OBESITY - FURTHER COURSE OF THE DISEASE; COMPLICATIONS AND TERMINATION.
Even at a more advanced stage of the disease obesity may persist for years almost unchanged, differing individually by the preponder ance of one or another symptom. The patients may perhaps reach a great age and death result from an intercurrent disease. In the ma jority of cases the malady advances with a gradual alteration of the subjective and objective symptoms and not rarely with a proportion ate increase of the inconveniences.
While in the early stages the disturbances were chiefly mechani cal, clue to the masses of fat accumulated in the body, later on degen erative processes develop by degrees in the various organs and influ ence the symptomatology more or less in accordance with them.
The blood suffers soonest by the prevailing nutritive disturbances. At first its hemoglobin contents diminish slowly but steadily, and with the increasing irregularities in the excretion of water by the urine and the invariably abundant ingestion of fluids the composition of the blood alters also in other ways. The specific gravity by de grees becomes more and more variable, reaching the lowest point of the normal limit and finally sinking below it, while the specific gravity of the serum is often before that time found subnormal. The ple thoric character is lost and the blood approaches more or less rapidly a condition of ancumia and hydrcemia until the obesity has changed completely into the hydmmic form. Owing to the diminution of the hcemoglobiu in the blood the oxidation processes are first re duced, as is the case from the start in the anemic form ; the fat-form ing substances are less perfectly burned up and are more largely deposited as fat. Since in progressive obesity, as stated above, the appetite often lessens, fat may be continually deposited even in cases in which the ingestion of fat and carbohydrates is not very great.
On the heart the fatty deposits increase steadily, spread from the sulci farther and farther over the surface, and penetrate between the muscular bundles into the substance of the organ. Tinder the pres
sure of the growing masses of fat the nutrition of the heart muscle suffers, the fibres atrophy in part or undergo fatty degeneration; the power of resistance of the muscle against the rising iutracardial pres sure decreases, the existing dilatation increases, and owing to the nutritive disturbances present the compensatory hypertrophy no longer suffices. Thus the heart becomes gradually less able to re spond to the demands made upon its function. - Besides, thG lack of oxygen in the blood, as in the aimnic form, influences the restitution of the inogen decomposed by the contractions, and reduces the capacity not only of the voluntary muscles but also, and especially, that of the heart muscle.
The contractions of the heart become ever less energetic, the weak impulse cannot be felt, the heart sounds are faint and often barely perceptible ; the pulse is small, thin, frequent, and traces dicrotic and subdicrotic curves. The heart strives to make up for the loss of power and amplitude of the contractions by increasing their number so as to propel the blood. In this way the work of the heart becomes ever less efficient. The arteries are filled less and the stagnation in the venous apparatus increases. Arterial anremia and venous hyper form constant symptoms. With the increasing weakness of the heart the organ also presents greater irritability manifested by ir regularities in its movements—alternate accentuated contractions and palpitations proceeding even to stormy heart action—either spon taneously produced, i.e., without demonstrable external agency, or from insignificant causes such as slight physical exertion, excitement, etc. The arterial anannia and the lack of haemoglobin in the blood on the other hand are bound to lead to marked disturbances in the re spiratory apparatus, shortness of breath and dyspncea, which are in creased still more by the restricted thoracic movements, the shallow inspirations.