LIBRARY ASS'N MEMPHIS MEDICAL MONTHLY. VOL. XII. MEMPHIS, JANUARY, 1892. No. 1 Original Communications, MALARIAL HEMATURIA THE OLD AND NEW THEORY. W. P. BARTON, M.D., MALONE'S LANDING, MISS. Malarial hematuria is a disease dependent upon a "pathological condition" the result of malaria. The etiology of the disease primarily is the same as that of other malarial troubles, whether acute or chronic-the malarial germ. But the disease is only indirectly dependent upon this etiology, and owes its existence more to the "secondary condition" produced by the development of the germ than to the development itself. This condition involves the whole system and not special organs, as many partial observers would have us think; for he who can see in a hematuric patient an affected liver or spleen to the exclusion of the rest of the human economy, is a man who "sees through a glass darkly." He sees the truth but not the whole truth. The most plausible etiological explanation of this condition and the one most generally accepted at present, I believe, is this: The malarial germ entering the body by what avenue soever affects the organism through the blood only. In the red corpuscle it finds a nidus, and, in true parasitic style, not only makes this little body its home, but its food also. In the red corpuscle we have life, in a destruction of it we have death, in a partial destruction we have a living death. What true cachexia can simulate a living death more closely than the VOL. XII - 1 advanced stage of malarial toxemia? Upon a healthy state of the red corpuscle depends the health of tissue, and upon healthy tissue depends the health of the man. Without organic derangement there is probably no disease; for even so-called functional diseases must depend either directly or indirectly upon organic changes. In this special pathology we find this state of affairs. The malarial germ entering the red corpuscle there develops, destroying the corpuscle and producing a chemical change that at certain periods produces paroxysms known as intermittents. This paroxysm, whatever may be its modus operandi, is only the manifestation of a nervous explosion dependent entirely upon the development of the germ, so far as we are at present able to judge. This is the primary disease pure and simple; for even its congener, the remittent, must have something more for its origin than the mere explosion. The effect of malarial poison like that of most others is primary and reflex or secondary, and after a paroxysm there is a reflex derangement. The red corpuscle being destroyed, there is no longer an agent of nutrition, and, of course, degeneration must at once follow. The most delicate tissue is the first to suffer, this being the nerve; unfortunately so; for upon wellnourished nerves depends the regeneration of the red corpuscle itself. Herein is the foundation of the whole trouble. After the corpuscles are destroyed in quantities sufficient to vitiate nerve nutrition, the other tissues, being dependent, quickly sympathize, and the reflex is general. Let the cause continue to act, and it is easy to see the consequence. Each day lessens the resisting power, and each day in direct proportion increases the virulence of the poison. The effect of this poison, like many others not necessarily selective, soon centralizes. That is, if the liver is the weak organ in a given subject, the liver is the organ that suffers most; and so on with all the parts in their turn. A crop of boils is a matter of common observation, traceable directly to this centralization of malarial poison upon the follicles of the skin. But this centralization is by no means constant. He who has not seen a man dying of chronic malarial poison, when all of the functions of the body seemed affected only in degree, has had small experience; for there is nothing of a grave nature more common in practice than a state of chronic malarial poison where the equilibrium of all functions is perfectly preserved. So much for the etiology of the "condition." The pathology is direct and reflex, so to speak. As has been shown, the red corpuscle suffers a direct change, removing it at once from a physiological state. In this transition is generated the pigment of malarial cachexia, and in a greater or less quantity hemoglobin is set free, which in hematuria plays so important a part, at least symptomatically. The nerve system must next suffer from malnutrition, and, possibly, from direct intoxication. But further than this, it is doubtful whether the poison has a direct influence. The malnutrition of the great vasomotor system of nerves will explain all other changes that go to produce and define this "pathological condition" necessary for the development of malarial hematuria. The organ, whatever it may be, that regenerates red corpuscles, is unable to perform its function from lack of nerve force, producing anemia, the nerve force of the liver is insufficient for the performance of its duties, that force which controls the mucific glands of the alimentary canal is wanting, the lymphatics cease normal action from the same cause, and we have general depression. This is roughly the pathology of the "condition." For morbid anatomy, there must be changes in the microtissue as well as in the blood. The coats of the vessels, either from lack of tone or from organic changes become loose and thin; the blood watery and charged with debris courses sluggishly, making congestion an easy possibility. Many cases present gross lesions, such as adenitis, pigment deposits, etc. The symptomatology is familiar to all. Chills and fever or remittent fever is generally the first manifestation of the intoxication. Febris simplex or no fever may be the history. Anemia more or less marked, languor, a capricious appetite, alternately voracious and wanting; nausea when the liver suffers most; a coated tongue, either white or dirty whitesometimes brown; offensive breath; highly colored urine; constipation and diarrhea, often alternating; loss of flesh; slight jaundice, cerulean eye, and in many cases a clear, transparent, waxy appearance of the skin. This latter symptom is one of a very advanced stage. This is the "pathological condition" requisite for the development of malarial hematuria. So far, I believe, all are agreed. But here the advocates of the two most prominent theories concerning the exciting cause of the disease diverge; nay, are diametrically opposed to each other. I will notice briefly each theory, and then undertake the self-imposed task of "deciding among doctors." Having the "pathological condition," the old and generally accepted theory is, that hematuria is the direct product of a nervous explosion immediately excited by malarial development, just as an intermittent paroxysm is. That the explosion spends its force upon the coats of the blood vessels in such a way through the vasomotor centers that the debris with which the blood is charged is forced through the attenuated vessel wall, producing the characteristic symptoms, hemoglobinuria and icterus. That hematuria results, perhaps, because the delicate vessel walls of the inner kidney are more assailable than any other group, being required to transmit more blood in the process of elimination than any other of equal caliber. But that the so-called hemorrhage will not be confined to this set of capillaries if other parts present conditions favorable for such a phenomenon. Such a manifestation is often seen in blisters drawn upon the bodies of hematuric patients. That the delicate tissues of the uriniferous tubules and malpighian tufts are so injured by this process, that if continued for a sufficient time they will lose power to perform their function, and as a natural consequence there is a retention of that most potent poison, urea, in the blood, which is responsible for all other mischief done; nausea, heart failure, etc., being only symptoms. I am aware of many personal engraftments and supplements to this theory, but I give it in the main. The new theory of such vast possibilities differs so widely from the old, not in its view of the pathology, but in that it introduces a new etiological element: namely, quinine. Holding that quinine is essential to the development of the disease. That quinine, by its known effect upon the vasomotor centers and especially by its selective effect upon the functional capillaries of the kidneys, finding the pathological condition ripe |