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Clinical Pathology

Method of Gastric Analysis

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To evaluate gastric acid secretion, the stomach's acid output is measured both in a fasting state and post the administration of a stimulating drug. The Basal Acid Output (BAO) represents the quantity of hydrochloric acid (HCl) secreted without external stimuli (visual, olfactory, or auditory). The Maximum Acid Output (MAO) quantifies the HCl secreted by the stomach when stimulated by pentagastrin, calculated from the initial four 15-minute samples post-stimulation. For assessing the greatest possible acid secretory capacity, the Peak Acid Output (PAO) is derived from the two highest consecutive 15-minute samples, preferred for its enhanced reproducibility. The acidity level is determined through titration methods.

Collection of Sample

All medications influencing gastric acid secretion, including antacids, anticholinergics, cholinergics, H2-receptor antagonists, antihistamines, tranquilizers, antidepressants, and carbonic anhydrase inhibitors, must be withheld for 24 hours before the examination. Proton pump inhibitors require discontinuation 5 days prior to the test. To ensure accurate results, patients should be in a relaxed state, devoid of any sensory stimulation sources.

No food or drink is allowed after midnight preceding the test. Gastric juice can be obtained through an oral or nasogastric tube, either during endoscopy or through aspiration.

The commonly used oral or nasogastric tube (depicted in Figure 1) is a flexible, narrow-diameter tube with a weighted bulbous end, facilitating gastric juice entry through perforations. Its radiopaque feature allows precise positioning in the stomach's most dependent part under fluoroscopic or X-ray guidance. Lubricated for ease, the tube can be introduced via the mouth or nose while the patient is seated or reclined on the left side. Markings on the tube's outer surface correspond to distances from the teeth: 40 cm (tip to cardioesophageal junction), 50 cm (body of stomach), 57 cm (pyloric antrum), and 65 cm (duodenum). Tube placement can be verified by fluoroscopy or the ‘water recovery test’, where the recovery of over 90% of introduced water indicates proper placement. Typically, the tube is positioned in the antrum, and a syringe is attached for gastric juice aspiration.

Oral or nasogastric Ryles tube
Figure 1: Oral or nasogastric Ryle’s tube. The tube is marked at 40, 50, 57, and 65 cm with radiopaque lines for accurate placement. The tip is bulbous and contains a small weight of lead to assist the passage during intubation and to know the position under fluoroscopy or X-ray guidance. There are four perforations or eyes to aspirate contents from the stomach through a syringe attached to the base.

For BAO Estimation: Samples are collected in the morning after a 12-hour overnight fast. Initial gastric secretion accumulated overnight is aspirated and discarded. Subsequently, gastric secretions are aspirated at 15-minute intervals for 1 hour, resulting in a total of 4 consecutive samples. All samples undergo centrifugation to remove particulate matter. Each 15-minute sample is analyzed for volume, pH, and acidity. The acid output in the four samples is totaled and expressed as the concentration of acid in milliequivalents per hour or in mmol per hour.

After Gastric Juice Collection for BAO Determination: Following this, the patient receives a subcutaneous or intramuscular injection of pentagastrin (6 μg/kg of body weight). Immediately afterward, gastric secretions are aspirated at 15-minute intervals for 1 hour for the estimation of MAO or PAO. MAO is calculated from the first four 15-minute samples after stimulation, while PAO is derived from two consecutive 15-minute samples showing the highest acidity.

Titration

 

Box 1: Determination of basal acid output, maximum acid output, and peak acid output
  1. Basal acid output (BAO) = Total acid content in all four 15-minute basal samples in mEq/L
  2. Maximum acid output (MAO) = Total acid content in all four 15-minute post-pentagastrin samples in mEq/L
  3. Peak acid output (PAO) = Sum of two consecutive 15-minute post-pentagastrin samples showing highest acidity ×2 (mEq/L)

Gastric acidity assessment involves titration, where the endpoint is determined by observing the change in color of the indicator solution or reaching the desired pH.

In this process, 0.1 N sodium hydroxide, an alkali solution, is incrementally added from a graduated vessel (burette) to a known volume of acid (gastric juice) until the equivalence point of the reaction is achieved. The concentration of acid is then determined based on the concentration and volume of alkali required for neutralizing the specific volume of gastric juice. Acid concentration is expressed in milliequivalents per liter or mmol per liter.

