II. Diagnosis and Treatment

II. Diagnosis and Treatment (---) Clinical Diagnosis

1. Diagnostic criteria for acute gastritis (1) Acute simple gastritis ① History of exposure to various physicochemical irritants, such as excessive consumption of strong alcoholic beverages, intake of certain medications, eating overly coarse food, overeating, or consuming food contaminated with bacteria or bacterial toxins; ② Clinical symptoms: sudden onset, usually within hours or 24 hours after improper diet; manifestations include upper abdominal discomfort or pain, nausea, vomiting, and loss of appetite; patients with bacterial infections often present with fever, and those with concomitant enteritis may experience abdominal pain and diarrhea; gastroscopic examination reveals gastric mucosal congestion, edema, exudation, petechial bleeding, or focal erosions, with neutrophil and monocyte infiltration observed in the mucosal biopsy. (2) Acute erosive gastritis ① Often associated with severe infections, extensive burns, craniocerebral trauma, major surgery, shock, or other precipitating factors such as medication use, overwork, or psychological stress; ② Clinical symptoms: abrupt onset, primarily presenting as upper gastrointestinal bleeding—hematemesis or melena—with severe cases potentially leading to shock; gastroscopy performed within 24–48 hours after bleeding reveals multiple erosions and bleeding, characteristic acute gastric mucosal lesions, serving as the main basis for diagnosis.
2. Diagnostic criteria for chronic gastritis Currently, endoscopic findings are the primary diagnostic criterion: (1) Superficial gastritis ① Gastric mucosa exhibits alternating red and white areas or a mottled appearance; ② There are patchy or linear areas of redness, with the former having indistinct borders and appearing bright red; ③ Some areas show edema and congestion; ④ The periphery of erosions often displays inflammatory signs, with a white coating on the erosion surface; increased mucus secretion that adheres tightly to the mucosa and is difficult to remove; the most prominent lesion location is the gastric antrum, which may be diffuse or localized and scattered. Pathological biopsy indicates that in superficial gastritis, the glandular structures remain intact without reduction. (2) Atrophic gastritis ① Atrophic gastric mucosa appears pale, grayish-white, grayish-yellow, or grayish-green; ② Blood vessels are clearly visible—mild atrophy shows small intramucosal vessels, while severe atrophy reveals large submucosal vessels resembling tree branches, colored red or purplish-blue; normal vessels in the gastric fundus and cardia can also be seen; ③ The extent of atrophy may be diffuse, localized, or uneven, resulting in an irregular mucosal surface with some areas appearing granular or nodular, known as verrucous gastritis.
3. Diagnostic criteria for peptic ulcer disease (1) Typical symptoms of peptic ulcer disease include mid-to-upper abdominal pain and acid regurgitation; the relationship between pain onset and postprandial timing serves as a clinical basis for differentiating gastric from duodenal ulcers. Gastric ulcer pain usually occurs about half an hour after a meal, whereas duodenal ulcer pain often occurs on an empty stomach. In recent years, with the widespread use of acid-suppressing drugs and nonsteroidal anti-inflammatory drugs (NSAIDs), many peptic ulcers present without obvious symptoms, with upper gastrointestinal bleeding being the initial symptom in some cases. (2) Gastroscopy and upper gastrointestinal barium meal examination Gastroscopy and upper gastrointestinal barium meal examination are the primary methods for diagnosing peptic ulcer disease. During gastroscopy, attention should be paid to the ulcer's location, morphology, size, depth, stage, and the condition of the surrounding mucosa. Patients with gastric ulcers should undergo routine histopathological examination. NSAID-related ulcers are more common in the stomach, distributed around the pylorus, antrum, and gastric fundus, with diverse morphologies and sizes ranging from 0.2 to 3 cm, often presenting as multiple, superficial ulcers. (3) Urease test and carbon-13 breath test Routine urease testing or carbon-13 breath testing is conducted for peptic ulcer disease to determine whether Helicobacter pylori infection is present. (II) Western Medical Treatment
