2. Symptomatic Treatment

① Stomach or abdominal pain: can use antispasmodics, such as belladonna compound 10ml, 3 times daily, oral; atropine 0.3–0.6mg, 3 times daily, oral; propantheline 15mg, 3 times daily, oral; 654-2 10mg, 3 times daily, oral. In severe cases, subcutaneous injection of atropine 0.5mg or intramuscular injection of 654-2 10mg.

② For severe vomiting, can administer metoclopramide 10mg, 3 times daily, oral or intramuscular; domperidone 10mg, 3 times daily, oral.

③ For cases caused by bacterial infection, can appropriately use anti-inflammatory drugs and antibiotics, such as berberine (0.5g), terramycin (0.5g), furazolidone (Litelin) (0.1g), gentamicin (40,000 units), all of which can be used 3–4 times daily, oral. For those with diarrhea, use pipemidic acid or flupimic acid 0.2–0.4g, 3 times daily, oral. For those who cannot take orally, administer via non-gastrointestinal routes (intramuscular injection or intravenous drip).

④ For those who experience significant dehydration due to severe vomiting, diarrhea, or massive gastric bleeding, can administer intravenous drip of 5% glucose and saline (in a 1:2 ratio) or balanced solution, with the volume determined by the degree of dehydration; for those with acidosis, appropriately administer 0.5% sodium bicarbonate intravenously.

VI. Prognosis and Outcome

Acute simple gastritis is a self-limiting disease, meaning that as long as the cause is removed, the body has the ability to repair itself and recover. Whether treated with TCM and herbal medicine or with Western symptomatic treatment, most patients can regain health in the short term. However, if the cause is not removed and the gastric mucosa is repeatedly irritated for a long time, the lesion may persist and develop into chronic gastritis, or even lead to peptic ulcers.

Appendix 1: Acute Corrosive Gastritis

<!-- translated-chunk:3/16 -->

Acute corrosive gastritis is an acute injury of the gastric mucosa caused by accidental ingestion or swallowing of corrosive agents such as nitric acid, hydrochloric acid, sulfuric acid, lye, caustic potash or sodium, mercuric chloride, carbolic acid, arsenic, and phosphorus. The severity of the lesion depends on factors such as the nature of the corrosive agent, its concentration, the dose administered, whether the stomach was empty at the time of ingestion, the duration of ingestion, the presence of vomiting, and the availability of emergency treatment. In mild cases, there is congestion, edema, and increased mucus secretion in the gastric mucosa; in severe cases, erosion, ulcers, necrosis, and even perforation may occur. Immediately after ingesting a corrosive agent, intense pain arises in the mouth, pharynx, retrosternal area, and upper abdomen, often accompanied by nausea and vomiting; in severe cases, hematemesis, hypotension, shock, esophageal or gastric perforation, and even death from poisoning may occur. There is marked tenderness in the upper abdomen, with abdominal muscle rigidity. When gastric perforation occurs as a complication, signs of acute peritonitis may appear. After contact with the corrosive agent, the lips, oral cavity, and pharyngeal mucosa may develop scabs of varying colors. Following the acute phase, cicatricial stenosis of the esophagus, cardia, or pylorus may form.

This disease is a serious toxic condition that requires prompt and aggressive emergency treatment. Protein solution should be administered immediately; fasting and gastric lavage are contraindicated, and intravenous fluids should be given. In cases of shock, active resuscitation is necessary. For patients with severe pain, morphine or pethidine can be used for analgesia; however, these analgesics may mask perforation, so precautions must be taken to avoid delaying treatment. To prevent infection, antibacterial drugs may be prescribed.

Appendix 2. Acute Suppurative Gastritis

Acute suppurative gastritis is a severe, full-thickness purulent disease of the gastric wall caused by bacterial infection in the bloodstream. The most common causative agent is hemolytic streptococcus, followed by staphylococcus and Escherichia coli. Since the 1930s, with the successive introduction of sulfonamides and antibiotics into clinical practice, this disease has become extremely rare.

Chapter 3 Chronic Gastritis

Section 1 Overview

Chronic gastritis, as the name suggests, refers to chronic inflammation occurring in the stomach. Based on etiology, it can be divided into primary and secondary types. Secondary gastritis can be regarded as a reactive change in the gastric mucosa resulting from systemic diseases in other parts of the body; for example, cor pulmonale, cardiac insufficiency, portal hypertension due to cirrhosis, and severe anemia can all lead to inflammatory reactions such as congestion and edema of the gastric mucosa. What people commonly refer to as chronic gastritis, however, is inflammation of the gastric mucosa caused by nonspecific (i.e., uncertain) factors, known as primary chronic gastritis. In fact, chronic gastritis is merely a general clinical diagnostic term; as early as 1950, foreign scholars had already classified it into chronic superficial gastritis and chronic atrophic gastritis. In 1973, based on differences in the site of lesion, it was further divided into Type A and Type B: Type A refers to lesions primarily located in the gastric body, while Type B refers to lesions mainly in the gastric antrum. Chinese scholars in 1982 classified chronic gastritis into three types—superficial, atrophic, and hypertrophic—but the hypertrophic type was gradually abandoned due to insufficient evidence. At the same time, they proposed the AB mixed type, meaning that in some cases the lesion sites are difficult to clearly separate and often involve both the gastric antrum and the gastric body. Since 1983, it has also been increasingly proven that Helicobacter pylori (HP) plays a significant role in the pathogenesis of chronic gastritis and peptic ulcer disease.

