptor antagonists and can strongly inhibit acid to pH>7.0, causing complete acid deficiency, denaturing and inactivating pepsin, and promoting ulcer healing. The high healing rate of DU and esophagitis is related to the strong inhibition of pepsin. In fact, this drug can be considered as the final medical treatment for peptic ulcer. With proper dosage and optimal acid inhibition, there is almost no case of peptic ulcer that does not respond to it. This fact confirms the old adage that “no acid means no ulcer”. In addition, it is the drug of choice for the treatment of hypersecretory states, such as Zollinger-Ellison syndrome.
Prostaglandins: Prostaglandin E is a major factor in cytoprotection, but has not been shown experimentally or clinically to be more effective than antisecretory agents in promoting healing of chronic ulcers. It is used to prevent mucosal damage, especially in patients treated with non-steroidal anti-inflammatory agents (NSAIDs), and its concomitant use significantly reduces the incidence of gastrointestinal mucosal erosions and ulcers.
(5) Antacids: This is the oldest class of anti-ulcer drugs that reduce gastric acid by chemical neutralization. It is no less important than H2 receptor antagonists in the treatment of peptic ulcer. For example, chewable tablets containing aluminum hydroxide and magnesium sulfate.
(6) Antibacterial therapy: The application of antibacterial drugs to clear H. pylori infection can promote ulcer healing and reduce recurrence, especially for certain intractable ulcers, which often have better results. The clinical application is often combined, such as: trimethyl dicron complex bismuth, tetracycline or hydroxybenzyl penicillin and metronidazole, etc. At present, the application of antimicrobial agents is considered necessary in the treatment of peptic ulcer.
(7) Others: Proglumide, octreotide, sandostatin, and furazolidone (dysentery) are used as dopamine promoters and have therapeutic effects on peptic ulcer. It has an inhibitory effect on H. pylori, which may also be one of its therapeutic mechanisms.
(8) Diet therapy: Before the introduction of H2 receptor antagonists, diet therapy used to be the only or main treatment for peptic ulcer. In 1901, Lengartz pointed out the importance of small and frequent meals. Later, the Syppy diet (consisting of milk, eggs, cream, and later some “soft” non-stimulating foods) was introduced and was used clinically for decades. The widespread use of antacids and H2 receptor antagonists has reduced the status of diet therapy. Despite the great achievements of other treatments, there is still a need for dietary guidance of patients. Its value has been re-evaluated in recent years.
2.2 New avenues in the treatment of peptic ulcers.
The improved understanding of mucosal defense mechanisms has made it possible to open up new avenues of treatment.
2.2.1 Improvement of microcirculation.
Vasospasm and nonvascular smooth muscle (and possibly mucosal muscle layer) contraction may be the primary mechanism of some types of gastric damage, which in turn is mediated in part by vasoactive and mass. If the mechanism can be elucidated, it can be prevented and treated by its receptor antagonists or synthetic inhibitors. The support of certain vasodilators may improve microcirculation, thereby enhancing the mucosal barrier and the ability to handle acid.
2.2.2 Improvement of neural mechanisms.
It is known that nerve afferent reflexes may play an important role in superficial mucosal damage. In individuals sensitive to peptic ulcers, this neural reflex is impaired and the epithelium is abnormally “leaky” so that acid diffusion is increased or the epithelium is unable to tolerate “normal” acid. Therefore, the use of drugs that regulate neural reflexes and reactivity may enhance the protective effect of the mucosa.
2.2.3 Modulation of immune response.
The chronicity of peptic ulcers may be related to the inability of the mucosal immune system to clear antigens. Application of immunomodulatory drugs may help to clear antigens and thus block their development. Many drugs are known to accelerate antigen healing, such as: interleukin 1β, platelet-derived growth factor, transfer growth factor, and epidermal growth factor. In addition, care should be taken to avoid alcohol, smoking and drugs that have an irritating and damaging effect on the mucosa. Most ulcers heal within 12 to 15 weeks after the above treatment. The recurrence rate of ulcers is about 25% to 60% within 5 years after stopping the medication, most of which is seen within six months.
