Achylia Gastrica

ACHYLIA GASTRICA, gastric a. (from Greek a-negative particle, and chylos-juice), a pathological state in which the stomach constantly and persistently secretes almost no gastric juice; this state corresponds to a well-known clinical symptom complex. The history of the doctrine of achylia is closely connected with the development of the doctrine of the so-called atrophy of the gastric mucosa. In 1877, the English physician Fenwick, based on four cases verified by autopsy, first described primary atrophy of the gastric mucosa as an independent severe disease form. Following this, many works appeared pointing to the connection between pernicious anemia and atrophy of the gastric mucosa. A careful anatomical and histological study of the gastric mucosa in gastritis indicated the possibility of primary atrophic catarrh leading to the complete loss of the glandular apparatus, the so-called anadenia (Ewald). In 1879, Van der Welden first pointed out the absence of free hydrochloric acid in gastric cancer as a symptom pathognomonic for this disease. Statistics give the following figures for achylia in gastric cancer: Kelling in 75% (1909), Boas in 82% (1907), Rovsing in 98.5%, Schütz in 75% (1908); on average, 80%. Smaller figures are given by the statistics of the Mayo Clinic in America, based on cases operated on over three years: achlorhydria was observed in 53.72%, lowered hydrochloric acid in 15.87%, in general, secretory insufficiency in 69.50%; normal secretion was found in 17.42% and increased in 4.58%. Friedenwald in 100 cases of cancer (1924) upon single examination after a test breakfast found achlorhydria in 79%. The same cases upon fractional examination gave the following: achylia in 52%, hypochlorhydria in 16%, normal acidity in 26%, hyperchlorhydria in 6%. As can be seen from the cited data, gastric cancers can proceed even with increased gastric secretion, especially the so-called sequential cancers following a round gastric ulcer. In cancerous lesions of other and even organs distant from the stomach, many authors have described atrophy of the gastric mucosa with the absence of hydrochloric acid in the gastric juice. The drop in the secretory function of the stomach in these cancers can be considered a consequence of cancerous cachexia. A general decline in nutrition can also cause achylia (cases of atrophy of advanced age, in senile marasm, and in debilitating diseases—tuberculosis, kidney disease, liver disease). Recent work has clarified that in chronic cholecystopathies, hypochylia or achylia are frequent symptoms. It must be pointed out that at the beginning of the process, normal or even increased acidity is often observed, but, over time, gallstone disease exerts a depressing effect on gastric secretion and causes a secondary atrophic process. This sign can serve as an aid in disputed differential diagnosis between duodenal ulcer and cholecystitis. In syphilis, in its febrile period, a decrease in secretion and even gastric achylia is often observed. Neugebauer performed a study of gastric juice in 200 syphilitic recruits and found subacidity in 62% and achylia in 18%. Knowing that the majority of changes in the parenchymal tissue of the stomach depend on post-mortem influences, to avoid rapid putrefaction, C. Faber (C. Faber, Copenhagen) and Lange used the following method in their studies. Directly after the patient's death, they injected 500-600 cubic centimeters of a 10 percent formalin solution into various places in the abdominal cavity; the mucosal changes found by them represent the picture of diffuse gastritis with a tendency to atrophy (gastritis progressiva atrophicans). Pathogenesis. Of particular importance for elucidating the pathogenesis of achylia were the works of Einhorn and Martius. Einhorn speaks of functional deviation of gastric secretion under the influence of disorders on the part of the nervous system and considers this anomaly a purely nervous affliction. The basis for this is, on the one hand, the absence of anatomical changes in many cases of gastric achylia, and on the other hand, the frequency of this deviation in neurasthenics. Martius does not consider achylia a symptom of neurasthenia, based on anatomical changes found in pieces of the mucosal membrane. Martius, however, views his cases not as the consequences of prolonged gastric catarrh, but as an innate, often familial, functional weakness of the organ. It is interesting to note that, according to the data of the Russian author Vogranik (1925), in a newborn up to two weeks old there is no free hydrochloric acid in the stomach; under certain pathological conditions (atrophy, colitis), a sharp extinction of gastric secretion occurs, almost to achylia, but in case of recovery, secretion is restored again. To