THE CAUSES AND IMPORTANCE OF DIGESTIVE DISTURBANCES IN PULMONARY TUBERCULOSIS.* By C. B. VAN ZANT, M.D., My only and yet, I trust, sufficient apology, for appearing before this society, with so old and trite a theme is simply its great importance. For many years, the physicians of Colorado have been afforded an excellent opportunity for studying pulmonary tuberculosis in all of its phases. In this study, this truth has impressed itself-that of all the protean conditions affecting the progress of these lung cases, none is more frequent or important than perversion of the digestive functions. In view of this fact, we desire to use the brief time at our disposal in an inquiry as to the bearing of these derangements of the alimentary tract on the pulmonary and general condition of these patients. First-As to casual relations. This we shall consider under the following two queries: (a) Are dyspeptics more prone to develop tuberculosis than others? (b) Are tuberculous subjects more prone to develop digestive derangements than others? (a) To the question, "Are dyspeptics more prone to develop phthisis than others?" the answer seems to be distinctly in the affirmative. Osler says "diseases of the stomach and intestines increase the susceptibility to tuberculosus infection." Again he says: "Among the most characteristic of the types of onset of pulmonary tuberculosis are those cases with dyspeptic symptoms, forming a large and important group. The patients may or may not naturally have had feeble digestion. They begin to show marked signs of dyspepsia and become pale, lose flesh and look chlorotic before any pulmonary symptoms are manifest." * Read before the Colorado State Medical Society, June, 1900. In this view of digestive disorders indirectly predisposing to tuberculosis, Osler has the support of Von Ziemssen, Ransome, Woodhead, Burr and others who might be mentioned. Whatever our conclusions from our reading may be, we all have been impressed with the frequent presence of anorexia, nausea, vomiting and indigestion in our lung cases long before we were able to make out any pulmonary affection. In weighing this aspect of the matter it has seemed to me that we might explain the development of pulmonary tuberculosis which apparently follows gastric and intestinal defects, on one of the following three grounds: First-Remembering that the vagi are a common source of innervation of both the respiratory and alimentary tracts, and that they contain trophic, as well as motor, vaso-motor, sensory and secretory fibres, some may possibly be able to accept the theory of Mays of Philadelphia, namely, that the digestive and indirectly the pulmonary conditions, are due to trophic or nutritional changes in these parts following a diseased condition of the vagi themselves. This theory lends itself nicely to an explanation of the related pulmonary and digestive disorders and only lacks one element to make it alluring, that is, proof. Secondly, and without doubt, the defective general nutrition consequent upon indigestion furnishes a large factor in indirectly predisposing dyspeptics to tuberculous disease. Again, if the precedent gastric condition be one of hypochlorhydria the usual bactericidal function of the gastric juice is diminished or lost and invasion of the system by way of the alimentary tract is thereby rendered more easy. In addition to this, the antiseptic effect normally exerted both on the stomach and intestinal contents by the H Cl of the gastric juice is diminished in such cases, and many kinds of fermentative processes are per mitted to develop. The bacteria back of these processes not only rob their host of his needed nourishment, but poison him by their excreta. Following in the footsteps of Von Ziemssen, who in the '80's laid great stress on the protective action of the acidity of the gastric juice against tuberculous infection, Burr has recently drawn especial attention to this feature of our subject. With subacidity of the gastric secretion, the intestines, he believes, become a veritable culture tube for micro-organisms, giving rise to toxins, ptomaines and toxalbumins, which ultimately reach the lungs and there embarrass respiration, weaken the lining cells of the alveoli and the capillaries. Thus, in his judgment, it predisposes to serious lung trouble. Hence arises the importance of using every precaution against alimentary auto-intoxication in cases predisposed to phthisis, and this remark applies as well to the reinfection of cases already tuberculous by the swallowing of their sputa. We will now take up our second question: Does pulmonary tuberculosis predispose to a secondary indigestion? If so, how? By most of our authorities an affirmative answer is given to this inquiry and the experience of all here will doubtless bear out the same assertion. What then, is the nature or cause of these secondary alimentary derangements? They may be entirely functional in character, and as a rule this is probably the case. Thus the activity of the gastric glands may be functionally disturbed by the profound anaemia of tuberculosis; by the hectic fever; by reflex irritation through the vagus from the lung; by neurasthenia; by various neurotic causes. Upon these latter nervous factors Immermann and others lay great stress. Again, the glands may be normal in their activity, while the musculature of the digestive truct may be the part at fault, leading to motor insufficiency. On the other hand, in many cases of slow onset of digestive trouble in lung cases, the symptoms may represent organic changes in the alimentary tract. Tubercular lesions in the stomach such as ulcer, are rare; in the intestine, common, and here they prove a notable source of indigestion and distress. 'Dilatation of the stomach is an occasional condition in phthisis. As acknowledged by all, however, the commonest diseased condition of the stomach, in these cases, is chronic gastritis. According to Pepper, Osler, Percy Kidd and others, the lung condition distinctly predisposes to this affection. It has been my own experience in a limited number of these cases of secondary gastric disorder in tuberculosis, to find by examining the gastric contents, etc., that the condition was often one of chronic gastritis. The subacidity was generally quite marked; the amount of mucus considerable; fermentative changes were present, and motor insufficiency was common. The vomiting which is so often a troublesome symptom in tuberculosis is frequently excited by fits of coughing which are apt to arise after meals and which Kidd believes are the result of hyperaesthesia of the vagus. Habershon refers the vomiting to four different causes: (a) Pressure on vagi by caseous glands. (b) Stimulation of peripheral branches of the vagi in the lungs, pharynx or stomach. (c) Mechanical causes. (d) Central causes, such as tuberculous meningitis. |