The statistics in Table 1, based on 320 cases, include 179 reported in September, 1915.

From the standpoint of anatomic conditions encountered, Table 2 is of interest.

Table 3, arranged under the headings of hours during which the patients were kept in the chair, is of interest. A consideration of this table and the explanatory note shows that in about 20 per cent of the

cases labor lasted only one hour or less after the patient was put in the chair. In one case fifteen minutes apparently sufficed, though here the cervix was almost fully dilated at the time, while in eighteen cases in which the cervix was only 1 or a few fingers dilated, less than one hour was required.

In the next group of cases, the patients with abnormal pelves, Table 4 gives the important features.

If we consider the primiparas in this group and their behavior with the obstetric chair, we observe the data given in Table 5.

Considering the first portion of this table, namely, the primiparas with normal pelves, an analysis and consideration gives the features presented in Table 6.

Reference to the last part of this table, that referring to the progress in the chair, taken in conjunction with the notes appended, shows that interference was necessary in six cases because of abnormalities of fetal position: 3 right occipitoposterior presentation, 1 left occipitotranverse TABLE 8.-ABNORMALITIES IN MULTIPARAS.

presentation, 1 prolapsed cord, 1 twin; and in 8 cases because of abnormalities in the mother: 1 lobar pneumonia, 2 eclampsia, 2 prominent spines, 3 rigid cervix.

In the remaining nineteen where operative interference was resorted

to, excluding five where notes of the progress were not made, there were fourteen cases where uterine inertia prevented delivery.

It will thus be seen that in twenty-one primiparas where conditions anatomically might have presupposed, or rendered necessary, operative interference, spontaneous delivery occurred. In other words, in about 37 per cent of fifty-six cases the obstetric chair apparently obviated the necessity of any other artificial aid. Of these twenty-one cases, fifteen were in the first stage of labor and six in the second. In two cases the pat en s were kept in the chair five and six hours, respectively, while

in nine cases one hour sufficed to effect delivery, six cases needed two hours and seven cases needed three hours for spontaneous delivery. The average duration of the entire labor in these cases was about twenty-one hours, while the average time in the chair was about two and one-half hours.

Of the twenty-nine multiparas with normal pelves, all but one was delivered spontaneously. Of the nine multiparas with abnormal pelves, Table 7 shows the important points.

In only two cases of the multiparas spontaneously delivered was the patient in the chair for more than two hours. A brief table of this series of cases, arranged with reference to the occurrence of abnormal positions and presentations and the resulting deliveries, is of decided interest (Table 8.)

From this table it will be seen that in almost 50 per cent of twentythree cases of right occipitoposterior positions, in one case of a total of four left occipitoposterior positions, in cases of transverse and in one case of chin posterior, spontaneous delivery occurred.

With regard to the case with the face presentation, the effect of the chair was to cause a rotation forward to a left mento-anterior position, and then to effect spontaneous delivery.

A brief survey of these tables, limited as is the number of cases on which they are based, cannot but bring home the distinct advantage the use of the obstetric chair offers, especially too in those cases in which, for some abnormality in the fetus or mother, operative interference seems to be indicated.

ACIDOSIS AS A FACTOR IN THE TOXEMIAS OF PREGNANCY.1

BY

J. R. LOSEE M. D. and DONALD D. VAN SLYKE Ph.D. From the Lying-in Hospital and the Hospital of the Rockefeller Institute for Medical Research, New York.

ALTHOUGH no general agreement has been reached concerning the nature of the substance causing the toxemias of pregnancy, two explanations have claimed special consideration Ewing and Wolf', noting the anatomical changes of the liver in eclampsia, the facts that leucine and tyrosine had been reported in eclamptic urines, and that they themselves often found a decrease in urea and an increase in the "undetermined nitrogen" fraction of the urine suggested that the amino-acids were incompletely catabolized in the degenerated liver, and were the cause of both the toxemia and the abnormal nitrogen distribution. Later Murlin and Bailey 2, also working in the Cornell laboratory, attacked the same problem with the aid of Sorensen's formol titration method, which is specific for amines and amino-acids. They decided that not only the amino-acid fraction, but also the other nitrogen fractions of the urine are likely to be within the limits of normal variation both before and immediately after the convulsions of eclampsia, and that consequently the nitrogen distribution in the urine offers no reliable means for either diagnosing the preeclamptic state or indicating the nature of the toxin.

1. Read at a meeting of the Section on Obstetrics and Gynecology of the New York Academy of Medicine, December 27, 1916.

The other explanation is that abnormal acids in the blood are responsible for the toxemia. It is known that even in normal pregnancy a slight degree of acidosis is indicated by the carbon dioxide content of the alveolar air3, and it was not illogical to suggest that an intensification of the acidosis might be a factor in the cause of eclampsia. Zweifel1, not only designated acidosis as the cause of eclampsia, but identified the specific acid as sarcolactic. This he found to be three times as concentrated in blood form the umbilical cord as in the venous blood of the mother, and he interpreted the results as proof that the mother is intoxicated by lactic acid formed in the fetus. Hasselbach and Gammeltoft3, found also that in two out of four cases of eclampsia examined by them the "regulated" hydrogen iron concentration of the blood was abnormally high, the values for P at normal CO, tension being 7.17 and 7.22, instead of the normal 7.45.

H

It seemed to the writers desirable to test the acidosis hypothesis quantitatively on a number of cases, in order to ascertain whether a degree of acidosis unusual for pregnancy regularly accompanies eclampsia, and whether the intensity of the acidosis is sufficient to account for the symptoms and ultimate coma noted. It seemed also not without interest to test with the gasometric method the proportion of amino-acid nitrogen in the urine in eclampsia, since the results of previous investigations on amino-acids in the urines of pregnancy, which have been performed with the help of the formol titration method, have not been entirely in agreement. While Hasselbach and Gammeltoft found the proportion of aminoacid nitrogen normal (2-3 per cent of the total nitrogen) in normal pregnancy, Falk and Hesky, with the same method, report results running chiefly between 3 and 7 per cent, 73 per cent of the cases showing figures above the ordinary limits observed in non-pregnant women. Falk and Hesky also noted in pregnancy a similar increase in peptide nitrogen, which varied from 2 to 7 per cent, non-pregnant women showing figures of from 1 to 2 per cent. Murlin and Bailey did not determine the peptide nitrogen but found in their three cases of normal pregnancy amino-acid nitrogen figures of 3.3, 5.1, and 4.3 per cent of the total nitrogen, figures which, like those of Falk and Hesky, are somewhat above the normal.

We have determined in the urine the "total amino-acid nitrogen", which includes the nitrogen of the free amino-acids and also that of the amino-acids conjugated in such forms as peptides and hippuric acid. In normal individuals this nitrogen runs from 1.5 to 3.5 per cent of the total nitrogen. Consequently the excretion of any considerable amount of amino acids either free or conjugated would cause a marked rise in this figure. We have also determined the proportion of the total nitrogen in the form of urea, ammonia and albumin.

As a further index of the amino-acid metabolism we have determined in a number of cases the amino-acid nitrogen of the blood, since the