Taking all these understandings into account, if we want to gain a comprehensive understanding of chronic gastritis, we must consider the following aspects: ① the site of onset—whether in the gastric body (Type A), the gastric antrum (Type B), or a mixed type (AB); ② the degree of lesion—superficial or atrophic, each further subdivided into mild, moderate, and severe grades; ③ the activity of inflammation—whether in the active phase or the quiescent phase; if in the active phase, it is also necessary to determine whether the lesion is localized or diffuse; ④ whether there is dysplasia (also called atypical hyperplasia, i.e., abnormal proliferation of gastric mucosal cells or the presence of atypical cells with different morphology from normal gastric mucosal cells), or intestinal metaplasia (i.e., when the gastric mucosa transforms into epithelial tissue similar to that of the small or large intestine); the simultaneous presence of dysplasia and intestinal metaplasia indicates that chronic gastritis has entered the precancerous stage; ⑤ whether HP is present.

Compared with chronic atrophic gastritis, chronic superficial gastritis is more common, accounting for about 80% of all cases of chronic gastritis. The typical age of onset is between 31 and 50 years old. Most patients with chronic superficial gastritis are either asymptomatic or have only mild symptoms, such as varying degrees of indigestion and discomfort in the upper abdomen after eating. Some patients experience dull pain in the upper abdomen, often related to diet—feeling better on an empty stomach but worse after eating, especially when consuming cold, hard, or spicy foods, which can trigger or exacerbate the pain, or when exposed to cold or emotional stress. Other symptoms may include nausea, vomiting, bloating, and decreased appetite. Chronic atrophic gastritis, on the other hand, accounts for only 10–30% of all cases of chronic gastritis, with an incidence of just 2% in the general population. The typical age of onset is after 40, peaking around 60. The characteristic feature of the lesion is atrophy of the gastric mucosal glands, either localized or widespread, with a reduction in their number and a corresponding decrease in secretory function. The main clinical symptoms are dull or distending pain in the upper abdomen, or simply a feeling of fullness or discomfort, often exacerbated after meals, accompanied by indigestion, loss of appetite, and belching. Due to glandular atrophy and reduced secretory function, digestion is impaired and absorption is affected, so patients with chronic atrophic gastritis often become progressively thinner and develop anemia, making them prone to being suspected of having gastric cancer and causing psychological distress. However, if chronic atrophic gastritis in the gastric antrum is accompanied by intestinal metaplasia and dysplasia (atypical hyperplasia), it may indicate a precancerous state; according to relevant statistics, gastric cancer is often associated with atrophic gastritis.

Although chronic superficial gastritis and chronic atrophic gastritis are two different pathological types of gastritis, they can coexist in the same stomach, and one can even transform into the other. For example, if the factors causing damage to the gastric mucosa persist, superficial gastritis can develop into atrophic gastritis; conversely, if the damaging factors are removed, some atrophic lesions may disappear or alleviate.

In general, the severity of subjective symptoms in chronic gastritis does not necessarily correlate with the extent of the lesion. Some cases of mild chronic superficial gastritis may actually have quite severe symptoms, while those with very severe atrophic gastritis may only exhibit mild subjective symptoms. This underscores the importance of confirming the diagnosis of chronic gastritis and determining the extent of the lesion through gastroscopy and gastric mucosal biopsy; otherwise, relying solely on clinical symptoms to infer the condition would be highly incomplete.

The causes of chronic gastritis are diverse. Broadly speaking, they can be summarized into the following aspects:

(1) Failure to treat acute gastritis in a timely manner or improper treatment leads to prolonged illness or recurrent attacks, eventually developing into chronic gastritis. This illustrates that the long-term persistence of any factor capable of causing acute gastritis is a major cause of chronic gastritis. Unhealthy dietary habits, such as eating too quickly, preferring excessively hot food, or regularly consuming spicy foods, raw and cold foods, coarse and hard foods, strong tea, and strong alcohol, as well as excessive smoking or long-term use of salicylate drugs like aspirin, can repeatedly irritate or damage the gastric mucosa, ultimately leading to chronic gastritis. Long-term chronic foci of infection in the oral cavity, nasal cavity, and pharynx can also produce bacteria and toxins that contribute to chronic inflammation of the gastric mucosa. In particular, recent research has found that Helicobacter pylori may be one of the main causative factors of chronic gastritis. In addition, long-term mental depression and excessive fatigue can also easily lead to chronic gastritis; traditional Chinese medicine’s concept of “excessive anger harms the liver, liver qi invades the stomach, overthinking harms the spleen, and overwork harms the spleen” further supports this point. Under the repeated influence of these factors, central nervous system dysfunction occurs, leading to spasm of visceral vascular smooth muscle, impairment of gastrointestinal secretion and motility, and malnutrition of the gastric wall, thereby causing chronic inflammation of the gastric mucosa.

(2) Bile reflux: Due to dysfunction of the pyloric sphincter or post-gastric surgery, bile may reflux into the stomach, destroying the protective layer of the gastric mucosa and allowing hydrogen ions secreted by the stomach to re-enter the mucosa, triggering pathological reactions and potentially leading to chronic gastritis. Since the gastric antrum is the first to be affected by bile reflux, chronic antral gastritis accounts for a considerable proportion of chronic gastritis cases, and clinically it is often simply referred to as bile-reflux gastritis.

(3) Immune factors: Research has found that in the blood of some patients with chronic atrophic gastritis, antibodies against parietal cells in the gastric mucosa are present, indicating that autoimmune reactions exist within the bodies of chronic gastritis patients and that immune regulation is disrupted. This is also one of the important factors among the many causes of chronic gastritis that deserves attention.

Section 2 Diagnosis