Lange noted that, out of 25 pregnan cies in which the usual hypertrophy of the thyroid did not occur, albtuninuria occurred in 20. Large doses of thy roidin were administered to pregnant women in whom the physiological en largement of the gland had occurred, and a marked diminution in the size of the gland resulted. One might therefore eonclude that the normal hypertrophy of the thyroid gland in pregnancy is the result of a demand for extra secretion to meet the wants of increased metab olism. With a continuous supply of artificial secretion the gland NN'aS re lieved of the additional strain and re sumed its former size. lIallion observed similar effects. H. O. Nicholson (Lancet, June 29, 1901).
Of all the theories advanced as to the cause of eclampsia and the pre-eclamptic state. none have appealed to us as strongly as that which takes into con sideration urinary inadequacy, with the attendant diminution of the secretion of the solid elements of the urine. In other words, with an ever-increasintt experience, we feel as morally sure as clinical experience will allow us that this dire condition is due to the poison ing. of the system by urea or one of its con.?.eners. S. Marx (3Ied. Examiner and Praet., March, 1903).
The idea that it is a renal disease seems to be abandoned, and it is now g.euerally attributed to the circulation of poisons in the blood, either from the alimentary canal or due to metabolism in the body of the mother or of the fcetus, or of both. In health such poi sons are either at once expelled front the body or rendered innocuous by its natural organs of defense,—the liver, kidneys, thyroid, and other glands,— but a breakdown of any one of these throws the whole ineehauism out of gear. In most pregnant woinen the de fensive power proves adequate; in some, though there is disturbance of function in early months, adjustment results and the .symptoms of intoxication pass off; ill a few the poisons accumulate, and. eclampsia or other serious troubles result. Fothergill (Practitioner, Feb., 1003).
As in the course of more extended knowledge, the etiological factor of eelampsia was recognized as being asso ciated with hydrremia of the blood and with toxremia, not alone has the pressure theory been exploded, but so also have the vague and insufficient terms uremia and urincenzia been discountenanced by the modern writer, teacher, and practi tioner.
During pregnancy the blood alters both in quantity and quality. There is an increase in the white cells and a de crease in the red. Albumin and iron fall below the normal. The blood becomes more watery, so to speak.
Careful histological studies made of the various organs in a large number of cases of puerperal eclampsia. In the vessels were found large multinueleated cells, which were considered to be cells derived from the placenta, and also multiple capillary thrombosis. From these facts the conclusion drawn that the disease is essentially due to the pres ence in the blood of a coagulating fer ment formed either by the degeneration of the free placental cells found in the blood or by degenerative changes in the placenta itself. Schmorl (Virchow's Archiv; St: Louis Med. and Surg. Jour., May, '96).
Chamberlent, working under the direc tion of Tarnier, in 1892 performed a series of experiments on the blood of eclamptic women and published the fol lowing conclusions:— 1. Pregnancy tends to the retention of poisons in the body, for the urine of the pregnant woman is less poisonous than normal.
2. In eclampsia the elimination of physiological poisons is hindered, and the urine is less poisonous than normal. It is also less poisonous than the urine of normally pregnant women.
3. The blood-serum of the eclamptic is considerably more poisonous Mini nor mal, and its toxicity is in direct pro portion to that of the urine.
The poison is by some believed to have its origin in the fcetus and placenta; but the commonly-accepted view is tha.t the poison is of maternal origin from im paired metabolism, together with reten tion from impaired eliminative capacity of the kidneys.
The albuminuria of cclampsia is prob ably secondary, following the direct ac tion of the poison on the renal epithelial cells. in the effort at elimination. Its almost universal presence in the eclamp tic renders it a sign of some importance. Only about one-eighth of eclamptics sub sequently deyelop nephritis, the albumin disappearing from the urine in from a few weeks to a few months after the attack, depending largely on the hygienic conditions which surround the patient.
While a patient with nephritis may and does sometimes have eclainpsia, it is by no means the invariable rule. J. L. Rothrock (Northwestern Lancet, Nov. 15, '97).