The cases of the subacute type are by far the most numerous. From this it is evident that the acute or pernicious type of the malady is, in most cases, only an exaggeration of the subacute, as observed in some other diseases, notably rheumatism and those of marsh malarial origin. The term pernicious is, strictly speaking, applicable to the wet form of the disease only, as the dry form is rarely, if ever, rapidly fatal. A marked case of wet beriberi is always to be regarded as dangerous, from the suddenness with which pernicious symptoms often declare themselves. In these the anasarca (which, as has been stated, constitutes the leading clinical difference between the two forms of the malady) plays an important rôle. It often happens that in the course of a few hours the local oedema in the extremities and the slight puffiness of the face become general and extreme, and the neck is enormously swollen by the distension of the veins, both deep and superficial. The pleural and pericardial sacs are more or less distended with serum, thus mechanically embarrassing the action of the organs they contain. The action of the heart now becomes laborious, the lungs oedematous and filled with coarse râles, and a terrible sense of suffocation comes over the patient, causing him to seek relief by constant change of position. The stomach is irritable, a greenish-yellow fluid is vomited, and death closes the scene. The acute stage of dry beriberi, on the contrary, is characterized by a rapid diminution of the fluids of the body and muscular atrophy.
The annual appearance in the same individual of either wet or dry beriberi, and its long continuance, constitute the chronic type of the disease.
MORBID ANATOMY.—The morbid anatomical changes in beriberi vary considerably with its form. Few, if any, observers claim seriously to have found in either the wet or dry form of the disease evidences of acute inflammatory action in any of the tissues or organs. The blood undoubtedly undergoes important morbid changes, whereby its nutritive and oxygenating power is impaired, indicating that this is a disease of inanition. This shows itself most markedly in necrobiotic and degenerative changes, especially in the muscular tissues, which are the seat of the leading morbid phenomena in all stages of both forms of this disease. The respiratory, digestive, and glandular systems rarely undergo morbid changes other than those of a secondary or passive kind, such as engorgement with serum and venous blood.
The condition of the organs contained in the cranial and spinal cavities is variable and inconstant. According to some observers, the substance of the brain and spinal cord is hardened. The greater number by far, however, have found it more or less softened.6 The heart in wet beriberi is habitually large and flabby, its muscular tissue softened and of a pale-yellow and macerated appearance. Its cavities are engorged with dark blood, sometimes fluid, but more often clotted. These clots are often voluminous in the right heart, semi-fibrinous, and extend into the pulmonary artery and great venous trunks, which are enormously enlarged. The cardiac muscular tissue I always found to have undergone metamorphic changes, varying from granular clouding to advanced fatty degeneration.7 The tissue of the paralyzed voluntary muscles undergoes degenerative changes in both forms of the disease. In the extreme atrophy of dry beriberi I have not unfrequently found many of the sarcolemma sheaths completely emptied of their contents. The power of regeneration in these cases is often wonderfully displayed by an almost complete restoration of the lost elements, and, in a corresponding degree, of the function of the part.
6 The former condition was undoubtedly observed in autopsies made of the dry or atrophic form of the disease, though this fact is not mentioned. The latter, or softened, condition of the cerebro-spinal contents belongs to the wet form of the disease (my own cases being of this kind). I regard this softening as not ante-mortem, but as consecutive to serous imbibition (as observed by Eismann and Sanders in chlorosis), and as taking place during the last moments of life or after death, when the vital forces no longer oppose themselves to the mechanical disintegrating power of the fluid with which the nervous as well as all the other tissues of the body are engorged.
7 I believe this to be the condition of the heart-muscle in all cases of death from the wet form of beriberi. In this opinion I am supported by Oudenhoven and many of the Dutch observers.
It would appear that in wet beriberi the heart is first weakened by paresis of the cardiac ganglia, with consequent incomplete emptying of its cavities. This, in connection with rapid degenerative changes in its muscular tissue, causes the walls to yield to the blood-pressure, producing dilatation and tricuspid insufficiency, with regurgitation and consequent capillary stasis and dropsy. Vaso-motor nerve-paralysis, acting at the same time on the pulmonary artery and arterioles, and on other large arterial trunks, probably gives rise to the murmurs heard in them. In the dry form of the disease the vaso-motor nerve-paralysis is less pronounced, and the degenerative changes in the muscular tissue of the heart slower, while the marked decrease in the fluids of the system and the great failure of nutrition tend toward atrophic changes. From this it follows that we usually have, instead of a large dilated heart, a small weak one, with a narrow tricuspid orifice instead of a dilated one; little or no intercostal pulsation, and hence less cardiac dulness; no venous distension or capillary stasis, and hence no dropsy.
PROGNOSIS.—In temperate climates the prognosis of uncomplicated beriberi is favorable in a majority of cases. In seasons of its epidemic prevalence, however, all cases of the wet form of the disease must be carefully watched, as it not unfrequently happens that grave symptoms suddenly appear at a time when no danger has been anticipated. An unfavorable prognosis may be ventured when, in a case of wet beriberi, relief is not obtained by free purging or when vomiting sets in. In dry beriberi the termination in death is exceedingly rare as a direct result of the action of the poison producing the disease, so that when death does occur it is chiefly from exhaustion. The time of recovery depends on the amount of muscular degeneration, and also upon the season of the year when the attack occurred, as all cases of both forms of beriberi usually get well without treatment during the winter months.
TREATMENT.—The well-established fact of the influence of certain localities in the production of beriberi makes the removal of the patient from them a hygienic measure of great importance, and this is frequently the only treatment necessary if it can be done early. The effect of the change is often almost magical, especially if it be made to an elevated locality and among the mountains.
Diet is an important element in the treatment of beriberi. At the head of the list of foods to be avoided is rice. Coarsely prepared grains, such as wheat, barley, certain kinds of beans,8 apparently because of more or less laxative properties, are preferable as articles of food.