Lactology Foundation

Pain Originating from the Stomach and Small Intestine

Distribution
Pain originating from the stomach and small intestine can be generally classified as follows:
➤ acute and chronic gastritis
➤ functional gastric disorders (gastric irritation)
➤ ulcerous disease (duodenal ulcer, gastric ulcer)
➤ gastric carcinoma
➤ rare disorders
➤ complaints secondary to general diseases.

Diagnosis
The differential diagnosis is based on the medical history, clinical findings, imaging (endoscopy, radiological examination), and biopsy with a histological analysis.
A detailed medical history is particularly important in gastric diseases. Functional stomach disorders (irritable stomach) are characterized by their relatively indefinite character. They generally occur irregularly and have no periodicity. The pain is frequent
accentuated immediately after eating.
Endoscopy is most important for diagnosis of obscure epigastric pain, dysphagia, heartburn, and gastrointestinal bleeding. Another indication is an unclear iron deficiency anemia. Radiologic examinations are helpful, particularly in cases of paraesophageal hiatus hernia, motility disorders, Zenker diverticulitis, external compression, or stenoses that cannot be detected endoscopically. Endosonography can be used to detect intramural processes, especially the extent and depth of infiltration of neoplasms, as well as lymph node metastases.

Acute Gastritis
Clinical Features
The clinical picture with acute gastritis is characterized by a diffuse pressure that can increase to intense pain in the stomach region. Eating intensifies the pain. Vomiting often brings relief. The complaints resolve over a few hours to days. The stomach symptoms are frequently accompanied by intestinal manifestations (meteorism, diarrhea).
Erosive gastritis is an important cause of hemateme-
sis.
Causes
Apart from infections (primarily Helicobacter pylori, very rarely other bacterial [phlegmonous, mycobacterial, luetic gastritis], viral [herpes simplex virus, cytomegalovirus; particularly with AIDS], parasitic or fungal causes), the causes of acute gastritis are: food poisoning (Staphylococcus aureus toxin), alcohol, stress (surgery, serious trauma, shock) and in particular drugs, primarily nonsteroidal antirheumatics (e.g., salicylates, phenylbutazone, indomethacin), corticosteroids, and cytostatic drugs.

Typical period of the most common causes of chronic (recurring) upper abdominal pain

Differential Diagnosis
Gastritis is often interpreted as primary, although it is frequently an expression of a more general disease. The following diseases present with gastric complaints and must always be considered
in differential diagnosis:
➤ Any serious general disease can show symptoms indicating a stomach disease, such as nausea, belching, loss of appetite, and possibly vomiting.
➤ These symptoms are particularly frequent in chronic uremia.
➤ Acute or chronic liver diseases (e. g., due to chronic alcohol abuse) are frequently accompanied by gastric complaints.
➤ Congestive gastritis, as a manifestation of cardiac insufficiency or portal hypertension, must be considered in patients with cardiac or hepatic disease.
➤ Among drugs, "digitalis gastritis" in cardiac patients disappears a few days after stopping therapy.
➤ Allergic gastritis, as a consequence of hypersensitive reactions to food, particularly milk, chocolate, yeast, nuts, citrus fruit, strawberries, shellfish, etc., occurs primarily as part of a generalized gastrointestinal reaction with diarrhea and pain, in some cases combined with systemic symptoms (e. g., tachycardia, drop in blood pressure, asthma, headache, urticaria).

Type A, B and C gastritis must be distinguished.
Type A Gastritis
Type A gastritis (autoimmune gastritis) primarily affects the gastric body and fundus. It is caused by autoimmune processes. It is typically associated with pernicious anemia. Autoantibodies against parietal cells and intrinsic factor are typical. Gastrin is increased. The risk of developing a gastric carcinoma is significantly increased in chronic-atrophic type A gastritis. Endoscopic surveillance is therefore indicated.
Type B Gastritis
Type B gastritis (bacterial gastritis) is primarily localized in the gastric antrum and is typically caused by Helicobacter pylori (Hp). It is more common than type A gastritis and is associated with gastric ulcers, duodenal ulcer, and mucosa-associated lymphoid
tissue (MALT) lymphoma.
Type C Gastritis
Type C gastritis (chemical gastritis) is caused by chemical irritation, i. e., reflux of bile (bile gastritis) or duodenal contents (reflux gastritis) and most importantly drugs, in particular use of NSAIDs (NSAID gastropathy).
Rare Cases of Gastritis
Rare, chronic forms of gastritis are lymphocytic, eosinophilic, and granulomatous gastritis.

