Posterior wall perforated ulcer
Introduction
Introduction to posterior wall perforating ulcer Ulcer penetration refers to the deep penetration of the serosa layer, which locally causes inflammation and adhesion due to the blockage of adjacent tissues, or the ulcer penetrates into adjacent tissues to form a wrap-around hole. This is more common in the duodenal ulcer of the posterior wall, and it is rare for gastric ulcer to penetrate. More than half of them penetrate into the pancreas, followed by the stomach and liver ligaments. Duodenal ulcers can also penetrate into the gallbladder or common bile duct; gastric ulcers can penetrate into the transverse colon. basic knowledge The proportion of illness: 0.15% Susceptible people: no specific population Mode of infection: non-infectious Complications: shock acute peritonitis
Cause
Posterior wall perforating ulcer
Excessive secretion of gastric acid hydrochloric acid is the main component of gastric juice, secreted by parietal cells, regulated by nerves and body fluids. It is known that parietal cells contain three receptors, namely hirstamine receptors, cholinergic receptors and gastrin receptors, which receive histamine, acetylcholine and gastric secretion, respectively. Activation of the prime. When the surface cell surface receptor is bound by the corresponding substance, the second messenger in the cell is activated, thereby affecting gastric acid secretion. There are two major second messengers in parietal cells: cAMP and calcium. The receptor in the parietal cell membrane, after binding to histamine, is coupled to an excitatory GTP-binding protein that activates adenylate cyclase, which catalyzes the conversion of ATP to cAMP. cAMP then activates a protein kinase that phosphorylates an unrecognized intracellular protein that ultimately leads to activation of H+K+-ATPase (also known as a hydrogen ion pump or proton pump) in parietal cells, promoting acid secretion. The acetylcholine receptor and the gastrin receptor, after binding to acetylcholine and gastrin, respectively, are coupled to a GTP-binding protein to activate membrane-bound phospholipase C. The enzyme catalyzes the decomposition of phospholipids in the membrane to produce inositol trisphosphate (IP3) and diacylglycerol. IP3 promotes the release of calcium from the intracellular reservoir and activates H+K+-ATPase to promote H+ secretion. Acetylcholine also increases the permeability of the cell membrane to calcium. Gastrin and acetylcholine promote the release of histamine from enterochromaffin-like cells (ECL), which have synergistic effects with histamine. There is still somatostatin on the surface of parietal cells. After excitatory, it binds to the inhibitory membrane receptor Gi, and inhibits adenylate cyclase by inhibitory GTP-binding protein, thereby reducing intracellular cAMP levels. The secretion of H+ from parietal cells is reduced. Excitatory receptors in parietal cells, regardless of which stimulus is received, eventually pass through the second messenger, cAMP and Ca2+, which affects the secretory membrane structure at the apical cell wall and the proton pump, H+, K+-ATPase, which increases H+ secretion. Or reduce and induce the disease.
Prevention
Posterior wall perforation ulcer prevention
1. Patients with a history of ulcers should be treated actively, standardizedly, and systematically to prevent complications of ulcer disease: perforation of ulcer disease.
2, eliminate the cause and control symptoms, promote ulcer healing, prevent recurrence and avoid complications.
3, usually eat foods that are easy to digest, eat less meals, avoid overeating, dinner should not be too full, usually insist on eating low-fat foods, such as lean meat and low-fat dairy products.
4, strengthen physical exercise, enhance physical fitness, reduce risk factors such as smoking, alcohol, and improve their immunity.
Complication
Posterior wall perforation ulcer complications Complications, shock, acute peritonitis
1, shock: severe chemical stimulation after perforation can cause shock symptoms. The patient developed irritability, shortness of breath, fast pulse, and unstable blood pressure. As the degree of abdominal pain is reduced, the situation can be stabilized. Thereafter, as bacterial peritonitis worsens, the condition worsens, and in severe cases, infection (poisoning) shock can occur.
2, acute peritonitis: full abdominal muscle tension as a plate, tenderness is significant, refused to press, the whole abdomen can lead to rebound pain. Laboratory examination: visible white blood cells increased, generally acute perforation cases, white blood cell count between 15,000 ~ 20,000 / mm3, neutrophils increased; hemoglobin and red blood cell count due to varying degrees of dehydration, also increased. Exploratory abdominal puncture, the liquid is taken for microscopic examination, such as seeing full-field white blood cells or pus, which is described as inflammatory ascites, is evidence for the diagnosis of peritonitis. It is also possible to determine the content of ammonia, and if it exceeds 3 g/ml, it means that there is gastrointestinal perforation.
Symptom
Posterior wall perforation ulcer symptoms common symptoms back pain infectious fever secondary infection
The most prominent manifestation of posterior wall perforating ulcer is back pain. The most common cause of clinically intractable duodenal ulcer is that the posterior duodenal ulcer penetrates into the pancreas. If so, the rhythm and cycle of the original ulcer pain At the beginning, the patient complained of back pain, usually in the lower thoracic vertebrae and the midline of the lumbar vertebrae. It is often similar to the radiation pain of the pancreas. This back pain begins with the appearance of pain in the anterior abdominal wall. After taking milk or antacid Can be alleviated, and later with the deeper development of penetration, this back pain may become more durable than the previous ulcer pain, when eating or taking antacids can not alleviate, although this penetrating ulcer often affects the pancreas, However, it rarely causes hemorrhagic pancreatitis, and may also cause elevated serum amylase and typical pain, but the clinical manifestations of acute pancreatitis rarely occur. If the pain is intractable, but only mild back pain, at this time It is difficult to distinguish whether there is penetrating ulcer. At this time, clinicians tend to ignore the diagnosis of the disease. The best way is to stop the patient once they have food. Pain, you should consider this complication.
Examine
Examination of posterior wall perforated ulcer
The ulcer penetrates into the pancreas and may have elevated serum amylase.
X-ray inspection
(1) Abdominal X-ray film: When the ulcer penetrates the gallbladder or the common bile duct forms a fistula, there is gas in the biliary tract.
(2) Gastrointestinal barium meal imaging: It can show that the fistula tube enters the transverse colon or bile duct, and the lateral slice can show penetrability.
(3) CT examination: a mass in the pancreas, a pseudocyst, or gas in the pancreatic duct is a sign that the pancreas is worn. The gastric ulcer penetrates into the liver, showing that the contour of the serosal surface of the stomach wall is unclear and close to the stomach wall. There is a liquid low-density shadow at the edge of the connected liver, which can have gas inside, and can form a small gas-liquid plane with low-density edges blurred (Fig. 1).
2. Fiber endoscope
See deep ulcers (small shadows) suspicious penetrating, large gastric ulcers with high and low unevenness are benign, have penetrated into the pancreas.
Diagnosis
Diagnosis and identification of posterior wall perforating ulcer
A history of gastroduodenal ulcer and back pain can be considered for the diagnosis of the disease. If the symptoms are not typical, it depends on endoscopy, and X-ray barium meal examination is also helpful if the duodenal bulb is only slightly deformed. Without obvious scar formation, the posterior wall penetrating ulcer is not considered; on the other hand, the obvious duodenal bulb deformation without the exact ulcer wall penetration may be the posterior wall penetration. The favorable evidence, in addition to the detection of serum amylase may be helpful in some cases.
