Perforative ulcers at the posterior wall

　　The occurrence of perforative ulcers at the posterior wall is related to excessive gastric acid secretion.

　　Hydrochloric acid is the main component of gastric juice, secreted by parietal cells and regulated by the nervous and humoral systems. It is known that there are three receptors in parietal cells, namely histamine receptors, cholinergic receptors, and gastrin receptors, which respectively accept the activation of histamine, acetylcholine, and gastrin. Once the surface receptors of parietal cells are bound by corresponding substances, the intracellular second messenger is activated, thereby affecting the secretion of gastric acid.

　　There are two main second messengers in parietal cells: cAMP and calcium. After the intracellular receptors of parietal cells bind to histamine, they couple with excitatory GTP-binding proteins to activate adenylate cyclase, which catalyzes the conversion of ATP to cAMP. cAMP then activates a protein kinase, causing an as yet unknown intracellular protein to be phosphorylated, ultimately leading to the secretion of H⁺K⁺-ATPase (also known as hydrogen ion pump or proton pump) is activated, promoting acid secretion. After acetylcholine receptors and gastrin receptors bind to acetylcholine and gastrin respectively, they couple with GTP-binding proteins, activating membrane-bound phospholipase C. This enzyme catalyzes the hydrolysis of phospholipids within the membrane, generating inositol triphosphate (IP3) and diacylglycerol. Inositol triphosphate (IP3) stimulates the release of calcium from intracellular stores, and then activates H⁺K⁺-ATPase promotes the secretion of H+ ions. Acetylcholine can also increase the permeability of the cell membrane to calcium.

　　Gastrin and acetylcholine can promote the release of histamine by enterochromaffin-like cells (ECL), and they have a synergistic effect with histamine. There is also a somatostatin substance on the surface of parietal cells, which, upon excitation, binds to the inhibitory membrane receptor Gi, inhibits adenylate cyclase through inhibitory GTP-binding protein, thereby reducing the intracellular cAMP level, causing parietal cells to secrete H⁺.

　　Parietal cell receptors are excited, regardless of the stimulus received, they ultimately pass through the second messenger cAMP and Ca2⁺, affecting the secretory membrane structure at the apical part of parietal cells and the proton pump H⁺K⁺-ATPase, causing H⁺Increased or decreased secretion can trigger the onset of the disease.

　　Perforative ulcers at the posterior wall can complicate with shock and acute peritonitis, with the following symptoms.

　　22. Shock:The severe chemical stimulation after perforation can cause shock symptoms. The patient may appear restless, shallow breathing, a rapid pulse, and unstable blood pressure. As the pain of the abdomen decreases, the situation can become stable. Later, as bacterial peritonitis becomes more severe, the condition can become worse again, and severe cases can lead to infectious (toxic) shock.

　　20. Acute peritonitis:The whole abdominal muscle is tense like a board, with significant tenderness, resistance to pressure, and rebound pain in the whole abdomen. Laboratory examination shows an increase in white blood cells. In general, the white blood cell count in cases of acute perforation is between 15,000 and 20,000/mm3, with an increase in neutrophils; hemoglobin and red blood cell count also increase due to varying degrees of dehydration. A tentative abdominal puncture can be performed, and the extracted fluid can be examined under a microscope. If the field is full of white blood cells or pus balls, it indicates inflammatory ascites, which is evidence of peritonitis. It can also be measured for ammonia content, if it exceeds 3μg/ml, it indicates gastrointestinal perforation.

　　The most prominent manifestation of posterior wall perforating ulcers is back pain. The most common cause of refractory duodenal ulcers in clinical practice is the deep penetration of posterior duodenal ulcers into the pancreas. If so, the rhythm and periodicity of the original ulcer pain will change.

　　At first, the patient reports back pain, usually a little to the right of the midline of the lower thoracic and lumbar vertebrae. It often radiates like pancreas pain. Initially, this back pain appeared with the appearance of anterior abdominal wall pain, which can be relieved by drinking milk or antacids. Later, as the penetration deepens, this back pain may become more persistent than the previous ulcer pain. At this time, eating or taking antacids cannot relieve the pain.

　　Although this penetrating ulcer often involves the pancreas, it rarely causes hemorrhagic pancreatitis. It may also cause an increase in serum amylase levels and typical pain, but the clinical manifestations of acute pancreatitis are rarely present.

　　If the pain is only manifested as persistent, and there is only mild back pain, it is relatively difficult to distinguish whether there is a penetrating ulcer at this time. At this time, clinical doctors are often prone to ignore the diagnosis of the disease, and the best way is to consider this complication once the patient has persistent pain that cannot be relieved by eating.

　　The prevention of posterior wall perforating ulcers mainly focuses on the prevention of the cause, and the specific preventive measures are described as follows.

　　9. Patients with a history of ulcer disease should be treated actively, systematically, and in accordance with the rules to prevent the occurrence of ulcer disease perforation.

　　8. Eliminate the cause and control the symptoms, promote ulcer healing, prevent recurrence, and avoid complications.

　　7. In daily life, eat easily digestible foods, eat small and frequent meals, and avoid overeating. Do not eat too heavily at dinner. Adhere to eating low-fat foods in daily life, such as lean meat and low-fat dairy products.

　　6. Strengthen physical exercise, enhance physical fitness, reduce risk factors such as smoking and excessive alcohol consumption, and improve self-immunity.

　　The examination of posterior wall perforating ulcers includes serum enzyme blood tests, X-ray examination, and fiberoptic endoscopy. The specific examination methods are described as follows.