4. Treatment of acute gastritis (1) Pharmacotherapy For abdominal pain, antispasmodics such as belladonna tablets at 10 mg three times daily, propantheline at 15 mg three times daily, or 654-2 at 10 mg three times daily may be administered. For nausea and vomiting, metoclopramide at 5–10 mg three times daily or domperidone at 10 mg three times daily can be given. For bacterial infections, berberine at 0.3 g three to four times daily or gentamicin at 40,000 units four times daily may be prescribed; patients with diarrhea can choose flupentixol at 0.2 g three times daily. The course of treatment generally lasts 3–5 days depending on the condition. For patients with gastric mucosal erosion or bleeding, H2-receptor antagonists or proton pump inhibitors that suppress gastric acid secretion, or aluminum hydroxide preparations with gastric mucosal protective effects, can be used. In case of massive hemorrhage, comprehensive resuscitative measures should be implemented. (2) Treatment of dehydration, electrolyte imbalance, and acidosis For mild cases, patients are advised to drink plenty of water or take oral rehydration salts; for severe cases, physiological saline and 5% glucose solution can be administered intravenously in a ratio of 2:3, followed by appropriate potassium supplementation after urination. Patients with acidosis are given an appropriate dose of 5% sodium bicarbonate.
5. Treatment of chronic gastritis (1) Pharmacotherapy ① Eliminate or weaken aggravating factors: including eradication of Helicobacter pylori; acid suppression or neutralization therapy; corresponding treatments and management for bile reflux and NSAID use. ② Enhance gastric mucosal defense: applicable to patients with gastric mucosal erosion, bleeding, or obvious symptoms. Medications include colloidal bismuth preparations with Helicobacter pylori eradication effects, aluminum carbonate preparations with both acid-neutralizing and bile salt adsorption functions, and aluminum hydroxide preparations with purely mucosal protective effects. ③ Prokinetic agents: such as domperidone and metoclopramide. (2) Surgical treatment Chronic gastritis patients, regardless of whether they have atrophic or superficial gastritis, should primarily receive medical treatment; surgical intervention is generally not recommended. However, for chronic atrophic gastritis accompanied by severe dysplasia, where there is a potential risk of malignancy, surgical treatment should be considered immediately, followed by continued postoperative follow-up. For mild to moderate dysplasia, traditional Chinese medicine treatment can still reverse the condition, eliminating the need for surgery.
6. Treatment of peptic ulcer disease (1) Treatment strategy for peptic ulcers For gastric or duodenal ulcers diagnosed through endoscopy or X-ray examination, the first step is to determine whether Helicobacter pylori infection is present. Patients positive for Helicobacter pylori should first undergo anti-Helicobacter pylori treatment, and if necessary, continue with acid-suppression therapy for another 2–4 weeks after completing anti-Helicobacter pylori treatment. For Helicobacter pylori-negative ulcers, including NSAID-related ulcers, conventional treatment can be followed: taking any H2-receptor antagonist or proton pump inhibitor. The treatment course for gastric ulcers is 4–6 weeks, while for duodenal ulcers it is 6–8 weeks. Gastric mucosal protectants can also be used instead of acid-suppressing agents for treating duodenal ulcers. As for maintenance therapy, the decision should be made based on factors such as ulcer recurrence frequency, patient age, NSAID use, smoking habits, presence of other serious diseases, and history of ulcer complications. Regarding surgical treatment, due to advances in medical therapy, it is currently only indicated for a very small number of patients with complications. (2) Pharmacotherapy ① Eradicate Helicobacter pylori. Currently, no single drug can effectively eradicate Helicobacter pylori, so treatment regimens combining acid-suppressing agents, antibiotics, and synergistic bismuth preparations have been developed. For eradicating Helicobacter pylori in peptic ulcers, a standard regimen involves one proton pump inhibitor combined with clarithromycin, amoxicillin (or tetracycline), metronidazole (or tinidazole), and furazolidone—forming a triple therapy. The standard dosage of acid-suppressing drugs used in Helicobacter pylori eradication treatment is shown in the table below: clarithromycin 25–500 mg, amoxicillin or tetracycline 500–1000 mg, metronidazole 400 mg, furazolidone 100 mg, administered twice daily. The typical course of Helicobacter pylori eradication treatment is 7 days. H2-receptor antagonists can be used instead of proton pump inhibitors to reduce costs, but the efficacy will also decrease. For those who fail initial treatment, a quadruple therapy consisting of a proton pump inhibitor, colloidal bismuth subsalicylate (240 mg twice daily), and two antibiotics can be employed. Commonly used acid-suppressing drugs

Drug | > Dosage per tablet | > Treatment for ulcers | > Eradication of Helicobacter pylori | > ( mg ) | > | > Standard dosage ( mg ) | | > Standard dosage( | | | > mg) | Proton pump inhibitors

Omeprazole | > 20 | > 20 qd | > 20 bid Lansoprazole | > 30 | > 30 qd | > 30 bid Continued table

Drug | > Dosage per tablet ( mg ) | > Treatment for ulcers | > Eradication of Helicobacter pylori | | > Standard dosage | > Standard dosage ( mg ) Pantoprazole | > 40 | > 40 qd | > 40 bid Rabeprazole | | | Esomeprazole | > 20 | > 20 qd | > 20 bid H2 receptor antagonists