Diagnosis: Chronic gastritis can only be confirmed by histology. There is no clear relationship to typical clinical symptoms. The majority of patients with histologically demonstrated chronic gastritis are asymptomatic.

Irritable Stomach (Functional Dyspepsia)
Continuous epigastric pain, loss of appetite, nausea, and frequent vomiting are the main symptoms. Eating tends to exacerbate the symptoms and there is generally no periodicity or diurnal rhythm. This information from the medical history generally distinguishes this complaint from an ulcer. The lack of the typical endoscopic changes with irritable stomach is decisive for differential diagnosis.

Ménétrier disease (giant hypertrophic gastritis) is characterized by bulging rigid stomach folds (similar in appearance to the brain). It is caused by massive foveolar hyperplasia.
Secondary inflammatory changes also frequently occur. Clinically, patients complain of epigastric pain and vomiting. Frequently, a protein loss occurs (exudative enteropathy) resulting in hypoproteinemic edema. The cause of the disease is unknown. It may be difficult to differentiate it from intramural solid tumors.

Ulcers
The central feature of ulcers is infection with Helicobacter pylori (Hp). There has been a radical change in the understanding of ulcers. The eradication of the Hp infection in patients with ulcers not only heals the acute lesion but generally prevents recurrence and complications of ulcers. Only about 10% of patients infected with Hp in industrialized countries develop an ulcer, but 95% of patients with a duodenal ulcer are infected with Hp This indicates that Hp infection alone is not sufficient to cause an ulcer. Hp generates conditions that, together with additional risk factors, cause an ulcer: stress, smoking, and a genetic predisposition.
Helicobacter pylori Detection
The presence of Hp can be confirmed:
➤ histologically by Giemsa or Warthin−Starry staining of gastric antrum biopsies
➤ by urease activity either with a fast urease test in the biopsy specimen or an exhalation test with 13C or 14C-labeled urea
➤ by culture from gastric antrum biopsies
➤ by serology: serology is, however, not generally useful, because Hp colonizes approximately 10% of persons under 30 and approximately 60% of persons of 60 years, while only 10% of infected persons develop an ulcer.

Clinical Features and Differential Diagnosis
Strongly localized pain is characteristic of ulcers, as compared to irritable stomach and acute gastritis. In acute gastritis a diffuse pain upon palpation is generally present in the epigastric region. Many patients with ulcers can point to the exact location of the spontaneous pain and the pain upon palpation. The maximum pain is to the left of the abdominal mid-line with gastric ulcers and to the right with duodenal ulcers.
The character of the pain is important in differential diagnosis versus biliary colic (period and diurnal rhythm of the pain). The pain characteristics and the diurnal rhythm typical for ulcers are particularly important. A biliary colic lasts for one to three
days, ulcer pain for three to five weeks. Ulcer pain generally disappears after eating within a few minutes while biliary pain does not. Ulcer pain is virtually never accompanied by nausea while nausea is very frequent with biliary diseases. Appetite is not affected, unlike gastritis and carcinoma. If the character of the pain is not typical in spite of other signs of an ulcer, the possi-
bility of complications must be considered:
➤ with continuous and back pain: penetration
➤ with nausea and vomiting: stenosis. An ulcer episode, like acute gastritis, can be triggered by stress situations (surgery, serious trauma), alcohol abuse, or drugs (including NSAIDs).
Ulcers occur at all ages, particularly after puberty.
Carcinoma incidence increases with age but can also be observed in 20- to 30-year-olds.

Diagnosis
The mainstay of ulcer diagnosis is endoscopy. Multiple biopsies from and around the ulcer are key for differentiating benign from malignant stomach ulcers.
Radiologic diagnosis is no longer common, but when performed, an ulcer niche, may be visible under tangential setting as a contrast agent bulge in the region of the gastric curvature. The ulcer niche is visible as a persistent contrast spot in the direct frontal view.
About 85% of ulcer niches are on the minor curvature of the stomach. The remaining 15% occur at the major curvature, the dorsal wall (back pain), and in the pyloric region. Gastric carcinomas can also form niches. Indirect ulcer signs are spastic retractions on the wall opposite the ulcer, referred to as ulcer fingers. They are not specific for ulcers, because they are also observed with various tumors. After healing an hourglass stomach may develop, which results from shrinkage of the minor curvature by scar tissue and spastic retraction of the major curvature.