　　One, Serological examination

　　The ulcer penetrates into the pancreas, and there may be an increase in serum amylase levels.

　　Two: X-ray examination

　　1. Abdominal X-ray film:When the ulcer penetrates the gallbladder or common bile duct to form a fistula, gas can be seen in the bile duct.

　　2. Gastrointestinal barium meal examination:It can show the fistula entering the transverse colon or bile duct, and the lateral view can show penetration.

　　3. CT examination:The presence of masses, pseudocysts within the pancreas, or gas in the pancreatic duct is a sign of pancreatic rupture. Gastric ulcer penetration into the liver is manifested by unclear contours of the serosal surface of the gastric wall, and a fluid hypodense shadow appears at the edge of the liver closely connected to the gastric wall, which may contain gas and can form small gas-liquid levels, with blurred low-density edges.

　　Three: Fiberoptic endoscopy

　　Deep ulcers (fossa shadow) are suspected to be penetrating. Large gastric ulcers with uneven surfaces are mostly benign and have penetrated into the pancreas.

　　When an acute attack of posterior wall perforating ulcer occurs, it is important to fast to avoid stimulating the local condition. Pay attention to eating easily digestible food, eat less and more often, and avoid overeating. It is not advisable to eat too much for dinner. In daily life, adhere to eating low-fat foods such as lean meat and low-fat dairy products. Avoid smoking and drinking. Specific dietary precautions are described below.

　　One: Diet宜 for patients with posterior wall perforating ulcers

　　1. Eat easily digestible, high in calories, rich in protein and vitamins.

　　2. Eat more foods rich in vitamin A, B, and C, such as fresh vegetables and fruits.

　　Two: Diet taboos for patients with posterior wall perforating ulcers

　　1. Quit smoking and drinking.

　　2. Avoid eating刺激性 food.

　　3. Eat less sweet and sour foods and fruits.

　　4. Eat less food that is easy to cause bloating.

　　Perforated ulcer at the posterior wall is difficult to treat. If proton pump inhibitors and eradication therapy for Helicobacter pylori are applied and the ulcer still does not heal, it is a sign for selective surgery. The surgical options include vagotomy of the vagus nerve trunk or proximal gastric vagotomy, or vagotomy combined with gastric antrum resection. Many surgeons believe that penetration usually represents a severe harmful ulcerative disease, and vagotomy combined with gastric antrum resection is superior to proximal gastric vagotomy. However, conclusive data is currently unavailable.

　　If the patient has a penetrating duodenal ulcer (DU) and the surgeon is to perform vagotomy with gastric antrum resection, the surgeon must carefully evaluate the two structural complications of the duodenum with chronic ulceration before beginning the resection. First, check and judge the severity of inflammation or scarring in the first part of the duodenum, as cutting this type of duodenum can make it difficult to suture or anastomose the duodenal stump. The second structural change that must be assessed is the severity of shortening of the first part of the duodenum. In severe ulcerative disease, shortening is severe, bringing the ampulla closer to the pylorus. In this case, it is possible to injure the common bile duct and the ampulla when the duodenum is cut. Experienced doctors will avoid performing gastric antrum resection in the presence of these two unfavorable conditions for anastomosis. Vagotomy combined with gastrojejunal anastomosis (avoiding pyloroplasty) is another option, but this surgery can cause unsatisfactory consequences such as dumping syndrome and diarrhea. Different types of treatment require different approaches, as described below.

　　1. Penetrating Gastric Ulcer

　　The surgical choice for penetrating benign gastric ulcer is Billroth I gastric antrum resection. The base of this ulcer is usually large and involves the pancreas. During the antrum resection, the base of the ulcer is not separated, and the stomach is sharply dissected around the peripheral edge of the penetration. In type I ulcers, additional distal gastric resection and truncal vagotomy do not reduce the long-term recurrence rate, so antral resection is sufficient. Unless it is a prepyloric ulcer, there is no need to increase truncal vagotomy. Patients with prepyloric ulcers often have similar gastric acid secretion as DU, and increasing vagotomy is beneficial to prevent recurrence.

　　2. Penetration and Biliary Fistula

　　When the fistula forms between the duodenal ulcer (DU) and the gallbladder or common bile duct, truncal vagotomy combined with antral resection can effectively treat the ulcer disease by using a gastric jejuno-anastomosis to bypass the fistula. However, this method can only be used in patients where the proximal duodenum can be transected and the duodenal stump can be safely closed. If not, the gallbladder is resected directly to handle the fistula, the common bile duct is drained with a T-tube, and the duodenal fistula is closed. Additionally, a large omentum is used to strengthen the dressing, and postcapillary venous microvessels (PGV) or truncal vagotomy combined with jejuno-anastomosis are adopted.

　　3. Gastric Colonic Fistula

　　The best treatment for a gastric colonic fistula caused by benign gastric ulcer is the combined resection of the gastric antrum and the involved transverse colon, and anastomosis of the stomach to the duodenum. Mechanical and antibiotic bowel preparation is required before surgery. Unless there is an accidental abscess, colostomy is not needed.

　　4. Gastric Jejuno-Colonic Fistula

　　Patients with gastric jejuno-colonic fistula often have malnutrition. Preoperative preparation requires total parenteral nutrition, broad-spectrum antibiotics to control diarrhea, and H2 receptor antagonists or proton pump inhibitors for treatment. Sufficient bowel preparation is also provided, including the primary resection of the gastric jejuno-colonic fistula, and anastomosis of the stomach to the jejunum or duodenum, jejuno-jejunal anastomosis, and colo-colonic anastomosis.