understand the pathogenesis of functional achylia, it is necessary to take into account the laws of the secretory function of the stomach established by I. P. Pavlov and his school. Gastric secretion, according to these data, consists of three successive phases: psychic (the significance of conditioned reflexes), reflex-chemical, and intestinal. Essential significance also belongs to the works of C. Faber, Lubarsch, Lange, and others, who found in achylia, on the one hand, histological changes indicating a progressive atrophic process, and on the other hand, the same authors speak of the possibility of gastric achylia with a completely normal structure of the gastric mucosa. Trükcsecsy emphasizes in the pathogenesis of achylia the significance of a disease of that nervous apparatus which governs the separation of gastric juice. The structure and conditions of the correct activity of this apparatus are extremely complex. The psychic state, conditioned reflexes, the act of chewing, etc., all this can inhibit the secretion of gastric juice. In addition to influences via the vagus nerves, a special nervous apparatus is embedded in the stomach wall itself, the conditions of activity of which we do not know precisely, but which can also exert a depressing effect on gastric secretion. Finally, we can speak of a lack in the blood of substances that are the source of hydrochloric acid formation, or of the presence in the blood of substances interfering with this act, although, in relation to the latter, there is no direct proof of their existence. As a result, the pathogenesis of gastric achylia must be recognized as very complex, with both cases of achylia with an anatomical substrate and functional achylia without a clearly expressed anatomical substrate being possible. Types of Achylia. All gastric achylias can be divided into two groups. The first, large group includes all secondary forms. Many diseases accompanied by general exhaustion often lead to achylia. In the first place here, one should place the physiological state of the organism in senile marasm. Special significance must be assigned, furthermore, to gastric cancer with atrophic catarrh and malignant tumors of various organs, in which cachexia and general nutritional decline provide a reason for the occurrence of achylia. The question of the connection of gastric achylia with pernicious anemia, as well as, in a number of cases, with such diseases as syphilis, tuberculosis, chronic cholecystopathies, kidney diseases, etc., must also be referred here. Depending on the underlying disease in the first group, forms of benign and malignant achylia are distinguished. The second group includes primary independent forms of gastric achylia, in which the stomach is affected independently of other diseases. This group includes achylia gastrica simplex described by Martius, which breaks down into two subgroups. In cases of one subgroup, changes with the character of progressive gastritis are expressed in the gastric mucosa, while in cases of the other, the mucosa appears normal. In "anatomical" achylia, various stages of chronic gastritis are observed, and sometimes the anatomical changes are so weakly expressed that it is impossible to explain the complete drop in secretion by them. Two cases of widespread total progressive atrophy of the gastrointestinal tract, leading to a fatal outcome, have been published in the literature (Konchalovsky). To explain progressive atrophy developing independently (primarily) over an extensive extent of the entire digestive tract, one must take into account, on the one hand, the congenital weakness of the digestive organs, and on the other, the trophic influence of the autonomic nervous system on this process. It is clear that with such a wide spread of the process, there can be no question of a compensatory function of the unaffected parts of the digestive tube. A significant disorder of the absorptive function of the intestine further contributes here to the progressive decline in nutrition. In functional achylia, which is encountered most frequently in young subjects, a return to normal secretion and even a transition to the reverse state—hypersecretion—is possible. Such fluctuations in gastric secretion are known as heterochylia (Hemmeter). Symptomatology. Attention should be paid to various constitutional anomalies of an anatomical and functional character (e.g., a tendency to Quincke's edema). Serious significance can hardly be ascribed to subjective symptoms. Achylia gastrica can often give no subjective sensations at all, provided there is good compensatory function of the pancreas and intestine. Still, patients often complain of heaviness and a feeling of fullness in the epigastric region. Heartburn is frequent—a phenomenon that seems paradoxical.