Free acidity signifies the concentration of HCl present in a free, uncombined form in the solution. The volume of alkali added to the gastric juice until Topfer’s reagent (an earlier-added indicator) changes color or when the pH reaches 3.5 is a measure of free acidity. A screening test for free HCl in gastric juice involves observing a red color after adding Topfer’s reagent to an aliquot. The presence of free HCl excludes the diagnosis of pernicious anemia (achlorhydria).

Combined acidity encompasses HCl combined with proteins and mucin, including small amounts of weak acids in gastric juice.

Total acidity is the summation of free and combined acidity. The amount of alkali added to gastric juice until phenolphthalein indicator (previously added to the gastric juice) changes color is indicative of total acidity (Box 1).

Interpretation of Results

  1. Volume: Normal total volume is 20-100 ml (usually < 50 ml). Causes of increased volume of gastric juice are—
    • Delayed emptying of stomach: pyloric stenosis
    • Increased gastric secretion: duodenal ulcer, Zollinger-Ellison syndrome.
  2. Color: Normal gastric secretion is colorless, with a faintly pungent odor. Fresh blood (due to trauma, or recent bleeding from ulcer or cancer) is red in color. Old hemorrhage produces a brown, coffee-ground like appearance (due to formation of acid hematin). Bile regurgitation produces a yellow or green color.
  3. pH: Normal pH is 1.5 to 3.5. In pernicious anemia, pH is greater than 7.0 due to absence of HCl.
  4. Basal acid output:
    • Normal: Up to 5 mEq/hour.
    • Duodenal ulcer: 5-15 mEq/hour.
    • Zollinger-Ellison syndrome: >20 mEq/hour.
    Normal BAO is seen in gastric ulcer and in some patients with duodenal ulcer.
  5. Peak acid output:
    • Normal: 1-20 mEq/hour.
    • Duodenal ulcer: 20-60 mEq/hour.
    • Zollinger-Ellison syndrome: > 60 mEq/hour.
    • Achlorhydria: 0 mEq/hour.
    • Normal PAO is seen in gastric ulcer and gastric carcinoma. Values up to 60 mEq/hour can occur in some normal individuals and in some patients with Zollinger-Ellison syndrome.
    • In pernicious anemia, there is no acid output due to gastric mucosal atrophy. Achlorhydria should be diagnosed only if there is no free HCl even after maximum stimulation.
  6. Ratio of basal acid output to peak acid output (BAO/PAO):
    • Normal: < 0.20 (or < 20%).
    • Gastric or duodenal ulcer: 0.20-0.40 (20-40%).
    • Duodenal ulcer: 0.40-0.60 (40-60%).
    • Zollinger-Ellison syndrome: > 0.60 (> 60%).
    • Normal values occur in gastric ulcer or gastric carcinoma.

Alterations in gastric acid output are linked to various conditions, as outlined in Table 1.

Importantly, the values of acid output, while significant, should not be considered diagnostic in isolation. Correlation with clinical, radiological, and endoscopic features is essential for a comprehensive evaluation.

Table 1: Causes of alterations in gastric acid output
Increased gastric acid outputDecreased gastric acid output
  • Duodenal ulcer
  • Zollinger-Ellison syndrome
  • Hyperplasia of antral G cells
  • Systemic mastocytosis
  • Basophilic leukemia
  • Chronic atrophic gastritis
    1. Pernicious anemia
    2. Rheumatoid arthritis
    3. Thyrotoxicosis
  • Gastric ulcer
  • Gastric carcinoma
  • Chronic renal failure
  • Post-vagotomy
  • Post-antrectomy

References

  • Burtis CA, Ashwood ER (Eds). Tietz Fundamentals of Clinical Chemistry, 4th ed. Philadelphia: WB Saunders Co, 1996.
  • Drossman DA, Shaheen NJ, Grimm IS (Eds). Handbook of Gastroenterologic Procedures (4th Ed). Philadelphia: Lippincott Williams and Wilkins, 2005.
  • Rosenfeld L. Gastric tubes, meals, acid, and analysisrise and decline. Clin Chem 1997;43:837-42.
  • Wallach J. Interpretation of Diagnostic tests (7th Ed). Philadelphia. Lippincott: Williams and Wilkins, 2000.
  • Wolfe MM, Soll AH. The physiology of gastric acid secretion. N Engl J Med 1988;319:1707-14.
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