Instrumental diagnostics
To confirm the diagnosis in modern practice, imaging techniques are used. The primary method (gold standard) is recognized as fibroesophagogastroduodenoscopy (FEGDS). It serves several purposes simultaneously: it allows for the precise determination of the ulcer's location and size, obtaining material to detect Helicobacter pylori infection, and performing histological verification. Biopsy is critically important for differential diagnosis. There is an important clinical nuance: gastric ulcers, especially those located on the greater curvature, may appear completely benign on X-rays, yet histological analysis reveals cancer.
The second method is X-ray examination using a barium sulfate suspension as contrast. The main pathognomonic radiological sign of the disease is the "niche" sign, which occurs when the ulcer defect fills with the contrast medium. Nevertheless, the method has severe limitations. It has low specificity, as X-rays do not allow distinguishing a simple ulcer from malignant transformation. Furthermore, if the patient already has scarring deformities of the mucous membrane, it is extremely difficult for the physician to assess healing dynamics.
Assessment of the functional state of the stomach
To measure the level of secretion, fractional gastric sounding is used. The detection of hypersecretion requires searching for the root cause, as the factors increasing acidity are quite diverse:
- Surgical: status post small bowel resection, resulting in the loss of inhibitory intestinal factors.
- Metabolic: hypercalcemia of any origin.
- Neurological: various brain injuries that stimulate vagus nerve (n. vagus) tone.
- Pancreatogenic: pancreatitis or mechanical obstruction of the pancreatic ducts.
Special attention is deserved by Zollinger-Ellison syndrome. Its essence lies in the presence of a gastrinoma—a pancreatic tumor that autonomously produces gastrin. This specific condition produces the most powerful hypersecretion. Clinically, the syndrome manifests with extremely high gastric juice acidity, frequent relapses of peptic ulcers, pain, severe dyspepsia, and progressive clinical deterioration. Diagnosis is based on radioimmunoassay (determining elevated blood gastrin levels) and locating the tumor itself using abdominal ultrasound or CT.
Acute complications of peptic ulcer disease
Complicated course is observed in one-fifth of patients. The most acute conditions include perforation and bleeding.
Perforation is characterized by a specific pain syndrome: the patient experiences sharp, sudden "dagger-like" abdominal pain. The consequence of such organ wall perforation is the rapid and fulminant development of acute peritonitis.
Bleeding most commonly complicates the course of ulcers localized in the duodenum. The clinical feature of this complication is that it is not always accompanied by a vivid clinical picture (such as hematemesis). Occult, paucisymptomatic forms are possible. In such cases, bleeding can only be diagnosed by laboratory means—using the fecal occult blood test.
Chronic complications: stenosis and penetration
If the ulcer is located in the pyloric channel or the initial part of the duodenum, its healing can lead to pyloric stenosis. As the lumen narrows, the nature of the pain changes: eating no longer brings relief to the patient; on the contrary, it increases discomfort and pain. The leading symptom becomes persistent, large-volume "projectile" vomiting. Due to the loss of a huge amount of gastric juice, hypochloremia develops (a decrease in blood chlorine levels), which leads to secondary renal failure. Upon palpation and percussion of the epigastrium, the physician may detect a characteristic "succussion splash". For accurate diagnosis and to rule out gastric cancer or pyloric hypertrophy, FEGDS with biopsy is mandatory.
Penetration represents the spread of the infiltrative-destructive ulcer process beyond the organ wall. The ulcer literally grows into the thickness of adjacent structures (liver, omentum, pancreas). Penetration can be suspected by the typical clinical triad:
- Persistent, unrelenting pain.
- Onsets of low-grade fever.
- Laboratory markers of inflammation (specifically, an elevated ESR).
Briefly: answers to topical questions
What are the stages of the clinical course of pyloric stenosis?
The clinical course of pyloric stenosis includes the decompensated stage.
- Decompensated stage — patient emaciation progresses, accompanied by electrolyte disturbances.
Additionally, as stenosis progresses, the nature of the pain changes (eating no longer brings relief and increases discomfort), persistent large-volume ("projectile") vomiting appears, and Vasilenko's sign ("late succussion splash") is detected.
What methods are used for non-invasive diagnosis of Helicobacter pylori infection?
For the non-invasive diagnosis of Helicobacter pylori infection, the following are used:
- 13C-urea breath test;
- stool tests: rapid immunochromatographic stool test for H. pylori, determination of H. pylori antigen in stool, molecular biological stool test for H. pylori;
- blood test: determination of antibodies to H. pylori.
What is the Forrest classification of peptic ulcer bleeding?
The Forrest classification of peptic ulcer bleeding distinguishes the following grades based on endoscopic findings:
- F1a, F1b — active bleeding. Characterized by a high risk of recurrence in case of successful endoscopic hemostasis.
- F2a, F2b — recent or stopped bleeding with signs of recent hemorrhage. Also assessed as a high recurrence risk state.
- F2c, F3 — stopped bleeding without signs of recent hemorrhage. Accompanied by a low risk of recurrence and treated conservatively.
The complication classification is easy to remember by the acronym P-B-S-P-M: Perforation, Bleeding, Stenosis, Penetration, Malignancy. And remember the penetration triad as P-L-E (Persistent pain, Low-grade fever, ESR).
Class and exam questions
How does pain change during the development of pyloric stenosis?
Unlike the typical course of an ulcer, in which food can reduce discomfort, in pyloric stenosis, food intake stretches the narrowed organ. This leads to the fact that food no longer brings relief, but only increases pain and discomfort.
Why is frequent vomiting dangerous in pyloric stenosis?
Large-volume ("projectile") vomiting leads to massive loss of gastric juice. This causes severe metabolic shifts, primarily hypochloremia, which provokes the development of secondary renal failure.
What else to study on this topic
- Mechanisms of the loss of inhibitory intestinal factors after small bowel resection.
- The effect of hypercalcemia on increasing gastric secretory function.
- Differential diagnosis of pyloric stenosis and pyloric hypertrophy during FEGDS.
- Radioimmunoassay method of diagnostics: principles of determining blood gastrin levels.
- Difficulties in assessing ulcer healing in the presence of mucosal scarring deformities.
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