Vomiting is comparatively rare. In other cases, pain attacks appear that simulate a round ulcer of the stomach. The diagnosis is established after examination of the gastric juice. On an empty stomach, the stomach is usually empty. Extremely characteristic is the appearance of the gastric contents after a Boas-Ewald test breakfast. Pieces of roll are completely unchanged; they appear as if chewed and coated with a mucous liquid. There is no odor. Regarding the mucus in the gastric contents, most authors believe that in simple functional forms, the amount of mucus may even be reduced, while in anatrophic catarrh, in certain stages of the latter, it may be increased. The reaction of the gastric contents is usually barely acid. Free hydrochloric acid is completely absent. The figures for total acidity in primary, simple achylia are also insignificant, usually from 4 to 10. In anatomical and secondary forms, these figures are sometimes higher (20–30), correspondingly determining bound hydrochloric acid, which indicates to us that in these cases we do not have complete anachlorhydria. There is no major fermentation in the stomach; volatile fatty acids, butyric and lactic acids are not detected in the gastric contents. The secretion of enzymes and the secretion of hydrochloric acid frequently do not run parallel. At the same time, the gastric glands lose the ability to secrete hydrochloric acid earlier and retain the enzyme-forming function longer. However, despite this, in almost all cases of gastric achylia, the enzymes ultimately disappear and are not detected by conventional methods. Only in rare cases are traces of them detected in functional forms. Blood in the gastric contents is usually not detected, except in cases where the mucous membrane is fragile. Under the microscope, starch appears undigested; thus, amylolytic processes also proceed poorly due to the undigested protein membrane binding the starch grains. Observations by a number of authors show that with certain modifications of the test meal, a greater secretagogue effect can be obtained. For example, with the administration of meat (Riegel meal), herring, alcoholic, and caffeinated breakfasts, traces of hydrochloric acid are obtained, and the total acidity figure sometimes increases. Obviously, secretion is not completely extinguished here. Such cases rather pertain to functional forms in which there is no complete anadenia. Recently, Katsch and Kalk proposed using the histamine test; with subcutaneous administration of this agent, acidity can be activated after a test breakfast and thus "absolute" achylias can be distinguished from functional forms and heterochylias. The motor function of the stomach in gastric achylia is usually increased. This rapid emptying of the stomach seemingly compensates for the lack of secretion and allows intestinal enzymes to develop their vicarious activity sooner. Marzius considers this increased motor function in achylia to be a reliable differential sign from gastric cancer. However, observation shows that in many cases of achylia, especially in women, one has to deal with a dropped and atonic stomach, in which case, of course, the motor function of the stomach cannot be increased. The fragility of the mucosa during gastric sounding, noted by earlier authors, is not characteristic of achylia. In chronic gastritis, especially with stagnation in the portal vein (in liver cirrhosis), looseness and bleeding of the mucous membrane are often present—yet more often occult bleeding causes one to suspect gastric cancer. Bearing in mind the circumstance that gastric achylia often proceeds without any symptoms thanks to the vicarious function of the intestine, it is natural to expect the appearance of intestinal symptoms when the latter is impaired, which is why diarrhea is a frequent companion of achylia. Its pathogenesis is explained differently. Some attribute its origin to the irritating influence of undigested and poorly processed food parts, others to the flooding of the intestine with bacteria due to the loss of the disinfecting properties of the gastric juice, and still others to concomitant catarrh of the intestines. In general, the character of the stool in achylia changes sharply; its amount increases, and unchanged connective tissue, undigested muscle fibers (lientery), and much fat are found in it. Clinical signs of increased intestinal fermentation (gases, bloating, foul-smelling stools, an increase in urinary indican, etc.) are often present. Among objective symptoms, attention should be paid to the tongue, which frequently has atrophic papillae and is smooth (Hunterian glossitis), as in pernicious anemia. In view of the fact that gastric achylia is often a consequence of chronic cholecystopathy, modern authors (Berg) note tenderness of the gallbladder upon palpation in achylics. Diagnosis. The physician's primary task in establishing a diagnosis is to separate secondary forms from primary, or independent ones. If the patient is of advanced age, if severe general diseases are present (malignant anemia, syphilis, tuberculosis, chronic cholecystitis, nephritis, etc.), if