2.3 Surgical treatment.
In the past, the aim of surgical treatment was to prevent recurrence of ulcers, but now it has evolved to eradicate the disorder so that the patient can live as normal a life as possible and reduce mortality and recurrence rates. However, theoretically, no single procedure is so perfect that it can be adapted to the objective reality of ulcer disease, which is so variable. Each procedure has its own advantages and, if properly applied, can lead to good results. In the meantime, scholars are still trying to explore new avenues. In addition, for many surgeons, there is a general emphasis on surgery and neglect of postoperative pharmacotherapy to maintain outcomes; in particular, the lack of understanding of the impact of H. pylori makes the treatment of this disease in the surgical field still incomplete.
2.3.1 Indications.
① Where the patient has a long history of disease and malignancy cannot be excluded clinically, the cancer rate is generally estimated to be no more than 1.5%. The problem is that some gastric ulcers are themselves malignant. Grossman reported 638 cases of benign ulcers with a 7-year follow-up, and 3.9% were malignant. Therefore, even if no cancer cells are found on biopsy, surgery should be considered if the ulcer does not heal for a long time, especially if the ulcer is huge, with a diameter of 2.5 cm or more.
②If the ulcer does not heal after 12 to 15 weeks of drug treatment. For example, compound ulcer patients, accounting for about 20%. Due to the pyloric drainage disorder and gastric retention caused by duodenal ulcer first, it is difficult for internal treatment to be effective, and it is also prone to secondary complications such as bleeding, obstruction and perforation.
(3) Recurrence of ulcers after the completion of treatment and discontinuation of the drug. Especially those who relapse after 6 months to 12 months are suspected to have ulcer quality.
④Those with comorbidities during treatment (e.g., pyloric obstruction, perforation, or severe bleeding).
⑤ Penetrating ulcers.
2.3.2 Choice of surgical procedure.
There are many surgical options available, each with its own advantages and disadvantages. Specifically, the majority of the stomach has a long history of resection. It is designed to lower acid and promote ulcer healing by removing the acid-producing area of the stomach. However, there are more postoperative complications, such as nutritional disorders and disabling sequelae caused by surgery for small gastric syndrome, which are difficult to fully recover from. In addition, the surgical trauma to the patient is also greater. The highly selective vagotomy was also designed and perfected by reducing the overproduction of gastric acid. The scope of the procedure has been significantly limited, and postoperative complications have been significantly reduced. However, the problem of high recurrence rate has emerged. The key to surgical treatment is the strict selection of the indications (selection of the procedure according to the cause and mechanism of individual pathogenesis) and the delicate operation to prevent complications in order to improve the surgical efficacy.
2.3.2.1 Major gastrectomy (Billoroth operation).
In 1881, Theodor Billroth (1829-1894), a German, pioneered the use of major gastrectomy to treat a patient with gastric cancer. The following year, Von Rydigier used it to treat ulcer disease. This was the beginning of surgical treatment of peptic ulcers. The procedure at that time was a pyloric resection with gastroduodenal anastomosis. It was later found that the ulcer recurred quickly after this procedure, so the scope of the procedure was expanded to 66%-75% of the distal stomach. In view of the distance between the stomach and the duodenal stump after extensive resection, in 1884, Billtoth invented a major gastrectomy with gastrojejunostomy; these were called Billroth I and II surgery. Since both of them can meet the purpose of surgical treatment of ulcer disease, which is to “cure the ulcer, eliminate the symptoms and prevent recurrence”, they were soon widely adopted. As for the ulcer itself, it is best to remove it, but its removal is not a necessary prerequisite for the cure of ulcer disease. It has been shown that an open ulcer can gradually heal on its own if food no longer passes through it. By 1930, a major gastrectomy was considered the standard procedure for the treatment of ulcer disease.
In the mid-1950s in China, major gastrectomy had been largely popularized in the majority of urban and rural hospitals, and good results had been achieved. So far, according to the statistics of a large group of cases in China, the near and long-term results of major gastrectomy for ulcer disease can reach 90%-95%. The operative mortality rate is 0.5% to 1.0%, and the recurrence rate does not exceed 1% to 2%. In recent years, due to the improvement of technology, the number of Billroth Ⅰ is gradually increasing.