Duodenal Ulcer
More than 95% of duodenal ulcers occur in the duodenum
bulb. Untreated they are characterized by spontaneous healing and recurrence. 60% of untreated cases recur within one year and 80−90% within two years. 95−100% are associated with Hp infection.
The main symptom is pain, which typically occurs 90 minutes to three hours postprandial and is relieved by eating (food relief). Asymptomatic ulcers are common.
Complications are penetration, particularly into the pancreas (constant pain in the back), stomach outlet obstruction (pain increased postprandially, vomiting), perforation, and hemorrhage.
Postbulbar ulcers are rare. The clinical symptoms correspond to the classical duodenal ulcer, but postbulbar ulcers bleed more frequently.

Gastric Ulcer
The peak incidence of gastric ulcers is in the sixth decade of life and thus about 10 years later than with duodenal ulcers. Men are affected more frequently than women. Benign gastric ulcers are most commonly localized adjacent to the corpus−antrum border. Gastric erosions and ulcers are often caused by NSAIDs. Gastric ulcers not associated with NSAIDs are generally caused by Hp infection. The pain is less typical than in duodenal ulcers and increases after eating. Nausea and vomiting occur even without gastric outlet obstruction, in contrast to the duodenal ulcer. Asymptomatic courses are common.

Ulcer Associated with Other Diseases
Peptic Ulcer. A peptic ulcer, particularly a duodenal ulcer, is frequently observed in patients with:
➤ cirrhosis of the liver
➤ chronic obstructive jaundice
➤ chronic pancreatitis
➤ chronic lung disease, especially emphysema
➤ chronic renal insufficiency
➤ general arteriosclerosis
➤ polycythemia vera
➤ hyperparathyroidism
➤ systemic mastocytosis.
Peptic ulcers, including gastric ulcers, are frequently observed:
➤ with NSAID use
➤ in smokers
➤ after chemotherapy.

Stress-induced Erosions
Stress-induced erosions and ulcers are often multiple and frequently occur in areas of the stomach with high activity, after shock, massive burns (Curling ulcer), sepsis, and after serious trauma.
Hemorrhage is frequent, particularly in patients on respirators and with coagulation disorders.
Cushing Ulcer
Gastric ulcers frequently occur after brain trauma, brain surgery, or in patients with elevated brain pressure (Cushing ulcer).
Zollinger-Ellison Syndrome
Ulcers are a complication of Zollinger-Ellison syndrome.
Gastrinomas (most frequently originating from non-beta-pancreatic islet cells or duodenal G cells), through overproduction of gastrin, increase secretion of gastric acid and are thus responsible for the formation of ulcers. Zollinger-Ellison syndrome should be considered in the following situations:
➤ peptic ulcers with atypical localization (esophagus, postbulbus, jejunal), multiple occurrence (approximately 10%), and resistance to treatment.
➤ aqueous diarrhea, with or without steatorrhea, with or without hypokalemia and its consequences
➤ gastric hypersecretion and increased serum gastrin levels.
➤ prominent gastric mucosa folds, as with Ménétrier
disease
➤ 25% of cases are associated with multiple endocrine
adenomatosis type I (Wermer syndrome). Zollinger-Ellison syndrome must be considered in patients with signs of hyperparathyroidism or hypophyseal tumor. The family medical history is particularly important in view of the inheritance.
➤ Fasting serum gastrin levels are elevated. Massive hy-
perchlorhydria and hypergastrinemia (> 1000 pg/mL) are diagnostic. Increased serum gastrin levels are also found in achlorhydria (e.g., pernicious anemia, after vagotomy, stomach resection).
In Zollinger-Ellison syndrome serum gastrin levels increase significantly in response to calcium infusion or after secretin administration. These provocation tests are useful for identification of Zollinger-Ellison syndrome in patients with borderline serum gastrin levels (200-1000 pg/mL).