the symptoms of achylia do not occupy a preeminent place in the course of the disease, then one must think that the gastric affliction is consecutive or secondary. In recognizing secondary achylia on the basis of existing symptoms, one can judge to a certain extent about the malignant or benign form. The character of the underlying disease plays the main role here. There are signs for differentiating cancerous achylia from simple ones: good motor function of the stomach often excludes cancer; the X-ray picture, persistent occult bleeding, and serological reactions allow for the diagnosis of cancerous achylia. When excluding secondary achylia, its primary, independent forms also require a certain differentiation. Sometimes it is difficult to distinguish functional achylia forms, in which there are no anatomical changes on the gastric mucosa, from forms with signs of progressive atrophic gastritis. Examination of the secretory function of the stomach by the fractional method using various modifications of the test meal with repeated feeding (alcoholic, caffeinated, Leporsky vegetable breakfast, Zimnitsky method) makes it possible to establish the degree of fading of secretion and to represent secretion in the form of secretion curves and chlorine curves. Subcutaneous administration of histamine (0.0005)—according to Katsch and Kalk—or adrenaline (1:1,000 – 1.0) according to Zimnitsky and Arinkin before a test meal makes it possible in some cases to activate dormant secretion. For the same purpose, intramuscular injection of a 1% Neutral Red solution is used (Glaerner, Wittgenstein), which in the case of achylia is either not excreted by the gastric juice at all or is excreted with a significant delay. With normal secretion, coloring of the gastric contents occurs after 15–20 minutes. With these new methods in primary forms, we can more easily differentiate "absolute" achylias (anadenia) with low monotonous curves from functional forms. Often, however, it is difficult to establish the boundary between anatomical and functional achylia. The prognosis in secondary forms depends on the underlying affliction. In the primary form, the prognosis in many cases is favorable, especially in functional forms. In anadenias, if the vicarious function of the intestine is good, the affliction may proceed unnoticed; with successive damage to the intestines by an atrophic process, the prognosis is serious. Prophylaxis in secondary forms addresses the underlying affliction; in primary forms, if we are dealing with functional achylia, a regimen that regulates the functions of the nervous system is necessary. Regarding anatomical forms (anadenias), it is important to prescribe a diet that prevents the development of atrophic gastritis (spicy, coarse, and pungent foods, as well as alcoholic beverages, are prohibited). Treatment. The main task is to support the motor function of the stomach and by all means ensure that the compensatory activity of the intestine is not disrupted. According to the majority of authors, it is impossible to artificially replace the lost secretory function of the stomach. However, the administration of hydrochloric acid proves useful in many cases. Hydrochloric acid stimulates gastric secretion, converts proenzymes of the gastric juice into active enzymes, exhibits an antiseptic effect in the stomach, improves amylorrhexis in the stomach, etc. Hydrochloric acid is prescribed during meals at 10–15 drops or more per dose in a large volume of water (¾ of a glass). The administration of artificial enzymes—pepsin, pancreon—is hardly rational (the fragility of the composition of these preparations). Natural gastric juice (gasterin), obtained experimentally in the laboratory of Prof. I. P. Pavlov, acts wonderfully on digestion, reducing unpleasant subjective symptoms and eliminating dyspeptic phenomena; naturally, it does not restore secretion to normal. The basis of treatment for achylia is a rational diet. Here the physician's task is to provide food prepared for intestinal digestion. Sufficiently comminuted food is given in fractional portions. The exclusion of protein food is by no means obligatory and must be strictly individualized. Some patients tolerate a meat diet perfectly, given good pancreatic digestion. It is necessary to dietetically spare the functions of the intestine, upon which the disease has placed increased enzymatic work.

Various dairy dishes, porridges, vegetables with an adequate vitamin content, and light sweet dishes are usually well tolerated. Quite a few dietary regimens have been proposed for sufferers of achylia. However, it is more correct to say that all pre-made diets are of less therapeutic importance than a careful, individual account by the patient himself regarding which types of food he tolerates. Essential importance also attaches to various auxiliary procedures: gastric lavage with a physiological NaCl solution, the prescription of salt-alkali mineral waters, preferably at a spa (Essentuki), and so forth. General strengthening treatment, along with measures affecting the nervous system, helps the cause.