①Billroth Ⅰ: It is the preferred operation for gastric ulcer. It is very suitable for type I gastric ulcer. Generally, 50% of the stomach (so-called hemi-gastrectomy) is sufficient.
Theoretically, this procedure has the following advantages.
a. Removal of the ulcer and the surrounding area of gastritis; b. Removal of the sinus portion of the stomach, removing the susceptible area and the gastrin-producing area; c. Simple surgical operation, more in line with the physiological anatomy. There are fewer postoperative complications due to gastrointestinal dysfunction.
②Billroth II: suitable for the treatment of gastric and duodenal ulcers in various conditions; especially in duodenal ulcers, this procedure is recommended. Note that the extent of gastrectomy must be greater than 60%; if less than 50% is removed or only part of the sinus is cut down, it will definitely lead to anastomotic ulceration.
The advantages of this procedure are
a. Adequate stomach can be resected without excessive anastomotic tension; b. The recurrence rate of postoperative ulcers is low; c. Food and gastric juice can enter the jejunum directly after surgery, and even difficult-to-resect duodenal ulcers can heal.
Disadvantages of this procedure.
a. The surgical operation is more complicated than Billroth II; b. The gastrojejunal anastomosis changes the normal anatomical and physiological relationship, and there are more postoperative complications. These include: small stomach syndrome, diarrhea, dumping syndrome, reflux gastritis or esophagitis, anastomotic ulcer, input collaterals syndrome, output collaterals obstruction, and pancreatitis.
Commonly used procedures.
a, gastrectomy, postcolonic gastrojejunostomy (Hoffmeister method); this procedure should be preferred for anyone who cannot use the Billroth I style.
b. BPolya method; c. Gastrectomy and anterior colonic gastrojejunostomy (Moynihan method); this procedure is used when the Hoffmeister method is not available due to transverse colon mesenteric variation.
d. V. Eiselsberg method, etc.
There are certain postoperative complications associated with each procedure. The good and bad of the procedure is relative and should be chosen at discretion.
2.3.2.2 Various vagotomies of the stomach.
Sir Benjamin Brodie was the first to discover the importance of the vagus meridian in promoting gastric secretory activity and in his studies on dogs in 1814. in 1925 Eugen Bircher (1882-1956) first recommended a selective vagotomy for the treatment of peptic ulcers. However, it has not received much attention from the clinical surgical community. This type of surgery mainly eliminates the nerve phase and was originally only indicated for duodenal ulcers. Postoperative gastrin levels are often elevated, which seems to be detrimental to gastric ulcers, but there is a benefit to ulcer healing from the aim of reducing gastric acid secretion. In gastric ulcers, it is more suitable for type II and III gastric ulcers. It must be noted that the ulcer is first excluded as malignant to avoid delaying treatment. Because of the increased risk of gastric mucosal carcinogenesis due to duodenal and jejunal fluid reflux after major gastrectomy (Augerinos, 1990); and Watanapa (1992), who demonstrated in a rat experiment that duodenal fluid reflux has a pancreatic carcinogenic effect. In recent years, vagotomy has received attention and application from surgeons all over the world. This type of surgery has the advantages of high safety and few sequelae, but the recurrence rate of postoperative ulcers is generally high. Most scholars report that the recurrence rate is 5% to 7%. For this reason, there are many clinical improvement options available.
Clinical surgeons tend to perform various vagotomies with drainage (pyloromyotomy or pyloroplasty). In order to reduce the incidence of postoperative complications, especially serious complications. The procedures associated with vagotomy are
①Vagus nerve trunk dissection: In 1943 Dragstedt first created the vagus nerve trunk dissection to treat ulcer disease. This method is easy to operate and the resection is complete. However, postoperative gastric emptying obstruction, retention of gastric contents, and other visceral secretion and motor dysfunction were left behind and have been abandoned.
Selective vagotomy was studied by Wertheimert and Lartarjet in 1922, and in 1948, Jackson and Franksson used this procedure in duodenal surgery. This procedure preserved the left hepatobiliary branch and the right abdominal branch of the vagus nerve. Therefore, no other visceral function rate disturbance occurs, but there is still the disadvantage of retention of gastric contents.
③Highly selective vagotomy: (High Selective Vagogomy) also known as mural cell or proximal gastric vagotomy, acid secretion vagotomy or superselective vagotomy: first proposed by Jlhnston and William in 1969. This procedure only cuts the crow’s claw nerve that branches the pyloric sinus and duodenum, leaving the function of the pylorus and pyloric sinus normal, without the need for additional gastric drainage surgery. The procedure is less invasive, has fewer complications, and is more anatomically correct. In 1970, Johnston and Amdrup reported early clinical results of applying highly selective vagotomy without additional gastric drainage, preserving the whole stomach and its emptying function; the operative mortality rate was low, and postoperative complications and gastrointestinal symptoms were few, thus rapidly gaining widespread use. The efficacy is related to the ulcer site, the presence of combined pyloric obstruction, and the surgeon’s operating experience. Complications: splenic injury (1.4%-4% for splenectomy), esophageal perforation (0.7%-1.6%) and necrotic perforation of the gastric lesser curvature (0.036%-2.8%) due to technical shortcomings; diarrhea (0%-7%) and dumping syndrome (0-4%) due to altered gastrointestinal function. Dewer observed that the rates of bile reflux and gastritis after selective vagotomy were significantly lower than those of other procedures. Most reported no surgical death, with some reporting a mortality rate of 0.4% to 0.9%. The cause of death is mostly in elderly patients with combined cardiopulmonary disease. The high recurrence rate is a major drawback of this procedure, with Johnston reporting a range of 3% to 30%, with an average of 8%. Most recurrences occur within 1a to 3a after surgery, and there are reports of proportional recurrence and follow-up time. In addition, the high operative requirements are a major obstacle to the popularization of this procedure. Most authors report poor outcomes with highly selective vagotomy for type III ulcers, with a recurrence rate of 16% to 44%. This is significantly higher than that of duodenal ulcers.
The gastric drainage problem was also addressed on the basis of ④ selective vagotomy slices. Among them, the removal of the pyloric sinus removes the cephalic and gastric phases of gastric acid secretion. Thus both vagotomy and removal of the large part of the stomach have the double advantage. However, this procedure is too large and is only indicated for cases with high fasting acid excretion and maximum acid excretion.
Vagotomy with sinus resection was proposed by Franksson and Jakson in 1948.
(vi) Vagotomy plus pyloroplasty. 1948 by Franksson and Jakson. The recurrence rate of duodenal ulcer after surgery is about 10%.
2.3.2.3 Roux-en-Y type gastrointestinal anastomosis.
To prevent duodenal fluid reflux after Bllroth-type surgery, it is mostly considered as the procedure of choice for secondary surgery. Because of the possibility of ulcer recurrence, vagotomy should be added to this procedure. Some authors advocate using this procedure instead of the conventional gastrojejunostomy, but no large number of cases have been reported.
2.3.3 Laparoscopy in peptic ulcer.
Application in the treatment: this is a remarkable development in general surgery in recent years. this technique was first used in surgery in the 80s. Due to the improvement of instruments and auxiliary techniques, this technique was soon appreciated and widely used by surgeons. Hill and Barker used this method to perform selective vagotomy (posterior vagal trunk and anterior hyper-selective vagotomy) to achieve satisfactory results of acid reduction without affecting gastric emptying. This procedure is expected to be accepted by general surgeons because it is less invasive, easier to perform, and has a faster postoperative recovery.
2.3.4 Application of endoscopy in the diagnosis and treatment of peptic ulcer.
The main application of endoscopy in the treatment of peptic ulcer at present is hemostasis. Its most prominent methods are thermal coagulation and injection therapy. Recent studies have shown that endoscopic treatment significantly reduces the mortality rate in cases of bleeding (by 30%). It reduces the rebleeding rate by 69% and the emergency surgery rate by 62%.